FN Thomson Reuters Web of Science™ VR 1.0 PT J AU Lafuente, EM van Puijenbroek, AAFL Constantine, E Berezovskaya, A Freeman, GJ Nadler, LM Boussiotis, VA AF Lafuente, EM van Puijenbroek, AAFL Constantine, E Berezovskaya, A Freeman, GJ Nadler, LM Boussiotis, VA TI RIAM, a novel Rap1-interacting adaptor molecule, couples Rap1 to the cytoskeleton via the Ena/VASP family proteins and the actin regulator profilin. SO BLOOD LA English DT Meeting Abstract CT 44th Annual Meeting of the American-Society-of-Hematology CY DEC 06-10, 2002 CL PHILADELPHIA, PENNSYLVANIA SP Amer Soc Hematol C1 Dana Farber Canc Inst, Boston, MA 02115 USA. RI Lafuente, Esther M/K-5684-2014 OI Lafuente, Esther M/0000-0001-8466-1022 NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2002 VL 100 IS 11 MA 30 BP 11A EP 12A PN 1 PG 2 WC Hematology SC Hematology GA 614JK UT WOS:000179184700031 ER PT J AU Takeyama, K Aguiar, RCT He, CY Kutok, JL Aster, JC Shipp, MA AF Takeyama, K Aguiar, RCT He, CY Kutok, JL Aster, JC Shipp, MA TI BRAP and Deltex1, 2 and 3: A novel family of RING finger proteins with ubiquitin E3 ligase activity. SO BLOOD LA English DT Meeting Abstract CT 44th Annual Meeting of the American-Society-of-Hematology CY DEC 06-10, 2002 CL PHILADELPHIA, PENNSYLVANIA SP Amer Soc Hematol C1 Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02115 USA. Brigham & Womens Hosp, Dept Pathol, Boston, MA 02115 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2002 VL 100 IS 11 MA 33 BP 12A EP 12A PN 1 PG 1 WC Hematology SC Hematology GA 614JK UT WOS:000179184700034 ER PT J AU Forkert, R Tao, C Sharpless, NE Adams, GB Rodrigues, N Depinho, RA Scadden, DT AF Forkert, R Tao, C Sharpless, NE Adams, GB Rodrigues, N Depinho, RA Scadden, DT TI Cyclin dependent kinase inhibitor, p16(INK4a), differentially affects hematopoietic stem cells under homeostatic versus stress conditions. SO BLOOD LA English DT Meeting Abstract CT 44th Annual Meeting of the American-Society-of-Hematology CY DEC 06-10, 2002 CL PHILADELPHIA, PENNSYLVANIA SP Amer Soc Hematol C1 Harvard Univ, Massachusetts Gen Hosp, Ctr Canc, Sch Med, Charlestown, MA USA. Harvard Univ, Massachusetts Gen Hosp, Partner AIDS Res Ctr, Sch Med, Charlestown, MA USA. Universitaetsklinikum Bonn, Med Poliklin, Bonn, Germany. Univ Pittsburgh, Inst Canc, Pittsburgh, PA 15260 USA. Harvard Univ, Sch Med, Dana Farber Canc Inst, Boston, MA 02115 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2002 VL 100 IS 11 MA 90 BP 27A EP 27A PN 1 PG 1 WC Hematology SC Hematology GA 614JK UT WOS:000179184700091 ER PT J AU Yuan, YZ Shen, HM Ying, S Lu, Q Li, L Scadden, DT Franklin, DS Tao, C AF Yuan, YZ Shen, HM Ying, S Lu, Q Li, L Scadden, DT Franklin, DS Tao, C TI Enhanced self-renewal of hematopoietic stem cells in the absence of the distinct cyclin-dependent kinase inhibitor, p18(INK4c). SO BLOOD LA English DT Meeting Abstract CT 44th Annual Meeting of the American-Society-of-Hematology CY DEC 06-10, 2002 CL PHILADELPHIA, PENNSYLVANIA SP Amer Soc Hematol C1 Univ Pittsburgh, Sch Med, Pittsburgh Canc Inst, Pittsburgh, PA 15261 USA. Univ Pittsburgh, Sch Med, Dept Radiat Oncol, Pittsburgh, PA USA. Harvard Univ, Massachusetts Gen Hosp, Ctr Canc, Sch Med, Boston, MA 02114 USA. Harvard Univ, Sch Med, AIDS Res Ctr, Boston, MA USA. Purdue Univ, Dept Biol Sci, W Lafayette, IN 47907 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2002 VL 100 IS 11 MA 91 BP 28A EP 28A PN 1 PG 1 WC Hematology SC Hematology GA 614JK UT WOS:000179184700092 ER PT J AU Min, Y Heck, S Iwasaki, H Akashi, K Graf, T AF Min, Y Heck, S Iwasaki, H Akashi, K Graf, T TI Probing hematopoietic lineage plasticity reveals infidelity of myeloid gene expression in long term repopulating stem cells. SO BLOOD LA English DT Meeting Abstract CT 44th Annual Meeting of the American-Society-of-Hematology CY DEC 06-10, 2002 CL PHILADELPHIA, PENNSYLVANIA SP Amer Soc Hematol C1 Albert Einstein Coll Med, Dept Dev & Mol Biol, Bronx, NY 10467 USA. Harvard Univ, Sch Med, Dana Farber Canc Inst, Dept Canc Immunol & AIDS, Boston, MA 02115 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2002 VL 100 IS 11 MA 99 BP 30A EP 30A PN 1 PG 1 WC Hematology SC Hematology GA 614JK UT WOS:000179184700100 ER PT J AU Okuda, K Sato, Y Sonoda, Y Griffin, JD AF Okuda, K Sato, Y Sonoda, Y Griffin, JD TI Signal transduction and cellular function of the TEL/ARG oncoprotein. SO BLOOD LA English DT Meeting Abstract CT 44th Annual Meeting of the American-Society-of-Hematology CY DEC 06-10, 2002 CL PHILADELPHIA, PENNSYLVANIA SP Amer Soc Hematol C1 Kyoto Prefectural Univ Med, Kyoto, Japan. Int Med Ctr Japan, Tokyo, Japan. Dana Farber Canc Inst, Boston, MA 02115 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2002 VL 100 IS 11 MA 101 BP 30A EP 30A PN 1 PG 1 WC Hematology SC Hematology GA 614JK UT WOS:000179184700102 ER PT J AU Langenau, DM Traver, D Ferrando, AA Kutok, J Aster, JC Kanki, JP Shuo, L Prochownik, EV Trede, N Zon, LI Look, AT AF Langenau, DM Traver, D Ferrando, AA Kutok, J Aster, JC Kanki, JP Shuo, L Prochownik, EV Trede, N Zon, LI Look, AT TI Myc-induced T-cell leukemia in transgenic zebrafish. SO BLOOD LA English DT Meeting Abstract CT 44th Annual Meeting of the American-Society-of-Hematology CY DEC 06-10, 2002 CL PHILADELPHIA, PENNSYLVANIA SP Amer Soc Hematol C1 Harvard Univ, Sch Med, Dana Farber Canc Inst, Boston, MA 02115 USA. Harvard Univ, Childrens Hosp, Sch Med, Boston, MA 02115 USA. Brigham & Womens Hosp, Boston, MA 02115 USA. Univ Calif Los Angeles, Inst Mol Med & Genet, Los Angeles, CA 90024 USA. Childrens Hosp Pittsburgh, Pittsburgh, PA 15213 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2002 VL 100 IS 11 MA 110 BP 32A EP 32A PN 1 PG 1 WC Hematology SC Hematology GA 614JK UT WOS:000179184700111 ER PT J AU Liu, TX Howlett, NG Moreau, L Kanki, JP D'Andrea, AD Look, AT AF Liu, TX Howlett, NG Moreau, L Kanki, JP D'Andrea, AD Look, AT TI Cloning and characterizatoin of the zebrafish homologue of the Fanconi Anemia protein, FANCD2. SO BLOOD LA English DT Meeting Abstract CT 44th Annual Meeting of the American-Society-of-Hematology CY DEC 06-10, 2002 CL PHILADELPHIA, PENNSYLVANIA SP Amer Soc Hematol C1 Harvard Univ, Sch Med, Dana Farber Canc Inst, Dept Pediat Oncol, Boston, MA 02115 USA. NR 0 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 NOV 16 PY 2002 VL 100 IS 11 MA 151 BP 43A EP 43A PN 1 PG 1 WC Hematology SC Hematology GA 614JK UT WOS:000179184700152 ER PT J AU Tzachanis, D Lafuente, EM Li, LQ Berezovskaya, A Freeman, GJ Nadler, LM Boussiotis, VA AF Tzachanis, D Lafuente, EM Li, LQ Berezovskaya, A Freeman, GJ Nadler, LM Boussiotis, VA TI The evolutionarily conserved, secreted protein twisted gastrulation (TSG) is an inducible selective inhibitor of preactivated T lymphocytes. SO BLOOD LA English DT Meeting Abstract CT 44th Annual Meeting of the American-Society-of-Hematology CY DEC 06-10, 2002 CL PHILADELPHIA, PENNSYLVANIA SP Amer Soc Hematol C1 Dana Farber Canc Inst, Boston, MA 02115 USA. RI Lafuente, Esther M/K-5684-2014 OI Lafuente, Esther M/0000-0001-8466-1022 NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2002 VL 100 IS 11 MA 174 BP 49A EP 49A PN 1 PG 1 WC Hematology SC Hematology GA 614JK UT WOS:000179184700175 ER PT J AU Fan, ZS Beresford, P Oh, D Lieberman, J AF Fan, ZS Beresford, P Oh, D Lieberman, J TI The tumor suppressor NM23-H1 is the granzyme a-activated DNase and the nucleosome assembly protein SET is its inhibitor. SO BLOOD LA English DT Meeting Abstract CT 44th Annual Meeting of the American-Society-of-Hematology CY DEC 06-10, 2002 CL PHILADELPHIA, PENNSYLVANIA SP Amer Soc Hematol C1 Harvard Univ, Sch Med, Ctr Blood Res, Boston, MA 02115 USA. Harvard Univ, Sch Med, Dept Pediat, Boston, MA 02115 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2002 VL 100 IS 11 MA 3705 BP 59B EP 59B PN 2 PG 1 WC Hematology SC Hematology GA 614JL UT WOS:000179184800248 ER PT J AU Mikkola, HKA Klintman, J Yang, H Hock, H Schlaeger, TM Fujiwara, Y Orkin, SH AF Mikkola, HKA Klintman, J Yang, H Hock, H Schlaeger, TM Fujiwara, Y Orkin, SH TI Adult hematopoiesis in the absence of stem cell transcription factor SCL/tal1. SO BLOOD LA English DT Meeting Abstract CT 44th Annual Meeting of the American-Society-of-Hematology CY DEC 06-10, 2002 CL PHILADELPHIA, PENNSYLVANIA SP Amer Soc Hematol C1 Childrens Hosp, Boston, MA 02115 USA. Dana Farber Canc Inst, Boston, MA 02115 USA. Howard Hughes Med Inst, Boston, MA 02115 USA. NR 0 TC 0 Z9 0 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 NOV 16 PY 2002 VL 100 IS 11 MA 211 BP 59A EP 59A PN 1 PG 1 WC Hematology SC Hematology GA 614JK UT WOS:000179184700212 ER PT J AU Iwasaki, H Mizuno, S Wells, RA Akashi, K AF Iwasaki, H Mizuno, S Wells, RA Akashi, K TI GATA-1 instructs commitment and transdifferentiation into megakaryocyte and erythroid lineages, counteracting myelomenocytic differentiation programs. SO BLOOD LA English DT Meeting Abstract CT 44th Annual Meeting of the American-Society-of-Hematology CY DEC 06-10, 2002 CL PHILADELPHIA, PENNSYLVANIA SP Amer Soc Hematol C1 Harvard Univ, Sch Med, Dana Farber Canc Inst, Dept Canc Immunol & AIDS, Boston, MA 02115 USA. Ontario Canc Inst, Dept Cell & Mol Biol, Toronto, ON M4X 1K9, Canada. NR 0 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 NOV 16 PY 2002 VL 100 IS 11 MA 216 BP 60A EP 60A PN 1 PG 1 WC Hematology SC Hematology GA 614JK UT WOS:000179184700217 ER PT J AU Duprez, EA Iwasaki-Arai, J Geary, K Somoza, C Murray, R Akashi, K Tenen, DG AF Duprez, EA Iwasaki-Arai, J Geary, K Somoza, C Murray, R Akashi, K Tenen, DG TI PU.1 deficiency blocks the production of common myeloid and common lymphoid progenitors in both adult and fetal liver myelopoiesis. SO BLOOD LA English DT Meeting Abstract CT 44th Annual Meeting of the American-Society-of-Hematology CY DEC 06-10, 2002 CL PHILADELPHIA, PENNSYLVANIA SP Amer Soc Hematol C1 Harvard Univ, Sch Med, Harvard Inst Med, Boston, MA USA. Dana Farber Canc Inst, Dept Canc Immunol & AIDS, Boston, MA 02115 USA. EOS Biotech, San Francisco, CA USA. RI duprez, estelle/R-2357-2016 NR 0 TC 5 Z9 5 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 NOV 16 PY 2002 VL 100 IS 11 MA 219 BP 61A EP 61A PN 1 PG 1 WC Hematology SC Hematology GA 614JK UT WOS:000179184700220 ER PT J AU Iwasaki-Arai, J Pu, Z Huettner, CS Fenyus, M Lekstrom-Himes, J Tenen, DG Akashi, K AF Iwasaki-Arai, J Pu, Z Huettner, CS Fenyus, M Lekstrom-Himes, J Tenen, DG Akashi, K TI C/EBP alpha deficiency in hematopoiesis induces accumulation of non-malignant myeloblasts mimicking acute myelogenous leukemia. SO BLOOD LA English DT Meeting Abstract CT 44th Annual Meeting of the American-Society-of-Hematology CY DEC 06-10, 2002 CL PHILADELPHIA, PENNSYLVANIA SP Amer Soc Hematol C1 Harvard Univ, Sch Med, Dana Farber Canc Inst, Dept Canc Immunol & AIDS, Boston, MA 02115 USA. Harvard Univ, Sch Med, Harvard Inst Med, Boston, MA USA. NIAID, LHD, Bethesda, MD 20892 USA. NR 0 TC 8 Z9 8 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 NOV 16 PY 2002 VL 100 IS 11 MA 218 BP 61A EP 61A PN 1 PG 1 WC Hematology SC Hematology GA 614JK UT WOS:000179184700219 ER PT J AU Yunes, JA Costa, LF Sallan, SE Nadler, LM Cardoso, AA AF Yunes, JA Costa, LF Sallan, SE Nadler, LM Cardoso, AA TI Interleukin-7 promotes the survival of bone marrow endothelial cells. SO BLOOD LA English DT Meeting Abstract CT 44th Annual Meeting of the American-Society-of-Hematology CY DEC 06-10, 2002 CL PHILADELPHIA, PENNSYLVANIA SP Amer Soc Hematol C1 Harvard Univ, Sch Med, Dana Farber Canc Inst, Boston, MA 02115 USA. Univ Lisbon, Sch Med, Inst Mol Med, P-1699 Lisbon, Portugal. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2002 VL 100 IS 11 MA 227 BP 63A EP 63A PN 1 PG 1 WC Hematology SC Hematology GA 614JK UT WOS:000179184700228 ER PT J AU Scheijen, B Ngo, HT Kang, H Griffin, JD AF Scheijen, B Ngo, HT Kang, H Griffin, JD TI FLT3 receptors with internal tandem duplications signal through AKT/PKB and forkhead (Foxo) transcription factors to regulate genes controlling cell cycle progression and viability. SO BLOOD LA English DT Meeting Abstract CT 44th Annual Meeting of the American-Society-of-Hematology CY DEC 06-10, 2002 CL PHILADELPHIA, PENNSYLVANIA SP Amer Soc Hematol C1 Dana Farber Canc Inst, Boston, MA 02115 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2002 VL 100 IS 11 MA 232 BP 64A EP 64A PN 1 PG 1 WC Hematology SC Hematology GA 614JK UT WOS:000179184700233 ER PT J AU Weng, AP Nam, Y Wolfe, MS Pear, WS Griffin, JD Blacklow, SC Aster, JC AF Weng, AP Nam, Y Wolfe, MS Pear, WS Griffin, JD Blacklow, SC Aster, JC TI Growth suppression of pre-T acute lymphoblastic leukemia cells by inhibition of NOTCH signaling. SO BLOOD LA English DT Meeting Abstract CT 44th Annual Meeting of the American-Society-of-Hematology CY DEC 06-10, 2002 CL PHILADELPHIA, PENNSYLVANIA SP Amer Soc Hematol C1 Brigham & Womens Hosp, Boston, MA 02115 USA. Univ Penn, Sch Med, Philadelphia, PA 19104 USA. Dana Farber Canc Inst, Boston, MA 02115 USA. RI Weng, Andrew/I-5015-2014 NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2002 VL 100 IS 11 MA 235 BP 65A EP 65A PN 1 PG 1 WC Hematology SC Hematology GA 614JK UT WOS:000179184700236 ER PT J AU Li, AH Zuckerman, D Zuckerman, A Silverman, LB Sallan, SE Gribben, JG AF Li, AH Zuckerman, D Zuckerman, A Silverman, LB Sallan, SE Gribben, JG TI Sequence analysis of clonal IgH and TCR gene rearrangements in children with acute lymphoblastic leukemia at diagnosis and at relapse: Implications for clinical utility of PCR based methods of minimal residual disease detection. SO BLOOD LA English DT Meeting Abstract CT 44th Annual Meeting of the American-Society-of-Hematology CY DEC 06-10, 2002 CL PHILADELPHIA, PENNSYLVANIA SP Amer Soc Hematol C1 Harvard Univ, Childrens Hosp, Dana Farber Canc Inst, Sch Med, Boston, MA 02115 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2002 VL 100 IS 11 MA 246 BP 68A EP 68A PN 1 PG 1 WC Hematology SC Hematology GA 614JK UT WOS:000179184700247 ER PT J AU Rubio, MT Bronson, RT Sykes, M AF Rubio, MT Bronson, RT Sykes, M TI Role of recipient STAT6 in graft-versus-host disease. SO BLOOD LA English DT Meeting Abstract CT 44th Annual Meeting of the American-Society-of-Hematology CY DEC 06-10, 2002 CL PHILADELPHIA, PENNSYLVANIA SP Amer Soc Hematol C1 Harvard Univ, Massachusetts Gen Hosp, Sch Med, Transplantat Biol Res Ctr, Boston, MA USA. Harvard Univ, Dana Farber Canc Inst, Sch Med, Boston, MA USA. Harvard Univ, Harvard Canc Res Ctr, Sch Med, Boston, MA USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2002 VL 100 IS 11 MA 262 BP 72A EP 72A PN 1 PG 1 WC Hematology SC Hematology GA 614JK UT WOS:000179184700263 ER PT J AU Shohet, JL Albrecht, RM Esnault, S Lauer, JL Pratoomtong, C Malter, JS Denes, FS von Andrian, U Shobet, SB AF Shohet, JL Albrecht, RM Esnault, S Lauer, JL Pratoomtong, C Malter, JS Denes, FS von Andrian, U Shobet, SB TI Cell adhesion to the lumenal surfaces or small diameter plasma-treated polyethylene tubing. SO BLOOD LA English DT Meeting Abstract CT 44th Annual Meeting of the American-Society-of-Hematology CY DEC 06-10, 2002 CL PHILADELPHIA, PENNSYLVANIA SP Amer Soc Hematol C1 Univ Wisconsin, Lab Med & Pathol, Madison, WI USA. Harvard Univ, Sch Med, Ctr Blood Res, Boston, MA 02115 USA. Univ Calif San Francisco, Lab Med, San Francisco, CA 94143 USA. NR 0 TC 1 Z9 1 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 NOV 16 PY 2002 VL 100 IS 11 MA 3759 BP 72B EP 72B PN 2 PG 1 WC Hematology SC Hematology GA 614JL UT WOS:000179184800302 ER PT J AU Bellucci, R Wu, CJ Munshi, NC Chiaretti, S Alyea, EP Anderson, KC Ritz, J AF Bellucci, R Wu, CJ Munshi, NC Chiaretti, S Alyea, EP Anderson, KC Ritz, J TI Antibody response against overexpressed target antigens associated with the graft-vs-myeloma response after donor lymphocyte infusion. SO BLOOD LA English DT Meeting Abstract CT 44th Annual Meeting of the American-Society-of-Hematology CY DEC 06-10, 2002 CL PHILADELPHIA, PENNSYLVANIA SP Amer Soc Hematol C1 Harvard Univ, Sch Med, Dana Farber Canc Inst, Dept Adult Oncol, Boston, MA 02115 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2002 VL 100 IS 11 MA 266 BP 73A EP 73A PN 1 PG 1 WC Hematology SC Hematology GA 614JK UT WOS:000179184700267 ER PT J AU Cutler, C Lee, S Greenberg, P Deeg, J Antin, J Perez, W Keating, A Weisdorf, D Horowitz, M AF Cutler, C Lee, S Greenberg, P Deeg, J Antin, J Perez, W Keating, A Weisdorf, D Horowitz, M TI A decision analysis of allogeneic stem cell transplantation for MDS: Delayed transplantation for low risk MDS is associated with improved outcome. SO BLOOD LA English DT Meeting Abstract CT 44th Annual Meeting of the American-Society-of-Hematology CY DEC 06-10, 2002 CL PHILADELPHIA, PENNSYLVANIA SP Amer Soc Hematol C1 Dana Farber Canc Inst, Boston, MA 02115 USA. Stanford Med Ctr & VA Hlth Care Syst, Int Myelodysplasia Risk Assessment Workshop, Palo Alto, CA USA. Fred Hutchinson Canc Res Ctr, Seattle, WA 98104 USA. Med Coll Wisconsin, Int Bone Marrow Transplant Registry, Acute Leukemia Writing Comm, Milwaukee, WI 53226 USA. NR 0 TC 6 Z9 7 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 NOV 16 PY 2002 VL 100 IS 11 MA 270 BP 74A EP 75A PN 1 PG 2 WC Hematology SC Hematology GA 614JK UT WOS:000179184700271 ER PT J AU Jagadeeswaran, R Benz, EJ Huang, SC AF Jagadeeswaran, R Benz, EJ Huang, SC TI Protein 4.1R is required for microtubule aster formation in mammalian mitotic extract. SO BLOOD LA English DT Meeting Abstract CT 44th Annual Meeting of the American-Society-of-Hematology CY DEC 06-10, 2002 CL PHILADELPHIA, PENNSYLVANIA SP Amer Soc Hematol C1 Dana Farber Canc Inst, Boston, MA 02115 USA. RI Jagadeeswaran, Ramasamy/C-9987-2013 NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2002 VL 100 IS 11 MA 288 BP 79A EP 79A PN 1 PG 1 WC Hematology SC Hematology GA 614JK UT WOS:000179184700289 ER PT J AU Hock, H Hamblen, MJ Rooke, HM Traver, D Bronson, RT Cameron, S Orkin, SH AF Hock, H Hamblen, MJ Rooke, HM Traver, D Bronson, RT Cameron, S Orkin, SH TI The zinc-finger transcription factor Gfi-1 is required for neutrophil differentiation and refines the identity of the myeloid lineages. SO BLOOD LA English DT Meeting Abstract CT 44th Annual Meeting of the American-Society-of-Hematology CY DEC 06-10, 2002 CL PHILADELPHIA, PENNSYLVANIA SP Amer Soc Hematol C1 Childrens Hosp, Div Hematol Oncol, Boston, MA 02115 USA. Dana Farber Canc Inst, Boston, MA 02115 USA. Howard Hughes Med Inst, Boston, MA 02115 USA. Harvard Univ, Sch Med, Dept Pathol, Boston, MA 02115 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2002 VL 100 IS 11 MA 290 BP 80A EP 80A PN 1 PG 1 WC Hematology SC Hematology GA 614JK UT WOS:000179184700291 ER PT J AU Stegmaier, K Ross, KN O'Malley, S Stockwell, BR Golub, TR AF Stegmaier, K Ross, KN O'Malley, S Stockwell, BR Golub, TR TI Manipulating leukemia gene expression programs via chemical genomics. SO BLOOD LA English DT Meeting Abstract CT 44th Annual Meeting of the American-Society-of-Hematology CY DEC 06-10, 2002 CL PHILADELPHIA, PENNSYLVANIA SP Amer Soc Hematol C1 Dana Farber Canc Inst, Boston, MA 02115 USA. Whitehead Inst Biomed Res, Cambridge, MA 02142 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2002 VL 100 IS 11 MA 305 BP 83A EP 83A PN 1 PG 1 WC Hematology SC Hematology GA 614JK UT WOS:000179184700306 ER PT J AU Armstrong, SA Kung, AL Mahon, ME Golub, TR Griffin, JD Korsmeyer, SJ AF Armstrong, SA Kung, AL Mahon, ME Golub, TR Griffin, JD Korsmeyer, SJ TI Inhibition of FLT3 in MLL: Validation of a therapeutic target discovered by gene expression based leukemia classification. SO BLOOD LA English DT Meeting Abstract CT 44th Annual Meeting of the American-Society-of-Hematology CY DEC 06-10, 2002 CL PHILADELPHIA, PENNSYLVANIA SP Amer Soc Hematol C1 Harvard Univ, Sch Med, Dana Farber Canc Inst, Boston, MA 02115 USA. Whitehead Inst Genome Res, Cambridge, MA USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2002 VL 100 IS 11 MA 306 BP 84A EP 84A PN 1 PG 1 WC Hematology SC Hematology GA 614JK UT WOS:000179184700307 ER PT J AU Stone, RM Klimek, V DeAngelo, DJ Nimer, S Estey, E Galinsky, I Neuberg, D Yap, A Fox, EA Gilliland, DG Griffin, J AF Stone, RM Klimek, V DeAngelo, DJ Nimer, S Estey, E Galinsky, I Neuberg, D Yap, A Fox, EA Gilliland, DG Griffin, J TI PKC412, an oral FLT3 inhibitor, has activity in mutant FLT3 acute myeloid leukemia (AML): A phase II clinical trial. SO BLOOD LA English DT Meeting Abstract CT 44th Annual Meeting of the American-Society-of-Hematology CY DEC 06-10, 2002 CL PHILADELPHIA, PENNSYLVANIA SP Amer Soc Hematol C1 Dana Farber Canc Inst, Boston, MA 02115 USA. Mem Sloan Kettering Canc Ctr, New York, NY 10021 USA. Univ Texas, MD Anderson Canc Ctr, Houston, TX 77030 USA. Novartis Pharma AG, BU Oncol, Basel, Switzerland. NR 0 TC 22 Z9 22 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 NOV 16 PY 2002 VL 100 IS 11 MA 316 BP 86A EP 86A PN 1 PG 1 WC Hematology SC Hematology GA 614JK UT WOS:000179184700317 ER PT J AU Massey, G Zipursky, A Doyle, JJ Taub, J Chang, MN Ravindranath, Y Weinstein, HJ AF Massey, G Zipursky, A Doyle, JJ Taub, J Chang, MN Ravindranath, Y Weinstein, HJ TI A prospective study of the natural history of transient leukemia (TL) in neonates with Down syndrome (DS): A Pediatric Oncolocy Group (POG) study. SO BLOOD LA English DT Meeting Abstract CT 44th Annual Meeting of the American-Society-of-Hematology CY DEC 06-10, 2002 CL PHILADELPHIA, PENNSYLVANIA SP Amer Soc Hematol C1 Virginia Commonwealth Univ, Med Coll Virginia, Dept Pediat, Richmond, VA 23298 USA. Hosp Sick Children, Div Pediat Hematol Oncol, Toronto, ON M5G 1X8, Canada. Childrens Hosp Michigan, Div Pediat Oncol, Detroit, MI 48201 USA. Univ Florida, COG Stat Off, Gainesville, FL 32611 USA. Massachusetts Gen Hosp, Dept Pediat, Boston, MA 02114 USA. NR 0 TC 3 Z9 3 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 NOV 16 PY 2002 VL 100 IS 11 MA 321 BP 87A EP 87A PN 1 PG 1 WC Hematology SC Hematology GA 614JK UT WOS:000179184700322 ER PT J AU Sekeres, MA Dodge, RK Bloomfield, CD Larson, RA Stone, RM AF Sekeres, MA Dodge, RK Bloomfield, CD Larson, RA Stone, RM TI Racial differences in prognostic factors and outcome in acute myeloid leukemia (AML): A cancer and leukemia group B (CALGB) study. SO BLOOD LA English DT Meeting Abstract CT 44th Annual Meeting of the American-Society-of-Hematology CY DEC 06-10, 2002 CL PHILADELPHIA, PENNSYLVANIA SP Amer Soc Hematol C1 Cleveland Clin Fdn, Cleveland, OH 44195 USA. Ctr Stat, Canc & Leukemia Grp B, Chicago, IL USA. Ohio State Univ, Columbus, OH 43210 USA. Univ Chicago, Chicago, IL 60637 USA. Dana Farber Canc Inst, Boston, MA 02115 USA. NR 0 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 NOV 16 PY 2002 VL 100 IS 11 MA 323 BP 88A EP 88A PN 1 PG 1 WC Hematology SC Hematology GA 614JK UT WOS:000179184700324 ER PT J AU Sekeres, MA Stone, RM Zahrieh, D Neuberg, D DeAngelo, DJ Galinsky, I Morrison, VA Lee, SJ AF Sekeres, MA Stone, RM Zahrieh, D Neuberg, D DeAngelo, DJ Galinsky, I Morrison, VA Lee, SJ TI Treatment decision-making and quality of life in older adults with acute myeloid leukemia (AML) or advanced myelodysplastic syndrome (aMDS). SO BLOOD LA English DT Meeting Abstract CT 44th Annual Meeting of the American-Society-of-Hematology CY DEC 06-10, 2002 CL PHILADELPHIA, PENNSYLVANIA SP Amer Soc Hematol C1 Cleveland Clin Fdn, Cleveland, OH 44195 USA. Dana Farber Canc Inst, Boston, MA 02115 USA. Minneapolis VA Med Ctr, Minneapolis, MN USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2002 VL 100 IS 11 MA 328 BP 89A EP 89A PN 1 PG 1 WC Hematology SC Hematology GA 614JK UT WOS:000179184700329 ER PT J AU Aguiar, RCT Takeyama, K He, C Mitra, J Klein, U Dalla-Favera, R Wilkinson, K Shipp, MA AF Aguiar, RCT Takeyama, K He, C Mitra, J Klein, U Dalla-Favera, R Wilkinson, K Shipp, MA TI The DLBCL risk-related BAL-1 protein functions as a repressor of transcription. SO BLOOD LA English DT Meeting Abstract CT 44th Annual Meeting of the American-Society-of-Hematology CY DEC 06-10, 2002 CL PHILADELPHIA, PENNSYLVANIA SP Amer Soc Hematol C1 Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02115 USA. Columbia Univ, Inst Canc Genet, New York, NY 10027 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2002 VL 100 IS 11 MA 333 BP 91A EP 91A PN 1 PG 1 WC Hematology SC Hematology GA 614JK UT WOS:000179184700334 ER PT J AU Gricks, CS Zauls, AJ Zahrieh, D Chiaretti, S Krackhardt, AM Neuberg, D Gribben, JG AF Gricks, CS Zauls, AJ Zahrieh, D Chiaretti, S Krackhardt, AM Neuberg, D Gribben, JG TI Gene expression profiling demonstrates differential regulation of genes controlling cell cycle progression following CD40 activation in healthy B cells compared to CLL cells. SO BLOOD LA English DT Meeting Abstract CT 44th Annual Meeting of the American-Society-of-Hematology CY DEC 06-10, 2002 CL PHILADELPHIA, PENNSYLVANIA SP Amer Soc Hematol C1 Harvard Univ, Sch Med, Dana Farber Canc Inst, Boston, MA 02115 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2002 VL 100 IS 11 MA 366 BP 99A EP 99A PN 1 PG 1 WC Hematology SC Hematology GA 614JK UT WOS:000179184700367 ER PT J AU Fonseca, R Blood, EA Paz, NG Picken, EB Davila, RS Oken, MM Kyle, RA Dewald, GW Ahmann, GJ Van Wier, SA Henderson, KJ Bailey, RJ Greipp, PR AF Fonseca, R Blood, EA Paz, NG Picken, EB Davila, RS Oken, MM Kyle, RA Dewald, GW Ahmann, GJ Van Wier, SA Henderson, KJ Bailey, RJ Greipp, PR TI Two major cytogenetic subtypes of multiple myeloma (MM) can be discerned, hyperdiploid-MM and non-hyperdiploid-MM, the latter with a strong association with IgH translocations (IgH-TRX). SO BLOOD LA English DT Meeting Abstract CT 44th Annual Meeting of the American-Society-of-Hematology CY DEC 06-10, 2002 CL PHILADELPHIA, PENNSYLVANIA SP Amer Soc Hematol C1 Mayo Clin, Dept Lab Med & Pathol, Rochester, MN USA. Dana Farber Canc Inst, Dept Biostat Sci, Boston, MA 02115 USA. Mayo Clin & Mayo Grad Sch Med, Mayo Clin, Rochester, MN USA. Abbott NW Hosp, Minneapolis, MN 55407 USA. ECOG, Boston, MA USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2002 VL 100 IS 11 MA 370 BP 100A EP 100A PN 1 PG 1 WC Hematology SC Hematology GA 614JK UT WOS:000179184700371 ER PT J AU Davies, FE Dring, AM Cheng, L Rawstron, AC Shammas, M Hideshima, T Chauhan, D Tai, IT Auclair, D Robinson, E Wong, WH Munshi, NC Morgan, GJ Anderson, KC AF Davies, FE Dring, AM Cheng, L Rawstron, AC Shammas, M Hideshima, T Chauhan, D Tai, IT Auclair, D Robinson, E Wong, WH Munshi, NC Morgan, GJ Anderson, KC TI The molecular basis of the transition of MGUS to multiple myeloma. SO BLOOD LA English DT Meeting Abstract CT 44th Annual Meeting of the American-Society-of-Hematology CY DEC 06-10, 2002 CL PHILADELPHIA, PENNSYLVANIA SP Amer Soc Hematol C1 Univ Leeds, Acad Dept Haematol & Oncol, Leeds LS2 9JT, W Yorkshire, England. Dana Farber Canc Inst, Dept Adult Oncol, Boston, MA 02115 USA. Harvard Univ, Sch Publ Hlth, Dept Biostat, Boston, MA 02115 USA. NR 0 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 NOV 16 PY 2002 VL 100 IS 11 MA 377 BP 102A EP 102A PN 1 PG 1 WC Hematology SC Hematology GA 614JK UT WOS:000179184700378 ER PT J AU Richardson, P Jagannath, S Schlossman, R Weller, E Zeldenrust, S Rajumar, VS Alsina, M Desikan, RK Mitsiades, C Kelly, K Doss, D McKenney, M Shepard, T Rich, R Warren, D Freeman, A Deocampo, R Doucet, K Knight, R Balinski, K Zeldis, J Dalton, W Hideshima, T Anderson, K AF Richardson, P Jagannath, S Schlossman, R Weller, E Zeldenrust, S Rajumar, VS Alsina, M Desikan, RK Mitsiades, C Kelly, K Doss, D McKenney, M Shepard, T Rich, R Warren, D Freeman, A Deocampo, R Doucet, K Knight, R Balinski, K Zeldis, J Dalton, W Hideshima, T Anderson, K TI A multi-center, randomized, phase II study to evaluate the efficacy and safety of two CDC-5013 dose regimens when used alone or in combination with dexamethasone (Dex) for the treatment of relapsed or refractory multiple myeloma (MM). SO BLOOD LA English DT Meeting Abstract CT 44th Annual Meeting of the American-Society-of-Hematology CY DEC 06-10, 2002 CL PHILADELPHIA, PENNSYLVANIA SP Amer Soc Hematol C1 Dana Farber Canc Inst, Boston, MA 02115 USA. St Vincents Catholic Med Ctr, New York, NY USA. Mayo Clin, Rochester, MN USA. Univ S Florida, H Lee Moffitt Canc Ctr, Tampa, FL 33682 USA. Celgene, Warren, NJ USA. NR 0 TC 29 Z9 30 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 NOV 16 PY 2002 VL 100 IS 11 MA 386 BP 104A EP 105A PN 1 PG 2 WC Hematology SC Hematology GA 614JK UT WOS:000179184700387 ER PT J AU Richardson, P Barlogie, B Berenson, J Traynor, A Singhal, S Jagannath, S Irwin, D Rajkumar, V Srkalovic, G Alsina, M Alexanian, R Siegel, D Orlowski, RZ Kuter, D Limentani, SA Lee, S Esseltine, DL Kauffman, M Adams, J Schenkein, DP Anderson, KC AF Richardson, P Barlogie, B Berenson, J Traynor, A Singhal, S Jagannath, S Irwin, D Rajkumar, V Srkalovic, G Alsina, M Alexanian, R Siegel, D Orlowski, RZ Kuter, D Limentani, SA Lee, S Esseltine, DL Kauffman, M Adams, J Schenkein, DP Anderson, KC TI A phase II multicenter study of the proteasome inhibitor bortezomib (VELCADE (TM), formerly PS-341) in multiple myeloma patients (pts) with relapsed/refractory disease. SO BLOOD LA English DT Meeting Abstract CT 44th Annual Meeting of the American-Society-of-Hematology CY DEC 06-10, 2002 CL PHILADELPHIA, PENNSYLVANIA SP Amer Soc Hematol C1 Dana Farber Canc Inst, Boston, MA 02115 USA. Univ Arkansas, Little Rock, AR 72204 USA. Cedars Sinai Med Ctr, Los Angeles, CA 90048 USA. Northwestern Univ, Med Ctr, Chicago, IL 60611 USA. St Vincents Catholic Med Ctr, New York, NY USA. Alta Bates Comprehens Canc Ctr, Berkeley, CA USA. Mayo Clin, Rochester, MN USA. Cleveland Clin Fdn, Cleveland, OH 44195 USA. Univ S Florida, H Lee Moffitt Canc Ctr, Tampa, FL 33682 USA. Univ Texas, MD Anderson Canc Ctr, Houston, TX 77030 USA. Carol G Simon Canc Ctr, Morristown, NJ USA. Univ N Carolina, Chapel Hill, NC 27515 USA. Massachusetts Gen Hosp, Boston, MA 02114 USA. Charlotte Med Clin, Charlotte, NC USA. Millennium Pharmaceut Inc, Cambridge, MA USA. NR 0 TC 29 Z9 30 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 NOV 16 PY 2002 VL 100 IS 11 MA 385 BP 104A EP 104A PN 1 PG 1 WC Hematology SC Hematology GA 614JK UT WOS:000179184700386 ER PT J AU Mitsiades, N Mitsiades, CS Richardson, PG Poulaki, V Fanourakis, G Tai, YT Chauhan, D Schlossman, R Munshi, NC Hideshima, T Anderson, KC AF Mitsiades, N Mitsiades, CS Richardson, PG Poulaki, V Fanourakis, G Tai, YT Chauhan, D Schlossman, R Munshi, NC Hideshima, T Anderson, KC TI The proteasome inhibitor PS-341 potentiates sensitivity of multiple myeloma cells to conventional chemotherapeutic agents: Therapeutic applications. SO BLOOD LA English DT Meeting Abstract CT 44th Annual Meeting of the American-Society-of-Hematology CY DEC 06-10, 2002 CL PHILADELPHIA, PENNSYLVANIA SP Amer Soc Hematol C1 Harvard Univ, Sch Med, Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02115 USA. Harvard Univ, Massachusetts Eye & Ear Infirm, Sch Med, Boston, MA USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2002 VL 100 IS 11 MA 390 BP 105A EP 106A PN 1 PG 2 WC Hematology SC Hematology GA 614JK UT WOS:000179184700391 ER PT J AU Catley, L Weisberg, E Tai, YT Lin, B Mitsiades, N Hideshima, T LeBlanc, R Shringapure, R Burger, R Mitsiades, C Chauhan, D Schlossman, R Munshi, N Richardson, P Griffin, J Anderson, K AF Catley, L Weisberg, E Tai, YT Lin, B Mitsiades, N Hideshima, T LeBlanc, R Shringapure, R Burger, R Mitsiades, C Chauhan, D Schlossman, R Munshi, N Richardson, P Griffin, J Anderson, K TI LAQ824 is a novel histone deacetylase inhibitor with significant activity against multiple myeloma: Results of a pre-clinical evaluation in vitro and in vivo. SO BLOOD LA English DT Meeting Abstract CT 44th Annual Meeting of the American-Society-of-Hematology CY DEC 06-10, 2002 CL PHILADELPHIA, PENNSYLVANIA SP Amer Soc Hematol C1 Dana Farber Canc Inst, Boston, MA 02115 USA. RI Catley, Laurence/E-5313-2013 NR 0 TC 3 Z9 4 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 NOV 16 PY 2002 VL 100 IS 11 MA 391 BP 106A EP 106A PN 1 PG 1 WC Hematology SC Hematology GA 614JK UT WOS:000179184700392 ER PT J AU Mitsiades, CS Mitsiades, N Poulaki, V Fanourakis, G Hideshima, T Chauhan, D Munshi, NC Anderson, KC AF Mitsiades, CS Mitsiades, N Poulaki, V Fanourakis, G Hideshima, T Chauhan, D Munshi, NC Anderson, KC TI Hsp90 inhibitors prolong survival in a SCID/NOD mice model of diffuse multiple myeloma: Therapeutic implications. SO BLOOD LA English DT Meeting Abstract CT 44th Annual Meeting of the American-Society-of-Hematology CY DEC 06-10, 2002 CL PHILADELPHIA, PENNSYLVANIA SP Amer Soc Hematol C1 Harvard Univ, Sch Med, Dana Farber Canc Inst, Jerome Lipper Multiple Myeloma Ctr,Dept Med Oncol, Boston, MA 02115 USA. NR 0 TC 7 Z9 7 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 NOV 16 PY 2002 VL 100 IS 11 MA 392 BP 106A EP 106A PN 1 PG 1 WC Hematology SC Hematology GA 614JK UT WOS:000179184700393 ER PT J AU Richardson, PG Soiffer, R Antin, JH Vredenburgh, J Kurtzberg, J Martin, PL Hockenbery, D Steinbach, G Murray, K Vogelsang, G Chen, A Warren, DL Momtaz, P Wei, LJ Jin, Z Rifai, N Bradwin, G Iacobelli, M McDonald, GB Guinan, EC AF Richardson, PG Soiffer, R Antin, JH Vredenburgh, J Kurtzberg, J Martin, PL Hockenbery, D Steinbach, G Murray, K Vogelsang, G Chen, A Warren, DL Momtaz, P Wei, LJ Jin, Z Rifai, N Bradwin, G Iacobelli, M McDonald, GB Guinan, EC TI Defibrotide (DF) appears effective and safe in a phase II, randomized study of patients (pts) with severe veno-occlusive disease (VOD) and multi-system organ failure (MOF) post stem cell transplantation (SCT). SO BLOOD LA English DT Meeting Abstract CT 44th Annual Meeting of the American-Society-of-Hematology CY DEC 06-10, 2002 CL PHILADELPHIA, PENNSYLVANIA SP Amer Soc Hematol C1 Massachusetts Gen Hosp, Boston, MA 02114 USA. Dana Farber Canc Inst, Boston, MA 02115 USA. Childrens Hosp, Boston, MA 02115 USA. Harvard Univ, Sch Publ Hlth, Boston, MA 02115 USA. Columbia Univ, New York, NY 10027 USA. Duke Univ, Med Ctr, Durham, NC 27706 USA. Johns Hopkins Oncol Ctr, Baltimore, MD USA. Fred Hutchinson Canc Res Ctr, Seattle, WA 98104 USA. Gentium SpA, Como, Italy. NR 0 TC 7 Z9 7 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 NOV 16 PY 2002 VL 100 IS 11 MA 414 BP 112A EP 112A PN 1 PG 1 WC Hematology SC Hematology GA 614JK UT WOS:000179184700415 ER PT J AU Alyea, EP Hochberg, EP Neuberg, D Canning, CM Parikh, B Soiffer, RJ Ritz, J AF Alyea, EP Hochberg, EP Neuberg, D Canning, CM Parikh, B Soiffer, RJ Ritz, J TI Long term follow-up of CD4+ donor lymphocyte infusions for patients with relapsed chronic myelogenous leukemia after allogeneic transplantation. SO BLOOD LA English DT Meeting Abstract CT 44th Annual Meeting of the American-Society-of-Hematology CY DEC 06-10, 2002 CL PHILADELPHIA, PENNSYLVANIA SP Amer Soc Hematol C1 Dana Farber Canc Inst, Boston, MA 02115 USA. Brigham & Womens Hosp, Dept Med, Boston, MA 02115 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2002 VL 100 IS 11 MA 424 BP 115A EP 115A PN 1 PG 1 WC Hematology SC Hematology GA 614JK UT WOS:000179184700425 ER PT J AU Italiano, JE Shivdasani, RA Hartwig, JH AF Italiano, JE Shivdasani, RA Hartwig, JH TI Cytoskeletal mechanics of platelet formation. SO BLOOD LA English DT Meeting Abstract CT 44th Annual Meeting of the American-Society-of-Hematology CY DEC 06-10, 2002 CL PHILADELPHIA, PENNSYLVANIA SP Amer Soc Hematol C1 Brigham & Womens Hosp, Dept Med, Boston, MA 02115 USA. Dana Farber Canc Inst, Dept Adult Oncol, Boston, MA 02115 USA. Dana Farber Canc Inst, Dept Canc Biol, Boston, MA 02115 USA. Harvard Univ, Sch Med, Boston, MA USA. NR 0 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 NOV 16 PY 2002 VL 100 IS 11 MA 495 BP 132A EP 132A PN 1 PG 1 WC Hematology SC Hematology GA 614JK UT WOS:000179184700496 ER PT J AU Adams, GB Calvi, LM Weibrecht, KW Olson, DP Knight, MC Schipani, E Divieti, P Kronenberg, HM Scadden, DT AF Adams, GB Calvi, LM Weibrecht, KW Olson, DP Knight, MC Schipani, E Divieti, P Kronenberg, HM Scadden, DT TI Interaction of bone and bone marrow: Expansion of hematopoietic stem cells in vivo and in vitro through activation of the PTH/PTHrP receptor in bone marrow stromal cells. SO BLOOD LA English DT Meeting Abstract CT 44th Annual Meeting of the American-Society-of-Hematology CY DEC 06-10, 2002 CL PHILADELPHIA, PENNSYLVANIA SP Amer Soc Hematol C1 Harvard Univ, Massachusetts Gen Hosp, Sch Med, Partners AIDS Res Ctr, Boston, MA 02114 USA. Harvard Univ, Massachusetts Gen Hosp, Sch Med, MGH Canc Ctr, Boston, MA 02114 USA. Harvard Univ, Massachusetts Gen Hosp, Sch Med, Endocrine Unit, Boston, MA 02114 USA. NR 0 TC 0 Z9 0 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 NOV 16 PY 2002 VL 100 IS 11 MA 501 BP 134A EP 134A PN 1 PG 1 WC Hematology SC Hematology GA 614JK UT WOS:000179184700502 ER PT J AU Hsieh, JJD Ernst, P Erdjument-Bromage, H Tempst, P Korsmeyer, S AF Hsieh, JJD Ernst, P Erdjument-Bromage, H Tempst, P Korsmeyer, S TI Proteolytic cleavage of MLL generates a complex of N- and C-terminal fragments that confers protein stability and subnuclear localization. SO BLOOD LA English DT Meeting Abstract CT 44th Annual Meeting of the American-Society-of-Hematology CY DEC 06-10, 2002 CL PHILADELPHIA, PENNSYLVANIA SP Amer Soc Hematol C1 Dana Farber Canc Inst, Boston, MA 02115 USA. Mem Sloan Kettering Canc Ctr, Program Mol Biol, New York, NY 10021 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2002 VL 100 IS 11 MA 514 BP 137A EP 137A PN 1 PG 1 WC Hematology SC Hematology GA 614JK UT WOS:000179184700515 ER PT J AU Roumiantsev, S Krause, DS Neumann, CA Dimitri, C Asiedu, F Daley, GQ Cross, NCP Van Etten, RA AF Roumiantsev, S Krause, DS Neumann, CA Dimitri, C Asiedu, F Daley, GQ Cross, NCP Van Etten, RA TI Stem cell myeloproliferative disease and T-lymphoma induced in mice by the ZNF198-FGFR1 fusion gene of human 8p11 myeloproliferative syndrome. SO BLOOD LA English DT Meeting Abstract CT 44th Annual Meeting of the American-Society-of-Hematology CY DEC 06-10, 2002 CL PHILADELPHIA, PENNSYLVANIA SP Amer Soc Hematol C1 Harvard Univ, Sch Med, Ctr Blood Res, Boston, MA 02115 USA. Harvard Univ, Sch Med, Dept Genet, Boston, MA USA. Whitehead Inst Biomed Res, Cambridge, MA 02142 USA. Salisbury Dist Hosp, Wessex Reg Genet Lab, Salisbury, Wilts, England. NR 0 TC 0 Z9 0 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 NOV 16 PY 2002 VL 100 IS 11 MA 529 BP 141A EP 141A PN 1 PG 1 WC Hematology SC Hematology GA 614JK UT WOS:000179184700530 ER PT J AU Barata, JT Cardoso, AA Brandao, J Nadler, LM Boussiotis, VA AF Barata, JT Cardoso, AA Brandao, J Nadler, LM Boussiotis, VA TI PI3K/PKB(Akt) is the dominant pathway regulating interleukin-7 mediated survival, activation and cell cycle progression of T cell acute lymphoblastic leukemia (T-ALL) cells. SO BLOOD LA English DT Meeting Abstract CT 44th Annual Meeting of the American-Society-of-Hematology CY DEC 06-10, 2002 CL PHILADELPHIA, PENNSYLVANIA SP Amer Soc Hematol C1 Univ Lisbon, Inst Mol Biol, P-1699 Lisbon, Portugal. Dana Farber Canc Inst, Boston, MA 02115 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2002 VL 100 IS 11 MA 570 BP 152A EP 152A PN 1 PG 1 WC Hematology SC Hematology GA 614JK UT WOS:000179184700571 ER PT J AU Ferrando, AA Neuberg, D Dodge, RK Paietta, E Larson, RA Wiernik, PH Rowe, JM Bloomfield, CD Caligiuri, MA Look, AT AF Ferrando, AA Neuberg, D Dodge, RK Paietta, E Larson, RA Wiernik, PH Rowe, JM Bloomfield, CD Caligiuri, MA Look, AT TI Adult T-cell ALL patients whose lymphoblasts express the HOX11 oncogene have an excellent prognosis when treated with chemotherapy and are not candidates for allogeneic bone marrow transplantaton in first remission. SO BLOOD LA English DT Meeting Abstract CT 44th Annual Meeting of the American-Society-of-Hematology CY DEC 06-10, 2002 CL PHILADELPHIA, PENNSYLVANIA SP Amer Soc Hematol C1 Harvard Univ, Sch Med, Dana Farber Canc Inst, Dept Pediat Oncol, Boston, MA 02115 USA. Harvard Univ, Sch Med, Dana Farber Canc Inst, Biostat Sci Dept, Boston, MA 02115 USA. Duke Univ, Med Ctr, Dept Biostat, Durham, NC 27706 USA. Our Lady Mercy Med Ctr, Bronx, NY USA. Univ Chicago Hosp, Chicago, IL 60637 USA. Rambam Med Ctr, Dept Hematol & Bone Marrow Transplantat, Haifa, Israel. Ohio State Univ, Med Ctr, Columbus, OH 43210 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2002 VL 100 IS 11 MA 578 BP 154A EP 154A PN 1 PG 1 WC Hematology SC Hematology GA 614JK UT WOS:000179184700579 ER PT J AU Friedberg, JW Neuberg, D Bendell, C Miyata, S McCauley, M Fisher, DC Takvorian, T Canellos, GP AF Friedberg, JW Neuberg, D Bendell, C Miyata, S McCauley, M Fisher, DC Takvorian, T Canellos, GP TI Phase I study of gemcitabine added to doxorubicin, bleomycin, and vinblastine for the treatment of de novo Hodgkin's disease (HD): Increased pulmonary toxicity compared with ABVD. SO BLOOD LA English DT Meeting Abstract CT 44th Annual Meeting of the American-Society-of-Hematology CY DEC 06-10, 2002 CL PHILADELPHIA, PENNSYLVANIA SP Amer Soc Hematol C1 Univ Rochester, James P Wilmot Canc Ctr, Rochester, NY 14627 USA. Dana Farber Canc Inst, Boston, MA 02115 USA. Rush Presbyterian St Lukes Med Ctr, Chicago, IL 60612 USA. Massachusetts Gen Hosp, Boston, MA 02114 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2002 VL 100 IS 11 MA 596 BP 159A EP 159A PN 1 PG 1 WC Hematology SC Hematology GA 614JK UT WOS:000179184700597 ER PT J AU Song, HD Liu, TX Wu, XY Zhou, Y Sun, XJ Chen, SJ Chen, Z Look, TA Zon, LI AF Song, HD Liu, TX Wu, XY Zhou, Y Sun, XJ Chen, SJ Chen, Z Look, TA Zon, LI TI Gene expression profiling in the zebrafish kidney marrow tissue. SO BLOOD LA English DT Meeting Abstract CT 44th Annual Meeting of the American-Society-of-Hematology CY DEC 06-10, 2002 CL PHILADELPHIA, PENNSYLVANIA SP Amer Soc Hematol C1 Shanghai Med Univ 2, State Key Lab Med Genom, Shanghai, Peoples R China. Shanghai Med Univ 2, Ruijin Hosp, Shanghai Inst Hematol, Shanghai, Peoples R China. Dana Farber Canc Inst, Dept Pediat Oncol, Boston, MA 02115 USA. Childrens Hosp, Dept Med, Div Hematol Oncol, Boston, MA 02115 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2002 VL 100 IS 11 MA 4131 BP 161B EP 161B PN 2 PG 1 WC Hematology SC Hematology GA 614JL UT WOS:000179184800674 ER PT J AU Shelley, CS Da Silva, N Bharti, AK AF Shelley, CS Da Silva, N Bharti, AK TI The promoter of the gene encoding the leukocyte anti-adhesion molecule CD43 is repressed by the single-stranded DNA binding proteins hnRNP-K and Pur alpha SO BLOOD LA English DT Meeting Abstract CT 44th Annual Meeting of the American-Society-of-Hematology CY DEC 06-10, 2002 CL PHILADELPHIA, PENNSYLVANIA SP Amer Soc Hematol C1 Harvard Univ, Massachusetts Gen Hosp, Sch Med, Renal Unit, Charlestown, MA USA. Dana Farber Canc Inst, Boston, MA 02115 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2002 VL 100 IS 11 MA 4137 BP 162B EP 162B PN 2 PG 1 WC Hematology SC Hematology GA 614JL UT WOS:000179184800680 ER PT J AU Cortes, JE Daley, G Talpaz, M O'Brien, S Garcia-Manero, G Giles, F Faderl, S Pate, O Zaknoen, S Kantarjian, H AF Cortes, JE Daley, G Talpaz, M O'Brien, S Garcia-Manero, G Giles, F Faderl, S Pate, O Zaknoen, S Kantarjian, H TI Pilot study of SCH66336 (Lonafarnib), a farnesyl transferase inhibitor (FTI), in patients with chronic myeloid leukemia (CML) in chronic or accelerated phase resistant or refractory to imatinib. SO BLOOD LA English DT Meeting Abstract CT 44th Annual Meeting of the American-Society-of-Hematology CY DEC 06-10, 2002 CL PHILADELPHIA, PENNSYLVANIA SP Amer Soc Hematol C1 Univ Texas, MD Anderson Canc Ctr, Houston, TX 77030 USA. Whitehead Inst, Boston, MA USA. Massachusetts Gen Hosp, Boston, MA 02114 USA. Schering Plough Corp, Res Inst, Kenilworth, NJ 07033 USA. NR 0 TC 13 Z9 13 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 NOV 16 PY 2002 VL 100 IS 11 MA 614 BP 164A EP 164A PN 1 PG 1 WC Hematology SC Hematology GA 614JK UT WOS:000179184700615 ER PT J AU Mauro, MJ O'Dwyer, ME Stone, RM Walker, T Wiese, A Druker, BJ AF Mauro, MJ O'Dwyer, ME Stone, RM Walker, T Wiese, A Druker, BJ TI Preliminary evaluation of the combination of imatinib mesylate (Gleevec) with low dose Ara-C as initial therapy for newly diagnosed chronic phase CML. SO BLOOD LA English DT Meeting Abstract CT 44th Annual Meeting of the American-Society-of-Hematology CY DEC 06-10, 2002 CL PHILADELPHIA, PENNSYLVANIA SP Amer Soc Hematol C1 Oregon Hlth Sci Univ, Portland, OR 97201 USA. Dana Farber Canc Inst, Boston, MA 02115 USA. NR 0 TC 4 Z9 4 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 NOV 16 PY 2002 VL 100 IS 11 MA 617 BP 165A EP 165A PN 1 PG 1 WC Hematology SC Hematology GA 614JK UT WOS:000179184700618 ER PT J AU Mitsiades, CS Mitsiades, N Kung, AL Shringapurne, R Poulaki, V Richardson, PG Liberman, TA Munshi, NC Loukopoulos, D Anderson, KC AF Mitsiades, CS Mitsiades, N Kung, AL Shringapurne, R Poulaki, V Richardson, PG Liberman, TA Munshi, NC Loukopoulos, D Anderson, KC TI The IGF/IGF-1R system is a major therapeutic target for multiple myeloma, other hematologic malignancies and solid tumors. SO BLOOD LA English DT Meeting Abstract CT 44th Annual Meeting of the American-Society-of-Hematology CY DEC 06-10, 2002 CL PHILADELPHIA, PENNSYLVANIA SP Amer Soc Hematol C1 Harvard Univ, Sch Med, Dana Farber Canc Inst, Jerome Lipper Multiple Myloma Ctr, Boston, MA 02115 USA. Harvard Univ, Sch Med, Dana Farber Canc Inst, Dept Cell Biol, Boston, MA 02115 USA. Harvard Univ, Sch Med, Harvard Inst Med, Boston, MA USA. Univ Athens, Sch Med, Dept Internal Med 1, GR-11527 Athens, Greece. NR 0 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 NOV 16 PY 2002 VL 100 IS 11 MA 637 BP 170A EP 170A PN 1 PG 1 WC Hematology SC Hematology GA 614JK UT WOS:000179184700638 ER PT J AU Baek, KH Kim, YS Kim, MS Choi, HK Lim, SK Shin, JM D'Andrea, AD AF Baek, KH Kim, YS Kim, MS Choi, HK Lim, SK Shin, JM D'Andrea, AD TI An IL-3-induced deubiquitinating enzyme in B-lymphocytes. SO BLOOD LA English DT Meeting Abstract CT 44th Annual Meeting of the American-Society-of-Hematology CY DEC 06-10, 2002 CL PHILADELPHIA, PENNSYLVANIA SP Amer Soc Hematol C1 Pochon CHA Univ, CHA Gen Hosp, Coll Med, Therapy Res Inst, Seoul, South Korea. Harvard Univ, Sch Med, Dana Farber Canc Inst, Dept Pediat Oncol, Boston, MA 02115 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2002 VL 100 IS 11 MA 4186 BP 172B EP 172B PN 2 PG 1 WC Hematology SC Hematology GA 614JL UT WOS:000179184800729 ER PT J AU Antin, JH Edwin, AP Kim, H Parikh, B Cutler, C Ho, VT Lee, SJ Soiffer, RJ AF Antin, JH Edwin, AP Kim, H Parikh, B Cutler, C Ho, VT Lee, SJ Soiffer, RJ TI Combination sirolimus, tacrolimus, and methotrexate to prevent graft-vs-host disease (GVHD) after unrelated donor or mismatched family-member marrow transplantation. SO BLOOD LA English DT Meeting Abstract CT 44th Annual Meeting of the American-Society-of-Hematology CY DEC 06-10, 2002 CL PHILADELPHIA, PENNSYLVANIA SP Amer Soc Hematol C1 Dana Farber Canc Inst, Boston, MA 02115 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2002 VL 100 IS 11 MA 654 BP 174A EP 175A PN 1 PG 2 WC Hematology SC Hematology GA 614JK UT WOS:000179184700655 ER PT J AU Sackstein, R Antin, JH Soiffer, R Spitzer, T Gonzalez, S AF Sackstein, R Antin, JH Soiffer, R Spitzer, T Gonzalez, S TI Use of laser reflectance confocal microscopy to diagnose acute cutaneous graft-versus-host disease (GVHD). SO BLOOD LA English DT Meeting Abstract CT 44th Annual Meeting of the American-Society-of-Hematology CY DEC 06-10, 2002 CL PHILADELPHIA, PENNSYLVANIA SP Amer Soc Hematol C1 Brigham & Womens Hosp, Boston, MA 02115 USA. Massachusetts Gen Hosp, Boston, MA 02114 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2002 VL 100 IS 11 MA 653 BP 174A EP 174A PN 1 PG 1 WC Hematology SC Hematology GA 614JK UT WOS:000179184700654 ER PT J AU Serna, DS Zhang, MJ Baker, KS Eapen, M Horowitz, MM Klein, JP Lee, SJ Rizzo, JD Loberiza, FR AF Serna, DS Zhang, MJ Baker, KS Eapen, M Horowitz, MM Klein, JP Lee, SJ Rizzo, JD Loberiza, FR TI Trends in survival rates by race after allogeneic hematopoietic stem cell transplantation for leukemia in the United States and Canada. SO BLOOD LA English DT Meeting Abstract CT 44th Annual Meeting of the American-Society-of-Hematology CY DEC 06-10, 2002 CL PHILADELPHIA, PENNSYLVANIA SP Amer Soc Hematol C1 Med Coll Wisconsin, Int Bone Marrow Transplant Registry, Milwaukee, WI 53226 USA. Med Coll Wisconsin, Div Biostat, Milwaukee, WI 53226 USA. Univ Minnesota, Pediat Blood & Marrow Transplant Program, Minneapolis, MN 55455 USA. Dana Farber Canc Inst, Ctr Outcomes & Policy Res, Boston, MA 02115 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2002 VL 100 IS 11 MA 696 BP 186A EP 186A PN 1 PG 1 WC Hematology SC Hematology GA 614JK UT WOS:000179184700697 ER PT J AU Zinkel, SS Ong, CC Ferguson, DO Iwasaki, H Akashi, K Bronson, RT Kutok, JL Alt, FW Korsmeyer, SJ AF Zinkel, SS Ong, CC Ferguson, DO Iwasaki, H Akashi, K Bronson, RT Kutok, JL Alt, FW Korsmeyer, SJ TI Pro-apoptotic BID is required for myeloid homeostasis and tumor suppression. SO BLOOD LA English DT Meeting Abstract CT 44th Annual Meeting of the American-Society-of-Hematology CY DEC 06-10, 2002 CL PHILADELPHIA, PENNSYLVANIA SP Amer Soc Hematol C1 Harvard Univ, Sch Med, Dana Farber Canc Inst, Howard Hughes Med Inst,Dept Pathol, Boston, MA 02115 USA. Harvard Univ, Sch Med, Dana Farber Canc Inst, Howard Hughes Med Inst,Dept Med, Boston, MA 02115 USA. Harvard Univ, Childrens Hosp, Sch Med,Dept Genet, Howard Hughes Med Inst,Div Immunol,Ctr Blood Res, Boston, MA 02115 USA. Harvard Univ, Sch Med, Dana Farber Canc Inst, Dept Pathol, Boston, MA 02115 USA. Harvard Univ, Sch Med, Dana Farber Canc Inst, Dept Canc Immunol & AIDS, Boston, MA 02115 USA. Harvard Univ, Brigham & Womens Hosp, Sch Med, Div Genet, Boston, MA 02115 USA. Harvard Univ, Brigham & Womens Hosp, Sch Med, Dept Pathol, Boston, MA 02115 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2002 VL 100 IS 11 MA 716 BP 191A EP 191A PN 1 PG 1 WC Hematology SC Hematology GA 614JK UT WOS:000179184700717 ER PT J AU De Angelo, DJ Schiffer, C Stone, R Amrein, P Fernandez, H Bradstock, K Tallman, M Foran, J Juliusson, G Liu, D Paul, C Russo, D Stenke, L Leopold, L Stevenson, D Richie, M Berger, M AF De Angelo, DJ Schiffer, C Stone, R Amrein, P Fernandez, H Bradstock, K Tallman, M Foran, J Juliusson, G Liu, D Paul, C Russo, D Stenke, L Leopold, L Stevenson, D Richie, M Berger, M TI Interim analysis of a phase II study of the safety and efficacy of gemtuzumab ozogamicin (Mylotarg (R)) given in combination with cytarabine and daunorubicin to patients < 60 years old with untreated acute myeloid leukemia. SO BLOOD LA English DT Meeting Abstract CT 44th Annual Meeting of the American-Society-of-Hematology CY DEC 06-10, 2002 CL PHILADELPHIA, PENNSYLVANIA SP Amer Soc Hematol C1 Dana Farber Canc Inst, Boston, MA 02115 USA. Wayne State Univ, Sch Med, Detroit, MI 48202 USA. Massachusetts Gen Hosp, Boston, MA 02114 USA. Univ Miami, Miami, FL 33152 USA. Westmead Hosp, Westmead, NSW 2145, Australia. Northwestern Univ, Sch Med, Chicago, IL USA. Univ Nebraska, Sch Med, Omaha, NE 68198 USA. Linkoping Univ, S-58183 Linkoping, Sweden. New York Med Coll, Valhalla, NY 10595 USA. Huddinge Univ Hosp, S-14186 Huddinge, Sweden. Udine Univ Hosp, Udine, Italy. Karolinska Hosp, S-10401 Stockholm, Sweden. Wyeth Ayerst Res, Collegeville, PA USA. RI Russo, Domenico/C-3947-2011 NR 0 TC 13 Z9 14 U1 0 U2 3 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 NOV 16 PY 2002 VL 100 IS 11 MA 745 BP 198A EP 199A PN 1 PG 2 WC Hematology SC Hematology GA 614JK UT WOS:000179184700746 ER PT J AU De Angelo, DJ Yu, DH Dodge, RK Coutre, SE Mitchell, BS Stone, RM Stopeck, AT Larson, RA AF De Angelo, DJ Yu, DH Dodge, RK Coutre, SE Mitchell, BS Stone, RM Stopeck, AT Larson, RA TI A phase II study of 2-amino-beta-D-arabinosyl-6-methoxy-9H-purine (506U78) in patients with relapsed or refractory T-lineage acute lymphoblastic leukemia (ALL) or lymphoblastic lymphoma (LBL): CALGB study 19801. SO BLOOD LA English DT Meeting Abstract CT 44th Annual Meeting of the American-Society-of-Hematology CY DEC 06-10, 2002 CL PHILADELPHIA, PENNSYLVANIA SP Amer Soc Hematol C1 Dana Farber Canc Inst, Boston, MA 02115 USA. Duke Univ, CALGB Stat Ctr, Durham, NC 27706 USA. Stanford Univ, Sch Med, Stanford, CA 94305 USA. Univ N Carolina, Chapel Hill, NC 27515 USA. Univ Arizona, Arizona Canc Ctr, Tucson, AZ USA. SW Oncol Grp, San Antonio, TX USA. Canc & Leukemia Grp B, Chicago, IL USA. RI Russo, Domenico/C-3947-2011 NR 0 TC 13 Z9 14 U1 0 U2 3 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 NOV 16 PY 2002 VL 100 IS 11 MA 743 BP 198A EP 198A PN 1 PG 1 WC Hematology SC Hematology GA 614JK UT WOS:000179184700744 ER PT J AU Letai, A Bassik, MC Walensky, L Sorcinelli, MD Weiler, S Korsmeyer, SJ AF Letai, A Bassik, MC Walensky, L Sorcinelli, MD Weiler, S Korsmeyer, SJ TI Distinct BH3 domains either sensitize or activate mitochondrial apoptosis serving as prototype cancer therapeutics. SO BLOOD LA English DT Meeting Abstract CT 44th Annual Meeting of the American-Society-of-Hematology CY DEC 06-10, 2002 CL PHILADELPHIA, PENNSYLVANIA SP Amer Soc Hematol C1 Dana Farber Canc Inst, Boston, MA 02115 USA. NR 0 TC 0 Z9 0 U1 1 U2 4 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2002 VL 100 IS 11 MA 749 BP 200A EP 200A PN 1 PG 1 WC Hematology SC Hematology GA 614JK UT WOS:000179184700750 ER PT J AU Lan, L Jie, Y Levin, L Qin, L Weir, E Mann, RB Borowitz, MJ Mueller, N Mauch, PM Diehl, LF Herman, JG Ambinder, RF AF Lan, L Jie, Y Levin, L Qin, L Weir, E Mann, RB Borowitz, MJ Mueller, N Mauch, PM Diehl, LF Herman, JG Ambinder, RF TI Viral DNA in serum and plasma of patients with Epstein-Barr Virus (EBV)-associated Hodgkin's lymphoma (HL) may be tumor derived and appears years before diagnosis. SO BLOOD LA English DT Meeting Abstract CT 44th Annual Meeting of the American-Society-of-Hematology CY DEC 06-10, 2002 CL PHILADELPHIA, PENNSYLVANIA SP Amer Soc Hematol C1 Johns Hopkins Univ, Sch Med, Kimmel Canc Ctr, Baltimore, MD USA. Walter Reed Army Inst Res, Silver Spring, MD USA. Univ Massachusetts, Sch Med, Worcester, MA USA. Harvard Sch Publ Hlth, Boston, MA USA. Harvard Univ, Sch Med, Dana Farber Canc Inst, Boston, MA 02115 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2002 VL 100 IS 11 MA 753 BP 201A EP 201A PN 1 PG 1 WC Hematology SC Hematology GA 614JK UT WOS:000179184700754 ER PT J AU Wu, EX Aguiar, RCT Savage, KJ Kutok, JL Wang, FF Aster, JC Shipp, MA AF Wu, EX Aguiar, RCT Savage, KJ Kutok, JL Wang, FF Aster, JC Shipp, MA TI PKC beta: A rational therapeutic target in diffuse large B-cell lymphoma. SO BLOOD LA English DT Meeting Abstract CT 44th Annual Meeting of the American-Society-of-Hematology CY DEC 06-10, 2002 CL PHILADELPHIA, PENNSYLVANIA SP Amer Soc Hematol C1 Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02115 USA. Brigham & Womens Hosp, Dept Pathol, Boston, MA 02115 USA. NR 0 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 NOV 16 PY 2002 VL 100 IS 11 MA 757 BP 202A EP 202A PN 1 PG 1 WC Hematology SC Hematology GA 614JK UT WOS:000179184700758 ER PT J AU Mohi, MG Sattler, M Li, SG Van Etten, RA Gu, HH Griffin, JD Neel, BG AF Mohi, MG Sattler, M Li, SG Van Etten, RA Gu, HH Griffin, JD Neel, BG TI Gab2 is required for transformation and leukemogenesis by Bcr/Abl. SO BLOOD LA English DT Meeting Abstract CT 44th Annual Meeting of the American-Society-of-Hematology CY DEC 06-10, 2002 CL PHILADELPHIA, PENNSYLVANIA SP Amer Soc Hematol C1 Harvard Univ, Beth Israel Deaconess Med Ctr, Sch Med, Dept Med,Canc Biol Program, Boston, MA 02215 USA. Dana Farber Canc Inst, Dept Adult Oncol, Boston, MA 02115 USA. Harvard Univ, Sch Med, Ctr Blood Res, Dept Genet, Boston, MA 02115 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2002 VL 100 IS 11 MA 764 BP 204A EP 204A PN 1 PG 1 WC Hematology SC Hematology GA 614JK UT WOS:000179184700765 ER PT J AU Smith, KM Van Etten, RA AF Smith, KM Van Etten, RA TI Oligomerization of Bcr-Abl via the Bcr coiled-coil domain overcomes intramolecular inhibition by the SH3 domain through autophosphorylation. SO BLOOD LA English DT Meeting Abstract CT 44th Annual Meeting of the American-Society-of-Hematology CY DEC 06-10, 2002 CL PHILADELPHIA, PENNSYLVANIA SP Amer Soc Hematol C1 Harvard Univ, Sch Med, Ctr Blood Res, Boston, MA 02115 USA. Harvard Univ, Sch Med, Dept Genet, Boston, MA USA. NR 0 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 NOV 16 PY 2002 VL 100 IS 11 MA 766 BP 204A EP 204A PN 1 PG 1 WC Hematology SC Hematology GA 614JK UT WOS:000179184700767 ER PT J AU Shammas, MA Reis, RJS Ayyadevara, S Thaden, J Davies, F Morgan, G Cheng, L Anderson, KC Munshi, NC AF Shammas, MA Reis, RJS Ayyadevara, S Thaden, J Davies, F Morgan, G Cheng, L Anderson, KC Munshi, NC TI Molecular mechanisms of genomic instability in multiple myeloma. SO BLOOD LA English DT Meeting Abstract CT 44th Annual Meeting of the American-Society-of-Hematology CY DEC 06-10, 2002 CL PHILADELPHIA, PENNSYLVANIA SP Amer Soc Hematol C1 Boston VA Hlth Care Syst, W Roxbury, MA USA. Harvard Univ, Sch Med, Boston, MA USA. Dana Farber Canc Inst, Boston, MA 02115 USA. Univ Arkansas Med Sci, Dept Geriatr, Little Rock, AR 72205 USA. Univ Arkansas Med Sci, Dept Biochem & Mol Biol, Little Rock, AR 72205 USA. Cent Arkansas Vet Hlth Care Syst, Dept Geriatr, Little Rock, AR USA. Univ Leeds, Leeds LS2 9JT, W Yorkshire, England. Leeds Gen Infirmary, Leeds, W Yorkshire, England. RI Shmookler Reis, Robert/C-4112-2009 NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2002 VL 100 IS 11 MA 780 BP 208A EP 208A PN 1 PG 1 WC Hematology SC Hematology GA 614JK UT WOS:000179184700781 ER PT J AU Treon, SP Wasi, P Emmanouilides, CA Frankel, SR Kimby, E Lister, A Morel, P Kelliher, A Branagan, A Preffer, F Anderson, KC AF Treon, SP Wasi, P Emmanouilides, CA Frankel, SR Kimby, E Lister, A Morel, P Kelliher, A Branagan, A Preffer, F Anderson, KC TI Combination therapy with rituximab and fludarabine is highly active in Waldenstrom's macroglobulinemia. SO BLOOD LA English DT Meeting Abstract CT 44th Annual Meeting of the American-Society-of-Hematology CY DEC 06-10, 2002 CL PHILADELPHIA, PENNSYLVANIA SP Amer Soc Hematol C1 Dana Farber Canc Inst, Boston, MA 02115 USA. McMaster Univ, Med Ctr, Hamilton, ON L8S 4L8, Canada. Univ Calif Los Angeles, Med Ctr, Los Angeles, CA 90024 USA. Greenebaum Canc Ctr, Baltimore, MD USA. Karolinska Inst, S-10401 Stockholm, Sweden. St Bartholomews Hosp & Canc Res, London, England. Ctr Hosp Schaffner, Lens, France. Massachusetts Gen Hosp, Boston, MA 02114 USA. NR 0 TC 9 Z9 9 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 NOV 16 PY 2002 VL 100 IS 11 MA 794 BP 211A EP 211A PN 1 PG 1 WC Hematology SC Hematology GA 614JK UT WOS:000179184700795 ER PT J AU Miklos, DB Kim, HT Zorn, E Hochberg, EP Guo, LX Mattes-Ritz, A Soiffer, RJ Antin, JH Ritz, J AF Miklos, DB Kim, HT Zorn, E Hochberg, EP Guo, LX Mattes-Ritz, A Soiffer, RJ Antin, JH Ritz, J TI Antibody response to H-Y minor histocompatibility antigen DBY is detected in male patients after allogeneic stem cell transplantation and in normal female donors. SO BLOOD LA English DT Meeting Abstract CT 44th Annual Meeting of the American-Society-of-Hematology CY DEC 06-10, 2002 CL PHILADELPHIA, PENNSYLVANIA SP Amer Soc Hematol C1 Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02115 USA. Dana Farber Canc Inst, Dept Biostat, Boston, MA 02115 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2002 VL 100 IS 11 MA 802 BP 213A EP 214A PN 1 PG 2 WC Hematology SC Hematology GA 614JK UT WOS:000179184700803 ER PT J AU Monahan, PE Rabinowitz, JE Elia, JR Yi, T Ntziachristo, V Sorg, BS Dewhirst, MW Weissleder, R Samulski, RJ AF Monahan, PE Rabinowitz, JE Elia, JR Yi, T Ntziachristo, V Sorg, BS Dewhirst, MW Weissleder, R Samulski, RJ TI Gene expression profiling of AAV serotype 1-5 vectors in adult and neonatal animals using in vivo bioluminescence imaging. SO BLOOD LA English DT Meeting Abstract CT 44th Annual Meeting of the American-Society-of-Hematology CY DEC 06-10, 2002 CL PHILADELPHIA, PENNSYLVANIA SP Amer Soc Hematol C1 Univ N Carolina, Gene Therapy Ctr, Chapel Hill, NC 27515 USA. Massachusetts Gen Hosp, Charlestown, MA USA. Duke Univ, Durham, NC 27706 USA. NR 0 TC 0 Z9 0 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 NOV 16 PY 2002 VL 100 IS 11 MA 826 BP 220A EP 220A PN 1 PG 1 WC Hematology SC Hematology GA 614JK UT WOS:000179184700827 ER PT J AU Abel, GA Kuter, DJ AF Abel, GA Kuter, DJ TI Association of thrombocytopenia with continuous venovenous hemofiltration. SO BLOOD LA English DT Meeting Abstract CT 44th Annual Meeting of the American-Society-of-Hematology CY DEC 06-10, 2002 CL PHILADELPHIA, PENNSYLVANIA SP Amer Soc Hematol C1 Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Med, Boston, MA USA. Harvard Univ, Massachusetts Gen Hosp, Sch Med, Div Hematol & Oncol, Boston, MA USA. NR 0 TC 0 Z9 0 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 NOV 16 PY 2002 VL 100 IS 11 MA 830 BP 221A EP 221A PN 1 PG 1 WC Hematology SC Hematology GA 614JK UT WOS:000179184700831 ER PT J AU Huang, SC Liu, ES Hui, C Benz, EJ AF Huang, SC Liu, ES Hui, C Benz, EJ TI Comparative analysis of cis-elements regulating protein 4.1R exon 16 splicing in cells that predominantly include or exclude exon 16 in vivo. SO BLOOD LA English DT Meeting Abstract CT 44th Annual Meeting of the American-Society-of-Hematology CY DEC 06-10, 2002 CL PHILADELPHIA, PENNSYLVANIA SP Amer Soc Hematol C1 Dana Farber Canc Inst, Boston, MA 02115 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2002 VL 100 IS 11 MA 841 BP 223A EP 224A PN 1 PG 2 WC Hematology SC Hematology GA 614JK UT WOS:000179184700842 ER PT J AU Zhou, AY Huang, SC Benz, EJ AF Zhou, AY Huang, SC Benz, EJ TI Regulatory cis-elements governing protein 4.1R exon 17a splicing in skeletal muscle. SO BLOOD LA English DT Meeting Abstract CT 44th Annual Meeting of the American-Society-of-Hematology CY DEC 06-10, 2002 CL PHILADELPHIA, PENNSYLVANIA SP Amer Soc Hematol C1 Dana Farber Canc Inst, Boston, MA 02115 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2002 VL 100 IS 11 MA 846 BP 224A EP 225A PN 1 PG 2 WC Hematology SC Hematology GA 614JK UT WOS:000179184700847 ER PT J AU Migliaccio, AR Rana, RA Sanchez, M Lorenzini, R Centurione, L Bianchi, L Vannucchi, AM Migliaccio, G Orkin, S AF Migliaccio, AR Rana, RA Sanchez, M Lorenzini, R Centurione, L Bianchi, L Vannucchi, AM Migliaccio, G Orkin, S TI A new function for GATA-1 as regulator of mast cell differentiation revealed by the phenotype of the GATA-1 knock down mouse. SO BLOOD LA English DT Meeting Abstract CT 44th Annual Meeting of the American-Society-of-Hematology CY DEC 06-10, 2002 CL PHILADELPHIA, PENNSYLVANIA SP Amer Soc Hematol C1 Univ Chieti, Dept Biomorphol, Chieti, Italy. Ist Super Sanita, Biochim Clin Lab, I-00161 Rome, Italy. Ist Super Sanita, Cell Biol Lab, I-00161 Rome, Italy. Ist Super Sanita, SQSA, I-00161 Rome, Italy. Univ Florence, I-50121 Florence, Italy. Harvard Univ, Sch Med, Dana Farber Canc Inst, Dept Pediat Oncol, Boston, MA 02115 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2002 VL 100 IS 11 MA 913 BP 242A EP 242A PN 1 PG 1 WC Hematology SC Hematology GA 614JK UT WOS:000179184700914 ER PT J AU Germeshausen, M Ballmaier, M Schulze, H Welte, K AF Germeshausen, M Ballmaier, M Schulze, H Welte, K TI Heterogeneity in expression of mutated versus wild type neutrophil elastase mRNA in patients with congenital and cyclic neutropenia. SO BLOOD LA English DT Meeting Abstract CT 44th Annual Meeting of the American-Society-of-Hematology CY DEC 06-10, 2002 CL PHILADELPHIA, PENNSYLVANIA SP Amer Soc Hematol C1 Hannover Med Sch, Hannover, Germany. Dana Farber Canc Inst, Boston, MA 02115 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2002 VL 100 IS 11 MA 922 BP 244A EP 244A PN 1 PG 1 WC Hematology SC Hematology GA 614JK UT WOS:000179184700923 ER PT J AU Sansores-Garcia, L Nigam, R Agrawal, A Siddiqi, T Adachi, R AF Sansores-Garcia, L Nigam, R Agrawal, A Siddiqi, T Adachi, R TI Localization, interaction and function of Munc-18 proteins and Syntaxins in mast cell exocytosis. SO BLOOD LA English DT Meeting Abstract CT 44th Annual Meeting of the American-Society-of-Hematology CY DEC 06-10, 2002 CL PHILADELPHIA, PENNSYLVANIA SP Amer Soc Hematol C1 Baylor Coll Med, Houston, TX 77030 USA. Houston VA Med Ctr, Houston, TX USA. RI Agrawal, Anurag/A-7312-2009 NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2002 VL 100 IS 11 MA 926 BP 245A EP 245A PN 1 PG 1 WC Hematology SC Hematology GA 614JK UT WOS:000179184700927 ER PT J AU Hsu, K Liu, TX Rhodes, J Kanki, JP Look, AT AF Hsu, K Liu, TX Rhodes, J Kanki, JP Look, AT TI Expression of green fluorescent protein (GFP) in transgenic zebrafish embryos under the control of the zebrafish MPO promoter. SO BLOOD LA English DT Meeting Abstract CT 44th Annual Meeting of the American-Society-of-Hematology CY DEC 06-10, 2002 CL PHILADELPHIA, PENNSYLVANIA SP Amer Soc Hematol C1 Harvard Univ, Sch Med, Dana Farber Canc Inst, Dept Pediat Oncol, Boston, MA 02115 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2002 VL 100 IS 11 MA 931 BP 246A EP 246A PN 1 PG 1 WC Hematology SC Hematology GA 614JK UT WOS:000179184700932 ER PT J AU Kroll, MH Resendiz, JC Ji, GL Berndt, MC Feng, SJ AF Kroll, MH Resendiz, JC Ji, GL Berndt, MC Feng, SJ TI Purinergic P2Y(12) receptor blockade inhibits shear-induced platelet aggregation by inhibiting phosphatidylinositol 3-kinase. SO BLOOD LA English DT Meeting Abstract CT 44th Annual Meeting of the American-Society-of-Hematology CY DEC 06-10, 2002 CL PHILADELPHIA, PENNSYLVANIA SP Amer Soc Hematol C1 VA Med Ctr, Houston, TX USA. Baylor Coll Med, Houston, TX 77030 USA. Rice Univ, Houston, TX 77251 USA. Wihuri Res Inst, SF-00140 Helsinki, Finland. Monash Univ, Clayton, Vic 3168, Australia. RI Berndt, Michael/D-5580-2012 NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2002 VL 100 IS 11 MA 959 BP 252A EP 252A PN 1 PG 1 WC Hematology SC Hematology GA 614JK UT WOS:000179184700960 ER PT J AU Endoh, M Ogawa, M Orkin, S Nishikawa, S AF Endoh, M Ogawa, M Orkin, S Nishikawa, S TI SCL/tal-1 dependent process determines a competence to select the definitive hematopoietic lineage prior to endothelial differentiation. SO BLOOD LA English DT Meeting Abstract CT 44th Annual Meeting of the American-Society-of-Hematology CY DEC 06-10, 2002 CL PHILADELPHIA, PENNSYLVANIA SP Amer Soc Hematol C1 Kyoto Univ, Fac Med, Dept Mol Genet, Kyoto, Japan. Kumamoto Univ, Inst Mol Embryol & Genet, Dept Cell Differentiat, Kumamoto, Japan. Dana Farber Canc Inst, Dept Pediat Oncol, Boston, MA 02115 USA. Harvard Univ, Childrens Hosp, Sch Med, Boston, MA 02115 USA. Howard Hughes Med Inst, Boston, MA 02115 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2002 VL 100 IS 11 MA 1129 BP 294A EP 294A PN 1 PG 1 WC Hematology SC Hematology GA 614JK UT WOS:000179184701129 ER PT J AU Rodrigues, NP Tao, C Ying, S Forkert, R Cohen, KS Vyas, P Scadden, DT AF Rodrigues, NP Tao, C Ying, S Forkert, R Cohen, KS Vyas, P Scadden, DT TI Stem cells deficient in p21Cip1/Waf1 compete poorly in establishing long-term bone marrow hematopoiesis. SO BLOOD LA English DT Meeting Abstract CT 44th Annual Meeting of the American-Society-of-Hematology CY DEC 06-10, 2002 CL PHILADELPHIA, PENNSYLVANIA SP Amer Soc Hematol C1 Harvard Univ, Massachusetts Gen Hosp, Sch Med, MGH Canc Ctr, Boston, MA USA. Harvard Univ, Massachusetts Gen Hosp, Sch Med, AIDS Res Ctr, Boston, MA USA. Univ Pittsburgh, Inst Canc, Pittsburgh, PA 15260 USA. Univ Oxford, Weatherall Inst Mol Med, MRC Hematol Unit, Oxford OX1 2JD, England. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2002 VL 100 IS 11 MA 1130 BP 294A EP 294A PN 1 PG 1 WC Hematology SC Hematology GA 614JK UT WOS:000179184701130 ER PT J AU Banerji, L Glassford, J Soeiro, R Skarell, SM Holman, M Klaus, GGB Koyasu, S Lam, EWF AF Banerji, L Glassford, J Soeiro, R Skarell, SM Holman, M Klaus, GGB Koyasu, S Lam, EWF TI The B-cell receptor (BCR) targets cyclin D2 via Btk and the p85 alpha subunit of PI3-K to induce cell cycle progression in primary mouse B-cells. SO BLOOD LA English DT Meeting Abstract CT 44th Annual Meeting of the American-Society-of-Hematology CY DEC 06-10, 2002 CL PHILADELPHIA, PENNSYLVANIA SP Amer Soc Hematol C1 Univ London Imperial Coll Sci Technol & Med, Sch Med, Dept Canc Med, London, England. Natl Inst Med Res, Dept Cellular Immunol, London NW7 1AA, England. Keio Univ, Sch Med, Dept Microbiol, Tokyo 160, Japan. Harvard Univ, Sch Med, Dana Farber Canc Inst, Boston, MA 02115 USA. NR 0 TC 0 Z9 0 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 NOV 16 PY 2002 VL 100 IS 11 MA 1158 BP 300A EP 300A PN 1 PG 1 WC Hematology SC Hematology GA 614JK UT WOS:000179184701158 ER PT J AU Kamizono, S Wu, WS Ferrando, AA Look, AT AF Kamizono, S Wu, WS Ferrando, AA Look, AT TI Increased apoptosis of hematopoietic stem and progenitor cells after DNA damage in mice lacking slug. SO BLOOD LA English DT Meeting Abstract CT 44th Annual Meeting of the American-Society-of-Hematology CY DEC 06-10, 2002 CL PHILADELPHIA, PENNSYLVANIA SP Amer Soc Hematol C1 Harvard Univ, Sch Med, Dana Farber Canc Inst, Boston, MA 02115 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2002 VL 100 IS 11 MA 1171 BP 303A EP 303A PN 1 PG 1 WC Hematology SC Hematology GA 614JK UT WOS:000179184701171 ER PT J AU Wu, WS Kamizono, S Iwasaki, H Akashi, K Look, AT AF Wu, WS Kamizono, S Iwasaki, H Akashi, K Look, AT TI Slug is a negative regulator of gamma-irradiation-induced apoptosis in hematopoietic stem and progenitor cells. SO BLOOD LA English DT Meeting Abstract CT 44th Annual Meeting of the American-Society-of-Hematology CY DEC 06-10, 2002 CL PHILADELPHIA, PENNSYLVANIA SP Amer Soc Hematol C1 Harvard Univ, Sch Med, Dana Farber Canc Inst, Boston, MA 02115 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2002 VL 100 IS 11 MA 1168 BP 303A EP 303A PN 1 PG 1 WC Hematology SC Hematology GA 614JK UT WOS:000179184701168 ER PT J AU Ferrando, AA Armstrong, SA Neuberg, DS Sallan, SE Silverman, LB Korsmeyer, SJ Look, AT AF Ferrando, AA Armstrong, SA Neuberg, DS Sallan, SE Silverman, LB Korsmeyer, SJ Look, AT TI Gene expression signatures in MLL-rearranged B-precursor and T lineage acute leukemias: Dominance of HOX dysregulation. SO BLOOD LA English DT Meeting Abstract CT 44th Annual Meeting of the American-Society-of-Hematology CY DEC 06-10, 2002 CL PHILADELPHIA, PENNSYLVANIA SP Amer Soc Hematol C1 Harvard Univ, Sch Med, Dana Farber Canc Inst, Boston, MA 02115 USA. Harvard Univ, Sch Med, Dana Farber Canc Inst, Howard Hughes Med Inst, Boston, MA 02115 USA. Childrens Hosp, Boston, MA 02115 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2002 VL 100 IS 11 MA 1201 BP 310A EP 310A PN 1 PG 1 WC Hematology SC Hematology GA 614JK UT WOS:000179184701201 ER PT J AU Chiaretti, S Ding, BY Gentleman, R Mauro, FR Guarini, A Gaidano, G Ritz, J Foa, R AF Chiaretti, S Ding, BY Gentleman, R Mauro, FR Guarini, A Gaidano, G Ritz, J Foa, R TI Gene expression profiling in chronic lymphocityc leukemia (CLL): Correlation with disease stability and progression, and p53 mutations. SO BLOOD LA English DT Meeting Abstract CT 44th Annual Meeting of the American-Society-of-Hematology CY DEC 06-10, 2002 CL PHILADELPHIA, PENNSYLVANIA SP Amer Soc Hematol C1 Harvard Univ, Sch Med, Dana Farber Canc Inst, Ctr Hematol Oncol, Boston, MA 02115 USA. Harvard Univ, Sch Med, Dana Farber Canc Inst, Dept Biostat Sci, Boston, MA 02115 USA. Univ Roma La Sapienza, Dept Cellular Biotechnol & Hematol, I-00185 Rome, Italy. Univ Eastern Piedmont, Dept Med Sci, Novara, Italy. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2002 VL 100 IS 11 MA 1216 BP 314A EP 314A PN 1 PG 1 WC Hematology SC Hematology GA 614JK UT WOS:000179184701216 ER PT J AU Hayashi, T Anderson, KC Steven, SP AF Hayashi, T Anderson, KC Steven, SP TI Rituximab induced antibody dependent cell mediated cytotoxicity (ADCC) is enhanced by thalidomide and its analogue revimid. SO BLOOD LA English DT Meeting Abstract CT 44th Annual Meeting of the American-Society-of-Hematology CY DEC 06-10, 2002 CL PHILADELPHIA, PENNSYLVANIA SP Amer Soc Hematol C1 Dana Farber Canc Inst, Boston, MA 02115 USA. Harvard Univ, Sch Med, Dept Med, Boston, MA USA. NR 0 TC 2 Z9 2 U1 2 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 NOV 16 PY 2002 VL 100 IS 11 MA 4800 BP 314B EP 314B PN 2 PG 1 WC Hematology SC Hematology GA 614JL UT WOS:000179184801343 ER PT J AU Shimamura, A Macari, TJ Svenson, JL D'Andrea, AD AF Shimamura, A Macari, TJ Svenson, JL D'Andrea, AD TI A screen for acquired Fanconi anemia pathway defects in acute myeloid leukemia. SO BLOOD LA English DT Meeting Abstract CT 44th Annual Meeting of the American-Society-of-Hematology CY DEC 06-10, 2002 CL PHILADELPHIA, PENNSYLVANIA SP Amer Soc Hematol C1 Dana Farber Canc Inst, Boston, MA 02115 USA. NR 0 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 NOV 16 PY 2002 VL 100 IS 11 MA 1256 BP 324A EP 324A PN 1 PG 1 WC Hematology SC Hematology GA 614JK UT WOS:000179184701256 ER PT J AU Speckhart, SA Christianson, TA Lensch, MW Bagby, GC AF Speckhart, SA Christianson, TA Lensch, MW Bagby, GC TI Screening for Fanconi pathway dysfunction using low numbers of CD34+ cells. SO BLOOD LA English DT Meeting Abstract CT 44th Annual Meeting of the American-Society-of-Hematology CY DEC 06-10, 2002 CL PHILADELPHIA, PENNSYLVANIA SP Amer Soc Hematol C1 Oregon Hlth Sci Univ, Inst Canc, Portland, OR 97201 USA. Portland VA Med Ctr, Mol Hematopoiesis Lab, Portland, OR USA. MIT, Whitehead Inst Biomed Res, Boston, MA USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2002 VL 100 IS 11 MA 1255 BP 324A EP 324A PN 1 PG 1 WC Hematology SC Hematology GA 614JK UT WOS:000179184701255 ER PT J AU Gallagher, RE Lee, SJ Sankoorikal, BJ Wiernik, PH Tallman, MS AF Gallagher, RE Lee, SJ Sankoorikal, BJ Wiernik, PH Tallman, MS CA Eastern Cooperative Oncology Grp TI Independent prognostic significance of FLT3 internal tandem duplication (ITD) mutations in acute promyelocytic leukemia (APL) patients treated on ECOG protocol E2491. SO BLOOD LA English DT Meeting Abstract CT 44th Annual Meeting of the American-Society-of-Hematology CY DEC 06-10, 2002 CL PHILADELPHIA, PENNSYLVANIA SP Amer Soc Hematol C1 Albert Einstein Canc Ctr, Bronx, NY USA. Dana Farber Canc Inst, Boston, MA 02115 USA. Our Lady Mercy Med Ctr, Bronx, NY USA. Northwestern Univ, Sch Med, Chicago, IL 60611 USA. Eastern Cooperat Oncol Grp, Brookline, MA USA. NR 0 TC 9 Z9 9 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 NOV 16 PY 2002 VL 100 IS 11 MA 1265 BP 326A EP 326A PN 1 PG 1 WC Hematology SC Hematology GA 614JK UT WOS:000179184701265 ER PT J AU Heinrich, MC Druker, BJ Curtin, PT Paquette, R Sawyers, CL De Angelo, DJ Gilliland, GD Stone, RM Caliguiri, MA Byrd, JC Heaney, ML Nimer, SD Romanko, KP Lambing, JL Lokker, NA Giese, NA Gretler, DD AF Heinrich, MC Druker, BJ Curtin, PT Paquette, R Sawyers, CL De Angelo, DJ Gilliland, GD Stone, RM Caliguiri, MA Byrd, JC Heaney, ML Nimer, SD Romanko, KP Lambing, JL Lokker, NA Giese, NA Gretler, DD TI A "first in man" study of the safety and PK/PD of an oral FLT3 inhibitor (MLN518) in patients with AML or high risk myelodysplasia. SO BLOOD LA English DT Meeting Abstract CT 44th Annual Meeting of the American-Society-of-Hematology CY DEC 06-10, 2002 CL PHILADELPHIA, PENNSYLVANIA SP Amer Soc Hematol C1 Oregon Hlth Sci Univ, Portland, OR 97201 USA. Univ Calif Los Angeles, Med Ctr, Los Angeles, CA 90024 USA. Dana Farber Canc Inst, Boston, MA 02115 USA. Ohio State Univ, Med Ctr, Columbus, OH 43210 USA. Mem Sloan Kettering Canc Ctr, New York, NY 10021 USA. Millennium Pharmaceut Inc, San Francisco, CA USA. RI Sawyers, Charles/G-5327-2016 NR 0 TC 11 Z9 12 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 NOV 16 PY 2002 VL 100 IS 11 MA 1305 BP 336A EP 337A PN 1 PG 2 WC Hematology SC Hematology GA 614JK UT WOS:000179184701305 ER PT J AU Savage, KJ Weng, AP Kutok, JL Pinkus, G Gribben, JG AF Savage, KJ Weng, AP Kutok, JL Pinkus, G Gribben, JG TI Loss of CD20 expression following treatment with anti-CD20 monoclonal antibody in chronic lymphocytic leukemia. SO BLOOD LA English DT Meeting Abstract CT 44th Annual Meeting of the American-Society-of-Hematology CY DEC 06-10, 2002 CL PHILADELPHIA, PENNSYLVANIA SP Amer Soc Hematol C1 Dana Farber Canc Inst, Boston, MA 02115 USA. Harvard Univ, Brigham & Womens Hosp, Sch Med, Boston, MA 02115 USA. RI Weng, Andrew/I-5015-2014 NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2002 VL 100 IS 11 MA 5013 BP 364B EP 364B PN 2 PG 1 WC Hematology SC Hematology GA 614JL UT WOS:000179184801555 ER PT J AU Friedberg, JW Dong, DA Li, SG Kim, H Stephans, K Noonan, K Neuberg, D Gribben, JG Freedman, AS Takvorian, T Battle, TE Frank, DA AF Friedberg, JW Dong, DA Li, SG Kim, H Stephans, K Noonan, K Neuberg, D Gribben, JG Freedman, AS Takvorian, T Battle, TE Frank, DA TI Oral fludarabine (FMP) is highly active in patients (pts) with previously untreated chronic lymphocytic leukemia (CLL), and leads to increased STAT1 levels in vivo. SO BLOOD LA English DT Meeting Abstract CT 44th Annual Meeting of the American-Society-of-Hematology CY DEC 06-10, 2002 CL PHILADELPHIA, PENNSYLVANIA SP Amer Soc Hematol C1 Univ Rochester, James P Wilmot Canc Ctr, Rochester, NY 14627 USA. Dana Farber Canc Inst, Boston, MA 02115 USA. Massachusetts Gen Hosp, Boston, MA 02114 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2002 VL 100 IS 11 MA 1504 BP 388A EP 388A PN 1 PG 1 WC Hematology SC Hematology GA 614JK UT WOS:000179184701505 ER PT J AU Davies, FE Dring, AM Cheng, L Rawstron, AC Shammas, M Chauhan, D Hideshima, T Tai, IT Auclair, D Robinson, E Wong, WH Munshi, NC Anderson, KC Morgan, GJ AF Davies, FE Dring, AM Cheng, L Rawstron, AC Shammas, M Chauhan, D Hideshima, T Tai, IT Auclair, D Robinson, E Wong, WH Munshi, NC Anderson, KC Morgan, GJ TI Presentation myeloma patients with a MGUS gene expression pattern have a trend towards an imporved surivial. SO BLOOD LA English DT Meeting Abstract CT 44th Annual Meeting of the American-Society-of-Hematology CY DEC 06-10, 2002 CL PHILADELPHIA, PENNSYLVANIA SP Amer Soc Hematol C1 Univ Leeds, Acad Dept Haematol & Oncol, Leeds LS2 9JT, W Yorkshire, England. Dana Farber Canc Inst, Dept Adult Oncol, Boston, MA 02115 USA. Harvard Univ, Sch Publ Hlth, Dept Biostat, Boston, MA 02115 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2002 VL 100 IS 11 MA 1511 BP 389A EP 390A PN 1 PG 2 WC Hematology SC Hematology GA 614JK UT WOS:000179184701512 ER PT J AU Fonseca, R Blood, EA Oken, MM Kyle, RA Dewald, GW Van Wier, SA Henderson, KJ Greipp, PR AF Fonseca, R Blood, EA Oken, MM Kyle, RA Dewald, GW Van Wier, SA Henderson, KJ Greipp, PR TI Isotype switch mediated IgH translocations (IgH-TRX) in multiple myeloma (MM) are recurrent, frequently unbalanced and favored with clonal evolution. SO BLOOD LA English DT Meeting Abstract CT 44th Annual Meeting of the American-Society-of-Hematology CY DEC 06-10, 2002 CL PHILADELPHIA, PENNSYLVANIA SP Amer Soc Hematol C1 Mayo Clin, Dept Lab Med & Pathol, Rochester, MN USA. Dana Farber Canc Inst, Dept Biostat Sci, Boston, MA 02115 USA. Abbott NW Hosp, Minneapolis, MN USA. ECOG, Boston, MA USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2002 VL 100 IS 11 MA 1508 BP 389A EP 389A PN 1 PG 1 WC Hematology SC Hematology GA 614JK UT WOS:000179184701509 ER PT J AU Mitsiades, CS Mitsiades, N Bailey, C Gu, XS Joseph, M Fanourakis, G Munshi, NC Poulaki, V Liberman, TA Anderson, KC AF Mitsiades, CS Mitsiades, N Bailey, C Gu, XS Joseph, M Fanourakis, G Munshi, NC Poulaki, V Liberman, TA Anderson, KC TI Gene expression and proteomic profiling of drug-treated multiple myeloma (MM) cells: Mechanisms of drug-responsiveness vs. resistance and rationale for design of novel combination therapies for MM. SO BLOOD LA English DT Meeting Abstract CT 44th Annual Meeting of the American-Society-of-Hematology CY DEC 06-10, 2002 CL PHILADELPHIA, PENNSYLVANIA SP Amer Soc Hematol C1 Harvard Univ, Sch Med, Dana Farber Canc Inst, Jerome Lipper Multiple Myeloma Ctr,Dept Med Oncol, Boston, MA 02115 USA. Harvard Univ, Sch Med, Harvard Inst Med, Boston, MA USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2002 VL 100 IS 11 MA 1509 BP 389A EP 389A PN 1 PG 1 WC Hematology SC Hematology GA 614JK UT WOS:000179184701510 ER PT J AU Munshi, NC Chauhan, D Shammas, MA Auclair, D Davies, F Mitsiades, N Mitsiades, C Kim, RS Cheng, L Hideshima, T Anderson, KC AF Munshi, NC Chauhan, D Shammas, MA Auclair, D Davies, F Mitsiades, N Mitsiades, C Kim, RS Cheng, L Hideshima, T Anderson, KC TI Identification of dysregulated genes in myeloma using a genetically identical twin samples. SO BLOOD LA English DT Meeting Abstract CT 44th Annual Meeting of the American-Society-of-Hematology CY DEC 06-10, 2002 CL PHILADELPHIA, PENNSYLVANIA SP Amer Soc Hematol C1 Boston VA Hlth Care Syst, W Roxbury, MA USA. Dana Farber Canc Inst, Boston, MA 02115 USA. Harvard Univ, Sch Med, Boston, MA USA. Univ Leeds, Leeds LS2 9JT, W Yorkshire, England. Gen Infirm, Leeds LS1 3EX, W Yorkshire, England. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2002 VL 100 IS 11 MA 1539 BP 396A EP 396A PN 1 PG 1 WC Hematology SC Hematology GA 614JK UT WOS:000179184701540 ER PT J AU Grosman, DD Borges, V Vasir, D Wu, ZK Anderson, K Richardson, P Munshi, N Kufe, D Avigan, D AF Grosman, DD Borges, V Vasir, D Wu, ZK Anderson, K Richardson, P Munshi, N Kufe, D Avigan, D TI Dendritic cell (DC)-tumor fusions generated with mature as compared to immature DC potently induce myeloma specific immunity. SO BLOOD LA English DT Meeting Abstract CT 44th Annual Meeting of the American-Society-of-Hematology CY DEC 06-10, 2002 CL PHILADELPHIA, PENNSYLVANIA SP Amer Soc Hematol C1 Beth Israel Deaconess Med Ctr, Boston, MA 02215 USA. Dana Farber Canc Inst, Boston, MA 02115 USA. NR 0 TC 2 Z9 3 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 NOV 16 PY 2002 VL 100 IS 11 MA 1551 BP 399A EP 399A PN 1 PG 1 WC Hematology SC Hematology GA 614JK UT WOS:000179184701552 ER PT J AU Hayashi, T Hideshima, T Akiyama, M Raje, N Chauhan, D Anderson, KC AF Hayashi, T Hideshima, T Akiyama, M Raje, N Chauhan, D Anderson, KC TI Ex vivo induction of multiple myeloma-specific cytotoxic T lymphocytes. SO BLOOD LA English DT Meeting Abstract CT 44th Annual Meeting of the American-Society-of-Hematology CY DEC 06-10, 2002 CL PHILADELPHIA, PENNSYLVANIA SP Amer Soc Hematol C1 Dana Farber Canc Inst, Dept Adult Oncol, Boston, MA 02115 USA. Harvard Univ, Sch Med, Dept Med, Boston, MA USA. NR 0 TC 1 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 NOV 16 PY 2002 VL 100 IS 11 MA 1554 BP 400A EP 400A PN 1 PG 1 WC Hematology SC Hematology GA 614JK UT WOS:000179184701555 ER PT J AU Shaffer, JM Kraus, A Preffer, F Dombkowski, D McAfee, SL Dey, BR Saidman, S Colby, C Sachs, DH Spitzer, TR Sykes, M AF Shaffer, JM Kraus, A Preffer, F Dombkowski, D McAfee, SL Dey, BR Saidman, S Colby, C Sachs, DH Spitzer, TR Sykes, M TI Peripheral blood stem cell transplantation leads to enhanced T cell recovery compared to BMT in patients with advanced hematological malignancies receiving HLA-identical transplantation with non-myeloablative conditioning. SO BLOOD LA English DT Meeting Abstract CT 44th Annual Meeting of the American-Society-of-Hematology CY DEC 06-10, 2002 CL PHILADELPHIA, PENNSYLVANIA SP Amer Soc Hematol C1 Harvard Univ, Massachusetts Gen Hosp, Sch Med, Boston, MA USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2002 VL 100 IS 11 MA 1593 BP 410A EP 410A PN 1 PG 1 WC Hematology SC Hematology GA 614JK UT WOS:000179184701594 ER PT J AU Soiffer, RJ Alyea, EP Kim, H Parikh, B Ho, V Hochberg, E Levin, J Fisher, DC Lee, SJ Antin, JH AF Soiffer, RJ Alyea, EP Kim, H Parikh, B Ho, V Hochberg, E Levin, J Fisher, DC Lee, SJ Antin, JH TI Engraftment, graft-vs-host disease (GVHD), and survival after CD8+T cell depleted allogeneic peripheral blood stem cell transplantation (PBSCT). SO BLOOD LA English DT Meeting Abstract CT 44th Annual Meeting of the American-Society-of-Hematology CY DEC 06-10, 2002 CL PHILADELPHIA, PENNSYLVANIA SP Amer Soc Hematol C1 Dana Farber Canc Inst, Div Med Oncol, Boston, MA 02115 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2002 VL 100 IS 11 MA 1619 BP 418A EP 418A PN 1 PG 1 WC Hematology SC Hematology GA 614JK UT WOS:000179184701620 ER PT J AU Ho, VT Zahrieh, D Neuberg, D Munoz, M Foss, F Steckel, S Lee, SJ Cutler, C Alyea, EP Soiffer, RJ Antin, JH AF Ho, VT Zahrieh, D Neuberg, D Munoz, M Foss, F Steckel, S Lee, SJ Cutler, C Alyea, EP Soiffer, RJ Antin, JH TI Safety and efficacy of denileukin diftitox (ONTAK) in patients with steroid refractory graft-versus-host disease (GVHD) after allogeneic hematopoietic stem cell transplantation (HSCT). SO BLOOD LA English DT Meeting Abstract CT 44th Annual Meeting of the American-Society-of-Hematology CY DEC 06-10, 2002 CL PHILADELPHIA, PENNSYLVANIA SP Amer Soc Hematol C1 Dana Farber Canc Inst, Boston, MA 02115 USA. Brigham & Womens Hosp, Dept Med, Boston, MA 02115 USA. Dana Farber Canc Inst, Dept Biostat, Boston, MA 02115 USA. Tufts Univ New England Med Ctr, Dept Hematol Oncol, Boston, MA 02111 USA. Ligand Pharmaceut Inc, Boston, MA USA. Harvard Univ, Sch Med, Boston, MA USA. NR 0 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 NOV 16 PY 2002 VL 100 IS 11 MA 1638 BP 423A EP 423A PN 1 PG 1 WC Hematology SC Hematology GA 614JK UT WOS:000179184701639 ER PT J AU Dey, BR McAfee, SL Colby, C Sackstein, R Saidman, S Tarbell, N Sachs, DH Sykes, M Spitzer, TR AF Dey, BR McAfee, SL Colby, C Sackstein, R Saidman, S Tarbell, N Sachs, DH Sykes, M Spitzer, TR TI Comparison of outcomes after transplantation of peripheral blood stem cells (PBSCT) versus bone marrow (BMT) following an identical non-myeloablative conditioning regimen. SO BLOOD LA English DT Meeting Abstract CT 44th Annual Meeting of the American-Society-of-Hematology CY DEC 06-10, 2002 CL PHILADELPHIA, PENNSYLVANIA SP Amer Soc Hematol C1 Massachusetts Gen Hosp, Dept Med, Boston, MA 02114 USA. Massachusetts Gen Hosp, Dept Pathol, Boston, MA 02114 USA. Massachusetts Gen Hosp, Dept Radiol, Boston, MA 02114 USA. Massachusetts Gen Hosp, Transplant Biol Res Ctr, Boston, MA 02114 USA. NR 0 TC 1 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 NOV 16 PY 2002 VL 100 IS 11 MA 1641 BP 424A EP 424A PN 1 PG 1 WC Hematology SC Hematology GA 614JK UT WOS:000179184701642 ER PT J AU Lee, CK McCoy, J Anderson, KC Kyle, R Crowley, J Tricot, G Barlogie, B AF Lee, CK McCoy, J Anderson, KC Kyle, R Crowley, J Tricot, G Barlogie, B TI Long-term follow-up of previously untreated symptomatic myeloma patients treated with myeloablative therapy and sibling-matched allogeneic transplantation of the SWOG study 9321. SO BLOOD LA English DT Meeting Abstract CT 44th Annual Meeting of the American-Society-of-Hematology CY DEC 06-10, 2002 CL PHILADELPHIA, PENNSYLVANIA SP Amer Soc Hematol C1 Univ Arkansas Med Sci, Myeloma Inst Res & Therapy, Little Rock, AR 72205 USA. Fred Hutchinson Canc Res Ctr, Seattle, WA 98104 USA. Dana Farber Canc Inst, Boston, MA 02115 USA. Mayo Clin, Rochester, MN USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2002 VL 100 IS 11 MA 1644 BP 424A EP 424A PN 1 PG 1 WC Hematology SC Hematology GA 614JK UT WOS:000179184701645 ER PT J AU Robertson, MJ Bierman, P Bolwell, BJ Shea, TC Pecora, AL Manna, L Fox, V McAfee, S AF Robertson, MJ Bierman, P Bolwell, BJ Shea, TC Pecora, AL Manna, L Fox, V McAfee, S TI Safety and biological activity of siplizumab (AlloMune (R) component II: MEDI-507) in non-myeloablative allogeneic peripheral blood stem cell transplantation (NMAT) for refractory non-Hodgkin's lymphoma (NHL). SO BLOOD LA English DT Meeting Abstract CT 44th Annual Meeting of the American-Society-of-Hematology CY DEC 06-10, 2002 CL PHILADELPHIA, PENNSYLVANIA SP Amer Soc Hematol C1 Indiana Univ, Med Ctr, Indianapolis, IN USA. Univ Nebraska, Med Ctr, Omaha, NE USA. Cleveland Clin, Cleveland, OH 44106 USA. Univ N Carolina, Med Ctr, Chapel Hill, NC 27515 USA. Hackensack Univ, Ctr Med, Hackensack, NJ USA. Biotransplant Inc, Charlestown, MA USA. Massachusetts Gen Hosp, Boston, MA 02114 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2002 VL 100 IS 11 MA 1651 BP 426A EP 426A PN 1 PG 1 WC Hematology SC Hematology GA 614JK UT WOS:000179184701652 ER PT J AU Galimi, F Noll, M Kanazawa, Y D'Andrea, AD Grompe, M Bagby, GG Wagner, JE Verma, IM AF Galimi, F Noll, M Kanazawa, Y D'Andrea, AD Grompe, M Bagby, GG Wagner, JE Verma, IM TI Gene therapy of Fanconi Anemia by lentiviral vectors. SO BLOOD LA English DT Meeting Abstract CT 44th Annual Meeting of the American-Society-of-Hematology CY DEC 06-10, 2002 CL PHILADELPHIA, PENNSYLVANIA SP Amer Soc Hematol C1 Oregon Hlth Sci Univ, Dept Mol & Med Genet, Portland, OR 97201 USA. Salk Inst Biol Studies, Genet Lab, La Jolla, CA USA. Dana Farber Canc Inst, Dept Pediat Oncol, Boston, MA 02115 USA. Univ Minnesota, Pediat MBT Program, Minneapolis, MN 55455 USA. RI Galimi, Francesco/J-4238-2012 NR 0 TC 0 Z9 0 U1 1 U2 3 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 NOV 16 PY 2002 VL 100 IS 11 MA 1694 BP 438A EP 438A PN 1 PG 1 WC Hematology SC Hematology GA 614JK UT WOS:000179184701695 ER PT J AU McDermott, DF Vasir, D Hess, V Joyce, RM Levine, JD Uhl, L Fardy, L Giallombardo, N Hurley, D Ottaway, J We, ZK Borges, V Avigan, DE AF McDermott, DF Vasir, D Hess, V Joyce, RM Levine, JD Uhl, L Fardy, L Giallombardo, N Hurley, D Ottaway, J We, ZK Borges, V Avigan, DE TI Non-myeloablative stem cell transplantation for metastatic solid tumors: Feasibility, clinical results and immune reconstitution. SO BLOOD LA English DT Meeting Abstract CT 44th Annual Meeting of the American-Society-of-Hematology CY DEC 06-10, 2002 CL PHILADELPHIA, PENNSYLVANIA SP Amer Soc Hematol C1 Beth Israel Deaconess Med Ctr, Boston, MA 02215 USA. Dana Farber Canc Inst, Boston, MA 02115 USA. NR 0 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 NOV 16 PY 2002 VL 100 IS 11 MA 5415 BP 460B EP 460B PN 2 PG 1 WC Hematology SC Hematology GA 614JL UT WOS:000179184801957 ER PT J AU Konecke, C Alexander, S Shaffer, J Dey, B Preffer, F Colby, C Hope, J Spitzer, TR Sykes, M AF Konecke, C Alexander, S Shaffer, J Dey, B Preffer, F Colby, C Hope, J Spitzer, TR Sykes, M TI Lack of correlation between KIR mismatches, rejection and NK cell reactivity after non-myeloablative HLA mismatched hematopoietic cell transplantation. SO BLOOD LA English DT Meeting Abstract CT 44th Annual Meeting of the American-Society-of-Hematology CY DEC 06-10, 2002 CL PHILADELPHIA, PENNSYLVANIA SP Amer Soc Hematol C1 Harvard Univ, Massachusetts Gen Hosp, Sch Med, Boston, MA 02115 USA. Biotransplant Inc, Charlestown, MA USA. RI Koenecke, Christian/C-3138-2009 OI Koenecke, Christian/0000-0001-7025-1735 NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2002 VL 100 IS 11 MA 5423 BP 462B EP 462B PN 2 PG 1 WC Hematology SC Hematology GA 614JL UT WOS:000179184801965 ER PT J AU Lutskiy, MI Rosen, FS Remold-O'Donnell, E AF Lutskiy, MI Rosen, FS Remold-O'Donnell, E TI Spontaneous correction of the T-cell defect in patients with the Wiskott-Aldrich syndrome. SO BLOOD LA English DT Meeting Abstract CT 44th Annual Meeting of the American-Society-of-Hematology CY DEC 06-10, 2002 CL PHILADELPHIA, PENNSYLVANIA SP Amer Soc Hematol C1 Ctr Blood Res, Boston, MA 02115 USA. Harvard Univ, Sch Med, Dept Pediat, Boston, MA 02115 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2002 VL 100 IS 11 MA 1802 BP 465A EP 465A PN 1 PG 1 WC Hematology SC Hematology GA 614JK UT WOS:000179184701803 ER PT J AU Park, JY Kob, M Smyrl, M Rodigina, TV Prodeus, AP Rosen, FS Shcherbina, A Remold-O'Donnell, E AF Park, JY Kob, M Smyrl, M Rodigina, TV Prodeus, AP Rosen, FS Shcherbina, A Remold-O'Donnell, E TI Altered lymphocyte subpopulations in patients with the Wiskott-Aldrich syndrome. SO BLOOD LA English DT Meeting Abstract CT 44th Annual Meeting of the American-Society-of-Hematology CY DEC 06-10, 2002 CL PHILADELPHIA, PENNSYLVANIA SP Amer Soc Hematol C1 Ctr Blood Res, Boston, MA 02115 USA. Harvard Univ, Sch Med, Dept Pediat, Boston, MA 02115 USA. Res Inst Pediat Hematol, Moscow, Russia. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2002 VL 100 IS 11 MA 1804 BP 465A EP 465A PN 1 PG 1 WC Hematology SC Hematology GA 614JK UT WOS:000179184701805 ER PT J AU Feng, SJ Xin, L Kroll, MH AF Feng, SJ Xin, L Kroll, MH TI Pathological shear stress stimulates alpha IIb beta 3-dependent tyrosine kinase signaling. SO BLOOD LA English DT Meeting Abstract CT 44th Annual Meeting of the American-Society-of-Hematology CY DEC 06-10, 2002 CL PHILADELPHIA, PENNSYLVANIA SP Amer Soc Hematol C1 VA Med Ctr, Houston, TX USA. Baylor Coll Med, Houston, TX 77030 USA. Rice Univ, Houston, TX 77251 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2002 VL 100 IS 11 MA 1841 BP 474A EP 475A PN 1 PG 2 WC Hematology SC Hematology GA 614JK UT WOS:000179184701842 ER PT J AU Feng, SJ Xin, L Kroll, MH AF Feng, SJ Xin, L Kroll, MH TI Peptide from the filamin A binding domain of platelet glycoprotein Ib alpha inhibits ristocetin- and shear-induced platelet aggregation. SO BLOOD LA English DT Meeting Abstract CT 44th Annual Meeting of the American-Society-of-Hematology CY DEC 06-10, 2002 CL PHILADELPHIA, PENNSYLVANIA SP Amer Soc Hematol C1 VA Med Ctr, Houston, TX USA. Baylor Coll Med, Houston, TX 77030 USA. Rice Univ, Houston, TX 77251 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2002 VL 100 IS 11 MA 1842 BP 475A EP 475A PN 1 PG 1 WC Hematology SC Hematology GA 614JK UT WOS:000179184701843 ER PT J AU Kroll, MH Resendiz, JC Feng, SJ Ji, GL AF Kroll, MH Resendiz, JC Feng, SJ Ji, GL TI von Willebrand factor binding to platelet glycoprotein Ib-IX-V stimulates the assembly of an alpha-actinin based signaling complex. SO BLOOD LA English DT Meeting Abstract CT 44th Annual Meeting of the American-Society-of-Hematology CY DEC 06-10, 2002 CL PHILADELPHIA, PENNSYLVANIA SP Amer Soc Hematol C1 VA Med Ctr, Houston, TX USA. Baylor Coll Med, Houston, TX 77030 USA. Rice Univ, Houston, TX 77251 USA. Wihuri Res Inst, SF-00140 Helsinki, Finland. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2002 VL 100 IS 11 MA 1843 BP 475A EP 475A PN 1 PG 1 WC Hematology SC Hematology GA 614JK UT WOS:000179184701844 ER PT J AU Richards, MK Liu, FL Iwasaki, H Akashi, K Link, DC AF Richards, MK Liu, FL Iwasaki, H Akashi, K Link, DC TI The use of a competitive repopulation assay to investigate G-CSF receptor signals in hematopoiesis. SO BLOOD LA English DT Meeting Abstract CT 44th Annual Meeting of the American-Society-of-Hematology CY DEC 06-10, 2002 CL PHILADELPHIA, PENNSYLVANIA SP Amer Soc Hematol C1 Washington Univ, Sch Med, Div Oncol, St Louis, MO 63130 USA. Dana Farber Canc Inst, Dept Canc Immunol & AIDS, Boston, MA 02115 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2002 VL 100 IS 11 MA 1974 BP 506A EP 506A PN 1 PG 1 WC Hematology SC Hematology GA 614JK UT WOS:000179184701975 ER PT J AU Hui, Z Degar, BA Forget, BG AF Hui, Z Degar, BA Forget, BG TI Embryonic stem cells homozygous for disruption of the Pitx2 homeodomain gene can contribute fully to the hematopoietic system in chimeric mice. SO BLOOD LA English DT Meeting Abstract CT 44th Annual Meeting of the American-Society-of-Hematology CY DEC 06-10, 2002 CL PHILADELPHIA, PENNSYLVANIA SP Amer Soc Hematol C1 Yale Univ, Sch Med, New Haven, CT 06520 USA. Dana Farber Canc Ctr, Boston, MA USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2002 VL 100 IS 11 MA 1978 BP 507A EP 507A PN 1 PG 1 WC Hematology SC Hematology GA 614JK UT WOS:000179184701979 ER PT J AU Wang, ZY Cohen, K Ying, S Mole, P Dombkowski, D Scadden, DT AF Wang, ZY Cohen, K Ying, S Mole, P Dombkowski, D Scadden, DT TI EphB4 facilitates hemangioblast formation and enhances hematopoietic and vasculogenic differentiation. SO BLOOD LA English DT Meeting Abstract CT 44th Annual Meeting of the American-Society-of-Hematology CY DEC 06-10, 2002 CL PHILADELPHIA, PENNSYLVANIA SP Amer Soc Hematol C1 Harvard Univ, Massachusetts Gen Hosp, Sch Med, Expt Hematol AIDS Res Ctr, Boston, MA USA. Harvard Univ, Massachusetts Gen Hosp, Sch Med, MGH Canc Ctr, Boston, MA USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2002 VL 100 IS 11 MA 1976 BP 507A EP 507A PN 1 PG 1 WC Hematology SC Hematology GA 614JK UT WOS:000179184701977 ER PT J AU Stier, S Ko, Y Forkert, R Lutz, C Gruenewald, E Neuhaus, T Tao, C Dombkowski, D Rittling, SR Scadden, DT AF Stier, S Ko, Y Forkert, R Lutz, C Gruenewald, E Neuhaus, T Tao, C Dombkowski, D Rittling, SR Scadden, DT TI Osteopontin affects the hematopoietic stem cell pool in vivo. SO BLOOD LA English DT Meeting Abstract CT 44th Annual Meeting of the American-Society-of-Hematology CY DEC 06-10, 2002 CL PHILADELPHIA, PENNSYLVANIA SP Amer Soc Hematol C1 Harvard Univ, Massachusetts Gen Hosp, Sch Med, AIDS Res Ctr,MGH Canc Ctr, Boston, MA USA. Univ Bonn, Med Poliklin, D-5300 Bonn, Germany. Rutgers State Univ, Dept Cell Biol & Neurosci, Piscataway, NJ 08855 USA. NR 0 TC 0 Z9 0 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 NOV 16 PY 2002 VL 100 IS 11 MA 1986 BP 509A EP 509A PN 1 PG 1 WC Hematology SC Hematology GA 614JK UT WOS:000179184701987 ER PT J AU Qiu, JH Takagi, Y Harada, J Teramoto, T Rodrigues, N Moskowitz, MA Scadden, DT Tao, C AF Qiu, JH Takagi, Y Harada, J Teramoto, T Rodrigues, N Moskowitz, MA Scadden, DT Tao, C TI p21(cip1/waf11) regulates neural precursors in vivo similarly as demonstrated in hematopoietic stem cells. SO BLOOD LA English DT Meeting Abstract CT 44th Annual Meeting of the American-Society-of-Hematology CY DEC 06-10, 2002 CL PHILADELPHIA, PENNSYLVANIA SP Amer Soc Hematol C1 Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Radiol, Boston, MA USA. Harvard Univ, Massachusetts Gen Hosp, Sch Med, Ctr Neurosci, Boston, MA USA. Harvard Univ, Massachusetts Gen Hosp, Sch Med, Ctr AIDS Res, Boston, MA USA. Harvard Univ, Massachusetts Gen Hosp, Sch Med, MGH Canc Ctr, Boston, MA USA. Univ Pittsburgh, Sch Med, Dept Radiat Oncol, Pittsburgh, PA 15260 USA. Univ Pittsburgh, Sch Med, Pittsburgh Canc Inst, Pittsburgh, PA 15261 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2002 VL 100 IS 11 MA 2020 BP 517A EP 517A PN 1 PG 1 WC Hematology SC Hematology GA 614JK UT WOS:000179184702021 ER PT J AU Palomero, T Berghmans, S Langenau, DM Rhodes, J Ferrando, AA Kanki, JP Look, AT AF Palomero, T Berghmans, S Langenau, DM Rhodes, J Ferrando, AA Kanki, JP Look, AT TI Genetic screen for mutations affecting Hox11 regulation and/or spleen development. SO BLOOD LA English DT Meeting Abstract CT 44th Annual Meeting of the American-Society-of-Hematology CY DEC 06-10, 2002 CL PHILADELPHIA, PENNSYLVANIA SP Amer Soc Hematol C1 Dana Farber Canc Inst, Dept Pediat Oncol, Boston, MA 02115 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2002 VL 100 IS 11 MA 2098 BP 535A EP 535A PN 1 PG 1 WC Hematology SC Hematology GA 614JK UT WOS:000179184702099 ER PT J AU Xu, K Chung, D Glasow, A Guidez, F Monks, A Stegmaier, K Golub, TR Zelent, A Waxman, S AF Xu, K Chung, D Glasow, A Guidez, F Monks, A Stegmaier, K Golub, TR Zelent, A Waxman, S TI Specific dithiophene analogs potentiate ATRA induction of acute promyelocytic leukemia cell differentiation and gene expression in vivo. SO BLOOD LA English DT Meeting Abstract CT 44th Annual Meeting of the American-Society-of-Hematology CY DEC 06-10, 2002 CL PHILADELPHIA, PENNSYLVANIA SP Amer Soc Hematol C1 Inst Canc Res, Leukaemia Res Fund Ctr, London SW3 6JB, England. NCI, SAIC Frederick, Frederick, MD USA. Dana Farber Canc Inst, Dept Pediat Oncol, Boston, MA 02115 USA. Mt Sinai Sch Med, Dept Med, New York, NY USA. RI Guidez, Fabien/B-3750-2009 NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2002 VL 100 IS 11 MA 2125 BP 541A EP 541A PN 1 PG 1 WC Hematology SC Hematology GA 614JK UT WOS:000179184702126 ER PT J AU Yee, KWH O'Farrell, AM Town, AR Cherrington, JM Heinrich, MC AF Yee, KWH O'Farrell, AM Town, AR Cherrington, JM Heinrich, MC TI FLT3 inbibitor SU11248 displays synergistic effects with cytarabine and daunorubicin on FLT3 ITD leukemia cell lines. SO BLOOD LA English DT Meeting Abstract CT 44th Annual Meeting of the American-Society-of-Hematology CY DEC 06-10, 2002 CL PHILADELPHIA, PENNSYLVANIA SP Amer Soc Hematol C1 Oregon Hlth Sci Univ, Portland, OR 97201 USA. Portland VA Med Ctr, Portland, OR USA. SUGEN Inc, Dept Preclin & Translat Med, San Francisco, CA USA. NR 0 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 NOV 16 PY 2002 VL 100 IS 11 MA 2129 BP 542A EP 542A PN 1 PG 1 WC Hematology SC Hematology GA 614JK UT WOS:000179184702130 ER PT J AU Yang, XF Yan, Y Phan, LY Fan, Y Talpaz, M Wu, CJ Ritz, J AF Yang, XF Yan, Y Phan, LY Fan, Y Talpaz, M Wu, CJ Ritz, J TI A novel mechanism of alternative promoter and splicing regulates the immunogenicity of tumor antigen CML66-L. SO BLOOD LA English DT Meeting Abstract CT 44th Annual Meeting of the American-Society-of-Hematology CY DEC 06-10, 2002 CL PHILADELPHIA, PENNSYLVANIA SP Amer Soc Hematol C1 Baylor Coll Med, Houston, TX 77030 USA. Univ Texas, MD Anderson Canc Ctr, Houston, TX 77030 USA. Dana Farber Canc Inst, Ctr Hematol Oncol, Boston, MA 02115 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2002 VL 100 IS 11 MA 2156 BP 549A EP 549A PN 1 PG 1 WC Hematology SC Hematology GA 614JK UT WOS:000179184702157 ER PT J AU Yang, XP Galinsky, I DeAngelo, DJ Sternberg, D Stone, RM AF Yang, XP Galinsky, I DeAngelo, DJ Sternberg, D Stone, RM TI Apoptosis suppression by FLT3 activated via an internal tandem duplication mutation (ITD) requires both the MEK/ERK and PI3K/Akt signalling pathways. SO BLOOD LA English DT Meeting Abstract CT 44th Annual Meeting of the American-Society-of-Hematology CY DEC 06-10, 2002 CL PHILADELPHIA, PENNSYLVANIA SP Amer Soc Hematol C1 Dana Farber Canc Inst, Boston, MA 02115 USA. Brigham & Womens Hosp, Boston, MA 02115 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2002 VL 100 IS 11 MA 2159 BP 549A EP 550A PN 1 PG 2 WC Hematology SC Hematology GA 614JK UT WOS:000179184702160 ER PT J AU Kriangkum, J Taylor, BJ Treon, SP Reiman, T Mant, MJ Belch, AR Pilarski, LM AF Kriangkum, J Taylor, BJ Treon, SP Reiman, T Mant, MJ Belch, AR Pilarski, LM TI IgH sequence analysis of Waldenstrom's macroglobulinemia: Clonal mu and delta transcripts are coexpressed in WM B cells with no evidence of class switching. SO BLOOD LA English DT Meeting Abstract CT 44th Annual Meeting of the American-Society-of-Hematology CY DEC 06-10, 2002 CL PHILADELPHIA, PENNSYLVANIA SP Amer Soc Hematol C1 Univ Alberta, Cross Canc Inst, Edmonton, AB T6G 2M7, Canada. Dana Farber Canc Inst, Boston, MA 02115 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2002 VL 100 IS 11 MA 2233 BP 568A EP 568A PN 1 PG 1 WC Hematology SC Hematology GA 614JK UT WOS:000179184702234 ER PT J AU Treon, SP Fox, EA Hansen, M Verselis, S Branagan, A Touroutoglou, N Maloney, DG Frankel, SR Anderson, KC Emmanouilides, C Kimby, E AF Treon, SP Fox, EA Hansen, M Verselis, S Branagan, A Touroutoglou, N Maloney, DG Frankel, SR Anderson, KC Emmanouilides, C Kimby, E TI Polymorphisms in Fc gamma RIIIa (CD16) receptor expression are associated with clinical response to rituximab in Waldenstrom's macroglobulinemia. SO BLOOD LA English DT Meeting Abstract CT 44th Annual Meeting of the American-Society-of-Hematology CY DEC 06-10, 2002 CL PHILADELPHIA, PENNSYLVANIA SP Amer Soc Hematol C1 Dana Farber Canc Inst, Mol Diagnost Lab, Boston, MA 02115 USA. Nevada Canc Ctr, Las Vegas, NV USA. Fred Hutchinson Canc Res Ctr, Seattle, WA 98104 USA. Greenebaum Canc Ctr, Baltimore, MD USA. Univ Calif Los Angeles, Med Ctr, Los Angeles, CA 90024 USA. Karolinska Inst, S-10401 Stockholm, Sweden. NR 0 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 NOV 16 PY 2002 VL 100 IS 11 MA 2251 BP 573A EP 573A PN 1 PG 1 WC Hematology SC Hematology GA 614JK UT WOS:000179184702252 ER PT J AU Wu, CJ Chen, LY Kutok, JL Canning, CM Alyea, EP Yang, XF Soiffer, RJ Ritz, J AF Wu, CJ Chen, LY Kutok, JL Canning, CM Alyea, EP Yang, XF Soiffer, RJ Ritz, J TI CML28 and CML66 are GVL-associated antigens that are highly expressed in proliferating cells. SO BLOOD LA English DT Meeting Abstract CT 44th Annual Meeting of the American-Society-of-Hematology CY DEC 06-10, 2002 CL PHILADELPHIA, PENNSYLVANIA SP Amer Soc Hematol C1 Dana Farber Canc Inst, Ctr Hematol Oncol, Boston, MA 02115 USA. Baylor Coll Med, Dept Med, Houston, TX 77030 USA. NR 0 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 NOV 16 PY 2002 VL 100 IS 11 MA 2285 BP 581A EP 582A PN 1 PG 2 WC Hematology SC Hematology GA 614JK UT WOS:000179184702286 ER PT J AU Sattler, M Pride, YB Gramlich, JL Quinnan, LR Salgia, R Lipkowitz, S Griffin, JD AF Sattler, M Pride, YB Gramlich, JL Quinnan, LR Salgia, R Lipkowitz, S Griffin, JD TI CBL-B is a negative regulator of transformation by BCR/ABL. SO BLOOD LA English DT Meeting Abstract CT 44th Annual Meeting of the American-Society-of-Hematology CY DEC 06-10, 2002 CL PHILADELPHIA, PENNSYLVANIA SP Amer Soc Hematol C1 Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02115 USA. NCI, Dept Genet, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2002 VL 100 IS 11 MA 2290 BP 583A EP 583A PN 1 PG 1 WC Hematology SC Hematology GA 614JK UT WOS:000179184702291 ER PT J AU Mayerhofer, M Hauswirth, AW Valent, P Pickl, WF Sperr, WR Griffin, JD Sillaber, C AF Mayerhofer, M Hauswirth, AW Valent, P Pickl, WF Sperr, WR Griffin, JD Sillaber, C TI BCR/ABL induces expression of VEGF through a pathway involving PI3-kinase and the rapamycin-sensitive regulator of cell cycle progression, mTOR. SO BLOOD LA English DT Meeting Abstract CT 44th Annual Meeting of the American-Society-of-Hematology CY DEC 06-10, 2002 CL PHILADELPHIA, PENNSYLVANIA SP Amer Soc Hematol C1 Univ Vienna, Dept Internal Med 1, Div Hematol & Hemostaseol, A-1010 Vienna, Austria. Univ Vienna, Inst Immunol, A-1010 Vienna, Austria. Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02115 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2002 VL 100 IS 11 MA 2300 BP 585A EP 585A PN 1 PG 1 WC Hematology SC Hematology GA 614JK UT WOS:000179184702301 ER PT J AU Gorgun, G Gribben, JG AF Gorgun, G Gribben, JG TI Induction of autologous Th1 response against CLL cells by addition of exogenous interferon during generation of antigen presenting cells gamma. SO BLOOD LA English DT Meeting Abstract CT 44th Annual Meeting of the American-Society-of-Hematology CY DEC 06-10, 2002 CL PHILADELPHIA, PENNSYLVANIA SP Amer Soc Hematol C1 Harvard Univ, Sch Med, Dana Farber Canc Inst, Boston, MA 02115 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2002 VL 100 IS 11 MA 2323 BP 591A EP 591A PN 1 PG 1 WC Hematology SC Hematology GA 614JK UT WOS:000179184702325 ER PT J AU Kay, NE Bone, ND Pittner, BT Jelinek, DF Leland, P Frank, DA Battle, TE Puri, RK AF Kay, NE Bone, ND Pittner, BT Jelinek, DF Leland, P Frank, DA Battle, TE Puri, RK TI Plasma membrane IL-4 receptors can be targeted to eliminate B-chronic lymphocytic leukemia B cells. SO BLOOD LA English DT Meeting Abstract CT 44th Annual Meeting of the American-Society-of-Hematology CY DEC 06-10, 2002 CL PHILADELPHIA, PA SP Amer Soc Hematol C1 Mayo Clin, Div Hematol, Rochester, MN USA. Dana Farber Canc Inst, Boston, MA 02115 USA. CBER, Bethesda, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2002 VL 100 IS 11 MA 2324 BP 591A EP 591A PN 1 PG 1 WC Hematology SC Hematology GA 614JK UT WOS:000179184702326 ER PT J AU Mitsiades, CS Mitsiades, N Poulaki, V Fanourakis, G Richardson, PG Shringapurne, R Akiyama, M Chauhan, D Hideshima, T Treon, SP Munshi, NC Dimopoulos, MA Anderson, KC AF Mitsiades, CS Mitsiades, N Poulaki, V Fanourakis, G Richardson, PG Shringapurne, R Akiyama, M Chauhan, D Hideshima, T Treon, SP Munshi, NC Dimopoulos, MA Anderson, KC TI HMG-CoA inhibitors (statins) induce growth arrest, apoptosis of multiple myeloma (MM) and Waldenstrom's macroglobulinemia (WM) cells and enhance their sensitivity to conventional or novel therapies. Molecular profiling of HMG-CoA inhibition in MM/WM and framework for translation to therapeutic application. SO BLOOD LA English DT Meeting Abstract CT 44th Annual Meeting of the American-Society-of-Hematology CY DEC 06-10, 2002 CL PHILADELPHIA, PENNSYLVANIA SP Amer Soc Hematol C1 Harvard Univ, Sch Med, Dana Farber Canc Inst, Dept Med Oncol,Jerome Lipper Multiple Myeloma Ctr, Boston, MA 02115 USA. Harvard Univ, Massachusetts Eye & Ear Infirm, Sch Med, Boston, MA USA. Univ Athens, Sch Med, Alexandra Gen Hosp, Dept Clin Therapeut, GR-11527 Athens, Greece. NR 0 TC 2 Z9 3 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 NOV 16 PY 2002 VL 100 IS 11 MA 2349 BP 597A EP 598A PN 1 PG 2 WC Hematology SC Hematology GA 614JK UT WOS:000179184702351 ER PT J AU Mitsiades, CS Mitsiades, N Hideshima, T Poulaki, V Chauhan, D Munshi, NC Treon, SP Pilarski, LM Anderson, KC AF Mitsiades, CS Mitsiades, N Hideshima, T Poulaki, V Chauhan, D Munshi, NC Treon, SP Pilarski, LM Anderson, KC TI Whole-body real-time fluorescence imaging of disseminated GFP plus lesions in a SCID/NOD model of multiple myeloma: Implications for evaluations of novel therapies. SO BLOOD LA English DT Meeting Abstract CT 44th Annual Meeting of the American-Society-of-Hematology CY DEC 06-10, 2002 CL PHILADELPHIA, PENNSYLVANIA SP Amer Soc Hematol C1 Harvard Univ, Sch Med, Dana Farber Canc Inst, Dept Med Oncol,Jerome Lipper Multiple Myeloma Ctr, Boston, MA 02115 USA. Harvard Univ, Massachusetts Eye & Ear Infirm, Sch Med, Boston, MA USA. Univ Alberta, Cross Canc Inst, Edmonton, AB T6G 2M7, Canada. NR 0 TC 2 Z9 3 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 NOV 16 PY 2002 VL 100 IS 11 MA 2348 BP 597A EP 597A PN 1 PG 1 WC Hematology SC Hematology GA 614JK UT WOS:000179184702350 ER PT J AU Greipp, PR Kumar, S Blood, EA Rue, M Jacobson, J Therneau, TM Larson, DR Anderson, KC Oken, MM Kyle, RA AF Greipp, PR Kumar, S Blood, EA Rue, M Jacobson, J Therneau, TM Larson, DR Anderson, KC Oken, MM Kyle, RA TI A simple classification to identify poor-risk untreated myeloma. SO BLOOD LA English DT Meeting Abstract CT 44th Annual Meeting of the American-Society-of-Hematology CY DEC 06-10, 2002 CL PHILADELPHIA, PENNSYLVANIA SP Amer Soc Hematol C1 Mayo Clin, Rochester, MN USA. Dana Farber Canc Inst, Boston, MA 02115 USA. SW Oncol Grp, Ctr Stat, Seattle, WA USA. Abbott NW Hosp, Minneapolis, MN 55407 USA. ECOG, Boston, MA USA. RI Kumar, Shaji/A-9853-2008 OI Kumar, Shaji/0000-0001-5392-9284 NR 0 TC 0 Z9 0 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 NOV 16 PY 2002 VL 100 IS 11 MA 2351 BP 598A EP 598A PN 1 PG 1 WC Hematology SC Hematology GA 614JK UT WOS:000179184702353 ER PT J AU Chauhan, D Li, GL Hideshima, T Podar, K Catley, L LeBlanc, R Mitsiades, N Mitsiades, C Richardson, P Saxena, S Anderson, KC AF Chauhan, D Li, GL Hideshima, T Podar, K Catley, L LeBlanc, R Mitsiades, N Mitsiades, C Richardson, P Saxena, S Anderson, KC TI Heat shock protein-27 confers drug-resistance in multiple myeloma cells. SO BLOOD LA English DT Meeting Abstract CT 44th Annual Meeting of the American-Society-of-Hematology CY DEC 06-10, 2002 CL PHILADELPHIA, PENNSYLVANIA SP Amer Soc Hematol C1 Dana Farber Canc Inst, Boston, MA 02115 USA. Lovelace Resp Res Inst, Albuquerque, NM USA. RI Catley, Laurence/E-5313-2013 NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2002 VL 100 IS 11 MA 2369 BP 602A EP 602A PN 1 PG 1 WC Hematology SC Hematology GA 614JK UT WOS:000179184702371 ER PT J AU Machida, K Nollau, P Thompson, CM Lin, B Anderson, KC Patel, N Mayer, BJ AF Machida, K Nollau, P Thompson, CM Lin, B Anderson, KC Patel, N Mayer, BJ TI Profiling of hematopoietic malignancies by Src Homology 2 (SH2) domain binding pattern. SO BLOOD LA English DT Meeting Abstract CT 44th Annual Meeting of the American-Society-of-Hematology CY DEC 06-10, 2002 CL PHILADELPHIA, PENNSYLVANIA SP Amer Soc Hematol C1 Univ Connecticut, Ctr Hlth, Farmington, CT USA. Harvard Univ, Sch Med, Dana Farber Canc Inst, Boston, MA 02115 USA. Universitatsklinikum Hamburg Eppendorf, Hamburg, Germany. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2002 VL 100 IS 11 MA 2374 BP 603A EP 603A PN 1 PG 1 WC Hematology SC Hematology GA 614JK UT WOS:000179184702376 ER PT J AU Chauhan, D Li, GL Sattler, M Catley, L LeBlanc, R Mitsiades, N Mitsiades, C Munshi, N Richardson, P Hideshima, T Anderson, KC AF Chauhan, D Li, GL Sattler, M Catley, L LeBlanc, R Mitsiades, N Mitsiades, C Munshi, N Richardson, P Hideshima, T Anderson, KC TI Differential oxidative stress responses during 2-methoxyestradiol (2ME2) and dexamthasone (Dex)-induced apoptosis in multiple myeloma (MM) cells. SO BLOOD LA English DT Meeting Abstract CT 44th Annual Meeting of the American-Society-of-Hematology CY DEC 06-10, 2002 CL PHILADELPHIA, PENNSYLVANIA SP Amer Soc Hematol C1 Dana Farber Canc Inst, Jerome Lipper Multiple Myeloma Ctr, Boston, MA 02115 USA. RI Catley, Laurence/E-5313-2013 NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2002 VL 100 IS 11 MA 2389 BP 607A EP 607A PN 1 PG 1 WC Hematology SC Hematology GA 614JK UT WOS:000179184702391 ER PT J AU Marty, FM Lee, S Alyea, E Soiffer, RJ Antin, JH Baden, LR AF Marty, FM Lee, S Alyea, E Soiffer, RJ Antin, JH Baden, LR TI Risk of non-Candida invasive fungal infections in allogeneic bone marrow transplant patients who received infliximab to control severe Graft v. Host Disease. SO BLOOD LA English DT Meeting Abstract CT 44th Annual Meeting of the American-Society-of-Hematology CY DEC 06-10, 2002 CL PHILADELPHIA, PENNSYLVANIA SP Amer Soc Hematol C1 Brigham & Womens Hosp, Boston, MA 02115 USA. Dana Farber Canc Inst, Adult Oncol Stem Cell Transplant Serv, Boston, MA 02115 USA. NR 0 TC 3 Z9 3 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 NOV 16 PY 2002 VL 100 IS 11 MA 2476 BP 628A EP 629A PN 1 PG 2 WC Hematology SC Hematology GA 614JK UT WOS:000179184702478 ER PT J AU Spitzer, TR McAfee, SL Dey, BR Colby, C Hope, J Grossberg, H Preffer, F Saidman, S Shaffer, J Alexander, SI Sachs, DH Sykes, M AF Spitzer, TR McAfee, SL Dey, BR Colby, C Hope, J Grossberg, H Preffer, F Saidman, S Shaffer, J Alexander, SI Sachs, DH Sykes, M TI Ex vivo T-cell depleted non-myeloablative haploidentical transplantation for advanced hematologic malignancy. SO BLOOD LA English DT Meeting Abstract CT 44th Annual Meeting of the American-Society-of-Hematology CY DEC 06-10, 2002 CL PHILADELPHIA, PENNSYLVANIA SP Amer Soc Hematol C1 Massachusetts Gen Hosp, Dept Med, Boston, MA 02114 USA. Massachusetts Gen Hosp, Dept Pathol, Boston, MA 02114 USA. Massachusetts Gen Hosp, Transplant Biol Res Ctr, Boston, MA 02114 USA. BioTransplant Inc, Charlestown, MA USA. NR 0 TC 0 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 NOV 16 PY 2002 VL 100 IS 11 MA 2513 BP 638A EP 638A PN 1 PG 1 WC Hematology SC Hematology GA 614JK UT WOS:000179184702515 ER PT J AU Soulier, J Leblanc, T Larghero, J Shimamura, A Dastot, H Guardiola, P Baruchel, A Sigaux, F D'Andrea, AD Gluckman, E AF Soulier, J Leblanc, T Larghero, J Shimamura, A Dastot, H Guardiola, P Baruchel, A Sigaux, F D'Andrea, AD Gluckman, E TI Efficiency of a specific diagnosis test for Fanconi Anemia. SO BLOOD LA English DT Meeting Abstract CT 44th Annual Meeting of the American-Society-of-Hematology CY DEC 06-10, 2002 CL PHILADELPHIA, PENNSYLVANIA SP Amer Soc Hematol C1 Hop St Louis, Dept Hematol, Paris, France. Hop St Louis, Inst Univ Hematol, Paris, France. Dana Farber Canc Inst, Dept Pediat Oncol, Boston, MA 02115 USA. NR 0 TC 0 Z9 0 U1 1 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 NOV 16 PY 2002 VL 100 IS 11 MA 2592 BP 659A EP 659A PN 1 PG 1 WC Hematology SC Hematology GA 614JK UT WOS:000179184702594 ER PT J AU Clark, JJ Geva, A Zhang, YX Manning, JM Neufeld, EJ AF Clark, JJ Geva, A Zhang, YX Manning, JM Neufeld, EJ TI Characterization of a novel dominant sickling hemoglobin (Hb Jamaica Plain, beta(Glu6Val,Leu68Phe)) reveals marked elevation of P-50 in the presence of 2,3 DPG. SO BLOOD LA English DT Meeting Abstract CT 44th Annual Meeting of the American-Society-of-Hematology CY DEC 06-10, 2002 CL PHILADELPHIA, PENNSYLVANIA SP Amer Soc Hematol C1 Childrens Hosp, Div Hematol, Boston, MA USA. Dana Farber Canc Inst, Boston, MA 02115 USA. Northeastern Univ, Boston, MA 02115 USA. RI Neufeld, Ellis/F-9331-2011 NR 0 TC 0 Z9 0 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 NOV 16 PY 2002 VL 100 IS 11 MA 2601 BP 661A EP 661A PN 1 PG 1 WC Hematology SC Hematology GA 614JK UT WOS:000179184702603 ER PT J AU Tzachanis, D van Puijenbroek, AAFL Berezovskaya, A Nadler, LM Boussiotis, VA AF Tzachanis, D van Puijenbroek, AAFL Berezovskaya, A Nadler, LM Boussiotis, VA TI Activated Rap1 induces a molecular and functional phenotype of regulatory T cells. SO BLOOD LA English DT Meeting Abstract CT 44th Annual Meeting of the American-Society-of-Hematology CY DEC 06-10, 2002 CL PHILADELPHIA, PENNSYLVANIA SP Amer Soc Hematol C1 Dana Farber Canc Inst, Boston, MA 02115 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2002 VL 100 IS 11 MA 2640 BP 670A EP 671A PN 1 PG 2 WC Hematology SC Hematology GA 614JK UT WOS:000179184702642 ER PT J AU LeBlanc, R Hideshima, T Hayashi, T Catley, LP Burger, R Shringarpure, R Cheema, P Richardson, P Anderson, KC Munshi, NC AF LeBlanc, R Hideshima, T Hayashi, T Catley, LP Burger, R Shringarpure, R Cheema, P Richardson, P Anderson, KC Munshi, NC TI Thalidomide analogue IMiD3 provides T cell co-stimulation through B7-CD28 pathway. SO BLOOD LA English DT Meeting Abstract CT 44th Annual Meeting of the American-Society-of-Hematology CY DEC 06-10, 2002 CL PHILADELPHIA, PENNSYLVANIA SP Amer Soc Hematol C1 Dana Farber Canc Inst, Boston, MA 02115 USA. VA Boston Healthcare Syst, Boston, MA 02115 USA. RI Catley, Laurence/E-5313-2013 NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2002 VL 100 IS 11 MA 2642 BP 671A EP 671A PN 1 PG 1 WC Hematology SC Hematology GA 614JK UT WOS:000179184702644 ER PT J AU Haining, WN Kohane, DS Bergwelt, N Anderson, DG Cardoso, A Alves, P Kosmatopoulos, K Langer, R Nadler, LM AF Haining, WN Kohane, DS Bergwelt, N Anderson, DG Cardoso, A Alves, P Kosmatopoulos, K Langer, R Nadler, LM TI pH-triggered microparticles enhance peptide antigen delivery to dendritic cells: Implications for tumor vaccines. SO BLOOD LA English DT Meeting Abstract CT 44th Annual Meeting of the American-Society-of-Hematology CY DEC 06-10, 2002 CL PHILADELPHIA, PENNSYLVANIA SP Amer Soc Hematol C1 Dana Farber Canc Inst, Boston, MA 02115 USA. Massachusetts Gen Hosp Children, Boston, MA USA. MIT, Dept Chem Engn, Cambridge, MA 02139 USA. Inst Gustave Roussy, INSERM487, Paris, France. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2002 VL 100 IS 11 MA 2648 BP 672A EP 673A PN 1 PG 2 WC Hematology SC Hematology GA 614JK UT WOS:000179184702650 ER PT J AU Avigan, D Vasir, D Gong, JL Wu, ZK Borges, V Uhl, L Smith, T Schadt, K Tetreault, JC Giallombardo, N Kufe, D AF Avigan, D Vasir, D Gong, JL Wu, ZK Borges, V Uhl, L Smith, T Schadt, K Tetreault, JC Giallombardo, N Kufe, D TI Vaccination with dendritic cell (DC)-breast cancer fusions induces tumor specific immunity and clinical response in patients with metastatic breast cancer. SO BLOOD LA English DT Meeting Abstract CT 44th Annual Meeting of the American-Society-of-Hematology CY DEC 06-10, 2002 CL PHILADELPHIA, PENNSYLVANIA SP Amer Soc Hematol C1 Beth Israel Deaconess Med Ctr, Boston, MA 02215 USA. Dana Farber Canc Inst, Boston, MA 02115 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2002 VL 100 IS 11 MA 2651 BP 673A EP 673A PN 1 PG 1 WC Hematology SC Hematology GA 614JK UT WOS:000179184702653 ER PT J AU LeBlanc, R Butch, AW Hideshima, T Hayashi, T Kessler, B Shringarpure, R Burger, R Catley, LP Anderson, KC Munshi, NC AF LeBlanc, R Butch, AW Hideshima, T Hayashi, T Kessler, B Shringarpure, R Burger, R Catley, LP Anderson, KC Munshi, NC TI Dendritic cells efficiently internalize and process exogenous peptides despite proteasome inhibition. SO BLOOD LA English DT Meeting Abstract CT 44th Annual Meeting of the American-Society-of-Hematology CY DEC 06-10, 2002 CL PHILADELPHIA, PENNSYLVANIA SP Amer Soc Hematol C1 Dana Farber Canc Inst, Boston, MA 02115 USA. Univ Calif Los Angeles, Los Angeles, CA 90024 USA. Harvard Univ, Sch Med, Dept Cell Biol, Boston, MA USA. VA Boston Healthcare Syst, Boston, MA USA. RI Catley, Laurence/E-5313-2013 NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2002 VL 100 IS 11 MA 2656 BP 674A EP 674A PN 1 PG 1 WC Hematology SC Hematology GA 614JK UT WOS:000179184702658 ER PT J AU Rubio, MT Shaffer, J Fudaba, Y Sykes, M AF Rubio, MT Shaffer, J Fudaba, Y Sykes, M TI Use of CFSE and intracellular cytokine staining to detect CD8 T cell response to exogenous protein antigen presented by monocyte-derived human dendritic cells: Differential effects of PGE2 on antigen presentation to CD4 versus CD8 T cells. SO BLOOD LA English DT Meeting Abstract CT 44th Annual Meeting of the American-Society-of-Hematology CY DEC 06-10, 2002 CL PHILADELPHIA, PENNSYLVANIA SP Amer Soc Hematol C1 Harvard Univ, Massachusetts Gen Hosp, Sch Med, Transplantat Biol Res Ctr, Boston, MA USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2002 VL 100 IS 11 MA 2659 BP 675A EP 675A PN 1 PG 1 WC Hematology SC Hematology GA 614JK UT WOS:000179184702661 ER PT J AU Hong, W Pastore, Y Pool, L Schafer, AI Prchal, J AF Hong, W Pastore, Y Pool, L Schafer, AI Prchal, J TI Gain-of function mutation of human erythropoietin receptor in mice decreases neointimal formation. SO BLOOD LA English DT Meeting Abstract CT 44th Annual Meeting of the American-Society-of-Hematology CY DEC 06-10, 2002 CL PHILADELPHIA, PENNSYLVANIA SP Amer Soc Hematol C1 Baylor Coll Med, VA Med Ctr, Dept Med, Houston, TX 77030 USA. Baylor Coll Med, VA Med Ctr, Texas Childrens Canc Ctr, Houston, TX 77030 USA. NR 0 TC 0 Z9 0 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 NOV 16 PY 2002 VL 100 IS 11 MA 2681 BP 680A EP 681A PN 1 PG 2 WC Hematology SC Hematology GA 614JK UT WOS:000179184702683 ER PT J AU Hoffmeister, KM Isaac, NA Josefsson, EC Wagner, DD Clausen, H Stossel, TP Hartwig, JH AF Hoffmeister, KM Isaac, NA Josefsson, EC Wagner, DD Clausen, H Stossel, TP Hartwig, JH TI Mechanism, significance and repair of cold-mediated platelet clearance. SO BLOOD LA English DT Meeting Abstract CT 44th Annual Meeting of the American-Society-of-Hematology CY DEC 06-10, 2002 CL PHILADELPHIA, PENNSYLVANIA SP Amer Soc Hematol C1 Brigham & Womens Hosp, Div Hematol, Boston, MA 02115 USA. Univ Copenhagen, Sch Dent, DK-1168 Copenhagen, Denmark. Harvard Univ, Sch Med, Ctr Blood Res, Boston, MA 02115 USA. Harvard Univ, Sch Med, Div Pathol, Boston, MA USA. NR 0 TC 0 Z9 0 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 NOV 16 PY 2002 VL 100 IS 11 MA 2784 BP 707A EP 707A PN 1 PG 1 WC Hematology SC Hematology GA 614JK UT WOS:000179184702786 ER PT J AU Xi, H Akashi, K Jie, C Iwasaki, H Chao, N Zhang, JW Haug, J Li, LH AF Xi, H Akashi, K Jie, C Iwasaki, H Chao, N Zhang, JW Haug, J Li, LH TI Transcriptional accessibility for multi-tissue and multi-hematopoietic lineage genes during early hematopoiesis. SO BLOOD LA English DT Meeting Abstract CT 44th Annual Meeting of the American-Society-of-Hematology CY DEC 06-10, 2002 CL PHILADELPHIA, PENNSYLVANIA SP Amer Soc Hematol C1 Stowers Inst Med Res, Kansas City, MO USA. Harvard Univ, Sch Med, Dana Farber Canc Inst, Boston, MA 02115 USA. Univ Missouri, Kansas City, MO 64110 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2002 VL 100 IS 11 MA 2812 BP 714A EP 714A PN 1 PG 1 WC Hematology SC Hematology GA 614JK UT WOS:000179184702814 ER PT J AU Okuno, Y Radomska, HS Huettner, CS Iwasaki, H Akashi, K Tenen, DG AF Okuno, Y Radomska, HS Huettner, CS Iwasaki, H Akashi, K Tenen, DG TI Mapping critical cis-elements necessary for human CD34 gene expression. SO BLOOD LA English DT Meeting Abstract CT 44th Annual Meeting of the American-Society-of-Hematology CY DEC 06-10, 2002 CL PHILADELPHIA, PENNSYLVANIA SP Amer Soc Hematol C1 Kumamoto Univ, Sch Med, Dept Internal Med 2, Kumamoto 860, Japan. Harvard Univ, Sch Med, Harvard Inst Med, Boston, MA USA. Harvard Univ, Sch Med, Dana Farber Canc Inst, Dept Canc Immunol & AIDS, Boston, MA 02115 USA. NR 0 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 NOV 16 PY 2002 VL 100 IS 11 MA 2839 BP 720A EP 720A PN 1 PG 1 WC Hematology SC Hematology GA 614JK UT WOS:000179184702841 ER PT J AU Carlesso, N Chora, A Cruz, E Cristina, FL Goumnerov, B Rahme, L Aster, JC Cardoso, AA Scadden, DT AF Carlesso, N Chora, A Cruz, E Cristina, FL Goumnerov, B Rahme, L Aster, JC Cardoso, AA Scadden, DT TI Notch 1 and Jagged2 expression in the bone marrow microenvironment are modulated by inflammatory stimuli in vitro and in vivo. SO BLOOD LA English DT Meeting Abstract CT 44th Annual Meeting of the American-Society-of-Hematology CY DEC 06-10, 2002 CL PHILADELPHIA, PENNSYLVANIA SP Amer Soc Hematol C1 Harvard Univ, Massachusetts Gen Hosp, Sch Med, Charlestown, MA USA. Brigham & Womens Hosp, Boston, MA 02115 USA. Dana Farber Canc Inst, Boston, MA 02115 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2002 VL 100 IS 11 MA 2884 BP 730A EP 731A PN 1 PG 2 WC Hematology SC Hematology GA 614JK UT WOS:000179184702886 ER PT J AU Yee, KWH Braziel, RM O'Farrell, AM McGreevey, LS Haley, A Town, AR Griffith, DJ Cherrington, JM Heinrich, MC AF Yee, KWH Braziel, RM O'Farrell, AM McGreevey, LS Haley, A Town, AR Griffith, DJ Cherrington, JM Heinrich, MC TI SU11248 inhibits activation loop mutants of FLT3. SO BLOOD LA English DT Meeting Abstract CT 44th Annual Meeting of the American-Society-of-Hematology CY DEC 06-10, 2002 CL PHILADELPHIA, PENNSYLVANIA SP Amer Soc Hematol C1 Oregon Hlth Sci Univ, Portland, OR 97201 USA. Portland VA Med Ctr, Portland, OR USA. SUGEN Inc, Dept Preclin & Translat Med, San Francisco, CA USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2002 VL 100 IS 11 MA 2922 BP 739A EP 739A PN 1 PG 1 WC Hematology SC Hematology GA 614JK UT WOS:000179184702924 ER PT J AU Berghmans, S Murphey, R Wienholds, E Morris, JP Schulte-Merker, S Plasterk, RHA Zon, LI Look, AT AF Berghmans, S Murphey, R Wienholds, E Morris, JP Schulte-Merker, S Plasterk, RHA Zon, LI Look, AT TI Developing a model to study p53 carcinogenesis in zebrafish (Danio rerio). SO BLOOD LA English DT Meeting Abstract CT 44th Annual Meeting of the American-Society-of-Hematology CY DEC 06-10, 2002 CL PHILADELPHIA, PENNSYLVANIA SP Amer Soc Hematol C1 Harvard Univ, Sch Med, Dana Farber Canc Inst, Dept Pediat Oncol, Boston, MA 02115 USA. Harvard Univ, Childrens Hosp, Sch Med, Dept Med, Boston, MA 02115 USA. Netherlands Inst Dev Biol, Hubrecht Lab, NL-3584 CT Utrecht, Netherlands. ARTEMIS Pharmaceut GmbH, Exelis Deutschland, Tubingen, Germany. Childrens Hosp, Howard Hughes Med Inst, Boston, MA 02115 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2002 VL 100 IS 11 MA 2930 BP 741A EP 741A PN 1 PG 1 WC Hematology SC Hematology GA 614JK UT WOS:000179184702932 ER PT J AU Schoch, C Schnittger, S Look, AT Gilliland, DG Tenen, DG Behre, G Haferlach, T Hiddemann, W AF Schoch, C Schnittger, S Look, AT Gilliland, DG Tenen, DG Behre, G Haferlach, T Hiddemann, W TI Additional genetic abnormalities in AML t(8;21)/AML1-ETO. SO BLOOD LA English DT Meeting Abstract CT 44th Annual Meeting of the American-Society-of-Hematology CY DEC 06-10, 2002 CL PHILADELPHIA, PENNSYLVANIA SP Amer Soc Hematol C1 Lab Leukemia Diagnost, Dept Internal Med 3, Munich, Germany. Dana Farber Canc Inst, Boston, MA 02115 USA. Brigham & Womens Hosp, Boston, MA 02115 USA. Harvard Univ, Sch Med, Harvard Inst Med, Boston, MA USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2002 VL 100 IS 11 MA 2971 BP 751A EP 751A PN 1 PG 1 WC Hematology SC Hematology GA 614JK UT WOS:000179184702973 ER PT J AU Li, AH Neuberg, D Zuckerman, D Zuckerman, A Silverman, LB Sallan, SE Gribben, JG AF Li, AH Neuberg, D Zuckerman, D Zuckerman, A Silverman, LB Sallan, SE Gribben, JG TI Utilization of Ig heavy-chain variable, diversity and joining gene segments in childhood acute lymphoblastic leukemia. SO BLOOD LA English DT Meeting Abstract CT 44th Annual Meeting of the American-Society-of-Hematology CY DEC 06-10, 2002 CL PHILADELPHIA, PENNSYLVANIA SP Amer Soc Hematol C1 Harvard Univ, Sch Med, Childrens Hosp, Dana Farber Canc Inst, Boston, MA USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2002 VL 100 IS 11 MA 3009 BP 760A EP 761A PN 1 PG 2 WC Hematology SC Hematology GA 614JK UT WOS:000179184703011 ER PT J AU Costa, LF Sallan, SE Nadler, LM Cardoso, AA AF Costa, LF Sallan, SE Nadler, LM Cardoso, AA TI Leukemia stimulation of bone marrow endothelium activates the mTOR signaling pathway and is blocked by Rapamycin. SO BLOOD LA English DT Meeting Abstract CT 44th Annual Meeting of the American-Society-of-Hematology CY DEC 06-10, 2002 CL PHILADELPHIA, PENNSYLVANIA SP Amer Soc Hematol C1 Harvard Univ, Sch Med, Dana Farber Canc Inst, Boston, MA 02115 USA. Univ Lisbon, Sch Med, Inst Mol Med, P-1699 Lisbon, Portugal. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2002 VL 100 IS 11 MA 3014 BP 762A EP 762A PN 1 PG 1 WC Hematology SC Hematology GA 614JK UT WOS:000179184703016 ER PT J AU Friedberg, JW Fischman, A Neuberg, D Kim, H Takvorian, T Mauch, PM Canellos, GP Van den Abbeele, AD AF Friedberg, JW Fischman, A Neuberg, D Kim, H Takvorian, T Mauch, PM Canellos, GP Van den Abbeele, AD TI FDG-PET is superior to gallium scintigraphy in the staging and follow-up of patients with de novo Hodgkin's disease: A prospective, blinded comparison. SO BLOOD LA English DT Meeting Abstract CT 44th Annual Meeting of the American-Society-of-Hematology CY DEC 06-10, 2002 CL PHILADELPHIA, PENNSYLVANIA SP Amer Soc Hematol C1 Univ Rochester, James P Wilmot Canc Ctr, Rochester, NY 14627 USA. Dana Farber Canc Inst, Boston, MA 02115 USA. Massachusetts Gen Hosp, Boston, MA 02114 USA. Brigham & Womens Hosp, Boston, MA 02115 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2002 VL 100 IS 11 MA 3037 BP 768A EP 768A PN 1 PG 1 WC Hematology SC Hematology GA 614JK UT WOS:000179184703039 ER PT J AU Stone, R Yu, DH Stock, W Hars, V Linker, C DeAngelo, D Shea, T Marcucci, G Larson, R AF Stone, R Yu, DH Stock, W Hars, V Linker, C DeAngelo, D Shea, T Marcucci, G Larson, R TI A phase II trial of homoharringtonine (HHT) in combination with low-dose cytarabine (Iodac) via continuous intravenous infusion (CIVI) for newly diagnosed patients (pts) with chronic myeloid leukemia (CML): CALGB 19804. SO BLOOD LA English DT Meeting Abstract CT 44th Annual Meeting of the American-Society-of-Hematology CY DEC 06-10, 2002 CL PHILADELPHIA, PENNSYLVANIA SP Amer Soc Hematol C1 Dana Farber Canc Inst, Boston, MA 02115 USA. Duke Univ, CALGB Stat Ctr, Durham, NC 27706 USA. Univ Chicago, Chicago, IL 60637 USA. Univ Calif San Francisco, San Francisco, CA 94143 USA. Univ N Carolina, Chapel Hill, NC 27515 USA. Ohio State Univ, Columbus, OH 43210 USA. NR 0 TC 0 Z9 0 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 NOV 16 PY 2002 VL 100 IS 11 MA 3101 BP 784A EP 785A PN 1 PG 2 WC Hematology SC Hematology GA 614JK UT WOS:000179184703103 ER PT J AU List, AF DeAngelo, D O'Brien, S Cortes, J Wilson, J Sugrue, MM Zhu, YL Statkevich, P Baum, C Zaknoen, S AF List, AF DeAngelo, D O'Brien, S Cortes, J Wilson, J Sugrue, MM Zhu, YL Statkevich, P Baum, C Zaknoen, S TI Phase I study of continuous oral administration of lonafarnib (Sarasar (TM)) in patients with advanced hematologic malignancies. SO BLOOD LA English DT Meeting Abstract CT 44th Annual Meeting of the American-Society-of-Hematology CY DEC 06-10, 2002 CL PHILADELPHIA, PENNSYLVANIA SP Amer Soc Hematol C1 Univ Arizona, Arizona Canc Ctr, Tucson, AZ USA. Dana Farber Canc Inst, Boston, MA 02115 USA. Royal Victoria Infirm, Newcastle Upon Tyne NE1 4LP, Tyne & Wear, England. Univ Texas, MD Anderson Canc Ctr, Houston, TX 77030 USA. Schering Plough Corp, Res Inst, Kenilworth, NJ 07033 USA. NR 0 TC 19 Z9 20 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 NOV 16 PY 2002 VL 100 IS 11 MA 3120 BP 789A EP 789A PN 1 PG 1 WC Hematology SC Hematology GA 614JK UT WOS:000179184703122 ER PT J AU Cortes, J Holyoake, TL Silver, RT Simonsson, B DeAngelo, D Turner, AR Maloisel, F O'Brien, S List, AF Nielsen, JL Reiffers, J Baccarani, M Wilson, J Sugrue, MM Baum, CM Zaknoen, SL AF Cortes, J Holyoake, TL Silver, RT Simonsson, B DeAngelo, D Turner, AR Maloisel, F O'Brien, S List, AF Nielsen, JL Reiffers, J Baccarani, M Wilson, J Sugrue, MM Baum, CM Zaknoen, SL TI Continuous oral lonafarnib (Sarasar (TM)) for the treatment of patients with advanced hematologic malignancies: A phase II study. SO BLOOD LA English DT Meeting Abstract CT 44th Annual Meeting of the American-Society-of-Hematology CY DEC 06-10, 2002 CL PHILADELPHIA, PENNSYLVANIA SP Amer Soc Hematol C1 Univ Texas, MD Anderson Canc Ctr, Houston, TX 77030 USA. Glasgow Royal Infirm, Glasgow G4 0SF, Lanark, Scotland. Cornell Univ, Weill Med Coll, New York, NY USA. Univ Uppsala Hosp, Uppsala, Sweden. Dana Farber Canc Inst, Boston, MA 02115 USA. Cross Canc Inst, Edmonton, AB T6G 1Z2, Canada. Hospices Civils Strasbourg, Strasbourg, France. Royal Victoria Infirm, Newcastle Upon Tyne NE1 4LP, Tyne & Wear, England. Univ Arizona, Arizona Canc Ctr, Tucson, AZ USA. Med Haematol Afd B, Aarhus, Denmark. Hop Haut Leveque, Pessac, France. Univ Bologna, I-40126 Bologna, Italy. Schering Plough Res Inst, Kenilworth, NJ USA. NR 0 TC 12 Z9 13 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 NOV 16 PY 2002 VL 100 IS 11 MA 3132 BP 793A EP 793A PN 1 PG 1 WC Hematology SC Hematology GA 614JK UT WOS:000179184703134 ER PT J AU Gotlib, J Malone, JM DeAngelo, DJ Stone, RM Gilliland, DG Clark, J Tefferi, A Alam, R Schrier, SL Coutre, SE AF Gotlib, J Malone, JM DeAngelo, DJ Stone, RM Gilliland, DG Clark, J Tefferi, A Alam, R Schrier, SL Coutre, SE TI Imatinib mesylate (GLEEVEC (TM)) induces rapid and complete hematologic remissions in patients with idiopathic hypereosinophilic syndrome (HES) without evidence of BCR-ABL or activating mutations in C-KIT and platelet-derived growth factor receptor-beta (PDGFR-beta). SO BLOOD LA English DT Meeting Abstract CT 44th Annual Meeting of the American-Society-of-Hematology CY DEC 06-10, 2002 CL PHILADELPHIA, PENNSYLVANIA SP Amer Soc Hematol C1 Stanford Univ, Med Ctr, Stanford, CA 94305 USA. Dana Farber Canc Inst, Boston, MA 02115 USA. Howard Hughes Med Inst, Boston, MA 02115 USA. Mayo Clin, Rochester, MN USA. Univ Texas, Med Branch, Galveston, TX 77550 USA. NR 0 TC 10 Z9 11 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 NOV 16 PY 2002 VL 100 IS 11 MA 3152 BP 798A EP 798A PN 1 PG 1 WC Hematology SC Hematology GA 614JK UT WOS:000179184703154 ER PT J AU Podar, K Tai, YT Cole, CE Hideshima, T Sattler, M Hamblin, A Mitsiades, N Schlossman, R Munshi, N Chauhan, D Anderson, KC AF Podar, K Tai, YT Cole, CE Hideshima, T Sattler, M Hamblin, A Mitsiades, N Schlossman, R Munshi, N Chauhan, D Anderson, KC TI Essential role of lipid rafts in IL-6- and IGF-I-triggered Akt-1/PKB mediated survival of multiple myeloma cells. SO BLOOD LA English DT Meeting Abstract CT 44th Annual Meeting of the American-Society-of-Hematology CY DEC 06-10, 2002 CL PHILADELPHIA, PENNSYLVANIA SP Amer Soc Hematol C1 Dana Farber Canc Inst, Dept Adult Oncol, Boston, MA 02115 USA. Univ Michigan, Dept Internal Med, Ann Arbor, MI 48109 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2002 VL 100 IS 11 MA 3181 BP 806A EP 806A PN 1 PG 1 WC Hematology SC Hematology GA 614JK UT WOS:000179184703183 ER PT J AU Akiyama, M Hideshima, T Hayashi, T Tai, TT Mitsiades, CS Mitsiades, N Chauhan, D Richardson, P Munshi, NC Anderson, KC AF Akiyama, M Hideshima, T Hayashi, T Tai, TT Mitsiades, CS Mitsiades, N Chauhan, D Richardson, P Munshi, NC Anderson, KC TI Nuclear factor kappa B (NF-kappa B) p65 mediates nuclear translocation of telomerase reverse transcriptase (hTERT) protein in human multiple myeloma cell line. SO BLOOD LA English DT Meeting Abstract CT 44th Annual Meeting of the American-Society-of-Hematology CY DEC 06-10, 2002 CL PHILADELPHIA, PENNSYLVANIA SP Amer Soc Hematol C1 Dana Farber Canc Inst, Jerome Lipper Multiple Myeloma Ctr, Dept Med Oncol, Boston, MA 02115 USA. VA Boston Healthcare Syst, W Roxbury, MA USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2002 VL 100 IS 11 MA 3194 BP 809A EP 809A PN 1 PG 1 WC Hematology SC Hematology GA 614JK UT WOS:000179184703196 ER PT J AU Shammas, MA Reis, RJS Koley, H Goyal, RK Hurley, LH Anderson, KC Munshi, NC AF Shammas, MA Reis, RJS Koley, H Goyal, RK Hurley, LH Anderson, KC Munshi, NC TI Telomerase inhibition and apoptotic cell death following telomestatin treatment of multiple myeloma. SO BLOOD LA English DT Meeting Abstract CT 44th Annual Meeting of the American-Society-of-Hematology CY DEC 06-10, 2002 CL PHILADELPHIA, PENNSYLVANIA SP Amer Soc Hematol C1 Boston VA Hlth Care Syst, W Roxbury, MA USA. Dana Farber Canc Inst, Boston, MA 02115 USA. Univ Arkansas Med Sci, Dept Geriatr, Little Rock, AR 72205 USA. Univ Arkansas Med Sci, Dept Biochem & Mol Biol, Little Rock, AR 72205 USA. Cent Arkansas Vet Hlth Care Syst, Dept Geriatr, Little Rock, AR USA. Univ Arizona, Arizona Canc Ctr, Tucson, AZ 85721 USA. Univ Arizona, Coll Pharm, Tucson, AZ 85721 USA. Harvard Univ, Sch Med, Boston, MA USA. RI Shmookler Reis, Robert/C-4112-2009 NR 0 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 NOV 16 PY 2002 VL 100 IS 11 MA 3201 BP 810A EP 810A PN 1 PG 1 WC Hematology SC Hematology GA 614JK UT WOS:000179184703203 ER PT J AU Tai, YT Podar, K Mitsiades, N Lin, B Mitsiades, C Gupta, D Akiyama, M Catley, L Hideshima, T Burger, R Munshi, NC Treon, SP Anderson, KC AF Tai, YT Podar, K Mitsiades, N Lin, B Mitsiades, C Gupta, D Akiyama, M Catley, L Hideshima, T Burger, R Munshi, NC Treon, SP Anderson, KC TI CD40 induces human multiple myeloma cell migration via phosphatidylinositol 3-kinase/AKT/NF-kB signaling. SO BLOOD LA English DT Meeting Abstract CT 44th Annual Meeting of the American-Society-of-Hematology CY DEC 06-10, 2002 CL PHILADELPHIA, PENNSYLVANIA SP Amer Soc Hematol C1 Dana Farber Canc Inst, Boston, MA 02115 USA. RI Catley, Laurence/E-5313-2013 NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2002 VL 100 IS 11 MA 3202 BP 810A EP 811A PN 1 PG 2 WC Hematology SC Hematology GA 614JK UT WOS:000179184703204 ER PT J AU Mitsiades, CS Mitsiades, N Fanourakis, G Shringapurne, R Bailey, C Gu, XS Joseph, M Munshi, NC Liberman, T Anderson, KC AF Mitsiades, CS Mitsiades, N Fanourakis, G Shringapurne, R Bailey, C Gu, XS Joseph, M Munshi, NC Liberman, T Anderson, KC TI Gene expression and proteomic profiling of multiple myeloma (MM) cells co-cultured with bone marrow (BM) stromal cells or stimulated with BM-derived cytokines: Implications for therapeutic targeting of the BM milieu in MM. SO BLOOD LA English DT Meeting Abstract CT 44th Annual Meeting of the American-Society-of-Hematology CY DEC 06-10, 2002 CL PHILADELPHIA, PENNSYLVANIA SP Amer Soc Hematol C1 Harvard Univ, Sch Med, Dana Farber Canc Inst, Jerome Lipper Multiple Myeloma Ctr, Boston, MA 02115 USA. Harvard Inst Med, Beth Israel Deaconess Med Ctr, Boston, MA USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2002 VL 100 IS 11 MA 3206 BP 811A EP 812A PN 1 PG 2 WC Hematology SC Hematology GA 614JK UT WOS:000179184703208 ER PT J AU Jagannath, S Barlogie, B Berenson, J Siegel, D Irwin, D Richardson, PG Alexanian, R Limentani, SA Alsina, M Lee, S Esseltine, DL Kauffman, M Adams, J Schenkein, DP Anderson, KC AF Jagannath, S Barlogie, B Berenson, J Siegel, D Irwin, D Richardson, PG Alexanian, R Limentani, SA Alsina, M Lee, S Esseltine, DL Kauffman, M Adams, J Schenkein, DP Anderson, KC TI A phase II multicenter randomized study of the proteasome inhibitor bortezomib (VELCADE (TM), formerly PS-341) in multiple myeloma (MM) patients (pts) relapsed after front-line therapy. SO BLOOD LA English DT Meeting Abstract CT 44th Annual Meeting of the American-Society-of-Hematology CY DEC 06-10, 2002 CL PHILADELPHIA, PENNSYLVANIA SP Amer Soc Hematol C1 St Vincents Catholic Med Ctr, New York, NY USA. Univ Arkansas, Little Rock, AR 72204 USA. Cedars Sinai Med Ctr, Los Angeles, CA 90048 USA. Carol G Simon Canc Ctr, Morristown, NJ USA. Alta Bates Comprehens Canc Ctr, Berkeley, CA USA. Dana Farber Canc Inst, Boston, MA 02115 USA. Univ Texas, MD Anderson Canc Ctr, Houston, TX 77030 USA. Charlotte Med Clin, Charlotte, NC USA. Univ S Florida, H Lee Moffitt Canc Ctr, Tampa, FL 33682 USA. Millennium Pharmaceut Inc, Cambridge, MA USA. NR 0 TC 6 Z9 7 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 NOV 16 PY 2002 VL 100 IS 11 MA 3207 BP 812A EP 812A PN 1 PG 1 WC Hematology SC Hematology GA 614JK UT WOS:000179184703209 ER PT J AU Hideshima, T Akiyama, M Hayashi, T Richardson, PG Schlossman, RL Chauhan, D Anderson, KC AF Hideshima, T Akiyama, M Hayashi, T Richardson, PG Schlossman, RL Chauhan, D Anderson, KC TI Targeting p38 MAPK inhibits multiple myeloma cell growth in the bone marrow milieu. SO BLOOD LA English DT Meeting Abstract CT 44th Annual Meeting of the American-Society-of-Hematology CY DEC 06-10, 2002 CL PHILADELPHIA, PENNSYLVANIA SP Amer Soc Hematol C1 Dana Farber Canc Inst, Jerome Lipper Multiple Myeloma Ctr, Boston, MA 02115 USA. NR 0 TC 1 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 NOV 16 PY 2002 VL 100 IS 11 MA 3214 BP 813A EP 813A PN 1 PG 1 WC Hematology SC Hematology GA 614JK UT WOS:000179184703216 ER PT J AU Hideshima, T Hayashi, T Akiyama, M Chauhan, D Richardson, PG Mitsiades, C Mitsiades, N Munshi, NC Singer, JW Anderson, KC AF Hideshima, T Hayashi, T Akiyama, M Chauhan, D Richardson, PG Mitsiades, C Mitsiades, N Munshi, NC Singer, JW Anderson, KC TI Induction of apoptosis by lysophosphatidic acid acyltransferase (LPAAT)-beta inhibitors in multiple myeloma (MM). SO BLOOD LA English DT Meeting Abstract CT 44th Annual Meeting of the American-Society-of-Hematology CY DEC 06-10, 2002 CL PHILADELPHIA, PENNSYLVANIA SP Amer Soc Hematol C1 Dana Farber Canc Inst, Jerome Lipper Multiple Myeloma Ctr, Boston, MA 02115 USA. Cell Therapeut Inc, Seattle, WA USA. NR 0 TC 1 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 NOV 16 PY 2002 VL 100 IS 11 MA 3213 BP 813A EP 813A PN 1 PG 1 WC Hematology SC Hematology GA 614JK UT WOS:000179184703215 ER PT J AU Richardson, P Jagannath, S Schlossman, R Alsina, M Desikan, RK Blood, E Weller, E Mitsiades, C Hideshima, T Davies, F Doss, D Freeman, A Bosch, J Patin, J Dalton, W Anderson, KC AF Richardson, P Jagannath, S Schlossman, R Alsina, M Desikan, RK Blood, E Weller, E Mitsiades, C Hideshima, T Davies, F Doss, D Freeman, A Bosch, J Patin, J Dalton, W Anderson, KC TI Thalidomide for relapsed multiple myeloma after high dose therapy and stem cell transplantation: Results of an open-label, multicenter phase two study of efficacy, toxicity and correlation with biological activity. SO BLOOD LA English DT Meeting Abstract CT 44th Annual Meeting of the American-Society-of-Hematology CY DEC 06-10, 2002 CL PHILADELPHIA, PENNSYLVANIA SP Amer Soc Hematol C1 Dana Farber Canc Inst, Boston, MA 02115 USA. Celgene, Warren, NJ USA. St Vincents Catholic Med Ctr, New York, NY USA. Univ S Florida, H Lee Moffitt Canc Ctr, Tampa, FL 33682 USA. NR 0 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 NOV 16 PY 2002 VL 100 IS 11 MA 3212 BP 813A EP 813A PN 1 PG 1 WC Hematology SC Hematology GA 614JK UT WOS:000179184703214 ER PT J AU Treon, SP Emmanouilides, CA Kimby, E Branagan, A Mitsiades, C Anderson, KC Frankel, SR AF Treon, SP Emmanouilides, CA Kimby, E Branagan, A Mitsiades, C Anderson, KC Frankel, SR TI Pre-therapy serum IgM levels predict clinical response to extended rituximab in Waldenstrom's macroglobulinemia. SO BLOOD LA English DT Meeting Abstract CT 44th Annual Meeting of the American-Society-of-Hematology CY DEC 06-10, 2002 CL PHILADELPHIA, PENNSYLVANIA SP Amer Soc Hematol C1 Dana Farber Canc Inst, Boston, MA 02115 USA. Univ Calif Los Angeles, Med Ctr, Los Angeles, CA 90024 USA. Karolinska Inst, S-10401 Stockholm, Sweden. Greenebaum Canc Ctr, Baltimore, MD USA. NR 0 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 NOV 16 PY 2002 VL 100 IS 11 MA 3211 BP 813A EP 813A PN 1 PG 1 WC Hematology SC Hematology GA 614JK UT WOS:000179184703213 ER PT J AU Hideshima, T Mitsiades, C Akiyama, M Hayashi, T Chauhan, D Richardson, PG Schlossman, RL Podar, K Munshi, NC Mitsiades, N Anderson, KC AF Hideshima, T Mitsiades, C Akiyama, M Hayashi, T Chauhan, D Richardson, PG Schlossman, RL Podar, K Munshi, NC Mitsiades, N Anderson, KC TI Molecular mechanisms mediating anti-myeloma activity of proteasome inhibitor PS-341. SO BLOOD LA English DT Meeting Abstract CT 44th Annual Meeting of the American-Society-of-Hematology CY DEC 06-10, 2002 CL PHILADELPHIA, PENNSYLVANIA SP Amer Soc Hematol C1 Dana Farber Canc Inst, Jerome Lipper Multiple Myeloma Ctr, Boston, MA 02115 USA. NR 0 TC 0 Z9 0 U1 1 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 NOV 16 PY 2002 VL 100 IS 11 MA 3215 BP 814A EP 814A PN 1 PG 1 WC Hematology SC Hematology GA 614JK UT WOS:000179184703217 ER PT J AU Hayashi, T Hideshima, T Akiyama, M Munshi, N Chauhan, D Anderson, KC AF Hayashi, T Hideshima, T Akiyama, M Munshi, N Chauhan, D Anderson, KC TI Mechanisms whereby immunomedulatory analogs of thalidomide augment autologous NK cell anti-myeloma immunity. SO BLOOD LA English DT Meeting Abstract CT 44th Annual Meeting of the American-Society-of-Hematology CY DEC 06-10, 2002 CL PHILADELPHIA, PENNSYLVANIA SP Amer Soc Hematol C1 Dana Farber Canc Inst, Dept Adult Oncol, Boston, MA 02115 USA. Harvard Univ, Sch Med, Dept Med, Boston, MA 02115 USA. NR 0 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 NOV 16 PY 2002 VL 100 IS 11 MA 3219 BP 815A EP 815A PN 1 PG 1 WC Hematology SC Hematology GA 614JK UT WOS:000179184703221 ER PT J AU Mitsiades, N Mitsiades, CS Poulaki, V Chauhan, D Fanourakis, G Gu, XS Bailey, C Joseph, M Libermann, TA Richardson, PG Munshi, NC Hideshima, T Anderson, KC AF Mitsiades, N Mitsiades, CS Poulaki, V Chauhan, D Fanourakis, G Gu, XS Bailey, C Joseph, M Libermann, TA Richardson, PG Munshi, NC Hideshima, T Anderson, KC TI Delineation of the apoptotic cascade induced by the proteasome inhibitor PS-341 in human multiple myeloma cells using microarray profiling and functional analysis: Clinical implications. SO BLOOD LA English DT Meeting Abstract CT 44th Annual Meeting of the American-Society-of-Hematology CY DEC 06-10, 2002 CL PHILADELPHIA, PENNSYLVANIA SP Amer Soc Hematol C1 Harvard Univ, Sch Med, Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02115 USA. Harvard Univ, Massachusetts Eye & Ear Infirm, Sch Med, Boston, MA USA. Harvard Inst Med, Beth Israel Deaconess Med Ctr, Genom Ctr, Boston, MA USA. NR 0 TC 0 Z9 0 U1 1 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 NOV 16 PY 2002 VL 100 IS 11 MA 3221 BP 815A EP 815A PN 1 PG 1 WC Hematology SC Hematology GA 614JK UT WOS:000179184703223 ER PT J AU Mitsiades, N Mitsiades, CS Poulaki, V Fanourakis, G Chauhan, D Munshi, NC Hideshima, T Anderson, KC AF Mitsiades, N Mitsiades, CS Poulaki, V Fanourakis, G Chauhan, D Munshi, NC Hideshima, T Anderson, KC TI The proteasome inhibitor PS-341 modulates VEGF secretion and activity in multiple myeloma. SO BLOOD LA English DT Meeting Abstract CT 44th Annual Meeting of the American-Society-of-Hematology CY DEC 06-10, 2002 CL PHILADELPHIA, PENNSYLVANIA SP Amer Soc Hematol C1 Harvard Univ, Sch Med, Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02115 USA. Harvard Univ, Massachusetts Eye & Ear Infirm, Sch Med, Boston, MA USA. NR 0 TC 0 Z9 0 U1 1 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 NOV 16 PY 2002 VL 100 IS 11 MA 3220 BP 815A EP 815A PN 1 PG 1 WC Hematology SC Hematology GA 614JK UT WOS:000179184703222 ER PT J AU Mitsiades, N Mitsiades, CS Poulaki, V Fanourakis, G Schlossman, R Munshi, NC Richardson, PG Anderson, KC AF Mitsiades, N Mitsiades, CS Poulaki, V Fanourakis, G Schlossman, R Munshi, NC Richardson, PG Anderson, KC TI Histone deacetylase (HDAC) inhibitors in the treatment of multiple myeloma (MM): Mechanisms of action and therapeutic applications. SO BLOOD LA English DT Meeting Abstract CT 44th Annual Meeting of the American-Society-of-Hematology CY DEC 06-10, 2002 CL PHILADELPHIA, PENNSYLVANIA SP Amer Soc Hematol C1 Harvard Univ, Sch Med, Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02115 USA. Harvard Univ, Massachusetts Eye & Ear Infirm, Sch Med, Boston, MA USA. NR 0 TC 0 Z9 0 U1 1 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 NOV 16 PY 2002 VL 100 IS 11 MA 3222 BP 815A EP 815A PN 1 PG 1 WC Hematology SC Hematology GA 614JK UT WOS:000179184703224 ER PT J AU Akiyama, M Hideshima, T Hayashi, T Tai, TT Shammas, M Gryaznov, S Anderson, KC Munshi, NC AF Akiyama, M Hideshima, T Hayashi, T Tai, TT Shammas, M Gryaznov, S Anderson, KC Munshi, NC TI The effect of telomerase inhibitor oligonucleotide N3 '-P5 ' phosphoramidate in human multiple myeloma cell lines. SO BLOOD LA English DT Meeting Abstract CT 44th Annual Meeting of the American-Society-of-Hematology CY DEC 06-10, 2002 CL PHILADELPHIA, PENNSYLVANIA SP Amer Soc Hematol C1 Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02115 USA. VA Boston Healthcare Syst, W Roxbury, MA USA. Geron Corp, Menlo Pk, CA USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2002 VL 100 IS 11 MA 3226 BP 816A EP 816A PN 1 PG 1 WC Hematology SC Hematology GA 614JK UT WOS:000179184703228 ER PT J AU Kim, YM Sachs, T Bronson, R Sykes, M AF Kim, YM Sachs, T Bronson, R Sykes, M TI FTY720 provides a new approach for separating graft-versus host disease (GvHD) from graft-versus-tumor effects. SO BLOOD LA English DT Meeting Abstract CT 44th Annual Meeting of the American-Society-of-Hematology CY DEC 06-10, 2002 CL PHILADELPHIA, PENNSYLVANIA SP Amer Soc Hematol C1 Harvard Univ, Massachusetts Gen Hosp, Sch Med, Transplantat Biol Res Ctr, Boston, MA USA. Harvard Univ, Sch Med, Dept Pathol, Boston, MA 02115 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2002 VL 100 IS 11 MA 3234 BP 818A EP 818A PN 1 PG 1 WC Hematology SC Hematology GA 614JK UT WOS:000179184703236 ER PT J AU Lin, BK Catley, LP LeBlanc, R Gupta, D Burger, R Tai, YT Podar, K Wartmann, M Griffin, JD Anderson, KC AF Lin, BK Catley, LP LeBlanc, R Gupta, D Burger, R Tai, YT Podar, K Wartmann, M Griffin, JD Anderson, KC TI EPO906 (Epothilone B) inhibits cell growth and survival of multiple myeloma cells in the bone marrow microenvironment, in vitro and in vivo. SO BLOOD LA English DT Meeting Abstract CT 44th Annual Meeting of the American-Society-of-Hematology CY DEC 06-10, 2002 CL PHILADELPHIA, PENNSYLVANIA SP Amer Soc Hematol C1 Dana Farber Canc Inst, Jerome Lipper Multiple Myeloma Ctr, Dept Adult Oncol, Boston, MA 02115 USA. Harvard Univ, Sch Med, Dept Med, Boston, MA USA. Novartis Pharma AG, Business Unit Oncol, Basel, Switzerland. RI Catley, Laurence/E-5313-2013 NR 0 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 NOV 16 PY 2002 VL 100 IS 11 MA 3233 BP 818A EP 818A PN 1 PG 1 WC Hematology SC Hematology GA 614JK UT WOS:000179184703235 ER PT J AU Krause, DS Van Etten, RA AF Krause, DS Van Etten, RA TI Adoptive immunotherapy of BCR-ABL-induced chronic myeloid leukemia-like myeloproliferative disease in a murine model. SO BLOOD LA English DT Meeting Abstract CT 44th Annual Meeting of the American-Society-of-Hematology CY DEC 06-10, 2002 CL PHILADELPHIA, PENNSYLVANIA SP Amer Soc Hematol C1 Harvard Univ, Sch Med, Ctr Blood Res, Boston, MA 02115 USA. Harvard Univ, Sch Med, Dept Genet, Boston, MA USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2002 VL 100 IS 11 MA 3251 BP 823A EP 823A PN 1 PG 1 WC Hematology SC Hematology GA 614JK UT WOS:000179184703253 ER PT J AU Friedberg, JW Li, SG Kim, H Neuberg, D Boyd, K Daley, H Fisher, DC Monroy, R Spitzer, TR Freedman, AS AF Friedberg, JW Li, SG Kim, H Neuberg, D Boyd, K Daley, H Fisher, DC Monroy, R Spitzer, TR Freedman, AS TI High-dose chemotherapy, autologous stem cell transplantation (ASCT) and ex vivo lymphoma cell purging using B-cell high density microparticles (HDM) cell separation system: PCR does not accurately predict disease recurrence in patients (pts) with follicular non-Hodgkin's lymphoma (FL). SO BLOOD LA English DT Meeting Abstract CT 44th Annual Meeting of the American-Society-of-Hematology CY DEC 06-10, 2002 CL PHILADELPHIA, PENNSYLVANIA SP Amer Soc Hematol C1 Univ Rochester, James P Wilmot Canc Ctr, Rochester, NY 14627 USA. Dana Farber Canc Inst, Boston, MA 02115 USA. Biotransplant Inc, Charlestown, MA USA. Massachusetts Gen Hosp, Boston, MA 02114 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2002 VL 100 IS 11 MA 3296 BP 835A EP 835A PN 1 PG 1 WC Hematology SC Hematology GA 614JK UT WOS:000179184703298 ER PT J AU Menzin, J Lang, K Earle, C Glendenning, A AF Menzin, J Lang, K Earle, C Glendenning, A TI Treatment patterns and outcomes among elderly patients with chronic myeloid leukemia: An analysis of linked SEER-Medicare data. SO BLOOD LA English DT Meeting Abstract CT 44th Annual Meeting of the American-Society-of-Hematology CY DEC 06-10, 2002 CL PHILADELPHIA, PENNSYLVANIA SP Amer Soc Hematol C1 Boston Hlth Econ Inc, Waltham, MA USA. Dana Farber Canc Inst, Boston, MA 02115 USA. Novartis Pharmaceut Corp, E Hanover, NJ USA. NR 0 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 NOV 16 PY 2002 VL 100 IS 11 MA 3450 BP 875A EP 875A PN 1 PG 1 WC Hematology SC Hematology GA 614JK UT WOS:000179184703452 ER PT J AU Henault, RG Eugenio, KR Kelliher, AF Alexis, AF Alexis, G Conlin, PR AF Henault, RG Eugenio, KR Kelliher, AF Alexis, AF Alexis, G Conlin, PR TI Transmitting clinical recommendations for diabetes care via e-mail SO AMERICAN JOURNAL OF HEALTH-SYSTEM PHARMACY LA English DT Editorial Material ID PATIENT-PHYSICIAN COMMUNICATION C1 VABHS, Dept Pharm, Brockton, MA USA. St Lukes Hosp, Dept Pharm, New Bedford, MA USA. Harvard Univ, Sch Med, Dept Med, Boston, MA 02115 USA. RP Henault, RG (reprint author), VABHS, Dept Pharm, Brockton, MA USA. NR 9 TC 2 Z9 2 U1 0 U2 1 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 NOV 15 PY 2002 VL 59 IS 22 BP 2166 EP + PG 3 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA 614KT UT WOS:000179188600005 PM 12455299 ER PT J AU Malhotra, A Huang, YQ Fogel, RB Pillar, G Edwards, JK Kikinis, R Loring, SH White, DP AF Malhotra, A Huang, YQ Fogel, RB Pillar, G Edwards, JK Kikinis, R Loring, SH White, DP TI The male predisposition to pharyngeal collapse - Importance of airway length SO AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE LA English DT Article DE apnea; finite element; length; sleep; upper airway ID OBSTRUCTIVE SLEEP-APNEA; WAKING GENIOGLOSSAL ELECTROMYOGRAM; QUANTITATIVE FOLLOW-UP; MUSCLE-ACTIVITY; NORMAL MEN; GENDER DIFFERENCES; HEALTHY-MEN; SOFT-TISSUE; PRESSURE; WOMEN AB Obstructive sleep apnea is an important disorder because of both its prevalence and its cardiovascular and neurocognitive sequelae. Despite the fact that male sex is a major risk factor for this disorder, the mechanisms underlying this predisposition are unclear. To understand the pathophysiologic basis of the male predisposition for pharyngeal collapse, we performed a detailed analysis of the anatomic and physiologic features of the upper airway in a cohort of normal and near-normal subjects (equal number of men and women). Although no important physiologic (genioglossal electromyogram, airflow resistance) differences were observed between sexes, a number of anatomic differences were apparent. The pharyngeal airway length was substantially longer in men compared with women. There was also an increased cross-sectional area of the soft palate and an increased airway volume in men compared with women. Using signal-averaged anatomic data from male and female subjects, we developed representative male and female finite element airway models. This model demonstrated the male airway to be substantially more collapsible than the female airway, solely on the basis of anatomic differences. This study suggests that the male predisposition to pharyngeal collapse is anatomically based, primarily as the result of an increased length of vulnerable airway as well as increased soft palate size. C1 Brigham & Womens Hosp, Dept Med, Div Sleep Med, Boston, MA 02115 USA. Brigham & Womens Hosp, Dept Med, Div Pulm & Crit Care Med, Boston, MA 02115 USA. Massachusetts Gen Hosp, Boston, MA 02114 USA. Harvard Univ, Sch Med, Boston, MA 02114 USA. RP Malhotra, A (reprint author), Brigham & Womens Hosp, Dept Med, Div Sleep Med, 221 Longwood Bldg,RF 486, Boston, MA 02115 USA. FU NCRR NIH HHS [MO1 RR02635]; NHLBI NIH HHS [1 P50 HL60292, R01 HL48531, T32 HL07633] NR 68 TC 166 Z9 168 U1 0 U2 9 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 NOV 15 PY 2002 VL 166 IS 10 BP 1388 EP 1395 DI 10.1164/rccm.2112072 PG 8 WC Critical Care Medicine; Respiratory System SC General & Internal Medicine; Respiratory System GA 613DM UT WOS:000179116500017 PM 12421747 ER PT J AU Otto, MW AF Otto, MW TI Learning and "unlearning" fears: Preparedness, neural pathways, and patients SO BIOLOGICAL PSYCHIATRY LA English DT Editorial Material ID PANIC DISORDER; NEGATIVE BELIEFS; SOCIAL PHOBIA; EXPOSURE; THERAPY; ANXIETY C1 Massachusetts Gen Hosp, Cognit Behav Therapy Program, Boston, MA 02114 USA. Harvard Univ, Sch Med, Cognit Behav Therapy Program, Boston, MA 02114 USA. RP Otto, MW (reprint author), Massachusetts Gen Hosp, Cognit Behav Therapy Program, WACC-812,15 Parkman St, Boston, MA 02114 USA. NR 18 TC 14 Z9 14 U1 0 U2 2 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD NOV 15 PY 2002 VL 52 IS 10 BP 917 EP 920 AR PII S0002-3223(02)01719-5 DI 10.1016/S0006-3223(02)01719-5 PG 4 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA 615GW UT WOS:000179238300001 PM 12437932 ER PT J AU Kuter, DJ Begley, CG AF Kuter, DJ Begley, CG TI Recombinant human thrombopoietin: basic biology and evaluation of clinical studies SO BLOOD LA English DT Review ID HUMAN MEGAKARYOCYTE GROWTH; ACUTE MYELOID-LEUKEMIA; C-MPL LIGAND; COLONY-STIMULATING FACTOR; PHASE-I TRIAL; PROPHYLACTIC PLATELET TRANSFUSIONS; HEMATOPOIETIC STEM-CELLS; FACTOR PEG-RHUMGDF; CHEMOTHERAPY-INDUCED THROMBOCYTOPENIA; CARBOPLATIN-INDUCED THROMBOCYTOPENIA AB Thrombocytopenia is a common medical problem for which the main treatment is platelet transfusion. Given the increasing use of platelets and the declining donor population, identification of a safe and effective platelet growth factor could improve the management of thrombocytopenia. Thrombopoietin (TPO), the c-Mpl ligand, is the primary physiologic regulator of megakaryocyte and platelet development. Since the purification of TPO in 1994, 2 recombinant forms of the c-Mpl ligand-recombinant human thrombopoletin (rhTPO) and pegylated recombinant human megakaryocyte growth and development factor (PEG-rHuMGDF)-have undergone extensive clinical investigation. Both have been shown to be potent stimulators of megakaryocyte growth and platelet production and are biologically active in reducing the thrombocytopenia of nonmyeloablative chemotherapy. However, neither TPO has demonstrated benefit in stem cell transplantation or leukemia chemotherapy. Other clinical studies have investigated the use of TPO in treating chronic nonchemotherapy-induced thrombocytopenia associated with myelodysplastic syndromes, idiopathic thrombocytopenic purpura, thrombocytopenia due to human immunodeficiency virus, and liver disease. Based solely on animal studies, TPO may be effective in reducing surgical thrombocytopenia and bleeding, ex vivo expansion of pluripotent stem cells, and as a radioprotectant. Ongoing and future studies will help define the clinical role of recombinant TPO and TPO mimetics in the treatment of chemotherapy- and nonchemotherapy-induced thrombocytopenia. C1 Harvard Univ, Massachusetts Gen Hosp, Sch Med, Hematol Oncol Unit, Boston, MA 02114 USA. Univ Western Australia, Ctr Child Hlth Res, Perth, WA, Australia. Western Australian Inst Med Res, Perth, WA, Australia. RP Kuter, DJ (reprint author), Harvard Univ, Massachusetts Gen Hosp, Sch Med, Hematol Oncol Unit, 100 Blossom St, Boston, MA 02114 USA. FU NHLBI NIH HHS [HL61272, HL54838] NR 157 TC 206 Z9 229 U1 1 U2 9 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 NOV 15 PY 2002 VL 100 IS 10 BP 3457 EP 3469 DI 10.1182/blood.V100.10.3457 PG 13 WC Hematology SC Hematology GA 613YE UT WOS:000179158500004 PM 12411315 ER PT J AU Antin, JH Weisdorf, D Neuberg, D Nicklow, R Clouthier, S Lee, SJ Alyea, E McGarigle, C Blazar, BR Sonis, S Soiffer, RJ Ferrara, JLM AF Antin, JH Weisdorf, D Neuberg, D Nicklow, R Clouthier, S Lee, SJ Alyea, E McGarigle, C Blazar, BR Sonis, S Soiffer, RJ Ferrara, JLM TI Interleukin-1 blockade does not prevent acute graft-versus-host disease: results of a randomized, double-blind, placebo-controlled trial of interleukin-1 receptor antagonist in allogeneic bone marrow transplantation SO BLOOD LA English DT Article ID CYTOKINE GENE-EXPRESSION; PERIPHERAL-BLOOD; CELLS; MICE AB Acute graft-versus-host disease (GVHD) is thought to derive from direct T-cell injury of target tissues through perforin/granzyme, Fas/FasL interactions, and the effects of inflammatory cytokines. Animal models and some clinical trials support the notion that inhibition of inflammatory mediators such as Interleukin-1 (IL-1), tumor necrosis factor alpha, and interferon gamma may ameliorate or prevent GVHD. We hypothesized that blockade of IL-1 during the period of initial T-cell activation would reduce the risk of severe GVHD. We tested this hypothesis In a double-blind, placebo-controlled randomized trial of recombinant human IL-1 receptor antagonist (IL-1 Ra) in 186 patients undergoing allogeneic stem cell transplantation. Randomization was stratified by degree of histocompatibility and stem cell source. All patients were conditioned with cyclophosphamide and total body irradiation. GVHD prevention consisted of cyclosporine and methotrexate in all patients. Recombinant human IL-1 Ra or saline placebo was given from day -4 to day +10. Randomization was stratified according to GVHD risk. The 2 groups were well-matched for pretreatment characteristics. Moderate to severe GVHD (grades B-D) developed in 57 (61%) of 94 patients receiving IL-1Ra and in 51 (59%) of 86 patients on placebo (P = .88). There was no difference in hematologic recovery, transplantation-related toxicity, event-free survival, or overall survival. We conclude that blockade of IL-1 using IL-1Ra during conditioning and 10 days immediately after transplantation is not sufficient to reduce GVHD or toxicity or to improve survival. C1 Brigham & Womens Hosp, Dana Farber Canc Inst, Dept Med Oncol & Biostat Sci, Boston, MA 02115 USA. Brigham & Womens Hosp, Dept Med, Boston, MA 02115 USA. Brigham & Womens Hosp, Dept Surg, Boston, MA 02115 USA. Univ Minnesota, Dept Med, Blood & Marrow Transplant Program, Minneapolis, MN 55455 USA. Univ Minnesota, Dept Pediat, Blood & Marrow Transplant Program, Minneapolis, MN 55455 USA. RP Antin, JH (reprint author), Dana Farber Canc Inst, 44 Binney St, Boston, MA 02115 USA. FU FDA HHS [FD-R-001704] NR 16 TC 85 Z9 86 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 NOV 15 PY 2002 VL 100 IS 10 BP 3479 EP 3483 DI 10.1182/blood-2002-03-0985 PG 5 WC Hematology SC Hematology GA 613YE UT WOS:000179158500006 PM 12393661 ER PT J AU Da Silva, N Bharti, A Shelley, CS AF Da Silva, N Bharti, A Shelley, CS TI hnRNP-K and Pur alpha act together to repress the transcriptional activity of the CD43 gene promoter SO BLOOD LA English DT Article ID WISKOTT-ALDRICH SYNDROME; NUCLEAR RIBONUCLEOPROTEIN-K; SINGLE-STRANDED-DNA; T-CELL ACTIVATION; LYMPHOCYTE SURFACE SIALOGLYCOPROTEIN; RNA-BINDING-PROTEINS; SIALOPHORIN CD43; HUMAN LEUKOSIALIN; MAJOR SIALOGLYCOPROTEIN; MONOCLONAL-ANTIBODY AB CD43 is an abundant, heavily glycosylated molecule expressed specifically on the surface of leukocytes and platelets. When leukocytes are at rest, CD43 acts to prevent both homotypic and heterotypic Interactions. However, during leukocyte activation CD43 expression is repressed, facilitating the intercellular contact required for chemotaxis, phagocytosis, aggregation, adhesion to endothelium, and transendothelial migration. Consequently, CD43 repression plays a vital role both in Innate and acquired immunity. Here we report that a dramatic down-regulation of CD43 mRNA levels occurs during activation of the leukocytic cell line K562. This repression coincides with repression of the transcriptional activity of the CD43 gene promoter. We have determined that heterogeneous nuclear ribonucleoprotein K (hnRNP-K) and Puralpha act together to mediate repression of the CD43 promoter during K562 activation. The hnRNP-K molecule and Pura bind single-stranded DNA. Therefore, exposure of single-stranded structures within the CD43 promoter probably plays a major role in effecting CD43 repression. C1 Harvard Univ, Massachusetts Gen Hosp, Sch Med, Renal Unit, Charlestown, MA 02129 USA. Dana Farber Canc Inst, Boston, MA 02115 USA. RP Shelley, CS (reprint author), Harvard Univ, Massachusetts Gen Hosp, Sch Med, Renal Unit, 149 13th St, Charlestown, MA 02129 USA. FU NIDDK NIH HHS [DK43351, DK50779] NR 87 TC 30 Z9 30 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 NOV 15 PY 2002 VL 100 IS 10 BP 3536 EP 3544 DI 10.1182/blood.V100.10.3536 PG 9 WC Hematology SC Hematology GA 613YE UT WOS:000179158500015 PM 12411317 ER PT J AU Mayerhofer, M Valent, P Sperr, WR Griffin, JD Sillaber, C AF Mayerhofer, M Valent, P Sperr, WR Griffin, JD Sillaber, C TI BCR/ABL induces expression of vascular endothelial growth factor and its transcriptional activator, hypoxia inducible factor-1 alpha, through a pathway involving phosphoinositide 3-kinase and the mammalian target of rapamycin SO BLOOD LA English DT Article ID FACTOR UP-REGULATION; KINASE-C-ZETA; BCR-ABL; TUMOR ANGIOGENESIS; MYELODYSPLASTIC SYNDROMES; HEMATOPOIETIC-CELLS; DISTINCT MECHANISMS; SIGNALING PATHWAY; AKT PROTOONCOGENE; TRANSFORMED-CELLS AB Recent data suggest that vascular endothelial growth factor (VEGF), a cytokine involved in autocrine growth of tumor cells and tumor angiogenesis, is up-regulated and plays a potential role In myelogenous leukemias. In chronic myelogenous leukemia (CML), VEGF is expressed at high levels in the bone marrow and peripheral blood. We show here that the CML-assoclated oncogene BCR/ABL induces VEGF gene expression in growth factor-dependent Ba/F3 cells. Whereas starved cells were found to contain only baseline levels of VEGF mRNA, Ba/F3 cells induced to express BCR/ABL exhibited substantial amounts of VEGF mRNA. BCR/ABL also induced VEGF promoter activity and increased VEGF protein levels in Ba/F3 cells. Moreover, BCR/ABL was found to promote the expression of functionally active hypoxia-inducible factor-1 (HIF-1), a major transcriptional regulator of VEGF gene expression. BCR/ABL-induced VEGF gene expression was counteracted by the phosphoinositide 3-kinase (PI3-kinase) inhibitor LY294002 and rapamycin, an antagonist of mammalian target of rapamycin (mTOR), but not by inhibition Of the mitogen-activated protein kinase pathway. Similarly, BCR/ABL-dependent HIF-1alpha expression was inhibited by the addition of LY294002 and rapamycin. Together, our data show that BCR/ABL induces VEGF- and HIF-1alpha gene expression through a pathway involving PI3-kinase and mTOR. BCR/ABL-induced VEGF expression may contribute to the pathogenesis and increased angiogenesis in CML. C1 Univ Vienna, Dept Internal Med 1, Div Hematol & Hemostaseol, AKH Wien, A-1097 Vienna, Austria. Harvard Univ, Sch Med, Dana Farber Canc Inst, Dept Adult Oncol, Boston, MA 02115 USA. RP Sillaber, C (reprint author), Univ Vienna, Dept Internal Med 1, Div Hematol & Hemostaseol, AKH Wien, Wahringer Gurtel 18-20, A-1097 Vienna, Austria. NR 58 TC 198 Z9 208 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 NOV 15 PY 2002 VL 100 IS 10 BP 3767 EP 3775 DI 10.1182/blood-2002-01-0109 PG 9 WC Hematology SC Hematology GA 613YE UT WOS:000179158500044 PM 12393646 ER PT J AU Weinstein, DA Roy, CN Fleming, MD Loda, MF Wolfsdorf, JI Andrews, NC AF Weinstein, DA Roy, CN Fleming, MD Loda, MF Wolfsdorf, JI Andrews, NC TI Inappropriate expression of hepcidin is associated with iron refractory anemia: implications for the anemia of chronic disease SO BLOOD LA English DT Article ID PEPTIDE; MICE; GENE; INFECTION; OVERLOAD; LIVER; MOUSE AB The anemia of chronic disease is a prevalent, poorly understood condition that afflicts patients with a wide variety of diseases, including infections, malignancies, and rheumatologic disorders. It is characterized by a blunted erythropoietin response by erythroid precursors, decreased red blood cell survival, and a defect in iron absorption and macrophage iron retention, which interrupts iron delivery to erythroid precursor cells. We noted that patients with large hepatic adenomas had severe iron refractory anemia similar to that observed in anemia of chronic disease. This anemia resolved spontaneously after adenoma resection or liver transplantation. We investigated the role of the adenomas in the pathogenesis of the anemia and found that they produce inappropriately high levels of hepcidin mRNA. Hepcidin is a peptide hormone that has been implicated in controlling the release of iron from cells. We conclude that hepcidin plays a major, causative role in the anemia observed in our subgroup of patients with hepatic adenomas, and we speculate that it is important in the pathogenesis of the anemia of chronic disease in general. C1 Harvard Univ, Sch Med, Childrens Hosp, Boston, MA USA. Brigham & Womens Hosp, Boston, MA 02115 USA. Dana Farber Canc Inst, Boston, MA 02115 USA. Harvard Univ, Sch Med, Childrens Hosp, Howard Hughes Med Inst, Boston, MA USA. RP Andrews, NC (reprint author), Childrens Hosp Boston, Div Hematol Oncol, Enders 720,300 Longwood Ave, Boston, MA 02115 USA. OI Andrews, Nancy/0000-0003-0243-4462 FU NCRR NIH HHS [M01RR02172]; NHLBI NIH HHS [T32-HL07623-15]; PHS HHS [K08-03600] NR 26 TC 374 Z9 410 U1 2 U2 17 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 NOV 15 PY 2002 VL 100 IS 10 BP 3776 EP 3781 DI 10.1182/blood-2002-04-1260 PG 6 WC Hematology SC Hematology GA 613YE UT WOS:000179158500045 PM 12393428 ER PT J AU Montanez, S Daws, LC Gould, GG Gerhardt, GA Frazer, A AF Montanez, S Daws, LC Gould, GG Gerhardt, GA Frazer, A TI Differential in vivo clearance of serotonin in rat dorsal raphe nucleus and CA3 region SO BRAIN RESEARCH LA English DT Article DE serotonin transporter; dorsal raphe nucleus; CA3; chronoamperometry; rat ID NOREPINEPHRINE UPTAKE SITES; IN-VIVO; QUANTITATIVE AUTORADIOGRAPHY; EXTRACELLULAR SEROTONIN; DOPAMINE UPTAKE; ELECTRON-MICROSCOPY; REUPTAKE INHIBITORS; PREFRONTAL CORTEX; SUBSTANTIA-NIGRA; MESSENGER-RNA AB In vivo chronoamperometric recordings were used to determine if the majority of serotonin transporters (SERTs) in the dorsal raphe nucleus (DRN) are functionally active. This was achieved by comparing the clearance of exogenously applied serotonin (5-HT) from the extracellular fluid (ECF) of the DRN to that in the CA3 region of the hippocampus, an area with lower SERT density. Serotonin was pressure ejected into these regions in anesthetized rats and reproducible electrochemical signals measured by carbon fiber microelectrodes were recorded. Consistent with SERT density as measured by [H-3]cyanoimipramine binding in these brain regions (DRN>>CA3), clearance of 5-HT was significantly faster in DRN compared to that in the CA3 region. The selective serotonin reuptake inhibitor, fluvoxamine, prolonged 5-HT clearance in both CA3 and DRN. It is known that the norepinephrine transporter (NET) contributes to clearance of 5-HT in the dentate gyrus (DG) but not in CA3. Given that the DRN receives noradrenergic innervation, it was also determined if the NET contributes to 5-HT clearance in the DRN. Destruction of the NET with the neurotoxin 6-hydroxydopamine failed to alter 5-HT clearance parameters in the DRN. These data support the hypothesis that serotonin transporters are functionally active in the DRN, that serotonin clearance is mediated primarily by the SERT in the DRN and that the faster clearance of 5-HT from this region is related to its greater density of functional SERTs. (C) 2002 Elsevier Science B.V. All rights reserved. C1 Univ Texas, Hlth Sci Ctr, Div Alcohol & Drug Addict, Dept Psychiat, San Antonio, TX 78229 USA. Univ Texas, Hlth Sci Ctr, Dept Pharmacol, San Antonio, TX 78229 USA. S Texas Vet Hlth Care Syst, San Antonio, TX 78284 USA. Univ Kentucky, Dept Anat & Neurobiol, Ctr Sensor Technol, Lexington, KY 40536 USA. RP Montanez, S (reprint author), Univ Texas, Hlth Sci Ctr, Div Alcohol & Drug Addict, Dept Psychiat, 7703 Floyd Curl Dr,MS 7792, San Antonio, TX 78229 USA. OI Gould, Georgianna/0000-0002-5470-8763 FU NIMH NIH HHS [MH01245, MH57001] NR 45 TC 16 Z9 16 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0006-8993 J9 BRAIN RES JI Brain Res. PD NOV 15 PY 2002 VL 955 IS 1-2 BP 236 EP 244 AR PII S0006-8993(02)03470-4 DI 10.1016/S0006-8993(02)03470-4 PG 9 WC Neurosciences SC Neurosciences & Neurology GA 618NU UT WOS:000179424800028 PM 12419542 ER PT J AU D'Amico, AV AF D'Amico, AV TI How to compare results after surgery or radiation for localized prostate carcinoma - Prostate specific antigen (PSA) outcome (no), posttreatment PSA doubling time (maybe), or survival (yes)? SO CANCER LA English DT Editorial Material ID EXTERNAL-BEAM RADIATION; RADICAL PROSTATECTOMY; DEFINITIVE RADIOTHERAPY; CLINICAL UTILITY; CANCER; THERAPY; RECURRENCE; PROGRESSION; BIOPSIES C1 Brigham & Womens Hosp, Dept Radiat Oncol L2, Boston, MA 02115 USA. Harvard Univ, Sch Med, Dana Farber Canc Inst, Boston, MA 02115 USA. RP D'Amico, AV (reprint author), Brigham & Womens Hosp, Dept Radiat Oncol L2, 75 Francis St, Boston, MA 02115 USA. NR 18 TC 6 Z9 6 U1 0 U2 0 PU JOHN WILEY & SONS INC PI HOBOKEN PA 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 0008-543X J9 CANCER JI Cancer PD NOV 15 PY 2002 VL 95 IS 10 BP 2041 EP 2043 DI 10.1002/cncr.10912 PG 3 WC Oncology SC Oncology GA 611HH UT WOS:000179010200001 PM 12412155 ER PT J AU Hogarty, MD Winter, CL Liu, XY Guo, C White, PS Look, AT Brodeur, GM Maris, JM AF Hogarty, MD Winter, CL Liu, XY Guo, C White, PS Look, AT Brodeur, GM Maris, JM TI No evidence for the presence of an imprinted neuroblastoma suppressor gene within chromosome sub-band 1p36.3 SO CANCER RESEARCH LA English DT Article ID MYC AMPLIFICATION; DELETION; REGION; EXPRESSION; ORIGIN; TUMORS; P73; HETEROZYGOSITY; IDENTIFICATION; LOCI AB Deletion of the distal short arm of chromosome 1 occurs in 35% of primary neuroblastomas (NBs). These deletions tend to be large and extend to the telomere, but a common region within sub-band 1p36.3 is consistently lost. Despite intensive investigation, no candidate tumor suppressor gene within this region has been shown to undergo tumor-specific mutation consistent with biallelic inactivation. In addition, initial studies demonstrated preferential loss of the maternally inherited 1p homologue in NBs with 1p loss of heterozygosity (LOH) without MYCN amplification. This has led to the widely accepted hypothesis that a genomically imprinted NB suppressor gene is the target of 1p deletion in this subset. To test this hypothesis we have studied 293 primary NBs for LOH within 1p36.3 and determined the parental origin of the deleted 1p homologue. LOH within 1p36.3 was demonstrated in 55 NBs (19%). Of these, 29 occurred in tumors without MYCN amplification: 13 had deletion of the maternally inherited 1p, whereas 16 had deletion of the paternally inherited 1p (P = 0.58). These data strongly refute a parent-of-origin effect for 1p deletions in NB and exclude the existence of an imprinted NB suppressor locus in this region. C1 Childrens Hosp Philadelphia, Div Oncol, Philadelphia, PA 19104 USA. Univ Penn, Sch Med, Dept Pediat, Philadelphia, PA 19104 USA. Dana Farber Canc Inst, Dept Pediat Oncol, Boston, MA 02115 USA. RP Hogarty, MD (reprint author), Childrens Hosp Philadelphia, Div Oncol, 9 N ARC,3615 Civic Ctr Blvd, Philadelphia, PA 19104 USA. FU NCI NIH HHS [R01CA78745, U01-CA30969]; PHS HHS [U1078966] NR 27 TC 6 Z9 7 U1 1 U2 3 PU AMER ASSOC CANCER RESEARCH PI BIRMINGHAM PA PO BOX 11806, BIRMINGHAM, AL 35202 USA SN 0008-5472 J9 CANCER RES JI Cancer Res. PD NOV 15 PY 2002 VL 62 IS 22 BP 6481 EP 6484 PG 4 WC Oncology SC Oncology GA 616QV UT WOS:000179315200027 PM 12438240 ER PT J AU Recio, JA Noonan, FP Takayama, H Anver, MR Duray, P Rush, WL Lindner, G De Fabo, EC DePinho, RA Merlino, G AF Recio, JA Noonan, FP Takayama, H Anver, MR Duray, P Rush, WL Lindner, G De Fabo, EC DePinho, RA Merlino, G TI Ink4a/Arf deficiency promotes ultraviolet radiation-induced melanomagenesis SO CANCER RESEARCH LA English DT Article ID HEPATOCYTE GROWTH-FACTOR; FACTOR SCATTER FACTOR; COMPARATIVE GENOMIC HYBRIDIZATION; MALIGNANT-MELANOMA; CUTANEOUS MELANOMA; FACTOR/SCATTER FACTOR; SPORADIC MELANOMA; TUMOR-SUPPRESSOR; TRANSGENIC MICE; MET RECEPTOR AB Cutaneous malignant melanoma (CMM), already known for its highly aggressive behavior and resistance to conventional therapy, has evolved into a health crisis by virtue of a dramatic elevation in incidence. The underlying genetic basis for CMM, as well as the fundamental role for UV radiation in its etiology, is now widely accepted. However, the only bona fide genetic locus to emerge from extensive analysis of CMM suppressor candidates is INK4a/ARF at 9p21, which is lost frequently in familial and occasionally in somatic CMM. The functional relationship between INK4a/ARF and UV radiation in the pathogenesis of CMM is largely unknown. Recently, we reported that hepatocyte growth factor/scatter factor (HGF/SF)-transgenic mice develop melanomas after a single erythemal dose of neonatal UV radiation, supporting epidemiological data implicating childhood sunburn in CMM. Here we show that neonatal UV irradiation induces a full spectrum of melanocyte pathology from early premalignant lesions through distant metastases. Cutaneous melanomas arise with histopathological and molecular pathogenetic features remarkably similar to CMM, including loss of ink4a/arf. A role for ink4a/arf in UV-induced melanomagenesis was directly assessed by placing the HGF/SF transgene on a genetic background devoid of ink4a/arf. Median time to melanoma development induced by UV radiation was only 50 days in HGF/SF ink4a/arf(-/-) mice, compared with 152 and 238 days in HGF/SF ink4a/arf(+/-) and HGF/SF ink4a/arf(+/+) mice, respectively. These studies provide experimental evidence that ink4a/arf plays a critical role in UV-induced melanomagenesis and strongly suggest that sunburn is a highly significant risk factor, particularly in families harboring germ-line mutations in INK4a/ARF. C1 NCI, Mol Biol Lab, Bethesda, MD 20892 USA. George Washington Univ, Sch Med, Dept Immunol & Dermatol, Washington, DC 20037 USA. Sci Applicat Int Corp, Pathol Histotechnol Lab, NCI, Frederick, MD 21702 USA. NCI, Pathol Lab, Bethesda, MD 20892 USA. Armed Forces Inst Pathol, Dept Dermatopathol, Washington, DC 20306 USA. Univ Hamburg, Hosp Eppendorf, Dept Dermatol, D-20246 Hamburg, Germany. Harvard Univ, Sch Med, Dana Farber Canc Inst, Dept Adult Oncol Med & Genet, Boston, MA 02115 USA. RP Merlino, G (reprint author), NCI, Mol Biol Lab, Bldg 37,Room 5002, Bethesda, MD 20892 USA. FU NCI NIH HHS [CA-92258, N0I-CO-56000] NR 62 TC 70 Z9 72 U1 0 U2 3 PU AMER ASSOC CANCER RESEARCH PI BIRMINGHAM PA PO BOX 11806, BIRMINGHAM, AL 35202 USA SN 0008-5472 J9 CANCER RES JI Cancer Res. PD NOV 15 PY 2002 VL 62 IS 22 BP 6724 EP 6730 PG 7 WC Oncology SC Oncology GA 616QV UT WOS:000179315200060 PM 12438273 ER PT J AU Wulfkuhle, JD Sgroi, DC Krutzsch, H McLean, K McGarvey, K Knowlton, M Chen, S Shu, HJ Sahin, A Kurek, R Wallwiener, D Merino, MJ Petricoin, EF Zhao, YM Steeg, PS AF Wulfkuhle, JD Sgroi, DC Krutzsch, H McLean, K McGarvey, K Knowlton, M Chen, S Shu, HJ Sahin, A Kurek, R Wallwiener, D Merino, MJ Petricoin, EF Zhao, YM Steeg, PS TI Proteomics of human breast ductal carcinoma in situ SO CANCER RESEARCH LA English DT Article ID SURGICAL-ADJUVANT-BREAST; TRANS-GOLGI NETWORK; IN-SITU; LOCAL RECURRENCE; HYDROGEN-PEROXIDE; FOLLOW-UP; CONSERVING THERAPY; ESTROGEN-RECEPTOR; HORMONE RECEPTORS; TUMOR PROGRESSION AB We report the first proteomic analysis of matched normal ductal/ lobular units and ductal carcinoma in situ (DCIS) of the human breast. An understanding of the transition from normal epithelium to the first definable stage of cancer at the functional level of protein expression is hypothesized to contribute to improved detection, prevention, and treatment. Ten sets of two-dimensional gels were evaluated, containing either matched normal ductal/lobular units or DCIS from either whole tissue sections or up to 100,000 laser capture microdissected epithelial cells. Differential protein expression was confirmed by image analysis. Protein spots (315) were excised and subjected to mass spectrometry sequencing. Fifty-seven proteins were differentially expressed between normal ductal/ lobular units and DCIS. Differences in overall protein expression levels and posttranslational processing were evident. Ten differentially expressed proteins were validated in independent DCIS specimens, and 14 of 15 proteomic trends from two-dimensional gel analyses were confirmed by standard inummohistochemical analysis using a limited independent tumor cohort. Many of the proteins identified were previously unconnected with breast cancer, including proteins regulating the intracellular trafficking of membranes, vesicles, cancer preventative agents, proteins, ions, and fatty acids. Other proteomic identifications related to cytoskeletal architecture, chaperone function, the microenvironment, apoptosis, and genomic instability. Proteomic analysis of DCIS revealed differential expression patterns distinct from previous nucleic acid-based studies and identified new facets of the earliest stage of breast cancer progression. C1 NCI, Womens Canc Sect, Pathol Lab, Bethesda, MD 20892 USA. Massachusetts Gen Hosp, Mol Pathol Unit, Boston, MA 02129 USA. Harvard Univ, Sch Med, Dept Pathol, Boston, MA 02129 USA. NCI, Pathol Lab, Bethesda, MD 20892 USA. Univ Texas, SW Med Ctr, Dept Biochem, Dallas, TX 75390 USA. Univ Texas, MD Anderson Canc Ctr, Dept Pathol, Houston, TX 77030 USA. Univ Tubingen, Dept Obstet & Gynecol, D-72076 Tubingen, Germany. US FDA, Ctr Biol Evaluat & Res, NCI, Clin Proteom Program,Div Therapeut Prot, Bethesda, MD 20892 USA. RP Steeg, PS (reprint author), NCI, Womens Canc Sect, Pathol Lab, Bldg 10,Room 2A33, Bethesda, MD 20892 USA. FU NCI NIH HHS [CA 85146] NR 69 TC 188 Z9 200 U1 2 U2 6 PU AMER ASSOC CANCER RESEARCH PI BIRMINGHAM PA PO BOX 11806, BIRMINGHAM, AL 35202 USA SN 0008-5472 J9 CANCER RES JI Cancer Res. PD NOV 15 PY 2002 VL 62 IS 22 BP 6740 EP 6749 PG 10 WC Oncology SC Oncology GA 616QV UT WOS:000179315200062 PM 12438275 ER PT J AU Hare, CB Vu, MP Grunfeld, C Lampiris, HW AF Hare, CB Vu, MP Grunfeld, C Lampiris, HW TI Simvastatin-nelfinavir interaction implicated in rhabdomyolysis and death SO CLINICAL INFECTIOUS DISEASES LA English DT Article ID COA REDUCTASE INHIBITORS; PROTEASE INHIBITORS; DISEASE AB We report the first death associated with rhabdomyolysis in a patient treated with a statin and a protease inhibitor, which produced a significant drug-drug interaction. C1 Univ Calif San Francisco, Div Infect Dis, Posit Hlth Program, San Francisco, CA 94110 USA. Univ Calif San Francisco, Dept Med, San Francisco, CA 94110 USA. San Francisco Vet Adm Med Ctr, Serv Pharm, San Francisco, CA USA. San Francisco Vet Adm Med Ctr, Metab Sect, San Francisco, CA USA. San Francisco Vet Adm Med Ctr, Div Infect Dis, San Francisco, CA USA. RP Hare, CB (reprint author), Univ Calif San Francisco, Div Infect Dis, Posit Hlth Program, 3180 18th St,Ste 305, San Francisco, CA 94110 USA. NR 14 TC 43 Z9 48 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 1058-4838 J9 CLIN INFECT DIS JI Clin. Infect. Dis. PD NOV 15 PY 2002 VL 35 IS 10 BP E111 EP E112 DI 10.1086/344179 PG 2 WC Immunology; Infectious Diseases; Microbiology SC Immunology; Infectious Diseases; Microbiology GA 611PM UT WOS:000179027000024 PM 12410494 ER PT J AU Freund, C Kuhne, R Yang, HL Park, S Reinherz, EL Wagner, G AF Freund, C Kuhne, R Yang, HL Park, S Reinherz, EL Wagner, G TI Dynamic interaction of CD2 with the GYF and the SH3 domain of compartmentalized effector molecules SO EMBO JOURNAL LA English DT Article DE CD2; GYF domain; lipid rafts; NMR; SH3 domain ID T-CELL ACTIVATION; PROLINE-RICH SEQUENCES; SIGNAL-TRANSDUCTION; CYTOPLASMIC DOMAIN; TYROSINE KINASES; PHOSPHOLIPASE-C; LIPID RAFTS; SRC; P59(FYN); PALMITOYLATION AB Intracellular protein interaction domains are essential for eukaryotic signaling. In T cells, the CD2BP2 adaptor binds two membrane-proximal proline-rich motifs in the CD2 cytoplasmic tail via its GYF domain, thereby regulating interleukin-2 production. Here we present the structure of the GYF domain in complex with a CD2 tail peptide. Unlike SH3 domains, which use two surface pockets to accommodate proline residues of ligands, the GYF domain employs phylogenetically conserved hydrophobic residues to create a single interaction surface. NMR analysis shows that the Fyn but not the Lck tyrosine kinase SH3 domain competes with CD2BP2 GYF-domain binding to the same CD2 proline-rich sequence in vitro. To test the in vivo significance of this competition, we used co-immunoprecipitation experiments and found that CD2BP2 is the ligand of the membrane-proximal proline-rich tandem repeat of CD2 in detergent-soluble membrane compartments, but is replaced by Fyn SH3 after CD2 is translocated into lipid rafts upon CD2 ectodomain clustering. This unveils the mechanism of a switch of CD2 function due to an extracellular mitogenic signal. C1 Forshungsinst Mol Pharmakol, Prot Engn Grp, D-13125 Berlin, Germany. Forshungsinst Mol Pharmakol, Mol Modeling Grp, D-13125 Berlin, Germany. Free Univ Berlin, D-13125 Berlin, Germany. Harvard Univ, Sch Med, Dana Farber Canc Inst, Immunobiol Lab, Boston, MA 02115 USA. Harvard Univ, Sch Med, Dept Med, Boston, MA 02115 USA. Harvard Univ, Sch Med, Dept Biol Chem & Mol Pharmacol, Boston, MA 02115 USA. RP Freund, C (reprint author), Forshungsinst Mol Pharmakol, Prot Engn Grp, Robert Rossle Str 10, D-13125 Berlin, Germany. FU NCRR NIH HHS [RR 00995]; NIAID NIH HHS [AI 37581, AI 19807, R01 AI019807, R01 AI037581, R37 AI019807, R56 AI019807]; NIGMS NIH HHS [GM 47467, P01 GM047467] NR 39 TC 54 Z9 57 U1 0 U2 4 PU OXFORD UNIV PRESS PI OXFORD PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND SN 0261-4189 J9 EMBO J JI Embo J. PD NOV 15 PY 2002 VL 21 IS 22 BP 5985 EP 5995 DI 10.1093/emboj/cdf602 PG 11 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA 618YZ UT WOS:000179446900005 PM 12426371 ER PT J AU Chen, ZY Shie, JL Tseng, CC AF Chen, ZY Shie, JL Tseng, CC TI STAT1 is required for IFN-gamma-mediated gut-enriched Kruppel-like factor expression SO EXPERIMENTAL CELL RESEARCH LA English DT Article DE KLF4; growth arrest; GAS; GKLF promoter; interferon-gamma ID ZINC-FINGER PROTEIN; INTERFERON-GAMMA; TRANSCRIPTIONAL ACTIVATION; GENE; RECEPTOR; CELLS; PROMOTER; GROWTH; PHOSPHORYLATION; PATHWAYS AB Gut-enriched Kruppel-like factor (GKLF/KLF4), a member of the Kruppel-like factor family of transcription factors, has recently been shown to be associated with growth arrest in the colonic mucosa. Our laboratory has previously demonstrated that GKLF is one of the down-stream targets of interferon-gamma (IFN-gamma) in colon cancer cells, but the signaling pathway regulating GKLF expression is not known. In this report, we showed that IFN-gamma increased GKLF and interferon regulatory factor-1 mRNA levels in a parallel fashion and these effects were abolished in STAT1 knockout mouse fibroblast cell lines, indicating that STAT1 mediated IFN-gamma-stimulated GKLF gene expression. IFN-gamma treatment induced phosphorylation of STAT1 and IFN-gamma-induced GKLF mRNA expression was attenuated by tyrosine protein kinase inhibitors, suggesting that phosphorylation of STAT1 played an essential role in this process. To further evaluate the effect of STAT1 on GKLF gene expression, a 2622-bp mouse GKLF promoter was isolated from a liver genomic library. In a transient transfection system, IFN-gamma treatment increased GKLF promoter activity by 3.5-fold. Sequential deletion and mutation analysis of the GKLF promoter has identified the sequence between -1675 and -1580, a region containing a GAS element, to be essential for IFN-gamma function. By electrophoretic mobility gel shift assay, nuclear extracts from IFN-gamma-stimulated HT-29 cells were found to bind to the GAS motif on the GKLF promoter and this protein-DNA complex was supershifted by the STAT1 antiserum. These results indicate that IFN-gamma-induced GKLF expression required phosphorylated STAT1 and that these effects were mediated, in part, through interaction of STAT1 with the GAS element on the GKLF promoter. (C) 2002 Elsevier Science (USA). C1 Boston Univ, Sch Med, Gastroenterol Sect, Boston, MA 02118 USA. VA Boston Healthcare Syst, Gastroenterol Sect, Boston, MA 02118 USA. RP Tseng, CC (reprint author), Boston Univ, Sch Med, Gastroenterol Sect, EBRC X-513,650 Albany St, Boston, MA 02118 USA. FU NCI NIH HHS [R01CA82593] NR 28 TC 18 Z9 21 U1 0 U2 0 PU ACADEMIC PRESS INC ELSEVIER SCIENCE PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA SN 0014-4827 J9 EXP CELL RES JI Exp. Cell Res. PD NOV 15 PY 2002 VL 281 IS 1 BP 19 EP 27 DI 10.1006/excr.2002.5633 PG 9 WC Oncology; Cell Biology SC Oncology; Cell Biology GA 617TY UT WOS:000179378000003 PM 12441126 ER PT J AU Choi, NC Fischman, AJ Niemierko, A Ryu, JS Lynch, T Wain, J Wright, C Fidias, P Mathisen, D AF Choi, NC Fischman, AJ Niemierko, A Ryu, JS Lynch, T Wain, J Wright, C Fidias, P Mathisen, D TI Dose-response relationship between probability of pathologic tumor control and glucose metabolic rate measured with FDG pet after preoperative chemoradiotherapy in locally advanced non-small-cell lung cancer SO INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS LA English DT Article DE lung cancer; FDG PET; dose-response relationship ID POSITRON-EMISSION-TOMOGRAPHY; THERAPY-ONCOLOGY-GROUP; PHASE-I/II TRIAL; RADIATION-THERAPY; ACCELERATED RADIOTHERAPY; COMPUTED-TOMOGRAPHY; F-18 DEOXYGLUCOSE; IMPROVED SURVIVAL; NORMAL TISSUE; CARCINOMA AB Purpose: To determine the dose-response relationship between the probability of tumor control on the basis of pathologic tumor response (pTCP) and the residual metabolic rate of glucose (MRglc) in response to preoperative chemoradiotherapy in locally advanced non-small-cell lung cancer and to define the level of residual MRglc that corresponds to pTCP 50% and pTCP greater than or equal to95%. Methods and Materials: Quantitative dynamic 18F-2-fluoro-2-deoxy-D-glucose (18F-FDG) positron emission tomography was performed to measure regional wMRglc at the primary lesion before and 2 weeks after preoperative chemoradiotherapy in an initial group of 13 patients with locally advanced NSCLC. A simplified kinetic method was developed subsequently from the initial dynamic study and used in the subsequent 16 patients. The preoperative radiotherapy programs consisted of (1) a split course of 42 Gy in 28 fractions within a period of 28 days using a twice-daily treatment schedule for Stage IIIA(N2) NSCLC (n = 18) and (2) standard once-daily radiation schedule of 45-63 Gy in 25-35 fractions during a 5-7-week period (n = 11). The preoperative chemotherapy regimens included two cycles of cisplatin, vinblastine, and 5-fluorouracil (n = 24), cisplatin and etoposide (n = 2), and cisplatin, Taxol, and 5-fluorouracil (n = 3). Patients free of tumor progression after preoperative chemoradiotherapy underwent surgery. The degree of residual MRglc measured 2 weeks after preoperative chemoradiotherapy and 2 weeks before surgery was correlated with the pathologic tumor response. The relationship between MRglc and pTCP was modeled using logistic regression. Results: Of 32 patients entered into the study, 29 (16 men and 13 women; 30 lesions) were evaluated for the correlation between residual MRgIc and pathologic tumor response. Three patients did not participate in the second study because of a steady decline in general condition. The median age was 60 years (range 42-78). One of the 29 patients had two separate lesions, and MRglc was measured in each separately. The tumor histologic types included squamous cell carcinoma (n = 9), adenocarcinoma In = 13), large cell carcinoma (n = 6), and poorly differentiated carcinoma (n = 2). The extent of the primary and nodal disease was as follows: Stage IIB (T3N0M0), Pancoast tumor (n = 2); Stage IIIA, T2-T3N2M0 (n = 18); Stage IIIB: T1-T3N3M0 (n = 5) and T4N0M0 (n = 2); a second lesion, T1 (n = 1); and localized stump recurrence (n = 2). A pathologically complete response was obtained in 14 (47%) of the 30 lesions. The remaining 16 lesions had residual cancer. The mean baseline value of the maximal MRglc was 0.333 +/- 0.087 mumol/min/g (n = 16), and it was reduced to 0.0957 +/- 0.059 mumol/min/g 2 weeks after chemoradiotherapy (p = 0.011). The correlation between residual MRglc and pTCP was made using an increment value of 0.02 mumol/min/g between the maximal and minimal values of MRgIc. A pathologically complete response was obtained in 6 of 6 patients with residual MRglc of less than or equal to0.050 mumol/min/g, 3 of 4 with less than or equal to0.070, 4 of 7 with less than or equal to0.090, 0 of 4 with less than or equal to0.110, 1 of 3 with less than or equal to0.130, and 0 of 6 with less than or equal to0.130 mumol/min/g. The fitted logistic model showed that residual MRglc corresponding to pTCP 50% and pTCP greater than or equal to95% was 0.076 and less than or equal to0.040 mumol/min/g, respectively. Conclusion: The correlation between the gradient of residual MRgIc after chemoradiotherapy and pTCP is an inverse dose-response relationship. Residual MRglc of 0.076 and less than or equal to0.040 mumol/min/g, representing pTCP 50% and pTCP greater than or equal to95%, respectively, may be useful surrogate markers for the tumor response to radiotherapy or chemoradiotherapy in lung cancer. (C) 2002 Elsevier Science Inc. C1 Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Radiat Oncol, Boston, MA 02114 USA. Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Radiol, Boston, MA 02114 USA. Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Med, Boston, MA 02114 USA. Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Surg, Boston, MA 02114 USA. RP Choi, NC (reprint author), Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Radiat Oncol, 100 Blossom St, Boston, MA 02114 USA. NR 69 TC 75 Z9 79 U1 0 U2 4 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 NOV 15 PY 2002 VL 54 IS 4 BP 1024 EP 1035 AR PII S0360-3016(02)03038-9 DI 10.1016/S0360-3016(02)03038-9 PG 12 WC Oncology; Radiology, Nuclear Medicine & Medical Imaging SC Oncology; Radiology, Nuclear Medicine & Medical Imaging GA 613FR UT WOS:000179122400006 PM 12419428 ER PT J AU Haddad, LA Smith, N Bowser, M Niida, Y Murthy, V Gonzalez-Agosti, C Ramesh, V AF Haddad, LA Smith, N Bowser, M Niida, Y Murthy, V Gonzalez-Agosti, C Ramesh, V TI The TSC1 tumor suppressor hamartin interacts with neurofilament-L and possibly functions as a novel integrator of the neuronal cytoskeleton SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID GROWTH CONE MORPHOLOGY; TUBEROUS SCLEROSIS; CELL-GROWTH; EMBRYONIC LETHALITY; GENE-PRODUCTS; COMPLEX; EXPRESSION; MOTILITY; MUTATION; RADIXIN AB Tuberous sclerosis complex, an autosomal dominant disease caused by mutations in either TSC1 or TSC2, is characterized by the development of hamartomas in a variety of organs. The proteins encoded by TSC1 and TSC2, hamartin and tuberin, respectively, associate with each other forming a tight complex. Here we show that hamartin binds the neurofilament light chain and it is possible to recover the hamartin-tuberin complex over the neurofilament light chain rod domain spanning amino acids 93-156 by affinity precipitation. Homologous rod domains in other intermediate filaments such as neurofilament medium chain, a-inter-nexin, vimentin, and desmin are not able to bind hamartin. In cultured cortical neurons, hamartin and tuberin co-localize with neurofilament light chain preferentially in the proximal to central growth cone region. Interestingly, in the distal part of the growth cone hamartin overlaps with the ezrin-radixin-moesin family of actin binding proteins, and we have validated the interaction of hamartin with moesin. These results demonstrate that hamartin may anchor neuronal intermediate filaments to the actin cytoskeleton, which may be critical for some of the CNS functions of the hamartin-tuberin complex, and abolishing this through mutations in TSC1 or TSC2 may lead to certain neurological manifestations associated with the disease. C1 Massachusetts Gen Hosp, Ctr Canc, Mol Neurogenet Unit, Charlestown, MA 02129 USA. RP Ramesh, V (reprint author), Massachusetts Gen Hosp, Ctr Canc, Mol Neurogenet Unit, Bldg 149,13th St,Rm 6222, Charlestown, MA 02129 USA. EM ramesh@helix.mgh.harvard.edu RI Haddad, Luciana/D-8002-2012 FU NINDS NIH HHS [NS24279, NS41917] NR 42 TC 45 Z9 48 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 EI 1083-351X J9 J BIOL CHEM JI J. Biol. Chem. PD NOV 15 PY 2002 VL 277 IS 46 BP 44180 EP 44186 DI 10.1074/jbc.M207211200 PG 7 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA 615XE UT WOS:000179272000084 PM 12226091 ER PT J AU Zhao, MJ Tang, D Lechpammer, S Hoffman, A Asea, A Stevenson, MA Calderwood, SK AF Zhao, MJ Tang, D Lechpammer, S Hoffman, A Asea, A Stevenson, MA Calderwood, SK TI Double-stranded RNA-dependent protein kinase (pkr) is essential for thermotolerance, accumulation of HSP70, and stabilization of ARE-containing HSP70 mRNA during stress SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID HEAT-SHOCK PROTEINS; AU-RICH ELEMENTS; MESSENGER-RNA; TRANSCRIPTIONAL ACTIVATION; 3'-UNTRANSLATED REGION; BINDING-PROTEINS; C-FOS; GENE; STABILITY; FACTOR-1 AB We have investigated the role of the double-stranded RNA-dependent protein kinase gene (pkr) in the regulation of the heat shock response. We show that the pkr gene is essential for efficient activation of the heat shock response and that pkr disruption profoundly inhibits heat shock protein 70 (HSP70) synthesis and blocks the development of thermotolerance. Despite these profound effects, pkr disruption did not markedly affect the activation of heat shock factor 1 by heat and did not reduce the rate of transcription of the HSP70 gene after heat shock. However, despite the lack of effect of pkr disruption on HSP70 gene transcription, we found a significant decrease in the expression of HSP70 mRNA in pkr-/- cells after heat shock. Kinetic studies of mRNA turnover suggested a block in the thermal stabilization of HSP70 mRNA in pkr-/- cells. As the thermal stabilization of HSP70 mRNA is thought to involve cis-acting A+U rich (ARE) elements in the 3'-untranslated region (UTR), we examined a potential role for pkr in this process. We found that a reporter beta-galactosidase mRNA destabilized by introduction of a functional ARE into the 3'-UTR became stabilized by heat but only in cells containing an intact pkr gene. Our studies suggest therefore that pkr plays a significant role in the stabilization of mRNA species containing ARE destruction sequences in the 3'-UTR and through this mechanism, contributes to the regulation of the heat shock response and other processes. C1 Boston Univ, Sch Med, Boston, MA 02118 USA. Harvard Univ, Sch Med, Dana Farber Canc Inst, Dept Radiat Oncol, Cambridge, MA 02138 USA. Harvard Univ, Sch Med, Beth Israel Deaconess Med Ctr, Dept Radiat Oncol, Boston, MA 02115 USA. CALTECH, Pasadena, CA 91125 USA. RP Calderwood, SK (reprint author), Boston Med Ctr, Ctr Mol Stress Response, 88 E Newton St,E645, Boston, MA 02118 USA. RI Asea, Alexzander/I-4112-2013 OI Asea, Alexzander/0000-0003-3592-3481 FU NCI NIH HHS [CA47407-11, CA77465, CA83890-01] NR 45 TC 34 Z9 35 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 NOV 15 PY 2002 VL 277 IS 46 BP 44539 EP 44547 DI 10.1074/jbc.M208408200 PG 9 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA 615XE UT WOS:000179272000126 PM 12207033 ER PT J AU Obin, M Lee, BY Meinke, G Bohm, A Lee, RH Gaudet, R Hopp, JA Arshavsky, VY Willardson, BM Taylor, A AF Obin, M Lee, BY Meinke, G Bohm, A Lee, RH Gaudet, R Hopp, JA Arshavsky, VY Willardson, BM Taylor, A TI Ubiquitylation of the transducin beta gamma subunit complex - Regulation by phosducin SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID UBIQUITIN-CONJUGATING ENZYME; ROD OUTER SEGMENTS; HETEROTRIMERIC G-PROTEINS; DEPENDENT PROTEOLYSIS; PHOTORECEPTOR CELLS; ALPHA-SUBUNIT; 3RD FORM; IN-VIVO; IDENTIFICATION; DEGRADATION AB G proteins (Galphabetagamma) are essential signaling molecules, which dissociate into Galpha and Gbetagamma upon activation by heptahelical membrane receptors. We have identified the betagamma subunit complex of the photoreceptor-specific G protein, transducin (T), as a target of the ubiquitin-proteasome pathway. Ubiquitylated species of the transducin gamma-subunit (Tgamma) but not the alpha- or beta-subunits were assembled de novo in bovine photoreceptor preparations. In addition, Tgamma was exclusively ubiquitylated when Tbetagamma was dissociated from Talpha. Ubiquitylation of Tbetagamma on Tgamma was selectively catalyzed by human ubiquitin-conjugating enzymes UbcH5 and UbcH7 and was coincident with degradation of the entire Tbetagamma subunit complex in vitro by a mechanism requiring ATP and the proteasome. We also show that Tbetagamma association with phosducin, a photoreceptor-specific protein of unknown physiological function, blocks Tbetagamma ubiquitylation and subsequent degradation. Phosphorylation of phosducin by Ca2+/calmodulin-dependent protein kinase II, which inhibits phosducin-Tbetagamma complex formation, completely restored Toy ubiquitylation and degradation. We conclude that Tbetagamma is a substrate of the ubiquitin-proteasome pathway and suggest that phosducin serves to protect Tbetagamma following the light-dependent dissociation of Talphabetagamma. C1 Tufts Univ, JMUSDA, HNRCA, Lab Nutr & Vis Res, Boston, MA 02111 USA. Tufts Ctr Vis Res, Boston, MA 02111 USA. Brigham Young Univ, Dept Chem & Biochem, Provo, UT 84602 USA. Boston Biomed Res Inst, Watertown, MA 02472 USA. Jules Stein Eye Inst, Sepulveda, CA 90095 USA. Greater Los Angeles Healthcare Syst, Sepulveda, CA 90095 USA. Harvard Univ, Dept Mol & Cellular Biol, Boston, MA 02138 USA. Harvard Univ, Sch Med, Dept Ophthalmol, Boston, MA 02114 USA. Massachusetts Eye & Ear Infirm, Boston, MA 02114 USA. RP Obin, M (reprint author), Tufts Univ, JMUSDA, HNRCA, Lab Nutr & Vis Res, 711 Washington St, Boston, MA 02111 USA. RI Gaudet, Rachelle/I-4133-2014 OI Gaudet, Rachelle/0000-0002-9177-054X FU NEI NIH HHS [EY10336, EY11704, EY12287, EY13250, P30 EY13078] NR 61 TC 50 Z9 50 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 NOV 15 PY 2002 VL 277 IS 46 BP 44566 EP 44575 DI 10.1074/jbc.M205308200 PG 10 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA 615XE UT WOS:000179272000129 PM 12215439 ER PT J AU Chen, WY Garber, JE Higham, S Schneider, KA Davis, KB Deffenbaugh, AM Frank, TS Gelman, RS Li, FP AF Chen, WY Garber, JE Higham, S Schneider, KA Davis, KB Deffenbaugh, AM Frank, TS Gelman, RS Li, FP TI BRCA1/2 genetic testing in the community setting SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Article; Proceedings Paper CT 35th Annual Meeting of the American-Society-of-Clinical-Oncology CY MAY 13-18, 1999 CL ATLANTA, GA SP Amer Soc Clin Oncol ID OVARIAN-CANCER SUSCEPTIBILITY; POPULATION-BASED SAMPLE; BREAST-CANCER; PSYCHOLOGICAL DISTRESS; PROPHYLACTIC SURGERY; HEREDITARY BREAST; FAMILY HISTORY; WOMEN; MUTATIONS; RISK AB Purpose: BRCA 1/2 genetic testing has been commercially available in the United States since 1996. Most published reports described BRCA 1/2 testing as research studies at large academic centers, but less is known about testing in the community. This study evaluates the process and early outcomes of BRCA 1/2 genetic testing as a clinical service in the community setting. Methods: Surveys were mailed to women in the United States whose health care providers ordered BRCA 1/2 genetic testing from Myriad Genetic Laboratories from August 1998 through July 2000. Women tested at 149 large academic centers were excluded. Main outcome measures were demographic characteristics, recall of and satisfaction with the genetic testing process, and likelihood of pursuing cancer prevention strategies. Results: Among the 646 respondents, 414 (64%) had a personal history of cancer and 505 (78%) had at least one first-degree relative with breast and/or ovarian cancer. Most subjects (82%) recalled discussions of informed consent before testing (median time, 30 minutes). Genetic results were conveyed during an office visit (57%), by telephone (39%), or by mail (3%). More than 75% of respondents were "very satisfied with the counseling received." Cancer-free subjects with a germline mutation were more likely to consider prevention strategies after receiving the genetic results. Conclusion: Virtually all respondents had a personal and/or family history of breast/ovarian cancer. Although pretest and posttest communications were not standardized, overall satisfaction with clinical breast cancer genetic testing was high. Additional follow-up will provide data on future cancer prevention practices and cancer incidence. (C) 2002 by American Society of Clinical Oncology. C1 Dana Farber Canc Inst, Dept Adult Oncol, Boston, MA 02115 USA. Dana Farber Canc Inst, Dept Biostat Sci, Boston, MA 02115 USA. Brigham & Womens Hosp, Channing Lab, Boston, MA 02115 USA. Harvard Univ, Sch Med, Boston, MA 02115 USA. UCL, Clin Operat Res Unit, London WC1E 6BT, England. Myriad Genet Labs Inc, Salt Lake City, UT USA. RP Chen, WY (reprint author), Dana Farber Canc Inst, Dept Adult Oncol, 44 Binney St, Boston, MA 02115 USA. EM wendy_chen@dfci.harvard.edu FU NCI NIH HHS [CA06516] NR 41 TC 34 Z9 34 U1 1 U2 3 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 NOV 15 PY 2002 VL 20 IS 22 BP 4485 EP 4492 DI 10.1200/JCO.2002.08.147 PG 8 WC Oncology SC Oncology GA 615VG UT WOS:000179267200013 PM 12431973 ER PT J AU Meyers, JH Ryu, A Monney, L Nguyen, K Greenfield, EA Freeman, GJ Kuchroo, VK AF Meyers, JH Ryu, A Monney, L Nguyen, K Greenfield, EA Freeman, GJ Kuchroo, VK TI Cutting edge: CD94/NKG2 is expressed on Th1 but not Th2 cells and costimulates Th1 effector functions SO JOURNAL OF IMMUNOLOGY LA English DT Article ID T-CELLS; MOLECULAR-CLONING; RECEPTORS; LYMPHOCYTES; MICE; DIVERSITY; ANTIGEN; QA-1(B); CD8(+); NKG2A AB Th1 and Th2 cells can be phenotypically distinguished by very few cell surface markers. To identify cell surface molecule that are specifically expressed on Th1 cells, we have generated a panel of mAbs that specifically bind the surfaces of in, urine Th1 but not Th2 cells. One of these Abs identified the NK cell receptor CD94 as a molecule also specifically expressed on the surface of Th1 cells. As in NK cells, CD94 is expressed on Th1 cells together with members of the NKG2 family of including NKG2A, C, and E. Cross-linking these receptors on differentiated Th1 tells in vitro costimulates proliferation and cytokine production with a potency similar to that obtained b cross-linking CD28. We propose that CD94 KG heterodimers may costimulate effector functions of differentiated Th1 cells. C1 Ctr Neurol Dis, Boston, MA 02115 USA. Brigham & Womens Hosp, Dept Neurol, Ctr Neurol Dis, Boston, MA 02115 USA. Harvard Univ, Sch Med, Dana Farber Canc Inst, Dept Adult Oncol, Boston, MA 02115 USA. RP Kuchroo, VK (reprint author), Ctr Neurol Dis, 77 Ave Louis Pasteur,HIM Rm 710, Boston, MA 02115 USA. FU NIAID NIH HHS [P01AI39671-01A1]; NINDS NIH HHS [R01 NS 30843, R01 NS 35685, P01 NS 38037-01A1] NR 25 TC 19 Z9 21 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 NOV 15 PY 2002 VL 169 IS 10 BP 5382 EP 5386 PG 5 WC Immunology SC Immunology GA 614CG UT WOS:000179170300002 PM 12421909 ER PT J AU Noessner, E Gastpar, R Milani, V Brandl, A Hutzler, PJS Kuppner, MC Roos, M Kremmer, E Asea, A Calderwood, SK Issels, RD AF Noessner, E Gastpar, R Milani, V Brandl, A Hutzler, PJS Kuppner, MC Roos, M Kremmer, E Asea, A Calderwood, SK Issels, RD TI Tumor-derived heat shock protein 70 peptide complexes are cross-presented by human dendritic cells SO JOURNAL OF IMMUNOLOGY LA English DT Article ID CYTOTOXIC T-LYMPHOCYTES; RECEPTOR-MEDIATED ENDOCYTOSIS; GP96 INDUCES MATURATION; NATURAL-KILLER-CELLS; MELANOMA-CELLS; CUTTING EDGE; IN-VIVO; CHAPERONED PEPTIDES; ANTITUMOR IMMUNITY; STRESS PROTEINS AB Our study demonstrates that tumor-derived heat shock protein (HSP)70 chaperones a tyrosinase peptide and mediates its transfer to human immature dendritic cells (DCs) by receptor-dependent uptake. Human tumor-derived HSP70 peptide complexes (HSP70-PC) thus have the immunogenic potential to instruct DCs to cross-present endogenously expressed, nonmutated, and tumor antigenic peptides that are shared among tumors of the melanocytic lineage for T cell recognition. T cell stimulation by HSP70-instructed DCs is dependent on the Ag bound to HSP70 in that only DCs incubated with HSP70-PC purified from tyrosinase-positive (HSP70-PC/tyr(+)) but not from tyrosinase-negative (HSP70-PC/tyr(-)) melanoma cells resulted in the specific activation of the HLA-A*0201-restricted tyrosinase peptide-specific cytotoxic T cell clone. HSP70-PC-mediated T cell stimulation is very efficient, delivering the tyrosinase peptide at concentrations as low as 30 ng/ml of HSP70-PC for T cell recognition. Receptor-dependent binding of HSP70-PC and active cell metabolism are prerequisites for MHC class I-restricted cross-presentation and T cell stimulation. T cell stimulation does not require external DC maturation signals (e.g., exogenously added TNF-alpha), suggesting that signaling DC maturation is an intrinsic property of the HSP70-PC itself and related to receptor-mediated binding. The cross-presentation of a shared human tumor Ag together with the exquisite efficacy are important new aspects for HSP70-based immunotherapy in clinical anti-cancer vaccination strategies, and suggest a potential extension of HSP70-based vaccination protocols from a patient-individual treatment modality to its use in an allogeneic setting. C1 Univ Munich, Clin Cooperat Grp Hyperthermie, Munich, Germany. Univ Munich, Inst Mol Immunol, GSF Natl Res Ctr Environm & Hlth, Munich, Germany. Univ Munich, Klinikum Grosshadern, Med Klin 3, Munich, Germany. GSF Natl Res Ctr Environm & Hlth, Inst Pathol, Neuherberg, Germany. Dana Farber Canc Inst, Dept Radiat Oncol, Boston, MA 02115 USA. Harvard Univ, Sch Med, Boston, MA 02115 USA. RP Noessner, E (reprint author), Univ Munich, Klinikum Univ Regensburg, Dept Hematol & Oncol, D-93053 Regensburg, Germany. RI Asea, Alexzander/I-4112-2013 OI Asea, Alexzander/0000-0003-3592-3481 NR 58 TC 157 Z9 177 U1 1 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 NOV 15 PY 2002 VL 169 IS 10 BP 5424 EP 5432 PG 9 WC Immunology SC Immunology GA 614CG UT WOS:000179170300010 PM 12421917 ER PT J AU Reid, RR Woodcock, S Shimabukuro-Vornhagen, A Austen, WG Kobzik, L Zhang, M Hechtman, HB Moore, FD Carroll, MC AF Reid, RR Woodcock, S Shimabukuro-Vornhagen, A Austen, WG Kobzik, L Zhang, M Hechtman, HB Moore, FD Carroll, MC TI Functional activity of natural antibody is altered in Cr2-deficient mice SO JOURNAL OF IMMUNOLOGY LA English DT Article ID INTESTINAL ISCHEMIA-REPERFUSION; RECOGNIZE PHOSPHATIDYL CHOLINE; COMPLEMENT RECEPTOR TYPE-1; B-1 CELL-DEVELOPMENT; T-DEPENDENT ANTIGEN; REMOTE ORGAN INJURY; B-CELLS; DEFICIENT MICE; AFFINITY MATURATION; IGG AUTOANTIBODIES AB The major source of natural IgM Abs are B-1 cells, which differ from conventional B cells in their anatomic location, cell surface phenotype, restricted usage of particular V, genes and limited use of N-region addition during V-D-J rearrangement. The origin of B-1 cells is unclear. However, they are capable of self-renewal and their development is sensitive to signaling via the B cell receptor, as genetic defects that impair the strength of the signal often result in limited development. These findings suggest that B-1 cells require either an intrinsic signal, or contact with Ag, for positive selection and expansion and/or maintenance in the periphery. In support of interaction with cognate Ag, deficiency in the complement receptors CD21/CD35 results in a 30-40% decrease in the CD5(+) B-1 population. To determine whether this reduction reflects a loss of certain specificities or simply a proportional decline in the repertoire, we examined peritoneal B cells isolated from Cr2(+) and Cr2(def) mice for recognition of a B-1 cell Ag, i.e., phosphatidylcholine, and assayed for injury in an IgM natural Ab-dependent model of reperfusion injury. We found a similar frequency of phosphatidylcholine-specific CD5(+) B-1 cells in the two strains of mice. By contrast, the Cr2(def) mice have reduced injury in the IgM-dependent model of reperfusion injury. Reconstitution of the deficient mice with pooled IgM or adoptive transfer of Cr2(+) peritoneal B cells restored injury. These results suggest that complement receptors CD21/CD35 are important in maintenance of the B-1 cell repertoire to some, but not all, specificities. C1 Ctr Blood Res, Boston, MA 02115 USA. Harvard Univ, Sch Med, Dept Pathol, Boston, MA 02115 USA. Harvard Univ, Sch Med, Dept Pediat, Boston, MA 02115 USA. Harvard Univ, Sch Med, Dept Surg, Boston, MA 02115 USA. Brigham & Womens Hosp, Boston, MA 02115 USA. RP Carroll, MC (reprint author), Ctr Blood Res, 200 Longwood Ave, Boston, MA 02115 USA. FU NIGMS NIH HHS [P01 GM 52585] NR 59 TC 72 Z9 76 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 NOV 15 PY 2002 VL 169 IS 10 BP 5433 EP 5440 PG 8 WC Immunology SC Immunology GA 614CG UT WOS:000179170300011 PM 12421918 ER PT J AU Gadieva, M Verschoor, A Brockman, MA Jezak, H Shen, LM Knipe, DM Carroll, MC AF Gadieva, M Verschoor, A Brockman, MA Jezak, H Shen, LM Knipe, DM Carroll, MC TI Macrophage-derived complement component C4 can restore humoral immunity in C4-deficient mice SO JOURNAL OF IMMUNOLOGY LA English DT Article ID FOLLICULAR DENDRITIC CELLS; HERPES-SIMPLEX VIRUS; T-DEPENDENT ANTIGEN; ANTIBODY-RESPONSE; EXTRAHEPATIC EXPRESSION; ACQUIRED-IMMUNITY; GERMINAL CENTER; LYMPHOCYTES-B; MESSENGER-RNA; C3 AB Mice with a disrupted C4 locus (C4(-/-)) have an impaired immune response to thymus-dependent Ags. To test the role of bone marrow-derived C4 in humoral immunity, we reconstituted deficient animals with wild-type bone marrow or an enriched fraction of bone marrow-derived macrophages. C4 chimeras were immunized with 4-hydroxy-3-nitrophenyl, conjugated to keyhole limpet hemocyanin (NP5- KLH) or infected with HSV-1, and the Ab response was evaluated. Wild-type bone marrow rescued the humoral immune response to both Ags, i.e., the soluble Ag and HSV-1, demonstrating that local C4 production is sufficient for humoral responses. Although the C4 chimeric animals lacked detectable C4 in their sera, C4 mRNA was identified in splenic sections by in situ hybridization, and C4 protein deposits were identified in the germinal center areas of splenic follicles by immunofluorescence staining. Macrophages derived from bone marrow produced sufficient C4 protein to restore the humoral response to NP5-KLH in C4-deficient animals when administered along with Ag. Cell-sorting experiments, followed by C4-specific RT-PCR, identified splenic macrophages; (CD11b(+), CD11c(-)) as a cellular source for C4 synthesis within the spleen. C1 Ctr Blood Res, Boston, MA 02115 USA. Harvard Univ, Sch Med, Dept Pediat, Boston, MA 02115 USA. Harvard Univ, Sch Med, Dept Pathol, Boston, MA 02115 USA. Harvard Univ, Sch Med, Dept Microbiol & Mol Genet, Boston, MA 02115 USA. RP Carroll, MC (reprint author), Ctr Blood Res, 221 Longwood Ave,LMRC501, Boston, MA 02115 USA. EM carroll@cbr.med.harvard.edu OI Brockman, Mark/0000-0001-6432-1426 NR 50 TC 0 Z9 0 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 NOV 15 PY 2002 VL 169 IS 10 BP 5489 EP 5495 PG 7 WC Immunology SC Immunology GA 614CG UT WOS:000179170300017 ER PT J AU Weber, DA Attinger, A Kemball, CC Wigal, JL Pohl, J Xiong, Y Reinherz, EL Cheroutre, H Kronenberg, M Jensen, PE AF Weber, DA Attinger, A Kemball, CC Wigal, JL Pohl, J Xiong, Y Reinherz, EL Cheroutre, H Kronenberg, M Jensen, PE TI Peptide-independent folding and CD8 alpha alpha binding by the nonclassical class I molecule thymic leukemia antigen SO JOURNAL OF IMMUNOLOGY LA English DT Article ID MAJOR HISTOCOMPATIBILITY COMPLEX; DELTA T-CELL; CRYSTAL-STRUCTURE; MOUSE; STABILITY; EXPRESSION; QA-1(B); LYMPHOCYTES; RECOGNITION; LIBRARIES AB The nonclassical class I molecule, thymic leukemia JL), has been shown to be expressed on intestinal epithelial cells and to interact with CD8(+) intraepithelial T lymphocytes. We generated recombinant soluble TL (T18(d)) H chains in bacteria as inclusion bodies and refolded them with beta(2)-microglobulin in the presence or absence of a random peptide library. Using a mAb, HD168, that recognizes a conformational epitope on native TL molecules, we observed that protein folds efficiently in the absence of peptide. Circular dichroism analysis demonstrated that TL molecules have structural features similar to classical class I molecules. Moreover, thermal denaturation experiments indicated that the melting temperature for peptide-free TL is similar to values reported previously for conventional class I-peptide complexes. Our results also show that CD8cea binding is not dependent on either TL-associated peptide or TL glycosylation. C1 Emory Univ, Sch Med, Dept Pathol & Lab Med, Atlanta, GA 30322 USA. Emory Univ, Sch Med, Dept Pathol, Atlanta, GA 30322 USA. Emory Univ, Micorchem Facil, Atlanta, GA 30322 USA. La Jolla Inst Allergy & Immunol, Div Dev Immunol, San Diego, CA 92121 USA. Dana Farber Canc Inst, Immunobiol Lab, Boston, MA 02115 USA. RP Jensen, PE (reprint author), Emory Univ, Sch Med, Dept Pathol & Lab Med, Woodruff Mem Bldg,Room 7-309,1639 Pierce Dr, Atlanta, GA 30322 USA. FU NIAID NIH HHS [AI 50263, AI 30554, AI 33614, AI 45022] NR 46 TC 27 Z9 27 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 NOV 15 PY 2002 VL 169 IS 10 BP 5708 EP 5714 PG 7 WC Immunology SC Immunology GA 614CG UT WOS:000179170300043 PM 12421950 ER PT J AU Delgado, JC Baena, A Thim, S Goldfeld, AE AF Delgado, JC Baena, A Thim, S Goldfeld, AE TI Ethnic-specific genetic associations with pulmonary tuberculosis SO JOURNAL OF INFECTIOUS DISEASES LA English DT Article; Proceedings Paper CT 13th International Congress of Histocompatibility and Immunogenetics CY MAY 18-22, 2002 CL SEATTLE, WASHINGTON ID CEREBRAL MALARIA; MYCOBACTERIUM-TUBERCULOSIS; PROMOTER REGION; NRAMP1 GENE; RECEPTOR DEFICIENCY; ACTIVE TUBERCULOSIS; SUSCEPTIBILITY; POLYMORPHISM; INFECTION; FREQUENCY AB Several susceptibility-associated genetic polymorphisms have been proposed to explain differential susceptibility to tuberculosis (TB) disease progression in different populations. Here, polymorphisms in the natural resistance-associated macrophage protein 1 (NRAMP1), vitamin D receptor, tumor necrosis factor-alpha, interleukin (IL)-1, and IL-10 genes were evaluated in 358 Cambodian patients with pulmonary TB and 106 tuberculin-positive control subjects. Heterozygosity for the -1082 polymorphism of the IL-10 promoter and heterozygosity for 2 linked polymorphic NRAMP1 variants, D543N and 3' untranslated region, were associated with TB susceptibility and resistance, respectively. Other polymorphisms associated with differential susceptibility to TB were not associated with susceptibility or resistance to TB in Cambodians. The novel pattern of genetic associations with susceptibility and resistance to TB detected in Cambodia is consistent with the conclusion that unique environmental and natural selective factors have resulted in the development of ethnic-specific host genetic factors associated with TB susceptibility and resistance worldwide. C1 Brigham & Womens Hosp, Ctr Blood Res, Boston, MA 02115 USA. Brigham & Womens Hosp, Dept Pathol, Boston, MA 02115 USA. Brigham & Womens Hosp, Dept Med, Boston, MA 02115 USA. Cambodian Hlth Committee, Phnom Penh, Cambodia. RP Goldfeld, AE (reprint author), Ctr Blood Res, 800 Huntington Ave, Boston, MA 02115 USA. FU NHLBI NIH HHS [HL-67471, HL-59838] NR 45 TC 168 Z9 176 U1 0 U2 1 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 NOV 15 PY 2002 VL 186 IS 10 BP 1463 EP 1468 DI 10.1086/344891 PG 6 WC Immunology; Infectious Diseases; Microbiology SC Immunology; Infectious Diseases; Microbiology GA 609EQ UT WOS:000178891000011 PM 12404162 ER PT J AU Elbert, T Sterr, A Rockstroh, B Pantev, C Muller, MM Taub, E AF Elbert, T Sterr, A Rockstroh, B Pantev, C Muller, MM Taub, E TI Expansion of the tonotopic area in the auditory cortex of the blind SO JOURNAL OF NEUROSCIENCE LA English DT Article DE tonotopic map; auditory cortex; reorganization; blind; MEG ID EVENT-RELATED POTENTIALS; CROSS-MODAL PLASTICITY; ADULT OWL MONKEYS; CONGENITALLY BLIND; BRAILLE READERS; FREQUENCY REPRESENTATION; CORTICAL REPRESENTATION; SOMATOSENSORY CORTEX; ACTIVATION PATTERNS; SIGHTED SUBJECTS AB A part of the core area of the auditory cortex was examined in nine blind and10 sighted individuals by magnetic source imaging and was found to be enlarged by a factor of 1.8 in the blind compared with the sighted humans. Moreover, the latency of the N1m component of the auditory-evoked magnetic response was significantly decreased in the blind. The development of use-dependent cortical reorganization may be a consequence of the absence of visual input in combination with enhanced auditory activity generated by the long-term concentration by blind individuals on nonvisual cues to interact appropriately with the environment. It is consistent with and well suited to mediate the demonstrated increased ability of the blind to accurately localize acoustic sources in peripheral auditory fields and to decode speech. C1 Univ Konstanz, Dept Psychol, D-78457 Constance, Germany. Univ Liverpool, Dept Psychol, Liverpool L69 7ZA, Merseyside, England. Rotman Res Inst Neurosci, Toronto, ON M6A 2E1, Canada. Univ Alabama, Dept Psychol, Birmingham, AL 35294 USA. Birmingham Vet Affairs Med Ctr, Birmingham, AL 35233 USA. RP Elbert, T (reprint author), Univ Konstanz, Dept Psychol, POB D25, D-78457 Constance, Germany. RI Elbert, Thomas/C-8556-2009 NR 44 TC 84 Z9 86 U1 0 U2 2 PU SOC NEUROSCIENCE PI WASHINGTON PA 11 DUPONT CIRCLE, NW, STE 500, WASHINGTON, DC 20036 USA SN 0270-6474 J9 J NEUROSCI JI J. Neurosci. PD NOV 15 PY 2002 VL 22 IS 22 BP 9941 EP 9944 PG 4 WC Neurosciences SC Neurosciences & Neurology GA 613TF UT WOS:000179147000033 PM 12427851 ER PT J AU Gurvits, TV Lasko, NB Repak, AL Metzger, LJ Orr, SP Pitman, RK AF Gurvits, TV Lasko, NB Repak, AL Metzger, LJ Orr, SP Pitman, RK TI Performance on visuospatial copying tasks in individuals with chronic posttraumatic stress disorder SO PSYCHIATRY RESEARCH LA English DT Article DE stress disorders; copy figure test; neurologic examinatior; form perception; psychomotor performance ID SIGNS AB The ability to copy figures was evaluated in 41 subjects with chronic posttraumatic stress disorder (PTSD) and 27 trauma-exposed. non-PTSD comparison subjects. Individuals with PTSD demonstrated significantly impaired performance. However, after adjusting for pre-trauma variables. there was only a marginally significant association between figure-copying performance and PTSD. These findings are consistent with pre-trauma visual-spatial impairment as being among the risk factors for chronic PTSD. (C) 2002 Elsevier Science Ireland Ltd. All rights reserved. C1 VA Res Serv, Manchester, NH 03104 USA. Massachusetts Gen Hosp, Dept Psychiat, Boston, MA 02114 USA. Harvard Univ, Sch Med, Boston, MA USA. RP Gurvits, TV (reprint author), VA Res Serv, 718 Smyth Rd, Manchester, NH 03104 USA. NR 14 TC 15 Z9 16 U1 0 U2 1 PU ELSEVIER SCI IRELAND LTD PI CLARE PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE, IRELAND SN 0165-1781 J9 PSYCHIAT RES JI Psychiatry Res. PD NOV 15 PY 2002 VL 112 IS 3 BP 263 EP 268 AR PII S0165-1781(02)00234-2 DI 10.1016/S0165-1781(02)00234-2 PG 6 WC Psychiatry SC Psychiatry GA 630KA UT WOS:000180105000009 PM 12450636 ER PT J AU Le, SV Yamaguchi, DJ McArdle, CA Tachiki, K Pisegna, JR Germano, P AF Le, SV Yamaguchi, DJ McArdle, CA Tachiki, K Pisegna, JR Germano, P TI PAC1 and PACAP expression, signaling, and effect on the growth of HCT8, human colonic tumor cells SO REGULATORY PEPTIDES LA English DT Article DE pituitary adenylate cyclase-activating polypeptide; pituitary adenylate cyclase-activating polypeptide type 1 receptor; HCT8 cells; colon cancer growth ID CYCLASE-ACTIVATING POLYPEPTIDE; GASTRIC-ACID SECRETION; LUNG-CANCER CELLS; ADENYLATE-CYCLASE; FAS-LIGAND; I RECEPTOR; HYPOTHALAMIC POLYPEPTIDE; MOLECULAR-CLONING; SPLICE VARIANTS; T-LYMPHOCYTES AB The pituitary adenylate cyclase-activating polypeptide (PACAP) type 1 receptor (PAC1) is a heptahelical, G protein-coupled receptor that has been shown to be expressed by non-squamous lung cancer and breast cancer cell lines, and to be coupled to the growth of these tumors. We have previously shown that PACAP and its receptor, PAC1, are expressed in rat colonic tissue. In this study, we used polyclonal antibodies directed against the COOH terminal of PAC1, as well as fluorescently labeled PACAP, Fluor-PACAP, to demonstrate the expression of PAC1 on HCT8 human colonic tumor cells, using FACS analysis and confocal laser scanning microscopy. Similarly, anti-PACAP polyclonal antibodies were used to confirm the expression of PACAP hormone by this cell line. We then investigated the signal transduction properties of PAC1 in these tumor cells. PACAP-38 elevated intracellular cAMP levels in a dose-dependent manner, with a half-maximal (EC50) stimulation of approximately 3 nM. In addition, PACAP-38 stimulation caused an increase in cytosolic Ca2+ concentration [Ca2+](i), which was partially inhibited by the PACAP antagonist, PACAP-(6-38). Finally, we studied the potential role of PACAP upon the growth of these tumor cells. We found that PACAP-38, but not VIP, increased the number of viable HCT8 cells, as measured by MTT activity. We also demonstrated that HCT8 cells expressed the Fas receptor (Fas-R/CD95), which was subsequently down-regulated upon activation with PACAP-38, further suggesting a possible role for PACAP in the growth and survival of these tumor cells. These data indicate that HCT8 human colon tumor cells express PAC1 and produce PACAP hormone. Furthermore, PAC1 activation is coupled to adenylate cyclase, increase cytosolic [Ca2+](i), and cellular proliferation. Therefore, PACAP is capable of increasing the number of viable cells and regulating Fas-R expression in a human colonic cancer cell line, suggesting that PACAP might play a role in the regulation of colon cancer growth and modulation of T lymphocyte anti-tumoral response via the Fas-R/Fas-L apoptotic pathway. (C) 2002 Published by Elsevier Science B.V. C1 Univ Calif Los Angeles, VA Greater Los Angeles Healthcare Syst, Digest Dis Res Ctr, CURE, Los Angeles, CA 90073 USA. Univ Calif Los Angeles, Dept Med, Los Angeles, CA 90073 USA. Univ Bristol, Res Ctr Neuroendocrinol, Bristol BS2 8HW, Avon, England. RP Germano, P (reprint author), Univ Calif Los Angeles, VA Greater Los Angeles Healthcare Syst, Digest Dis Res Ctr, CURE, Bldg 115,Room 313,11301 Wilshire Blvd, Los Angeles, CA 90073 USA. NR 48 TC 23 Z9 24 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0167-0115 J9 REGUL PEPTIDES JI Regul. Pept. PD NOV 15 PY 2002 VL 109 IS 1-3 BP 115 EP 125 AR PII S0167-0115(02)00194-5 DI 10.1016/S0167-0115(02)00194-5 PG 11 WC Endocrinology & Metabolism; Physiology SC Endocrinology & Metabolism; Physiology GA 614WA UT WOS:000179213400017 PM 12409223 ER PT J AU Anderson, MS Venanzi, ES Klein, L Chen, ZB Berzins, SP Turley, SJ von Boehmer, H Bronson, R Dierich, A Benoist, C Mathis, D AF Anderson, MS Venanzi, ES Klein, L Chen, ZB Berzins, SP Turley, SJ von Boehmer, H Bronson, R Dierich, A Benoist, C Mathis, D TI Projection of an immunological self shadow within the thymus by the aire protein SO SCIENCE LA English DT Article ID CANDIDIASIS-ECTODERMAL DYSTROPHY; T-CELL TOLERANCE; AUTOIMMUNE REGULATOR AIRE; EPITHELIAL-CELLS; SUBCELLULAR LOCATION; IMMUNE TOLERANCE; GENE-EXPRESSION; BINDING PROTEIN; STROMAL CELLS; ANTIGEN AB Humans expressing a defective form of the transcription factor AIRE (autoimmune regulator) develop multiorgan autoimmune disease. We used aire-deficient mice to test the hypothesis that this transcription factor regulates autoimmunity by promoting the ectopic expression of peripheral tissue restricted antigens in medullary epithelial cells of the thymus. This hypothesis proved correct. The mutant animals exhibited a defined pro. le of autoimmune diseases that depended on the absence of aire in stromal cells of the thymus. Aire-deficient thymic medullary epithelial cells showed a specific reduction in ectopic transcription of genes encoding peripheral antigens. These findings highlight the importance of thymically imposed "central" tolerance in controlling autoimmunity. C1 Joslin Diabet Ctr, Sect Immunol & Immunogenet, Boston, MA 02115 USA. Brigham & Womens Hosp, Dept Med, Boston, MA 02115 USA. Harvard Univ, Sch Med, Boston, MA 02115 USA. Dana Farber Canc Inst, Boston, MA 02115 USA. ULP, CNRS, INSERM, Inst Genet & Biol Mol & Cellualire, F-67404 Strasbourg, France. RP Benoist, C (reprint author), Joslin Diabet Ctr, Sect Immunol & Immunogenet, Boston, MA 02115 USA. RI Klein, Ludger/G-8785-2011 FU NCI NIH HHS [T32CA70083-05]; NIDDK NIH HHS [2 P30 DK36836-16, 2T32 DK07260-26, KO8-DK59958-01A1, R01 DK60027-01] NR 37 TC 1285 Z9 1326 U1 6 U2 55 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 NOV 15 PY 2002 VL 298 IS 5597 BP 1395 EP 1401 DI 10.1126/science.1075958 PG 8 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA 615AF UT WOS:000179223100044 PM 12376594 ER PT J AU Kumagai, N O'Neil, JJ Barth, RN LaMattina, JC Utsugi, R Moran, SG Yamamoto, S Vagefi, PA Kitamura, H Kamano, C Sachs, DH Yamada, Y AF Kumagai, N O'Neil, JJ Barth, RN LaMattina, JC Utsugi, R Moran, SG Yamamoto, S Vagefi, PA Kitamura, H Kamano, C Sachs, DH Yamada, Y TI Vascularized islet-cell transplantation in miniature swine. I. Preparation of vascularized islet kidneys SO TRANSPLANTATION LA English DT Article ID MAJOR HISTOCOMPATIBILITY COMPLEX; PANCREAS TRANSPLANTATION; THYMIC TRANSPLANTATION; DIABETES-MELLITUS; TOLERANCE; COMPLICATIONS; ALLOGRAFTS; INDUCTION; BARRIER AB Background. Whereas clinical pancreatic transplantation has been highly successful in correcting the hyperglycemia of insulin-dependent diabetes mellitus (type 1), the results of islet transplantation have been disappointing. This discrepancy may be because of, at least in part, nonspecific loss of islets during the time required for revascularization. To test this hypothesis, we have designed composite kidney grafts containing vascularized autologous islets that can be used to compare the engraftment potential of vascularized versus nonvascularized islet tissue. Methods. (1) Islet-cell isolation: miniature swine underwent either partial pancreatectomy to isolate autologous islets or total pancreatectomy to isolate minor antigen-mismatched islets. Islets were purified from excised pancreatic tissue by enzymatic digestion and discontinuous density gradient purification. Isolated islets were cultured for 3 days before transplant. (2) Creation of vascularized islet kidneys UK): autologous islets alone (n=6), minor-mismatched islets alone (n=3), and minor-mismatched islets plus simultaneous autologous thymic tissue (n=3) were transplanted beneath the renal capsule of juvenile miniature swine. Minor antigen-mismatched islets were also transplanted into both the vascularized thymic graft of a thymokidney (to produce a thymo-islet kidney [TIK]) and the contralateral native kidney (n=3) and both the host thymus and beneath the renal capsule (n=2). All recipients receiving minor-mismatched islets were treated with a 12-day intravenous (M course of either cyclosporine A (CsA) at 10 mg/kg per day or FK506 at 0.15 mg/kg per day. (3) Assessment of Function: to evaluate the function of the transplanted islets, three animals bearing TIK and IK underwent total pancreatectomy 3 months following islet transplantation. Results. (1) Islet-cell yields: an average of 254,960 51,879 (4,452 932 islet equivalents [IEQ]/ gram of pancreas) and 374,410 9,548 (4,183+/-721 IEQ/gram of pancreas) viable islets were obtained by partial pancreatectomy and complete pancreatectomy, respectively. (2) Creation of IK: autologous islets engrafted indefinitely, whereas recipients of minor-mismatched islets alone rejected the islets within 2 months. However, when minor-mismatched islets were implanted into both the thymokidney and the contralateral kidney of animals bearing a thymokidney, the islets engrafted indefinitely in both sites (>3 months). Simultaneous implantation of islets into the host thymus and under the renal capsule also led to permanent engraftment of minor-mismatched islets. (3) Function of vascularized islets: three animals with both a TIK and an IK in place for 3 months underwent total pancreatectomy. All three animals maintained normoglycemia thereafter. In two of these animals, the IKs were removed 2 months after the pancreatectomy, and in both cases normoglycemia was maintained thereafter by the TIK. Conclusions. The implantation of islets beneath the autologous renal capsule permitted the establishment of a vascular supply and thereby supported normal-islet-cell growth and function. The presence of thymic tissue beneath the autologous renal capsule facilitated the engraftment of minor-mismatched islets, and such grafts achieved results similar to autologous islet transplants. Therefore, the ability to create vascularized islet grafts may provide a strategy for successful islet transplantation across allogeneic and potentially across xenogeneic barriers. C1 Massachusetts Gen Hosp, Transplantat Biol Res Ctr, Boston, MA 02129 USA. Joslin Diabet Ctr, Dept Islet Transplantat & Cell Biol, Boston, MA 02215 USA. Massachusetts Gen Hosp, Dept Pathol, Boston, MA 02129 USA. RP Yamada, Y (reprint author), Massachusetts Gen Hosp, Transplantat Biol Res Ctr, MGH-E,Bldg 149-9019,13th St, Boston, MA 02129 USA. RI Barth, Rolf/B-2542-2014; LaMattina, John/B-2976-2014 OI LaMattina, John/0000-0001-7016-0382 NR 26 TC 18 Z9 19 U1 0 U2 1 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0041-1337 J9 TRANSPLANTATION JI Transplantation PD NOV 15 PY 2002 VL 74 IS 9 BP 1223 EP 1230 DI 10.1097/01.TP.0000035880.84249.41 PG 8 WC Immunology; Surgery; Transplantation SC Immunology; Surgery; Transplantation GA 615WN UT WOS:000179270500005 PM 12451257 ER PT J AU Gleit, ZL Cameron, AM Fuchimoto, Y Melendy, E Monajati, L Coburn, RC Sachs, DH Huang, CA AF Gleit, ZL Cameron, AM Fuchimoto, Y Melendy, E Monajati, L Coburn, RC Sachs, DH Huang, CA TI Persistent chimerism despite antidonor MHC in vitro responses in miniature swine following allogeneic hematopoietic cell transplantation SO TRANSPLANTATION LA English DT Article ID BONE-MARROW TRANSPLANTATION; INTRATHYMIC CLONAL DELETION; SKIN ALLOGRAFT TOLERANCE; POSITIVE T-CELLS; MONOCLONAL-ANTIBODIES; MIXED CHIMERISM; CLASS-I; LYMPHOCYTES; ANTIGEN; COMPLEX AB Background. T-cell chimerism predominates in miniature swine receiving hematopoietic-cell transplantation without myelosuppressive conditioning. Several chimeric recipients have become hyporesponsive to donor-major histocompatibility complex (MHC) in vitro and accepted donor-matched renal transplants without immunosuppression. However, some retained antidonor in vitro responses and subsequently rejected donor renal allografts despite the persistence of peripheral blood chimerism. In this study, we characterize the donor cells in both "tolerant" and "nontolerant" chimeric miniature swine. Methods. Peripheral blood chimerism was determined by flow cytometry. In vitro antidonor responsiveness was determined by mixed lymphocyte reaction (MLR) and cell-mediated lymphocytotoxicity (CML). Donor cells were separated from chimeras by immunomagnetic bead separation and used as stimulators or targets in CML assays. Phenotypic analysis of donor cells in chimeras was performed using flow cytometry. Results. Peripheral blood chimerism stabilized beyond 100 days and was made up almost entirely of T cells. PBMC from nontolerant chimeras could be stimulated in vitro to kill donor cells isolated from the mixed chimera itself. In contrast, PBMC from tolerant chimeras hyporesponsive to donor-type cells could not be stimulated in vitro to kill their own sorted donor cells. Conclusions. The in vivo persistence of donor T cells in mixed chimeric animals with in vitro antidonor responsiveness is not caused by an inability of these cells to be killed but rather by the poor stimulating capacity of these donor T cells. The nature of donor T cells that persist in the face of in vitro antidonor responses, has important implications for them induction of transplant tolerance by way of the generation of mixed chimerism. C1 Harvard Univ, Massachusetts Gen Hosp, Sch Med, Transplantat Biol Res Ctr, Boston, MA 02129 USA. RP Huang, CA (reprint author), Columbia Univ, Coll Phys & Surg, New York, NY 10032 USA. FU NCI NIH HHS [1R01 CA79989-01A1]; NHLBI NIH HHS [1R01 HL63430-01]; NIAID NIH HHS [1F32AI-10306] NR 32 TC 12 Z9 12 U1 0 U2 1 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0041-1337 J9 TRANSPLANTATION JI Transplantation PD NOV 15 PY 2002 VL 74 IS 9 BP 1260 EP 1266 DI 10.1097/01.TP.0000035882.90503.CE PG 7 WC Immunology; Surgery; Transplantation SC Immunology; Surgery; Transplantation GA 615WN UT WOS:000179270500011 PM 12451263 ER PT J AU Magro, CM Deng, A Pope-Harman, A Waldman, WJ Collins, AB Adams, PW Kelsey, M Ross, P AF Magro, CM Deng, A Pope-Harman, A Waldman, WJ Collins, AB Adams, PW Kelsey, M Ross, P TI Humorally mediated posttransplantation septal capillary injury syndrome as a common form of pulmonary allograft rejection: A hypothesis SO TRANSPLANTATION LA English DT Article ID LUNG-TRANSPLANT RECIPIENTS; HUMAN CARDIAC ALLOGRAFTS; NECROSIS-FACTOR-ALPHA; VIII RELATED ANTIGEN; PERITUBULAR CAPILLARIES; HYPERACUTE REJECTION; COMPLEMENT FRAGMENT; LUPUS-ERYTHEMATOSUS; C4D DEPOSITS; ANTIBODIES AB Background. Cellular immunity is the reputed mechanism of lung allograft failure. Humoral immunity is not a commonly recognized pathway. Material and Methods. We describe 22 patients who developed a posttransplantation septal capillary injury syndrome in the absence of panel-reactive antibodies. Factor VIII levels served as an index of microvascular injury. Routine light microscopic studies were performed in a total of 73 biopsies; 54 biopsy specimens were analyzed for deposition of C1q, C4d, C5b-9, and immunoglobulin (IgG, IgM, and IgA). Indirect immunofluorescent testing to assess for antiendothelial cell antibodies was performed using patient serum and human pulmonary microvascular endothelial cell cultures as substrate. Control samples were based on patients who were clinically well at the time of the biopsy. Results. All presented with a deterioration in respiratory function. All patients had elevated factor VIII levels; the levels were significantly greater compared with pretransplantation baseline values (P=<0.03). The biopsy specimens were remarkable for septal capillary necrosis with significant septal capillary deposition of C1q, C3, C4d, and/or C5b-9 along with immunoglobulin, including IgG, with variable endothelial cell localization. The degree of septal capillary necrosis was significantly less in posttransplantation patients who were clinically doing well (P<0.0001) as was the degree of C1q, C3, C4d, and C5b-9 (P<0.05). Indirect antiendothelial cell antibody studies were positive in most patients. Treatment interventions included plasmapheresis, resulting in functional improvement: the postpheresis biopsy specimens showed a reduction in both the degree of septal capillary injury (P<0.0003) and the amount of C1q, C3, C4d, and C5b-9 deposition (P<0.05). Conclusions. Septal capillary injury accompanied by direct and indirect immunofluorescent evidence of humoral immunity is a frequent finding on transbronchial biopsies. The findings suggest that humoral immunity to endothelial-based alloantigen is a common occurrence in lung grafts and may be a critical factor in chronic graft dysfunction. C1 Ohio State Univ, Div Cardiothorac Surg, Columbus, OH 43210 USA. Ohio State Univ, Dept Pathol, Columbus, OH 43210 USA. Ohio State Univ, Div Pulm Crit Med, Columbus, OH 43210 USA. Harvard Univ, Massachusetts Gen Hosp, Sch Med, Immunopathol Unit, Boston, MA USA. Ohio State Univ, Clin Histocompatibil Lab, Columbus, OH 43210 USA. RP Ross, P (reprint author), Ohio State Univ, Div Cardiothorac Surg, N816 Doan Hall,410 W 10th Ave, Columbus, OH 43210 USA. NR 29 TC 52 Z9 52 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0041-1337 J9 TRANSPLANTATION JI Transplantation PD NOV 15 PY 2002 VL 74 IS 9 BP 1273 EP 1280 DI 10.1097/01.TP.00000313936.05322.D9 PG 8 WC Immunology; Surgery; Transplantation SC Immunology; Surgery; Transplantation GA 615WN UT WOS:000179270500013 PM 12451265 ER PT J AU Port, FK Bragg-Gresham, JL Metzger, RA Dykstra, DM Gillespie, BW Young, EW Delmonico, FL Wynn, JJ Merion, RM Wolfe, RA Held, PJ AF Port, FK Bragg-Gresham, JL Metzger, RA Dykstra, DM Gillespie, BW Young, EW Delmonico, FL Wynn, JJ Merion, RM Wolfe, RA Held, PJ TI Donor characteristics associated with reduced graft survival: An approach to expanding the pool of kidney donors SO TRANSPLANTATION LA English DT Article ID ORGAN DONATION; TRANSPLANTS; SPAIN AB Background. Availability of cadaveric kidneys for transplantation is far below the growing need, leading to longer waiting time and more deaths while waiting. Methods. Using national data from 1995 to 2000, we evaluated graft survival by donor characteristics and the rate of discard of retrieved organs, with the goal of increasing use of kidneys that are associated with increased risk of graft failure, that is, expanded donor kidneys. Results. Cox models identified four donor factors that independently predicted significantly higher relative risk of graft loss compared with a low-risk group. These factors included donor age, cerebrovascular accident as the cause of death, renal insufficiency (serum creatinine >1.5 mg/dL), and history of hypertension. Expanded donor kidneys were defined as those with relative risk of graft loss greater than 1.70 and included all donors aged 60 years and older and those aged 50 to 59 years with at least two of the other three conditions (cerebrovascular cause of death, renal insufficiency, hypertension). The expanded donor group accounted for 14.8% of transplanted kidneys. Among organs procured from expanded donors, 38% were discarded versus 9% for all other kidneys. The risk of graft loss of expanded donor kidneys was increased in both older and younger recipients but to a greater extent in those recipients older than 50 years. Conclusion. By identifying donor factors associated with graft failure, these analyses may help to expand the number of transplanted kidneys by increasing the utilization of retrieved cadaveric kidneys. C1 Univ Renal Res & Educ Assoc, URREA, Sci Registry Transplant Recipients, Ann Arbor, MI 48103 USA. TransLife Florida Hosp, Med Ctr, Orlando, FL USA. Univ Michigan, Sch Publ Hlth, Dept Biostat, Ann Arbor, MI 48109 USA. Dept Vet Affairs Med Ctr, Ann Arbor, MI USA. Univ Michigan, Div Nephrol, Ann Arbor, MI 48109 USA. Massachusetts Gen Hosp, Boston, MA 02114 USA. Med Coll Georgia, Augusta, GA 30912 USA. Univ Michigan, Hlth Syst, Dept Surg, Div Transplantat, Ann Arbor, MI 48109 USA. Univ Michigan, Kidney Epidemiol & Cost Ctr, Ann Arbor, MI 48109 USA. RP Port, FK (reprint author), Univ Renal Res & Educ Assoc, URREA, Sci Registry Transplant Recipients, 315 W Huron,Suite 260, Ann Arbor, MI 48103 USA. NR 12 TC 384 Z9 394 U1 0 U2 7 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0041-1337 J9 TRANSPLANTATION JI Transplantation PD NOV 15 PY 2002 VL 74 IS 9 BP 1281 EP 1286 DI 10.1097/01.TP.0000034060.18738.0B PG 6 WC Immunology; Surgery; Transplantation SC Immunology; Surgery; Transplantation GA 615WN UT WOS:000179270500014 PM 12451266 ER PT J AU Ellison, MD McBride, MA Taranto, SE Delmonico, FL Kauffman, HM AF Ellison, MD McBride, MA Taranto, SE Delmonico, FL Kauffman, HM TI Living kidney donors in need of kidney transplants: A report from the organ procurement and transplantation network SO TRANSPLANTATION LA English DT Article AB Background. Our aim was to use the Organ Procurement and Transplantation Network (OPTN) database to determine the number of renal waitlist candidates who previously had been living donors. Methods. All living renal donors in the OPTN database were cross-checked against the renal waitlist history files. Additionally, renal transplant programs were contacted that had listed candidates as qualified for four additional allocation points available to patients who previously had donated an organ. Confirmatory phone calls to transplant programs yielded additional cases previously unreported to the United Network for Organ Sharing. Results. A total of 56 previous living donors were identified as having been subsequently listed for cadaveric kidney transplantation. Forty-three have received transplants; 36 currently have functioning grafts. One died after transplantation. Two candidates died while waiting. Conclusions. Living renal donation has long-term risks that may not be apparent in the short term. The numbers here reported underestimate the actual number of living donors with renal failure, because they include only patients listed for a kidney transplant. To determine risk factors for postdonation renal failure long-term living-donor follow-up data are needed. C1 Harvard Univ, Massachusetts Gen Hosp, Boston, MA 02115 USA. RP Ellison, MD (reprint author), United Network Organ Sharing, 1100 Boulders Pkwy,Suite 500, Richmond, VA 23225 USA. NR 7 TC 113 Z9 119 U1 0 U2 4 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0041-1337 J9 TRANSPLANTATION JI Transplantation PD NOV 15 PY 2002 VL 74 IS 9 BP 1349 EP 1351 DI 10.1097/01.TP.0000034031.95427.2A PG 3 WC Immunology; Surgery; Transplantation SC Immunology; Surgery; Transplantation GA 615WN UT WOS:000179270500025 PM 12451277 ER PT J AU Hahn, WC Weinberg, RA AF Hahn, WC Weinberg, RA TI Mechanisms of disease: Rules for making human tumor cells. SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Review ID PROTEIN PHOSPHATASE 2A; MAMMARY EPITHELIAL-CELLS; TRANSFORMED HUMAN-CELLS; HARVEY-RAS ONCOGENE; A-ALPHA SUBUNIT; LARGE T-ANTIGEN; TELOMERASE ACTIVITY; GENE-EXPRESSION; HUMAN CANCER; MULTISTAGE CARCINOGENESIS C1 Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02115 USA. Brigham & Womens Hosp, Dept Med, Boston, MA 02115 USA. Whitehead Inst Biomed Res, Cambridge, England. MIT, Dept Biol, Cambridge, England. RP Hahn, WC (reprint author), Dana Farber Canc Inst, Dept Med Oncol, 44 Binney St, Boston, MA 02115 USA. FU NCI NIH HHS [K01CA94223, R01 CA78461] NR 123 TC 572 Z9 599 U1 3 U2 36 PU MASSACHUSETTS MEDICAL SOC/NEJM 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 NOV 14 PY 2002 VL 347 IS 20 BP 1593 EP 1603 DI 10.1056/NEJMra021902 PG 11 WC Medicine, General & Internal SC General & Internal Medicine GA 614KL UT WOS:000179187800008 PM 12432047 ER PT J AU Hawighorst, T Oura, H Streit, M Janes, L Nguyen, L Brown, LF Oliver, G Jackson, DG Detmar, M AF Hawighorst, T Oura, H Streit, M Janes, L Nguyen, L Brown, LF Oliver, G Jackson, DG Detmar, M TI Thrombospondin-1 selectively inhibits early-stage carcinogenesis and angiogenesis but not tumor lymphangiogenesis and lymphatic metastasis in transgenic mice SO ONCOGENE LA English DT Article DE TSP-1; VEGF; Prox1; LYVE-1; chemoprevention ID ENDOTHELIAL GROWTH-FACTOR; CARCINOMA CELL-LINE; MULTISTAGE CARCINOGENESIS; SKIN CARCINOGENESIS; VESSEL MATURATION; MOUSE SKIN; CANCER; PROMOTES; PROGRESSION; EXPRESSION AB The roles played by the endogenous angiogenesis inhibitor thrombospondin-1 (TSP-1) in the early stages of multi-step carcinogenesis and in the control of hematogenous versus lymphatic metastasis are unknown. To investigate these issues we compared tumor development in normal mice and in transgenic mice with targeted overexpression of TSP-1 in the epidermis following a standard two-step chemical skin carcinogenesis regimen. Overexpression of TSP-1 resulted in delayed and reduced development of premalignant epithelial. hyperplasias, but did not inhibit the malignant conversion to squamous cell carcinomas. TSP-1 overexpression also suppressed tumor angiogenesis and distant organ metastasis, but failed to inhibit tumor-associated lymphangiogenesis or lymphatic tumor spread to regional lymph nodes. Concomitant with these results, we found that the endothelial TSP-1 receptor CD36 was mostly absent from cutaneous lymphatic vessels. Our findings indicate the potential use of TSP-1 for the prevention of premalignant stages of tumorigenesis and are likely to have implications for the further development of anti-angiogenic cancer therapies. C1 Massachusetts Gen Hosp, Dept Dermatol, CBRC, Charlestown, MA 02129 USA. Harvard Univ, Sch Med, Charlestown, MA 02129 USA. Beth Israel Deaconess Med Ctr, Dept Pathol, Boston, MA 02215 USA. Harvard Univ, Sch Med, Boston, MA 02215 USA. St Jude Childrens Res Hosp, Dept Genet, Memphis, TN 38105 USA. John Radcliffe Hosp, Inst Mol Med, IMCR Human Immunol Unit, Oxford OX3 9DS, England. RP Detmar, M (reprint author), Massachusetts Gen Hosp, Dept Dermatol, CBRC, Bldg 149,13st St, Charlestown, MA 02129 USA. EM michael.detmar@cbrc2.mgh.harvard.edu FU NCI NIH HHS [CA69184, CA91861, CA86410]; NEI NIH HHS [EY12162]; NIGMS NIH HHS [GM58462] NR 42 TC 58 Z9 62 U1 0 U2 0 PU NATURE PUBLISHING GROUP PI LONDON PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND SN 0950-9232 J9 ONCOGENE JI Oncogene PD NOV 14 PY 2002 VL 21 IS 52 BP 7945 EP 7956 DI 10.1038/sj.onc.1205956 PG 12 WC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity GA 612VY UT WOS:000179097200004 PM 12439745 ER PT J AU Burgio, KL Goode, PS Locher, JL Umlauf, MG Roth, DL Richter, HE Varner, RE Lloyd, LK AF Burgio, KL Goode, PS Locher, JL Umlauf, MG Roth, DL Richter, HE Varner, RE Lloyd, LK TI Behavioral training with and without biofeedback in the treatment of urge incontinence in older women - A Randomized controlled trial SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION LA English DT Article ID URINARY-INCONTINENCE; BLADDER; EFFICACY AB Context Previous research on urge urinary incontinence has demonstrated that multicomponent behavioral training with biofeedback is safe and effective, yet it has not been established whether biofeedback is an essential component that heightens therapeutic efficacy. Objective To examine the role of biofeedback in a multicomponent behavioral training program for urge incontinence in community-dwelling older women. Design Prospective, randomized controlled trial conducted from April 1, 1995, to March 30, 2001. Setting University-based outpatient continence clinic in the United States. Patients A volunteer sample of 222 ambulatory, nondemented, community-dwelling women aged 55 to 92 years with urge incontinence or mixed incontinence with urge as the predominant pattern. Patients were stratified by race, type of incontinence (urge only vs mixed), and severity (frequency of accidents). Interventions Patients were randomly assigned to receive 8 weeks (4 visits) of bio-feedback-assisted behavioral training (n=73), 8 weeks (4 visits) of behavioral training fee without biofeedback (verbal feedback based on vaginal palpation; n=74), or 8 weeks, of self-administered behavioral treatment using a self-help booklet (control condition; n=75). Main Outcome Measures Reduction in the number of incontinence episodes as documented in bladder diaries, patients' perceptions and satisfaction, and changes in quality of life. Results Intention-to-treat analysis showed that behavioral training with biofeedback yielded a mean 63.1% reduction (SD, 42.7%) in incontinence, verbal feedback a mean 69.4% reduction (SD; 32.7%), and the self-help booklet a mean 58.6% reduction (SD, 38.8%). The 3 groups were not significantly different from each other (P=.23). The groups differed significantly regarding patient satisfaction: 75.0% of the biofeedback group, 85.5% of the verbal feedback group, and 55.7% of the self-help booklet group reported being completely satisfied with treatment (P=.001). Significant improvements were seen across all 3 groups on 3 quality-of-life instruments, with no significant between-group differences. Conclusions Biofeedback to teach pelvic floor muscle control, verbal feedback based on vaginal palpation, and a self-help booklet in a first-line behavioral training program all;achieved comparable improvements in urge incontinence in community-dwelling older women. Patients' perceptions of treatment were significantly better for the 2 behavioral training interventions. C1 Dept Vet Affairs Med Ctr, Birmingham Atlanta Geriatr Res Educ & Clin Ctr, Birmingham, AL USA. Univ Alabama, Sch Med, Birmingham, AL USA. Univ Alabama, Ctr Aging, Birmingham, AL USA. Univ Alabama, Sch Nursing, Birmingham, AL USA. Univ Alabama, Sch Publ Hlth, Birmingham, AL 35294 USA. RP Burgio, KL (reprint author), Birmingham Vet Affairs Med Ctr, GRECC-11G,700 19th St S, Birmingham, AL 35233 USA. FU NIA NIH HHS [AG R0108010] NR 24 TC 134 Z9 136 U1 3 U2 9 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 USA SN 0098-7484 J9 JAMA-J AM MED ASSOC JI JAMA-J. Am. Med. Assoc. PD NOV 13 PY 2002 VL 288 IS 18 BP 2293 EP 2299 DI 10.1001/jama.288.18.2293 PG 7 WC Medicine, General & Internal SC General & Internal Medicine GA 614JZ UT WOS:000179186400028 PM 12425706 ER PT J AU Hung, J Guerrero, JL Handschumacher, MD Supple, G Sullivan, S Levine, RA AF Hung, J Guerrero, JL Handschumacher, MD Supple, G Sullivan, S Levine, RA TI Reverse ventricular remodeling reduces ischemic mitral regurgitation - Echo-guided device application in the beating heart SO CIRCULATION LA English DT Article DE ischemia; mitral valve; ventricles; regurgitation; echocardiography ID PAPILLARY-MUSCLE DYSFUNCTION; 3-DIMENSIONAL ECHOCARDIOGRAPHIC RECONSTRUCTION; ACUTE MYOCARDIAL-INFARCTION; DILATED CARDIOMYOPATHY; ORIFICE AREA; MECHANISM; INSIGHTS; VOLUME; FLOW; GEOMETRY AB Background-In ischemic mitral regurgitation (MR), mitral leaflet closure is restricted by ventricular remodeling with displacement of the papillary muscles (PMs). Therapy is uncertain because ring annuloplasty does not alleviate PM displacement. We tested the hypothesis that echo-guided PM repositioning using an external device can reduce MR without compromising left ventricular (LV) function. Methods and Results-We studied 10 sheep with ischemic MR produced by circumflex ligation with inferior infarction, 6 acutely and 4 eight weeks after myocardial infarction (MI). A Dacron patch containing an inflatable balloon was placed over the PMs and adjusted under echo guidance to reverse LV remodeling and reposition the infarcted PM. 3D echo assessed mitral valve geometric changes. In 7 sheep, sonomicrometry and Millar catheters assessed changes in end-systolic and end-diastolic pressure-volume relationships, and microspheres were injected to assess coronary flow. Moderate MR after MI resolved with patch application alone (n=3) or echo-guided balloon inflation, which repositioned the infarcted PM, decreasing the PM tethering distance from 31.1+/-2.5 min after MI to 26.8+/-1.8 with patch (P<0.01; baseline=25.5+/-1.5). LV contractility was unchanged (end-systolic slope=3.4+/-1.6 mm Hg/mL with patch versus 2.8+/-1.6 after MI). Although there was a nonsignificant trend for a mild increase in stiffness constant (0.07+/-0.05 mL(-1) versus 0.05+/-0.03 after MI, P=0.06), LV end-diastolic pressure was unchanged as MR resolved. Coronary flow to noninfarcted regions was not reduced. Conclusions-An external device that repositions the PMs can reduce ischemic MR without compromising LV function. This relatively simple technique can be applied under echo guidance in the beating heart. C1 Harvard Univ, Massachusetts Gen Hosp, Sch Med, Cardiac Ultrasound Lab, Boston, MA 02114 USA. Harvard Univ, Massachusetts Gen Hosp, Sch Med, Surg Cardiovasc Lab, Boston, MA 02114 USA. RP Levine, RA (reprint author), Harvard Univ, Massachusetts Gen Hosp, Sch Med, Cardiac Ultrasound Lab, 55 Fruit St, Boston, MA 02114 USA. FU NHLBI NIH HHS [5R01HL38176-09, 1K24HL67434-01, K23 HL04504-01] NR 35 TC 97 Z9 100 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0009-7322 J9 CIRCULATION JI Circulation PD NOV 12 PY 2002 VL 106 IS 20 BP 2594 EP 2600 DI 10.1161/01.CIR.0000038363.83133.6D PG 7 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 617BH UT WOS:000179339300029 PM 12427657 ER PT J AU Rollins, YD Filley, CM McNutt, JT Chahal, S Kleinschmidt-DeMasters, BK AF Rollins, YD Filley, CM McNutt, JT Chahal, S Kleinschmidt-DeMasters, BK TI Fulminant ascending paralysis as a delayed sequela of diethylene glycol (Sterno) ingestion SO NEUROLOGY LA English DT Article; Proceedings Paper CT 78th Annual Meeting of the American-Association-of-Neuropathologists CY JUN 20-23, 2002 CL DENVER, COLORADO SP Amer Assoc Neuropathol ID CHILDREN; EPIDEMIC AB The authors report a 57-year-old man who survived 18 days after swallowing an 8-oz. can of Sterno in a suicide attempt. Two days after ingestion, he developed confusion and acute renal failure requiring hemodialysis, followed on day 8 by a delayed but rapidly evolving ascending paralysis. Pathologic examination showed severe demyelination, with lesser axonal damage, of virtually all cranial and peripheral nerves sampled and sparing of central myelin. The diethylene glycol in the Sterno was considered responsible for this intoxication. C1 Univ Colorado, Hlth Sci Ctr, Dept Neurol, Denver, CO 80262 USA. Univ Colorado, Hlth Sci Ctr, Dept Pathol, Denver, CO 80262 USA. Denver Vet Affairs Med Ctr, Denver, CO USA. RP Kleinschmidt-DeMasters, BK (reprint author), Univ Colorado, Hlth Sci Ctr, Dept Neurol, Denver, CO 80262 USA. NR 10 TC 20 Z9 20 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0028-3878 J9 NEUROLOGY JI Neurology PD NOV 12 PY 2002 VL 59 IS 9 BP 1460 EP 1463 PG 4 WC Clinical Neurology SC Neurosciences & Neurology GA 613LT UT WOS:000179134300038 PM 12427908 ER PT J AU Cole, AJ Dichter, M AF Cole, AJ Dichter, M TI Neuroprotection and antiepileptogenesis - Overview, definitions, and context SO NEUROLOGY LA English DT Editorial Material ID ELECTROGRAPHIC SEIZURES; RATS; PILOCARPINE C1 Massachusetts Gen Hosp, MGH Epilepsy Serv, Boston, MA 02114 USA. Harvard Univ, Sch Med, Dept Neurol, Boston, MA 02115 USA. Univ Penn, Sch Med, Dept Neurol, Philadelphia, PA 19104 USA. Univ Penn, Sch Med, Dept Pharmacol, Philadelphia, PA 19104 USA. David Mahoney Inst Neurol Sci, Philadelphia, PA USA. Penn Epilepsy Ctr, Philadelphia, PA USA. RP Cole, AJ (reprint author), Massachusetts Gen Hosp, MGH Epilepsy Serv, VBK-830,Fruit St, Boston, MA 02114 USA. NR 9 TC 7 Z9 8 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0028-3878 J9 NEUROLOGY JI Neurology PD NOV 12 PY 2002 VL 59 IS 9 SU 5 BP S1 EP S2 PG 2 WC Clinical Neurology SC Neurosciences & Neurology GA 614QG UT WOS:000179200400001 PM 12428024 ER PT J AU Dichter, MA Cole, AJ AF Dichter, MA Cole, AJ TI Neuroprotection and antiepileptogenesis - Where are we now? SO NEUROLOGY LA English DT Article C1 Univ Penn, Dept Neurol, Sch Med, Philadelphia, PA 19104 USA. Univ Penn, Dept Pharmacol, Sch Med, Philadelphia, PA 19104 USA. David Mahoney Inst Neurol Sci, Philadelphia, PA USA. Penn Epilepsy Ctr, Philadelphia, PA USA. Harvard Univ, Sch Med, Dept Neurol, Massachusetts Gen Hosp,MGH Epilepsy Serv, Boston, MA 02115 USA. RP Dichter, MA (reprint author), Univ Penn, Dept Neurol, Sch Med, 3 West Gates,3400 Spruce St, Philadelphia, PA 19104 USA. NR 0 TC 2 Z9 2 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0028-3878 J9 NEUROLOGY JI Neurology PD NOV 12 PY 2002 VL 59 IS 9 SU 5 BP S36 EP S38 PG 3 WC Clinical Neurology SC Neurosciences & Neurology GA 614QG UT WOS:000179200400008 PM 12428031 ER PT J AU Rebel, VI Kung, AL Tanner, EA Yang, H Bronson, RT Livingston, DM AF Rebel, VI Kung, AL Tanner, EA Yang, H Bronson, RT Livingston, DM TI Distinct roles for CREB-binding protein and p300 in hematopoietic stem cell self-renewal SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article ID IN-VITRO; CBP; DIFFERENTIATION; OVEREXPRESSION; CBP/P300; DEFECTS; HOXB4; LEVEL; MOUSE; VIVO AB Hematopoietic stem cells (HSC) are tightly regulated through, as yet, undefined mechanisms that balance self-renewal and differentiation. We have identified a role for the transcriptional coactivators CREB-binding protein (CBP) and p300 in such HSC fate decisions. A full dose of CBP, but not p300, is crucial for HSC self-renewal. Conversely, p300, but not CBP, is essential for proper hematopoietic differentiation. Furthermore, in chimeric mice, hematologic malignancies emerged from both CBP-/- and p300(-1-) cell populations. Thus, CBP and p300 play essential but distinct roles in maintaining normal hematopoiesis, and, in mice, both are required for preventing hematologic tumorigenesis. C1 Dana Farber Canc Inst, Boston, MA 02115 USA. Harvard Univ, Sch Med, Dept Pathol, Boston, MA 02115 USA. RP Livingston, DM (reprint author), Dana Farber Canc Inst, 44 Binney St, Boston, MA 02115 USA. OI Kung, Andrew/0000-0002-9091-488X NR 27 TC 130 Z9 136 U1 0 U2 1 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD NOV 12 PY 2002 VL 99 IS 23 BP 14789 EP 14794 DI 10.1073/pnas.232568499 PG 6 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA 615AZ UT WOS:000179224800034 PM 12397173 ER PT J AU Le, DA Wu, YQ Huang, ZH Matsushita, K Plesnila, N Augustinack, JC Hyman, BT Yuan, JY Kuida, K Flavell, RA Moskowitz, MA AF Le, DA Wu, YQ Huang, ZH Matsushita, K Plesnila, N Augustinack, JC Hyman, BT Yuan, JY Kuida, K Flavell, RA Moskowitz, MA TI Caspase activation and neuroprotection in caspase-3-deficient mice after in vivo cerebral ischemia and in vitro oxygen glucose deprivation SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article ID NITRIC-OXIDE SYNTHASE; CELL-DEATH; POLY(ADP-RIBOSE) POLYMERASE; SIGNALING COMPLEX; NEURONAL DEATH; MUTANT MICE; APOPTOSIS; PROTEASE; BRAIN; IDENTIFICATION AB Caspase-3 is a major cell death effector protease in the adult and neonatal nervous system. We found a greater number and higher density of cells in the cortex of caspase-3(-/-) adult mice, consistent with a defect in developmental cell death. Caspase-3(-/-) mice were also more resistant to ischemic stress both in vivo and in vitro. After 2 h of ischemia and 48 h of reperfusion, cortical infarct volume was reduced by 55%, and the density of terminal deoxynucleotidyl-transferase-mediated dUTP nick end labeling-positive cells was decreased by 36% compared with wild type. When subjected to oxygen-glucose deprivation (2 h), cortical neurons cultured from mice deficient in caspase-3 expression were also more resistant to cell death by 59%. Mutant brains showed caspase-specific poly(ADP-ribose) polymerase cleavage product (85-kDa fragment) in vivo and in vitro, suggesting redundant mechanisms and persistence of caspase-mediated cell death. In the present study, we found that caspase-8 mediated poly(ADP-ribose) polymerase cleavage in caspase-3(-/-) neurons in vivo and in vitro. In addition, mutant neurons showed no evidence of compensatory activation by caspase-6 or caspase-7 after ischemia. Taken together, these data extend the pharmacological evidence supporting an important role for caspase-3 and caspase-8 as cell death mediators in mammalian cortex and indicate the potential advantages of targeting more than a single caspase family member to treat ischemic cell injury. C1 Harvard Univ, Sch Med, Stroke & Neurovasc Regulat Lab, Boston, MA 02114 USA. Harvard Univ, Massachusetts Gen Hosp, Sch Med, Alzheimers Dis Res Unit, Boston, MA 02114 USA. Harvard Univ, Sch Med, Dept Cell Biol, Boston, MA 02114 USA. Vertex Pharmaceut Inc, Cambridge, MA 02139 USA. Yale Univ, Sch Med, Immunol Sect, New Haven, CT 06510 USA. Yale Univ, Sch Med, Howard Hughes Med Inst, New Haven, CT 06510 USA. RP Moskowitz, MA (reprint author), Harvard Univ, Sch Med, Stroke & Neurovasc Regulat Lab, Boston, MA 02114 USA. RI Moskowitz, Michael/D-9916-2011 FU NINDS NIH HHS [1 R01 NS374141, K08 NS02162, NS 5 P50 NS 10828, P50 NS010828] NR 42 TC 186 Z9 207 U1 1 U2 9 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD NOV 12 PY 2002 VL 99 IS 23 BP 15188 EP 15193 DI 10.1073/pnas.232473399 PG 6 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA 615AZ UT WOS:000179224800103 PM 12415117 ER PT J AU Yang, J Liu, XQ Yue, GH Adamian, M Bulgakav, O Li, TS AF Yang, J Liu, XQ Yue, GH Adamian, M Bulgakav, O Li, TS TI Rootletin, a novel coiled-coil protein, is a structural component of the ciliary rootlet SO JOURNAL OF CELL BIOLOGY LA English DT Article DE photoreceptor; cilium; striated fiber; basal body; centriole ID PHOTORECEPTORS; EXPRESSION; TRANSPORT; FILAMENTS; CENTRIN; C-NAP1; CELLS AB The ciliary rootlet, first recognized over a century ago, is a prominent structure originating from the basal body at the proximal end of a cilium. Despite being the largest cytoskeleton, its structural composition has remained unknown. Here, we report a novel 220-kD protein, designated rootletin, found in the rootlets of ciliated cells. Recombinant rootletin forms detergent-insoluble filaments radiating from the centrioles and resembling rootlets found in vivo. An mAb widely used as a marker for vertebrate rootlets recognizes an epitope in rootletin. Rootletin has a globular head domain and a tail domain consisting of extended coiled-coil structures. Rootletin forms parallel in register homodimers and elongated higher order polymers mediated by the tail domain alone. The head domain may be required for targeting to the basal body and binding to a kinesin light chain. In retinal photoreceptors where rootlets appear particularly robust, rootlets extend from the basal bodies to the synaptic terminals and anchor ER membranes along their length. Our data indicate that rootlets are composed of homopolymeric rootletin protofilaments bundled into variably shaped thick filaments. Thus, rootletin is the long-sought structural component of the ciliary rootlet. C1 Harvard Univ, Massachusetts Eye & Ear Infirm, Sch Med, Berman Gund Lab Study Retinal Degenerat, Boston, MA 02114 USA. RP Li, TS (reprint author), Harvard Univ, Massachusetts Eye & Ear Infirm, Sch Med, Berman Gund Lab Study Retinal Degenerat, 243 Charles St, Boston, MA 02114 USA. FU NEI NIH HHS [EY10309, R01 EY010309] NR 27 TC 101 Z9 106 U1 0 U2 2 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 1114 FIRST AVE, 4TH FL, NEW YORK, NY 10021 USA SN 0021-9525 J9 J CELL BIOL JI J. Cell Biol. PD NOV 11 PY 2002 VL 159 IS 3 BP 431 EP 440 DI 10.1083/jcb.200207153 PG 10 WC Cell Biology SC Cell Biology GA 614VE UT WOS:000179211500006 PM 12427867 ER PT J AU Sui, JH Marasco, WA AF Sui, JH Marasco, WA TI Evidence against Ebola virus sGP binding to human neutrophils by a specific receptor SO VIROLOGY LA English DT Article ID GLYCOPROTEINS; MARBURG; ENTRY; GENE; RNA AB The issue of whether Ebola secretory glycoprotein (sGP) binds to human neutrophils via the IgG Fc receptor IIIb (FcgammaRIIlb, CD16b) or other receptors has been controversial. To clarify this, FACS analysis, an sGP absorption assay, and direct binding of I-125-sGP to neutrophils were performed. Results from FACS analysis demonstrated that limited washing conditions leads to the nonspecific formation of immune complexes on the neutrophil surface and this, but not a specific interaction between sGP and CD16b, is responsible for the previous observations. An sGP absorption assay also demonstrated that sGP is not specifically bound but is nonspecifically proteolysed by proteases released from neutrophils. Finally, there was no difference in I-125-sGP binding to neutrophils compared to other control cell types. Taken together, these results demonstrate that neutrophils do not express a specific receptor for Ebola virus sGR It is unlikely that sGP plays a role in the Ebola virus pathogenesis through interfering with the innate immunity by targeting neutrophils. (C) 2002 Elsevier Science (USA). C1 Harvard Univ, Sch Med, Dana Farber Canc Inst, Dept Canc Immunol & AIDS, Boston, MA 02115 USA. Harvard Univ, Sch Med, Dept Med, Boston, MA 02115 USA. RP Marasco, WA (reprint author), Harvard Univ, Sch Med, Dana Farber Canc Inst, Dept Canc Immunol & AIDS, 44 Binney St, Boston, MA 02115 USA. OI SUI, JIANHUA/0000-0002-1272-9662 NR 18 TC 24 Z9 27 U1 1 U2 5 PU ACADEMIC PRESS INC ELSEVIER SCIENCE PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA SN 0042-6822 J9 VIROLOGY JI Virology PD NOV 10 PY 2002 VL 303 IS 1 BP 9 EP 14 DI 10.1006/viro.2002.1715 PG 6 WC Virology SC Virology GA 625RF UT WOS:000179828800002 PM 12482654 ER PT J AU Atema, A Chene, P AF Atema, A Chene, P TI The gain of function of the p53 mutant Asp281Gly is dependent on its ability to form tetramers SO CANCER LETTERS LA English DT Article DE p53; gain of function; tetramerisation; chemoresistance; chemosensitivity ID MISSENSE MUTATION; SAOS-2 CELLS; DNA-BINDING; LI-FRAUMENI; DOMAIN; OLIGOMERIZATION; BETA-STRAND-326-333; CONFORMATION; EXPRESSION; PROTEINS AB The influence of tetramerisation on the properties of the p53 mutants is poorly understood. We describe here the influence of tetramerisation on the properties of the oncogenic mutant Asp281Gly. We show that despite being both nuclear the tetrameric Asp281Gly and the monomeric Asp281GlyLeu344Pro proteins have different properties: only Asp281 Gly stimulates the transcription of the multidrug resistance-1 gene promoter and induces cisplatin resistance in Saos-2 cells. Moreover, we identify a 130-kDa protein that specifically interacts with Asp281Gly but not with Asp281GlyLeu344Pro. This suggests that tetramerisation is important for the properties of the p53 mutants and that these properties might be mediated via protein-protein interactions. (C) 2002 Elsevier Science Ireland Ltd. All rights reserved. C1 Novartis, Oncol Dept, CH-4002 Basel, Switzerland. Dana Farber Canc Inst, Boston, MA 02115 USA. Harvard Univ, Sch Med, Boston, MA 02115 USA. RP Chene, P (reprint author), Novartis, Oncol Dept, K125 420, CH-4002 Basel, Switzerland. NR 22 TC 8 Z9 8 U1 0 U2 1 PU ELSEVIER SCI IRELAND LTD PI CLARE PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE, IRELAND SN 0304-3835 J9 CANCER LETT JI Cancer Lett. PD NOV 8 PY 2002 VL 185 IS 1 BP 103 EP 109 AR PII S0304-3835(02)00318-X DI 10.1016/S0304-3835(02)00318-X PG 7 WC Oncology SC Oncology GA 599GY UT WOS:000178326800013 PM 12142085 ER PT J AU Wang, XJ Xu, SQ Rivolta, C Li, LY Peng, GH Swain, PK Sung, CH Swaroop, A Berson, EL Dryja, TP Chen, SM AF Wang, XJ Xu, SQ Rivolta, C Li, LY Peng, GH Swain, PK Sung, CH Swaroop, A Berson, EL Dryja, TP Chen, SM TI Barrier to autointegration factor interacts with the cone-rod homeobox and represses its Transactivation function SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID BARDET-BIEDL-SYNDROME; DOMINANT RETINITIS-PIGMENTOSA; LEBER CONGENITAL AMAUROSIS; CRX TRANSCRIPTION FACTOR; GENE-EXPRESSION; RETROVIRAL DNA; LEUCINE-ZIPPER; HOMEODOMAIN PROTEIN; CRYSTAL-STRUCTURE; CELLULAR FACTOR AB Crx (cone-rod homeobox) is a homeodomain transcription factor implicated in regulating the expression of photoreceptor and pineal genes. To identify proteins that interact with Crx in the retina, we carried out a yeast two-hybrid screen of a retinal cDNA library. One of the identified clones encodes Baf (barrier to autointegration factor), which was previously shown to have a role in mitosis and retroviral integration. Additional biochemical assays provided supporting evidence for a Baf-Crx interaction. The Baf protein is detectable in all nuclear layers of the mouse retina, including the photo-receptors and the bipolar cells where Crx is expressed. Transient transfection assays with a rhodopsin-luciferase reporter in HEK293 cells demonstrate that overexpression of Baf represses Crx-mediated transactivation, suggesting that Baf acts as a negative regulator of Crx. Consistent with this role for Baf, an E80A mutation of CRX associated with cone-rod dystrophy has a higher than normal transactivation potency but a reduced interaction with Baf. Although our studies did not identify a causative Baf mutation in retinopathies, we suggest that Baf may contribute to the phenotype of a photoreceptor degenerative disease by modifying the activity of Crx. In view of the ubiquitous expression of Baf, we hypothesize that it may play a role in regulating tissue- or cell type-specific gene expression by interacting with homeodomain transcription factors. C1 Washington Univ, Sch Med, Dept Ophthalmol & Visual Sci, St Louis, MO 63110 USA. Washington Univ, Sch Med, Dept Mol Biol & Pharmacol, St Louis, MO 63110 USA. Harvard Univ, Massachusetts Eye & Ear Infirm, Sch Med, Ocular Mol Genet Inst, Boston, MA 02114 USA. Harvard Univ, Massachusetts Eye & Ear Infirm, Sch Med, Berman Gund Lab Study Retinal Degenerat, Boston, MA 02114 USA. Univ Michigan, Dept Ophthalmol & Visual Sci, Ann Arbor, MI 48105 USA. Univ Michigan, Dept Human Genet, Ann Arbor, MI 48105 USA. Cornell Univ, Weill Med Coll, Margaret M Dyson Vis Res Inst, Dept Cell Biol & Anat, New York, NY 10021 USA. RP Chen, SM (reprint author), Washington Univ, Sch Med, Dept Ophthalmol & Visual Sci, 660 S Euclid Ave,Campus Box 8096, St Louis, MO 63110 USA. OI Swaroop, Anand/0000-0002-1975-1141; Rivolta, Carlo/0000-0002-0733-9950 FU NEI NIH HHS [EY00169, EY02687, EY08683, EY11115, EY12543, R01 EY011307, R01 EY012543] NR 71 TC 92 Z9 93 U1 2 U2 7 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 NOV 8 PY 2002 VL 277 IS 45 BP 43288 EP 43300 DI 10.1074/jbc.M207952200 PG 13 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA 612MZ UT WOS:000179081200112 PM 12215455 ER PT J AU Wang, KC Kim, JA Sivasankaran, R Segal, R He, ZG AF Wang, KC Kim, JA Sivasankaran, R Segal, R He, ZG TI p75 interacts with the Nogo receptor as a co-receptor for Nogo, MAG and OMgp SO NATURE LA English DT Article ID NEUROTROPHIN RECEPTOR; AXON REGENERATION; RHO; PROTEIN; GROWTH; CNS; IDENTIFICATION; EXPRESSION; INHIBITION; OUTGROWTH AB In inhibiting neurite outgrowth, several myelin components, including the extracellular domain of Nogo-A (Nogo-66)(1), oligodendrocyte myelin glycoprotein (OMgp)(2) and myelin-associated glycoprotein (MAG)(3,4), exert their effects through the same Nogo receptor (NgR). The glycosyl phosphatidylinositol (GPI)-anchored nature of NgR indicates the requirement for additional transmembrane protein(s) to transduce the inhibitory signals into the interior of responding neurons. Here, we demonstrate that p75, a transmembrane protein known to be a receptor for the neurotrophin family of growth factors(5,6), specifically interacts with NgR. p75 is required for NgR-mediated signalling, as neurons from p75 knockout mice are no longer responsive to myelin and to each of the known NgR ligands. Blocking the p75-NgR interaction also reduces the activities of these inhibitors. Moreover, a truncated p75 protein lacking the intracellular domain, when overexpressed in primary neurons, attenuates the same set of inhibitory activities, suggesting that p75 is a signal transducer of the NgR-p75 receptor complex. Thus, interfering with p75 and its downstream signalling pathways may allow lesioned axons to overcome most of the inhibitory activities associated with central nervous system myelin. C1 Childrens Hosp, Div Neurosci, Boston, MA 02115 USA. Harvard Univ, Sch Med, Program Neurosci, Boston, MA 02115 USA. Dana Farber Canc Inst, Dept Pediat Oncol, Boston, MA 02115 USA. RP He, ZG (reprint author), Childrens Hosp, Div Neurosci, 300 Longwood Ave, Boston, MA 02115 USA. NR 25 TC 556 Z9 595 U1 1 U2 15 PU NATURE PUBLISHING GROUP PI LONDON PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND SN 0028-0836 J9 NATURE JI Nature PD NOV 7 PY 2002 VL 420 IS 6911 BP 74 EP 78 DI 10.1038/nature01176 PG 6 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA 612HJ UT WOS:000179068100039 PM 12422217 ER PT J AU Kemp, DM Lin, JC Ubeda, M Habener, JF AF Kemp, DM Lin, JC Ubeda, M Habener, JF TI NRSF/REST confers transcriptional repression of the GPR10 gene via a putative NRSE/RE-1 located in the 5 ' promoter region SO FEBS LETTERS LA English DT Article DE neuron-restrictive silencer factor; neuron-restrictive silencer element; GPR10 ID PROLACTIN-RELEASING PEPTIDE; NEURON-RESTRICTIVE SILENCER; PANCREATIC BETA-CELLS; SODIUM-CHANNEL GENE; RECEPTOR GENE; TISSUE DISTRIBUTION; COUPLED RECEPTOR; PROTEIN-KINASE; TARGET GENES; IN-VIVO AB The G protein-coupled receptor GPR10 is highly localized to areas of the brain. In an effort to reveal transcriptional determinants of this tissue specificity, we recognized a putative NRSE (neuron-restrictive silencer element) located in the 5' promoter region of the gene. The cognate NRSE binding protein NRSF (neuron-restrictive silencer factor) restricts gene expression to mature neurons and endocrine cells by repressing their transcription in non-neuronal/-endocrine cells. In cell lines where NRSF-mediated gene repression has been functionally established, the activity of the GPR10 promoter was repressed in a manner consistent with NRSE-dependent regulation. A specific point mutation to confer non-functionality of the NRSE revealed a 10-fold de-repression of reporter gene expression. In contrast, in the GPR10-expressing cell line GH3, mRNA transcripts of NRSF were undetectable and suppression of promoter activity was not observed. However, transfection of a rat NRSF expression vector resulted in significant repression of transcription, which was reversed by mutation of the NRSE. In conclusion, we demonstrate that the GPR10 gene is specifically regulated by NRSF, and suggest this to be a contributory factor in the tissue-specific distribution of GPR10 in vivo. (C) 2002 Federation of European Biochemical Societies. Published by Elsevier Science B.V. All rights reserved. C1 Harvard Univ, Massachusetts Gen Hosp, Sch Med, Howard Hughes Med Inst,Lab Mol Endocrinol, Boston, MA 02114 USA. RP Habener, JF (reprint author), Harvard Univ, Massachusetts Gen Hosp, Sch Med, Howard Hughes Med Inst,Lab Mol Endocrinol, 55 Fruit St WEL320, Boston, MA 02114 USA. NR 35 TC 8 Z9 8 U1 0 U2 2 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0014-5793 J9 FEBS LETT JI FEBS Lett. PD NOV 6 PY 2002 VL 531 IS 2 BP 193 EP 198 AR PII S0014-5793(02)03502-0 DI 10.1016/S0014-5793(02)03502-0 PG 6 WC Biochemistry & Molecular Biology; Biophysics; Cell Biology SC Biochemistry & Molecular Biology; Biophysics; Cell Biology GA 613HY UT WOS:000179127900016 PM 12417311 ER PT J AU Zandi, PP Carlson, MC Plassman, BL Welsh-Bohmer, KA Mayer, LS Steffens, DC Breitner, JCS AF Zandi, PP Carlson, MC Plassman, BL Welsh-Bohmer, KA Mayer, LS Steffens, DC Breitner, JCS CA Cache County Memory Study Investig TI Hormone replacement therapy and incidence of Alzheimer disease in older women - The Cache County Study SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION LA English DT Article ID COGNITIVE DECLINE; CONTROLLED TRIAL; ESTROGEN; RISK; DEMENTIA; AD; POPULATION; PREVALENCE; AGE AB Context Previous studies have shown a sex-specific increased risk of Alzheimer disease (AD) in women older than 80 years. Basic neuroscience findings suggest that hormone replacement therapy (HRT) could reduce a woman's risk of AD. Epidemiologic findings on AD and HRT are mixed. Objective To examine the relationship between use of HRT and risk of AD among elderly women. Design, Setting, and Participants Prospective study of incident dementia among 1357 men (mean age, 73.2 years) and 1889 women (mean age, 74.5 years) residing in a single county in Utah. Participants were first assessed in 1995-1997, with follow-up conducted in 1998-2000. History of women's current and former use of HRT, as well as of calcium and multivitamin supplements, was ascertained at the initial contact. Main Outcome Measure Diagnosis of incident AD. Results Thirty-five men (2.6%) and 88 women (4.7%) developed AD between the initial interview and time of the follow-up Q years). Incidence among women increased after age 80 years and exceeded the risk among men of similar age (adjusted hazard ratio [HR], 2.11.; 95% confidence interval [CI], 1.22-3.86). Women who used HRT had a reduced risk of AD (26 cases among 1066 women) compared with non-HRT users (58 cases among 800 women) (adjusted HR, 0.59; 95% CI, 0.36-0.96). Risk varied with duration of HRT use, so that a woman's sex-specific increase in risk disappeared entirely with more than 10 years of treatment Q cases among 427 women). Adjusted HRs were 0.41 (95% CI, 0.17-0.86) for HRT users compared with non users and 0.77 (95% CI, 0.31-1.67) compared with men. No similar effect was seen with calcium or multivitamin use. Almost all of the HRT-related reduction in incidence reflected former use of HRT (9 cases among 490 women; adjusted HR, 0.33 [95% CI, 0.15-0.65]). There was no effect with current HRT use (17 cases among 576 women; adjusted HR, 1.08 [95% CI, 0.59-1.91]) unless duration of treatment exceeded 10 years (6 cases among 344 women; adjusted HR, 0.55 [95% CI, 0.21-1.23]). Conclusions Prior HRT use is associated with reduced risk of AD, but there is no apparent benefit with current HRT use unless such use has exceeded 10 years. C1 VA Puget Sound Hlth Care Syst, GRECC S182, Seattle, WA 98108 USA. Johns Hopkins Univ, Sch Hyg & Publ Hlth, Dept Ment Hyg, Baltimore, MD USA. Duke Univ, Med Ctr, Dept Psychiat & Behav Sci, Durham, NC USA. Duke Univ, Med Ctr, Joseph & Kathleen Bryan Alzheimers Dis Res Ctr, Durham, NC USA. Banner Hlth Syst, Phoenix, AZ USA. Univ Washington, Sch Med, Dept Psychiat & Behav Sci, Seattle, WA 98195 USA. RP Breitner, JCS (reprint author), VA Puget Sound Hlth Care Syst, GRECC S182, 1660 S Columbian Way, Seattle, WA 98108 USA. FU NIA NIH HHS [R01-AG-11380] NR 32 TC 544 Z9 557 U1 5 U2 18 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 USA SN 0098-7484 J9 JAMA-J AM MED ASSOC JI JAMA-J. Am. Med. Assoc. PD NOV 6 PY 2002 VL 288 IS 17 BP 2123 EP 2129 DI 10.1001/jama.288.17.2123 PG 7 WC Medicine, General & Internal SC General & Internal Medicine GA 611ZJ UT WOS:000179048100022 PM 12413371 ER PT J AU Sedlis, SP Morrison, DA Lorin, JD Esposito, R Sethi, G Sacks, J Henderson, W Grover, F Ramanathan, KB Weiman, D Saucedo, J Antakli, T Paramesh, V Pett, S Vernon, S Blrjiniuk, V Welt, F Krucoff, M Wolfe, W Lucke, JC Mediratta, S Booth, D Murphy, E Ward, H Miller, L Kiesz, S Barbiere, C Lewis, D AF Sedlis, SP Morrison, DA Lorin, JD Esposito, R Sethi, G Sacks, J Henderson, W Grover, F Ramanathan, KB Weiman, D Saucedo, J Antakli, T Paramesh, V Pett, S Vernon, S Blrjiniuk, V Welt, F Krucoff, M Wolfe, W Lucke, JC Mediratta, S Booth, D Murphy, E Ward, H Miller, L Kiesz, S Barbiere, C Lewis, D CA Investigators Dept Vet Affairs Stu Angina Extremely Serious Operative TI Percutaneous coronary intervention versus coronary bypass graft surgery for diabetic patients with unstable angina and risk factors for adverse outcomes with bypass - Outcome of diabetic patients in the AWESOME randomized trial and registry SO JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY LA English DT Article; Proceedings Paper CT 50th Annual Scientific Session of the American College of Cardiology CY MAR 18-20, 2001 CL ORLANDO, FLORIDA SP Amer Coll Cardiol ID ACUTE MYOCARDIAL-INFARCTION; LONG-TERM SURVIVAL; REVASCULARIZATION-INVESTIGATION BARI; HOSPITAL RESOURCE UTILIZATION; ARTERY BYPASS; ECONOMIC-IMPACT; CARDIAC-SURGERY; DISEASE ERACI; FOLLOW-UP; ANGIOPLASTY AB OBJECTIVES This study compared survival after percutaneous coronary intervention (PCI) with survival after coronary artery bypass graft surgery (CABG) among diabetics in the Veterans Affairs AWESOME (Angina With Extremely Serious Operative Mortality Evaluation) study randomized trial and registry of high-risk patients. BACKGROUND Previous studies indicate that CABG may be superior to PCI for diabetics, but no comparisons have been made for diabetics at high risk for surgery. METHODS Over five years (1995 to 2000), 2,431 patients with medically refractory myocardial ischemia and at least one of five risk factors (prior CABG, myocardial infarction within seven days, left ventricular ejection fraction <0.35, age >70 years, or an intra-aortic balloon being required to stabilize) were identified. A total of 781 were acceptable for CABG and PCI, and 454 consented to be randomized. The 1,650 patients not acceptable for both CABG and PCI constitute the physician-directed registry, and the 327 who were acceptable but refused to be randomized constitute the patient-choice registry. Diabetes prevalence was 32% (144) among randomized patients, 27% (89) in the patient-choice registry, and 32% (525) in the physician-directed registry. The CABG and PCI survival rates were compared using Kaplan-Meier curves and log-rank tests. RESULTS The respective CABG and PCI 36-month survival rates for diabetic patients were 72% and 81% for randomized patients, 85% and 89% for patient-choice registry patients, and 73% and 71% for the physician-directed registry patients. None of the differences was statistically significant. CONCLUSIONS We conclude that PCI is a relatively safe alternative to CABG for diabetic patients with medically refractory unstable angina who are at high risk for CABG. (C) 2002 by the American College of Cardiology Foundation. C1 Vet Adm Med Ctr, Cardiol Sect, New York, NY 10010 USA. Tucson VA Med Ctr, Tucson, AZ USA. Edward Hines Jr Vet Adm Hosp, CSPCC, Hines, IL 60141 USA. Denver VA Med Ctr, Denver, CO USA. Memphis VA Med Ctr, Memphis, TN USA. Little Rock VA Med Ctr, Little Rock, AR USA. Albuquerque VA Med Ctr, Albuquerque, NM USA. W Roxbury VA Med Ctr, W Roxbury, MA USA. Durham VA Med Ctr, Durham, NC USA. Asheville VA Med Ctr, Asheville, NC USA. Lexington VA Med Ctr, Lexington, KY USA. Portland VA Med Ctr, Portland, OR USA. Minneapolis VA Med Ctr, Minneapolis, MN USA. San Antonio VA Med Ctr, San Antonio, TX USA. Kansas City VA Med Ctr, Kansas City, KS USA. RP Sedlis, SP (reprint author), Vet Adm Med Ctr, Cardiol Sect, 12W,423 E 23rd St, New York, NY 10010 USA. NR 50 TC 61 Z9 63 U1 0 U2 1 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0735-1097 J9 J AM COLL CARDIOL JI J. Am. Coll. Cardiol. PD NOV 6 PY 2002 VL 40 IS 9 BP 1555 EP 1566 AR PII S0735-1097(02)02346-X DI 10.1016/S0735-1097(02)02346-X PG 12 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA 610DY UT WOS:000178946500003 PM 12427406 ER PT J AU Washington, DL Stevens, CD Shekelle, PG Henneman, PL Brook, RH AF Washington, DL Stevens, CD Shekelle, PG Henneman, PL Brook, RH TI Next-day care for emergency department users with nonacute conditions - A randomized, controlled trial SO ANNALS OF INTERNAL MEDICINE LA English DT Article ID PUBLIC HOSPITAL EMERGENCY; DEPARTMENTS; CONSEQUENCES; PHYSICIAN; QUALITY; LEAVE; LIFE AB Background: Because of overcrowding and cost-control efforts, emergency departments are under pressure to refer patients with nonacute conditions to other settings. However, no validated systematic methods exist for safely performing such referrals. Objective: To determine the effects on health status and access to care of systematically referring patients with nonacute conditions to next-day primary care. Design: Randomized, controlled trial. Setting: An emergency department in a public hospital. Patients: 156 adults who used the emergency department on weekdays from 7:00 a.m. to 3:00 p.m. and met criteria for deferred care. The criteria applied to three symptom complexes that account for 33% of U.S. emergency department visits by adults. Intervention: Next-day care at the study site's primary care center or usual same-day care. Measurements: Self-reported health status and use of health services during 1-week follow-up. Results: Patients assigned to next-day care did not demonstrate clinically important disadvantages in health status or physician visits compared with usual care patients. In each group, more than 95% of patients were evaluated at least once by a physician, 4% sought health services after their initial evaluation, and no patients were hospitalized or died. At follow-up, both groups reported improved health status and fewer days in bed or with disability, although the deferred care group reported less improvement on all three measures. The 95% Cls were sufficiently narrow to exclude a clinically significant difference in self-reported health status. However, the possibility of 1 additional day in bed or with disability in the deferred care group could not be excluded. Conclusions: Clinically detailed standardized screening criteria can safely identify patients at public hospital emergency departments for referral to next-day care. However, larger studies are needed to assess the possibility of adverse effects. C1 Vet Affairs Greater Los Angeles Healthcare syst, Los Angeles, CA 90073 USA. Univ Calif Los Angeles, Los Angeles, CA USA. Harbor UCLA Med Ctr, Torrance, CA 90509 USA. RAND Hlth, Santa Monica, CA USA. Baystate Med Ctr, Springfield, MA USA. Tufts Univ, Sch Med, Boston, MA 02111 USA. RP Washington, DL (reprint author), Vet Affairs Greater Los Angeles Healthcare syst, 11301 Wilshire Blvd,111G, Los Angeles, CA 90073 USA. NR 30 TC 39 Z9 40 U1 0 U2 2 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 NOV 5 PY 2002 VL 137 IS 9 BP 707 EP 714 PG 8 WC Medicine, General & Internal SC General & Internal Medicine GA 612BA UT WOS:000179052400001 PM 12416944 ER PT J AU Piserchio, A Shimizu, N Gardella, TJ Mierke, DF AF Piserchio, A Shimizu, N Gardella, TJ Mierke, DF TI Residue 19 of the parathyroid hormone: Structural consequences SO BIOCHEMISTRY LA English DT Article ID NUCLEAR-MAGNETIC-RESONANCE; DISTANCE CONSTRAINTS; RECEPTOR-BINDING; NMR-SPECTROSCOPY; CONFORMATION; FRAGMENTS; PEPTIDES AB Residue 19 of the parathyroid hormone (PTH) has been shown to play an important role in both binding to and activation of the PTH receptor; specifically, Arg(19)-containing analogues have improved biological function over similar Glu(19) peptides {Shimizu et al. (2002) Biochemistry 41, 13224-13233}. Additionally the juxtamembrane portion of the receptor is involved in the different biological responses. Here, we determine the conformational preferences of PTH analogues to provide a structural basis for their biological actions. On the basis of circular dichroism results, the Arg(19) --> Glu(19) mutations within the context of both PTH(1-20) and PTH(1-34) analogues lead to increases in helix content, ranging from a 8-15% increase. High-resolution structures as determined by H-1 NMR and NOE-restrained molecular dynamics simulations clearly illustrate the difference between Arg(19) and Glu(19)-PTH(1-20), particularly with the extent and stability of the C-terminal helix. The Arg(19)-containing analogue has a well defined, stable alpha-helix from Ser(4)-Arg(19), while the Glu(19) analogue is less ordered at the C-terminus. On the basis of these observations, we propose that position 19 of PTH(1-20) must be alpha-helical for optimal interaction with the juxtamembrane portion of the receptor. This mode of binding extends the current view of PTH binding (indeed ligand binding for all class B GPCRs), which invokes a bihelical ligand with the C-terminus of the ligand interacting with the N-terminus of the receptor (responsible for binding) and the N-terminus of the ligand interacting with the seven-helical bundle (leading to receptor activation). C1 Brown Univ, Dept Mol Pharmacol, Div Biol & Med, Providence, RI 02912 USA. Brown Univ, Dept Chem, Providence, RI 02912 USA. Massachusetts Gen Hosp, Endocrine Unit, Boston, MA 02114 USA. Harvard Univ, Sch Med, Boston, MA 02114 USA. RP Mierke, DF (reprint author), Brown Univ, Dept Mol Pharmacol, Div Biol & Med, Providence, RI 02912 USA. FU NIDDK NIH HHS [DK-11794]; NIGMS NIH HHS [GM-54082] NR 34 TC 16 Z9 16 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 NOV 5 PY 2002 VL 41 IS 44 BP 13217 EP 13223 DI 10.1021/bi0261600 PG 7 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA 609QG UT WOS:000178916000012 PM 12403623 ER PT J AU Shimizu, M Shimizu, N Tsang, JC Petroni, BD Khatri, A Potts, JT Gardella, TJ AF Shimizu, M Shimizu, N Tsang, JC Petroni, BD Khatri, A Potts, JT Gardella, TJ TI Residue 19 of the parathyroid hormone (PTH) modulates ligand interaction with the juxtamembrane region of the PTH-1 receptor SO BIOCHEMISTRY LA English DT Article ID (PTH)/PTH-RELATED PEPTIDE RECEPTOR; TERMINAL EXTRACELLULAR DOMAIN; PHOTOAFFINITY CROSS-LINKING; PROTEIN-COUPLED RECEPTOR; PTH/PTHRP RECEPTOR; BINDING DOMAIN; CHIMERIC RECEPTORS; ACTIVATION; LOOP; CONFORMATION AB Recent data suggest that the binding of parathyroid hormone (PTH)-(1-34) to the PTH-1 receptor (PIR) involves a high-affinity interaction between the C-terminal (15-34) domain of the ligand and the amino-terminal extracellular (N) domain of the receptor and a low-affinity interaction between the N-terminal (I - 14) portion of PTH and the juxtamembrane (J) region of the receptor, with the latter interaction giving rise to signal transduction. We investigated whether residues C-terminal of position 14 in PTH(1-34) contribute to the J component of the interaction mechanism by comparing the capacity of PTH analogues N-terminally modified to improve J domain affinity and C-terminally truncated at position 14, 20, or 34 to stimulate cAMP formation in COS-7 cells transiently transfected with PIR-delNt, a PIR construct that lacks most of the N domain. In these cells, the potency of [M]PTH(1-34) (M = Ala(1,3,12),-Gln(10),Har(11),Trp(14),Arg(19)) was 120-fold greater than that of [M]PTH(1-14) (EC(50)s = 3.0 +/- 0.8 and 360 +/- 90 nM, respectively) but was equal to that of [M]PTH(1-20) (EC50 = 2.3 +/- 0.3 nM). Reverting the Arg19 substitution of [M]PTH(1-20) to the native Glu reduced cAMP signaling potency on PIR-delNt by 12-fold (EC50 of [M]PTH(1-20)-Glu(19) = 27 +/- 4 nM), and it decreased the analog's capacity to inhibit the binding of the J domain-selective radioligand, I-125-[Aib(1.3),Nle(8),M,Tyr(21)]ratPTH(1-21), to the full-length PIR stably expressed in LLC-PK1 cells by 40-fold. The Glu(19) --> Arg modification, however, did not affect the capacity of PTH(15-31) to inhibit the binding of the N domain-selective radioligand I-125-bPTH(3-34) to the full-length receptor. The overall data suggest that residues (15-20) of PTH, and particularly residue 19, contribute to the capacity of the N-terminal portion of the ligand to interact with the juxtamembrane region of the receptor. The NMR data presented in the accompanying, manuscript suggests that this role could involve intramolecular effects on secondary structure in the N-terminal portion of the ligand. C1 Massachusetts Gen Hosp, Endocrine Unit, Boston, MA 02114 USA. Harvard Univ, Sch Med, Boston, MA 02114 USA. RP Gardella, TJ (reprint author), Massachusetts Gen Hosp, Endocrine Unit, Boston, MA 02114 USA. FU NIDDK NIH HHS [DK-11794] NR 43 TC 20 Z9 21 U1 0 U2 0 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA SN 0006-2960 J9 BIOCHEMISTRY-US JI Biochemistry PD NOV 5 PY 2002 VL 41 IS 44 BP 13224 EP 13233 DI 10.1021/bi026162k PG 10 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA 609QG UT WOS:000178916000013 PM 12403624 ER PT J AU Ichinose, F Bloch, KD Wu, JC Zapol, WM Picard, MH Scherrer-Crosbie, M AF Ichinose, F Bloch, KD Wu, JC Zapol, WM Picard, MH Scherrer-Crosbie, M TI Pressure-overload-induced left ventricular hypertrophy and dysfunction are exacerbated by nitric oxide synthase 3 deficiency in mice SO CIRCULATION LA English DT Meeting Abstract CT American-Heart-Association Abstracts From Scientific Sessions CY NOV 17-20, 2002 CL CHICAGO, ILLINOIS SP Amer Heart Assoc C1 Massachusetts Gen Hosp, Boston, MA 02114 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 0009-7322 J9 CIRCULATION JI Circulation PD NOV 5 PY 2002 VL 106 IS 19 SU S MA 41 BP 9 EP 9 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 613QJ UT WOS:000179142700083 ER PT J AU Limbourg, FP Ho, K Huang, ZH Moskowitz, MA Liao, JK AF Limbourg, FP Ho, K Huang, ZH Moskowitz, MA Liao, JK TI Src mediates non-transcriptional activation of phosphoinositide 3-kinase and Akt by glucocorticoid receptor SO CIRCULATION LA English DT Meeting Abstract CT American-Heart-Association Abstracts From Scientific Sessions CY NOV 17-20, 2002 CL CHICAGO, ILLINOIS SP Amer Heart Assoc C1 Brigham & Womens Hosp, Cambridge, MA USA. Brigham & Womens Hosp, Boston, MA 02115 USA. Massachusetts Gen Hosp, Boston, MA 02114 USA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0009-7322 J9 CIRCULATION JI Circulation PD NOV 5 PY 2002 VL 106 IS 19 SU S MA 54 BP 11 EP 12 PG 2 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 613QJ UT WOS:000179142700096 ER PT J AU Mansour, M Houghtaling, C Keane, D Hajjar, R Ruskin, JN AF Mansour, M Houghtaling, C Keane, D Hajjar, R Ruskin, JN TI Atrial action potential duration prolongation by over-expression of the sodium-calcium exchanger using adenoviral gene transfer in goats SO CIRCULATION LA English DT Meeting Abstract CT American-Heart-Association Abstracts From Scientific Sessions CY NOV 17-20, 2002 CL CHICAGO, ILLINOIS SP Amer Heart Assoc C1 Massachusetts Gen Hosp, Cardiovasc Res Ctr, Boston, MA 02114 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 0009-7322 J9 CIRCULATION JI Circulation PD NOV 5 PY 2002 VL 106 IS 19 SU S MA 152 BP 31 EP 31 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 613QJ UT WOS:000179142700194 ER PT J AU Burger, PC Wagner, DD AF Burger, PC Wagner, DD TI Platelet P-selectin facilitates atherosclerotic lesion development SO CIRCULATION LA English DT Meeting Abstract CT American-Heart-Association Abstracts From Scientific Sessions CY NOV 17-20, 2002 CL CHICAGO, ILLINOIS SP Amer Heart Assoc C1 Ctr Blood Res, Boston, MA 02115 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 0009-7322 J9 CIRCULATION JI Circulation PD NOV 5 PY 2002 VL 106 IS 19 SU S MA 198 BP 40 EP 40 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 613QJ UT WOS:000179142700240 ER PT J AU Shannon, RP Nikolaidis, LA Hentosz, T Stolarski, C Elahi, D AF Shannon, RP Nikolaidis, LA Hentosz, T Stolarski, C Elahi, D TI Myocardial insulin resistance in advanced dilated cardiomyopathy is associated with unique insulin signaling abnormalities SO CIRCULATION LA English DT Meeting Abstract CT American-Heart-Association Abstracts From Scientific Sessions CY NOV 17-20, 2002 CL CHICAGO, ILLINOIS SP Amer Heart Assoc C1 Allegheny Gen Hosp, Pittsburgh, PA 15212 USA. Massachusetts Gen Hosp, Boston, MA 02114 USA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0009-7322 J9 CIRCULATION JI Circulation PD NOV 5 PY 2002 VL 106 IS 19 SU S MA 269 BP 54 EP 54 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 613QJ UT WOS:000179142700311 ER PT J AU Musi, N Xing, YQ Fujii, N Hirshman, MF Pomerleau, J Tian, R Goodyear, LJ AF Musi, N Xing, YQ Fujii, N Hirshman, MF Pomerleau, J Tian, R Goodyear, LJ TI Ischemia-stimulated glucose uptake is decreased in hearts from transgenic mice overexpressing a dominant negative alpha 2 AMPK SO CIRCULATION LA English DT Meeting Abstract CT American-Heart-Association Abstracts From Scientific Sessions CY NOV 17-20, 2002 CL CHICAGO, ILLINOIS SP Amer Heart Assoc C1 Joslin Diabet Ctr, Boston, MA 02215 USA. Brigham & Womens Hosp, Boston, MA 02115 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 0009-7322 J9 CIRCULATION JI Circulation PD NOV 5 PY 2002 VL 106 IS 19 SU S MA 272 BP 55 EP 55 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 613QJ UT WOS:000179142700314 ER PT J AU Aikawa, K Retzlaff, B Fish, B Levitz, M Walden, C Khan, SE Knopp, RH AF Aikawa, K Retzlaff, B Fish, B Levitz, M Walden, C Khan, SE Knopp, RH TI Dyslipidemia of insulin resistance and obesity: Gender differences SO CIRCULATION LA English DT Meeting Abstract CT American-Heart-Association Abstracts From Scientific Sessions CY NOV 17-20, 2002 CL CHICAGO, ILLINOIS SP Amer Heart Assoc C1 Univ Washington, NW Lipid Res Clin, Seattle, WA 98195 USA. Univ Washington, VA Puget Sound Hlth Care Syst, Seattle, WA 98195 USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0009-7322 J9 CIRCULATION JI Circulation PD NOV 5 PY 2002 VL 106 IS 19 SU S MA 377 BP 75 EP 75 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 613QJ UT WOS:000179142700419 ER PT J AU Friedrich, EB Olsen, D Scadden, DT Gerszten, RE AF Friedrich, EB Olsen, D Scadden, DT Gerszten, RE TI VCAM-1 and SDF-1 are critical determinants of primitive stem cell homing in vitro SO CIRCULATION LA English DT Meeting Abstract CT American-Heart-Association Abstracts From Scientific Sessions CY NOV 17-20, 2002 CL CHICAGO, ILLINOIS SP Amer Heart Assoc C1 Massachusetts Gen Hosp, Charlestown, MA 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 0009-7322 J9 CIRCULATION JI Circulation PD NOV 5 PY 2002 VL 106 IS 19 SU S MA 412 BP 82 EP 82 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 613QJ UT WOS:000179142700454 ER PT J AU Li, J Wu, JP Post, M Selike, FW Simons, M AF Li, J Wu, JP Post, M Selike, FW Simons, M TI The mechanism of the novel peptide PR39 in anti-apoptosis SO CIRCULATION LA English DT Meeting Abstract CT American-Heart-Association Abstracts From Scientific Sessions CY NOV 17-20, 2002 CL CHICAGO, ILLINOIS SP Amer Heart Assoc C1 Harvard Univ, Sch Med, BIDMC, Div Cardiothorac Surg, Boston, MA USA. Dartmouth Coll Sch Med, Dartmouth Hitchcock Med Ctr, Cardiol Sect, Lebanon, NH 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 0009-7322 J9 CIRCULATION JI Circulation PD NOV 5 PY 2002 VL 106 IS 19 SU S MA 464 BP 92 EP 92 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 613QJ UT WOS:000179142700506 ER PT J AU Yu, GS Pan, XY Gulick, T AF Yu, GS Pan, XY Gulick, T TI Mitochondrial carriers of nucleoside reverse transcriptase inhibitor (NRTI)-phosphates SO CIRCULATION LA English DT Meeting Abstract CT American-Heart-Association Abstracts From Scientific Sessions CY NOV 17-20, 2002 CL CHICAGO, ILLINOIS SP Amer Heart Assoc C1 Massachusetts Gen Hosp, Charlestown, MA 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 0009-7322 J9 CIRCULATION JI Circulation PD NOV 5 PY 2002 VL 106 IS 19 SU S MA 490 BP 97 EP 97 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 613QJ UT WOS:000179142700532 ER PT J AU Yu, GS Gulick, T AF Yu, GS Gulick, T TI Expression of COX subunit heart/muscle isoforms via NRF1 : Mef2 interactions SO CIRCULATION LA English DT Meeting Abstract CT American-Heart-Association Abstracts From Scientific Sessions CY NOV 17-20, 2002 CL CHICAGO, ILLINOIS SP Amer Heart Assoc C1 Massachusetts Gen Hosp, Charlestown, MA 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 0009-7322 J9 CIRCULATION JI Circulation PD NOV 5 PY 2002 VL 106 IS 19 SU S MA 489 BP 97 EP 97 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 613QJ UT WOS:000179142700531 ER PT J AU Beppu, H Ichinose, F Zapol, WM Li, E Bloch, KD AF Beppu, H Ichinose, F Zapol, WM Li, E Bloch, KD TI Haplo-insufficiency for the bone morphogenetic protein type II receptor (BMPR2) gene sensitizes mice to the pulmonary vascular changes cause by prolonged breathing at low oxygen levels SO CIRCULATION LA English DT Meeting Abstract CT American-Heart-Association Abstracts From Scientific Sessions CY NOV 17-20, 2002 CL CHICAGO, ILLINOIS SP Amer Heart Assoc C1 Massachusetts Gen Hosp, Charlestown, MA USA. Massachusetts Gen Hosp, Boston, MA 02114 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 0009-7322 J9 CIRCULATION JI Circulation PD NOV 5 PY 2002 VL 106 IS 19 SU S MA 555 BP 110 EP 110 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 613QJ UT WOS:000179142700597 ER PT J AU Chao, W Shen, Y Novikov, MS Li, L Ahn, YK Rosenzweig, A AF Chao, W Shen, Y Novikov, MS Li, L Ahn, YK Rosenzweig, A TI Adenoviral expression of dominant-negative Fas-associated death domain protein blocks cardiomyocyte apoptosis and reduces myocardial injury after transient ischemia SO CIRCULATION LA English DT Meeting Abstract CT American-Heart-Association Abstracts From Scientific Sessions CY NOV 17-20, 2002 CL CHICAGO, ILLINOIS SP Amer Heart Assoc C1 Massachusetts Gen Hosp, Charlestown, MA USA. Massachusetts Gen Hosp, Boston, MA 02114 USA. NR 0 TC 2 Z9 2 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0009-7322 J9 CIRCULATION JI Circulation PD NOV 5 PY 2002 VL 106 IS 19 SU S MA 657 BP 131 EP 131 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 613QJ UT WOS:000179142700694 ER PT J AU Cook, SA Novikov, MS Matsui, T Nagoshi, T Rosenzweig, A AF Cook, SA Novikov, MS Matsui, T Nagoshi, T Rosenzweig, A TI The zinc finger protein A20 inhibits NF-kappa B signaling in cardiac myocytes and reduces infarct size during ischemia-reperfusion injury SO CIRCULATION LA English DT Meeting Abstract CT American-Heart-Association Abstracts From Scientific Sessions CY NOV 17-20, 2002 CL CHICAGO, ILLINOIS SP Amer Heart Assoc C1 Massachusetts Gen Hosp, CVRC, Charlestown, MA 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 0009-7322 J9 CIRCULATION JI Circulation PD NOV 5 PY 2002 VL 106 IS 19 SU S MA 674 BP 134 EP 134 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 613QJ UT WOS:000179142700711 ER PT J AU Ammer, R Keane, D Aretz, T Ruskin, JN AF Ammer, R Keane, D Aretz, T Ruskin, JN TI Permanent atrial fibrillation induces apoptosis via p38 activation SO CIRCULATION LA English DT Meeting Abstract CT American-Heart-Association Abstracts From Scientific Sessions CY NOV 17-20, 2002 CL CHICAGO, ILLINOIS SP Amer Heart Assoc C1 Univ Klinikum Munster, Munster, Germany. Massachusetts Gen Hosp, Boston, MA 02114 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 0009-7322 J9 CIRCULATION JI Circulation PD NOV 5 PY 2002 VL 106 IS 19 SU S MA 782 BP 156 EP 156 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 613QJ UT WOS:000179142700824 ER PT J AU Nemoto, S Diwan, A DeFrietas, G Shi, SP Sivasubramanian, N AF Nemoto, S Diwan, A DeFrietas, G Shi, SP Sivasubramanian, N TI Mice deficient in the NF kappa B1 p50 subunit exhibit cardiac hypertrophy and altered function in the unstressed state SO CIRCULATION LA English DT Meeting Abstract CT American-Heart-Association Abstracts From Scientific Sessions CY NOV 17-20, 2002 CL CHICAGO, ILLINOIS SP Amer Heart Assoc C1 Baylor Coll Med, Houston VAMC, Houston, TX 77030 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 0009-7322 J9 CIRCULATION JI Circulation PD NOV 5 PY 2002 VL 106 IS 19 SU S MA 807 BP 160 EP 161 PG 2 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 613QJ UT WOS:000179142700849 ER PT J AU Xing, YQ Musi, N Fujii, N Goodyear, LJ Tian, R AF Xing, YQ Musi, N Fujii, N Goodyear, LJ Tian, R TI Inhibition of AMPK by overexpressing dominant negative alpha2-subunit in the heart exacerbates ATP depletion and LV dysfunction during ischemia SO CIRCULATION LA English DT Meeting Abstract CT American-Heart-Association Abstracts From Scientific Sessions CY NOV 17-20, 2002 CL CHICAGO, ILLINOIS SP Amer Heart Assoc C1 Brigham & Womens Hosp, Boston, MA USA. Joslin Diabet Ctr, Boston, MA 02215 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 0009-7322 J9 CIRCULATION JI Circulation PD NOV 5 PY 2002 VL 106 IS 19 SU S MA 815 BP 162 EP 162 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 613QJ UT WOS:000179142700857 ER PT J AU Leopold, J Zhang, YY Scribner, A Ruberg, F Stanton, R Loscalzo, J AF Leopold, J Zhang, YY Scribner, A Ruberg, F Stanton, R Loscalzo, J TI Glucose-6-phosphate dehydrogenase overexpression decreases endothelial oxidant stress and enhances nitric oxide synthase activity SO CIRCULATION LA English DT Meeting Abstract CT American-Heart-Association Abstracts From Scientific Sessions CY NOV 17-20, 2002 CL CHICAGO, ILLINOIS SP Amer Heart Assoc C1 Boston Univ, Sch Med, Boston, MA 02118 USA. Joslin Diabet Ctr, Boston, MA 02215 USA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0009-7322 J9 CIRCULATION JI Circulation PD NOV 5 PY 2002 VL 106 IS 19 SU S MA 819 BP 163 EP 163 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 613QJ UT WOS:000179142700861 ER PT J AU Zhao, DX Hu, YY Miller, G Luster, AD Mitchell, RN Libby, P AF Zhao, DX Hu, YY Miller, G Luster, AD Mitchell, RN Libby, P TI Association of chemokines IP-10 and I-TAC with human cardiac allograft vasculopathy (CAV) SO CIRCULATION LA English DT Meeting Abstract CT American-Heart-Association Abstracts From Scientific Sessions CY NOV 17-20, 2002 CL CHICAGO, ILLINOIS SP Amer Heart Assoc C1 Vanderbilt Univ, Med Ctr, Nashville, TN USA. Massachusetts Gen Hosp, Boston, MA 02114 USA. Brigham & Womens Hosp, Boston, MA 02115 USA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0009-7322 J9 CIRCULATION JI Circulation PD NOV 5 PY 2002 VL 106 IS 19 SU S MA 943 BP 188 EP 188 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 613QJ UT WOS:000179142700985 ER PT J AU Zhao, DX Hu, YY Miller, G Luster, AD Mitchell, RN AF Zhao, DX Hu, YY Miller, G Luster, AD Mitchell, RN TI Association of chemokines Mig and IP-10 with acute allograft rejection in human cardiac allografts SO CIRCULATION LA English DT Meeting Abstract CT American-Heart-Association Abstracts From Scientific Sessions CY NOV 17-20, 2002 CL CHICAGO, ILLINOIS SP Amer Heart Assoc C1 Vanderbilt Univ, Med Ctr, Nashville, TN USA. Massachusetts Gen Hosp, Boston, MA 02114 USA. Brigham & Womens Hosp, Boston, MA 02115 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 0009-7322 J9 CIRCULATION JI Circulation PD NOV 5 PY 2002 VL 106 IS 19 SU S MA 952 BP 190 EP 190 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 613QJ UT WOS:000179142700994 ER PT J AU Matsui, T Nagoshi, T Cook, SA Li, L Rosenzweig, A AF Matsui, T Nagoshi, T Cook, SA Li, L Rosenzweig, A TI Adenoviral gene transfer of glucose transporter-4 (GLUT4) is not sufficient to prevent hypoxia-induced cardiomyocyte apoptosis SO CIRCULATION LA English DT Meeting Abstract CT American-Heart-Association Abstracts From Scientific Sessions CY NOV 17-20, 2002 CL CHICAGO, ILLINOIS SP Amer Heart Assoc C1 Massachusetts Gen Hosp, CVRC, Charlestown, MA 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 0009-7322 J9 CIRCULATION JI Circulation PD NOV 5 PY 2002 VL 106 IS 19 SU S MA 977 BP 195 EP 195 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 613QJ UT WOS:000179142701019 ER PT J AU Fitzgerald, ML Short, G Morris, AL Rhee, JS Szostak, J Freeman, MW AF Fitzgerald, ML Short, G Morris, AL Rhee, JS Szostak, J Freeman, MW TI ABCA1 traffics to basolateral membranes and participates in PDZ protein-protein interactions SO CIRCULATION LA English DT Meeting Abstract CT American-Heart-Association Abstracts From Scientific Sessions CY NOV 17-20, 2002 CL CHICAGO, ILLINOIS SP Amer Heart Assoc C1 Harvard Univ, Sch Med, Massachusetts Gen Hosp, Boston, MA 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 0009-7322 J9 CIRCULATION JI Circulation PD NOV 5 PY 2002 VL 106 IS 19 SU S MA 1102 BP 219 EP 219 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 613QJ UT WOS:000179142701143 ER PT J AU Fitzgerald, ML Morris, AL Rhee, JMS Mendez, AJ Freeman, MW AF Fitzgerald, ML Morris, AL Rhee, JMS Mendez, AJ Freeman, MW TI Analysis of naturally occurring mutations in the large extracellular loops of ABCA1 suggest that a direct interaction with apoA-I is necessary but not sufficient for cholesterol efflux SO CIRCULATION LA English DT Meeting Abstract CT American-Heart-Association Abstracts From Scientific Sessions CY NOV 17-20, 2002 CL CHICAGO, ILLINOIS SP Amer Heart Assoc C1 Harvard Univ, Sch Med, Massachusetts Gen Hosp, Boston, MA USA. Univ Miami, Sch Med, Miami, FL 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 0009-7322 J9 CIRCULATION JI Circulation PD NOV 5 PY 2002 VL 106 IS 19 SU S MA 1108 BP 220 EP 220 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 613QJ UT WOS:000179142701149 ER PT J AU Cook, SA Matsui, T Li, L Rosenzweig, A AF Cook, SA Matsui, T Li, L Rosenzweig, A TI Transcriptional changes associated with chronic expression of activated Akt in the heart SO CIRCULATION LA English DT Meeting Abstract CT American-Heart-Association Abstracts From Scientific Sessions CY NOV 17-20, 2002 CL CHICAGO, ILLINOIS SP Amer Heart Assoc C1 Massachusetts Gen Hosp, CVRC, Charlestown, MA 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 0009-7322 J9 CIRCULATION JI Circulation PD NOV 5 PY 2002 VL 106 IS 19 SU S MA 1189 BP 236 EP 236 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 613QJ UT WOS:000179142701230 ER PT J AU Meiler, SE Li, L Cook, SA Kang, JX Rosenzweig, T AF Meiler, SE Li, L Cook, SA Kang, JX Rosenzweig, T TI The Fat-1 gene, a C. elegans fatty acid desaturase, alters lipid composition and inhibits inflammation of human endothelium by reducing the transcriptional activity of NF-kappa B (p65) SO CIRCULATION LA English DT Meeting Abstract CT American-Heart-Association Abstracts From Scientific Sessions CY NOV 17-20, 2002 CL CHICAGO, ILLINOIS SP Amer Heart Assoc C1 Massachusetts Gen Hosp, Program CV Gene Therapy, Cardiovasc Res Ctr, Charlestown, MA USA. Harvard Univ, Sch Med, Charlestown, MA USA. NR 0 TC 0 Z9 0 U1 1 U2 2 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0009-7322 J9 CIRCULATION JI Circulation PD NOV 5 PY 2002 VL 106 IS 19 SU S MA 1228 BP 243 EP 243 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 613QJ UT WOS:000179142701269 ER PT J AU Friedrich, EB Tager, AM Luster, AD Gerszten, RE AF Friedrich, EB Tager, AM Luster, AD Gerszten, RE TI Stromal derived factor-1 a triggers Th1 cell adhesion under flow conditions SO CIRCULATION LA English DT Meeting Abstract CT American-Heart-Association Abstracts From Scientific Sessions CY NOV 17-20, 2002 CL CHICAGO, ILLINOIS SP Amer Heart Assoc C1 Massachusetts Gen Hosp, Charlestown, MA 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 0009-7322 J9 CIRCULATION JI Circulation PD NOV 5 PY 2002 VL 106 IS 19 SU S MA 1231 BP 244 EP 244 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 613QJ UT WOS:000179142701272 ER PT J AU Nemoto, S Diwan, A DeFreitas, G Carabello, BA Mann, DL AF Nemoto, S Diwan, A DeFreitas, G Carabello, BA Mann, DL TI Post-translational processing of tumor necrosis factor (TNF) modulates LV function in transgenic mice with cardiac restricted overexpression of TNF SO CIRCULATION LA English DT Meeting Abstract CT American-Heart-Association Abstracts From Scientific Sessions CY NOV 17-20, 2002 CL CHICAGO, ILLINOIS SP Amer Heart Assoc C1 VA Med Ctr, Baylor Coll Med, Houston, TX USA. Baylor Coll Med, Winters Ctr Heart Failure Res, Houston, TX 77030 USA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0009-7322 J9 CIRCULATION JI Circulation PD NOV 5 PY 2002 VL 106 IS 19 SU S MA 1297 BP 258 EP 258 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 613QJ UT WOS:000179142701336 ER PT J AU Matsui, T Nagoshi, T Luptak, I Li, L Cook, SA Tian, R Rosenzweig, A AF Matsui, T Nagoshi, T Luptak, I Li, L Cook, SA Tian, R Rosenzweig, A TI Enhanced glucose uptake and glycogen storage in transgenic cardiac Akt mice SO CIRCULATION LA English DT Meeting Abstract CT American-Heart-Association Abstracts From Scientific Sessions CY NOV 17-20, 2002 CL CHICAGO, ILLINOIS SP Amer Heart Assoc C1 Massachusetts Gen Hosp, CVRC, Charlestown, MA USA. Brigham & Womens Hosp, Boston, MA 02115 USA. NR 0 TC 0 Z9 0 U1 1 U2 1 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0009-7322 J9 CIRCULATION JI Circulation PD NOV 5 PY 2002 VL 106 IS 19 SU S MA 1315 BP 262 EP 262 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 613QJ UT WOS:000179142701354 ER PT J AU Nemoto, S Razeghi, P Young, ME DeFreitas, G Taegtmeyer, H Carabello, BA AF Nemoto, S Razeghi, P Young, ME DeFreitas, G Taegtmeyer, H Carabello, BA TI Peroxisome proliferator-activated receptor (PPAR) agonists ameliorate LV dysfunction in experimental chronic mitral regurgitation (MR) SO CIRCULATION LA English DT Meeting Abstract CT American-Heart-Association Abstracts From Scientific Sessions CY NOV 17-20, 2002 CL CHICAGO, ILLINOIS SP Amer Heart Assoc C1 VA Med Ctr, Baylor Coll Med, Houston, TX USA. Univ Texas, Sch Med, Houston, TX 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 0009-7322 J9 CIRCULATION JI Circulation PD NOV 5 PY 2002 VL 106 IS 19 SU S MA 1320 BP 263 EP 263 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 613QJ UT WOS:000179142701359 ER PT J AU Ellinor, PT Yoerger, DM McGovern, BA Fishman, MC Ruskin, JN MacRae, CA AF Ellinor, PT Yoerger, DM McGovern, BA Fishman, MC Ruskin, JN MacRae, CA TI Familial aggregation in patients with lone atrial fibrillation SO CIRCULATION LA English DT Meeting Abstract CT American-Heart-Association Abstracts From Scientific Sessions CY NOV 17-20, 2002 CL CHICAGO, ILLINOIS SP Amer Heart Assoc C1 Massachusetts Gen Hosp, Charlestown, MA USA. Massachusetts Gen Hosp, Boston, MA 02114 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 0009-7322 J9 CIRCULATION JI Circulation PD NOV 5 PY 2002 VL 106 IS 19 SU S MA 1600 BP 319 EP 319 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 613QJ UT WOS:000179142701639 ER PT J AU Tawakol, A Elmaleh, D Gewirtz, H Brady, T Muller, JE Fischman, AJ Daghighian, F AF Tawakol, A Elmaleh, D Gewirtz, H Brady, T Muller, JE Fischman, AJ Daghighian, F TI Detection of macrophage-rich atherosclerotic lesions with 18F-FDG and a novel catheter-mounted beta probe SO CIRCULATION LA English DT Meeting Abstract CT American-Heart-Association Abstracts From Scientific Sessions CY NOV 17-20, 2002 CL CHICAGO, ILLINOIS SP Amer Heart Assoc C1 Massachusetts Gen Hosp, Boston, MA 02114 USA. IntraMed Imaging LLC, Los Angeles, CA 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 0009-7322 J9 CIRCULATION JI Circulation PD NOV 5 PY 2002 VL 106 IS 19 SU S MA 1656 BP 331 EP 331 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 613QJ UT WOS:000179142701695 ER PT J AU Marelli, AJ Sijbom, M Llberthson, R Child, JS Graham, T Day, M Hopkins, W Murphy, D Landzberg, M King, ME AF Marelli, AJ Sijbom, M Llberthson, R Child, JS Graham, T Day, M Hopkins, W Murphy, D Landzberg, M King, ME TI The international society for adult congenital cardiac disease registry: Genefic transmission rates in family clusters SO CIRCULATION LA English DT Meeting Abstract CT American-Heart-Association Abstracts From Scientific Sessions CY NOV 17-20, 2002 CL CHICAGO, ILLINOIS SP Amer Heart Assoc C1 McGill Univ, Ctr Hlth, Montreal, PQ, Canada. Massachusetts Gen Hosp, Boston, MA 02114 USA. Univ Calif Los Angeles, Med Ctr, Los Angeles, CA 90024 USA. Vanderbilt Univ, Nashville, TN USA. Univ Utah, Med Ctr, Salt Lake City, UT USA. Univ Vermont, Burlington, VT USA. Stanford Univ, Stanford, CA 94305 USA. Brigham & Womens Hosp, Boston, MA 02115 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 0009-7322 J9 CIRCULATION JI Circulation PD NOV 5 PY 2002 VL 106 IS 19 SU S MA 1790 BP 358 EP 359 PG 2 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 613QJ UT WOS:000179142701828 ER PT J AU Marelli, AJ Sijbom, M DeMoor, M Rouah, F Liberthson, R Child, JS Day, M Foster, E Graham, T Hopkins, W Murphy, D Landzberg, M King, ME AF Marelli, AJ Sijbom, M DeMoor, M Rouah, F Liberthson, R Child, JS Day, M Foster, E Graham, T Hopkins, W Murphy, D Landzberg, M King, ME TI The international society for adult congenital cardiac disease: Population profile of the first 1,245 patients - Operated vs unoperated outcomes SO CIRCULATION LA English DT Meeting Abstract CT American-Heart-Association Abstracts From Scientific Sessions CY NOV 17-20, 2002 CL CHICAGO, ILLINOIS SP Amer Heart Assoc C1 McGill Univ, Ctr Hlth, Montreal, PQ, Canada. Massachusetts Gen Hosp, Boston, MA 02114 USA. Univ Calif Los Angeles, Sch Med, Los Angeles, CA USA. Univ Utah, Med Ctr, Salt Lake City, UT USA. Univ Calif San Francisco, San Francisco, CA 94143 USA. Vanderbilt Univ, Nashville, TN USA. Univ Vermont, Burlington, VT USA. Stanford Univ, Stanford, CA 94305 USA. Brigham & Womens Hosp, Boston, MA 02115 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 0009-7322 J9 CIRCULATION JI Circulation PD NOV 5 PY 2002 VL 106 IS 19 SU S MA 1791 BP 359 EP 359 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 613QJ UT WOS:000179142701829 ER PT J AU Gibson, CM Murphy, SA Marble, SJ James, D Kalapanda, R Zeymer, U Giugliano, RP AF Gibson, CM Murphy, SA Marble, SJ James, D Kalapanda, R Zeymer, U Giugliano, RP TI Combination therapy with eptifibatide and TNK is associated with an improved rate of dye entry into the myocardium (TIMI Myocardial Frame Count) in ST elevation myocardial infarction (STEMI): An INTEGRITI substudy SO CIRCULATION LA English DT Meeting Abstract CT American-Heart-Association Abstracts From Scientific Sessions CY NOV 17-20, 2002 CL CHICAGO, ILLINOIS SP Amer Heart Assoc C1 TIMI Study Grp, Boston, MA USA. Clin Kassel, Kassel, Germany. Brigham & Womens Hosp, Boston, MA 02115 USA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0009-7322 J9 CIRCULATION JI Circulation PD NOV 5 PY 2002 VL 106 IS 19 SU S MA 1804 BP 363 EP 363 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 613QJ UT WOS:000179142701842 ER PT J AU Nikolaidis, LA Mankad, S Miske, G Elahi, D Shannon, RP AF Nikolaidis, LA Mankad, S Miske, G Elahi, D Shannon, RP TI Safety and efficacy of GLP-1 in acute myocardial infarction associated with left ventricular systolic dysfunction SO CIRCULATION LA English DT Meeting Abstract CT American-Heart-Association Abstracts From Scientific Sessions CY NOV 17-20, 2002 CL CHICAGO, ILLINOIS SP Amer Heart Assoc C1 Allegheny Gen Hosp, Pittsburgh, PA 15212 USA. Massachusetts Gen Hosp, Boston, MA 02114 USA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0009-7322 J9 CIRCULATION JI Circulation PD NOV 5 PY 2002 VL 106 IS 19 SU S MA 1810 BP 364 EP 364 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 613QJ UT WOS:000179142701848 ER PT J AU Masoudi, FA Plomondon, ME Magid, DJ Sales, AE Rumsfeld, JS AF Masoudi, FA Plomondon, ME Magid, DJ Sales, AE Rumsfeld, JS TI Renal dysfunction and mortality after acute coronary syndromes SO CIRCULATION LA English DT Meeting Abstract CT American-Heart-Association Abstracts From Scientific Sessions CY NOV 17-20, 2002 CL CHICAGO, ILLINOIS SP Amer Heart Assoc C1 Denver Hlth Med Ctr, Denver, CO USA. Denver VA Med Ctr, Denver, CO USA. Colorado Permanente Med Grp, Denver, CO USA. VA Puget Sound Hlth Care Syst, Seattle, WA USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0009-7322 J9 CIRCULATION JI Circulation PD NOV 5 PY 2002 VL 106 IS 19 SU S MA 1991 BP 401 EP 401 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 613QJ UT WOS:000179142702029 ER PT J AU Wylie, JV Cannon, CP Antman, EM Braunwald, E AF Wylie, JV Cannon, CP Antman, EM Braunwald, E TI A validated risk score predicts the development of congestive heart failure and correlates with B-type, natriuretic peptide after presentation with unstable angina or non-ST elevation myocardial infarction: Results from OPUS-TIMI 16 and TIMI 11B SO CIRCULATION LA English DT Meeting Abstract CT American-Heart-Association Abstracts From Scientific Sessions CY NOV 17-20, 2002 CL CHICAGO, ILLINOIS SP Amer Heart Assoc C1 Massachusetts Gen Hosp, Boston, MA 02114 USA. Brigham & Womens Hosp, Boston, MA 02115 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 0009-7322 J9 CIRCULATION JI Circulation PD NOV 5 PY 2002 VL 106 IS 19 SU S MA 1997 BP 402 EP 402 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 613QJ UT WOS:000179142702035 ER PT J AU Nikolaidis, LA Elahi, D Shannon, RP AF Nikolaidis, LA Elahi, D Shannon, RP TI Advanced dilated cardiomyopathy is associated with myocardial insulin resistance in conscious dogs SO CIRCULATION LA English DT Meeting Abstract CT American-Heart-Association Abstracts From Scientific Sessions CY NOV 17-20, 2002 CL CHICAGO, ILLINOIS SP Amer Heart Assoc C1 Allegheny Gen Hosp, Pittsburgh, PA 15212 USA. Massachusetts Gen Hosp, Boston, MA 02114 USA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0009-7322 J9 CIRCULATION JI Circulation PD NOV 5 PY 2002 VL 106 IS 19 SU S MA 2129 BP 428 EP 428 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 613QJ UT WOS:000179142702167 ER PT J AU Hoffmann, U Enzweiler, C Millea, R Titus, J Kwait, D Brady, TJ AF Hoffmann, U Enzweiler, C Millea, R Titus, J Kwait, D Brady, TJ TI Detection of acute myocardial infarction by multidetector CT in a porcine model of acute coronary occlusion SO CIRCULATION LA English DT Meeting Abstract CT American-Heart-Association Abstracts From Scientific Sessions CY NOV 17-20, 2002 CL CHICAGO, ILLINOIS SP Amer Heart Assoc C1 Massachusetts Gen Hosp, Boston, MA 02114 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 0009-7322 J9 CIRCULATION JI Circulation PD NOV 5 PY 2002 VL 106 IS 19 SU S MA 2193 BP 441 EP 441 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 613QJ UT WOS:000179142702231 ER PT J AU Messas, E Pouzet, B Touchot, B Guerrero, L Abdelhamid, H Desnos, M Menasche, P Hagege, A Levine, RA AF Messas, E Pouzet, B Touchot, B Guerrero, L Abdelhamid, H Desnos, M Menasche, P Hagege, A Levine, RA TI Efficacy of chordal cutting for reducing chronic ischemic mitral regurgitation SO CIRCULATION LA English DT Meeting Abstract CT American-Heart-Association Abstracts From Scientific Sessions CY NOV 17-20, 2002 CL CHICAGO, ILLINOIS SP Amer Heart Assoc C1 Fac Med Necker Enfants Malad Paris V, INSERM, EMI 0016, Paris, France. Hop Xavier Bichat, Paris, France. Harvard Univ, Massachusetts Gen Hosp, Sch Med, Boston, MA USA. Hosp Europeen Georges Pompidou, Serv Cardiol 1, Paris, France. Harvard Univ, Massachusetts Gen Hosp, Sch Med, Cardiac Ultrasound Lab, Boston, MA USA. Hop Xavier Bichat, Dept Cardiovasc Surg, Paris, France. Assistance Publ Hop Paris, Ecole Natl Chirurg, Paris, France. 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 0009-7322 J9 CIRCULATION JI Circulation PD NOV 5 PY 2002 VL 106 IS 19 SU S MA 2280 BP 460 EP 460 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 613QJ UT WOS:000179142702319 ER PT J AU Pagani, FD DerSimonian, H Zawadzka, A Jacoby, DB Dinsmore, J Wright, S Aretz, TH Wetzel, K Aaronson, KD AF Pagani, FD DerSimonian, H Zawadzka, A Jacoby, DB Dinsmore, J Wright, S Aretz, TH Wetzel, K Aaronson, KD TI Autologous skeletal myoblasts transplanted in ischemia damaged myocardium in humans: Histological analysis of cell survival and differentiation SO CIRCULATION LA English DT Meeting Abstract CT American-Heart-Association Abstracts From Scientific Sessions CY NOV 17-20, 2002 CL CHICAGO, ILLINOIS SP Amer Heart Assoc C1 Univ Michigan, Ann Arbor, MI 48109 USA. Diacrin Inc, Charlestown, MA USA. Univ Michigan, Ann Arbor, MI 48109 USA. Massachusetts Gen Hosp, Boston, MA 02114 USA. NR 0 TC 1 Z9 1 U1 0 U2 1 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0009-7322 J9 CIRCULATION JI Circulation PD NOV 5 PY 2002 VL 106 IS 19 SU S MA 2293 BP 463 EP 463 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 613QJ UT WOS:000179142702332 ER PT J AU Lachmann, JS Lewis, GD Systrom, DM Tawakol, A Shin, JT Dec, GW Semigran, MJ AF Lachmann, JS Lewis, GD Systrom, DM Tawakol, A Shin, JT Dec, GW Semigran, MJ TI Sildenafil improves hemodynamics and exercise tolerance in advanced heart failure SO CIRCULATION LA English DT Meeting Abstract CT American-Heart-Association Abstracts From Scientific Sessions CY NOV 17-20, 2002 CL CHICAGO, ILLINOIS SP Amer Heart Assoc C1 Massachusetts Gen Hosp, Boston, MA 02114 USA. NR 0 TC 3 Z9 3 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0009-7322 J9 CIRCULATION JI Circulation PD NOV 5 PY 2002 VL 106 IS 19 SU S MA 2323 BP 469 EP 469 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 613QJ UT WOS:000179142702361 ER PT J AU Mozaffarian, D Nye, RG AF Mozaffarian, D Nye, RG TI Statin therapy is associated with lower mortality in severe heart failure SO CIRCULATION LA English DT Meeting Abstract CT American-Heart-Association Abstracts From Scientific Sessions CY NOV 17-20, 2002 CL CHICAGO, ILLINOIS SP Amer Heart Assoc C1 VA Puget Sound Healthcare Syst, Seattle, WA USA. Pfizer, New London, CT USA. Univ Washington, Seattle, WA 98195 USA. RI Mozaffarian, Dariush/B-2276-2008 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 0009-7322 J9 CIRCULATION JI Circulation PD NOV 5 PY 2002 VL 106 IS 19 SU S MA 2329 BP 470 EP 471 PG 2 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 613QJ UT WOS:000179142702367 ER PT J AU Lewis, GD Koelling, TM Systrom, DM Zapol, WM Bloch, KD Dec, GW Semigran, MJ AF Lewis, GD Koelling, TM Systrom, DM Zapol, WM Bloch, KD Dec, GW Semigran, MJ TI Inhaled nitric oxide improves ventilatory efficiency in patients with severe heart failure and right ventricular dysfunction SO CIRCULATION LA English DT Meeting Abstract CT American-Heart-Association Abstracts From Scientific Sessions CY NOV 17-20, 2002 CL CHICAGO, ILLINOIS SP Amer Heart Assoc C1 Massachusetts Gen Hosp, Boston, MA 02114 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 0009-7322 J9 CIRCULATION JI Circulation PD NOV 5 PY 2002 VL 106 IS 19 SU S MA 2330 BP 471 EP 471 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 613QJ UT WOS:000179142702368 ER PT J AU Rumsfeld, JS Havranek, E Masoudi, FA Tooley, JF Peterson, ED Jones, P Spertus, JA AF Rumsfeld, JS Havranek, E Masoudi, FA Tooley, JF Peterson, ED Jones, P Spertus, JA TI Depressive symptoms are the strongest predictor of decline in health status in patients with heart failure SO CIRCULATION LA English DT Meeting Abstract CT American-Heart-Association Abstracts From Scientific Sessions CY NOV 17-20, 2002 CL CHICAGO, ILLINOIS SP Amer Heart Assoc C1 Denver VA Med Ctr, Denver, CO USA. Pharmacia Co, Skokie, IL USA. Duke Univ, Med Ctr, Durham, NC USA. UMKC, Mid Amer Heart Inst, Kansas City, MO USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0009-7322 J9 CIRCULATION JI Circulation PD NOV 5 PY 2002 VL 106 IS 19 SU S MA 2338 BP 472 EP 473 PG 2 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 613QJ UT WOS:000179142702376 ER PT J AU Al-Marayati, F Isselbacher, EM Mehta, RH Cooper, JV O'Gara, PT Sechtem, U Bossone, E Evangelista, A Oh, JK Nienaber, CA Eagle, KA AF Al-Marayati, F Isselbacher, EM Mehta, RH Cooper, JV O'Gara, PT Sechtem, U Bossone, E Evangelista, A Oh, JK Nienaber, CA Eagle, KA CA Int Registry Acute Aortic Dissecti TI Marfan syndrome: A distinct and highly lethal cause of aortic dissection; Lessons from the International Registry of Aortic Dissection (IRAD) SO CIRCULATION LA English DT Meeting Abstract CT American-Heart-Association Abstracts From Scientific Sessions CY NOV 17-20, 2002 CL CHICAGO, ILLINOIS SP Amer Heart Assoc C1 Univ Michigan, Med Ctr, Ann Arbor, MI USA. Massachusetts Gen Hosp, Boston, MA 02114 USA. Univ Michigan, Med Ctr, Ann Arbor, MI USA. Brigham & Womens Hosp, Boston, MA 02115 USA. Robert Bosch Med Ctr, Stuttgart, Germany. Inst Policlin San Donato, San Donato Milanese, Italy. Hosp Gen Valle Hebron, Barcelona, Spain. Mayo Clin, Rochester, MN USA. Univ Rostock, Rostock, Germany. Int Registry Acute Aort Dissect Invest, Ann Arbor, MI USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0009-7322 J9 CIRCULATION JI Circulation PD NOV 5 PY 2002 VL 106 IS 19 SU S MA 2342 BP 473 EP 473 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 613QJ UT WOS:000179142702380 ER PT J AU Ix, JH Mercado, N Shlipak, MG Boersma, E Lemos, PA Lindenboom, W O'Neill, WW Wijns, W Serruys, PW AF Ix, JH Mercado, N Shlipak, MG Boersma, E Lemos, PA Lindenboom, W O'Neill, WW Wijns, W Serruys, PW TI The effect of renal insufficiency on clinical outcomes after coronary revascularization in patients with multivessel disease: The Arterial Revascularization Therapies Study (ARTS) SO CIRCULATION LA English DT Meeting Abstract CT American-Heart-Association Abstracts From Scientific Sessions CY NOV 17-20, 2002 CL CHICAGO, ILLINOIS SP Amer Heart Assoc C1 Erasmus Univ, Ctr Thorax, NL-3000 DR Rotterdam, Netherlands. Univ Calif San Francisco, San Francisco VA Med Ctr, San Francisco, CA 94143 USA. Univ Hosp Digest & Cardialysis, Rotterdam, Netherlands. William Beaumont Hosp, Royal Oak, MI 48072 USA. Onze Lieve Vrouw Hosp, CV Ctr, Aalst, Belgium. RI Lemos, Pedro/G-5758-2013 OI Lemos, Pedro/0000-0002-6782-750X NR 0 TC 2 Z9 2 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0009-7322 J9 CIRCULATION JI Circulation PD NOV 5 PY 2002 VL 106 IS 19 SU S MA 2428 BP 492 EP 492 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 613QJ UT WOS:000179142702466 ER PT J AU Liu, HL Filippov, G Panella, SM Bloch, KD AF Liu, HL Filippov, G Panella, SM Bloch, KD TI Regulation of gene expression in rat pulmonary artery smooth muscle cells by nitric oxide - A microarray analysis SO CIRCULATION LA English DT Meeting Abstract CT American-Heart-Association Abstracts From Scientific Sessions CY NOV 17-20, 2002 CL CHICAGO, ILLINOIS SP Amer Heart Assoc C1 Massachusetts Gen Hosp, Charlestown, MA 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 0009-7322 J9 CIRCULATION JI Circulation PD NOV 5 PY 2002 VL 106 IS 19 SU S MA 2446 BP 495 EP 495 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 613QJ UT WOS:000179142702484 ER PT J AU Buck, T Plicht, B Hunold, P Levine, RA AF Buck, T Plicht, B Hunold, P Levine, RA TI Evaluation of the severity of mitral regurgitation: Benefit of regurgitant stroke volume and vena contracta quantification versus jet area grading SO CIRCULATION LA English DT Meeting Abstract CT American-Heart-Association Abstracts From Scientific Sessions CY NOV 17-20, 2002 CL CHICAGO, ILLINOIS SP Amer Heart Assoc C1 Univ Clin Essen, Essen, Germany. Massachusetts Gen Hosp, Boston, MA 02114 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 0009-7322 J9 CIRCULATION JI Circulation PD NOV 5 PY 2002 VL 106 IS 19 SU S MA 2493 BP 505 EP 505 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 613QJ UT WOS:000179142702531 ER PT J AU Hung, J Guerrero, JL Handschumacher, MD Papakostas, L Levine, RA AF Hung, J Guerrero, JL Handschumacher, MD Papakostas, L Levine, RA TI Persistent benefit of an echo-guided papillary muscle repositioning device to reduce ischemic mitral regurgitation SO CIRCULATION LA English DT Meeting Abstract CT American-Heart-Association Abstracts From Scientific Sessions CY NOV 17-20, 2002 CL CHICAGO, ILLINOIS SP Amer Heart Assoc C1 Massachusetts Gen Hosp, Boston, MA 02114 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 0009-7322 J9 CIRCULATION JI Circulation PD NOV 5 PY 2002 VL 106 IS 19 SU S MA 2497 BP 505 EP 506 PG 2 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 613QJ UT WOS:000179142702535 ER PT J AU Nesta, F Otsuji, Y Levine, RA Handshumacher, MD Leavitt, M Hung, J AF Nesta, F Otsuji, Y Levine, RA Handshumacher, MD Leavitt, M Hung, J TI Leaflet concavity: A rapid visual clue to the presence of ischemic mitral regurgitation SO CIRCULATION LA English DT Meeting Abstract CT American-Heart-Association Abstracts From Scientific Sessions CY NOV 17-20, 2002 CL CHICAGO, ILLINOIS SP Amer Heart Assoc C1 Massachusetts Gen Hosp, Boston, MA 02114 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 0009-7322 J9 CIRCULATION JI Circulation PD NOV 5 PY 2002 VL 106 IS 19 SU S MA 2496 BP 505 EP 505 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 613QJ UT WOS:000179142702534 ER PT J AU Wong, ML Staszewsky, L Anand, I Feliciano, N Hester, A Cohn, JN AF Wong, ML Staszewsky, L Anand, I Feliciano, N Hester, A Cohn, JN TI Stratification of baseline left ventricular dimension and ejection fraction determines response to valsartan in heart failure. Val-HeFT echocardiography study SO CIRCULATION LA English DT Meeting Abstract CT American-Heart-Association Abstracts From Scientific Sessions CY NOV 17-20, 2002 CL CHICAGO, ILLINOIS SP Amer Heart Assoc C1 VA Greater Los Angeles Hlth Care Syst, Los Angeles, CA USA. Inst Mario Negri, Milan, Italy. Univ Minnesota, Minneapolis, MN USA. Novartis Pharmaceut Corp, E Hanover, NJ 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 0009-7322 J9 CIRCULATION JI Circulation PD NOV 5 PY 2002 VL 106 IS 19 SU S MA 2526 BP 511 EP 512 PG 2 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 613QJ UT WOS:000179142702564 ER PT J AU Go, AS Hylek, EM Phillips, KA Chang, YC Henault, LE Capra, AM Jensvold, NG Selby, JV Singer, DE AF Go, AS Hylek, EM Phillips, KA Chang, YC Henault, LE Capra, AM Jensvold, NG Selby, JV Singer, DE TI Effectiveness and safety of warfarin to prevent thromboembolism among 13,559 patients with atrial fibrillation: How well do results of randomized trials apply to clinical practice? The ATRIA study SO CIRCULATION LA English DT Meeting Abstract CT American-Heart-Association Abstracts From Scientific Sessions CY NOV 17-20, 2002 CL CHICAGO, ILLINOIS SP Amer Heart Assoc C1 Permanente No CA, Oakland, CA USA. Massachusetts Gen Hosp, Boston, MA 02114 USA. NR 0 TC 3 Z9 3 U1 0 U2 1 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0009-7322 J9 CIRCULATION JI Circulation PD NOV 5 PY 2002 VL 106 IS 19 SU S MA 2545 BP 515 EP 515 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 613QJ UT WOS:000179142702583 ER PT J AU Ako, J Morino, Y Honda, Y Sonoda, S Terashima, M Jaeger, JL Palacios, IF Brown, CL Baim, DS Fitzgerald, PJ AF Ako, J Morino, Y Honda, Y Sonoda, S Terashima, M Jaeger, JL Palacios, IF Brown, CL Baim, DS Fitzgerald, PJ TI Incidence of incomplete stent apposition at baseline and follow-up: Interim analysis from the SIRIUS trial SO CIRCULATION LA English DT Meeting Abstract CT American-Heart-Association Abstracts From Scientific Sessions CY NOV 17-20, 2002 CL CHICAGO, ILLINOIS SP Amer Heart Assoc C1 Stanford Univ, Palo Alto, CA 94304 USA. Cordis Corp, Warren, NJ USA. Massachusetts Gen Hosp, Boston, MA 02114 USA. Fuqua Heart ACtr, Atlanta, GA USA. Brigham & Womens Hosp, Boston, MA 02115 USA. RI Honda, Yasuhiro/J-6227-2013 OI Honda, Yasuhiro/0000-0002-0102-7841 NR 0 TC 4 Z9 4 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0009-7322 J9 CIRCULATION JI Circulation PD NOV 5 PY 2002 VL 106 IS 19 SU S MA 2570 BP 520 EP 520 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 613QJ UT WOS:000179142702608 ER PT J AU Cai, JM Hatsukami, TS Ferguson, MS Yuan, C AF Cai, JM Hatsukami, TS Ferguson, MS Yuan, C TI The differentiation of stable and unstable carotid atherosclerotic plaque by in vivo high-resolution MR imaging SO CIRCULATION LA English DT Meeting Abstract CT American-Heart-Association Abstracts From Scientific Sessions CY NOV 17-20, 2002 CL CHICAGO, ILLINOIS SP Amer Heart Assoc C1 Univ Washington, Dept Radiol, Seattle, WA 98195 USA. Univ Washington, VA Puget Sound Hlth Care Syst, Surg Serv 112, Seattle, WA 98195 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 0009-7322 J9 CIRCULATION JI Circulation PD NOV 5 PY 2002 VL 106 IS 19 SU S MA 2590 BP 525 EP 525 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 613QJ UT WOS:000179142702628 ER PT J AU Carroll, DL Hamilton, GA McGovern, BA AF Carroll, DL Hamilton, GA McGovern, BA TI Quality of life in implanted cardioverter defibrillator recipients: The impact of a device shock SO CIRCULATION LA English DT Meeting Abstract CT American-Heart-Association Abstracts From Scientific Sessions CY NOV 17-20, 2002 CL CHICAGO, ILLINOIS SP Amer Heart Assoc C1 Massachusetts Gen Hosp, Boston, MA 02114 USA. Univ Oslo, Lancaster, MA 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 0009-7322 J9 CIRCULATION JI Circulation PD NOV 5 PY 2002 VL 106 IS 19 SU S MA 2667 BP 540 EP 540 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 613QJ UT WOS:000179142702705 ER PT J AU Xu, Y Lu, L Lee, J Greyson, C Kinugawa, K Long, C Schwartz, GG AF Xu, Y Lu, L Lee, J Greyson, C Kinugawa, K Long, C Schwartz, GG TI Acute treatment with a PPAR-gamma activator increases susceptibility to ventricular fibrillation in myocardial ischemia and reperfusion in pigs SO CIRCULATION LA English DT Meeting Abstract CT American-Heart-Association Abstracts From Scientific Sessions CY NOV 17-20, 2002 CL CHICAGO, ILLINOIS SP Amer Heart Assoc C1 Denver VA Med Ctr, Denver, CO USA. Univ Colorado, Hlth Sci Ctr, Denver, CO 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 0009-7322 J9 CIRCULATION JI Circulation PD NOV 5 PY 2002 VL 106 IS 19 SU S MA 2776 BP 562 EP 562 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 613QJ UT WOS:000179142702814 ER PT J AU Agoston, I Urbauer, D Deswal, A AF Agoston, I Urbauer, D Deswal, A TI Outcomes of diastolic heart failure in a racially balanced cohort SO CIRCULATION LA English DT Meeting Abstract CT American-Heart-Association Abstracts From Scientific Sessions CY NOV 17-20, 2002 CL CHICAGO, ILLINOIS SP Amer Heart Assoc C1 Baylor Coll Med, Winters Ctr Heart Failure Res, Houston, TX 77030 USA. Baylor Coll Med, VA Med Ctr, Houston, TX 77030 USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0009-7322 J9 CIRCULATION JI Circulation PD NOV 5 PY 2002 VL 106 IS 19 SU S MA 2801 BP 567 EP 567 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 613QJ UT WOS:000179142702839 ER PT J AU Hylek, EM Go, AS Chang, YC Phillips, KA Henault, LE Capra, AM Jensvold, NG Selby, JV Singer, DE AF Hylek, EM Go, AS Chang, YC Phillips, KA Henault, LE Capra, AM Jensvold, NG Selby, JV Singer, DE TI The impact of anticoagulation intensity on severity of stroke in atrial fibrillation: The AnTicoagulation and Risk Factors in Atrial Fibrillation (ATRIA) study SO CIRCULATION LA English DT Meeting Abstract CT American-Heart-Association Abstracts From Scientific Sessions CY NOV 17-20, 2002 CL CHICAGO, ILLINOIS SP Amer Heart Assoc C1 Massachusetts Gen Hosp, Boston, MA 02114 USA. Kaiser Permanente No Calif, Oakland, CA 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 0009-7322 J9 CIRCULATION JI Circulation PD NOV 5 PY 2002 VL 106 IS 19 SU S MA 2854 BP 577 EP 578 PG 2 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 613QJ UT WOS:000179142702892 ER PT J AU Murphy, SA Antman, EM de Lemos, JA Morrow, DA Sabatine, MS Wong, GC Kalapanda, R Marble, SJ James, D Gibson, CM AF Murphy, SA Antman, EM de Lemos, JA Morrow, DA Sabatine, MS Wong, GC Kalapanda, R Marble, SJ James, D Gibson, CM CA TIMI Study Grp TI A pattern of systolic flow reversal (pulsatile flow) is related to angiographic and clinical outcomes. A TIMI angiographic substudy SO CIRCULATION LA English DT Meeting Abstract CT American-Heart-Association Abstracts From Scientific Sessions CY NOV 17-20, 2002 CL CHICAGO, ILLINOIS SP Amer Heart Assoc C1 TIMI Study Grp, Boston, MA USA. Brigham & Womens Hosp, Boston, MA 02115 USA. Univ Texas, Hlth Sci Ctr, SW Med Sch, Dallas, TX 75235 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 0009-7322 J9 CIRCULATION JI Circulation PD NOV 5 PY 2002 VL 106 IS 19 SU S MA 2953 BP 597 EP 598 PG 2 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 613QJ UT WOS:000179142702991 ER PT J AU Gibson, CM Murphy, SA James, D Marble, SJ Wong, GC Kalapanda, R Kraimer, N Antman, EM AF Gibson, CM Murphy, SA James, D Marble, SJ Wong, GC Kalapanda, R Kraimer, N Antman, EM TI Facilitated angioplasty is associated with an improvement in the number of frames required for dye to fill the mycocardium (TIMI Myocardial Frame Count) in ST segment elevation myocardial infarction (STEMI) SO CIRCULATION LA English DT Meeting Abstract CT American-Heart-Association Abstracts From Scientific Sessions CY NOV 17-20, 2002 CL CHICAGO, ILLINOIS SP Amer Heart Assoc C1 TIMI Study Grp, Boston, MA USA. Brigham & Womens Hosp, Boston, MA 02115 USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0009-7322 J9 CIRCULATION JI Circulation PD NOV 5 PY 2002 VL 106 IS 19 SU S MA 2955 BP 598 EP 598 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 613QJ UT WOS:000179142702993 ER PT J AU Gibson, CM Giugliano, RP Roe, MT Murphy, SA Green, CL Morrow, DA Schweiger, MJ Miklin, JS Krucoff, M AF Gibson, CM Giugliano, RP Roe, MT Murphy, SA Green, CL Morrow, DA Schweiger, MJ Miklin, JS Krucoff, M CA TIMI Study Grp TI Impaired TIMI epicardial flow and myocardial perfusion grades are associated with increased time to ST segment recovery in ST segment elevation MI: An INTEGRITI substudy SO CIRCULATION LA English DT Meeting Abstract CT American-Heart-Association Abstracts From Scientific Sessions CY NOV 17-20, 2002 CL CHICAGO, ILLINOIS SP Amer Heart Assoc C1 TIMI Study Grp, Boston, MA USA. Brigham & Womens Hosp, Boston, MA 02115 USA. Duke Univ, Clin Res Inst, Durham, NC USA. Baystate Med Ctr, Springfield, MA USA. Luthern Med Ctr, Wheat Ridge, CO USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0009-7322 J9 CIRCULATION JI Circulation PD NOV 5 PY 2002 VL 106 IS 19 SU S MA 2954 BP 598 EP 598 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 613QJ UT WOS:000179142702992 ER PT J AU Palacios, IF de Moor, M Martin, F Sanchez, PL Inglessis, I King, MEE Hung, J Yoerger, DM Buonanno, F Demirjian, Z AF Palacios, IF de Moor, M Martin, F Sanchez, PL Inglessis, I King, MEE Hung, J Yoerger, DM Buonanno, F Demirjian, Z TI Percutaneous transcatheter closure of patent foramen ovale in patients with paradoxical embolism SO CIRCULATION LA English DT Meeting Abstract CT American-Heart-Association Abstracts From Scientific Sessions CY NOV 17-20, 2002 CL CHICAGO, ILLINOIS SP Amer Heart Assoc C1 Massachusetts Gen Hosp, Boston, MA 02114 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 0009-7322 J9 CIRCULATION JI Circulation PD NOV 5 PY 2002 VL 106 IS 19 SU S MA 3060 BP 619 EP 620 PG 2 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 613QJ UT WOS:000179142703099 ER PT J AU Olshansky, B Warner, A Solomon, A Sharma, A Platia, E O'Neill, G Feld, G Rosenfeld, L Akiyama, T Brodsky, M Ingalls, S Greene, HL AF Olshansky, B Warner, A Solomon, A Sharma, A Platia, E O'Neill, G Feld, G Rosenfeld, L Akiyama, T Brodsky, M Ingalls, S Greene, HL CA NHLBI AFFIRM Investigators TI Rate control in atrial fibrillation: A substudy of the AFFIRM trial SO CIRCULATION LA English DT Meeting Abstract CT American-Heart-Association Abstracts From Scientific Sessions CY NOV 17-20, 2002 CL CHICAGO, ILLINOIS SP Amer Heart Assoc C1 Univ Iowa, Iowa City, IA USA. VA Greater Los Angeles Hlth Care Syst, Los Angeles, CA USA. Georgetown Univ, Med Ctr, Washington, DC 20007 USA. Reg Cardiol Assoc, Med Grp, Sacramento, CA USA. Washington Hosp Ctr, Washington, DC 20010 USA. Univ Calif Davis, Sacramento, CA 95817 USA. Univ Calif Davis, Sacramento, CA 95817 USA. Mercy Gen Hosp, Sacramento, CA USA. Univ Calif San Diego, Med Ctr, San Diego, CA 92103 USA. Yale Univ, Sch Med, New Haven, CT USA. Univ Rochester, Med Ctr, Rochester, NY 14642 USA. Univ Calif Irvine, Irvine Med Ctr, Orange, CA 92668 USA. Axio Res Corp, Seattle, WA USA. NHLBI, AFFIRM Investigators, Bethesda, MD 20892 USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0009-7322 J9 CIRCULATION JI Circulation PD NOV 5 PY 2002 VL 106 IS 19 SU S MA 3125 BP 633 EP 634 PG 2 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 613QJ UT WOS:000179142703164 ER PT J AU Holmvang, G Witzke, CF Wetzel, C Inglessis, I Semigran, M Dec, GW Palacios, IF AF Holmvang, G Witzke, CF Wetzel, C Inglessis, I Semigran, M Dec, GW Palacios, IF TI Regional gadolinium-enhanced MRI analysis identifies patients with acute myocarditis SO CIRCULATION LA English DT Meeting Abstract CT American-Heart-Association Abstracts From Scientific Sessions CY NOV 17-20, 2002 CL CHICAGO, ILLINOIS SP Amer Heart Assoc C1 Massachusetts Gen Hosp, Boston, MA 02114 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 0009-7322 J9 CIRCULATION JI Circulation PD NOV 5 PY 2002 VL 106 IS 19 SU S MA 3220 BP 653 EP 653 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 613QJ UT WOS:000179142703259 ER PT J AU MacNeill, BD Shaw, JA Yabushita, H DeJoseph, D Kaufman, C Tearney, GJ Bouma, BE Dart, AM Mizuno, K Jang, IK AF MacNeill, BD Shaw, JA Yabushita, H DeJoseph, D Kaufman, C Tearney, GJ Bouma, BE Dart, AM Mizuno, K Jang, IK TI Lipid rich plaques display greater vessel distensibility than fibrous plaques: A combined optical coherence tomography and intravascular ultrasound study SO CIRCULATION LA English DT Meeting Abstract CT American-Heart-Association Abstracts From Scientific Sessions CY NOV 17-20, 2002 CL CHICAGO, ILLINOIS SP Amer Heart Assoc C1 Massachusetts Gen Hosp, Boston, MA 02114 USA. Baker Med Res Inst, Melbourne, Vic, Australia. NR 0 TC 1 Z9 1 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0009-7322 J9 CIRCULATION JI Circulation PD NOV 5 PY 2002 VL 106 IS 19 SU S MA 3237 BP 656 EP 656 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 613QJ UT WOS:000179142703276 ER PT J AU Tearney, GJ Yabushita, H Houser, SL Aretz, HT Jang, IK Schlendorf, KH Kauffman, CR Shishkov, M Halpern, EF Bouma, BE AF Tearney, GJ Yabushita, H Houser, SL Aretz, HT Jang, IK Schlendorf, KH Kauffman, CR Shishkov, M Halpern, EF Bouma, BE TI Optical coherence tomography is capable of quantifying macrophage content in atherosclerotic plaque fibrous caps SO CIRCULATION LA English DT Meeting Abstract CT American-Heart-Association Abstracts From Scientific Sessions CY NOV 17-20, 2002 CL CHICAGO, ILLINOIS SP Amer Heart Assoc C1 Massachusetts Gen Hosp, Boston, MA 02114 USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0009-7322 J9 CIRCULATION JI Circulation PD NOV 5 PY 2002 VL 106 IS 19 SU S MA 3238 BP 656 EP 656 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 613QJ UT WOS:000179142703277 ER PT J AU Jang, IK MacNeill, B Yabushita, H DeJoseph, D Kaufman, CR Bouma, BE Tearney, GJ AF Jang, IK MacNeill, B Yabushita, H DeJoseph, D Kaufman, CR Bouma, BE Tearney, GJ TI In-vivo visualization of coronary plaques in patients with non-ST elevation myocardial infarction/unstable angina using optical coherence tomography SO CIRCULATION LA English DT Meeting Abstract CT American-Heart-Association Abstracts From Scientific Sessions CY NOV 17-20, 2002 CL CHICAGO, ILLINOIS SP Amer Heart Assoc C1 Massachusetts Gen Hosp, Boston, MA 02114 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 0009-7322 J9 CIRCULATION JI Circulation PD NOV 5 PY 2002 VL 106 IS 19 SU S MA 3239 BP 657 EP 657 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 613QJ UT WOS:000179142703278 ER PT J AU Yabushita, H Bouma, BE Houser, SL Aretz, HT Jang, IK Kauffman, CR Schlendorf, KH Shishkov, M Halpern, EF Tearney, GJ AF Yabushita, H Bouma, BE Houser, SL Aretz, HT Jang, IK Kauffman, CR Schlendorf, KH Shishkov, M Halpern, EF Tearney, GJ TI Optical coherence tomography accurately identifies atherosclerotic plaque type SO CIRCULATION LA English DT Meeting Abstract CT American-Heart-Association Abstracts From Scientific Sessions CY NOV 17-20, 2002 CL CHICAGO, ILLINOIS SP Amer Heart Assoc C1 Massachusetts Gen Hosp, Boston, MA 02114 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 0009-7322 J9 CIRCULATION JI Circulation PD NOV 5 PY 2002 VL 106 IS 19 SU S MA 3240 BP 657 EP 657 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 613QJ UT WOS:000179142703279 ER PT J AU James, D Murphy, SA Wong, GG Morrow, DA Antman, EM McCabe, CH Marble, SJ Markovic, R Gibson, CM AF James, D Murphy, SA Wong, GG Morrow, DA Antman, EM McCabe, CH Marble, SJ Markovic, R Gibson, CM TI Increased AHA lesion complexity following thrombolytic administration is associated with mortality in ST elevation myocardial infarction SO CIRCULATION LA English DT Meeting Abstract CT American-Heart-Association Abstracts From Scientific Sessions CY NOV 17-20, 2002 CL CHICAGO, ILLINOIS SP Amer Heart Assoc C1 TIMI Study Grp, Boston, MA USA. Brigham & Womens Hosp, Boston, MA 02115 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 0009-7322 J9 CIRCULATION JI Circulation PD NOV 5 PY 2002 VL 106 IS 19 SU S MA 3256 BP 660 EP 660 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 613QJ UT WOS:000179142703295 ER PT J AU Murphy, SA Antman, EM McCabe, CH Wong, GC James, D Marble, SJ Kraimer, N Gibson, CM AF Murphy, SA Antman, EM McCabe, CH Wong, GC James, D Marble, SJ Kraimer, N Gibson, CM TI Rescue or adjunctive PCI of the culprit artery after lytic administration is associated with improvement in epicardial flow in the non-culprit artery SO CIRCULATION LA English DT Meeting Abstract CT American-Heart-Association Abstracts From Scientific Sessions CY NOV 17-20, 2002 CL CHICAGO, ILLINOIS SP Amer Heart Assoc C1 TIMI Study Grp, Boston, MA USA. Brigham & Womens Hosp, Boston, MA 02115 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 0009-7322 J9 CIRCULATION JI Circulation PD NOV 5 PY 2002 VL 106 IS 19 SU S MA 3255 BP 660 EP 660 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 613QJ UT WOS:000179142703294 ER PT J AU Gilon, D Mehta, RH Oh, JK Januzzi, JL Bossone, E Cooper, JV Smith, DE Nienaber, CA Isselbacher, EM AF Gilon, D Mehta, RH Oh, JK Januzzi, JL Bossone, E Cooper, JV Smith, DE Nienaber, CA Isselbacher, EM TI Clinical characteristics and in-hospital outcomes of patients with cardiac tamponade complicating acute type A aortic dissection SO CIRCULATION LA English DT Meeting Abstract CT American-Heart-Association Abstracts From Scientific Sessions CY NOV 17-20, 2002 CL CHICAGO, ILLINOIS SP Amer Heart Assoc C1 Hadassah Univ Hosp, IL-91120 Jerusalem, Israel. Univ Michigan Hlth Syst, Ann Arbor, MI USA. Mayo Clin, Rochester, MN USA. Massachusetts Gen Hosp, Boston, MA 02114 USA. Inst Policlin San Donato, San Donato Milanese, Italy. Univ Rostock, Rostock, Germany. 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 0009-7322 J9 CIRCULATION JI Circulation PD NOV 5 PY 2002 VL 106 IS 19 SU S MA 3315 BP 672 EP 672 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 613QJ UT WOS:000179142703353 ER PT J AU Baruch, L Heywood, T Krum, H Anand, I Glazer, R Cohn, JN AF Baruch, L Heywood, T Krum, H Anand, I Glazer, R Cohn, JN TI Efficacy of valsartan in elderly heart failure patients in Val-HeFT SO CIRCULATION LA English DT Meeting Abstract CT American-Heart-Association Abstracts From Scientific Sessions CY NOV 17-20, 2002 CL CHICAGO, ILLINOIS SP Amer Heart Assoc C1 Bronx Vet Adm Med Ctr, Bronx, NY USA. Loma Linda Univ, Med Ctr, Loma Linda, CA USA. Monash Univ, Sch Med, Melbourne, Vic 3004, Australia. VA Med Ctr Cardiol, Minneapolis, MN USA. Novartis Pharmaceut Corp, E Hanover, NJ USA. Univ Minnesota, Minneapolis, MN 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 0009-7322 J9 CIRCULATION JI Circulation PD NOV 5 PY 2002 VL 106 IS 19 SU S MA 3379 BP 685 EP 685 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 613QJ UT WOS:000179142703417 ER PT J AU Jang, IK MacNeill, BD Yabushita, H DeJoseph, D Kauffman, CR Tearney, GJ Bouma, BE AF Jang, IK MacNeill, BD Yabushita, H DeJoseph, D Kauffman, CR Tearney, GJ Bouma, BE TI In-vivo characterization of coronary plaques in patients with ST elevation acute myocardial infarction using optical coherence tomography (OCT) SO CIRCULATION LA English DT Meeting Abstract CT American-Heart-Association Abstracts From Scientific Sessions CY NOV 17-20, 2002 CL CHICAGO, ILLINOIS SP Amer Heart Assoc C1 Massachusetts Gen Hosp, Boston, MA 02114 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 0009-7322 J9 CIRCULATION JI Circulation PD NOV 5 PY 2002 VL 106 IS 19 SU S MA 3440 BP 698 EP 698 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 613QJ UT WOS:000179142703478 ER PT J AU Giri, S Rosenfield, K Eisenhauer, AC Rocha-Singh, K Jaff, M Prpic, R Popma, JJ AF Giri, S Rosenfield, K Eisenhauer, AC Rocha-Singh, K Jaff, M Prpic, R Popma, JJ TI A study to evaluate the safety and effectiveness of renal artery stenting after failed angioplasty: Acute and follow up results at quantitative renal angiography in the ASPIRE2 trial SO CIRCULATION LA English DT Meeting Abstract CT American-Heart-Association Abstracts From Scientific Sessions CY NOV 17-20, 2002 CL CHICAGO, ILLINOIS SP Amer Heart Assoc C1 Brigham & Womens Hosp, Boston, MA 02115 USA. Massachusetts Gen Hosp, Boston, MA 02114 USA. St Johns Hosp, Springfield, IL USA. Washington Hosp Ctr, Washington, DC 20010 USA. Harvard Clin Res Inst, Boston, MA USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0009-7322 J9 CIRCULATION JI Circulation PD NOV 5 PY 2002 VL 106 IS 19 SU S MA 3522 BP 714 EP 714 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 613QJ UT WOS:000179142703559 ER PT J AU Hylek, EM Go, AS Chang, YC Phillips, KA Henault, LE Capra, AM Jensvold, NG Selby, JV Singer, DE AF Hylek, EM Go, AS Chang, YC Phillips, KA Henault, LE Capra, AM Jensvold, NG Selby, JV Singer, DE TI Predictors of warfarin use post stroke in atrial fibrillation: The AnTicoagulation and risk factors in atrial fibrillation (ATRIA) study SO CIRCULATION LA English DT Meeting Abstract CT American-Heart-Association Abstracts From Scientific Sessions CY NOV 17-20, 2002 CL CHICAGO, ILLINOIS SP Amer Heart Assoc C1 Kaiser Permanente No CA, Oakland, CA USA. Massachusetts Gen Hosp, Boston, MA 02114 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 0009-7322 J9 CIRCULATION JI Circulation PD NOV 5 PY 2002 VL 106 IS 19 SU S MA 3586 BP 727 EP 728 PG 2 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 613QJ UT WOS:000179142703622 ER PT J AU Hylek, EM Regan, S McClelland, R Stewart, S Kopecky, SL AF Hylek, EM Regan, S McClelland, R Stewart, S Kopecky, SL TI Quality of anticoagulation control across age and indication among community-based practices in the United States: The anticoagulation consortium to improve outcomes nationally (ACTION) study SO CIRCULATION LA English DT Meeting Abstract CT American-Heart-Association Abstracts From Scientific Sessions CY NOV 17-20, 2002 CL CHICAGO, ILLINOIS SP Amer Heart Assoc C1 Massachusetts Gen Hosp, Boston, MA 02114 USA. Mayo Clin, Rochester, MN USA. McKesson HBOC Bioserv, Rockville, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0009-7322 J9 CIRCULATION JI Circulation PD NOV 5 PY 2002 VL 106 IS 19 SU S MA 3587 BP 728 EP 728 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 613QJ UT WOS:000179142703623 ER PT J AU Chen, EW Canto, JG Parsons, LS Every, NR Barron, HV AF Chen, EW Canto, JG Parsons, LS Every, NR Barron, HV TI Hospital variation of short term mortality following acute ST elevation myocardial infarction in the United States SO CIRCULATION LA English DT Meeting Abstract CT American-Heart-Association Abstracts From Scientific Sessions CY NOV 17-20, 2002 CL CHICAGO, ILLINOIS SP Amer Heart Assoc C1 Univ Calif San Francisco, San Francisco, CA 94143 USA. Univ Alabama, Birmingham, AL USA. Ovat Res Grp, Seattle, WA USA. VA Puget Sound Healthcare Syst, Seattle, WA USA. Univ Washington, Seattle, WA 98195 USA. Genentech Inc, San Francisco, CA 94080 USA. Univ Calif San Francisco, San Francisco, CA 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 0009-7322 J9 CIRCULATION JI Circulation PD NOV 5 PY 2002 VL 106 IS 19 SU S MA 3701 BP 753 EP 753 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 613QJ UT WOS:000179142703737 ER PT J AU Allen, LA O'Donnell, CJ Giugliano, RP Camargo, CA Lloyd-Jones, DM AF Allen, LA O'Donnell, CJ Giugliano, RP Camargo, CA Lloyd-Jones, DM TI Unstable angina guideline concordance predicts decreased mortality up to ten-years after hospitalization SO CIRCULATION LA English DT Meeting Abstract CT American-Heart-Association Abstracts From Scientific Sessions CY NOV 17-20, 2002 CL CHICAGO, ILLINOIS SP Amer Heart Assoc C1 Massachusetts Gen Hosp, Boston, MA 02114 USA. Brigham & Womens Hosp, Boston, MA 02115 USA. RI Lloyd-Jones, Donald/C-5899-2009 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 0009-7322 J9 CIRCULATION JI Circulation PD NOV 5 PY 2002 VL 106 IS 19 SU S MA 3743 BP 762 EP 762 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 613QJ UT WOS:000179142703779 ER PT J AU Chen, EW Canto, JG Parsons, LS Littrell, KA Every, NR Hochman, JS Ohman, EM Cheeks, M Barron, HV AF Chen, EW Canto, JG Parsons, LS Littrell, KA Every, NR Hochman, JS Ohman, EM Cheeks, M Barron, HV TI High hospital intra-aortic balloon counterpulsation volume is associated with lower mortality in acute myocardial infarction complicated by cardiogenic shook SO CIRCULATION LA English DT Meeting Abstract CT American-Heart-Association Abstracts From Scientific Sessions CY NOV 17-20, 2002 CL CHICAGO, ILLINOIS SP Amer Heart Assoc C1 Univ Calif San Francisco, San Francisco, CA 94143 USA. Univ Alabama, Birmingham, AL USA. Ovat Res Grp, Seattle, WA USA. Genentech Inc, San Francisco, CA 94080 USA. VA Puget Sound Healthcare Syst, Seattle, WA USA. Univ Washington, Seattle, WA 98195 USA. St Lukes Roosevelt Hosp, New York, NY USA. Columbia Univ, New York, NY USA. Univ N Carolina, Chapel Hill, NC USA. Univ Calif San Francisco, San Francisco, CA 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 0009-7322 J9 CIRCULATION JI Circulation PD NOV 5 PY 2002 VL 106 IS 19 SU S MA 3742 BP 762 EP 762 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 613QJ UT WOS:000179142703778 ER PT J AU Sonel, AF Good, CB Kelley, ME Wall, L Whittle, J AF Sonel, AF Good, CB Kelley, ME Wall, L Whittle, J TI What do borderline troponin elevations imply and do we listen? SO CIRCULATION LA English DT Meeting Abstract CT American-Heart-Association Abstracts From Scientific Sessions CY NOV 17-20, 2002 CL CHICAGO, ILLINOIS SP Amer Heart Assoc C1 VA Pittsburgh Healthcare Syst, Ctr Hlth Equity Res & Promot, Pittsburgh, PA USA. Univ Kansas, Kansas City, KS 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 0009-7322 J9 CIRCULATION JI Circulation PD NOV 5 PY 2002 VL 106 IS 19 SU S MA 3740 BP 762 EP 762 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 613QJ UT WOS:000179142703776 ER PT J AU Chen, EW Canto, JG Parsons, LS Every, NR Barron, HV AF Chen, EW Canto, JG Parsons, LS Every, NR Barron, HV TI Hospital variation of short-term mortality after acute ST-segment elevation myocardial infarction in the United States SO CIRCULATION LA English DT Meeting Abstract CT American-Heart-Association Abstracts From Scientific Sessions CY NOV 17-20, 2002 CL CHICAGO, ILLINOIS SP Amer Heart Assoc C1 Univ Calif San Francisco, San Francisco, CA 94143 USA. Univ Alabama, Birmingham, AL USA. Ovat Res Grp, Seattle, WA USA. VA Puget Sound Healthcare Syst, Seattle, WA USA. Univ Washington, Seattle, WA 98195 USA. Genentech Inc, San Francisco, CA 94080 USA. Univ Calif San Francisco, San Francisco, CA 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 0009-7322 J9 CIRCULATION JI Circulation PD NOV 5 PY 2002 VL 106 IS 19 SU S BP R EP R PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 613QJ UT WOS:000179142700028 ER PT J AU Ellinor, PT Yoerger, DM McGovern, BA Fishman, MC Ruskin, JN MacRae, CA AF Ellinor, PT Yoerger, DM McGovern, BA Fishman, MC Ruskin, JN MacRae, CA TI Familial aggregation in patients with lone atrial fibrillation SO CIRCULATION LA English DT Meeting Abstract CT American-Heart-Association Abstracts From Scientific Sessions CY NOV 17-20, 2002 CL CHICAGO, ILLINOIS SP Amer Heart Assoc C1 Massachusetts Gen Hosp, Boston, MA 02114 USA. Massachusetts Gen Hosp, Charlestown, MA 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 0009-7322 J9 CIRCULATION JI Circulation PD NOV 5 PY 2002 VL 106 IS 19 SU S BP U EP V PG 2 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 613QJ UT WOS:000179142700037 ER PT J AU Heller, S AF Heller, S TI Molecular screens for inner ear genes SO JOURNAL OF NEUROBIOLOGY LA English DT Article DE molecular screens; inner ear genes; hearing and balance ID CDNA LIBRARY; COCHLEAR GENE; NONSYNDROMIC DEAFNESS; EXPRESSION ANALYSIS; MAMMALIAN COCHLEA; CANDIDATE GENES; HAIR-CELLS; IDENTIFICATION; PROTEIN; CLONING AB Identification of the genes that encode proteins that are important for proper function of specific inner ear cell types is central to our understanding of the molecular basis of hearing and balance. Whereas the combination of electrophysiology and biophysics has resulted in an exquisite understanding of inner ear function, little is known about the proteins that confer these properties at the cellular level. Furthermore, the genes that control inner ear development, susceptibility to wear and tear, regeneration from damage, and age-related degeneration, are largely unknown. This review discusses tools that have been developed during the past few years to address this imbalance between a thorough physiologic characterization of inner ear function and a detailed understanding at a molecular level of the proteins involved in these functions. Creation of inner ear cDNA libraries has laid the foundation for the discovery of genes that are specifically expressed by cell types of the inner ear and that encode proteins that are important for molecular processes in these cells. In conjunction with expressed sequence tag database analysis, cDNA subtraction, and DNA arrays, functionally important genes, whose specific expression patterns are usually verified by gene expression analysis, can be identified. Discussion of these techniques takes into account the specific characteristics of the inner ear in relation to its study using molecular biological approaches.) (C) 2002 Wiley Periodicals, Inc. J Neurobiol 53: 265-275, 2002. C1 Harvard Univ, Sch Med, Dept Otolaryngol, Boston, MA 02114 USA. Harvard Univ, Sch Med, Neurosci Program, Boston, MA 02114 USA. RP Heller, S (reprint author), Massachusetts Eye & Ear Infirm, 243 Charles St, Boston, MA 02114 USA. FU NIDCD NIH HHS [DC00317, DC04563] NR 41 TC 12 Z9 13 U1 0 U2 0 PU JOHN WILEY & SONS INC PI HOBOKEN PA 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 0022-3034 J9 J NEUROBIOL JI J. Neurobiol. PD NOV 5 PY 2002 VL 53 IS 2 BP 265 EP 275 DI 10.1002/neu.10122 PG 11 WC Neurosciences SC Neurosciences & Neurology GA 608KZ UT WOS:000178846600012 PM 12382280 ER PT J AU Chen, ZY Corey, DP AF Chen, ZY Corey, DP TI Understanding inner ear development with gene expression profiling SO JOURNAL OF NEUROBIOLOGY LA English DT Article DE inner ear development; gene expression profiling; human and mouse genome projects ID HAIR-CELLS; SACCHAROMYCES-CEREVISIAE; CANDIDATE GENES; IDENTIFICATION; GENOME; LOCALIZATION; COLLAGEN; DISEASE; PROTEIN; DIFFERENTIATION AB Understanding the development of the inner ear requires knowing the spatial and temporal pattern of gene expression, and the functions of those gene products. In the last decade, hearing research has benefited tremendously from the progress of the human and mouse genome projects, as amply illustrated by the identification of many deafness genes in both human and mouse. However, the sheer amount of information generated from the genome project has far outpaced the rate at which it is utilized. Microarray technology offers " means to quantify the expression level of transcripts at " whole-genome scale. Cross-tissue comparisons will identify genes unique to the inner ear, which will expedite the identification of new deafness genes. Microdissection and subtraction after ablation of cell types can reveal genes expressed in certain cells, such as hair cells. Expression profiling of both inner ear and other tissues, under a variety of conditions (such as during development, with drug treatment or in knock-out animals), can be used for cluster analysis to group genes of similar expression. Coexpression can suggest functional pathways and interactions between known genes, and can identify new genes in a structure or pathway. In this review we give examples for both transcription factors and cochlear structures. (C) 2002 Wiley Periodicals, Inc. J Neurobiol 53: 276-285, 2002. C1 Harvard Univ, Sch Med, Dept Neurobiol, Boston, MA 02115 USA. Harvard Univ, Sch Med, Dept Neurol, Boston, MA 02115 USA. Massachusetts Gen Hosp, Neurol Serv, Boston, MA 02114 USA. Howard Hughes Med Inst, Chevy Chase, MD 20815 USA. RP Corey, DP (reprint author), Harvard Univ, Sch Med, Dept Neurobiol, Boston, MA 02115 USA. OI Corey, David/0000-0003-4497-6016 NR 52 TC 15 Z9 20 U1 0 U2 0 PU JOHN WILEY & SONS INC PI HOBOKEN PA 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 0022-3034 J9 J NEUROBIOL JI J. Neurobiol. PD NOV 5 PY 2002 VL 53 IS 2 BP 276 EP 285 DI 10.1002/neu.10125 PG 10 WC Neurosciences SC Neurosciences & Neurology GA 608KZ UT WOS:000178846600013 PM 12382281 ER PT J AU Barrington, RA Pozdnyakova, O Zafari, MR Benjamin, CD Carroll, MC AF Barrington, RA Pozdnyakova, O Zafari, MR Benjamin, CD Carroll, MC TI B lymphocyte memory: Role of stromal cell complement and Fc gamma RIIB receptors SO JOURNAL OF EXPERIMENTAL MEDICINE LA English DT Article DE B lymphocytes; memory; complement receptors; Fc gamma RIIB; follicular dendritic cells ID FOLLICULAR DENDRITIC CELLS; PRIMARY IMMUNE-RESPONSE; LIVED PLASMA-CELLS; AFFINITY MATURATION; GERMINAL-CENTERS; DEFICIENT MICE; IMMUNOLOGICAL MEMORY; CLONAL SELECTION; ANTIGEN-DRIVEN; CR2(-/-) MICE AB To dissect the influence of CD21/CD35 and FcgammaRIIB in antigen retention and Immoral memory, we used an adoptive transfer model in which antigen-primed B and T lymphocytes were given to sublethally irradiated wild-type mice or mice deficient in CD21/CD35 (Cr2(-/-)) or FcgammaRIIB receptors (FcgammaRIIB(-/-)). Cr2(-/-) chimeras showed impaired memory as characterized by a decrease in antibody titer, reduced frequency of antibody secreting cells, an absence of affinity maturation, and significantly reduced recall response. The impaired memory in Cr2(-/-) chimeras corresponded with the reduced frequency of antigen-specific memory B cells. Interestingly, FcgammaRIIB(-/-) chimeras showed a differential phenotype with impaired splenic but normal bone marrow responses. These data suggest that CD21/CD35 on stroma, including follicular dendritic cells, is critical to the maintenance of long-term B lymphocyte memory. C1 Harvard Univ, Sch Med, Ctr Blood Res, Boston, MA 02115 USA. Harvard Univ, Dept Pathol, Boston, MA 02115 USA. Biogen Inc, Cambridge, MA 02142 USA. RP Carroll, MC (reprint author), Harvard Univ, Sch Med, Ctr Blood Res, LMRC 502,221 Longwood Ave, Boston, MA 02115 USA. FU PHS HHS [A139246] NR 48 TC 91 Z9 93 U1 0 U2 3 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 1114 FIRST AVE, 4TH FL, NEW YORK, NY 10021 USA SN 0022-1007 J9 J EXP MED JI J. Exp. Med. PD NOV 4 PY 2002 VL 196 IS 9 BP 1189 EP 1199 DI 10.1084/jem.20021110 PG 11 WC Immunology; Medicine, Research & Experimental SC Immunology; Research & Experimental Medicine GA 613VC UT WOS:000179151300007 PM 12417629 ER PT J AU Magid, DJ Rhodes, KV Asplin, BR Steiner, JF Rumsfeld, JS AF Magid, DJ Rhodes, KV Asplin, BR Steiner, JF Rumsfeld, JS TI Designing a research agenda to improve the quality of emergency care SO ACADEMIC EMERGENCY MEDICINE LA English DT Article; Proceedings Paper CT AEM Consensus Conference on Assuring Quality CY MAY, 2002 CL ST LOUIS, MISSOURI DE quality; emergency medicine; research ID ACUTE MYOCARDIAL-INFARCTION; THROMBOLYTIC THERAPY; ADVERSE EVENTS; PROSPECTIVE VALIDATION; IMMEDIATE ANGIOPLASTY; HOSPITALIZED-PATIENTS; CORONARY ANGIOPLASTY; MEDICARE PATIENTS; CLINICAL-TRIAL; RULE AB A systematic approach to develop a research agenda for improving the quality of emergency care is presented. This approach is based on the six domains of quality outlined by the Institute of Medicine (effective, timely, efficient, safe, patient-centered, and equitable care) and a sequence of four research steps (evidence, synthesis, assessment, and intervention). Examples related to the care of patients with acute myocardial infarction are used to illustrate the proposed approach. Examples of other emergency medicine research topics relevant to the Institute of Medicine quality domains are also presented. Research to improve the quality of emergency care can benefit from a more systematic consideration of the domains of quality and the research steps necessary to generate evidence and inform quality improvement efforts in practice. C1 Colorado Permanente Med Grp, Clin Res Unit, Denver, CO USA. Univ Colorado, Hlth Sci Ctr, Denver, CO 80202 USA. Univ Chicago, Chicago, IL 60637 USA. Reg Hosp, St Paul, MN USA. Hlth Partners Res Fdn, St Paul, MN USA. Colorado Hlth Outcomes Program, Denver, CO USA. Denver VA Med Ctr, Denver, CO USA. RP Magid, DJ (reprint author), Colorado Permanente Clin Res Unit, POB 378066, Denver, CO 80237 USA. NR 63 TC 6 Z9 6 U1 0 U2 1 PU HANLEY & BELFUS INC PI PHILADELPHIA PA 210 S 13TH ST, PHILADELPHIA, PA 19107 USA SN 1069-6563 J9 ACAD EMERG MED JI Acad. Emerg. Med. PD NOV PY 2002 VL 9 IS 11 BP 1124 EP 1130 DI 10.1111/j.1553-2712.2002.tb01566.x PG 7 WC Emergency Medicine SC Emergency Medicine GA 614RC UT WOS:000179203100011 PM 12414460 ER PT J AU Mazor, KM Campbell, EG Field, T Purwono, U Peterson, D Lockwood, JH Weissman, JS Gurwitz, JH AF Mazor, KM Campbell, EG Field, T Purwono, U Peterson, D Lockwood, JH Weissman, JS Gurwitz, JH TI Managed care education: What medical students are telling us SO ACADEMIC MEDICINE LA English DT Article ID PHYSICIANS VIEWS; VALIDITY; RATINGS; COMPETENCES; SCHOOLS; FACULTY; HMOS AB Purpose. To examine graduating medical students' perceptions of the adequacy of instruction in managed care and in 11 curricular content areas identified by experts as a necessary part of managed care education. This study sought to determine whether medical students perceived these content areas as relevant to managed care and to evaluate the extent to which students' perceptions of the adequacy of instruction varied as a function of managed care penetration in the locations of their respective medical schools. Method. Data from the Association of American Medical Colleges' 1999 Medical School Graduation Questionnaire (GQ) were analyzed. Students' ratings of adequacy of instruction were summarized. Correlations between ratings of instruction in managed care and 11 related content areas were calculated, as well as correlations between managed care penetration in the locations of the students' schools and the proportion of students rating instruction as inadequate. Results. A majority, of 1999 medical school graduates (60%) rated instruction in managed care as inadequate; other content areas to which majorities of graduates gave inadequate ratings were practice management (72%), quality assurance (57%), medical care cost control (57%), and cost-effective medical practice (56%). Ratings in these four content areas were highly correlated with ratings of instruction in managed care. The correlation between managed care penetration and rating of instruction in managed care was statistically significant (r = -.37); correlations between managed care penetration and instruction in the other content areas were not. Conclusions. On the 1999 GQ, a majority of medical students responded that they felt they had not received adequate instruction in managed care. Further, the responses suggest that these - medical students defined managed care in terms of managing costs, rather than managing health care, or developing population-based approaches to the delivery of health care. C1 Univ Massachusetts, Sch Med, Meyers Primary Care Inst, Fallon Healthcare Syst, Worcester, MA 01605 USA. Harvard Univ, Sch Med, Dept Med, Inst Hlth Policy, Boston, MA USA. Massachusetts Gen Hosp, Boston, MA 02114 USA. Assoc Amer Med Coll, Washington, DC USA. RP Mazor, KM (reprint author), Univ Massachusetts, Sch Med, Meyers Primary Care Inst, Fallon Healthcare Syst, 630 Plantat St, Worcester, MA 01605 USA. OI Purwono, Urip/0000-0002-6629-8300 NR 27 TC 6 Z9 6 U1 0 U2 0 PU HANLEY & BELFUS INC PI PHILADELPHIA PA 210 S 13TH ST, PHILADELPHIA, PA 19107 USA SN 1040-2446 J9 ACAD MED JI Acad. Med. PD NOV PY 2002 VL 77 IS 11 BP 1128 EP 1133 DI 10.1097/00001888-200211000-00015 PG 6 WC Education, Scientific Disciplines; Health Care Sciences & Services SC Education & Educational Research; Health Care Sciences & Services GA 617MR UT WOS:000179365900012 PM 12431927 ER PT J AU Beinfeld, MT Bosch, JL Gazelle, GS AF Beinfeld, MT Bosch, JL Gazelle, GS TI Hospital costs of uterine artery embolization and hysterectomy for uterine fibroid tumors SO ACADEMIC RADIOLOGY LA English DT Article DE arteries, chemotherapeutic embolization; arteries, uterine; economics, medical; uterine neoplasms, therapy; uterus, surgery ID LEIOMYOMATA AB Rationale and Objectives. The purpose of this study was to compare the total actual hospital costs of uterine artery embolization (UAE) and hysterectomy for treatment of uterine fibroid tumors and to evaluate factors that might influence cost. Materials and Methods. Total actual hospital costs were collected from the institution's cost accounting system on patients who underwent UAE (n = 57) or hysterectomy (n = 300) for uterine fibroids between 1998 and 2001. Electronic medical records were reviewed to collect clinical information. Standard statistical techniques were used to determine which factors influenced hospital costs. Results. The mean total actual hospital costs of UAE were significantly higher than hysterectomy ($8,223 vs $6,046, P < .0001), but the mean length of stay was shorter (0.95 vs 2.6 days, P < .0001). In linear regression analyses, complications were predictive of increased costs of UAE; length of stay, complications, and laparoscopic hysterectomy were predictive of increased costs of hysterectomy. Conclusion. Hospital costs of UAE were higher than hysterectomy for the treatment of uterine fibroids, but the hospital stays were shorter. C1 Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Radiol, Boston, MA USA. Harvard Univ, Sch Publ Hlth, Dept Hlth Policy & Management, Boston, MA 02115 USA. Erasmus Univ, Med Ctr, Dept Epidemiol & Biostat, Rotterdam, Netherlands. RP Gazelle, GS (reprint author), DATA Grp, Zero Emerson Pl,Ste 2H, Boston, MA 02114 USA. NR 13 TC 13 Z9 14 U1 0 U2 1 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 NOV PY 2002 VL 9 IS 11 BP 1300 EP 1304 DI 10.1016/S1076-6332(03)80563-9 PG 5 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA 611NB UT WOS:000179023000008 PM 12449362 ER PT J AU Hartmann, C Johnk, L Kitange, G Wu, YH Ashworth, LK Jenkins, RB Louis, DN AF Hartmann, C Johnk, L Kitange, G Wu, YH Ashworth, LK Jenkins, RB Louis, DN TI A In-Silico generated transcript map of the 3.7 Mb D19S112-D19S246 candidate tumor suppressor region on the long arm of chromosome 19 SO ACTA NEUROPATHOLOGICA LA English DT Meeting Abstract CT Joint Meeting of the Belgian-Dutch-and-German-Societies/47th Annual Meeting of the Deutsche-Gesellschaft-fur-Neuropathologie CY OCT 09-12, 2002 CL AACHEN, GERMANY SP Belgian Dutch & German Soc, Deutsch Gesell Neuropathol C1 Massachusetts Gen Hosp, Dept Pathol, Mol Neurooncol Lab, Boston, MA 02114 USA. Massachusetts Gen Hosp, Neurosurg Serv, Boston, MA 02114 USA. Harvard Univ, Sch Med, Boston, MA USA. Mayo Clin & Mayo Fdn, Div Lab Genet, Rochester, MN 55905 USA. Lawrence Livermore Natl Lab, Livermore, CA USA. DOE Joint Genome Inst, Walnut Creek, CA USA. Humboldt Univ, Charite, Inst Neuropathol, Berlin, Germany. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SPRINGER PI NEW YORK PA 233 SPRING STREET, NEW YORK, NY 10013 USA SN 0001-6322 J9 ACTA NEUROPATHOL JI Acta Neuropathol. PD NOV PY 2002 VL 104 IS 5 BP 553 EP 553 PG 1 WC Clinical Neurology; Neurosciences; Pathology SC Neurosciences & Neurology; Pathology GA 606TX UT WOS:000178750700060 ER PT J AU Freudenreich, O Goff, DC AF Freudenreich, O Goff, DC TI Antipsychotic combination therapy in schizophrenia. A review of efficacy and risks of current combinations SO ACTA PSYCHIATRICA SCANDINAVICA LA English DT Review DE antipsychotic agents; schizophrenia; treatment outcome; drug therapy combination ID CLOZAPINE-RISPERIDONE COMBINATION; TREATMENT-RESISTANT SCHIZOPHRENIA; D-2 RECEPTOR OCCUPANCY; REFRACTORY SCHIZOPHRENIA; PIMOZIDE AUGMENTATION; DOUBLE-BLIND; OLANZAPINE; POLYPHARMACY; DRUG; COMBINATION/AUGMENTATION AB Objective: To review the literature on efficacy and risks of combining antipsychotics (atypical with atypical or conventional) and suggest a rationale and strategies for future clinical trials. Method: A computerized Medline search supplemented by an examination of cross-references and reviews was performed. Results: Empirical evidence for the efficacy of combining antipsychotics is too limited to draw firm conclusions. The practice of augmenting clozapine with more 'tightly bound' D2 receptor antagonists as exemplified by risperidone augmentation of clozapine has some empirical and theoretical support. The risks of augmentation strategies have not been studied systematically. No study has examined the economic impact of combination treatment. Conclusions: Further trials of antipsychotic combination therapies are needed before this currently unsupported practice can be recommended. Rationales for combination treatment include a broadening of the range of receptor activity or an increase in D2 receptor occupancy with certain atypical agents. Trial methodology needs to take into account subject characteristics, duration of treatment, optimization of monotherapy comparators, and appropriate outcome measures. C1 Massachusetts Gen Hosp, Dept Psychiat, MGH Schizophrenia Program, Freedom Trail Clin, Boston, MA 02114 USA. Harvard Univ, Sch Med, Boston, MA USA. RP Freudenreich, O (reprint author), Massachusetts Gen Hosp, Dept Psychiat, MGH Schizophrenia Program, Freedom Trail Clin, 25 Staniford St,2nd Floor, Boston, MA 02114 USA. NR 51 TC 161 Z9 166 U1 2 U2 4 PU BLACKWELL MUNKSGAARD PI COPENHAGEN PA 35 NORRE SOGADE, PO BOX 2148, DK-1016 COPENHAGEN, DENMARK SN 0001-690X J9 ACTA PSYCHIAT SCAND JI Acta Psychiatr. Scand. PD NOV PY 2002 VL 106 IS 5 BP 323 EP 330 DI 10.1034/j.1600-0447.2002.01331.x PG 8 WC Psychiatry SC Psychiatry GA 600DU UT WOS:000178376000002 PM 12366465 ER PT J AU Blais, MA Matthews, J Lipkis-Orlando, R O'Keefe, SM Jacobo, M Rivas-Vazquez, RA Summergrad, P AF Blais, MA Matthews, J Lipkis-Orlando, R O'Keefe, SM Jacobo, M Rivas-Vazquez, RA Summergrad, P TI Development and application of a brief multi-faceted tool for evaluating inpatient psychiatric care SO ADMINISTRATION AND POLICY IN MENTAL HEALTH LA English DT Article DE inpatient care; patient satisfaction; program evaluation; treatment outcome ID PATIENT SATISFACTION; HEALTH-CARE; PHASE MODEL; PSYCHOTHERAPY; RELIABILITY; OUTCOMES; QUALITY; SCALE AB Increasingly, hospitals are expected to monitor and document service delivery variables, such as treatment outcome and patient satisfaction with care, which are thought to be associated with the quality of care received by patients. Documenting the patient's collaboration in the treatment-planning process also has become more important. However, for many clinically oriented units, translating these expectations into a useable instrument and an efficient measurement procedure is a complex and difficult task. This paper outlines the development of a brief multi-faceted program evaluation instrument and assessment process for completing these tasks. The authors describe the rationale behind their approach to these measurement issues, and they introduce an instrument capable of effectively measuring both outcome and satisfaction. They also provide an overview of how they apply the instrument in their inpatient psychiatry service. The strengths and weakness of this assessment strategy are reviewed. C1 Massachusetts Gen Hosp, Inpatient Psychiat Serv, Boston, MA 02114 USA. Neurol Ctr S Florida, Partners Psychiat & Mental Hlth, Miami, FL USA. RP Blais, MA (reprint author), Massachusetts Gen Hosp, Inpatient Psychiat Serv, Blake 2,55 Fruit St, Boston, MA 02114 USA. NR 29 TC 8 Z9 9 U1 1 U2 3 PU KLUWER ACADEMIC-HUMAN SCIENCES PRESS PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013-1578 USA SN 0894-587X J9 ADM POLICY MENT HLTH JI Adm. Policy. Ment. Health PD NOV PY 2002 VL 30 IS 2 BP 159 EP 172 DI 10.1023/A:1022537218940 PG 14 WC Health Policy & Services; Public, Environmental & Occupational Health SC Health Care Sciences & Services; Public, Environmental & Occupational Health GA 661DW UT WOS:000181876800005 PM 12680619 ER PT J AU Xiang, SH Doka, N Choudhary, RK Sodroski, J Robinson, JE AF Xiang, SH Doka, N Choudhary, RK Sodroski, J Robinson, JE TI Characterization of CD4-induced epitopes on the HIV type 1 gp120 envelope glycoprotein recognized by neutralizing human monoclonal antibodies SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Article ID HUMAN-IMMUNODEFICIENCY-VIRUS; PROGRAMMED CELL-DEATH; CONFORMATIONAL-CHANGES; CHEMOKINE RECEPTORS; VARIABLE LOOPS; BINDING; CD4; INFECTION; CCR5; ENTRY AB The entry of human immunodeficiency virus (HIV-1) into target cells typically requires the sequential binding of the viral exterior envelope glycoprotein, gp120, to CD4 and a chemokine receptor. CD4 binding exposes gp120 epitopes recognized by CD4-induced (CD4i) antibodies, which can block virus binding to the chemokine receptor. We identified three new CD4i antibodies from an HIV-1-infected individual and localized their epitopes. These epitopes include a highly conserved gp120 beta-strand encompassing residues 419-424, which is also important for binding to the CCR5 chemokine receptor. All of the CD4i antibodies inhibited the binding of gp120-CD4 complexes to CCR5. CD4i antibodies and CD4 reciprocally induced each other's binding, suggesting that these ligands recognize a similar gp120 conformation. The CD4i antibodies neutralized laboratory-adapted HIV-1 isolates; primary isolates were more resistant to neutralization by these antibodies. Thus, all known CD4i antibodies recognize a common, conserved gp120 element overlapping the binding site for the CCR5 chemokine receptor. C1 Tulane Univ, Med Ctr, Dept Pediat, New Orleans, LA 70012 USA. Dana Farber Canc Inst, Dept Canc Immunol & AIDS, Boston, MA 02115 USA. Harvard Univ, Sch Med, Dept Pathol, Div AIDS, Boston, MA 02115 USA. Harvard Univ, Sch Publ Hlth, Dept Immunol & Infect Dis, Boston, MA 02115 USA. RP Robinson, JE (reprint author), Tulane Univ, Med Ctr, Dept Pediat, 1430 Tulane Ave, New Orleans, LA 70012 USA. FU NIAID NIH HHS [AI24030, AI24755, AI31783, AI41851, AI42848, AI46725] NR 51 TC 108 Z9 111 U1 0 U2 1 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 USA SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD NOV 1 PY 2002 VL 18 IS 16 BP 1207 EP 1217 DI 10.1089/08892220260387959 PG 11 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA 612FD UT WOS:000179063100006 PM 12487827 ER PT J AU Kemper, KJ Highfield, ES McLellan, M Ott, MJ Dvorkin, L Whelan, JS AF Kemper, KJ Highfield, ES McLellan, M Ott, MJ Dvorkin, L Whelan, JS TI Pediatric faculty development in integrative medicine SO ALTERNATIVE THERAPIES IN HEALTH AND MEDICINE LA English DT Article; Proceedings Paper CT Annual Meeting of the Pediatric-Academic-Societies CY MAY 04-07, 2002 CL BALTIMORE, MARYLAND SP Pediatr Acad Soc ID COMPLEMENTARY MEDICINE; HOLISTIC PEDIATRICS; ACUPUNCTURE; THERAPIES; ABC AB As more patients use complementary and alternative medical (CAM) therapies, faculty may he asked to teach trainees about topics requiring faculty development training. Our purpose in this study was to evaluate qualitatively and quantitatively a new faculty development program covering 4 key areas of CAM: herbs and dietary supplements, mind-body therapies, massage, and acupuncture. Faculty members (N = 6) volunteered for the program and were included in the study if they completed at least 3 of the 6 scheduled sessions. For each session, participants completed a pretest evaluating their knowledge and confidence about the topic, then they received background reading and focused discussion questions, Each session was a case-based, experiential seminar led by an expert in the content area. Participants completed post-session questionnaires measuring knowledge, confidence, and communication practices at the end of each session and at the end of the series of seminars. They also were asked for feedback and suggestions for the following year. All participants strongly agreed that they gained important knowledge; scores on tests about herbs increased from 62% at baseline to 84% at completion, and scores on knowledge of acupuncture increased from 60% before the session to 98% after. All participants strongly agreed that their confidence in talking with patients, colleagues, and trainees improved; on average, confidence scores improved an average of 1.8 out of a total of 5 possible points for all topics. Participants more frequently asked patients about their use of herbs (from 50% at baseline to 75% at the end) and increased the percentage of training encounters in which they discussed CAM with trainees or colleagues from 10% to 25%. We concluded that faculty development in integrative medicine is feasible and results in qualitative and quantitative improvements in knowledge, confidence, and clinical and teaching behaviors. C1 Wake Forest Univ, Sch Med, Winston Salem, NC 27109 USA. Childrens Hosp, Ctr Holist Pediat Educ & Res, Massage Program, Boston, MA 02115 USA. Dana Farber Canc Inst, Program Pain Symptom Management, Boston, MA 02115 USA. Massachusetts Coll Pharm & Allied Hlth Sci, Boston, MA USA. Massachusetts Gen Hosp, Consumer Hlth Reference Ctr, Boston, MA 02114 USA. RP Kemper, KJ (reprint author), Wake Forest Univ, Sch Med, Winston Salem, NC 27109 USA. FU NCCIH NIH HHS [R25 AT00538] NR 21 TC 10 Z9 10 U1 0 U2 0 PU INNOVISION COMMUNICATIONS PI ALISO VIEJO PA 101 COLUMBIA, ALISO VIEJO, CA 92656 USA SN 1078-6791 J9 ALTERN THER HEALTH M JI Altern. Ther. Health Med. PD NOV-DEC PY 2002 VL 8 IS 6 BP 70 EP 73 PG 4 WC Integrative & Complementary Medicine SC Integrative & Complementary Medicine GA 615TY UT WOS:000179264000011 PM 12440841 ER PT J AU Cooper, HA de Lemos, JA Morrow, DA Sabatine, MS Murphy, SA McCabe, CH Gibson, CM Antman, EM Braunwald, E AF Cooper, HA de Lemos, JA Morrow, DA Sabatine, MS Murphy, SA McCabe, CH Gibson, CM Antman, EM Braunwald, E TI Minimal ST-segment deviation: A simple, noninvasive method for identifying patients with a patent infarction-related artery after fibrinolytic administration SO AMERICAN HEART JOURNAL LA English DT Article ID ACUTE MYOCARDIAL-INFARCTION; THROMBOLYTIC THERAPY; ELEVATION RESOLUTION; RESCUE ANGIOPLASTY; RANDOMIZED TRIAL; STRONG PREDICTOR; EXTENT; IMMEDIATE; FLOW; REPERFUSION AB Background Because rescue intervention may improve the outcome of patients who fail to achieve epicardial reperfusion after fibrinolytic administration for acute ST-elevation myocardial infarction (STEMI), simple noninvasive measures of infarction-related. artery (IRA) potency are needed: The sum of ST-segment resolution (sum-STRES) has a high positive predictive value (PPV) for a patent IRA, but is quite time-consuming. Methods We retrospectively developed a very simple assessment that requires only the measurement of ST-segment deviation in a single electrocardiographic lead on a single electrocardiogram (ECG) 90 minutes after fibrinolytic administration. The ECG obtained immediately before fibrinolytic administration was reviewed as a means of selecting the single, lead with the greatest ST-segment deviation. The absolute magnitude of ST deviation was measured in this lead on the. 90-minute ECG. Minimal ST-segment deviation (MSTD) was defined as less than or equal to1 mm ST deviation for inferior infarctions and less than or equal to2 mm ST deviation for anterior infarctions. We compared the predictive value of this method with established but more complex ECG methods using data from the Thrombolysis In Myocardial Infarction (TIMI) 14 trial of low-dose fibrinolytic with full-dose glycoprotein IIb/IIIa inhibition. Results of the 604 patients with an evaluable ECG and angiographic data, 383 (63%) had MSTD. The presence of MSTD had a positive predictive value (PPV) of 91% for a patent IRA (TIMI flow grade 2 or 3). Results were similar for inferior; and anterior infarctions. MSTD was a means of identifying 90% of patients with complete sum-STRES. The PPV of MSTD compared favorably with that of standard measures of ST-segment resolution, but it required only a few seconds to perform. Conclusions The presence of MSTD at 90 minutes after fibrinolytic administration indicates a very high likelihood of IRA patency. MSTD may be helpful in identifying patients with STEMI treated by means of fibrinolytics who could safely avoid emergent coronary angiography. C1 Brigham & Womens Hosp, Div Cardiovasc, TIMI Study Grp, Boston, MA 02115 USA. Univ Texas, SW Med Ctr, Donald W Reynolds Cardiovasc Clin Res Ctr, Dallas, TX USA. Harvard Univ, Clin Res Inst, Boston, MA 02115 USA. RP Cooper, HA (reprint author), Brigham & Womens Hosp, Div Cardiovasc, TIMI Study Grp, 75 Francis St, Boston, MA 02115 USA. EM HACooper@partners.org NR 22 TC 12 Z9 13 U1 0 U2 0 PU MOSBY, INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 USA SN 0002-8703 J9 AM HEART J JI Am. Heart J. PD NOV PY 2002 VL 144 IS 5 BP 790 EP 795 DI 10.1067/mhj.2002.125618 PG 6 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA 615NJ UT WOS:000179252400008 PM 12422146 ER PT J AU Rumsfeld, JS Magid, DJ Plomondon, ME Spertus, JA O'Brien, MM Every, NR Sales, AE AF Rumsfeld, JS Magid, DJ Plomondon, ME Spertus, JA O'Brien, MM Every, NR Sales, AE TI Depression is associated with anginal frequency, anginal stability, physical limitation, and quality of life after acute coronary syndromes SO AMERICAN HEART JOURNAL LA English DT Meeting Abstract CT 3rd Scientific Forum on Quality of Care and Outcomes Research in Cardiovascular Disease and Stroke CY SEP 30-OCT 01, 2001 CL WASHINGTON, D.C. C1 Vet Adm Med Ctr, Denver, CO USA. St Lukes Hosp, Mid Amer Heart Inst, Kansas City, MO 64111 USA. VA Puget Sound Hlth Care Syst, Seattle, WA USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MOSBY, INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 USA SN 0002-8703 J9 AM HEART J JI Am. Heart J. PD NOV PY 2002 VL 144 IS 5 MA 31 BP 894 EP 894 PG 1 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA 615NJ UT WOS:000179252400053 ER PT J AU Furie, KL Schwamm, LH Little, EA Gleason, S O'Donnell, J Koroshetz, WJ AF Furie, KL Schwamm, LH Little, EA Gleason, S O'Donnell, J Koroshetz, WJ TI Quality of life after intracerebral hemorrhage SO AMERICAN HEART JOURNAL LA English DT Meeting Abstract CT 3rd Scientific Forum on Quality of Care and Outcomes Research in Cardiovascular Disease and Stroke CY SEP 30-OCT 01, 2001 CL WASHINGTON, D.C. C1 Massachusetts Gen Hosp, Boston, MA 02114 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MOSBY, INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 USA SN 0002-8703 J9 AM HEART J JI Am. Heart J. PD NOV PY 2002 VL 144 IS 5 MA 41 BP 899 EP 899 PG 1 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA 615NJ UT WOS:000179252400064 ER PT J AU Little, EA Furie, KL Hylek, EM Gleason, S Prady, S Lester, JE Schwamm, LH AF Little, EA Furie, KL Hylek, EM Gleason, S Prady, S Lester, JE Schwamm, LH TI Web-enabled warfarin maintenance dose prediction SO AMERICAN HEART JOURNAL LA English DT Meeting Abstract CT 3rd Scientific Forum on Quality of Care and Outcomes Research in Cardiovascular Disease and Stroke CY SEP 30-OCT 01, 2001 CL WASHINGTON, D.C. C1 Massachusetts Gen Hosp, Boston, MA 02114 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MOSBY, INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 USA SN 0002-8703 J9 AM HEART J JI Am. Heart J. PD NOV PY 2002 VL 144 IS 5 MA 47 BP 901 EP 902 PG 2 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA 615NJ UT WOS:000179252400070 ER PT J AU Samaha, FF Kimmel, SE Kizer, JR Goyal, A Wade, M Boden, WE AF Samaha, FF Kimmel, SE Kizer, JR Goyal, A Wade, M Boden, WE TI Usefulness of the TIMI risk score in predicting both short- and long-term outcomes in the Veterans Affairs Non-Q-Wave myocardial Infarction Strategies, In-Hospital (VANQWISH) Trial SO AMERICAN JOURNAL OF CARDIOLOGY LA English DT Article ID CONSERVATIVE MANAGEMENT STRATEGY; CORONARY SYNDROMES AB We sought to test the validity and clinical, utility of the Thrombolysis in Myocardial Infarction (TIMI) risk,score for patients who have non-O-wave myocardial infarction. A post hoc analysis of the Veterans Affairs Non-Q-Wave Infarction Strategies In-Hospital (VANQWISH) Trial was performed, wherein patients were assigned a TIMI risk score from which both 30-day and 12-month Outcomes (death, nonfatal myocardial infarction, or urgent revascularization) were assessed. At 30 days, the TIMI risk score showed a close match between observed and predicted probabilities of events after adjustment for overall event rates. The event rate at 30 days was 6%, for a score of 0 to 2, 10% for a score of 3, 13% for a score of 4, and 14% for a score of 5 to 7 (p = 0.003 and c statistic 0.59). Discriminative ability of the score was greater, in the conservative group at 30 days'(p = 0.0004, c statistic 0.67). The score remained modestly predictive of events at 1 year (c statistic 0.66). Conservative strategy. patients had better 30-day outcomes than the invasive strategy patients if their score was 0 to 2 (odds ratio 0.24, 95% confidence interval 0.08 to 0.76). No significant difference in outcomes between strategies was. detected for a score greater than or equal to3. The TIMI risk score provides moderate incremental prognostic information in high-risk patients, during both short- and long-term follow-up. (C) 2002 by Excerpta Medica, Inc. C1 Univ Penn, Dept Med, Div Cardiovasc, Philadelphia, PA 19104 USA. Univ Penn, Sch Med, Dept Biostat & Epidemiol, Philadelphia, PA 19104 USA. Univ Penn, Sch Med, Dept Med, Philadelphia, PA 19104 USA. Vet Affairs Med Ctr, Philadelphia, PA 19104 USA. Cornell Univ, Dept Med, Weill Coll, New York, NY USA. Cornell Univ, Dept Publ Hlth, Weill Coll, New York, NY USA. Vet Affairs Med Ctr, Syracuse, NY USA. Univ Connecticut, Div Cardiol, Hartford Hosp, Dept Med, Hartford, CT 06112 USA. RP Samaha, FF (reprint author), Vet Affairs Med Ctr, MC 111C,Univ & Woodland Ave, Philadelphia, PA 19104 USA. RI Goyal, Abhinav/J-5086-2012 OI Goyal, Abhinav/0000-0002-6286-2349 NR 12 TC 20 Z9 22 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 NOV 1 PY 2002 VL 90 IS 9 BP 922 EP 926 AR PII S0002-9149(02)02654-1 DI 10.1016/S0002-9149(02)02654-1 PG 5 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA 610ZC UT WOS:000178991100003 PM 12398955 ER PT J AU Gallik, DM Singer, I Meissner, MD Molnar, J Somberg, JC AF Gallik, DM Singer, I Meissner, MD Molnar, J Somberg, JC TI Hemodynamic and surface electrocardiographic effects of a now aqueous formulation of intravenous amiodarone SO AMERICAN JOURNAL OF CARDIOLOGY LA English DT Article ID POLYSORBATE-80; HEART; DOG AB Intravenous amiodarone is an effective antiarrhythmic agent. However, the standard formulation (Cordarone IV) frequently causes hypotension. Hemodynamic studies have attributed this adverse effect to the solvents employed. A newly developed aqueous formulation (Amio-Aqueous) lacks solvents and thus may not causes hypotension. This study evaluated the hemodynamic effects in a cardiac catheterization laboratory. Two boluses of 150-mg aqueous amiodarone were administered via a peripheral vein to 32 hemodynamically stable patients who underwent cardiac catheterization. Boluses were administered initially over 2 to 5 minutes and in the lost 9 patients over 2 minutes. Hemodynamic evaluation was performed and 12-lead electrocardiograms were obtained at baseline, immediately after each bolus, and following 30 minutes of observation. No patient developed hypotension. There were no significant changes in systolic and diastolic blood pressure (BP) following the boluses. Compared with baseline, heart rate (HR) significantly decreased 5 minutes after the second bolus (73 +/- 12 vs 67 +/- 11 beats/min, p < 0.05). Mean arterial BP increased (90 +/- 14 vs 100 +/- 16 mm Hg, p <0.05) and dp/dt decreased (1,599 +/- 645 vs 1,294 +/- 531 mm Hg/s p <0.05), whereas the PR, QT, and JT intervals increased (174 30 vs 182 331402 +/- 32 vs 424 +/- 35; 317 +/- 37 vs 336 +/- 32 ms, p <0.05, respectively) by the end of the 30-minute observation period. Amio-Aqueous possesses pharmacodynamic effects that have been attributed to amiodarone, whereas it lacks the hypotensive effect of the standard intravenous amiodarone formulation. Amio-Aqueous appears to be a safer alternative to Cordarone IV when rapid administration is indicated. (C) 2002 by Excerpta Medica, Inc. C1 W Los Angeles Vet Affairs Med Ctr, Los Angeles, CA 90073 USA. Univ Louisville, Louisville, KY 40292 USA. Sinai Grace Hosp, Detroit, MI USA. Acad Pharmaceut, Lake Bluff, IL USA. Rush Univ, Chicago, IL 60612 USA. RP Somberg, JC (reprint author), 21 N Skokie Valley Hwy,Suite G-3, Lake Bluff, IL 60044 USA. NR 17 TC 19 Z9 20 U1 1 U2 1 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 NOV 1 PY 2002 VL 90 IS 9 BP 964 EP 968 AR PII S0002-9149(02)02662-0 DI 10.1016/S0002-9149(02)02662-0 PG 5 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA 610ZC UT WOS:000178991100011 PM 12398963 ER PT J AU Lieber, CS Packer, L AF Lieber, CS Packer, L TI S-adenosylmethionine: molecular, biological, and clinical aspects - an introduction SO AMERICAN JOURNAL OF CLINICAL NUTRITION LA English DT Article; Proceedings Paper CT Symposium on S-Adenosylmethionine (SAMe) - From Molecular Mechanism to Clinical Implications CY MAR 07-10, 2001 CL SANTA BARBARA, CALIFORNIA SP Abbott Labs, Ross Prod Div DE homocysteine; membranes; methionine; methionine adenosyltransferase; nucleic acids; polyamines; S-adenosylmethionine ID METABOLISM; HOMOCYSTEINE; METHIONINE; LIVER AB In clinical research, a novel approach has emerged: some of the essential nutrients are being used to treat pathologic conditions. Many of these nutrients, including methionine, must first be activated in the liver or in other tissues before they can exert their key functions. However, this activating process is impaired in disease states and, as a consequence, nutritional requirements change. For instance, for methionine to act as the main cellular methyl donor, it must first be activated to S-adenosylmethionine (SAMe; also known as ademethionine). SAMe is required and is of fundamental importance for the metabolism of nucleic acids and polyamines, the structure and function of membranes, and as a precursor of glutathione. These processes are often seriously altered in various pathologic states addressed in this symposium, but they cannot be restored by simply administering methionine. For instance, in liver disease associated with impairment of the enzyme that activates methionine to SAMe, supplementation with methionine is useless and may even become toxic as it accumulates because it is not used. Accordingly, one must correct the lack of SAMe by bypassing the deficiency in enzyme activation; this is done by providing the product of the defective reaction, namely SAMe. Under these pathologic conditions, SAMe becomes crucial for the functioning of the cell. Thus SAMe, which is found in all living organisms, becomes the essential nutrient instead of methionine. This symposium reviewed the biological and corresponding molecular aspects of SAMe metabolism and the clinical consequences of its deficiency or supplementation in various tissues. C1 Bronx Vet Adm Med Ctr, Sect Liver Dis & Nutr, Bronx, NY 10468 USA. Mt Sinai Sch Med, Bronx, NY USA. Univ So Calif, Dept Mol Pharmacol & Toxicol, Sch Pharm, Los Angeles, CA USA. RP Lieber, CS (reprint author), Bronx Vet Adm Med Ctr, Sect Liver Dis & Nutr, 151-2,130 W Kingsbridge Rd, Bronx, NY 10468 USA. NR 12 TC 39 Z9 44 U1 0 U2 2 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 NOV PY 2002 VL 76 IS 5 BP 1148S EP 1150S PG 3 WC Nutrition & Dietetics SC Nutrition & Dietetics GA 609PE UT WOS:000178913500039 PM 12418492 ER PT J AU Mischoulon, D Fava, M AF Mischoulon, D Fava, M TI Role of S-adenosyl-L-methionine in the treatment of depression: a review of the evidence SO AMERICAN JOURNAL OF CLINICAL NUTRITION LA English DT Article; Proceedings Paper CT Symposium on S-Adenosylmethionine (SAMe) - From Molecular Mechanism to Clinical Implications CY MAR 07-10, 2001 CL SANTA BARBARA, CALIFORNIA SP Abbott Labs, Ross Prod Div DE SAMe; S-adenosyl-L-methionine; depression; antidepressants; alternative treatments; natural treatments ID AFFECTIVE-ILLNESS; MAJOR DEPRESSION; SWITCH MECHANISM; CLINICAL-TRIAL; ADENOSYLMETHIONINE; EFFICACY; DISTRESS; DISORDER; FOLATE; ONSET AB Major depression remains difficult to treat, despite the wide array of registered antidepressants available. In recent years there has been a surge in the popularity of natural or alternative medications. Despite this growing popularity, there is limited evidence for the effectiveness of many of these natural treatments. S-adenosyl-L-methionine (SAMe) is one of the better studied of the natural remedies. SAMe is a methyl donor and is involved in the synthesis of various neurotransmitters in the brain. Derived from the amino acid L-methionine through a metabolic pathway called the one-carbon cycle, SAMe has been postulated to have antidepressant properties. A small number of clinical trials with parenteral or oral SAMe have shown that, at doses of 200-1600 mg/d, SAMe is superior to placebo and is as effective as tricyclic antidepressants in alleviating depression, although some individuals may require higher doses. SAMe may have a faster onset of action than do conventional antidepressants and may potentiate the effect of tricyclic antidepressants. SAMe may also protect against the deleterious effects of Alzheimer disease. SAMe is well tolerated and relatively free of adverse effects, although some cases of mania have been reported in bipolar patients. Overall, SAMe appears to be safe and effective in the treatment of depression, but more research is needed to determine optimal doses. Head-to-head comparisons with newer antidepressants should help to clarify SAMe's place in the psychopharmacologic armamentarium. C1 Harvard Univ, Dept Psychiat, Sch Med, Massachusetts Gen Hosp,Depress Clin & Res Program, Boston, MA 02114 USA. RP Mischoulon, D (reprint author), Harvard Univ, Dept Psychiat, Sch Med, Massachusetts Gen Hosp,Depress Clin & Res Program, WAC-812,15 Parkman St, Boston, MA 02114 USA. NR 40 TC 71 Z9 75 U1 1 U2 11 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 NOV PY 2002 VL 76 IS 5 BP 1158S EP 1161S PG 4 WC Nutrition & Dietetics SC Nutrition & Dietetics GA 609PE UT WOS:000178913500041 PM 12420702 ER PT J AU Lieber, CS AF Lieber, CS TI S-adenosyl-L-methionine: its role in the treatment of liver disorders SO AMERICAN JOURNAL OF CLINICAL NUTRITION LA English DT Article; Proceedings Paper CT Symposium on S-Adenosylmethionine (SAMe) - From Molecular Mechanism to Clinical Implications CY MAR 07-10, 2001 CL SANTA BARBARA, CALIFORNIA SP Abbott Labs, Ross Prod Div DE S-adenosyl-L-methionine; SAMe; alcoholic liver injury; baboons; cholestasis; fibrosis; mitochondria; oxidative stress; liver disorders ID HEPATIC GLUTATHIONE; INTRAHEPATIC CHOLESTASIS; AMINO-ACIDS; ETHANOL; DISEASE; CIRRHOSIS; ALCOHOL; PATHOGENESIS; PLASMA; INJURY AB S-Adenosyl-L-methionine (SAMe) exerts many key functions in the liver, including serving as a precursor for cysteine, 1 of 3 amino acids of glutathione-the major physiologic defense mechanism against oxidative stress. SAMe is particularly important in opposing the toxicity of free oxygen radicals generated by various pathogens, including alcohol, which cause oxidative stress largely by the induction of cytochrome P4502E1 (CYP2E1) and by its metabolite acetaldehyde. SAMe also acts as the main methylating agent in the liver. The precursor of SAMe is methionine, one of the essential amino acids, which is activated by SAMe-synthetase (EC 2.5.1.6). Unfortunately, the activity of this enzyme is significantly decreased as a consequence of liver disease. Because of decreased utilization, methionine accumulates and, simultaneously, there is a decrease in SAMe that acquires the status of an essential nutrient and therefore must be provided exogenously as a supernutrient to compensate for its deficiency. Administration of this innocuous supernutrient results in many beneficial effects in various tissues, mainly in the liver, and especially in the mitochondria. This was shown in alcohol-fed baboons and in other experimental models of liver injury and in clinical trials, some of which are reviewed in other articles in this issue. C1 Bronx Vet Affairs Med Ctr, Mt Sinai Sch Med, Sect Liver Dis & Nutr, Bronx, NY 10468 USA. Bronx Vet Affairs Med Ctr, Alcohol Res Ctr, Sect Liver Dis & Nutr, Bronx, NY 10468 USA. RP Lieber, CS (reprint author), Bronx Vet Affairs Med Ctr, Mt Sinai Sch Med, Sect Liver Dis & Nutr, 151-2,130 W Kingsbridge Rd, Bronx, NY 10468 USA. FU NIAAA NIH HHS [AA11115, AA12867] NR 50 TC 72 Z9 80 U1 3 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 NOV PY 2002 VL 76 IS 5 BP 1183S EP 1187S PG 5 WC Nutrition & Dietetics SC Nutrition & Dietetics GA 609PE UT WOS:000178913500045 PM 12418503 ER PT J AU Brugge, WR AF Brugge, WR TI Fine needle aspiration of pancreatic masses: The clinical impact SO AMERICAN JOURNAL OF GASTROENTEROLOGY LA English DT Editorial Material ID ENDOSCOPIC ULTRASOUND; CARCINOMA; DIAGNOSIS; CANCER; BIOPSY C1 Massachusetts Gen Hosp, Boston, MA 02114 USA. RP Brugge, WR (reprint author), Massachusetts Gen Hosp, 55 Fruit St,Blake 452C, Boston, MA 02114 USA. NR 10 TC 7 Z9 9 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0002-9270 J9 AM J GASTROENTEROL JI Am. J. Gastroenterol. PD NOV PY 2002 VL 97 IS 11 BP 2701 EP 2702 PG 2 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA 613DH UT WOS:000179116100003 PM 12425535 ER PT J AU Ramirez, FC Padda, S Medlin, S Tarbell, H Leung, FW AF Ramirez, FC Padda, S Medlin, S Tarbell, H Leung, FW TI Reflectance spectrophotometry in the gastrointestinal tract: Limitations and new applications SO AMERICAN JOURNAL OF GASTROENTEROLOGY LA English DT Article ID MUCOSAL BLOOD-FLOW; PORTAL HYPERTENSIVE GASTROPATHY; ENDOSCOPIC ASSESSMENT; CIRRHOTIC-PATIENTS; GASTRIC-ULCER; HEMODYNAMICS; PERFUSION; INJURY; RESPONSES; HYPOXIA AB OBJECTIVES: Reflectance spectrophotometry (RS) assesses blood flow changes by measuring an index of Hb concentration (IHB) and index of Hb oxygen saturation (ISO2). We tested the following hypotheses: 1) endoscopic RS measurements obtained by two observers and with the aid of fiber optic and video endoscopes are similar, and 2) the method is suitable for documenting mesenteric venoconstriction associated with systemic hypoxia and blood flow autoregulation associated with hemorrhagic hypotension. METHODS: Study 1: two investigators obtained baseline gastric mucosal RS measurements in anesthetized rats (n = 3) before and after stepwise reduction of blood pressure induced by arterial hemorrhage. Study 2: subjects were examined by both fiber optic and video endoscopes. Endoscopic RS measurements were obtained at 20 cm from the anal verge. Study 3: video endoscope was used to obtain RS measurements in oxygen-dependent patients on and off oxygen treatment. Study 4: the procedures in study I were repeated in five additional rats by one of the investigators. RESULTS: Study 1: there was good agreement between the measurements of IHB and ISO2 between the two investigators. Study 2: video endoscope-assisted measurements were consistently lower. Study 3: cessation of oxygen treatment produced a significant drop in oxygen saturation (pulse oximetry), decline in ISO2, and rise in IHB. Study 4: when blood pressure varied between 90% and 40% of baseline, gastric mucosal blood flow (IHB) was maintained at similar to70% of baseline level. CONCLUSIONS: We confirmed that reproducible measurement can be obtained by different investigators using standardized techniques. Standardization of endoscopic equipment is also necessary to overcome the significant limitation of endoscopic equipment on RS measurements. RS measurements can document mesenteric venoconstriction associated with systemic hypoxia and blood flow autoregulation associated with hemorrhagic hypotension. (C) 2002 by Am. Coll. of Gastroenterology. C1 Carl T Hayden VA Med Ctr, Res Serv, Phoenix, AZ 85012 USA. Carl T Hayden VA Med Ctr, Med Serv, Phoenix, AZ 85012 USA. Vet Affairs Greater Los Angeles Healthcare Syst, Sepulveda Ambulatory Care Ctr, Los Angeles, CA USA. Vet Affairs Greater Los Angeles Healthcare Syst, Nursing Home, Los Angeles, CA USA. Univ Calif Los Angeles, Sch Med, Los Angeles, CA USA. RP Ramirez, FC (reprint author), Carl T Hayden VA Med Ctr, Res Serv, 650 E Indian Sch Rd, Phoenix, AZ 85012 USA. NR 31 TC 13 Z9 13 U1 1 U2 2 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0002-9270 J9 AM J GASTROENTEROL JI Am. J. Gastroenterol. PD NOV PY 2002 VL 97 IS 11 BP 2780 EP 2784 AR PII S0002-9270(02)05439-4 PG 5 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA 613DH UT WOS:000179116100021 PM 12425548 ER PT J AU Oslin, DW Pettinati, H Volpicelli, JR AF Oslin, DW Pettinati, H Volpicelli, JR TI Alcoholism treatment adherence - Older age predicts better adherence and drinking outcomes SO AMERICAN JOURNAL OF GERIATRIC PSYCHIATRY LA English DT Article ID ADDICTION SEVERITY INDEX; BEHAVIORAL TREATMENT; TREATMENT PROGRAMS; NALTREXONE; DEPENDENCE; RELIABILITY; ABUSE; DRINKERS; TRIAL AB Objective: Adherence to treatment has been demonstrated to be an important factor for remission from alcohol dependence. The authors compared therapy and medication adherence for treatment of alcohol dependence in older adults with adherence in younger adults. Methods: All subjects were participants in a randomized, double-blind, placebo-controlled efficacy trial of naltrexone for the treatment of alcohol dependence. All subjects received a medically-based psychosocial intervention focused on motivating patients to change and on adherence to treatment The therapy is non-confrontational and is delivered by a nurse-practitioner Results: Compared with younger adults, older adults bad greater attendance at therapy sessions and greater adherence to the medication. Age-group was the only pretreatment factor associated with adherence. The greater adherence in older adults translated to less relapse than in younger adults. Conclusion: Treatment for alcohol dependence can be effective for older adults. Older adults appear to respond well to a medically-oriented program that is supportive and individualized. In fact, findings from this study suggest that older adults can be treated in mixed-age treatment settings when psychotherapeutic strategies are used that are age-appropriate and delivered on an individual basis. C1 Univ Penn, Dept Psychiat, Sect Geriatr Psychiat, Philadelphia, PA 19104 USA. Univ Penn, Dept Psychiat, Ctr Study Addict, Philadelphia, PA 19104 USA. Philadelphia VA Med Ctr, Philadelphia, PA USA. RP Oslin, DW (reprint author), Univ Penn, Dept Psychiat, Sect Geriatr Psychiat, 3535 Market St,Room 3002, Philadelphia, PA 19104 USA. FU NIAAA NIH HHS [AA 07517] NR 34 TC 32 Z9 33 U1 5 U2 7 PU AMER PSYCHIATRIC PRESS, INC PI WASHINGTON PA 1400 K ST, N W, STE 1101, WASHINGTON, DC 20005 USA SN 1064-7481 J9 AM J GERIAT PSYCHIAT JI Am. J. Geriatr. Psychiatr. PD NOV-DEC PY 2002 VL 10 IS 6 BP 740 EP 747 PG 8 WC Geriatrics & Gerontology; Gerontology; Psychiatry SC Geriatrics & Gerontology; Psychiatry GA 614DC UT WOS:000179172200013 PM 12427583 ER PT J AU Suchin, EJ Cizman, B Connolly, BR DiBattista, WJ Agus, ZS AF Suchin, EJ Cizman, B Connolly, BR DiBattista, WJ Agus, ZS TI Pseudohyperphosphatemia in a hyperphosphatemic hemodialysis patient SO AMERICAN JOURNAL OF KIDNEY DISEASES LA English DT Article DE phosphorus; hyperphosphatemia; pseudohyperphosphaternia; hemodialysis (HD); analytical methods ID ROUTINE PHOTOMETRIC ANALYSIS; MULTIPLE-MYELOMA; INTERFERENCE; PHOSPHORUS AB Hyperphosphatemia is a predictable consequence of end-stage renal disease. Pseudohyperphosphatemia is a spurious elevation of serum phosphate in samples containing a substance that interferes with the laboratory assay for phosphate. The most common cause is a paraprotein in disorders such as Waldenstrom's macroglobulinemia and multiple myeloma. We report here a case of pseudohyperphosphatemia in a hyperphosphatemic patient with end-stage renal disease on long-term hemodialysis caused by a saline solution containing phosphorus used to dilute the patient's serum sample in the clinical chemistry laboratory. Investigations showed that the phosphorus most likely was introduced at the time of saline manufacture. Pseudohyperphosphatemia resulting from the manufacture and distribution of saline-containing phosphorus could be a cause of abnormally high serum phosphate measurements in hyperphosphatemic dialysis patients whose serum samples must be diluted in the laboratory. Such spuriously elevated results can lead to inappropriate changes in medications and subject patients to additional hemodialysis treatments. C1 Hosp Univ Penn, Renal Electrolyte & Hypertens Div, Philadelphia, PA 19104 USA. Philadelphia Vet Affairs Med Ctr, Dept Med, Renal Sect, Philadelphia, PA USA. Philadelphia Vet Affairs Med Ctr, Dept Lab Med, Philadelphia, PA USA. RP Agus, ZS (reprint author), Hosp Univ Penn, Renal Electrolyte & Hypertens Div, 700 Clin Res Bldg,415 Curie Blvd, Philadelphia, PA 19104 USA. NR 22 TC 3 Z9 3 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 USA SN 0272-6386 J9 AM J KIDNEY DIS JI Am. J. Kidney Dis. PD NOV PY 2002 VL 40 IS 5 AR E18 DI 10.1053/ajkd.2002.36351 PG 5 WC Urology & Nephrology SC Urology & Nephrology GA 611ZA UT WOS:000179047100036 PM 12407666 ER PT J AU Rosenzweig, JL Weinger, K Poirier-Solomon, L Rushton, M AF Rosenzweig, JL Weinger, K Poirier-Solomon, L Rushton, M TI Use of a disease severity index for evaluation of healthcare costs and management of comorbidities of patients with diabetes mellitus SO AMERICAN JOURNAL OF MANAGED CARE LA English DT Article ID IMPROVED GLYCEMIC CONTROL; ECONOMIC-BENEFITS; CARE; COMPLICATIONS; POPULATION; PROGRAM; MODEL; NIDDM AB yObjectives: To evaluate a stratification system for patients with diabetes mellitus according to severity of illness and care requirements and to correlate severity of illness with total medical and pharmaceutical cost's of care. Study Design, Patients, and Methods: A cohort of 697 patients with diabetes mellitus was followed in a diabetes clinic under a managed care plan. Patients were stratified according to severity of illness in 6 clinical areas: glycemic control, cardiovascular disease, peripheral vascular disease/peripheral neuropathy, eye disease, renal disease, and autonomic neuropathy. Stratification was based on clinical elements in patients' medical records related to diabetes mellitus care and its comorbidities. Total medical and pharmaceutical costs were identified for 508 patients who participated in the managed care program for at least 8 months. Results: Patients in high- and very high-risk categories for cardiovascular disease, peripheral vascular disease/peripheral neuropathy, eye disease, and renal disease had markedly increased medical and pharmaceutical costs compared with those in low-risk categories. Pharmaceutical costs for patients in the glycemic control clinical area show, a trend toward lower costs at higher risk. Pregnancy and depression were also associated with markedly increased healthcare costs. Patients who were in. multiple high- and very high-risk categories had dramatically increased medical costs, as much as 10-fold those of patients who were in none of these categories. Conclusions: A diabetes mellitus-specific risk stratification system related to required care intensity can be used to identify patients with high medical costs and can enable care providers to select patients for case management and triage into specific care programs. C1 Joslin Diabet Ctr, Off Dis Management, Boston, MA 02215 USA. RP Rosenzweig, JL (reprint author), Joslin Diabet Ctr, Off Dis Management, 1 Joslin Pl, Boston, MA 02215 USA. NR 29 TC 46 Z9 46 U1 0 U2 4 PU AMER MED PUBLISHING, M W C COMPANY PI JAMESBURG PA 241 FORSGATE DR, STE 102, JAMESBURG, NJ 08831 USA SN 1088-0224 J9 AM J MANAG CARE JI Am. J. Manag. Care PD NOV PY 2002 VL 8 IS 11 BP 950 EP 958 PG 9 WC Health Care Sciences & Services; Health Policy & Services; Medicine, General & Internal SC Health Care Sciences & Services; General & Internal Medicine GA 614LE UT WOS:000179190100004 PM 12437310 ER PT J AU Peabody, JW Luck, J AF Peabody, JW Luck, J TI When do developing countries adopt managed care policies and technologies? Part I: Policies, experience, and a framework of preconditions SO AMERICAN JOURNAL OF MANAGED CARE LA English DT Article ID HEALTH-CARE; LATIN-AMERICA; REFORM; PROSPECTS; SERVICES; COLOMBIA; SYSTEM; SECTOR; CHINA; HMOS AB Objective: For developing countries with constrained economic resources, managed care holds out the promise of,being able to control healthcare costs and reduce unnecessary utilization. However, little empirical evidence has been gathered about when managed care techniques can be applied to these countries and no framework considers the macroeconomic context. We propose. a, straightforward method to evaluate the economic and policy environment of a developing country to assess when managed care might be introduced. Study Design and, Methods: Analysis of available developing country health system and healthcare spending data, review of the available literature, and authors' experience evaluating healthcare reforms in developing,countries. Results: Many countries have implemented managed care techniques, which are driven by-policy efforts to increase quality or to control costs. Successful implementation of managed care, however, appears to depend on five major preconditions. One precondition is an adequately developed formal wage sector in which patients have a sufficient ability to pay for healthcare services. Another is an adequate labor supply of trained professionals to support managed care administration, foster competition, and use available information technology. Conclusions: Although managed care encompasses a range of incentives and arrangements, implementation in developing countries appears to depend on attaining macroeconomic preconditions. C1 Univ Calif San Francisco, Sch Med, San Francisco Vet Affairs Med Ctr, Inst Global Hlth, San Francisco, CA 94105 USA. RAND Corp, Santa Monica, CA 90407 USA. Univ Calif Los Angeles, Sch Publ Hlth, W Los Angeles Vet Affairs Med Ctr, Los Angeles, CA 90024 USA. RP Peabody, JW (reprint author), Univ Calif San Francisco, Sch Med, San Francisco Vet Affairs Med Ctr, Inst Global Hlth, 74 New Montgomery St,Suite 508, San Francisco, CA 94105 USA. NR 63 TC 3 Z9 3 U1 0 U2 1 PU AMER MED PUBLISHING, M W C COMPANY PI JAMESBURG PA 241 FORSGATE DR, STE 102, JAMESBURG, NJ 08831 USA SN 1088-0224 J9 AM J MANAG CARE JI Am. J. Manag. Care PD NOV PY 2002 VL 8 IS 11 BP 997 EP 1007 PG 11 WC Health Care Sciences & Services; Health Policy & Services; Medicine, General & Internal SC Health Care Sciences & Services; General & Internal Medicine GA 614LE UT WOS:000179190100008 PM 12437314 ER PT J AU Grady, D Yaffe, K Kristof, M Lin, F Richards, C Barrett-Connor, E AF Grady, D Yaffe, K Kristof, M Lin, F Richards, C Barrett-Connor, E TI Effect of postmenopausal hormone therapy on cognitive function: The heart and estrogen/progestin replacement study SO AMERICAN JOURNAL OF MEDICINE LA English DT Article ID ALZHEIMERS-DISEASE; ESTROGEN-TREATMENT; WORKING-MEMORY; WOMEN; DEMENTIA; TRIAL; HEALTH; APOE AB PURPOSE: To determine if hormone therapy results in better cognitive function in older postmenopausal women. SUBJECTS AND METHODS: The Heart and Estrogen/progestin Replacement Study (HERS) was a randomized, placebo-controlled trial involving 2763 women with coronary disease. Women were assigned randomly to conjugated estrogen (0.625 mg) plus medroxyprogesterone acetate (2.5 mg) in one tablet daily or identical placebo; they were followed for a mean (+/-SD) of 4.2 +/- 0.4 years. Participants at 10 of the 20 HERS centers were invited to enroll in the cognitive function substudy. At the end of the trial, we measured cognitive function in 517 women in the hormone group and 546 in the placebo group using six standard tests: the modified Mini-Mental Status Examination, Verbal Fluency, Boston Naming, Word List Memory, Word List Recall, and Trails B. Cognitive function was not measured at baseline. RESULTS: The mean age of participants at the time of cognitive function testing was 71 +/- 6 years. There were no differences in age-adjusted cognitive function test scores between the two treatment groups, except that women assigned to hormones scored worse on the Verbal Fluency test than women assigned to placebo (15.9 +/- 4.8 vs. 16.6 +/- 4.8, P = 0.02). Adjustment for other potential confounders and restriction of the analyses to women who had been adherent to study medication did not change the results. CONCLUSION: Among older postmenopausal women with coronary disease, 4 years of treatment with postmenopausal hormone therapy did not result in better cognitive function as measured on six standardized tests. Whether these results also apply to elderly women without coronary disease cannot be determined from this study. (C) 2002 by Excerpta Medica, Inc. C1 Univ Calif San Francisco, Dept Epidemiol & Biostat, San Francisco, CA 94115 USA. Univ Calif San Francisco, Dept Med, San Francisco, CA 94115 USA. Univ Calif San Francisco, Dept Psychiat, San Francisco, CA 94115 USA. San Francisco VA Med Ctr, San Francisco, CA USA. Wyeth Ayerst Res, Radnor, PA USA. Univ Calif San Diego, Dept Family & Prevent Med, San Diego, CA 92103 USA. RP Grady, D (reprint author), Univ Calif San Francisco, Dept Epidemiol & Biostat, 1635 Divisidero St,Suite 600, San Francisco, CA 94115 USA. NR 34 TC 132 Z9 139 U1 0 U2 0 PU EXCERPTA MEDICA INC PI NEW YORK PA 650 AVENUE OF THE AMERICAS, NEW YORK, NY 10011 USA SN 0002-9343 J9 AM J MED JI Am. J. Med. PD NOV PY 2002 VL 113 IS 7 BP 543 EP 548 AR PII S0002-9343(02)01270-6 DI 10.1016/S0002-9343(02)01270-6 PG 6 WC Medicine, General & Internal SC General & Internal Medicine GA 619BR UT WOS:000179453900002 PM 12459399 ER PT J AU Mangrulkar, RS Saint, S Chu, S Tierney, LM AF Mangrulkar, RS Saint, S Chu, S Tierney, LM TI What is the role of the clinical "pearl"? SO AMERICAN JOURNAL OF MEDICINE LA English DT Editorial Material ID EVIDENCE-BASED MEDICINE; EPIDEMIOLOGY C1 Univ Michigan, Dept Internal Med, Sch Med, Ann Arbor, MI 48109 USA. Ann Arbor VA Med Ctr, Ann Arbor, MI USA. Univ Calif San Francisco, Sch Med, San Francisco, CA 94143 USA. San Francisco VA Med Ctr, San Francisco, CA USA. RP Mangrulkar, RS (reprint author), Univ Michigan, Dept Internal Med, Sch Med, Ann Arbor, MI 48109 USA. NR 14 TC 5 Z9 5 U1 0 U2 0 PU EXCERPTA MEDICA INC PI NEW YORK PA 650 AVENUE OF THE AMERICAS, NEW YORK, NY 10011 USA SN 0002-9343 J9 AM J MED JI Am. J. Med. PD NOV PY 2002 VL 113 IS 7 BP 617 EP 624 AR PII S0002-9343(02)01353-0 DI 10.1016/S0002-9343(02)01353-0 PG 8 WC Medicine, General & Internal SC General & Internal Medicine GA 619BR UT WOS:000179453900019 PM 12459416 ER PT J AU Schaefer, PW Hunter, GJ He, J Hamberg, LM Sorensen, AG Schwamm, LH Koroshetz, WJ Gonzalez, RG AF Schaefer, PW Hunter, GJ He, J Hamberg, LM Sorensen, AG Schwamm, LH Koroshetz, WJ Gonzalez, RG TI Predicting cerebral ischemic infarct volume with diffusion and perfusion MR imaging SO AMERICAN JOURNAL OF NEURORADIOLOGY LA English DT Article; Proceedings Paper CT 86th Scientific Assembly and Annual Meeting of the Radiological-Society-of-North-America (RSNA) CY NOV 26-DEC 01, 2000 CL CHICAGO, ILLINOIS SP Radiol Soc N Amer ID HIGH-RESOLUTION MEASUREMENT; TRACER BOLUS PASSAGES; WEIGHTED MRI; BLOOD-VOLUME; ACUTE STROKE; HYPERACUTE STROKE; T2-WEIGHTED MRI; CONTRAST AGENTS; INJURY; BRAIN AB BACKGROUND AND PURPOSE: Diffusion and perfusion MR imaging have proved useful in the assessment of acute stroke. We evaluated the utility of these techniques in detecting acute ischemic infarction and in predicting final infarct size. METHODS: Diffusion and hemodynamic images were obtained in 134 patients within a mean of 12.3 hours of onset of acute ischemic stroke symptoms. We retrospectively reviewed patient radiology reports to determine the presence or absence of lesion identification on initial diffusion- (DW) and perfusion-weighted (PW) images. Radiologists were not blinded to the initial clinical assessment. For determination of sensitivity and specificity, the final discharge diagnosis was used as the criterion standard. Neurologists were not blinded to the DW or PW imaging findings. In 81 patients, acute lesions were compared with final infarct volumes. RESULTS: Sensitivities of DW imaging and cerebral blood volume (CBV), cerebral blood flow (CBF), and mean transit time (MTT) perfusion parameters were 94%, 74%, 84%, and 84%, respectively. Specificities of DW imaging, CBV, CBF, and MTT were 96%, 100%, 96%, and 96%, respectively. Results were similar in 93 patients imaged within 12 hours. In 81 patients with follow-up, regression analysis yielded r(2) = 0.9, slope = 1.24 for DW imaging; r(2) = 0.84, slope = 1.22 for CBV; r(2) = 0.35, slope = 0.44 for CBF; and r(2) = 0.22, slope = 0.32 for MTT, versus follow-up volume. A DW-CBV mismatch predicted additional lesion growth, whereas DW-CBF and DW-MTT mismatches did not. Results were similar in 60 patients imaged within 12 hours. CONCLUSION. Diffusion and hemodynamic images are sensitive and specific for detecting acute infarction. DW imaging and CBV best predict final infarct volume. DW-CBV mismatch predicts lesion growth into the CBV abnormality. CBF and MTT help identify additional tissue with altered perfusion but have lower correlation with final volume. C1 Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Radiol,Div Neuroradiol, Boston, MA 02114 USA. Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Neurol, Boston, MA 02114 USA. RP Schaefer, PW (reprint author), Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Radiol,Div Neuroradiol, Gray B285,Fruit St, Boston, MA 02114 USA. OI Schwamm, Lee/0000-0003-0592-9145 NR 38 TC 93 Z9 97 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 NOV-DEC PY 2002 VL 23 IS 10 BP 1785 EP 1794 PG 10 WC Clinical Neurology; Neuroimaging; Radiology, Nuclear Medicine & Medical Imaging SC Neurosciences & Neurology; Radiology, Nuclear Medicine & Medical Imaging GA 614PR UT WOS:000179199000035 PM 12427640 ER PT J AU Berg, AO AF Berg, AO CA US Preventive Services Task Force TI Newborn hearing screening: Recommendations and rationale SO AMERICAN JOURNAL OF NURSING LA English DT Article ID IDENTIFICATION; IMPAIRMENT C1 Univ Washington, Dept Family Med, Seattle, WA 98195 USA. Univ Texas, Hlth Sci Ctr, Sch Nursing, San Antonio, TX 78285 USA. Tri Cty Family Med, Cohocton, NY USA. Univ Rochester, Sch Med, Rochester, NY USA. Natl Initiat Childrens Healthcare Qual, Boston, MA USA. Univ Med & Dent New Jersey, New Jersey Med Sch, Dept Family Med, Newark, NJ 07103 USA. Harvard Pilgrim Hlth Care, Dept Ambulatory Care & Prevent, Boston, MA USA. Harvard Univ, Sch Med, Boston, MA 02115 USA. Univ Texas, Hlth Sci Ctr, Audie L Murphy Mem Vet Hosp, San Antonio, TX 78285 USA. Robert Wood Johnson Fdn, Princeton, NJ 08540 USA. Women & Infants Hosp Rhode Isl, Providence, RI 02908 USA. Univ Michigan, Sch Nursing, Ann Arbor, MI 48109 USA. CUNY Mt Sinai Sch Med, Div Gen Internal Med, New York, NY 10029 USA. CUNY Mt Sinai Sch Med, Med Serv Care Ctr, New York, NY 10029 USA. Mt Sinai Med Ctr, New York, NY 10029 USA. Merck & Co Inc, Outcomes Res & Management, W Point, PA USA. Columbia Univ, Coll Phys & Surg, Dept Obstet & Gynecol, New York, NY USA. Virginia Commonwealth Univ, Dept Family Practice, Fairfax, VA USA. RP Berg, AO (reprint author), Care of Atkins D, US Prevent Serv Task Force, Ctr Practice & Technol Assessment, Agcy Healthcare Res & Qual, 6010 Execut Blvd,Suite 300, Rockville, MD 20852 USA. NR 18 TC 1 Z9 1 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0002-936X J9 AM J NURS JI Am. J. Nurs. PD NOV PY 2002 VL 102 IS 11 BP 83 EP + PG 4 WC Nursing SC Nursing GA 615DZ UT WOS:000179231700033 PM 12436079 ER PT J AU Ufret-Vincenty, RL Chen, RJL Azar, DT AF Ufret-Vincenty, RL Chen, RJL Azar, DT TI Corneal flap displacement and drift in LASIK: Comparison of Hansatome and Automated Corneal Shaper microkeratomes SO AMERICAN JOURNAL OF OPHTHALMOLOGY LA English DT Article ID IN-SITU KERATOMILEUSIS; PHOTOREFRACTIVE KERATECTOMY; LASER; MANAGEMENT; COMPLICATIONS AB .PURPOSE: To describe and compare the displacement of corneal flaps created during laser in situ keratomileusis (LASIK) procedures performed with two different microkeratomes and analyze parameters (for example, pupil-to-hinge distance, drift during suction) that might affect the flap displacement or be influenced by flap displacement. . DESIGN: This work was based on a cross-sectional study design. . METHODS: Images copied from video recordings of 206 consecutive LASIK surgeries were analyzed to determine the distance from pupil center to corneal flap hinge (pupil to-hinge distance), the hinge size, the distance from the center of the pupil to the margins of the flap, and the positions of the suction ring before and after vacuum in corneal flaps created by the Hansatome and the Automated Corneal Shaper (ACS) microkeratomes. Accurate measurements of all these variables could be obtained in 121 eyes (Hansatome: n = 66, right eye (OD) = 27 eyes, left eye (OS) = 39 eyes; ACS: n = 55, OD = 25 eyes, OS = 30 eyes), which were included in the analysis. Formulas were derived to calculate from the measurements the magnitude and direction of the drift of the suction ring during vacuum and the final displacement of the corneal flap. .RESULTS: The mean +/- standard deviation (SD) drift of yes during suction with the Hansatome was 0.27 +/- 0.02 mm and with the ACS was 0.12 +/- 0.02 mm (P <.001). The Hansatome induced, on average, more biased (temporal vs random) drift than did the ACS. The mean final displacement of the center of the flap from the center of the pupil was of equal magnitude for the two instruments (0.37 +/- 0.02 mm and 0.36 +/- 0.02 mm with the Hansatome and ACS, respectively). . CONCLUSION: The drift induced by the Hansatome contributes to the horizontal component of the final decentration of the corneal flaps. This tendency for drift and the resultant decrease in pupil-to-hinge distance should be considered to minimize flap displacements during LASIK. (C) 2002 by Elsevier Science Inc. All rights reserved. C1 Harvard Univ, Massachusetts Eye & Ear Infirm, Sch Med, Dept Ophthalmol,Corneal Serv, Boston, MA 02114 USA. RP Azar, DT (reprint author), Harvard Univ, Massachusetts Eye & Ear Infirm, Sch Med, Dept Ophthalmol,Corneal Serv, 243 Charles St, Boston, MA 02114 USA. NR 16 TC 1 Z9 1 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 NOV PY 2002 VL 134 IS 5 BP 701 EP 706 AR PII S0002-9394(02)01675-6 DI 10.1016/S0002-9394(02)01675-6 PG 6 WC Ophthalmology SC Ophthalmology GA 614DT UT WOS:000179173600008 PM 12429246 ER PT J AU Cunha, IT Lim, PAC Henson, H Monga, T Qureshy, H Protas, EJ AF Cunha, IT Lim, PAC Henson, H Monga, T Qureshy, H Protas, EJ TI Performance-based gait tests for acute stroke patients SO AMERICAN JOURNAL OF PHYSICAL MEDICINE & REHABILITATION LA English DT Article DE physical performance; gait; qualitative measures; stroke survivors ID REHABILITATION; RECOVERY; SCALE; TRIAL AB Objective: Qualitative measures may not differentiate severity of deficits after an acute or subacute stroke. The aim of this study was to contrast the utility of performance-based gait tests with qualitative measures in a sample of acute stroke patients. Design: Twenty acute stroke subjects had their performance-based gait measured by gait speed, walking distance, gait energy expenditure, and gait energy cost. They were also qualitatively evaluated for cognition, functional outcomes, motor impairment, and Functional Ambulation Category. Results: Strong and significant correlations were observed among performance-based gait tests. Qualitative scales indicated moderate to minimal deficits in each domain evaluated although they were not, correlated among themselves, except for Functional Ambulation Category and FIM(TM) and FIM and Mini-Mental State Exam. Functional Ambulation Category correlated with performance-based gait tests. Conclusions: Performance-based gait tests are feasible to conduct during early recovery after a stroke and allow better discrimination among the patients than qualitative measures. C1 Texas Womans Univ, Sch Phys Therapy, Houston, TX USA. Houston Vet Affairs Med Ctr, Phys Med & Rehabil Dept, Houston, TX USA. Houston Vet Affairs Med Ctr, Rehabil Res & Dev Ctr Healthy Aging & Disabil, Houston, TX USA. Singapore Gen Hosp, Singapore 0316, Singapore. RP Protas, EJ (reprint author), 1130 John Freeman Blvd, Houston, TX 77030 USA. NR 29 TC 62 Z9 66 U1 1 U2 3 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0894-9115 J9 AM J PHYS MED REHAB JI Am. J. Phys. Med. Rehabil. PD NOV PY 2002 VL 81 IS 11 BP 848 EP 856 DI 10.1097/01.PHM.0000027423.96462.CF PG 9 WC Rehabilitation; Sport Sciences SC Rehabilitation; Sport Sciences GA 607FP UT WOS:000178781700008 PM 12394997 ER PT J AU Bode, BP Fuchs, BC Hurley, BP Conroy, JL Suetterlin, JE Tanabe, KK Rhoads, DB Abcouwer, SF Souba, WW AF Bode, BP Fuchs, BC Hurley, BP Conroy, JL Suetterlin, JE Tanabe, KK Rhoads, DB Abcouwer, SF Souba, WW TI Molecular and functional analysis of glutamine uptake in human hepatoma and liver-derived cells SO AMERICAN JOURNAL OF PHYSIOLOGY-GASTROINTESTINAL AND LIVER PHYSIOLOGY LA English DT Article DE amino acid transporter B-0; ASCT2; SN1; SN2; hepatocellular carcinoma; transport; system A ID AMINO-ACID TRANSPORTER; CULTURED HUMAN-FIBROBLASTS; TISSUE EXPRESSION PATTERN; HEPATOCELLULAR-CARCINOMA; SYSTEM ASC; MEMBRANE-VESICLES; RAT-LIVER; METABOLISM; LINE; CLONING AB Human hepatoma cells take up glutamine at rates severalfold faster than the system N-mediated transport rates observed in normal human hepatocytes. Amino acid inhibition, kinetic, Northern blotting, RT-PCR, and restriction enzyme analyses collectively identified the transporter responsible in six human hepatoma cell lines as amino acid transporter B-0 (ATB(0)), the human ortholog of rodent ASCT2. The majority of glutamine uptake in liver fibroblasts and an immortalized human liver epithelial cell line (THLE-5B) was also mediated by ATB(0). The 2.9-kb ATB(0) mRNA was equally expressed in all cell lines, whereas expression of the system A transporters ATA2 and ATA3 was variable. In contrast, the system N isoforms (SN1 and SN2) were expressed only in well-differentiated hepatomas. ATB(0) mRNA was also expressed in cirrhotic liver and adult and pediatric liver cancer biopsies but was not detectable in isolated human hepatocytes or fetal liver. Although the growth of all hepatomas was glutamine dependent, competitive inhibition of ATB(0) mediated glutamine uptake blocked proliferation only in poorly differentiated cells lacking SN1 or SN2 expression and exhibiting low glutamine synthetase mRNA levels. C1 St Louis Univ, Dept Biol, St Louis, MO 63103 USA. Harvard Univ, Sch Med, Boston, MA 02114 USA. Massachusetts Gen Hosp, Dept Surg, Surg Oncol Res Labs, Boston, MA 02114 USA. RP Bode, BP (reprint author), St Louis Univ, Dept Biol, 3507 Laclede Ave, St Louis, MO 63103 USA. FU NCI NIH HHS [1 R29 CA69505] NR 52 TC 54 Z9 56 U1 1 U2 7 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA SN 0193-1857 J9 AM J PHYSIOL-GASTR L JI Am. J. Physiol.-Gastroint. Liver Physiol. PD NOV PY 2002 VL 283 IS 5 BP G1062 EP G1073 DI 10.1152/ajpgi.00031.2002 PG 12 WC Gastroenterology & Hepatology; Physiology SC Gastroenterology & Hepatology; Physiology GA 604CX UT WOS:000178599100007 PM 12381519 ER PT J AU Chen, MC Solomon, TE Kui, R Soll, AH AF Chen, MC Solomon, TE Kui, R Soll, AH TI Apical EGF receptors regulate epithelial barrier to gastric acid: endogenous TGF-alpha is an essential facilitator SO AMERICAN JOURNAL OF PHYSIOLOGY-GASTROINTESTINAL AND LIVER PHYSIOLOGY LA English DT Article DE peptic ulcer; paracellular pathway; tight junctions; cell polarity ID EPIDERMAL GROWTH-FACTOR; CHIEF CELL MONOLAYERS; MOLECULAR PHYSIOLOGY; TIGHT JUNCTIONS; CULTURE; JUICE; PATHOPHYSIOLOGY; SURFACE; PERMEABILITY; PROTEINS AB In previous studies, we found that apical and basolateral EGF receptors (EGFR) on primary canine gastric monolayers decreased paracellular permeability, evident by increased transepithelial electrical resistance (TER) and decreased flux of [H-3]mannitol (MF). After studying monolayers in Ussing chambers, we now report that treatment with apical, but not basolateral, EGF enhanced tolerance to apical H+, evident by a slower decay in TER and an attenuated rise in MF. Enhanced tolerance to apical acid was evident within 10 min of treatment with apical EGF. Immunoneutralization of endogenous transforming growth factor (TGF)-alpha accelerated the drop in TER and the rise in MF in response to apical acidification; apical EGF reversed these effects. Study of monolayers cultured in Transwell inserts showed that immunoblockade of basolateral, but not apical, EGFR also impaired the resistance to apical acidification and enhanced MF. We conclude that apical EGFR regulates the barrier to apical acidification via effects on paracellular resistance. Although exogenous basolateral EGF has a less apparent effect on the barrier to acid, endogenous ligand active at basolateral EGFR plays an important role in maintaining the barrier to apical acid. Our data implicate a role for an apical EGFR ligand, which may be EGF or another member of the EGF family. C1 Univ Calif Los Angeles, Sch Med, Greater Los Angeles Vet Affairs Hlth Care Syst, CURE,Div Digest Dis, Los Angeles, CA 90073 USA. Univ Calif Los Angeles, Sch Med, Greater Los Angeles Vet Affairs Hlth Care Syst, Med & Res Serv, Los Angeles, CA 90073 USA. RP Soll, AH (reprint author), Vet Affairs Wadsworth Hosp Ctr, Bldg 115,Rm 215,11301 Wilshire Blvd, Los Angeles, CA 90073 USA. FU NIDDK NIH HHS [DK-19984, DK-30444] NR 35 TC 15 Z9 15 U1 1 U2 1 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA SN 0193-1857 J9 AM J PHYSIOL-GASTR L JI Am. J. Physiol.-Gastroint. Liver Physiol. PD NOV PY 2002 VL 283 IS 5 BP G1098 EP G1106 DI 10.1152/ajpgi.00507.2001 PG 9 WC Gastroenterology & Hepatology; Physiology SC Gastroenterology & Hepatology; Physiology GA 604CX UT WOS:000178599100011 PM 12381523 ER PT J AU Okolo, C Wong, T Moody, MW Nguyen, TD AF Okolo, C Wong, T Moody, MW Nguyen, TD TI Effects of bile acids on dog pancreatic duct epithelial cell secretion and monolayer resistance SO AMERICAN JOURNAL OF PHYSIOLOGY-GASTROINTESTINAL AND LIVER PHYSIOLOGY LA English DT Article DE taurocholate; iodide and rubidium efflux; pancreatitis; Ussing chamber; transepithelial resistance ID TAUROURSODEOXYCHOLIC ACID; CALCIUM; LINE; CONDUCTANCES; MORPHOLOGY; POTASSIUM; TRANSPORT; CURRENTS; SALTS; COLON AB Pancreatic duct epithelial cells (PDEC) mediate the secretion of fluid and electrolytes and are exposed to refluxed bile. In nontransformed cultured dog PDEC, which express many ion transport pathways of PDEC, 1 mM taurodeoxycholic acid (TDCA) stimulated an I-125(-) efflux inhibited by DIDS and 5-nitro-2-(3-phenylpropylamino) benzoic acid (NPPB) and a Rb-86(+) efflux inhibited by charybdotoxin. Inhibition by 1,2-bis(2-aminophenoxy)-ethane- N,N,N',N'-tetraacetic acid (BAPTA)-AM suggests mediation via increased intracellular Ca2+ concentration, whereas the absence of lactate dehydrogenase release excludes cellular toxicity. At 1 mM, TDCA stimulated a larger I-125(-) efflux than glycodeoxycholate; two dihydroxy bile acids, taurochenodeoxycholate and TDCA, were similarly effective, whereas a trihydroxy bile acid, taurocholate, was ineffective. In Ussing chambers, 1 mM serosal or 2 mM luminal TDCA stimulated an I-sc increase from confluent PDEC monolayers. TDCA also stimulated 1) a short-circuit current (I-sc) increase from basolaterally permeabilized PDEC subject to a serosal-to-luminal Cl- gradient that was inhibited by BAPTA-AM, DIDS, and NPPB and 2) an I-sc increase from apically permeabilized PDEC subject to a luminal-to-serosal K+ gradient inhibited by BAPTA-AM and charybdotoxin. Along with the efflux studies, these findings suggest that TDCA interacts directly with PDEC to stimulate Ca2+-activated apical Cl- channels and basolateral K+ channels. Monolayer transepithelial resistance was only minimally affected by 1 mM serosal and 2 mM luminal TDCA but decreased after exposure to higher TDCA concentrations (2 mM serosal and 4 mM luminal). A secretory role for bile acids should be considered in pancreatic diseases associated with bile reflux. C1 Univ Washington, Div Gastroenterol, Dept Med, VA Med Ctr,GI Sect, Seattle, WA 98108 USA. Vet Affairs Puget Sound Hlth Care Syst, Seattle, WA 98108 USA. RP Nguyen, TD (reprint author), Univ Washington, Div Gastroenterol, Dept Med, VA Med Ctr,GI Sect, S-111 Gastro,1660 S Columbian Way, Seattle, WA 98108 USA. FU NIDDK NIH HHS [DK-07742, R01-DK-55885] NR 23 TC 5 Z9 5 U1 0 U2 1 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA SN 0193-1857 J9 AM J PHYSIOL-GASTR L JI Am. J. Physiol.-Gastroint. Liver Physiol. PD NOV PY 2002 VL 283 IS 5 BP G1042 EP G1050 DI 10.1152/ajpgi.00436.2001 PG 9 WC Gastroenterology & Hepatology; Physiology SC Gastroenterology & Hepatology; Physiology GA 604CX UT WOS:000178599100005 PM 12381517 ER PT J AU Barbieri, R Triedman, JK Saul, JP AF Barbieri, R Triedman, JK Saul, JP TI Heart rate control and mechanical cardiopulmonary coupling to assess central volume: a systems analysis SO AMERICAN JOURNAL OF PHYSIOLOGY-REGULATORY INTEGRATIVE AND COMPARATIVE PHYSIOLOGY LA English DT Article DE baroreflex; cardiopulmonary reflex; hypovolemia; hypervolemia; respiration; blood pressure ID CENTRAL VENOUS-PRESSURE; BODY NEGATIVE-PRESSURE; BLOOD-PRESSURE; MODULATION; RESPONSES; REFLEX; VARIABILITY; CIRCULATION; REDUCTIONS; STRESS AB Small negative changes of central volume reduce cardiac output without significant alterations of arterial blood pressure (ABP), suggesting an adequate regulatory response. Furthermore, evidence has arisen supporting a Bainbridge reflex (tachycardia with hypervolemia) in humans. To investigate these phenomena, multivariate autoregressive techniques were used to evaluate the beat-to-beat interactions between respiration, R-R interval, and ABP at six levels of decreased and increased central volume. With reductions of central volume below control, baroreflex and respiratory sinus arrhythmia gains were reduced, while with increases of volume above control, gains increased for the first two levels but decreased again at the highest volume level, suggesting the presence of a Bainbridge reflex in healthy human subjects. The mechanical influence of respiration on central venous pressure (CVP) had an unexpected shift in phase at the point of mild central hypervolemia, with the expected negative relation at lower volumes (inspiration lowers CVP) but a positive relation at higher volumes (inspiration raises CVP). We conclude that multivariate techniques can quantify the relations between a variety of respiratory and hemodynamic parameters, allowing for the in vivo assessment of complex cardiorespiratory interactions during manipulations of central volume. The results identify the presence of a Bainbridge reflex in humans and suggest that short-term cardiovascular control is optimized at mild hypervolemia. C1 Med Univ S Carolina, Dept Pediat, Charleston, SC 29425 USA. Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Anesthesia & Crit Care, Boston, MA 02114 USA. Childrens Hosp, Dept Cardiol, Boston, MA 02115 USA. Harvard Univ, Sch Med, Boston, MA 02115 USA. RP Saul, JP (reprint author), 165 Ashley Ave,POB 250915, Charleston, SC 29425 USA. FU NHLBI NIH HHS [R01-HL-62385] NR 28 TC 59 Z9 62 U1 0 U2 5 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA SN 0363-6119 J9 AM J PHYSIOL-REG I JI Am. J. Physiol.-Regul. Integr. Comp. Physiol. PD NOV PY 2002 VL 283 IS 5 BP R1210 EP R1220 DI 10.1152/ajpregu.00127.2002 PG 11 WC Physiology SC Physiology GA 604HP UT WOS:000178613500026 PM 12376415 ER PT J AU Wu, MF John, J Maidment, N Lam, HA Siegel, JM AF Wu, MF John, J Maidment, N Lam, HA Siegel, JM TI Hypocretin release in normal and narcoleptic dogs after food and sleep deprivation, eating, and movement SO AMERICAN JOURNAL OF PHYSIOLOGY-REGULATORY INTEGRATIVE AND COMPARATIVE PHYSIOLOGY LA English DT Article DE cerebrospinal fluid; locomotor activity; feeding; orexin ID LOCUS-COERULEUS NEURONS; LATERAL HYPOTHALAMIC AREA; OREXIN MESSENGER-RNA; RETICULAR-FORMATION; BEHAVIORAL ORGANIZATION; UNRESTRAINED CAT; CONSCIOUS RATS; EXPRESSION; MICE; SECRETION AB Hypocretins (orexins) are recently discovered hypothalamic neuropeptides that have been implicated in the etiology of narcolepsy. The normal behavioral functions of these peptides are unclear, although a role in feeding has been suggested. We measured hypocretin-1 (Hcrt-1) in the cerebrospinal fluid of dogs during a variety of behaviors. We found that 48 h without food (24 h beyond normal 24-h fasting period) produced no significant change in Hcrt-1 levels nor did feeding after the deprivation. In contrast, 24 h of sleep deprivation produced on average a 70% increase in Hcrt-1 level compared with baseline levels. The amount of increase was correlated with the level of motor activity during the sleep-deprivation procedure. A 2-h period of exercise in the same dogs produced a 57% increase in Hcrt-1 levels relative to quiet waking levels, with the magnitude of the increase being highly correlated with the level of motor activity. The strong correlation between motor activity and Hcrt-1 release may explain some of the previously reported behavioral, physiological, and pathological phenomena ascribed to the Hcrt system. C1 Vet Affairs Greater Los Angeles Healthcare Syst S, North Hills, CA 91343 USA. Univ Calif Los Angeles, Brain Res Inst, Los Angeles, CA 90024 USA. Univ Calif Los Angeles, Dept Psychiat, Los Angeles, CA USA. RP Wu, MF (reprint author), Vet Affairs Greater Los Angeles Healthcare Syst S, North Hills, CA 91343 USA. FU NIMH NIH HHS [MH-64109]; NINDS NIH HHS [NS-14610] NR 64 TC 88 Z9 90 U1 0 U2 2 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA SN 0363-6119 J9 AM J PHYSIOL-REG I JI Am. J. Physiol.-Regul. Integr. Comp. Physiol. PD NOV PY 2002 VL 283 IS 5 BP R1079 EP R1086 DI 10.1152/ajpregu.00207.2002 PG 8 WC Physiology SC Physiology GA 604HP UT WOS:000178613500012 PM 12376401 ER PT J AU Kern, RS Liberman, RP Kopelowicz, A Mintz, J Green, MF AF Kern, RS Liberman, RP Kopelowicz, A Mintz, J Green, MF TI Applications of errorless learning for improving work performance in persons with schizophrenia SO AMERICAN JOURNAL OF PSYCHIATRY LA English DT Article; Proceedings Paper CT 16th Annual Meeting of the Society-for-Research-in-Psychopathology CY NOV 01-04, 2001 CL MADISON, WISCONSIN SP Soc Res Psychopathol ID SEVERE MENTAL-ILLNESS; SUPPORTED EMPLOYMENT; CONTROLLED TRIAL; MEMORY; REHABILITATION; DISORDERS; OUTPATIENTS; INDIVIDUALS; REMEDIATION; DEFICITS AB Objective: Until recently, few training methods used in the psychosocial rehabilitation of persons with schizophrenia have taken into account the neurocognitive deficits common to this illness. The present study tested a training method called errorless learning (which theoretically compensates for neurocognitive impairments) for efficacy at teaching entry-level job tasks to persons with serious and persistent mental illness. Method: Sixty-five unemployed, clinically stable outpatients with schizophrenia or schizoaffective disorder were randomly assigned to training by means of either errorless learning or conventional instruction for two entry-level job tasks (index card filing and toilet tank assembly). Training was conducted in small groups of four subjects for 90-120 minutes in a simulated workshop. Efficacy-as measured by accuracy, speed, and overall productivity-was assessed immediately after training and at a 3-month follow-up evaluation. Results: Significant group differences in accuracy that favored errorless learning were found on both job tasks. In terms of productivity, the errorless learning group was superior to the conventional instruction group on the card filing task, and differences for the tank assembly task approached significance. There were no significant group differences in speed. Both groups showed significant drops in accuracy and productivity on the tank assembly task from immediately after training to the 3-month follow-up evaluation; performance levels were more stable for both groups on the card filing task. Conclusions. Errorless learning appears to be a useful training method for establishing introductory high levels of performance in the work rehabilitation of persons with schizophrenia. Future studies may wish to test its long-term durability by embedding it within supported employment programs. C1 VA Greater Los Angeles Healthcare Syst, MIRECC, Los Angeles, CA 90073 USA. Univ Calif Los Angeles, Dept Psychiat & Biobehav Sci, Los Angeles, CA 90024 USA. Mental Illness Res Educ & Clin Ctr, MIRECC, Dept Vet Affairs, VISN 22, Los Angeles, CA USA. San Fernando Mental Hlth Ctr, San Fernando, CA USA. RP Kern, RS (reprint author), VA Greater Los Angeles Healthcare Syst, MIRECC, 210 A,11301 Wilshire Blvd, Los Angeles, CA 90073 USA. OI kopelowicz, alex/0000-0002-1728-4105 FU NIMH NIH HHS [MH-30911] NR 54 TC 52 Z9 53 U1 5 U2 8 PU AMER PSYCHIATRIC PRESS, INC PI WASHINGTON PA 1400 K ST, N W, STE 1101, WASHINGTON, DC 20005 USA SN 0002-953X J9 AM J PSYCHIAT JI Am. J. Psychiat. PD NOV PY 2002 VL 159 IS 11 BP 1921 EP 1926 DI 10.1176/appi.ajp.159.11.1921 PG 6 WC Psychiatry SC Psychiatry GA 613EY UT WOS:000179120300020 PM 12411229 ER PT J AU Kalra, MK Prasad, S Saini, S Blake, MA Varghese, J Halpern, EF Thrall, JH AF Kalra, MK Prasad, S Saini, S Blake, MA Varghese, J Halpern, EF Thrall, JH TI Clinical comparison of standard-dose and 50% reduced-dose abdominal CT: Effect on image quality SO AMERICAN JOURNAL OF ROENTGENOLOGY LA English DT Article ID COMPUTED-TOMOGRAPHY; HELICAL CT; REDUCTION; PITCH; MAS AB OBJECTIVE. We hypothesized that radiation doses for abdominal CT could be reduced by adjusting the dose for a patient's weight and cross-sectional abdominal dimensions, with the resultant scans still being of diagnostic quality. SUBJECTS AND METHODS. Using a multidetector CT scanner, we prospectively studied 39 patients who were 65 years and older who had a known history of cancer. After performing a diagnostic contrast-enhanced CT examination, we obtained four slices each (centered at the top of the right kidney) at a standard radiation dose (240-300 mA) and at a 50% reduced dose (120-150 mA) at a constant kilovoltage of 140. Scans were obtained during a single breath-hold, with a 2.5-mm detector configuration and a slice pitch of 6:1. Reconstructed slice thickness was 5 mm. In a blinded review, two radiologists rated the randomized CT scans for overall image quality and anatomic details of liver, spleen, adrenal glands, kidneys, pancreas, and abdominal wall, using a 5-point scale (1 = unacceptable, 2 = substandard, 3 = acceptable, 4 = above average, and 5 = superior). Patients' weight and abdominal circumference, area, and anteroposterior and transverse diameters were correlated with image quality of scans obtained at standard-dose and 50% reduced-dose CT Statistical analysis of the data was performed using Wilcoxon's signed rank test. RESULTS. Overall, the image quality score was significantly higher (p < 0.005) on the scans obtained with standard-dose CT. No statistically significant difference in image quality was noted in the 50% reduced- and standard-dose CT scans in patients who weighed less than 180 lb, or 81 kg, (p > 0.05) and who had a transverse abdominal diameter of less than 34.5 cm (p > 0.05), an anteroposterior diameter of less than 28 cm. (p > 0.05), a cross-sectional circumference of less than 105 cm (p > 0.05), and a cross-sectional area of less than 800 cm(2) (p > 0.05). Good interobserver agreement (p > 0.5) was found between the two reviewing radiologists. CONCLUSION. Abdominal CT scan quality appears to be acceptable even with a 50% reduction in radiation dose except in patients with large anthropometric measurements. A reduction in CT radiation dose is possible if the tube current is optimized for the patient's weight and abdominal dimensions. C1 Massachusetts Gen Hosp, Dept Radiol, Boston, MA 02114 USA. Harvard Univ, Sch Med, Boston, MA 02114 USA. RP Saini, S (reprint author), Massachusetts Gen Hosp, Dept Radiol, White 270-E,55 Fruit St, Boston, MA 02114 USA. NR 23 TC 97 Z9 117 U1 0 U2 4 PU AMER ROENTGEN RAY SOC PI RESTON PA 1891 PRESTON WHITE DR, SUBSCRIPTION FULFILLMENT, RESTON, VA 22091 USA SN 0361-803X EI 1546-3141 J9 AM J ROENTGENOL JI Am. J. Roentgenol. PD NOV PY 2002 VL 179 IS 5 BP 1101 EP 1106 PG 6 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA 606GG UT WOS:000178725800002 PM 12388481 ER PT J AU Smith, JJ Berlin, L AF Smith, JJ Berlin, L TI Malpractice issues in radiology - E-mail consultation SO AMERICAN JOURNAL OF ROENTGENOLOGY LA English DT Article ID PATIENT C1 Massachusetts Gen Hosp, Dept Radiol, Boston, MA 02114 USA. Harvard Univ, Sch Med, Boston, MA 02114 USA. Rush Med Coll, Chicago, IL 60612 USA. Rush N Shore Med Ctr, Dept Radiol, Skokie, IL 60076 USA. RP Berlin, L (reprint author), Massachusetts Gen Hosp, Dept Radiol, 32 Fruit St, Boston, MA 02114 USA. NR 9 TC 4 Z9 4 U1 0 U2 0 PU AMER ROENTGEN RAY SOC PI RESTON PA 1891 PRESTON WHITE DR, SUBSCRIPTION FULFILLMENT, RESTON, VA 22091 USA SN 0361-803X J9 AM J ROENTGENOL JI Am. J. Roentgenol. PD NOV PY 2002 VL 179 IS 5 BP 1133 EP 1136 PG 4 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA 606GG UT WOS:000178725800007 PM 12388486 ER PT J AU Ulbright, TM Srigley, JR Hatzianastassiou, DK Young, RH AF Ulbright, TM Srigley, JR Hatzianastassiou, DK Young, RH TI Leydig cell tumors of the testis with unusual features - Adipose differentiation, calcification with ossification, and spindle-shaped tumor cells SO AMERICAN JOURNAL OF SURGICAL PATHOLOGY LA English DT Article DE Leydig cell tumor; adipose metaplasia; osseous metaplasia; sarcomatoid tumor; testicular neoplasm ID SPERMATOCYTIC SEMINOMA; ADRENOGENITAL SYNDROME; TESTICULAR-TUMOR; SARCOMA AB We report 19 Leydig cell tumors (LCTs) of the testis with adipose differentiation (n = 12) and/or spindle cell growth (n = 8) in patients 28-70 years of age; three tumors with adipose differentiation showed psammomatous calcifications, two of which also had foci of ossification. In eight tumors fat-like cells apparently derived from lipid accumulation within neoplastic Leydig cells and appeared as focal to prominent clusters in a background of vacuolated, neoplastic Leydig cells. The fat-like cells were usually immunoreactive for Leydig cell markers (inhibin-a, calretinin, and melan-A) but were typically strongly positive for the adipose tissue marker, S-100 protein, supporting a hybrid cell phenotype. Four tumors had fat of stromal derivation. In two of these there were intermixed mature adipocytes, but in two others only lipoblastic cells were present. These four tumors lacked vacuolated, neoplastic Leydig cells, and the fat cells in the single case studied were negative for inhibin-alpha and melan-A but positive for S-100. Three of the 12 LCTs with adipose differentiation were clinically malignant, and each had several of the established malignant features. Eight tumors with spindle cells occurred in men 34-70 years of age. Two tumors had ill-defined fascicles of spindle cells, and three showed prominent edematous to myxoid areas with spindle-shaped tumor cells. Two additional tumors had a fibroma-like spindled component that blended with islands of more plump, polygonal to spindle-shaped Leydig cells. Finally, one tumor had foci resembling an unclassified sarcoma that merged with conventional LCT; the spindle cell component in this case did not react for Leydig cell markers in contrast to the spindle cells in five of the six other cases in which immunostains were performed. Spindle cell differentiation, by itself, did not appear to have prognostic significance. Of the six patients with available follow-up, two developed metastases, but their tumors had malignant features apart from spindle cells; the remaining four patients were disease free at a mean of 3.6 years. Awareness of these unusual patterns in LCTs may prevent misinterpretation of fat admixed with neoplastic Leydig cells as evidence of extratesticular growth (a criterion for malignant LCT) may help avoid misdiagnosis of a LCT as a testicular "tumor" of the adrenogenital syndrome (which may contain fat) and may prevent misdiagnosis of a LCT with spindle cells as a sarcoma or unclassified sex cord-stromal tumor. C1 Indiana Univ Hosp, Indianapolis, IN 46202 USA. Credit Valley Hosp, Mississauga, ON, Canada. McMaster Univ, Hamilton, ON, Canada. 401 Army Gen Hosp, Athens, Greece. Massachusetts Gen Hosp, Boston, MA 02114 USA. Harvard Univ, Sch Med, Boston, MA 02115 USA. RP Ulbright, TM (reprint author), Indiana Univ Hosp, 550 N Univ Blvd,Room 3465, Indianapolis, IN 46202 USA. NR 22 TC 33 Z9 33 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0147-5185 J9 AM J SURG PATHOL JI Am. J. Surg. Pathol. PD NOV PY 2002 VL 26 IS 11 BP 1424 EP 1433 DI 10.1097/00000478-200211000-00004 PG 10 WC Pathology; Surgery SC Pathology; Surgery GA 609YQ UT WOS:000178934300004 PM 12409718 ER PT J AU Washington, K Greenson, JK Montgomery, E Shyr, Y Crissinger, KD Polk, DB Barnard, J Lauwers, GY AF Washington, K Greenson, JK Montgomery, E Shyr, Y Crissinger, KD Polk, DB Barnard, J Lauwers, GY TI Histopathology of ulcerative colitis in initial rectal biopsy in children SO AMERICAN JOURNAL OF SURGICAL PATHOLOGY LA English DT Article DE ulcerative colitis; children; inflammatory bowel disease; histologic pattern ID INFLAMMATORY-BOWEL-DISEASE; SELF-LIMITED COLITIS; DIAGNOSIS; SPECIMENS; CRITERIA AB Definitive histologic diagnosis of ulcerative colitis relies upon mucosal architectural distortion and inflammation in the appropriate clinical setting. Although crypt branching, atrophy, and loss are usually present in first biopsies from adults with ulcerative colitis, it has been our impression that features of chronicity are often lacking in first biopsies from children. To test this hypothesis, initial rectal biopsies and follow-up biopsies and/or colonic resections from 53 children (age 15 months to 17 years) and 38 adults (age 21-76 years) with ulcerative colitis were examined in a blinded fashion for villiform surface, crypt atrophy, branching crypts, lamina propria inflammation, crypt abscesses, cryptitis,and basal plasma cells. Mucosal architecture was classified as normal, focally abnormal, or diffusely abnormal. Medical records were reviewed for confirmatory evidence of ulcerative colitis and for duration of symptoms before biopsy. In 87 of 91 biopsies, the lamina propria contained a mixed inflammatory infiltrate. Crypt abscesses and cryptitis were common in both groups. Initial biopsies from children were less likely to show diffuse architectural abnormalities (17 of 53, 32.1%) compared with biopsies from adults (22 of 38, 57.9% p < 0.05). Duration of symptoms before diagnosis was significantly shorter in children (mean 17.5 weeks) compared with adults (mean 54.9 weeks). In summary, initial rectal biopsies from children with ulcerative colitis are less likely to show diagnostic mucosal architectural distortion than biopsies from adults. This difference may be related to a shorter duration of symptoms before biopsy. C1 Vanderbilt Univ, Med Ctr, Dept Pathol, Nashville, TN 37232 USA. Vanderbilt Univ, Med Ctr, Dept Biostat, Nashville, TN 37232 USA. Vanderbilt Univ, Med Ctr, Dept Pediat, Nashville, TN 37232 USA. Univ Michigan, Hlth Syst, Dept Pathol, Ann Arbor, MI 48109 USA. Johns Hopkins Univ Hosp, Dept Pathol, Baltimore, MD 21287 USA. Univ S Alabama, Dept Pediat, Mobile, AL 36688 USA. Columbus Childrens Hosp, Columbus, OH USA. Ohio State Univ, Columbus, OH 43210 USA. Massachusetts Gen Hosp, Dept Pathol, Boston, MA 02114 USA. RP Washington, K (reprint author), Vanderbilt Univ, Med Ctr, Dept Pathol, C-3321 Med Ctr N, Nashville, TN 37232 USA. NR 14 TC 52 Z9 54 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0147-5185 J9 AM J SURG PATHOL JI Am. J. Surg. Pathol. PD NOV PY 2002 VL 26 IS 11 BP 1441 EP 1449 DI 10.1097/00000478-200211000-00006 PG 9 WC Pathology; Surgery SC Pathology; Surgery GA 609YQ UT WOS:000178934300006 PM 12409720 ER PT J AU Zembowicz, A Granter, SR McKee, PH Mihm, MC AF Zembowicz, A Granter, SR McKee, PH Mihm, MC TI Amelanotic cellular blue nevus - a hypopigmented variant of the cellular blue nevus: Clinicopathologic analysis of 20 cases SO AMERICAN JOURNAL OF SURGICAL PATHOLOGY LA English DT Article DE blue nevus; cellular blue nevus; amelanotic blue nevus; malignant blue nevus; melanoma; clear cell sarcoma ID MICROPHTHALMIA TRANSCRIPTION FACTOR; DESMOPLASTIC MALIGNANT-MELANOMA; SOFT PARTS; T(12-22) TRANSLOCATION; DISTINCTIVE VARIANT; SARCOMA; TENDONS; COMMON; BENIGN; IMMUNOREACTIVITY AB Blue nevus and its variants typically present as pigmented lesions. Dermal melanin is responsible for coloration and is an expected histologic finding. Herein, we report 20 cases of an unusual amelanotic variant of cellular blue nevus. Our series showed clinical demographics similar to pigmented counterparts. Thus, there was a predilection for young individuals with a mean age of 24 years (range 6-74 years). Both sexes were affected, with a female-to-male ratio of approximately 2:1. The lower back, distal extremities, and scalp were the most common sites of occurrence. Importantly, the lack of pigmentation resulted in an atypical clinical appearance. A diagnosis of blue nevus by the attending physician was not considered in any of the reported lesions. All of the tumors extended deep into the reticular dermis or subcutaneous fat with a mean thickness of 5.5 mm (range 1.7-11 mm). Ulceration was present in two lesions. Mild cytologic atypia and pleomorphism were present in five cases. Mitotic activity (up to 3 mitoses/mm(2)) was observed in I I lesions. A brisk lymphocytic host response was present in only one lesion. Tumor necrosis was not observed. Most, but not all, tumors showed reactivity for S-100 and HMB-45. Clinical follow-up (mean 32 months) was consistent with a benign course. Local recurrence was not observed after complete excision. None of the cases was associated with clinical evidence of lymph node or distant metastases. Recognition of amelanotic cellular blue nevus is important because the lack of expected pigmentation may result in clinical and pathologic diagnostic difficulty. In particular, amelanotic cellular blue nevus must be distinguished from malignant cellular blue nevus and other variants of melanoma. C1 Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Pathol, Boston, MA 02114 USA. Harvard Univ, Brigham & Womens Hosp, Sch Med, Dept Pathol, Boston, MA 02115 USA. RP Zembowicz, A (reprint author), Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Pathol, Warren 820,55 Fruit St, Boston, MA 02114 USA. NR 52 TC 15 Z9 16 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0147-5185 J9 AM J SURG PATHOL JI Am. J. Surg. Pathol. PD NOV PY 2002 VL 26 IS 11 BP 1493 EP 1500 DI 10.1097/00000478-200211000-00012 PG 8 WC Pathology; Surgery SC Pathology; Surgery GA 609YQ UT WOS:000178934300012 PM 12409726 ER PT J AU Delmonico, FL Wynn, JJ AF Delmonico, FL Wynn, JJ TI Managing the enlarging waiting list SO AMERICAN JOURNAL OF TRANSPLANTATION LA English DT Editorial Material C1 Harvard Univ, Sch Med, Dept Surg, Massachusetts Gen Hosp, Cambridge, MA 02138 USA. Med Coll Georgia, Dept Surg, Augusta, GA 30912 USA. RP Delmonico, FL (reprint author), Harvard Univ, Sch Med, Dept Surg, Massachusetts Gen Hosp, Cambridge, MA 02138 USA. NR 3 TC 6 Z9 11 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 NOV PY 2002 VL 2 IS 10 BP 889 EP 890 DI 10.1034/j.1600-6143.2002.21001.x PG 2 WC Surgery; Transplantation SC Surgery; Transplantation GA 620ZM UT WOS:000179564100001 PM 12482137 ER PT J AU Monnard, PA Deamer, DW AF Monnard, PA Deamer, DW TI Membrane self-assembly processes: Steps toward the first cellular life SO ANATOMICAL RECORD LA English DT Article DE cellular life; membrane; boundary structures; amphiphile vesicles ID MURCHISON CARBONACEOUS CHONDRITE; TRANSMEMBRANE ION CHANNELS; FATTY-ACID MEMBRANES; LIPID VESICLES; PHOSPHOLIPID-BILAYERS; REPLICATING MICELLES; REPRODUCING VESICLES; PREBIOTIC STRUCTURES; ENZYMATIC-SYNTHESIS; PEPTIDE NANOTUBES AB This review addresses the question of the origin of life, with emphasis on plausible boundary structures that may have initially provided cellular compartmentation. Some form of compartmentation is a necessary prerequisite for maintaining the integrity of interdependent molecular systems that are associated with metabolism, and for permitting variations required for speciation. The fact that lipid-bilayer membranes define boundaries of all contemporary living cells suggests that protocellular compartments were likely to have required similar, self-assembled boundaries. Amphiphiles such as short-chain fatty acids, which were presumably available on the early Earth, can self-assemble into stable vesicles that encapsulate hydrophilic solutes with catalytic activity. Their suspensions in aqueous media have therefore been used to investigate nutrient uptake across Simple membranes and encapsulated catalyzed reactions, both of which Would be essential processes in protocellular life forms. C1 Univ Calif Santa Cruz, Dept Chem & Biochem, Santa Cruz, CA 95064 USA. RP Monnard, PA (reprint author), Massachusetts Gen Hosp, Dept Mol Biol, 50 Blossom St, Boston, MA 02114 USA. EM monnard@molbio.mgh.harvard.edu NR 79 TC 117 Z9 125 U1 9 U2 57 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 0003-276X J9 ANAT RECORD JI Anat. Rec. PD NOV 1 PY 2002 VL 268 IS 3 BP 196 EP 207 DI 10.1002/ar.10154 PG 12 WC Anatomy & Morphology SC Anatomy & Morphology GA 608WN UT WOS:000178870800005 PM 12382318 ER PT J AU Gordon, SM Brahim, JS Dubner, R McCullagh, LM Sang, C Dionne, RA AF Gordon, SM Brahim, JS Dubner, R McCullagh, LM Sang, C Dionne, RA TI Attenuation of pain in a randomized trial by suppression of peripheral nociceptive activity in the immediate postoperative period SO ANESTHESIA AND ANALGESIA LA English DT Article ID PLASMA BETA-ENDORPHIN; RAT SPINAL-CORD; DORSAL HORN; PREEMPTIVE ANALGESIA; LOCAL-ANESTHESIA; INFLAMMATION; SURGERY; INFILTRATION; HYPERALGESIA; NEURONS AB Peripheral neuronal barrage from tissue injury produces central nervous system changes that contribute to the maintenance of postoperative pain. The therapeutic approaches to blocking these central changes remain controversial, because previous studies have not differentiated presurgical interventions from those administered after tissue injury, yet before pain onset. In this study, we evaluated the relative contributions of blockade of nociceptive input during surgery or during the immediate postoperative period on pain suppression. Subjects were randomly allocated to one of four groups: preoperative 2% lidocaine, postoperative 0.5% bupivacaine, both, or placebo injections. General anesthesia was induced and third molars extracted. Pain was assessed over 4 h and at 24 and 48 h. The P-endorphin in blood samples increased twofold during surgery, which is indicative of activation of the peripheral nociceptive barrage in response to painful stimuli. Pain was decreased in the immediate postoperative period in the bupivacaine groups, whereas it increased in the lidocaine group over time. Pain intensity was less 48 h after surgery in the groups whose postoperative pain was blocked by the administration of bupivacaine, but no effect was demonstrated for the preoperative administration of lidocaine alone. These results in the oral surgery pain model suggest that minimizing the peripheral nociceptive barrage during the immediate postoperative period decreases pain at later time periods. In contrast, blocking the intraoperative nociceptive barrage does not appear to contribute significantly to the subsequent reduction in pain. C1 Massachusetts Gen Hosp, Dept Anesthesia, Boston, MA 02114 USA. NIH, Dept Nursing, Ctr Clin, Bethesda, MD 20892 USA. Univ Maryland, Sch Dent, Baltimore, MD 21201 USA. Natl Inst Dent & Craniofacial Res, Bethesda, MD USA. RP Dionne, RA (reprint author), 10 Ctr Dr,Room 1N-117, Bethesda, MD 20892 USA. EM raymond.dionne@nih.gov NR 39 TC 16 Z9 17 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0003-2999 EI 1526-7598 J9 ANESTH ANALG JI Anesth. Analg. PD NOV PY 2002 VL 95 IS 5 BP 1351 EP 1357 DI 10.1213/01.ANE.0000033210.87385.AD PG 7 WC Anesthesiology SC Anesthesiology GA 609NV UT WOS:000178912600047 PM 12401625 ER PT J AU Cohen, SP Abdi, S AF Cohen, SP Abdi, S TI Venous malformations associated with central pain: Report of a case SO ANESTHESIA AND ANALGESIA LA English DT Article ID CENTRAL POSTSTROKE PAIN; NEUROPATHIC PAIN; THALAMIC PAIN; INJURY; MODEL; TRIAL; RAT C1 NYU, Sch Med, Dept Anesthesiol, New York, NY 10016 USA. Harvard Univ, Massachusetts Gen Hosp, Sch Med, MGH Pain Ctr,Dept Anesthesia & Crit Care, Boston, MA USA. Uniformed Serv Univ Hlth Sci, Bethesda, MD 20814 USA. Walter Reed Army Med Ctr, Dept Anesthesiol, Pain Management Ctr, Washington, DC 20307 USA. RP Cohen, SP (reprint author), NYU, Sch Med, Dept Anesthesiol, 550 1st Ave, New York, NY 10016 USA. NR 18 TC 4 Z9 4 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0003-2999 J9 ANESTH ANALG JI Anesth. Analg. PD NOV PY 2002 VL 95 IS 5 BP 1358 EP 1360 DI 10.1213/01.ANE.0000033100.62362.4A PG 3 WC Anesthesiology SC Anesthesiology GA 609NV UT WOS:000178912600048 PM 12401626 ER PT J AU Baboolal, HA Ichinose, F Ullrich, R Kawai, N Bloch, KD Zapol, WM AF Baboolal, HA Ichinose, F Ullrich, R Kawai, N Bloch, KD Zapol, WM TI Reactive oxygen species scavengers attenuate endotoxin-induced impairment of hypoxic pulmonary vasoconstriction in mice SO ANESTHESIOLOGY LA English DT Article; Proceedings Paper CT Annual Meeting of the American-Society-of-Anesthesiologists CY OCT 10-20, 2001 CL NEW ORLEANS, LA SP Amer Soc Anesthesiologists ID ACUTE LUNG INJURY; RESPIRATORY-DISTRESS SYNDROME; ACETYL-L-CYSTEINE; N-ACETYLCYSTEINE; SUPEROXIDE-DISMUTASE; SEPTIC SHOCK; MODEL; ANTIOXIDANTS; SURVIVAL; SHEEP AB Background: Sepsis and endotoxemia attenuate hypoxic pulmonary vasoconstriction (HPV), thereby impairing systemic oxygenation. Reactive oxygen species (ROS) are implicated in the pathogenesis of sepsis-induced lung injury. The authors investigated whether treatment with scavengers of ROS prevents impairment of HPV in mice challenged with endotoxin. Methods: The pulmonary vasoconstrictor response to left mainstem bronchus occlusion (LMBO) was studied in anesthetized mice 22 h after an intraperitoneal challenge with saline solution or 10 mg/kgEscherichia coli endotoxin. In some mice, challenge with saline solution or endotoxin was followed after 1 h with Intraperitoneal or intratracheal administration of the ROS scavengers N-acetylcysteine or EUK-8. Myeloperoxidase activity and nitric oxide synthase-2 gene expression were measured in lung tissues. Results. The LMBO increased left pulmonary vascular resistance by 106 +/- 24% in saline-challenged control mice but by only 23 +/- 12% (P < 0.05) in endotoxin-challenged mice. Intraperitoneal administration of N-acetylcysteine or EUK-8 1 h after endotoxin challenge attenuated the endotoxin-induced impairment of HPV (58 +/- 6% and 68 +/- 10%, respectively, bothP < 0.05 vs. endotoxin-challenged mice). Intratracheal administration of ROS scavengers 1 h after endotoxin challenge was equally effective but required lower doses than systemic treatment. Administration of the ROS scavengers 22 h after endotoxin challenge did not restore HPV. Conclusions: Administration of N-acetylcysteine or EUK-8 I h after endotoxin challenge in mice prevented the impairment of HPV after LMBO. Early therapy with ROS scavengers, either systemically or by inhalation, may provide a means to preserve HPV in sepsis-associated acute lung injury. C1 Harvard Univ, Dept Anesthesia & Crit Care, Massachusetts Gen Hosp, Sch Med, Boston, MA 02114 USA. Harvard Univ, Cardiovasc Res Ctr, Massachusetts Gen Hosp, Sch Med, Boston, MA 02114 USA. Harvard Univ, Div Cardiol,Dept Med, Massachusetts Gen Hosp, Sch Med, Boston, MA 02114 USA. RP Harvard Univ, Dept Anesthesia & Crit Care, Massachusetts Gen Hosp, Sch Med, 55 Fruit St, Boston, MA 02114 USA. EM ichinose@etherdome.mgh.harvard.edu FU NHLBI NIH HHS [HL-42397, HL-57172] NR 38 TC 26 Z9 26 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA SN 0003-3022 EI 1528-1175 J9 ANESTHESIOLOGY JI Anesthesiology PD NOV PY 2002 VL 97 IS 5 BP 1227 EP 1233 DI 10.1097/00000542-200211000-00028 PG 7 WC Anesthesiology SC Anesthesiology GA 611TV UT WOS:000179034600027 PM 12411809 ER PT J AU Lecamwasam, HS Katz, D Vlahakes, GJ Dzik, W Streckenbach, SC AF Lecamwasam, HS Katz, D Vlahakes, GJ Dzik, W Streckenbach, SC TI Cardiopulmonary bypass following severe transfusion-related acute lung injury SO ANESTHESIOLOGY LA English DT Article ID NONCARDIOGENIC PULMONARY-EDEMA; COMPLICATION; PLASMA C1 Massachusetts Gen Hosp, Dept Anesthesia & Crit Care, Dept Cardiac Surg, Boston, MA 02114 USA. Massachusetts Gen Hosp, Blood Transfus Serv, Boston, MA 02114 USA. Harvard Univ, Sch Med, Boston, MA USA. RP Streckenbach, SC (reprint author), Massachusetts Gen Hosp, Dept Anesthesia & Crit Care, Dept Cardiac Surg, 55 Fruit St, Boston, MA 02114 USA. NR 15 TC 2 Z9 2 U1 0 U2 1 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0003-3022 J9 ANESTHESIOLOGY JI Anesthesiology PD NOV PY 2002 VL 97 IS 5 BP 1311 EP 1312 DI 10.1097/00000542-200211000-00040 PG 2 WC Anesthesiology SC Anesthesiology GA 611TV UT WOS:000179034600039 PM 12411821 ER PT J AU Washington, DL Bird, CE AF Washington, DL Bird, CE TI Sex differences in disease presentation in the emergency department SO ANNALS OF EMERGENCY MEDICINE LA English DT Editorial Material ID ACUTE MYOCARDIAL-INFARCTION; GENDER DIFFERENCES; CHEST PAIN; PERSPECTIVE C1 VA Greater Los Angeles Healthcare Syst, Dept Med, Los Angeles, CA USA. RAND Hlth, Santa Monica, CA USA. RP Washington, DL (reprint author), 11301 Wilshire Blvd,111G, Los Angeles, CA 90073 USA. RI Bird, Chloe/C-7107-2008 NR 12 TC 3 Z9 3 U1 1 U2 1 PU MOSBY, INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 USA SN 0196-0644 J9 ANN EMERG MED JI Ann. Emerg. Med. PD NOV PY 2002 VL 40 IS 5 BP 461 EP 463 DI 10.1067/mem.2002.128859 PG 3 WC Emergency Medicine SC Emergency Medicine GA 609DX UT WOS:000178889300002 PM 12399787 ER PT J AU Weinberg, A Li, SB Palmer, M Tyler, KL AF Weinberg, A Li, SB Palmer, M Tyler, KL TI Quantitative CSFPCR in Epstein-Barr virus infections of the central nervous system SO ANNALS OF NEUROLOGY LA English DT Article ID POLYMERASE CHAIN-REACTION; CEREBROSPINAL-FLUID; NEUROLOGIC COMPLICATIONS; MONONUCLEOSIS; ENCEPHALITIS; DISEASES; PCR; MENINGOENCEPHALITIS; ANTIBODIES; DIAGNOSIS AB Acute Epstein-Barr virus (EBV) infection of the central nervous system (CNS) is associated with meningoencephalitis and other neurological syndromes and with CNS lymphomas (CNSLs). Diagnosis is based on serological studies and more recently on detection of EBV DNA in cerebrospinal fluid (CSF) by polymerase chain reaction (PCR). We measured EBV DNA toy quantitative PCR and EBV mRNA by RT-PCR in the CSF in patients with EBV-associated neurological disorders. EBV was identified as the cause of CNS infection in 28 patients: 14 with CNSL, 10 with encephalitis, and 4 with postinfectious neurological complications. CSF analysis showed that patients with CNSL had high EBV load (mean +/- standard error of 4.8 +/- 0.2 log(10) DNA copies/ml) and low leukocyte counts (22 +/- 7 cells/mul); encephalitis was characterized by high EBV load (4.2 +/- 0.3 log(10) DNA copies/ml) and high leukocyte counts (143 62 cells/mul); and patients with postinfectious complications showed low EBV load (3.0 +/- 0.2 log(10) DNA copies/ml) with high leukocyte counts (88 +/- 57 cells/mul). Lytic cycle EBV mRNA, a marker of viral replication, was identified in 10 CSF samples from patients with CNSL and encephalitis. These studies demonstrate the utility of quantitative CSF PCR and establish the presence of lyric cycle EBV mRNA in CSF of patients with EBV-associated neurological disease. C1 Univ Colorado, Hlth Sci Ctr, Dept Pediat, Denver, CO 80262 USA. Univ Colorado, Hlth Sci Ctr, Dept Med, Denver, CO 80262 USA. Univ Colorado, Hlth Sci Ctr, Dept Microbiol & Immunol, Denver, CO 80262 USA. Univ Colorado, Hlth Sci Ctr, Dept Neurol, Denver, CO 80262 USA. Denver Vet Affairs Med Ctr, Denver, CO USA. RP Weinberg, A (reprint author), Univ Colorado, Hlth Sci Ctr, Dept Pediat, Campus Box C227, Denver, CO 80262 USA. OI Tyler, Kenneth/0000-0003-3294-5888 FU NIAID NIH HHS [U01 AI 38858]; NICHD NIH HHS [N01HD 33162] NR 29 TC 73 Z9 76 U1 0 U2 3 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA SN 0364-5134 J9 ANN NEUROL JI Ann. Neurol. PD NOV PY 2002 VL 52 IS 5 BP 543 EP 548 DI 10.1002/ana.10321 PG 6 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA 609PK UT WOS:000178914000005 PM 12402250 ER PT J AU Herbert, MR Harris, GJ Adrien, KT Ziegler, DA Makris, N Kennedy, DN Lange, NT Chabris, CF Bakardjiev, A Hodgson, J Takeoka, M Tager-Flusberg, H Caviness, VS AF Herbert, MR Harris, GJ Adrien, KT Ziegler, DA Makris, N Kennedy, DN Lange, NT Chabris, CF Bakardjiev, A Hodgson, J Takeoka, M Tager-Flusberg, H Caviness, VS TI Abnormal asymmetry in language association cortex in autism SO ANNALS OF NEUROLOGY LA English DT Article ID INFERIOR PREFRONTAL CORTEX; PLANUM TEMPORALE ASYMMETRY; FUSIFORM FACE AREA; DEVELOPMENTAL DYSLEXIA; PARS TRIANGULARIS; ANATOMICAL ASYMMETRY; CEREBRAL STRUCTURE; ASPERGER-SYNDROME; STROKE PATIENTS; FUNCTIONAL MRI AB Autism is a neurodevelopmental disorder affecting cognitive, language, and social functioning. Although language and social communication abnormalities are characteristic, prior structural imaging studies have not examined language-related cortex in autistic and control subjects. Subjects included 16 boys with autism (aged 7-11 years), with nonverbal IQ greater than 80, and 15 age- and handedness-matched controls. Magnetic resonance brain images were segmented into gray and white matter; cerebral cortex was parcellated into 48 gyral-based divisions per hemisphere. Asymmetry was assessed a priori in language-related inferior lateral frontal and posterior superior temporal regions and assessed post hoc in all regions to determine specificity of asymmetry abnormalities. Boys with autism had significant asymmetry reversal in frontal language-related cortex: 27% larger on the right in autism and 17% larger on the left in controls. Only one additional region had significant asymmetry differences on post hoc analysis: posterior temporal fusiform gyrus (more left-sided in autism), whereas adjacent fusiform gyrus and temporooccipital inferior temporal gyrus both approached significance (more right-sided in autism). These inferior temporal regions are involved in visual face processing. In boys with autism, language and social/face processing-related regions displayed abnormal asymmetry. These structural abnormalities may relate to language and social disturbances observed in autism. C1 Massachusetts Gen Hosp, Ctr Morphometr Anal, Boston, MA 02114 USA. Massachusetts Gen Hosp, Radiol Comp Aided Diagnost Lab, Boston, MA 02114 USA. McLean Hosp, Brain Imaging Ctr, Belmont, MA 02178 USA. Boston Univ, Sch Med, Boston, MA 02215 USA. Childrens Hosp, Oakland, CA 94609 USA. Pennington Sch, Pennington, NJ USA. Keio Univ, Sch Med, Tokyo, Japan. RP Herbert, MR (reprint author), Massachusetts Gen Hosp, Ctr Morphometr Anal, CNY-149,Room 6012, Boston, MA 02114 USA. RI Tager-Flusberg, Helen/D-5265-2009; Kennedy, David/H-3627-2012 FU NIDA NIH HHS [DA 09467]; NIDCD NIH HHS [DC 03610]; NIMH NIH HHS [MH 57180]; NINDS NIH HHS [NS 02126, NS 37483, NS 20489, NS 34189] NR 80 TC 153 Z9 155 U1 8 U2 19 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA SN 0364-5134 J9 ANN NEUROL JI Ann. Neurol. PD NOV PY 2002 VL 52 IS 5 BP 588 EP 596 DI 10.1002/ana.10349 PG 9 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA 609PK UT WOS:000178914000011 PM 12402256 ER PT J AU Klein, C Liu, L Doheny, D Kock, N Muller, B Aguiar, PD Leung, J de Leon, D Bressman, SB Silverman, J Smith, C Danisi, F Morrison, C Walker, RH Velickovic, M Schwinger, E Kramer, PL Breakefield, XO Brin, MF Ozelius, LJ AF Klein, C Liu, L Doheny, D Kock, N Muller, B Aguiar, PD Leung, J de Leon, D Bressman, SB Silverman, J Smith, C Danisi, F Morrison, C Walker, RH Velickovic, M Schwinger, E Kramer, PL Breakefield, XO Brin, MF Ozelius, LJ TI epsilon-sarcoglycan mutations found in combination with other dystonia gene mutations SO ANNALS OF NEUROLOGY LA English DT Article ID D2 DOPAMINE-RECEPTOR; INHERITED MYOCLONUS-DYSTONIA; HIRSCHSPRUNG-DISEASE; RETINITIS-PIGMENTOSA; CHROMOSOME 7Q; MAJOR LOCUS; PERIPHERIN/RDS; 7Q21-Q31; FAMILIES; RET AB Myoclonus-dystonia is a movement disorder associated with mutations in the c-sarcoglycan gene (SGCE) in most families and in the DRD2 and DYT1 genes in two single families. In both of the latter families, we also found a mutation of SGCE. The molecular mechanisms through which the detected mutations may contribute to myoclonus-dystonia remain to be determined. C1 Med Univ Lubeck, Dept Neurol, D-23538 Lubeck, Germany. Med Univ Lubeck, Dept Human Genet, D-23538 Lubeck, Germany. Albert Einstein Coll Med, Dept Mol Genet, Bronx, NY 10461 USA. Mt Sinai Sch Med, Dept Neurol, New York, NY USA. Univ Fed Sao Paulo, Dept Neurol & Neurosurg, Sao Paulo, Brazil. Massachusetts Gen Hosp, Dept Neurol, Charlestown, MA USA. Harvard Univ, Sch Med, Charlestown, MA USA. Beth Israel Med Ctr, Dept Neurol, New York, NY 10003 USA. Vet Affairs Med Ctr, Dept Neurol, Bronx, NY USA. Oregon Hlth Sci Univ, Dept Neurol, Portland, OR 97201 USA. RP Ozelius, LJ (reprint author), Albert Einstein Coll Med, Dept Mol Genet, 1300 Morris Pk Ave, Bronx, NY 10461 USA. RI de Carvalho Aguiar, Patricia/B-2350-2013; de Carvalho Aguiar, Patricia/E-8520-2010 OI de Carvalho Aguiar, Patricia/0000-0003-2957-9573; de Carvalho Aguiar, Patricia/0000-0003-2957-9573 FU NINDS NIH HHS [NS 26656, NS 28384, NS 37409] NR 19 TC 69 Z9 72 U1 0 U2 3 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA SN 0364-5134 J9 ANN NEUROL JI Ann. Neurol. PD NOV PY 2002 VL 52 IS 5 BP 675 EP 679 DI 10.1002/ana.10358 PG 5 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA 609PK UT WOS:000178914000026 PM 12402271 ER PT J AU Suzuki, T Bless, DM Connor, NP Ford, CN Lee, K Inagi, K AF Suzuki, T Bless, DM Connor, NP Ford, CN Lee, K Inagi, K TI Age-related alterations in myosin heavy chain isoforms in rat intrinsic laryngeal muscles SO ANNALS OF OTOLOGY RHINOLOGY AND LARYNGOLOGY LA English DT Article; Proceedings Paper CT Meeting of the American-Broncho-Esophagological-Association CY MAY 14-15, 2001 CL PALM DESERT, CALIFORNIA SP Amer Broncho Esophagolog Assoc DE aging; lateral cricoarytenoid muscle; myosin heavy chain; posterior cricoarytenoid muscle; thyroarytenoid muscle ID SKELETAL-MUSCLE; FIBER-TYPE; EXPRESSION; MODULATION; VELOCITY; ATROPHY AB Deficits in voice and swallowing are found in the elderly, but the underlying neuromuscular mechanisms are unclear. A potential mechanism may be denervation-induced muscle fiber transformation to a slower-contracting type of muscle fiber. This study examined young, old, and denervated rat laryngeal muscles (lateral thyroarytenoid, lateral cricoarytenoid, and posterior cricoarytenoid) to examine differences in myosin heavy chain (MHC) composition. Results of sodium dodecyl sulfate-polyacrylamide gel electrophoresis analyses indicated that all muscles were composed predominately of type IIB MHC. With aging and denervation, type IIB was reduced and type IIX, a slower-contracting isoform, was increased in the lateral thyroarytenoid and lateral cricoarytenoid muscles. In the posterior cricoarytenoid muscle, the MHC composition was relatively unchanged. These findings suggest that aging may affect laryngeal adductory function by altering muscle fiber type composition to a slower-contracting isoform, in a manner similar to that observed with denervation. C1 Univ Wisconsin, Ctr Clin Sci, Dept Surg, Div Otolaryngol Head & Neck Surg, Madison, WI 53792 USA. William S Middleton Mem Vet Adm Med Ctr, Surg Serv, Madison, WI USA. Kitasato Univ, Sch Med, Dept Otolaryngol Head & Neck Surg, Kanagawa, Japan. Med Ctr Hosp, Kitasato Inst, Dept Otolaryngol Head & Neck Surg, Saitama, Japan. RP Connor, NP (reprint author), Univ Wisconsin, Ctr Clin Sci, Dept Surg, Div Otolaryngol Head & Neck Surg, Room K4-711,600 Highland Ave, Madison, WI 53792 USA. NR 35 TC 25 Z9 28 U1 0 U2 3 PU ANNALS PUBL CO PI ST LOUIS PA 4507 LACLEDE AVE, ST LOUIS, MO 63108 USA SN 0003-4894 J9 ANN OTO RHINOL LARYN JI Ann. Otol. Rhinol. Laryngol. PD NOV PY 2002 VL 111 IS 11 BP 962 EP 967 PG 6 WC Otorhinolaryngology SC Otorhinolaryngology GA 614EM UT WOS:000179175400002 PM 12450167 ER PT J AU Madihally, SV Toner, M Yarmush, ML Mitchell, RN AF Madihally, SV Toner, M Yarmush, ML Mitchell, RN TI Interferon gamma modulates trauma-induced muscle wasting and immune dysfunction SO ANNALS OF SURGERY LA English DT Article ID RAT SKELETAL-MUSCLE; THERMAL-INJURY; EXPRESSION; DISEASE; BURNS; CELLS; MICE; INTERLEUKIN-6; STIMULATION; CYTOKINES AB Objective To test the effect of burn injury in mice congenitally deficient in interferon gamma (IFN-gamma) and as well as in wild-type animals treated with IFN-gamma neutralizing antibody. Summary Background Data The mechanisms underlying muscle wasting following burn trauma are incompletely characterized, although the hypercatabolic state is a consequence of increased proteasomal degradation. Concurrently, burn injury results in an immunocompromised state, and subsequent infections are the leading cause of morbidity and mortality in these patients. IFN-gamma, best conceptualized as a macrophage activating protein, modulates a variety of biologic pathways potentially relevant to muscle wasting and immune dysfunction. Methods Mice received either a 20% total body surface area burn or a control sham treatment. At days 1, 2, and 7 following treatment, skeletal muscle, peripheral blood, and spleen were harvested from both groups. Protein synthesis and degradation rates were measured. Lymphocyte subpopulation expression of major histocompatibility complex I (MHC I) molecules was assessed by flow cytometry, and proliferation capacity was measured using mixed lymphocyte reaction. Results IFN-gamma is critically involved in burn-induced weight loss; moreover, absence of IFN-gamma virtually abolished skeletal muscle hypercatabolism following burn injury. Lymphocyte proliferation and MHC I expression in the setting of burn trauma are also normalized in the absence of IFN-gamma. Both antigen presentation and proliferation functions are independently affected. Conclusions IFN-gamma plays a fundamental role in mediating the hypercatabolic state of multiple cell types following burn trauma. C1 Brigham & Womens Hosp, Dept Pathol, Div Immunol, Boston, MA 02115 USA. Harvard Univ, Massachusetts Gen Hosp, Sch Med, Ctr Engn Med,Surg Serv, Boston, MA USA. Shriners Hosp Children, Boston, MA USA. RP Mitchell, RN (reprint author), Brigham & Womens Hosp, Dept Pathol, Div Immunol, 221 Longwood Ave,LMRC 515, Boston, MA 02115 USA. RI Madihally, Sundararajan/D-9285-2012 OI Madihally, Sundararajan/0000-0001-7498-5760 NR 34 TC 21 Z9 21 U1 0 U2 1 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0003-4932 J9 ANN SURG JI Ann. Surg. PD NOV PY 2002 VL 236 IS 5 BP 649 EP 657 DI 10.1097/01.SLA.0000032943.21932.F5 PG 9 WC Surgery SC Surgery GA 609YP UT WOS:000178934200016 PM 12409672 ER PT J AU Poole, AR Kobayashi, M Yasuda, T Laverty, S Mwale, F Kojima, T Sakai, T Wahl, C El-Maadawy, S Webb, G Tchetina, E Wu, W AF Poole, AR Kobayashi, M Yasuda, T Laverty, S Mwale, F Kojima, T Sakai, T Wahl, C El-Maadawy, S Webb, G Tchetina, E Wu, W TI Type II collagen degradation and its regulation in articular cartilage in osteoarthritis SO ANNALS OF THE RHEUMATIC DISEASES LA English DT Article; Proceedings Paper CT 4th International Symposium on Advances in Targeted Therapies CY APR 28-MAY 01, 2002 CL MANDELIEU, FRANCE ID CRUCIATE LIGAMENT TRANSECTION; MATRIX-METALLOPROTEINASE; CHONDROCYTE; CLEAVAGE; DAMAGE; DIFFERENTIATION; PROTEOGLYCAN; EXPRESSION; INHIBITOR; ARTHRITIS C1 McGill Univ, Shriners Hosp Children, Dept Surg, Montreal, PQ, Canada. McGill Univ, Shriners Hosp Children, Dept Med, Montreal, PQ, Canada. Kyoto Univ, Sch Med, Dept Orthopaed Surg, Kyoto 606, Japan. Univ Montreal, Fac Med Vet, Dept Clin Sci, St Hyacinthe, PQ J2S 7C6, Canada. Jewish Gen Hosp, Dept Orthopaed Surg, Montreal, PQ, Canada. Nagoya Univ, Sch Med, Dept Orthopaed Surg, Nagoya, Aichi, Japan. Glaxo Wellcome Res & Dev Ltd, Mol Cell Biol Unit, Stevenage SG1 2NY, Herts, England. Massachusetts Gen Hosp, Arthrit Unit, Boston, MA 02114 USA. RP Poole, AR (reprint author), McGill Univ, Shriners Hosp Children, Dept Surg, Montreal, PQ, Canada. EM rpoole@shriners.mcgill.ca RI KOJIMA, Toshihisa/I-7366-2014 NR 36 TC 72 Z9 73 U1 0 U2 3 PU BMJ PUBLISHING GROUP PI LONDON PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND SN 0003-4967 EI 1468-2060 J9 ANN RHEUM DIS JI Ann. Rheum. Dis. PD NOV PY 2002 VL 61 SU 2 BP 78 EP 81 PG 4 WC Rheumatology SC Rheumatology GA 609KZ UT WOS:000178903900020 ER PT J AU Mangi, AA Boeve, TJ Vlahakes, GJ Akins, CW Hilgenberg, AD Ruskin, JN McGovern, BM Torchiana, DF AF Mangi, AA Boeve, TJ Vlahakes, GJ Akins, CW Hilgenberg, AD Ruskin, JN McGovern, BM Torchiana, DF TI Surgical coronary revascularization and antiarrhythmic therapy in survivors of out-of-hospital cardiac arrest SO ANNALS OF THORACIC SURGERY LA English DT Article ID BYPASS GRAFT-SURGERY; VENTRICULAR ARRHYTHMIAS; HIGH-RISK; IMPLANTABLE DEFIBRILLATOR; SUDDEN-DEATH; PREVENTION; DISEASE AB Background. Patients who survive out-of-hospital cardiac arrest are at high risk for recurrent arrest. Coronary artery bypass grafting (CABG) confers a survival advantage, but it is unclear whether antiarrhythmic drugs or an implanted defibrillator confer added benefit. This study was designed to determine predictors for further treatment, survival, and therapeutic internal cardiac defibrillator (ICD) discharge in this patient population. Methods. One hundred and eight patients undergoing CABG after out-of-hospital cardiac arrest were identified over a 12-year period. Case records were retrospectively reviewed. Follow-up was obtained and predictors of outcome events were analyzed. Results. Fifty-four (50%) patients underwent CABG only. Fifty-four received additional treatment that included ICD placement in 23 (21%), antiarrhythmic medications in 19 (18%), or both in 12 (11%). Predictors of ICD placement included left ventricular ejection fraction (LVEF) less than 40% and perioperative intraaortic balloon counterpulsation. ICD or medical management increased survival in patients with LVEF <40%. Predictors of increased mortality included age >65 years, Cleveland Severity Score >8, and female gender. Predictors of therapeutic ICD discharge included age >65 years, reoperative CABG, LVEF <40%, and positive postoperative electrophysiological (EP) study. No patient with a negative postoperative EP study received an ICD, and none suffered sudden cardiac death during follow-up. Conclusions. Patients with coronary artery disease anatomically suitable for CABG who survive an acute out-of-hospital cardiac arrest should undergo EP testing after CABG. Approximately half of these patients are adequately treated by CABG alone. The remainder may benefit from ICD placement or medical antiarrhythmic management. (C) 2002 by The Society of Thoracic Surgeons. C1 Harvard Univ, Massachusetts Gen Hosp, Sch Med, Div Cardiac Surg, Boston, MA 02114 USA. Harvard Univ, Massachusetts Gen Hosp, Sch Med, Div Cardiol, Boston, MA 02114 USA. RP Torchiana, DF (reprint author), Harvard Univ, Massachusetts Gen Hosp, Sch Med, Div Cardiac Surg, Bullfinch 119,55 Fruit St, Boston, MA 02114 USA. NR 20 TC 4 Z9 4 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0003-4975 J9 ANN THORAC SURG JI Ann. Thorac. Surg. PD NOV PY 2002 VL 74 IS 5 BP 1510 EP 1516 AR PII S0003-4975(02)04086-9 DI 10.1016/S0003-4975(02)04086-9 PG 7 WC Cardiac & Cardiovascular Systems; Respiratory System; Surgery SC Cardiovascular System & Cardiology; Respiratory System; Surgery GA 615TG UT WOS:000179262300020 PM 12440601 ER PT J AU Giglia, JS Ollerenshaw, JD Dawson, PE Black, KS Abbott, WM AF Giglia, JS Ollerenshaw, JD Dawson, PE Black, KS Abbott, WM TI Cryopreservation prevents arterial allograft dilation SO ANNALS OF VASCULAR SURGERY LA English DT Article ID SAPHENOUS-VEIN; RECONSTRUCTION; PROSTHESES; EXPERIENCE; HOMOGRAFT; TERM AB Historically, immune-mediated degradation and subsequent aneurysm formation have limited the usefulness of cryopreserved arterial allografts. This study tested the hypothesis that modern cryopreserved arterial allografts are protected from immune-mediated dilation. Abdominal aortas were harvested from anesthetized rats (Lewis and Brown-Norway) for immediate implantation or cryopreservation. Subsequently, Lewis rats underwent infrarenal aortic replacement with either an acutely harvested or a cryopreserved graft. There were four experimental groups: (1) acutely harvested isografts (Iso; n = 6), (2) cryopreserved isografts (C-Iso; n 6), (3) cryopreserved allografts (C-Allo; n = 6), and (4) acutely harvested allografts (Allo; n 6). All grafts were explanted at 8 weeks. A video camera and edge detection software were used to measure systolic and diastolic in vivo graft diameter (d). Measurement of arterial blood pressure (p) allowed calculation of compliance (deltad/deltap). Tail-cuff plethysmography was used to assess graft patency at 1 week. Graft diameter and blood pressure measurements were repeated at harvest. All harvested grafts were examined histologically. Our results showed that cryopreservation prevented immune-mediated dilation in arterial allografts in our 8-week rat implant model. Furthermore, the compliance of the cryopreserved grafts and was similar to that of controls. Further investigation is needed to delineate the exact mechanism of these potential cliniclly significant findings. C1 Univ Cincinnati, Coll Med, Dept Surg, Div Vasc Surg, Cincinnati, OH 45267 USA. Cryolife Inc, Kennesaw, GA USA. Massachusetts Gen Hosp, Dept Surg, Div Vasc Surg, Boston, MA USA. RP Giglia, JS (reprint author), Univ Cincinnati, Coll Med, Dept Surg, Div Vasc Surg, 231 Albert Sabin Way,Med Sci Bldg,Rm 2363, Cincinnati, OH 45267 USA. FU NHLBI NIH HHS [1R43 HL 59029-01] NR 18 TC 12 Z9 13 U1 0 U2 2 PU SPRINGER-VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 USA SN 0890-5096 J9 ANN VASC SURG JI Ann. Vasc. Surg. PD NOV PY 2002 VL 16 IS 6 BP 762 EP 767 DI 10.1007/s10016-001-0072-1 PG 6 WC Surgery; Peripheral Vascular Disease SC Surgery; Cardiovascular System & Cardiology GA 632BD UT WOS:000180202400014 PM 12391500 ER PT J AU Ince, D Zhang, XM Silver, LC Hooper, DC AF Ince, D Zhang, XM Silver, LC Hooper, DC TI Dual targeting of DNA gyrase and topoisomerase IV: Target interactions of garenoxacin (BMS-284756, T-3811ME), a new desfluoroquinolone SO ANTIMICROBIAL AGENTS AND CHEMOTHERAPY LA English DT Article ID QUINOLONE RESISTANCE MUTATIONS; STAPHYLOCOCCUS-AUREUS; STREPTOCOCCUS-PNEUMONIAE; IN-VITRO; DES-F(6) QUINOLONE; FLUOROQUINOLONE RESISTANCE; DES-FLUORO(6) QUINOLONE; DETERMINING REGION; ESCHERICHIA-COLI; MECHANISMS AB We determined the target enzyme interactions of garenoxacin (BMS-284756, T-3811ME), a novel desfluoroquinolone, in Staphylococcus aureus by genetic and biochemical studies. We found garenoxacin to be four- to eightfold more active than ciprofloxacin against wild-type S. aureus. A single topoisomerase IV or gyrase mutation caused only a 2- to 4-fold increase in the MIC of garenoxacin, whereas a combination of mutations in both loci caused a substantial increase (128-fold). Overexpression of the NorA efflux pump had minimal effect on resistance to garenoxacin. With garenoxacin at twice the MIC, selection of resistant mutants (<7.4 x 10(-12) to 4.0 x 10(-11)) was 5 to 6 log units less than that with ciprofloxacin. Mutations inside or outside the quinolone resistance-determining regions (QRDR) of either topoisomerase IV, or gyrase, or both were selected in single-step mutants, suggesting dual targeting of topoisomerase IV and gyrase. Three of the novel mutations were shown by genetic experiments to be responsible for resistance. Studies with purified topoisomerase IV and gyrase from S. aureus also showed that garenoxacin had similar activity against topoisomerase IV and gyrase (50% inhibitory concentration, 1.25 to 2.5 and 1.25 mug/ml, respectively), and although its activity against topoisomerase IV was 2-fold greater than that of ciprofloxacin, its activity against gyrase was 10-fold greater. This study provides the first genetic and biochemical data supporting the dual targeting of topoisomerase IV and gyrase in S. aureus by a quinolone as well as providing genetic proof for the expansion of the QRDRs to include the 5' terminus of grlB and the 3' terminus of gyrA. C1 Harvard Univ, Massachusetts Gen Hosp, Sch Med, Div Infect Dis, Boston, MA 02114 USA. Harvard Univ, Massachusetts Gen Hosp, Sch Med, Med Serv, Boston, MA 02114 USA. RP Harvard Univ, Massachusetts Gen Hosp, Sch Med, Div Infect Dis, 55 Fruit St, Boston, MA 02114 USA. EM dhooper@partners.org FU NIAID NIH HHS [R01 AI023988, R01 AI23988] NR 56 TC 53 Z9 56 U1 0 U2 2 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA SN 0066-4804 EI 1098-6596 J9 ANTIMICROB AGENTS CH JI Antimicrob. Agents Chemother. PD NOV PY 2002 VL 46 IS 11 BP 3370 EP 3380 DI 10.1128/AAC.46.11.3370-3380.2002 PG 11 WC Microbiology; Pharmacology & Pharmacy SC Microbiology; Pharmacology & Pharmacy GA 606BK UT WOS:000178712800006 PM 12384338 ER PT J AU Wexler, HM Molitoris, D St John, S Vu, A Read, EK Finegold, SM AF Wexler, HM Molitoris, D St John, S Vu, A Read, EK Finegold, SM TI In vitro activities of faropenem against 579 strains of anaerobic bacteria SO ANTIMICROBIAL AGENTS AND CHEMOTHERAPY LA English DT Article ID CARBAPENEMASE GENE CFIA; BACTEROIDES-FRAGILIS; PSEUDOMONAS-AERUGINOSA; HYDROLYZING ENZYME; BETA-LACTAMASE; ORAL PENEM; IMIPENEM; RESISTANCE; EXPRESSION; OPRD AB The activity of faropenem, a new oral penem, was tested against 579 strains of anaerobic bacteria by using the NCCLS-approved reference method. Drugs tested included amoxicillin-clavulanate, cefoxitin, clindamycin, faropenem, imipenem, and metronidazole. Of the 176 strains of Bacteroides fragilis group isolates tested, two isolates had faropenem MICs of 64 mug/ml and imipenem MICs of >32 mug/ml. Faropenem had an MIC of 16 mug/ml for an additional isolate of B. fragilis; this strain was sensitive to imipenem (MIC of 1 mug/ml). Both faropenem and imipenem had MICs of less than or equal to4 mug/ml for all isolates of Bacteroides capillosus (10 isolates), Bacteroides splanchnicus (13 isolates), Bacteroides ureolyticus (11 isolates), Bilophila wadsworthia (11 isolates), Porphyromonas species (42 isolates), Prevotella species (78 isolates), Campylobacter species (25 isolates), Sutterella wadsworthensis (11 isolates), Fusobacterium nucleatum (19 isolates), Fusobacterium mortiferum/varium (20 isolates), and other Fusobacterium species (9 isolates). Faropenem and imipenem had MICs of 16 to 32 mug/ml for two strains of Clostridium difficile; the MICs for all other strains of Clostridium tested (69 isolates) were less than or equal to4 mug/ml. Faropenem had MICs of 8 and 16 mug/ml, respectively, for two strains of Peptostreptococcus anaerobius (MICs of imipenem were 2 mug/ml). MICs were less than or equal to4 mug/ml for all other strains of gram-positive anaerobic cocci (53 isolates) and non-spore-forming gram-positive rods (28 isolates). Other results were as expected and reported in previous studies. No metronidazole resistance was seen in gram-negative anaerobes other than S. wadsworthensis (18% resistant); 63% of gram-positive non-spore-forming rods were resistant. Some degree of clindamycin resistance was seen in most of the groups tested. C1 Vet Adm Greater Los Angeles Healthcare Syst, Med Serv, Los Angeles, CA 90073 USA. Vet Adm Greater Los Angeles Healthcare Syst, Res Serv, Los Angeles, CA 90073 USA. Univ Calif Los Angeles, Sch Med, Dept Med, Los Angeles, CA 90024 USA. Univ Calif Los Angeles, Sch Med, Dept Microbiol Mol Genet & Immunol, Los Angeles, CA 90024 USA. RP Wexler, HM (reprint author), Wadsworth Anaerobe Lab, Bldg 304,Room E3-224,VAGLAHS 692-151J, Los Angeles, CA 90073 USA. NR 19 TC 20 Z9 22 U1 0 U2 1 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA SN 0066-4804 J9 ANTIMICROB AGENTS CH JI Antimicrob. Agents Chemother. PD NOV PY 2002 VL 46 IS 11 BP 3669 EP 3675 DI 10.1128/AAC.46.11.3669-3675.2002 PG 7 WC Microbiology; Pharmacology & Pharmacy SC Microbiology; Pharmacology & Pharmacy GA 606BK UT WOS:000178712800057 PM 12384389 ER PT J AU Chung, JH Yano, K Lee, MK Youn, CS Seo, JY Kim, KH Cho, KH Eun, HC Detmar, M AF Chung, JH Yano, K Lee, MK Youn, CS Seo, JY Kim, KH Cho, KH Eun, HC Detmar, M TI Differential effects of photoaging vs intrinsic aging on the vascularization of human skin SO ARCHIVES OF DERMATOLOGY LA English DT Article ID TOPICAL TRETINOIN; GROWTH; ANGIOGENESIS AB Objective: To quantify the distinct effects of photoaging vs; intrinsic aging of human skin on cutaneous vascularization in the Korean population. Design: Case series. Setting: University hospital. Participants: A total of 21 healthy Korean volunteers from the third to the ninth decades of life. Intervention: Skin biopsy specimens were obtained from chronically sun-exposed and sun-protected skin of each participant. Main Outcome Measures: Frozen sections were stained for the platelet endothelial cell adhesion molecule CD31 (PECAM-1), and computer-assisted quantitative image analysis was performed to quantify cutaneous vascular density and vessel size. Results: Intrinsically aged and photoaged skin showed an age-dependent reduction of cutaneous vessel size. However, only photoaged skin exhibited significantly reduced numbers of dermal vessels, in particular in the subepidermal areas that displayed extensive matrix damage. Linear regression analysis revealed an inverse relation of vessel numbers and age in sun-damaged, but not in sun-protected, skin. Conclusions: In Korean skin, chronic photodamage results in a gradual decrease in the number and size of dermal vessels over several decades of sun exposure, most likely due to degenerative changes of the dermal extracellular matrix. Because the present investigation was restricted to ethnic Korean volunteers, future studies are needed to evaluate whether similar changes can be observed in whites. C1 Seoul Natl Univ Hosp, Dept Dermatol, Chongno Gu, Lab Cutaneous Aging Res,Clin Res Inst, Seoul 110744, South Korea. Seoul Natl Univ, Dept Dermatol, Coll Med, Seoul 151, South Korea. Massachusetts Gen Hosp, Cutaneous Biol Res Ctr, Dept Dermatol, Boston, MA 02114 USA. Harvard Univ, Sch Med, Cambridge, MA 02138 USA. RP Chung, JH (reprint author), Seoul Natl Univ Hosp, Dept Dermatol, Chongno Gu, Lab Cutaneous Aging Res,Clin Res Inst, 28 Yungon Dong, Seoul 110744, South Korea. RI Kim, Kyu Han/E-7814-2012; Chung, Jin Ho/C-3604-2011; Cho, Kwang Hyun/J-5661-2012; Eun, Hee Chul/J-5568-2012 FU NCI NIH HHS [CA69184, CA86410] NR 20 TC 49 Z9 51 U1 0 U2 2 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 USA SN 0003-987X J9 ARCH DERMATOL JI Arch. Dermatol. PD NOV PY 2002 VL 138 IS 11 BP 1437 EP 1442 DI 10.1001/archderm.138.11.1437 PG 6 WC Dermatology SC Dermatology GA 617UL UT WOS:000179379200006 PM 12437449 ER PT J AU Egan, RA Lessell, S AF Egan, RA Lessell, S TI A contribution to the natural history of optic nerve sheath meningiomas SO ARCHIVES OF OPHTHALMOLOGY LA English DT Article ID 3-DIMENSIONAL CONFORMAL RADIATION; SPONTANEOUS VISUAL IMPROVEMENT; THERAPY AB Objective: To describe the natural history of patients with primary optic nerve sheath meningioma (ONSM) who were cared for without intervention. Methods: A retrospective review of the medical records of 42 patients identified in the database of an academic neuro-ophthalmology unit who had been diagnosed with a unilateral ONSM. Twenty-five had been referred after treatment had been implemented, and 1 was blind at referral. The remaining 16 patients who were followed up with observation only are the focus of this study. Results: The study subjects were followed up for a mean of 6.2 years (range, 2-18 years). The mean follow-up from the time of the first symptom was 10.2 years (range, 3-28 years). No patient died or incurred neurological deficits other than vision loss. At diagnosis, 12 of 16 had a visual acuity of 20/100 or better; 11 had a visual acuity of 20/30 or better. At follow-up, 8 of 16 had a visual acuity of 20/100 or better; 6 had a visual acuity of 20/30 or better. Three patients had slight improvement. Visual fields remained stable in 4 patients and improved in the 3 patients whose visual acuity also improved. Conclusions: Some patients with ONSM have a stable course for many years, and a few may even show slight improvement. The routine application of radiation therapy may unnecessarily expose some patients to complications and should be reserved for those patients whose visual function declines under observation. C1 Oregon Hlth Sci Univ, Casey Eye Inst, Portland, OR 97201 USA. Harvard Univ, Massachusetts Eye & Ear Infirm, Sch Med, Boston, MA USA. RP Egan, RA (reprint author), Oregon Hlth Sci Univ, Casey Eye Inst, 3375 SW Terwilliger Blvd, Portland, OR 97201 USA. NR 9 TC 34 Z9 34 U1 0 U2 0 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 USA SN 0003-9950 J9 ARCH OPHTHALMOL-CHIC JI Arch. Ophthalmol. PD NOV PY 2002 VL 120 IS 11 BP 1505 EP 1508 PG 4 WC Ophthalmology SC Ophthalmology GA 614RE UT WOS:000179203400010 PM 12427064 ER PT J AU Rivolta, C Berson, EL Dryja, TP AF Rivolta, C Berson, EL Dryja, TP TI Paternal uniparental heterodisomy with partial isodisomy of chromosome 1 in a patient with retinitis pigmentosa mutation in without hearing loss and a missense the usher syndrome type II gene USH2A SO ARCHIVES OF OPHTHALMOLOGY LA English DT Article ID JUNCTIONAL EPIDERMOLYSIS-BULLOSA; LOW-PENETRANCE; DISOMY; RETINOBLASTOMA; ASSOCIATION; PEDIGREES AB Objective: To evaluate a form of nonmendelian inheritance in a patient with retinitis pigmentosa (RP). Methods: Direct DNA sequencing of the USH2A coding region and microsatellite analysis of polymorphic markers from chromosome 1 and other chromosomes. Results: A patient with RP without hearing loss caused by the homozygous mutation Cys759Phe in the USH2A gene on chromosome 1q was found to be the daughter of a noncarrier mother and a father who was heterozygous for this change. Further evaluation with microsatellite markers revealed that the patient had inherited 2 copies of chromosome 1 from her father and none from her mother. The paternally derived chromosome 1's were heteroallelic from the centromere of chromosome 1 to the proximal short and long arms. The distal regions of the short and long arms of chromosome 1 were homoallelic, including the region of 1q with the mutant USH2A allele. This genetic pattern is compatible with a phenomenon of uniparental primary heterodisomy with regions of homozygosity arising through a nondisjunction event during paternal meiosis 1 and subsequent trisomy rescue or gamete complementation. A paternal second cousin of the patient also had RP and also had an identical heterozygous mutation in the USH2A gene in the same codon. However, the analysis of an isocoding polymorphism 20 base pairs away and closely linked microsatellite markers in the patient and family members indicated that the 2 mutant alleles are unlikely to be identical by descent and that the 2 relatives fortuitously had RP and a mutation in the same codon of the USH2A gene. Conclusion: This family illustrates that recessive RP without hearing loss can rarely be inherited from only 1 unaffected carrier parent in a nonmendelian manner. Clinical Relevance: The genetic counseling of families with recessively inherited eye diseases must take into consideration the possibility that an unaffected heterozygous carrier can have an affected offspring homozygous for the same mutation, even if the carrier's spouse has wild-type alleles at the disease locus. C1 Harvard Univ, Massachusetts Eye & Ear Infirm, Sch Med, Ocular Mol Genet Inst, Boston, MA 02114 USA. Harvard Univ, Massachusetts Eye & Ear Infirm, Sch Med, Berman Gund Lab Study Retinal Degenerat, Boston, MA 02114 USA. RP Dryja, TP (reprint author), Harvard Univ, Massachusetts Eye & Ear Infirm, Sch Med, Ocular Mol Genet Inst, 243 Charles St, Boston, MA 02114 USA. FU NEI NIH HHS [EY00169, EY08683] NR 23 TC 26 Z9 27 U1 0 U2 2 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 USA SN 0003-9950 J9 ARCH OPHTHALMOL-CHIC JI Arch. Ophthalmol. PD NOV PY 2002 VL 120 IS 11 BP 1566 EP 1571 PG 6 WC Ophthalmology SC Ophthalmology GA 614RE UT WOS:000179203400019 PM 12427073 ER PT J AU Van Cott, EM Laposata, M Prins, MH AF Van Cott, EM Laposata, M Prins, MH TI Laboratory evaluation of hypercoagulability with venous or arterial thrombosis - Venous thromboembolism, myocardial infarction, stroke, and other conditions SO ARCHIVES OF PATHOLOGY & LABORATORY MEDICINE LA English DT Article; Proceedings Paper CT 36th Conference of the College-of-American-Pathologists CY NOV 09-11, 2001 CL ATLANDA, GEORGIA SP Coll Amer Pathol ID FACTOR-V-LEIDEN; C-REACTIVE PROTEIN; CORONARY-HEART-DISEASE; DEEP-VEIN THROMBOSIS; COAGULATION-FACTOR-V; MIDDLE-AGED MEN; METHYLENETETRAHYDROFOLATE REDUCTASE GENE; UNSTABLE ANGINA-PECTORIS; INDEPENDENT RISK FACTOR; PLASMA HOMOCYSTEINE CONCENTRATIONS AB Objective.-To provide recommendations for hypercoagulation testing for patients with venous, arterial, or neurovascular thrombosis, as reflected in the medical literature and the consensus opinion of recognized experts in the field. Data Sources, Extraction, and Synthesis.-The authors extensively examined the literature and current practices, and prepared a draft manuscript with preliminary recommendations. The draft manuscript was circulated to each of the expert participants (n = 30) in the consensus conference prior to the convening of the conference. The manuscript and recommendations were then presented at the conference for discussion. Recommendations were accepted if a consensus of the 28 experts attending the conference was reached. The discussions were also used to revise the manuscript into its final form. Conclusions.-The resulting article provides 17 recommendations for hypercoagulation testing in the setting of venous, arterial, or neurovascular thrombosis. The supporting evidence for test selection is analyzed and cited, and consensus recommendations for test selection are presented. Issues for which a consensus was not reached at the conference are also discussed. C1 Massachusetts Gen Hosp, Dept Pathol, Boston, MA 02114 USA. Univ Maasticht, Dept Clin Epidemiol, Maastricht, Netherlands. Harvard Univ, Sch Med, Dept Pathol, Boston, MA 02115 USA. RP Van Cott, EM (reprint author), Massachusetts Gen Hosp, Dept Pathol, 55 Fruit St, Boston, MA 02114 USA. NR 229 TC 44 Z9 46 U1 1 U2 2 PU COLLEGE AMER PATHOLOGISTS PI NORTHFIELD PA C/O KIMBERLY GACKI, 325 WAUKEGAN RD, NORTHFIELD, IL 60093-2750 USA SN 0003-9985 J9 ARCH PATHOL LAB MED JI Arch. Pathol. Lab. Med. PD NOV PY 2002 VL 126 IS 11 BP 1281 EP 1295 PG 15 WC Medical Laboratory Technology; Medicine, Research & Experimental; Pathology SC Medical Laboratory Technology; Research & Experimental Medicine; Pathology GA 614EA UT WOS:000179174300006 PM 12421136 ER PT J AU Brenner, BR Nowak-Gottl, U Kosch, A Manco-Johnson, M Laposata, M AF Brenner, BR Nowak-Gottl, U Kosch, A Manco-Johnson, M Laposata, M TI Diagnostic studies for thrombophilia in women on hormonal therapy and during pregnancy, and in children SO ARCHIVES OF PATHOLOGY & LABORATORY MEDICINE LA English DT Article; Proceedings Paper CT 36th Conference of the College-of-American-Pathologists CY NOV 09-11, 2001 CL ATLANDA, GEORGIA SP Coll Amer Pathol ID FACTOR-V-LEIDEN; ACTIVATED PROTEIN-C; PROTHROMBOTIC RISK-FACTORS; NEONATAL PURPURA FULMINANS; ORAL-CONTRACEPTIVE USERS; PORTAL-VEIN THROMBOSIS; VENOUS THROMBOEMBOLIC COMPLICATIONS; ACUTE LYMPHOBLASTIC-LEUKEMIA; CATHETER-RELATED THROMBOSIS; SEVERE HEMOPHILIA-A AB Objective.-To review the role of acquired and inherited prothrombotic risk factors that increase the risk of thrombosis in oral contraceptive users, during pregnancy, and in neonates, infants, and children; and to determine by the consensus opinion of recognized experts in the field which risk factors should be determined in which individuals at which time. Data Sources.-Review of the medical literature and current clinical practice by a panel of experts in the field of thrombophilia. Data Extraction and Synthesis.-The experts made an extensive review of the published literature and prepared a draft manuscript, which included preliminary recommendations. The draft manuscript was circulated to participants in the College of American Pathologists Conference XXXVI: Diagnostic Issues in Thrombophilia prior to the conference. The manuscript and recommendations were then presented at the conference for discussion. Recommendations were accepted if a consensus of the 26 experts attending the conference was reached. The results of the discussion were used to revise the manuscript into its final form. Conclusions.-This report reviews the options for testing for thrombophilic states in women using oral contraceptives, during pregnancy, and in neonates and children. General guidelines for testing in these clinical situations are provided, along with citation of the appropriate supporting literature. C1 Massachusetts Gen Hosp, Div Lab Med, Boston, MA 02114 USA. Univ Colorado, Hlth Sci Ctr, Denver, CO USA. Univ Childrens Hosp, Munster, Germany. Rambam Med Ctr, Inst Hematol, Haifa, Israel. RP Laposata, M (reprint author), Massachusetts Gen Hosp, Div Lab Med, Gray Bldg,Room 235,32 Fruit St, Boston, MA 02114 USA. NR 132 TC 32 Z9 33 U1 0 U2 1 PU COLLEGE AMER PATHOLOGISTS PI NORTHFIELD PA C/O KIMBERLY GACKI, 325 WAUKEGAN RD, NORTHFIELD, IL 60093-2750 USA SN 0003-9985 J9 ARCH PATHOL LAB MED JI Arch. Pathol. Lab. Med. PD NOV PY 2002 VL 126 IS 11 BP 1296 EP 1303 PG 8 WC Medical Laboratory Technology; Medicine, Research & Experimental; Pathology SC Medical Laboratory Technology; Research & Experimental Medicine; Pathology GA 614EA UT WOS:000179174300007 PM 12421137 ER PT J AU Jaffer, FA Tung, CH Gerszten, RE Weissleder, R AF Jaffer, FA Tung, CH Gerszten, RE Weissleder, R TI In vivo Imaging of thrombin activity in experimental thrombi with thrombin-sensitive near-infrared molecular probe SO ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY LA English DT Article DE thrombin; near-infrared imaging; optical fluorescence; molecular imaging; thrombosis ID CONTRAST AGENT; PLAQUES AB Objective-Thrombin, a serine protease, plays an important role in thrombosis as well as other cellular and developmental processes. In this study, we investigated the ability of a novel thrombin-activatable molecular probe to provide in vivo images of thrombin activity in experimental thrombi. Methods and Results-The thrombin probe consists of a near-infrared (NIR) fluorochrome attached to a delivery vehicle via a thrombin-specific oligopeptide substrate. In human blood, endogenous thrombin activated the thrombin probe and increased the fluorescence signal by 18-fold (P = 0.008). Hirudin, a specific thrombin inhibitor, suppressed probe activation by 82% (P = 0.007). Imaging of in vivo thrombin activity was then investigated in acute experimental murine thrombosis models up to 12 hours. After systemic thrombin probe injection, focal NIR fluorescence signal enhancement was rapidly detected within acute and subacute thrombi. In contrast, no thrombosis signal enhancement was seen in similar experiments with a control NIR fluorochrome, Conclusions-Thrombin activity can be imaged in vivo by using a novel thrombin-activatable and thrombin-specific NIR molecular probe. The thrombin probe could enhance the understanding of the role of thrombin in thrombogenesis and other homeostatic and pathological conditions. C1 Harvard Univ, Sch Med, Massachusetts Gen Hosp, Ctr Mol Imaging Res, Charlestown, MA 02139 USA. Harvard Univ, Sch Med, Massachusetts Gen Hosp, Ctr Immunol & Inflammatory Dis, Charlestown, MA 02139 USA. Massachusetts Gen Hosp, Dept Med, Div Cardiol, Boston, MA 02114 USA. RP Jaffer, FA (reprint author), Harvard Univ, Sch Med, Massachusetts Gen Hosp, Ctr Mol Imaging Res, 149 13th St,Room 5406, Charlestown, MA 02139 USA. OI Jaffer, Farouc/0000-0001-7980-384X; Tung, Ching-Hsuan/0000-0001-6648-6195 FU NCI NIH HHS [P50-CA-86355, R24-CA-92782, R33-CA-88365]; NHLBI NIH HHS [R01-HL-67768] NR 28 TC 82 Z9 89 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 NOV PY 2002 VL 22 IS 11 BP 1929 EP 1935 DI 10.1161/01.ATV.0000033089.56970.2D PG 7 WC Hematology; Peripheral Vascular Disease SC Hematology; Cardiovascular System & Cardiology GA 615QM UT WOS:000179258000032 PM 12426227 ER PT J AU Namjou, B Nath, SK Kilpatrick, J Kelly, JA Reid, J James, JA Harley, JB AF Namjou, B Nath, SK Kilpatrick, J Kelly, JA Reid, J James, JA Harley, JB TI Stratification of pedigrees multiplex for systemic lupus erythematosus and for self-reported rheumatoid arthritis detects a systemic lupus erythematosus susceptibility gene (SLER1) at 5p15.3 SO ARTHRITIS AND RHEUMATISM LA English DT Article ID AUTOIMMUNE-DISEASES; TELOMERASE ACTIVITY; REVISED CRITERIA; GENOME SCAN; LINKAGE; FAMILIES; CLASSIFICATION; MODELS; LOCUS AB Objective. Arthritis is a common manifestation in systemic lupus erythematosus (SLE), appearing in similar to85% of patients. Often, the polyarthritis at presentation of SLE cannot be distinguished from rheumatoid arthritis (RA) by physical examination or history. Indeed, physicians initially tell many SLE patients that they have RA (one source of "self-reported RA"), only to have SLE established later. In addition, RA aggregates in families with an SLE proband. We predicted that pedigrees multiplex for both SLE and for self-reported RA would better isolate particular genetic effects. If this proved to be true, we would then use the increased genetic homogeneity to more easily reveal genetic linkage. Methods. From a collection of 160 pedigrees multiplex for SLE, we selected 36 pedigrees that also contained greater than or equal to2 members with self-reported RA (19 pedigrees were African American, 14 were European American, and 3 were of other ethnic origin). Data from a genome scan of 307 microsatellite markers were evaluated for SLE linkage by contemporary genetic epidemiologic techniques. Results. The most significant evidence of linkage to SLE was obtained at 5p15.3 in the European American pedigrees by both parametric (logarithm of odds [LOD] score 6.2, P 9.3 X 10(-8)) and nonparametric (LOD score 6.9, P 1.7 X 10(-8)) methods. The bestfitting model for this putative SLE gene in this region was a recessive gene with a population frequency of 5% and with 50% penetrance in females and 15% penetrance in males at virtually 100% homogeneity. Conclusion. For a genetically complex disease phenotype, an unusually powerful linkage has been found with SLE at 5p15.3 in European American pedigrees multiplex for SLE and for self-reported RA. This result predicts the presence of a gene at the top of chromosome 5 in this subset of patients that is important for the pathogenesis of SLE. C1 Oklahoma Med Res Fdn, Oklahoma City, OK 73104 USA. Univ Oklahoma, Hlth Sci Ctr, Oklahoma City, OK USA. US Dept Vet Affairs, Med Ctr, Oklahoma City, OK USA. RP Harley, JB (reprint author), Oklahoma Med Res Fdn, 825 NE 13th St, Oklahoma City, OK 73104 USA. FU NCRR NIH HHS [RR-15577]; NIAID NIH HHS [AI-31584, AI-24717]; NIAMS NIH HHS [AR-12253, AR-42460, AR-45231] NR 42 TC 25 Z9 26 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA SN 0004-3591 J9 ARTHRITIS RHEUM JI Arthritis Rheum. PD NOV PY 2002 VL 46 IS 11 BP 2937 EP 2945 DI 10.1002/art.10588 PG 9 WC Rheumatology SC Rheumatology GA 615HJ UT WOS:000179239500015 PM 12428235 ER PT J AU Waldman, ID Faraone, SV AF Waldman, ID Faraone, SV TI A meta-analysis of linkage and association between the dopamine transporter gene (DAT1) and childhood ADHD SO BEHAVIOR GENETICS LA English DT Meeting Abstract C1 Harvard Univ, Sch Med, Massachusetts Gen Hosp, Dept Psychiat, W Bridgewater, MA 02376 USA. Emory Univ, Dept Psychol, Atlanta, GA 30322 USA. NR 0 TC 3 Z9 3 U1 0 U2 1 PU KLUWER ACADEMIC/PLENUM PUBL PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA SN 0001-8244 J9 BEHAV GENET JI Behav. Genet. PD NOV PY 2002 VL 32 IS 6 BP 487 EP 487 PG 1 WC Behavioral Sciences; Genetics & Heredity; Psychology, Multidisciplinary SC Behavioral Sciences; Genetics & Heredity; Psychology GA 607XC UT WOS:000178815200112 ER PT J AU Prodhan, P Kinane, TB AF Prodhan, P Kinane, TB TI Developmental paradigms in terminal lung development SO BIOESSAYS LA English DT Article ID RETINOIC ACID RECEPTORS; SONIC HEDGEHOG; FETAL LUNG; BRANCHING MORPHOGENESIS; FIBROBLAST-GROWTH; LIMB DEVELOPMENT; PDGF-A; BRONCHOPULMONARY DYSPLASIA; MICE BEARING; MOUSE LUNG AB Late lung development comprises the formation of the terminal sac followed by the subdivision of the terminal sac by septa into alveoli and results in the formation of the gas-exchange surface of the lung. This developmentally regulated process involves a complex epithelium-mesenchyme interaction via evolutionarily conserved molecular signaling pathways. In addition, there is a continuous process of vascular growth and development. Currently there are large gaps in our understanding of the molecular mechanisms involved in the formation of the gas-exchange surface. In this review, we attempt to integrate and reconcile the morphologic features in late lung development with what is known about the molecular basis for these processes. We describe the formation of the terminal sac and the subsequent formation of the septa, which divide the terminal sac into alveoli, in terms of the classically described developmental stages of induction, morphogenesis and differentiation. We believe that evolutionarily conserved pathways regulate this process and that morphogen gradients are likely to be a central mechanism. In addition, we highlight the importance of the molecular mechanisms involved in the simultaneous development of the vascular bed and its importance in the late development of the lungs. (C) 2002 Wiley Periodicals, Inc. C1 Massachusetts Gen Hosp, Dept Pediat, Pediat Intens Care Unit, Boston, MA 02114 USA. Harvard Univ, Sch Med, Boston, MA 02115 USA. Massachusetts Gen Hosp, Pediat Pulm Unit, Boston, MA 02114 USA. RP Kinane, TB (reprint author), Massachusetts Gen Hosp, Pediat Pulm Unit, Jackson 14,GRJ 1416,55 Fruit St, Boston, MA 02114 USA. NR 62 TC 29 Z9 31 U1 0 U2 1 PU COMPANY OF BIOLOGISTS LTD PI CAMBRIDGE PA BIDDER BUILDING CAMBRIDGE COMMERCIAL PARK COWLEY RD, CAMBRIDGE CB4 4DL, CAMBS, ENGLAND SN 0265-9247 J9 BIOESSAYS JI Bioessays PD NOV PY 2002 VL 24 IS 11 BP 1052 EP 1059 DI 10.1002/bies.10177 PG 8 WC Biochemistry & Molecular Biology; Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics GA 608YD UT WOS:000178874600010 PM 12386936 ER PT J AU Wilcox, MA Faraone, SV Su, J Van Eerdewegh, P Tsuang, MT AF Wilcox, MA Faraone, SV Su, J Van Eerdewegh, P Tsuang, MT TI Genome scan of three quantitative traits in schizophrenia pedigrees SO BIOLOGICAL PSYCHIATRY LA English DT Article DE schizophrenia; linkage; quantitative traits; Scale for the Assessment of Negative Symptoms; Scale for the Assessment of Positive Symptoms; genetics ID SUSCEPTIBILITY LOCUS; LINKAGE ANALYSIS; MILLENNIUM-CONSORTIUM; GENETIC-HETEROGENEITY; DIAGNOSTIC INTERVIEW; CHROMOSOMES 5Q; 10P; 6P; 6Q; PHENOTYPES AB Background: Twin and adoption studies have consistently implicated genes in the etiology of schizophrenia. Molecular genetic studies have found some consistent support for linkage to many regions of the genome. Despite these encouraging results, none of these findings have achieved genome-wide levels of statistical significance, and none have been consistently replicated. Methods: This report is a follow-up of a genome scan that analyzed linkage to the diagnosis of schizophrenia in a series of sibling pairs in the National Institute of Mental Health Genetics Initiative for Schizophrenia data. In this report, we use the same sample to assess linkage to three quantitative traits developed from the Scale for the Assessment of Negative Symptoms and the Scale for the Assessment of Positive Symptoms: positive, negative, and disorganized symptoms. Results: We show suggestive linkage to chromosomes 6, 9, and 20 for the disorganized trait and to chromosome 12 for the negative trait. We also show weak association with PAH (phenylalanine hydroxylase) on that chromosome. Conclusions: The findings on chromosome 6 replicate some prior findings, the other loci are novel. A larger sample would provide more power to detect both linkage and association for this complex disorder. (C) 2002 Society of Biological Psychiatry. C1 Boston Univ, Sch Med, Genet Program, Dept Med, Boston, MA 02215 USA. Harvard Univ, Sch Med, Dept Psychiat, Massachusetts Mental Hlth Ctr, Boston, MA 02115 USA. Massachusetts Gen Hosp, Psychiat Serv, Boston, MA 02114 USA. Harvard Univ, Inst Psychiat Epidemiol & Genet, Boston, MA 02115 USA. Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA. Genome Therapeut, Waltham, MA USA. RP Faraone, SV (reprint author), Harvard Univ, 4F S Main St 301, W Bridgewater, MA 02379 USA. OI Faraone, Stephen/0000-0002-9217-3982 FU NCRR NIH HHS [1 P41 RR03655]; NIMH NIH HHS [1 R01 MH41874-01, 1 R37 MH43518, 5 U01 MH46318, R01 MH44292, R01 MH59624, U01 MH46276, U01 MH46289] NR 33 TC 33 Z9 33 U1 1 U2 3 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD NOV 1 PY 2002 VL 52 IS 9 BP 847 EP 854 AR PII S0006-3223(02)01465-8 DI 10.1016/S0006-3223(02)01465-8 PG 8 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA 606RC UT WOS:000178746100001 PM 12399137 ER PT J AU Tung, CH Mueller, S Weissleder, R AF Tung, CH Mueller, S Weissleder, R TI Novel branching membrane translocational peptide as gene delivery vector SO BIOORGANIC & MEDICINAL CHEMISTRY LA English DT Article ID NUCLEAR-LOCALIZATION PROPERTIES; HIV-1 TAT PROTEIN; IN-VIVO; MAMMALIAN-CELLS; INTRACELLULAR DELIVERY; PLASMA-MEMBRANE; CELLULAR UPTAKE; DNA COMPLEXES; TRANSDUCTION; THERAPY AB A fragment of HIV-tat protein, RKKRRQRRR, has been shown to have membrane penetration and nuclear localization properties, which are critical attributes of gene therapy agents. In this study, we designed a series of arborizing tat peptides, containing 1-8 tat moieties, and evaluated them as transfection enhancers in a variety of cell lines. We found that all compounds complexed with plasmid DNA, but only the molecule containing 8 tat-peptide chains shows significant transfection capabilities. Using rhodamine labeled plasmid and eight tat-peptide complex, we were also able to demonstrate intracellular delivery of the complex by fluorescence microscopy. (C) 2002 Elsevier Science Ltd. All rights reserved. C1 Harvard Univ, Massachusetts Gen Hosp, Sch Med, Ctr Mol Imaging Res, Boston, MA 02129 USA. RP Tung, CH (reprint author), Harvard Univ, Massachusetts Gen Hosp, Sch Med, Ctr Mol Imaging Res, Boston, MA 02129 USA. OI Tung, Ching-Hsuan/0000-0001-6648-6195 FU NIDDK NIH HHS [R21DK55713] NR 49 TC 61 Z9 64 U1 0 U2 6 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 NOV PY 2002 VL 10 IS 11 BP 3609 EP 3614 AR PII S0968-0896(02)00248-1 DI 10.1016/S0968-0896(02)00248-1 PG 6 WC Biochemistry & Molecular Biology; Chemistry, Medicinal; Chemistry, Organic SC Biochemistry & Molecular Biology; Pharmacology & Pharmacy; Chemistry GA 599UN UT WOS:000178353700026 PM 12213476 ER PT J AU Richardson, PG Schlossman, RL Weller, E Hideshima, T Mitsiades, C Davies, F LeBlanc, R Catley, LP Doss, D Kelly, K McKenney, M Mechlowicz, J Freeman, A Deocampo, R Rich, R Ryoo, JJ Chauhan, D Balinski, K Zeldis, J Anderson, KC AF Richardson, PG Schlossman, RL Weller, E Hideshima, T Mitsiades, C Davies, F LeBlanc, R Catley, LP Doss, D Kelly, K McKenney, M Mechlowicz, J Freeman, A Deocampo, R Rich, R Ryoo, JJ Chauhan, D Balinski, K Zeldis, J Anderson, KC TI Immunomodulatory drug CC-5013 overcomes drug resistance and is well tolerated in patients with relapsed multiple myeloma SO BLOOD LA English DT Article ID MARROW STROMAL CELLS; BONE-MARROW; THERAPEUTIC APPLICATIONS; THALIDOMIDE ANALOGS; POTENT INHIBITORS; TNF-ALPHA; GROWTH; INTERLEUKIN-6; ACTIVATION; DEXAMETHASONE AB Thalidomide (Thai) can overcome drug resistance in multiple myeloma (MM) but is associated with somnolence, constipation, and neuropathy. In previous in vitro studies, we have shown that the potent immunomodulatory derivative of thalidomide (IMID) CC-5013 induces apoptosis or growth arrest even in resistant MM cell lines and patient cells, decreases binding of MM cells to bone marrow stromal cells (BMSCs), inhibits the production in the BM milieu of cytokines (interieukin-6 [IL-6], vascular endothelial growth factor [VEGF], tumor necrosis factor-alpha [TNF-alpha]) mediating growth and survival of MM cells, blocks angiogenesis, and stimulates host anti-MM natural killer (NK) cell immunity. Moreover, CC-5013 also inhibits tumor growth, decreases angiogenesis, and prolongs host survival in a human plasmacytoma mouse model. In the present study, we carried out a phase 1 CC-5013 dose-escalation (5 mg/d, 10 mg/d, 25 mg/d, and 50 mg/d) study in 27 patients (median age 57 years; range, 40-71 years) with relapsed and refractory relapsed MM. They received a median of 3 prior regimens (range, 2-6 regimens), including autologous stem cell transplantation and Thai in 15 and 16 patients, respectively. In 24 evaluable patients, no dose-limiting toxicity (DLT) was observed in patients treated at any dose level within the first 28 days; however, grade 3 myelosuppression developed after day 28 in all 13 patients treated with 50 mg/d CC-5013. In 12 patients, dose reduction to 25 mg/d was well tolerated and therefore considered the maximal tolerated dose (MTD). Importantly, no significant somnolence, constipation, or neuropathy has been seen in any cohort. Best responses of at least 25% reduction in paraprotein occurred in 17 (71%) of 24 patients (90% confidence interval [CI], 52%-85%), including 11 (46%) patients who had received prior Thai. Stable disease (less than 25% reduction in paraprotein) was observed in an additional 2 (8%) patients. Therefore, 17 (71%) of 24 patients (90% Cl, 52%-85%) demonstrated benefit from treatment. Our study therefore provides the basis for the evaluation of CC-5013, either alone or in combination, to treat patients with MM at earlier stages of disease. (C) 2002 by The American Society of Hematology. C1 Harvard Univ, Sch Med, Dana Farber Canc Inst, Jerome Lipper Multiple Myeloma Ctr, Boston, MA 02115 USA. Celgene, Warren, NJ USA. RP Anderson, KC (reprint author), Harvard Univ, Sch Med, Dana Farber Canc Inst, Jerome Lipper Multiple Myeloma Ctr, Mayer 557,44 Binney St, Boston, MA 02115 USA. EM kenneth_anderson@dfci.harvard.edu RI Catley, Laurence/E-5313-2013; Ain, Kenneth/A-5179-2012 OI Ain, Kenneth/0000-0002-2668-934X FU PHS HHS [P0-78378, R01 50947] NR 21 TC 563 Z9 581 U1 2 U2 16 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 NOV 1 PY 2002 VL 100 IS 9 BP 3063 EP 3067 DI 10.1182/blood-2002-03-0996 PG 5 WC Hematology SC Hematology GA 608AE UT WOS:000178822300003 PM 12384400 ER PT J AU Du, MQ Diss, TC Liu, HX Ye, HT Hamoudi, RA Cabecadas, J Dong, HY Harris, NL Chan, JKC Rees, JW Dogan, A Isaacson, PG AF Du, MQ Diss, TC Liu, HX Ye, HT Hamoudi, RA Cabecadas, J Dong, HY Harris, NL Chan, JKC Rees, JW Dogan, A Isaacson, PG TI KSHV- and EBV-associated germinotropic lymphoproliferative disorder SO BLOOD LA English DT Article ID SARCOMA-ASSOCIATED HERPESVIRUS; PRIMARY EFFUSION LYMPHOMA; MULTICENTRIC CASTLEMAN-DISEASE; KAPOSIS-SARCOMA; INTERLEUKIN-10; INVOLVEMENT; EXPRESSION; VIRUS; CELLS AB Kaposi sarcoma-associated herpesvirus (KSHV) is known to be associated with 3 distinct lymphoproliferative disorders: primary effusion lymphoma (PEL), multicentric Castleman disease (MCD), and MCD-associated plasmablastic lymphoma. We report 3 cases of a previously undescribed KSHV-associated lymphoproliferative disorder. The disease presented as localized lymphadenopathy and showed a favorable response to chemotherapy or radiotherapy. Histologically, the lymphoproliferation is characterized by plasmablasts that preferentially involved germinal centers of the lymphoid follicles, forming confluent aggregates. They were negative for CD20, CD27, CD79a, CD138, BCL6, and CD10 but showed monotypic kappa or lambda light chain. Clusters of CD10(+)CD20(+) residual follicle center cells were identified in some of the follicles. The plasmablasts were positive for both KSHV and EBV, and most of them also expressed viral interleukin-6 (vIL-6). Unexpectedly, molecular analysis of whole tissue sections or microdissected KSHV-positive aggregates demonstrated a polyclonal or oligoclonal pattern of immunoglobulin (Ig) gene rearrangement. The plasmablasts showed somatic mutation and intraclonal variation in the rearranged Ig genes, and one case expressed switched Ig heavy chain (IgA), suggesting that they originated from germinal center B cells. We propose calling this distinctive entity "KSHV-associated germinotropic lymphoproliferative disorder." C1 UCL, Royal Free & Univ Coll, Sch Med, Dept Histopathol, London WC1E 6JJ, England. Queen Elizabeth Hosp, Dept Pathol, Hong Kong, Hong Kong, Peoples R China. Massachusetts Gen Hosp, Dept Pathol, Boston, MA 02114 USA. Inst Portugues Oncol Francisco Gentil, Serv Anat Patol, Lisbon, Portugal. RP Du, MQ (reprint author), UCL, Royal Free & Univ Coll, Sch Med, Dept Histopathol, Rockefeller Bldg,Univ St, London WC1E 6JJ, England. EM m.du@ucl.ac.uk OI Cabecadas, Jose/0000-0001-6232-1596 NR 16 TC 98 Z9 111 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 NOV 1 PY 2002 VL 100 IS 9 BP 3415 EP 3418 DI 10.1182/blood-2002-02-0487 PG 4 WC Hematology SC Hematology GA 608AE UT WOS:000178822300048 PM 12384445 ER PT J AU Liu, XB Hill, P Haile, DJ AF Liu, XB Hill, P Haile, DJ TI Role of the ferroportin iron-responsive element in iron and nitric oxide dependent gene regulation SO BLOOD CELLS MOLECULES AND DISEASES LA English DT Article; Proceedings Paper CT Meeting on Molecular and Clinical Aspects of Human Iron Metabolism CY SEP 28-OCT 02, 2002 CL CHIEMESEE, GERMANY SP Deutsch Forsch Gemeinsch, Vifor Fresenium Med Care, Blood Cells Fdn, Schwarz pharma, Innova Med Biotech ID TRANSFERRIN RECEPTOR EXPRESSION; RNA-BINDING ACTIVITY; FERRITIN SYNTHESIS; INTERFERON-GAMMA; ACONITASE ACTIVITY; MOUSE MACROPHAGES; DIVALENT-CATIONS; J774 MACROPHAGES; CANCER-PATIENTS; DOWN-REGULATION AB The newly described iron transporter, ferroportin (MTP1, IREG1), is expressed in a variety of tissues including the duodenum and cells of the mononuclear phagocyte system (MPS). In the MPS, ferroportin is hypothesized to be a major exporter of iron scavenged from senescent erythrocytes. Changes in iron metabolism, including the sequestration of iron in the MPS, are characteristic of both acute and chronic inflammation and these conditions induce changes in ferroportin expression. In a mouse model of acute inflammation, LPS administration is associated with reduced MPS ferroportin protein and mRNA expression. In addition, the ferroportin 5' UTR also has an iron-responsive element that binds to the iron-response proteins, but whether there is a role for this IRE in inflammation induced regulation of ferroportin has been unclear. A luciferase reporter gene under the control of the mouse ferroportin promoter and 5' UTR was used to determine if this 5' UTR conferred IRE-dependent regulation on this reporter gene. Stimulation of reporter gene transfected RAW 264.7 cells (a mouse macrophage cell line) with LPS resulted in IRE-dependent inhibition of luciferase production. Inhibitors of nitric oxide synthase abrogated the IRE-dependent effect of LPS. In addition, direct treatment of RAW 264.7 and with NO donor S-nitroso-N-acetylpenicillamine resulted in IRE-dependent down-regulation of luciferase expression. The effect of NO was consistent with IRP1/IRE mediated translation block. There are most likely both inflammation-mediated transcriptional and post-transcriptional (IRE-dependent) mechanisms for inhibiting ferroportin expression in MPS cells. (C) 2002 Elsevier Science (USA). C1 Univ Texas, Hlth Sci Ctr, Dept Med, San Antonio, TX 78229 USA. S Texas Vet Hlth Syst, Audie Murphy Vet Adm Hosp, San Antonio, TX 78229 USA. RP Haile, DJ (reprint author), Univ Texas, Hlth Sci Ctr, Dept Med, 7703 Floyd Curl Dr, San Antonio, TX 78229 USA. NR 45 TC 53 Z9 54 U1 5 U2 6 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 NOV-DEC PY 2002 VL 29 IS 3 BP 315 EP 326 DI 10.1006/bcmd.2002.0572 PG 12 WC Hematology SC Hematology GA 660FC UT WOS:000181822300009 PM 12547222 ER PT J AU Husson, H Freedman, AS Cardoso, AA Schultze, J Munoz, O Strola, G Kutok, J Carideo, EG De Beaumont, R Caligaris-Cappio, F Ghia, P AF Husson, H Freedman, AS Cardoso, AA Schultze, J Munoz, O Strola, G Kutok, J Carideo, EG De Beaumont, R Caligaris-Cappio, F Ghia, P TI CXCL13 (BCA-1) is produced by follicular lymphoma cells: role in the accumulation of malignant B cells SO BRITISH JOURNAL OF HAEMATOLOGY LA English DT Article DE follicular lymphomas; CXCL13; CXCL12 ID CHEMOKINE RECEPTOR; FACTOR-I; EXPRESSION; FOLLICLES AB Follicular lymphomas (FLs) localize in lymphoid tissues and recapitulate the structure of normal secondary follicles. The chemokine/chemokine receptor pair CXCL13/ CXCR5 is required for the architectural organization of B cells within lymphoid follicles. In this study, we showed that CXCL13 was secreted by FL cells. FL cells expressed CXCR5 and migrated in response to CXCL13. Furthermore, we observed a synergistic effect between CXCL13 and CXCL12 (SDF-1), a chemokine produced by stromal cells in lymphoid tissues. The production of CXCL13 by FL cells and CXCL12 by stromal cells probably directs and participates in the accumulation of FL cells within specific anatomic sites. C1 Dana Farber Canc Inst, Dept Adult Oncol, Boston, MA 02115 USA. Harvard Univ, Sch Med, Dept Med, Boston, MA USA. Ist Ric & Cura Canc, Candiolo, TO, Italy. Univ Turin, Dept Biomed Sci & Human Oncol, Turin, Italy. Osped Mauriziano Umberto 1, Div Clin Immunol & Hematol, Turin, Italy. Harvard Univ, Sch Med, Dept Pathol, Boston, MA 02115 USA. Brigham & Womens Hosp, Dept Pathol, Boston, MA 02115 USA. RP Freedman, AS (reprint author), Dana Farber Canc Inst, Dept Adult Oncol, 44 Binney St, Boston, MA 02115 USA. RI Schultze, Joachim/D-7794-2011; Ghia, Paolo/K-7138-2016 OI Schultze, Joachim/0000-0003-2812-9853; Ghia, Paolo/0000-0003-3750-7342 FU NCI NIH HHS [CA66996] NR 12 TC 33 Z9 33 U1 0 U2 4 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 NOV PY 2002 VL 119 IS 2 BP 492 EP 495 DI 10.1046/j.1365-2141.2002.03832.x PG 4 WC Hematology SC Hematology GA 610LQ UT WOS:000178961900032 PM 12406091 ER PT J AU Rosenkranz, KM Sheridan, R AF Rosenkranz, KM Sheridan, R TI Management of the burned trauma patient: balancing conflicting priorities SO BURNS LA English DT Article AB Purpose: Approximately 5% of multiple trauma patients sustain concomitant bums. Complicated management issues arise in these patients as burn and trauma care often conflict. This study reviews 53 consecutive burned multiple trauma patients in order to examine common management conflicts and recommend appropriate compromises in caring for these difficult patients. Procedure: A retrospective review of 53 consecutive burn patients with coincident trauma admitted to The Massachusetts General Hospital (NIGH) from 1993-2001 was performed. Findings: In the study period, 53 patients were admitted to the Massachusetts General Hospital with concomitant burns and trauma. Of this group, 42 (79%) were male. Average age was 31.5 +/- 15.0. Mechanisms included I I motor vehicle collisions (MVC), 10 explosions, 10 electrocutions with subsequent falls, nine house fires, four motorcycle collisions (MCC), three pedestrian versus car accidents, two falls into fires, two plane crashes, and one each of a lawnmower accident and a patient drawn into a machine. Average burn size was 25.4% +/- 22.4. The most common traumatic injury was fracture (52). Management of fractures in burn patients and resuscitation in head injured burn patient represented the most common conflicts in patient care. There were five deaths (9.4%) in this series. Conclusions: Bums are a rare but significant complication in the trauma patient. Outcomes are dependent on rapid trauma evaluation as well as effective resuscitation and wound management. Given the complexities of their problems, these patients necessitate a balanced multidisciplinary approach to maximize their potential for full recovery. Thoughtful compromise between trauma and burn priorities is frequently necessary. (C) 2002 Elsevier Science Ltd and ISBI. All rights reserved. C1 Massachusetts Gen Hosp, Dept Surg, Shock Trauma Unit, Boston, MA 02114 USA. Massachusetts Gen Hosp, Burn Ctr, Boston, MA 02114 USA. Massachusetts Gen Hosp, Dartmouth Hitchcock Med Ctr, Dept Surg, Boston, MA 02114 USA. RP Sheridan, R (reprint author), Massachusetts Gen Hosp, Dept Surg, Shock Trauma Unit, MGH-GRB 1302,55 Fruit St, Boston, MA 02114 USA. NR 5 TC 17 Z9 17 U1 2 U2 2 PU ELSEVIER SCI LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND SN 0305-4179 J9 BURNS JI Burns PD NOV PY 2002 VL 28 IS 7 BP 665 EP 669 AR PII S0305-4179(02)00109-2 DI 10.1016/S0305-4179(02)00109-2 PG 5 WC Critical Care Medicine; Dermatology; Surgery SC General & Internal Medicine; Dermatology; Surgery GA 617VM UT WOS:000179381600008 PM 12417162 ER PT J AU Stone, RM AF Stone, RM TI The difficult problem of acute myeloid leukemia in the older adult SO CA-A CANCER JOURNAL FOR CLINICIANS LA English DT Article ID ACUTE MYELOGENOUS LEUKEMIA; COLONY-STIMULATING-FACTOR; ACUTE LYMPHOBLASTIC-LEUKEMIA; BONE-MARROW TRANSPLANTATION; REMISSION-INDUCTION CHEMOTHERAPY; COOPERATIVE-ONCOLOGY-GROUP; STEM-CELL TRANSPLANTATION; PHASE-III; CONSOLIDATION THERAPY; ELDERLY PATIENTS AB Acute myeloid leukemia (AML) in older adults is a biologically and clinically distinct entity. Based on analysis of cytogenetic and molecular data, it is known that leukemic cells in older patients are intrinsically resistant to standard chemotherapy. Due to comorbid disease and impaired bone marrow stem cell reserve, older adults tolerate myelosuppressive chemotherapy poorly, with a treatment-related mortality rate of 25 percent. About 35 percent of adults under age 40 are cured, but the complete remission rate (likelihood of temporary disease eradication) is 45 percent in those over age 60, considerably lower than the 75% rate among younger patients, and the possibility of long-term disease free survival is 20 percent in those achieving remission or less than 10 percent overall. Standard allogeneic bone marrow transplantation is too dangerous to be considered as a means to eradicate minimal residual disease after remission is obtained and myelointensive chemotherapy is not a beneficial post-remission strategy in this age cohort. These disappointing results call for more effective and less toxic therapeutic options. Advances in our understanding of the pathophysiology of AML and promising early clinical data suggest that the era of truly targeted therapy in this difficult disease may soon be a reality. C1 Harvard Univ, Sch Med, Dana Farber Canc Inst, Adult Acute Leukemia Program, Boston, MA 02115 USA. RP Stone, RM (reprint author), Harvard Univ, Sch Med, Dana Farber Canc Inst, Adult Acute Leukemia Program, 44 Binney St, Boston, MA 02115 USA. NR 60 TC 63 Z9 67 U1 0 U2 2 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0007-9235 J9 CA-CANCER J CLIN JI CA-Cancer J. Clin. PD NOV-DEC PY 2002 VL 52 IS 6 BP 363 EP 371 PG 9 WC Oncology SC Oncology GA 620XT UT WOS:000179559500005 PM 12469764 ER PT J AU Smith, MR Kaufman, D George, D Oh, WK Kazanis, M Manola, J Kantoff, PW AF Smith, MR Kaufman, D George, D Oh, WK Kazanis, M Manola, J Kantoff, PW TI Selective aromatase inhibition for patients with androgen-independent prostate carcinoma SO CANCER LA English DT Article DE prostatatic neoplasms; androgen-independent; aromatase; letrozole ID PHASE-II TRIAL; STEROID BINDING CHARACTERISTICS; CLINICAL-TRIALS; BREAST-CANCER; RECEPTOR; MUTATION; CELLS; TAMOXIFEN; THERAPY; DOMAIN AB BACKGROUND. First and second-generation aromatase inhibitors have shown activity in patients with androgen-independent prostate carcinoma. These early-generation aromatase inhibitors are nonselective, however, and inhibition of other steroidogenic enzymes may contribute to their reported clinical activity. The authors conducted a Phase II clinical study of letrozole to determine the safety and efficacy of a potent and selective third-generation aromatase inhibitor in men with androgen-independent prostate carcinoma. METHODS. Forty-three men with androgen-independent prostate carcinoma were treated with oral letrozole (2.5 mg daily). Treatment was continued until progressive disease or Grade 3 toxicity developed. Response and progressive disease were defined according to recommendations of the Prostate Specific Antigen Working Group. RESULTS. In total, 380 weeks of treatment were administered to the 43 study patients. The median duration of treatment was 8 weeks. Forty men discontinued treatment due to progressive disease. Only one patient responded to treatment with a sustained decrease > 50% in serum prostate specific antigen (PSA) levels. Three other patients experienced transient minor decreases (<50%) in serum PSA levels. There were no serious treatment-related adverse events. CONCLUSIONS. Selective aromatase inhibition with letrozole is not active in men with androgen-independent prostate carcinoma. C1 Massachusetts Gen Hosp, Dept Hematol Oncol, Boston, MA 02114 USA. Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02115 USA. RP Smith, MR (reprint author), Massachusetts Gen Hosp, Dept Hematol Oncol, Cox 640,100 Blossom St, Boston, MA 02114 USA. RI Oh, William/B-9163-2012 OI Oh, William/0000-0001-5113-8147 NR 23 TC 27 Z9 28 U1 0 U2 0 PU JOHN WILEY & SONS INC PI HOBOKEN PA 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 0008-543X J9 CANCER JI Cancer PD NOV 1 PY 2002 VL 95 IS 9 BP 1864 EP 1868 DI 10.1002/cncr.10844 PG 5 WC Oncology SC Oncology GA 607TV UT WOS:000178807600007 PM 12404279 ER PT J AU Cross, CK Harris, J Recht, A AF Cross, CK Harris, J Recht, A TI Race, socioeconomic status, and breast carcinoma in the US - What have we learned from clinical studies? SO CANCER LA English DT Article DE race; socioeconomic status (SES); breast carcinoma; African American; prognostic factors ID SURGICAL ADJUVANT BREAST; ESTROGEN-RECEPTOR STATUS; BLACK-WHITE DIFFERENCES; AFRICAN-AMERICAN FAMILIES; RACIAL-DIFFERENCES; CANCER SURVIVAL; PROGNOSTIC DISCRIMINANTS; CONSERVATION THERAPY; BRCA1 MUTATIONS; NATIONAL SURVEY AB BACKGROUND. Whether African-American women have biologically more aggressive breast carcinoma compared with white women and whether race acts as a significant independent prognostic factor for survival have not been determined. Alternatively, race merely may be a surrogate for socioeconomic status (SES). METHODS. A literature review was performed of clinical trials and retrospective studies in the U.S. that compared survival between white women and black women with breast carcinoma after adjustment for known prognostic factors (patient age, disease stage, lymph node status, and estrogen receptor status) to assess the impact of race and SES. RESULTS. Single institutional and clinical studies suggest that, when black patients are treated appropriately and other prognostic variables are controlled, their survival is similar to the survival of white patients. Twelve retrospective studies and 1 analysis of a clinical trial included SES and race as variables for survival. Only three of those studies revealed race as a significant prognostic factor for survival after adjusting for SES. CONCLUSIONS. SES replaces race as a predictor of worse outcome after women are diagnosed with breast carcinoma in many studies. However, black women present with more advanced disease that appear more aggressive biologically, and they present at a younger age compared with white women. Further research should be conducted concerning the precise elements of SES that account for the incidence of breast carcinoma, age at diagnosis, hormone receptor status, and survival to devise better strategies to improve outcome. (C) 2002 American Cancer Society. C1 Brigham & Womens Hosp, Dana Farber Canc Inst, Beth Israel Deaconess Med Ctr, Joint Ctr Radiat, Boston, MA 02115 USA. Harvard Univ, Sch Med, Boston, MA 02138 USA. Brigham & Womens Hosp, Dana Farber Canc Inst, Beth Israel Deaconess Med Ctr, Dept Radiat Oncol, Boston, MA 02115 USA. RP Cross, CK (reprint author), Brigham & Womens Hosp, Dana Farber Canc Inst, Beth Israel Deaconess Med Ctr, Joint Ctr Radiat, 75 Francis St,ASB-1,L2 Level, Boston, MA 02115 USA. NR 78 TC 53 Z9 53 U1 2 U2 5 PU JOHN WILEY & SONS INC PI HOBOKEN PA 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 0008-543X J9 CANCER JI Cancer PD NOV 1 PY 2002 VL 95 IS 9 BP 1988 EP 1999 DI 10.1002/cncr.10830 PG 12 WC Oncology SC Oncology GA 607TV UT WOS:000178807600022 PM 12404294 ER PT J AU Ren, XP Cao, C Zhu, LB Yoshida, K Kharbanda, S Weichselbaum, R Kufe, D AF Ren, XP Cao, C Zhu, LB Yoshida, K Kharbanda, S Weichselbaum, R Kufe, D TI Lyn tyrosine kinase inhibits nuclear export of the p53 tumor suppressor SO CANCER BIOLOGY & THERAPY LA English DT Article DE p53; Lyn tyrosine kinase; Mdm2; ubiquitination; proteosome; nuclear export ID C-ABL; DNA-DAMAGE; APOPTOTIC RESPONSE; IONIZING-RADIATION; MDM2; ACTIVATION; PROTEIN; CELLS; PHOSPHORYLATION; DEGRADATION AB The p53 tumor suppressor is activated in the cellular response to stress. Mdm2 inhibits p53-dependent transactivation and promotes degradation of p53 by the ubiquitin-proteosome pathway. The present studies demonstrate that p53 binds directly to the nuclear Lyn tyrosine kinase. Lyn increases p53 levels and stimulates p53-mediated transcription by a kinase-independent mechanism. The results also demonstrate that Lyn increases nuclear levels of ubiquitinated p53 by inhibiting export of p53 to the cytoplasm. In concert with these results, Lyn reverses Mdm2-mediated degradation of p53 and increases p53-dependent apoptosis. Our findings support a previously undefined role for nuclear Lyn in both activation and Mdm2-mediated regulation of p53. C1 Harvard Univ, Sch Med, Dana Farber Canc Inst, Boston, MA 02115 USA. Harvard Univ, Sch Med, Dept Cell Biol, Boston, MA 02115 USA. Univ Chicago, Dept Radiat & Cellular Oncol, Chicago, IL 60637 USA. RP Kufe, D (reprint author), Harvard Univ, Sch Med, Dana Farber Canc Inst, 44 Binney St, Boston, MA 02115 USA. NR 36 TC 9 Z9 9 U1 0 U2 0 PU LANDES BIOSCIENCE PI GEORGETOWN PA 810 SOUTH CHURCH STREET, GEORGETOWN, TX 78626 USA SN 1538-4047 J9 CANCER BIOL THER JI Cancer Biol. Ther. PD NOV-DEC PY 2002 VL 1 IS 6 BP 703 EP 708 PG 6 WC Oncology SC Oncology GA 672XT UT WOS:000182549600020 PM 12642697 ER PT J AU Sellers, WR Loda, M AF Sellers, WR Loda, M TI The EZH2 polycomb transcriptional repressor - a marker or mover of metastatic prostate cancer? SO CANCER CELL LA English DT Editorial Material ID GENE AB The recent finding of overexpression of the polycomb group transcriptional repressor EZH2 in prostate cancer raises the possibility that transcriptional regulation at the chromatin level may play a role in the development of the metastatic phenotype and suggests new avenues of exploration with respect to patient stratification and therapeutics. C1 Harvard Univ, Sch Med, Brigham & Womens Hosp, Dept Med Oncol,Dana Farber Canc Inst, Boston, MA 02115 USA. Harvard Univ, Sch Med, Brigham & Womens Hosp, Dept Med, Boston, MA 02115 USA. Harvard Univ, Sch Med, Brigham & Womens Hosp, Dept Pathol, Boston, MA 02115 USA. RP Sellers, WR (reprint author), Harvard Univ, Sch Med, Brigham & Womens Hosp, Dept Med Oncol,Dana Farber Canc Inst, Boston, MA 02115 USA. NR 14 TC 67 Z9 68 U1 0 U2 8 PU CELL PRESS PI CAMBRIDGE PA 1100 MASSACHUSETTS AVE, CAMBRIDGE, MA 02138 USA SN 1535-6108 J9 CANCER CELL JI Cancer Cell PD NOV PY 2002 VL 2 IS 5 BP 349 EP 350 DI 10.1016/S1535-6108(02)00187-3 PG 2 WC Oncology; Cell Biology SC Oncology; Cell Biology GA 618JQ UT WOS:000179415300002 PM 12450788 ER PT J AU Roberts, CWM Leroux, MM Fleming, MD Orkin, SH AF Roberts, CWM Leroux, MM Fleming, MD Orkin, SH TI Highly penetrant, rapid tumorigenesis through conditional inversion of the tumor suppressor gene Snf5 SO CANCER CELL LA English DT Article ID CELL-CYCLE ARREST; RHABDOID TUMORS; MICE; MUTATIONS; COMPLEX; COOPERATE; CANCER; MOUSE; BRG1; RB AB Recent data suggest the SWI/SNF chromatin remodeling complex may also act as a tumor suppressor. Utilizing a reversibly inactivating conditional allele, we demonstrate that loss of Snf5/Ini1/Baf47/SmarcB1, a core subunit of SWI/SNF, results in highly penetrant cancer predisposition with 100% of mice developing mature CD8(+) T cell lymphoma or rare rhabdoid tumors with a median onset of only 11 weeks. Notably, while loss of Snf5 predisposes to aggressive cancers, it is also required for survival of virtually all nonmalignant cells in vivo. Reversible gene targeting demonstrates a critical and specific role for Snf5 in tumor suppression, provides a novel system in which to explore the genetic pathways involved in tumor suppression by Swi/Snf, and should be of wide use in evaluating other essential tumor suppressor genes. C1 Dana Farber Canc Inst, Div Hematol Oncol, Boston, MA 02115 USA. Harvard Univ, Sch Med, Dept Pediat, Childrens Hosp, Boston, MA 02115 USA. Howard Hughes Med Inst, Boston, MA 02115 USA. Childrens Hosp, Dept Pathol, Boston, MA 02115 USA. Harvard Univ, Sch Med, Boston, MA 02115 USA. RP Orkin, SH (reprint author), Dana Farber Canc Inst, Div Hematol Oncol, Boston, MA 02115 USA. NR 38 TC 173 Z9 178 U1 0 U2 4 PU CELL PRESS PI CAMBRIDGE PA 1100 MASSACHUSETTS AVE, CAMBRIDGE, MA 02138 USA SN 1535-6108 J9 CANCER CELL JI Cancer Cell PD NOV PY 2002 VL 2 IS 5 BP 415 EP 425 DI 10.1016/S1535-6108(02)00185-X PG 11 WC Oncology; Cell Biology SC Oncology; Cell Biology GA 618JQ UT WOS:000179415300010 PM 12450796 ER PT J AU Mauceri, HJ Seetharam, S Beckett, MA Schumm, LP Koons, A Gupta, VK Park, JO Manan, A Lee, JY Montag, AG Kufe, DW Weichselbaum, RR AF Mauceri, HJ Seetharam, S Beckett, MA Schumm, LP Koons, A Gupta, VK Park, JO Manan, A Lee, JY Montag, AG Kufe, DW Weichselbaum, RR TI Angiostatin potentiates cyclophosphamide treatment of metastatic disease SO CANCER CHEMOTHERAPY AND PHARMACOLOGY LA English DT Article DE angiostatin; cyclophosphamide; Lewis lung carcinoma; metastasis ID LEWIS LUNG-CARCINOMA; GROWTH IN-VIVO; IONIZING-RADIATION; GENE-THERAPY; ANGIOGENESIS; CANCER; PROLIFERATION; TUMORS; AGENTS; CELLS AB Purpose: We examined the interaction between cyclophosphamide (CPA) and angiostatin (AS) on the growth of primary Lewis lung carcinoma (LLC) tumors and on the development of LLC pulmonary metastases. We studied the effects of AS and CPA on the stages of angiogenesis employing in vitro assays. Methods: Primary tumor growth and pulmonary metastases were measured to evaluate the effects of treatment with AS alone, CPA alone or the combination of CPA and AS. We examined the effects of CPA plus AS on endothelial cell (HUVEC) survival, migration and tube formation. Results: Combined treatment with CPA and AS did not significantly affect primary tumor growth when compared with CPA treatment alone. However, a significant decrease in the number of pulmonary metastases was observed following CPA plus AS treatment when compared with CPA treatment alone (P < 0.001). AS did not enhance CPA-mediated HUVEC cytotoxicity, and CPA failed to enhance AS-mediated inhibition of migration. However, tube formation was inhibited following combined treatment with CPA and AS when compared with either treatment alone. Conclusions: AS enhanced the antimetastatic effects of CPA without significantly influencing the effects of CPA on primary tumor growth. CPA plus AS inhibited tube formation, suggesting that interrupting specific steps in the angiogenesis process might be an effective approach to the treatment of subclimcal distant metastases. C1 Duchossois Ctr Adv Med, Dept Radiat & Cellular Oncol, Chicago, IL 60637 USA. Univ Chicago, Dept Hlth Studies, Chicago, IL 60637 USA. Univ Chicago, Dept Surg, Chicago, IL 60637 USA. Univ Chicago, Dept Pathol, Chicago, IL 60637 USA. Dana Farber Canc Inst, Div Pharmacol, Boston, MA 02115 USA. RP Weichselbaum, RR (reprint author), Duchossois Ctr Adv Med, Dept Radiat & Cellular Oncol, 5758 S Maryland Ave,MC 9006, Chicago, IL 60637 USA. NR 26 TC 15 Z9 17 U1 0 U2 0 PU SPRINGER-VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 USA SN 0344-5704 J9 CANCER CHEMOTH PHARM JI Cancer Chemother. Pharmacol. PD NOV PY 2002 VL 50 IS 5 BP 412 EP 418 DI 10.1007/s00280-002-0514-7 PG 7 WC Oncology; Pharmacology & Pharmacy SC Oncology; Pharmacology & Pharmacy GA 623DQ UT WOS:000179688400010 PM 12439600 ER PT J AU Wu, K Willett, WC Chan, JM Fuchs, CS Colditz, GA Rimm, EB Giovannucci, EL AF Wu, K Willett, WC Chan, JM Fuchs, CS Colditz, GA Rimm, EB Giovannucci, EL TI A prospective study on supplemental vitamin E intake and risk of colon cancer in women and men SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION LA English DT Article ID FOOD FREQUENCY QUESTIONNAIRE; COLORECTAL-CANCER; ALPHA-TOCOPHEROL; BETA-CAROTENE; ANTIOXIDANT VITAMINS; REPRODUCIBILITY; VALIDITY; TRIAL; CONSUMPTION; PREVENTION AB We conducted a prospective study on the association between supplemental vitamin E and colon cancer in 87,998 females from the Nurses' Health Study and 47, 344 males from the Health Professionals Follow-up Study. There was some suggestion that men with supplemental vitamin E intake of 300 IU/day or more may be at lower risk for colon cancer when compared with never users [multivariate relative risk (RR), 300-500 IU/day versus never users, 0.73 (95% confidence interval (CI), 0.52-1.03); greater than or equal to600 IU/day versus never users = 0.70 (95% CI 0.38-1.29)], but CIs included 1. In women, there was no evidence for an inverse association between vitamin E supplementation and risk of colon cancer. Our findings do not provide consistent support for an inverse association between supplemental vitamin E and colon cancer risk. Considering the paucity of epidemiological data on this association, further studies of vitamin E and colon cancer are warranted. C1 Harvard Univ, Sch Publ Hlth, Dept Nutr, Boston, MA 02115 USA. Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA. Harvard Univ, Brigham & Womens Hosp, Sch Med, Channing Lab,Dept Med, Boston, MA 02115 USA. Dana Farber Canc Inst, Div Med Oncol, Boston, MA 02115 USA. RP Wu, K (reprint author), Harvard Univ, Sch Publ Hlth, Dept Nutr, 665 Huntington Ave,Bldg 2, Boston, MA 02115 USA. RI Colditz, Graham/A-3963-2009 OI Colditz, Graham/0000-0002-7307-0291 FU NCI NIH HHS [CA 55075, CA 87969] NR 36 TC 34 Z9 35 U1 0 U2 3 PU AMER ASSOC CANCER RESEARCH PI BIRMINGHAM PA PO BOX 11806, BIRMINGHAM, AL 35202 USA SN 1055-9965 J9 CANCER EPIDEM BIOMAR JI Cancer Epidemiol. Biomarkers Prev. PD NOV PY 2002 VL 11 IS 11 BP 1298 EP 1304 PG 7 WC Oncology; Public, Environmental & Occupational Health SC Oncology; Public, Environmental & Occupational Health GA 615WL UT WOS:000179270300004 PM 12433706 ER PT J AU Monnier, J Laken, M Carter, CL AF Monnier, J Laken, M Carter, CL TI Patient and caregiver interest in Internet-based cancer services SO CANCER PRACTICE LA English DT Article DE cancer; caregiver; health information; Internet; online resource ID DIGITAL DIVIDE; BREAST-CANCER; INFORMATION AB PURPOSE: The primary goal of this study was to identify the needs for, the interest in, and the feasibility of the implementation of an Internet-based cancer services web site. Additionally, group differences (racial, patient vs caregiver, or rural vs urban) were identified that might influence the implementation of such a project. DESCRIPTION OF STUDY: Patients with cancer and caregivers (N = 319) in the waiting rooms of a cancer center located within a southeastern medical university completed questionnaires regarding their interest in Internet-based services. Topics included the likelihood of using Internet-based services, interest in home healthcare services delivered via a personal computer, and knowledge about and use of the Internet. RESULTS: Results indicated that most patient and caregiver respondents were interested in Internet-based cancer-related services such as information related to treatment (80%), conversations with physicians via the Internet (70%), and online support groups (65%). In addition, respondents reported that they would be likely to use such services (70%) and were interested in home healthcare services delivered via personal computers (60%). No group differences were found across ethnic groups, geographic settings, and patient status (patient vs caregivers) on these variables. Minorities, older individuals, and less educated individuals were less likely to have knowledge of and to have used the Internet. CLINICAL IMPLICATIONS: Patients with cancer and their caregivers are interested in supplementing in-person services with Internet-based services relating to their cancer treatment. Special efforts need to be made to reach ethnic minorities, the elderly, and those with less education with Internet-based programs. C1 Med Univ S Carolina, Dept Psychiat & Behav Sci, Charleston, SC 29425 USA. Ralph H Johnson Vet Affairs Med Ctr, Charleston, SC USA. Med Univ S Carolina, Coll Nursing, Charleston, SC 29425 USA. Med Univ S Carolina, Off Special Initiat, Charleston, SC 29425 USA. Med Univ S Carolina, Dept Radiat Oncol, Charleston, SC 29425 USA. Med Univ S Carolina, Hollings Canc Ctr, Charleston, SC 29425 USA. RP Monnier, J (reprint author), Med Univ S Carolina, Dept Psychiat & Behav Sci, POB 250861, Charleston, SC 29425 USA. NR 11 TC 47 Z9 47 U1 2 U2 10 PU BLACKWELL PUBLISHING INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 USA SN 1065-4704 J9 CANCER PRACT JI Cancer Pract. PD NOV-DEC PY 2002 VL 10 IS 6 BP 305 EP 310 DI 10.1046/j.1523-5394.2002.106005.x PG 6 WC Oncology; Health Care Sciences & Services; Nursing SC Oncology; Health Care Sciences & Services; Nursing GA 608MM UT WOS:000178850100008 PM 12406053 ER PT J AU Chang, Q Li, Y White, MF Fletcher, JA Xiao, S AF Chang, Q Li, Y White, MF Fletcher, JA Xiao, S TI Constitutive activation of insulin receptor substrate 1 is a frequent event in human tumors: Therapeutic implications SO CANCER RESEARCH LA English DT Article ID IGF-I RECEPTOR; SIGNAL-TRANSDUCTION; PHOSPHORYLATION SITES; HEMATOPOIETIC-CELLS; PROTEIN; GROWTH; IRS-1; OVEREXPRESSION; DIFFERENTIATION; TRANSFORMATION AB Insulin receptor substrate 1 (IRS-1) is a major substrate of insulin, insulin-like growth factors, and cytokine signaling and plays an important role in mediating apoptosis, cell differentiation, and cell transformation. We found that IRS-1 is constitutively activated in a variety of solid tumors, including breast cancers, leiomyomas, Wilms' tumors, rhabdomyosarcomas, liposarcomas, leiomyosarcomas, and adrenal cortical carcinomas. Blocking the constitutively activated IRS-1 signaling in breast cancer cells with a dominant-negative IRS-1, an IRS-1 with all 18 potential tyrosine-phosphorylation sites replaced by phenylalanines (F18), dramatically reduced cancer cell growth. Breast cancer cells that expressed F18 also formed smaller and far fewer colonies in soft agar culture than did the cells that did not express F18. These studies suggest that constitutive IRS-1 activation is a common phenomenon in tumors and that activated IRS-1 may present an attractive therapeutic target. C1 Brigham & Womens Hosp, Dept Pathol, Boston, MA 02115 USA. Joslin Diabet Ctr, Div Res, Boston, MA 02115 USA. RP Xiao, S (reprint author), Brigham & Womens Hosp, Dept Pathol, 75 Francis St, Boston, MA 02115 USA. NR 25 TC 97 Z9 100 U1 0 U2 0 PU AMER ASSOC CANCER RESEARCH PI BIRMINGHAM PA PO BOX 11806, BIRMINGHAM, AL 35202 USA SN 0008-5472 J9 CANCER RES JI Cancer Res. PD NOV 1 PY 2002 VL 62 IS 21 BP 6035 EP 6038 PG 4 WC Oncology SC Oncology GA 612EW UT WOS:000179062400009 PM 12414625 ER PT J AU Kijima, T Maulik, G Ma, PC Tibaldi, EV Turner, RE Rollins, B Sattler, M Johnson, BE Salgia, R AF Kijima, T Maulik, G Ma, PC Tibaldi, EV Turner, RE Rollins, B Sattler, M Johnson, BE Salgia, R TI Regulation of cellular proliferation, cytoskeletal function, and signal transduction through CXCR4 and c-kit in small cell lung cancer cells SO CANCER RESEARCH LA English DT Article ID HEMATOPOIETIC PROGENITOR CELLS; GASTROINTESTINAL STROMAL TUMOR; GROWTH-STIMULATING FACTOR; KINASE INHIBITOR STI571; FOCAL ADHESION PROTEINS; TYROSINE PHOSPHORYLATION; CHEMOKINE RECEPTORS; HIV-1 ENTRY; PHOSPHATIDYLINOSITOL 3-KINASE; MOLECULAR-CLONING AB The regulation of biological functions including cell growth, viability, migration, and adhesion of small cell lung cancer (SCLC) cells depends largely on the autocrine or paracrine stimulation of growth factor receptors and chemokine receptors. Stem cell factor (SCF) and its receptor c-Kit have been identified as important regulators of SCLC viability and are coexpressed in approximately 40-70% of SCLC specimens. In vitro, the inhibition of c-Kit tyrosine kinase activity by the small molecule tyrosine kinase inhibitor STI571 (Gleevec) abrogates cell growth. We have investigated the role of c-Kit and chemokine receptors in the regulation of cell migration and adhesion of SCLC cells. CXCR4, the chemokine receptor for stromal cell-derived factor-1alpha (SDF-1alpha), was found to be the major chemokine receptor commonly expressed in all of the 10 SCLC cell lines tested. SCF and SDF-1alpha increased cellular proliferation over a course of 72 h in both the c-Kit- and the CXCR4-positive NCI-H69 SCLC cell line. Recently, SDF-1alpha and CXCR4 have been shown to be important regulators of migration and metastasis in breast and ovarian cancer. We found that SDF-1alpha dramatically increased cell motility and adhesion in CXCR4-expressing NCI-H446 SCLC cells. In addition, SDF-1alpha altered cell morphology with increased formation of filopodia and neurite-like projections. In NCI-H69 SCLC cells, SCF and SDF-1alpha cooperatively induced morphological changes and activated downstream signaling pathways. Treatment of NCI-H69 cells with STI571 specifically inhibited the c-Kit signaling events of Akt and p70 S6 kinase, whereas SDF-1alpha-mediated activation of Akt or p70 S6 kinase was normal. In contrast, the phosphatidylinositol 3-kinase inhibitor, LY294002, prevented these cells from adhering and completely blocked SCF- and/or SDF-1alpha-induced Akt or p70 S6 kinase phosphorylation. These results demonstrate that the CXCR4 receptor is functionally expressed in SCLC cells and may, therefore, be involved in the pathogenesis of SCLC in vivo. Inhibition of both the CXCR4 and the c-Kit downstream events could be a promising therapeutic approach in SCLC. C1 Dana Farber Canc Inst, Dept Adult Oncol, Boston, MA 02115 USA. Dana Farber Canc Inst, Dept Immunol, Boston, MA 02115 USA. Brigham & Womens Hosp, Dept Med, Boston, MA 02115 USA. Harvard Univ, Sch Med, Boston, MA 02115 USA. Tufts Univ, New England Med Ctr, Div Hematol & Oncol, Boston, MA 02111 USA. RP Salgia, R (reprint author), Dana Farber Canc Inst, Dept Adult Oncol, Dana 1234B,44 Binney St, Boston, MA 02115 USA. NR 48 TC 216 Z9 233 U1 1 U2 9 PU AMER ASSOC CANCER RESEARCH PI BIRMINGHAM PA PO BOX 11806, BIRMINGHAM, AL 35202 USA SN 0008-5472 J9 CANCER RES JI Cancer Res. PD NOV 1 PY 2002 VL 62 IS 21 BP 6304 EP 6311 PG 8 WC Oncology SC Oncology GA 612EW UT WOS:000179062400045 PM 12414661 ER PT J AU Arellano, RS Gervais, DA Boland, GW Mueller, PR AF Arellano, RS Gervais, DA Boland, GW Mueller, PR TI Percutaneous reconstruction of isolated bile ducts: Combination of percutaneous and endoscopic biliary techniques SO CARDIOVASCULAR AND INTERVENTIONAL RADIOLOGY LA English DT Article DE bile ducts ID DRAINAGE; RESECTION; BILOMA AB Reconstruction of isolated biliary segments can be achieved using a combination of radiologic and endoscopic interventions. C1 Massachusetts Gen Hosp, Div Abdominal Imaging & Intervent Radiol, Dept Radiol, Boston, MA 02114 USA. RP Arellano, RS (reprint author), Massachusetts Gen Hosp, Div Abdominal Imaging & Intervent Radiol, Dept Radiol, White Bldg 270,55 Fruit St, Boston, MA 02114 USA. NR 7 TC 1 Z9 1 U1 0 U2 0 PU SPRINGER-VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 USA SN 0174-1551 J9 CARDIOVASC INTER RAD JI Cardiovasc. Interv. Radiol. PD NOV-DEC PY 2002 VL 25 IS 6 BP 527 EP 529 DI 10.1007/s00270-002-1935-8 PG 3 WC Cardiac & Cardiovascular Systems; Radiology, Nuclear Medicine & Medical Imaging SC Cardiovascular System & Cardiology; Radiology, Nuclear Medicine & Medical Imaging GA 631XZ UT WOS:000180194600013 PM 12042998 ER PT J AU Gervais, DA Arellano, RS Mueller, PR AF Gervais, DA Arellano, RS Mueller, PR TI Percutaneous radiofrequency ablation of nodal metastases SO CARDIOVASCULAR AND INTERVENTIONAL RADIOLOGY LA English DT Article DE radiofrequency ablation; tumor ablation; kidney neoplasm; prostate neoplasm; ovarian neoplasm; lymph node ID TISSUE ABLATION; COAGULATION NECROSIS; CLINICAL-EXPERIENCE; LIVER METASTASES; RADIO-FREQUENCY; MALIGNANCY; CANCER AB We report our experience with percutaneous image-guided radiofrequency (RF) ablation to treat isolated nodal metastases. Four patients underwent image-guided percutaneous RF ablation of metastatic disease involving retrocrural nodes, retroperitoneal nodes, or pelvic nodes. Coagulation necrosis was achieved in all cases. C1 Massachusetts Gen Hosp, Dept Radiol, Boston, MA 02114 USA. RP Gervais, DA (reprint author), Massachusetts Gen Hosp, Dept Radiol, White 270, Boston, MA 02114 USA. NR 12 TC 23 Z9 24 U1 0 U2 1 PU SPRINGER-VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 USA SN 0174-1551 J9 CARDIOVASC INTER RAD JI Cardiovasc. Interv. Radiol. PD NOV-DEC PY 2002 VL 25 IS 6 BP 547 EP 549 DI 10.1007/s00270-002-2661-y PG 3 WC Cardiac & Cardiovascular Systems; Radiology, Nuclear Medicine & Medical Imaging SC Cardiovascular System & Cardiology; Radiology, Nuclear Medicine & Medical Imaging GA 631XZ UT WOS:000180194600018 PM 12391519 ER PT J AU Ganesan, S Silver, DP Greenberg, RA Avni, D Drapkin, R Miron, A Mok, SC Randrianarison, V Brodie, S Salstrom, J Rasmussen, TP Klimke, A Marrese, C Marahrens, Y Deng, CX Feunteun, J Livingston, DM AF Ganesan, S Silver, DP Greenberg, RA Avni, D Drapkin, R Miron, A Mok, SC Randrianarison, V Brodie, S Salstrom, J Rasmussen, TP Klimke, A Marrese, C Marahrens, Y Deng, CX Feunteun, J Livingston, DM TI BRCA1 supports XIST RNA concentration on the inactive X chromosome SO CELL LA English DT Article ID MEIOTIC CELLS; BREAST-CANCER; ESTROGEN-RECEPTOR; DNA-REPAIR; TRANSCRIPTION; MUTATION; ASSOCIATION; PROTEINS; COMPLEX; CHROMATIN AB BRCA1, a breast and ovarian tumor suppressor, colocalizes with markers of the inactive X chromosome (Xi) on Xi in female somatic cells and associates with XIST RNA, as detected by chromatin immunoprecipitation. Breast and ovarian carcinoma cells lacking BRCA1 show evidence of defects in Xi chromatin structure. Reconstitution of BRCA1-deficient cells with wt BRCA1 led to the appearance of focal XIST RNA staining without altering XIST abundance. Inhibiting BRCA1 synthesis in a suitable reporter line led to increased expression of an otherwise silenced Xi-located GFP transgene. These observations suggest that loss of BRCA1 in female cells may lead to Xi perturbation and destabilization of its silenced state. C1 Harvard Univ, Sch Med, Dana Farber Canc Inst, Boston, MA 02115 USA. Brigham & Womens Hosp, Dept Obstet Gynecol & Reprod Biol, Lab Gynecol Oncol, Boston, MA 02115 USA. Inst Gustave Roussy, Lab Genet Oncol, Lab Vectorol & Transfert Genes, F-94805 Villejuif, France. NIDDKD, Genet Dev & Dis Branch 10 9N105, NIH, Bethesda, MD 20892 USA. Univ Calif Los Angeles, Dept Human Genet, Gonda Ctr, Los Angeles, CA 90095 USA. Univ Connecticut, Ctr Regenerat Biol, Storrs, CT 06269 USA. Univ Connecticut, Dept Anim Sci, Storrs, CT 06269 USA. RP Livingston, DM (reprint author), Harvard Univ, Sch Med, Dana Farber Canc Inst, 44 Binney St, Boston, MA 02115 USA. RI Drapkin, Ronny/E-9944-2016; deng, chuxia/N-6713-2016 OI Drapkin, Ronny/0000-0002-6912-6977; NR 52 TC 202 Z9 209 U1 2 U2 5 PU CELL PRESS PI CAMBRIDGE PA 1100 MASSACHUSETTS AVE, CAMBRIDGE, MA 02138 USA SN 0092-8674 J9 CELL JI Cell PD NOV 1 PY 2002 VL 111 IS 3 BP 393 EP 405 DI 10.1016/S0092-8674(02)01052-8 PG 13 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA 611HG UT WOS:000179010100011 PM 12419249 ER PT J AU Hahn, WC AF Hahn, William C. TI Empty Pockets Yield More Telomere Change SO CELL CYCLE LA English DT Editorial Material DE Telomeres; Retinoblastoma; p107; p130; Rb11; Rb12 C1 Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02115 USA. RP Hahn, WC (reprint author), Dana Farber Canc Inst, Dept Med Oncol, 44 Binney St,Dana 710C, Boston, MA 02115 USA. EM William_Hahn@dfci.harvard.edu FU NCI NIH HHS [K01 CA94223] NR 25 TC 0 Z9 0 U1 0 U2 0 PU TAYLOR & FRANCIS INC PI PHILADELPHIA PA 530 WALNUT STREET, STE 850, PHILADELPHIA, PA 19106 USA SN 1538-4101 EI 1551-4005 J9 CELL CYCLE JI Cell Cycle PD NOV-DEC PY 2002 VL 1 IS 6 BP 406 EP 407 DI 10.4161/cc.1.6.266 PG 2 WC Cell Biology SC Cell Biology GA V40QA UT WOS:000209491900011 PM 12548015 ER PT J AU Snider, GL AF Snider, GL TI Enhancement of exercise performance in COPD patients by Hyperoxia - A call for research SO CHEST LA English DT Article DE COPD; dyspnea; exercise; oxygen inhalation therapy; physical endurance ID OBSTRUCTIVE PULMONARY-DISEASE; AIR-FLOW LIMITATION; MILD HYPOXEMIA; LUNG-DISEASE; EXERTIONAL BREATHLESSNESS; SUPPLEMENTAL OXYGEN; HYPERINFLATION; ENDURANCE; ABILITY; O-2 AB This essay summarizes 16 reports, published since 1956, that describe the effects of hyperoxia on kexercise endurance in persons with COPD who have severe airflow obstruction (ie, FEV1 < 1.0 L or < 39% of predicted) and mild hypoxemia at rest (ie, Pao(2) > 62 mm Hg or arterial oxygen saturation [Sao(2)] measured by pulse oximetry of > 91%). The term hyperoxia is used because, in a proportion of study participants, oxygen administration increased exercise endurance in a dose-dependent fashion, up to a fraction of inspired oxygen of 0.5 or a flow of 100% O-2 of 6 L/min. The process appears to be dependent on an increase in Pao(2) rather than on the restoration of Sao(2) to normal levels. The results of pulmonary function tests were not predictive of response. Increased exercise performance was associated with a decrease in dyspnea, respiratory frequency, and minute ventilation. The slowing of respiratory frequency and the decrease in pulmonary air trapping likely accounted for the decrease in dyspnea. Slowing of the respiratory rate, which occurred at the expense of the retention of CO2, is most likely due to a by induced decrease in chemoreceptor ventilatory drive from the aortic and carotid bodies. Research is called for to determine the following: (1) the prevalence of COPD patients who have severe airflow limitation accompanied by mild hypoxemia; (2) the proportion of these patients who show improvements in exercise performance during a test of hyperoxic exercise; and (3) whether enhanced exercise performance during a brief test translates into a meaningful increase in the ability to perform the activities of daily living. C1 VA Boston Healthcare Syst, Boston, MA 02130 USA. RP Snider, GL (reprint author), VA Boston Healthcare Syst, 150 S Huntington Ave, Boston, MA 02130 USA. NR 28 TC 21 Z9 21 U1 0 U2 1 PU AMER COLL CHEST PHYSICIANS PI NORTHBROOK PA 3300 DUNDEE ROAD, NORTHBROOK, IL 60062-2348 USA SN 0012-3692 J9 CHEST JI Chest PD NOV PY 2002 VL 122 IS 5 BP 1830 EP 1836 DI 10.1378/chest.122.5.1830 PG 7 WC Critical Care Medicine; Respiratory System SC General & Internal Medicine; Respiratory System GA 617TH UT WOS:000179376600050 PM 12426288 ER PT J AU Kratz, A Lewandrowski, KB McDermott, S Chun, KY Lee-Lewandrowski, E AF Kratz, A Lewandrowski, KB McDermott, S Chun, KY Lee-Lewandrowski, E TI Performance of a point-of-care qualitative triple cardiac marker screen under controlled laboratory conditions and in an emergency department setting SO CLINICA CHIMICA ACTA LA English DT Article DE cardiac markers; laboratory technologists; point of care; acute coronary syndrome ID ACUTE MYOCARDIAL-INFARCTION; CREATINE-KINASE MB; TROPONIN-I; RELIABILITY; MYOGLOBIN; TRIAGE AB Background: The performance of point-of-care testing under controlled laboratory conditions may vary from results obtained in actual patient care settings. User errors are a major cause of this discrepancy. Methods: We studied the clinical performance of the Cardiac STATus (Spectral USA, Frederick, MD), a qualitative triple cardiac marker point-of-care test, under controlled laboratory conditions and in actual practice in an emergency department (ED) satellite laboratory. First-draw samples obtained from patients presenting to the hospital emergency department with chest pain were used for the study. Tests were performed in the chemistry research laboratory by a company product specialist or in an emergency department satellite laboratory by hospital staff. Test results were analyzed by correlation to the clinical discharge diagnosis. Results: In the emergency department, for the test system as a whole (any one or more marker(s) positive versus all three markers negative), sensitivity was 63%, specificity was 81%, positive predictive value was 26%, and negative predictive value was 95%. A manufacturer-supplied product specialist in a laboratory setting achieved very similar sensitivity, specificity, and positive and negative predictive values. Conclusions: The performance of this system under controlled laboratory conditions call be applied to estimate its performance at the point of care. (C) 2002 Elsevier Science B.V. All rights reserved. C1 Massachusetts Gen Hosp, Dept Pathol, Div Lab Med, Clin Chem Lab, Boston, MA 02114 USA. Harvard Univ, Sch Med, Boston, MA USA. RP Lee-Lewandrowski, E (reprint author), Massachusetts Gen Hosp, Dept Pathol, Div Lab Med, Clin Chem Lab, 55 Fruit St,Gray Bigelow 5, Boston, MA 02114 USA. NR 22 TC 2 Z9 2 U1 0 U2 1 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0009-8981 J9 CLIN CHIM ACTA JI Clin. Chim. Acta PD NOV PY 2002 VL 325 IS 1-2 BP 79 EP 85 AR PII S0009-8981(02)00253-X DI 10.1016/S0009-8981(02)00253-X PG 7 WC Medical Laboratory Technology SC Medical Laboratory Technology GA 610UD UT WOS:000178978600008 PM 12367769 ER PT J AU Perea, S Patterson, TF AF Perea, S Patterson, TF TI Antifungal resistance in pathogenic fungi SO CLINICAL INFECTIOUS DISEASES LA English DT Article ID HUMAN-IMMUNODEFICIENCY-VIRUS; IN-VITRO SUSCEPTIBILITY; MESSENGER-RNA LEVELS; CANDIDA-ALBICANS; AMPHOTERICIN-B; FLUCONAZOLE RESISTANCE; CRYPTOCOCCUS-NEOFORMANS; ASPERGILLUS-FUMIGATUS; INFECTED PATIENTS; OROPHARYNGEAL CANDIDIASIS AB Pathogenic fungi are the cause of life-threatening infections in an increasing number of immunocompromised patients. The intrinsic resistance to antifungal therapy observed in some genera, along with the development of resistance during treatment in others, is becoming a major problem in the management of these diseases. We reviewed the epidemiology of the most common systemic fungal infections for which antifungal resistance is a potential problem, the mechanisms of antifungal resistance, the correlation between in vitro susceptibility testing and clinical outcome, and the clinical implications of antifungal resistance. C1 Univ Texas, Hlth Sci Ctr, Div Infect Dis, Dept Med, San Antonio, TX 78229 USA. S Texas Vet Hlth Care Syst, Audie Murphy Div, San Antonio, TX USA. RP Patterson, TF (reprint author), Univ Texas, Hlth Sci Ctr, Div Infect Dis, Dept Med, Mail Code 7881,7703 Floyd Curl Dr, San Antonio, TX 78229 USA. NR 71 TC 113 Z9 126 U1 3 U2 5 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 1058-4838 J9 CLIN INFECT DIS JI Clin. Infect. Dis. PD NOV 1 PY 2002 VL 35 IS 9 BP 1073 EP 1080 DI 10.1086/344058 PG 8 WC Immunology; Infectious Diseases; Microbiology SC Immunology; Infectious Diseases; Microbiology GA 604VF UT WOS:000178641200012 PM 12384841 ER PT J AU Simmons, SF Ferrell, BA Schnelle, JF AF Simmons, SF Ferrell, BA Schnelle, JF TI Effects of a controlled exercise trial on pain in nursing home residents SO CLINICAL JOURNAL OF PAIN LA English DT Article DE assessment; exercise; nursing homes; pain ID RANDOMIZED TRIAL; RELIABILITY AB Objectives: To report preliminary data relevant to the effects of an exercise and toileting intervention on pain among incontinent nursing home (NH) residents. Design: A randomized controlled intervention trial. Setting and Participants: Fifty-one incontinent residents in one skilled NH. Intervention: The intervention was implemented by research staff for a total of 4 times a day (every 2 hours), 5 days a week, for 32 weeks. Residents were provided with incontinence care and assistance to either walk or, if nonambulatory, wheel their chairs, and to repeat sit-to-stand movements. Measurements: Pain was measured in two ways at baseline and again at 32 weeks: (1) a count of the number of verbal expressions and pain behaviors during a standardized physical performance assessment; and (2) a modified Geriatric Pain Measure administered in a one-on-one interview format. Results: There were significant differences between intervention and control groups on all physical performance measures over time, with the intervention group remaining stable and the control group showing a significant decline in sit-to-stand, walking, and wheelchair propulsion endurance. Both groups showed mild to moderate pain at baseline according to each of the two pain measures, while there were no significant changes in pain reports between groups over time based on either measure. There was, however, a trend for pain to increase in the intervention group. Conclusions: No significant changes in pain reports were attributable to exercise despite significant improvements in physical performance. In fact, there was a tendency for pain reports to increase with exercise. These preliminary findings suggest that exercise alone may be ineffective for pain management among incontinent NH residents. Care providers should consider that exercise to improve physical function may increase pain symptoms, requiring preemptive analgesia, other pain control strategies, or modified exercise techniques for this frail segment of the NH population. C1 Univ Calif Los Angeles, Jewish Home Aging, Borun Ctr Gerontol Res, Reseda, CA 91335 USA. Univ Calif Los Angeles, Sch Med, Dept Geriatr, Borun Ctr Gerontol Res, Los Angeles, CA USA. Vet Adm Greater Los Angeles Healthcare Syst, Speulveda Geriatr Res Educ & Clin Ctr, Sepulveda, CA USA. RP Simmons, SF (reprint author), Univ Calif Los Angeles, Jewish Home Aging, Borun Ctr Gerontol Res, 7150 Tampa Ave, Reseda, CA 91335 USA. FU NIA NIH HHS [AG10415, AG13013] NR 19 TC 18 Z9 18 U1 1 U2 1 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0749-8047 J9 CLIN J PAIN JI Clin. J. Pain PD NOV-DEC PY 2002 VL 18 IS 6 BP 380 EP 385 DI 10.1097/00002508-200211000-00006 PG 6 WC Anesthesiology; Clinical Neurology SC Anesthesiology; Neurosciences & Neurology GA 612PM UT WOS:000179084700006 PM 12441832 ER PT J AU Muratoglu, OK Bragdon, CR O'Connor, DO Perinchief, RS Jasty, M Harris, WH AF Muratoglu, OK Bragdon, CR O'Connor, DO Perinchief, RS Jasty, M Harris, WH TI Aggressive wear testing of a cross-linked polyethylene in total knee arthroplasty SO CLINICAL ORTHOPAEDICS AND RELATED RESEARCH LA English DT Article; Proceedings Paper CT Annual Meeting of the Knee-Society/Association of-Hip-and-Knee-Surgeons CY 2002 CL DALLAS, TEXAS SP Knee Soc, Assoc Hip & Knee Surgeons ID MOLECULAR-WEIGHT POLYETHYLENE; OXIDATION; FAILURE; UHMWPE AB Recently, highly cross-linked polyethylenes with high wear and oxidation resistance have been developed. These materials may improve the in vivo performance of polyethylene components used in total knee arthroplasty. To date, the in vitro knee wear testing of these new polyethylenes has been done under conditions of normal gait. However, their critical assessment also must include aggressive in vitro fatigue and wear testing. In the current study, an aggressive in vitro knee wear and device fatigue model simulating a tight posterior cruciate ligament balance during stair climbing was developed and used to assess the performance of one type of highly cross-linked polyethylene tibial knee insert in comparison with conventional polyethylene. The highly crosslinked inserts and one group of conventional inserts were tested after sterilization. One additional group of conventional inserts was subjected to accelerated aging before testing. The articular surfaces of the inserts were inspected visually for surface delamination, cracking, and pitting at regular intervals during the test. The aged conventional polyethylene inserts showed extensive delamination and cracking as early as 50,000 cycles. In contrast, the unaged conventional and highly cross-linked polyethylene inserts did not show any subsurface cracking or delamination at 0.5 million cycles. The appearance and location of delamination that occurred in the aged conventional inserts tested with the current model previously have been observed in vivo with posterior cruciate-sparing design knee arthroplasties with a tight posterior cruciate ligament. C1 Massachusetts Gen Hosp, Orthopaed Biomech & Biomat Lab, Boston, MA 02114 USA. RP Muratoglu, OK (reprint author), Massachusetts Gen Hosp, Orthopaed Biomech & Biomat Lab, Jackson 1206,55 Fruit St, Boston, MA 02114 USA. NR 14 TC 39 Z9 40 U1 0 U2 1 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0009-921X J9 CLIN ORTHOP RELAT R JI Clin. Orthop. Rel. Res. PD NOV PY 2002 IS 404 BP 89 EP 95 DI 10.1097/01.blo.0000036526.46246.6c PG 7 WC Orthopedics; Surgery SC Orthopedics; Surgery GA 615XR UT WOS:000179273100015 PM 12439243 ER PT J AU Li, GA Otterberg, E Sabbag, K Zayontz, S Johnson, T Rubash, H AF Li, GA Otterberg, E Sabbag, K Zayontz, S Johnson, T Rubash, H TI Biomechanics of posterior-substituting total knee arthroplasty: An in vitro study SO CLINICAL ORTHOPAEDICS AND RELATED RESEARCH LA English DT Article; Proceedings Paper CT Annual Meeting of the Knee-Society/Association of-Hip-and-Knee-Surgeons CY 2002 CL DALLAS, TEXAS SP Knee Soc, Assoc Hip & Knee Surgeons ID IN-SITU FORCES; ANTERIOR CRUCIATE LIGAMENT; KINEMATICS; MOTION; REPLACEMENT; PREDICTION; QUADRICEPS; DESIGN; PROSTHESIS; FLEXION AB The cam-spine system in posterior-substituting total knee arthroplasty was designed to improve posterior stability and to increase posterior femoral translation (rollback). Little is known on its effectiveness in the restoration of femoral rollback under functional loads. In the current study, the effect of cam-spine engagement on knee motion under simulated muscle loads was investigated using knees from cadavers. The translations of the lateral and medial femoral condyles of the knee before and after total knee arthroplasty were compared from 0degrees to 120degrees flexion. Cam-spine contact forces were measured under the same muscle loads. The posterior translations of both femoral condyles in the total knee arthroplasty were significantly lower than that of the native knee beyond full extension. Cam-spine engagement occurred between 60degrees and 90degrees flexion followed by an increase in posterior translation of both femoral condyles. However, the resultant femoral translation of the total knee arthroplasty was still lower than that of the native knee from 90degrees to 120degrees flexion. Knee motion after cam-spine engagement was independent of muscle loads, indicating the importance of the cam-spine mechanism at high flexion angles. Decreased posterior translation of both femoral condyles after total knee arthroplasty may be a limiting factor at high flexion. C1 Harvard Univ, Massachusetts Gen Hosp, Sch Med,Beth Israel Deaconess Med Ctr, Orthopaed Biomech Lab, Boston, MA 02115 USA. MIT, Dept Mech Engn, Cambridge, MA 02139 USA. Zimmer Inc, Warsaw, IN USA. RP Li, GA (reprint author), Orthopaed Biomech Lab, 330 Brooklin3 Ave,RN 115, Boston, MA 02215 USA. NR 36 TC 35 Z9 36 U1 0 U2 2 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0009-921X J9 CLIN ORTHOP RELAT R JI Clin. Orthop. Rel. Res. PD NOV PY 2002 IS 404 BP 214 EP 225 DI 10.1097/01.blo.0000030498.43495.db PG 12 WC Orthopedics; Surgery SC Orthopedics; Surgery GA 615XR UT WOS:000179273100035 PM 12439263 ER PT J AU Fogarty, CM Cyganowski, M Palo, WA Hom, RC Craig, WA AF Fogarty, CM Cyganowski, M Palo, WA Hom, RC Craig, WA TI A comparison of cefditoren pivoxil and amoxicillin/clavulanate in the treatment of community-acquired pneumonia: A multicenter, prospective, randomized, investigator-blinded, parallel-group study SO CLINICAL THERAPEUTICS LA English DT Article DE cefditoren; amoxicillin/clavulanate; CAP; pneumonia ID STREPTOCOCCUS-PNEUMONIAE; ORAL CEPHALOSPORIN; MANAGEMENT; GUIDELINES; CARE; RESISTANCE; ADULTS; AGENTS AB Background: Cefditoren pivoxil is a broad-spectrum cephalosporin that is approved for the treatment of pharyngitis, acute exacerbations of chronic bronchitis, and skin and skin-structure infections. Objective: This study was conducted to examine the efficacy and tolerability of cefditoren in the treatment of community-acquired pneumonia (CAP). Amoxicillin/clavulanate was chosen as a comparator because of its established efficacy and general acceptance as a standard of care in CAP. Methods: This multicenter, prospective, randomized, investigator-blinded, parallel-group trial compared oral cefditoren 200 and 400 mg BID with oral amoxicillin/clavulanate 875/125 mg BID for 14 days in adult outpatients with CAP. Results: Eight hundred two patients (404 men, 398 women; mean age, 50 years; age range, 12-93 years) with CAP were enrolled. Comparable clinical cure rates were observed among evaluable patients in all treatment groups at both the posttreatment and follow-up visits: 88.0% (125/142) for cefditoren 200 mg, 89.9% (143/159) for cefditoren 400 mg, and 90.3% (130/144) for amoxicillin/clavulanate at the posttreatment visit, and 86.5% (128/148), 86.8% (138/159), and 87.8% (129/147) for the respective groups at the follow-up visit. Of 82 Streptococcus pneumoniae strains isolated before treatment, 22 (26.8%) had reduced susceptibility to penicillin, 12 (14.6%) of them penicillin resistant. Overall eradication rates at the posttreatment visit for pathogens isolated from microbiologically evaluable patients were 84.0%, 88.6%, and 82.6% for cefditoren 200 mg, cefditoren 400 mg, and amoxicillin/clavulanate, respectively. In the respective treatmentgroups, 80.6%, 88.6%, and 88.0% of Haemophilus influenzae strains and 95.0%, 96.2%, and 89.5% of S pneumoniae strains were eradicated. The rates of resolution of or improvement in clinical signs and symptoms were comparable between treatment groups. The treatment regimens were well tolerated, with 4.9%, 3.0%, and 5.2% of patients in the respective treatment groups requiring discontinuation of study drug due to an adverse event. Conclusions: In this study in adult outpatients with CAP, both doses of cefditoren demonstrated equivalence to amoxicillin/clavulanate based on rates of clinical and microbiologic cure. All 3 regimens were effective in resolving or improving the clinical signs and symptoms of CAP. Both cefditoren and amoxicillin/clavulanate were well tolerated. C1 Spartanburg Pharmaceut Res, Spartanburg, SC 29307 USA. TAP Pharmaceut Prod Inc, Lake Forest, IL USA. William S Middleton Mem Vet Adm Med Ctr, Madison, WI USA. RP Fogarty, CM (reprint author), Spartanburg Pharmaceut Res, 126 Dillon Dr, Spartanburg, SC 29307 USA. NR 22 TC 22 Z9 24 U1 0 U2 2 PU EXCERPTA MEDICA INC PI NEW YORK PA 650 AVENUE OF THE AMERICAS, NEW YORK, NY 10011 USA SN 0149-2918 J9 CLIN THER JI Clin. Ther. PD NOV PY 2002 VL 24 IS 11 BP 1854 EP 1870 DI 10.1016/S0149-2918(02)80084-4 PG 17 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA 623MJ UT WOS:000179706900011 PM 12501879 ER PT J AU Chatmongkolchart, S Schettino, GPP Dillman, C Kacmarek, RM Hess, DR AF Chatmongkolchart, S Schettino, GPP Dillman, C Kacmarek, RM Hess, DR TI In vitro evaluation of aerosol bronchodilator delivery during noninvasive positive pressure ventilation: Effect of ventilator settings and nebulizer position SO CRITICAL CARE MEDICINE LA English DT Article DE mechanical ventilation; noninvasive positive pressure ventilation; aerosol therapy; nebulizer; asthma; chronic obstructive pulmonary disease ID OBSTRUCTIVE PULMONARY-DISEASE; SUPPORT; THERAPY AB Objective: Respiratory failure due to exacerbation of obstructive lung disease has been successfully treated with noninvasive positive pressure ventilation (NPPV). However, there have been no reports of factors affecting aerosol delivery during NPPV. Our objective was to determine the effect of ventilator settings and nebulizer position on albuterol delivery during NPPV. Design: Bench model study. Setting: University laboratory. Subjects: None. Interventions: A Respironics BiPAP S/T-D30 with a standard circuit was attached to a lung model simulating spontaneous breathing. Inspiratory/expiratory pressures of 10/5, 15/5, 20/5, 15/10, 20/10, and 25/10 cm H2O were tested at respiratory rates of 10 and 20/min. A nebulizer was filled with 5 mg of albuterol in 4 mL of solution, driven with 8 L/min oxygen, and placed at either a proximal (ventilator outlet) or distal (between leak port and lung model connection) position. Albuterol delivery was estimated by measuring the amount of the albuterol collected on a filter placed at the inlet of the lung model. Measurement and Main Results: Albuterol delivery varied from 5.2 +/- 0.4% to 24.5 +/- 1.3% of the nominal dose and was significantly affected by the position of the nebulizer, respiratory rate, and BiPAP settings (p <.001 in each case). The greatest albuterol delivery was observed with the nebulizer operating at the distal position and a respiratory rate of 20/min. At this respiratory rate and nebulizer placement, albuterol delivery increased with increasing inspiratory pressure levels and decreased as expiratory pressure levels were increased. Nebulizer flow did not affect function of the ventilator. Conclusions: At optimum nebulizer position (between the leak port and patient connection) and ventilator settings (high inspiratory pressure and low expiratory pressure), as much as 25% of the nominal albuterol dose may be delivered during NPPV. C1 Massachusetts Gen Hosp, Dept Anesthesia & Crit Care, Boston, MA 02114 USA. Massachusetts Gen Hosp, Dept Resp Care, Boston, MA 02114 USA. Harvard Univ, Sch Med, Boston, MA 02115 USA. Prince Songkla Univ, Dept Anesthesiol, Fac Med, Songkhla, Thailand. RP Hess, DR (reprint author), Massachusetts Gen Hosp, Dept Anesthesia & Crit Care, Ellison 401,55 Fruit St, Boston, MA 02114 USA. NR 13 TC 40 Z9 41 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0090-3493 J9 CRIT CARE MED JI Crit. Care Med. PD NOV PY 2002 VL 30 IS 11 BP 2515 EP 2519 DI 10.1097/01.CCM.0000034558.03726.66 PG 5 WC Critical Care Medicine SC General & Internal Medicine GA 616UZ UT WOS:000179322900018 PM 12441763 ER PT J AU Alston, TA AF Alston, TA TI Nitric oxide, fever, and brimstone: Babylon revisited SO CRITICAL CARE MEDICINE LA English DT Editorial Material DE aqua regia; glutathione; hemoglobin; nitric oxide; S-nitrosothiol; sickle cell disease; transnitrosylation ID INHIBITION C1 Harvard Univ, Sch Med, Massachusetts Gen Hosp,Cardiac Anesthesia Grp, Dept Anesthesia & Crit Care, Boston, MA 02114 USA. RP Alston, TA (reprint author), Harvard Univ, Sch Med, Massachusetts Gen Hosp,Cardiac Anesthesia Grp, Dept Anesthesia & Crit Care, Boston, MA 02114 USA. NR 10 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0090-3493 J9 CRIT CARE MED JI Crit. Care Med. PD NOV PY 2002 VL 30 IS 11 BP 2600 EP 2601 DI 10.1097/01.CCM.0000033269.65406.8D PG 2 WC Critical Care Medicine SC General & Internal Medicine GA 616UZ UT WOS:000179322900036 PM 12441781 ER PT J AU Sheridan, RL AF Sheridan, RL TI Burns SO CRITICAL CARE MEDICINE LA English DT Review DE burn wound; sepsis; postburn deformity; fluid resuscitation; inhalation injury ID HYPERBARIC-OXYGEN THERAPY; ACUTE INHALATION INJURY; MULTIPLE ORGAN FAILURE; LARGE CUTANEOUS BURNS; INTENSIVE-CARE UNIT; ACUTE HAND BURNS; GROWTH-HORMONE; THERMAL-INJURY; PEDIATRIC-PATIENTS; PERMISSIVE HYPERCAPNIA AB During the past 20 yrs, as burn care has evolved as a specialty of surgery, survival and outcome quality have soared. Public expectations for survival and long-term outcomes are at previously unprecedented levels. These changes are the result of a number of advances in aspects of burn care that have occurred in parallel and have fostered increasing regionalization of this resource- intensive activity into fewer specialized centers. These are complex hospitalizations and can be divided into four phases: initial evaluation and resuscitation, initial wound excision and biological closure, definitive wound closure, and rehabilitation and reconstruction. C1 Harvard Univ, Massachusetts Gen Hosp, Sch Med,Sumner Redstone Burn Ctr, Burn Surg Serv,Shriners Burns Hosp, Boston, MA 02114 USA. RP Sheridan, RL (reprint author), Harvard Univ, Massachusetts Gen Hosp, Sch Med,Sumner Redstone Burn Ctr, Burn Surg Serv,Shriners Burns Hosp, Boston, MA 02114 USA. NR 137 TC 46 Z9 48 U1 2 U2 9 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 NOV PY 2002 VL 30 IS 11 SU S BP S500 EP S514 DI 10.1097/01.CCM.0000034128.77577.30 PG 15 WC Critical Care Medicine SC General & Internal Medicine GA 617VH UT WOS:000179381200015 PM 12528792 ER PT J AU Walkes, JCM Earle, N Reardon, MJ Glaeser, DH Wall, MJ Huh, J Jones, JW Soltero, ER AF Walkes, JCM Earle, N Reardon, MJ Glaeser, DH Wall, MJ Huh, J Jones, JW Soltero, ER TI Outcomes in single versus bilateral internal thoracic artery grafting in coronary artery bypass surgery SO CURRENT OPINION IN CARDIOLOGY LA English DT Review ID STERNAL WOUND INFECTIONS; MAMMARY-ARTERY; SURVIVAL AB The authors analyzed the early outcomes in two groups of patients undergoing coronary artery bypass grafting (CABG) with single versus bilateral internal thoracic arteries (ITA) in their institution. One thousand sixty-nine patients underwent CABG with single or bilateral ITAs from 1990 to 2000. Of these patients, 911 (85.2%) had single ITA and 158 had bilateral ITA (14.8%). The incidence of tobacco abuse was 40.3% in the single ITA group and 56.7% in the double ITA group (P = 0.0001). The incidence of perioperative myocardial infarction, renal failure, reoperation for bleeding, stroke, or operative mortality did not differ in the two groups. There was a 4.4% incidence of mediastinitis in the bilateral ITA group versus 2.2% in the single ITA group (P = 0.0602). Early outcomes after bilateral ITA grafting for CABG are similar to single ITA grafting. Careful judgment should be exercised in selecting patients for bilateral ITA grafting, particularly if the patient smokes. (C) 2002 Lippincott Williams Wilkins, Inc. C1 Houston VA Med Ctr, Operat Care Line, Div Cardiothorac Surg, Houston, TX 77030 USA. Baylor Coll Med, Michael E DeBakey Dept Surg, Houston, TX 77030 USA. Univ Missouri, Dept Surg, Columbia, MO USA. RP Soltero, ER (reprint author), Houston VA Med Ctr, Operat Care Line, Div Cardiothorac Surg, 2002 Holcombe Blvd, Houston, TX 77030 USA. NR 18 TC 11 Z9 11 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0268-4705 J9 CURR OPIN CARDIOL JI Curr. Opin. Cardiol. PD NOV PY 2002 VL 17 IS 6 BP 598 EP 601 DI 10.1097/00001573-200211000-00003 PG 4 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA 635NU UT WOS:000180406300003 PM 12466700 ER PT J AU Moreno, PR Muller, JE AF Moreno, PR Muller, JE TI Identification of high-risk atherosclerotic plaques: a survey of spectroscopic methods SO CURRENT OPINION IN CARDIOLOGY LA English DT Review ID LASER-INDUCED FLUORESCENCE; NEAR-INFRARED SPECTROMETRY; RAMAN-SPECTROSCOPY; CORONARY-ARTERIES; HUMAN-TISSUE; DIAGNOSIS; SATURATION; C-13-NMR; AORTA C1 Univ Kentucky, Linda & Jack Gill Heart Inst, Lexington, KY USA. Harvard Univ, Sch Med, Massachusetts Gen Hosp, Div Cardiol, Boston, MA 02115 USA. Harvard Univ, Sch Med, Massachusetts Gen Hosp, CIMIT, Boston, MA 02115 USA. RP Moreno, PR (reprint author), 111B-CDD 1101 Vet Dr, Lexington, KY 40502 USA. NR 46 TC 24 Z9 25 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0268-4705 J9 CURR OPIN CARDIOL JI Curr. Opin. Cardiol. PD NOV PY 2002 VL 17 IS 6 BP 638 EP 647 DI 10.1097/00001573-200211000-00010 PG 10 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA 635NU UT WOS:000180406300010 PM 12466707 ER PT J AU Guha, S Kaunitz, JD AF Guha, S Kaunitz, JD TI Gastroduodenal mucosal defense: an integrated protective response SO CURRENT OPINION IN GASTROENTEROLOGY LA English DT Article ID EPIDERMAL GROWTH-FACTOR; ALKALINE SECRETION; HELICOBACTER-PYLORI; RAT DUODENUM; GASTRIC TOXICITY; GEL LAYER; ACID; CELLS; STOMACH; PATHOGENESIS AB The mechanisms by which the gastroducidenal mucosa maintains viability and normal functioning despite its intensely caustic environment have puzzled clinicians and investigators alike for at least 150 years. Protective mechanisms have been divided into three main categories: preepithelial (mucus and bicarbonate secretion), epithelial (cellular buffering, mucosal architecture and permeability), and postepithelial mechanisms (mucosal blood flow). Within each category are many other factors that bear on the ability of the mucosa to withstand constant changes of luminal pH. We will summarize some of the recent findings that pertain to the nature and regulation of these defense mechanisms in the context of a historical overview. Therapeutic implications of these findings will also be presented in the discussion of novel antiinflammatory compounds designed to upregulate simultaneously several defensive mechanisms, with the expectation that gastroduodenal damage will be minimized. (C) 2002 Lippincott Williams Wilkins, C1 W Los Angeles Vet Affairs Med Ctr, Greater Los Angeles Vet Affairs Healthcare Syst, Los Angeles, CA 90073 USA. Univ Calif Los Angeles, David Geffen Sch Med, Dept Med, Div Digest Dis, Los Angeles, CA 90024 USA. Univ Calif Los Angeles, David Geffen Sch Med, CURE, Digest Dis Res Ctr, Los Angeles, CA USA. RP Kaunitz, JD (reprint author), W Los Angeles Vet Affairs Med Ctr, Greater Los Angeles Vet Affairs Healthcare Syst, Bldg 114,Suite 217, Los Angeles, CA 90073 USA. NR 53 TC 4 Z9 4 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0267-1379 J9 CURR OPIN GASTROEN JI Curr. Opin. Gastroenterol. PD NOV PY 2002 VL 18 IS 6 BP 650 EP 657 DI 10.1097/00001574-200211000-00003 PG 8 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA 610ZN UT WOS:000178992100003 PM 17033343 ER PT J AU Walker, WA AF Walker, WA TI Editorial overview - Immunology SO CURRENT OPINION IN GASTROENTEROLOGY LA English DT Editorial Material C1 Massachusetts Gen Hosp, Mucosal Immunol Lab, Boston, MA 02129 USA. RP Walker, WA (reprint author), Massachusetts Gen Hosp, Mucosal Immunol Lab, Boston, MA 02129 USA. NR 7 TC 1 Z9 1 U1 0 U2 1 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0267-1379 J9 CURR OPIN GASTROEN JI Curr. Opin. Gastroenterol. PD NOV PY 2002 VL 18 IS 6 BP 688 EP 690 DI 10.1097/00001574-200211000-00009 PG 3 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA 610ZN UT WOS:000178992100009 PM 17033349 ER PT J AU Shi, HN Walker, WA AF Shi, HN Walker, WA TI T helper cell subclasses and clinical disease states SO CURRENT OPINION IN GASTROENTEROLOGY LA English DT Article ID IN-VIVO; RESPONSES; INFLAMMATION; INDUCTION; INFECTION; COLITIS; ATOPY; MICE AB The functionally different CD4(+) T helper cell subsets known as T helper 1 (Th1) and T helper 2 (Th2) display a unique and different cytokine profile. Abnormal skewing toward Th1 or Th2 cells has been suggested to play an important role in the pathogenesis of autoimmune disorders and in inflammatory and allergic diseases. The Th1/Th2 paradigm continues to serve as a model to understand the pathogenesis of several pathologic conditions and provides the rationale for the development of new strategies for treating and preventing these diseases. Over the past year, efforts have continued to increase our understanding of the mechanisms underlying the development and regulation of Th cells and their pathogenic role and therapeutic potential in the induction and treatment of clinic diseases. Several teams of researchers have further examined the association of Th1/Th2 inducing factors and allergic disease and intestinal inflammatory diseases. The protective effect of helminth infection on allergy and the role of regulatory T cells in both Th1 - and Th2-mediated diseases have been further examined. (C) 2002 Lippincott Williams Wilkins, Inc. C1 Massachusetts Gen Hosp, Mucosal Immumol Lab, Charlestown, MA 02129 USA. Harvard Univ, Sch Med, Charlestown, MA USA. RP Shi, HN (reprint author), Massachusetts Gen Hosp, Mucosal Immumol Lab, 114 16th St,Room 3504, Charlestown, MA 02129 USA. NR 33 TC 5 Z9 6 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0267-1379 J9 CURR OPIN GASTROEN JI Curr. Opin. Gastroenterol. PD NOV PY 2002 VL 18 IS 6 BP 711 EP 716 DI 10.1097/00001574-200211000-00013 PG 6 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA 610ZN UT WOS:000178992100013 PM 17033353 ER PT J AU Borges, VF Kufe, D Avigan, DE AF Borges, VF Kufe, D Avigan, DE TI Update on cancer vaccines SO CURRENT OPINION IN GASTROENTEROLOGY LA English DT Review ID COLONY-STIMULATING FACTOR; HUMAN DENDRITIC CELLS; CYTOTOXIC T-LYMPHOCYTES; CD34(+) HEMATOPOIETIC PROGENITORS; THERAPEUTIC ANTITUMOR IMMUNITY; COSTIMULATORY MOLECULE B7; TUMOR-CELLS; APOPTOTIC CELLS; TRANSGENIC MICE; MELANOMA-CELLS AB The development of vaccines to induce tumor-specific immunity in patients with cancer has as emerged as a major area of investigation. The identification of antigens uniquely expressed by tumor cells and a heightened understanding of tumor immunology have resulted in efforts to activate host immunity to recognize and reject tumor cells. Tumor-associated antigens and peptides, genes encoding tumor antigens, and modified whole tumor cells have been used in preclinical studies with provocative results. Potent antigen-presenting cells, known as dendritic cells, have also been modified using peptides, genetic material, or whole tumor cells to present tumor antigens in the context of co-stimulation to overcome tolerance and induce tumor-specific cell killing. Promising data generated from the preclinical evaluation of cancer vaccines have resulted in the initiation of clinical trials to define the associated toxicity profile, immunologic response, and clinical impact of this treatment approach. We summarize the preclinical and clinical experience in this expanding area of investigation. Cancer vaccines hold much promise; however, many unresolved questions remain in the effort to generate a clinically meaningful treatment strategy. (C) 2002 Lippincott Williams Wilkins, Inc. C1 Harvard Univ, Sch Med, Beth Israel Deaconess Med Ctr, Boston, MA 02215 USA. Dana Farber Canc Inst, Boston, MA 02115 USA. RP Avigan, DE (reprint author), Harvard Univ, Sch Med, Beth Israel Deaconess Med Ctr, 330 Brookline Ave,Kirsten 1, Boston, MA 02215 USA. NR 105 TC 2 Z9 2 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0267-1379 J9 CURR OPIN GASTROEN JI Curr. Opin. Gastroenterol. PD NOV PY 2002 VL 18 IS 6 BP 723 EP 731 DI 10.1097/00001574-200211000-00015 PG 9 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA 610ZN UT WOS:000178992100015 PM 17033355 ER PT J AU Dzik, WH AF Dzik, WH TI Leukoreduction of blood components SO CURRENT OPINION IN HEMATOLOGY LA English DT Article ID VIRAL ACTIVATION TRANSFUSION; WBC REDUCTION; UNIVERSAL LEUKOREDUCTION; LEUKOCYTE-DEPLETION; MULTICENTER; EXPERIENCE; RBCS; NO AB During the past year, blood component therapy witnessed two quite contradictory trends in the area of leukoreduction. On the one hand, the year saw widespread forced implementation of leukoreduction by several national blood suppliers, including the American Red Cross, who refused to sell hospitals nonleukoreduced blood. The forced implementation came at high cost to hospitals and with the strong endorsement of the US Food and Drug Administration, which stopped short of mandating universal leukoreduction in the United States. On the other hand, the year saw the publication of several pivotal clinical trials that failed to demonstrate significant patient benefit from the use of leukoreduced blood components. The emerging scientific and clinical evidence reviewed in this article demonstrates that leukoreduction technology is an effective means to reduce the risk of three complications of transfusion: HLA alloimmunization, cytomegalovirus transmission, and recurrent febrile nonhemolytic transfusion reactions. The application of the technology to all blood components does not appear to be warranted. (C) 2002 Lippincott Williams Wilkins, Inc. C1 Massachusetts Gen Hosp, Blood Transfus Serv, Boston, MA 02114 USA. Harvard Univ, Sch Med, Boston, MA 02215 USA. RP Dzik, WH (reprint author), Massachusetts Gen Hosp, Blood Transfus Serv, J-224,55 Fruit St, Boston, MA 02114 USA. NR 26 TC 38 Z9 39 U1 3 U2 3 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 NOV PY 2002 VL 9 IS 6 BP 521 EP 526 DI 10.1097/01.MOH.0000028593.70519.54 PG 6 WC Hematology SC Hematology GA 605RD UT WOS:000178690100010 PM 12394176 ER PT J AU Stowell, CP AF Stowell, CP TI Hemoglobin-based oxygen carriers SO CURRENT OPINION IN HEMATOLOGY LA English DT Article ID CROSS-LINKED HEMOGLOBIN; RED-CELL SUBSTITUTE; LIPOSOME-ENCAPSULATED HEMOGLOBIN; HUMAN POLYMERIZED HEMOGLOBIN; RECOMBINANT HUMAN HEMOGLOBIN; STROMA-REDUCED HEMOGLOBIN; ABDOMINAL AORTIC-SURGERY; ACUTE ISCHEMIC STROKE; BLOOD SUBSTITUTE; BOVINE HEMOGLOBIN AB Three types of materials have been studied as candidate blood substitutes: the perfluorocarbons, modified hemoglobins, and liposome-encapsulated hemoglobin. Progress has been greatest with the hemoglobin-based oxygen carriers. Hemoglobin is a highly active molecule; hence, modification has been required to avoid potential deleterious effects. Although there has been considerable progress toward bringing such a product to the clinic, its development has challenged understanding of oxygen delivery and use. The study of these molecules has provided new insights into basic physiologic processes. (C) 2002 Lippincott Williams Wilkins, Inc. C1 Massachusetts Gen Hosp, Blood Transfus Serv, Boston, MA 02114 USA. Harvard Univ, Sch Med, Boston, MA 02215 USA. RP Stowell, CP (reprint author), Massachusetts Gen Hosp, Blood Transfus Serv, GRJ148,55 Fruit St, Boston, MA 02114 USA. NR 77 TC 32 Z9 34 U1 2 U2 4 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 NOV PY 2002 VL 9 IS 6 BP 537 EP 543 DI 10.1097/01.MOH.0000031253.01532.8F PG 7 WC Hematology SC Hematology GA 605RD UT WOS:000178690100013 PM 12394179 ER PT J AU Tolkoff-Rubin, NE AF Tolkoff-Rubin, NE TI Of mice and men: the road to tolerance SO CURRENT OPINION IN NEPHROLOGY AND HYPERTENSION LA English DT Review ID DONOR BONE-MARROW; MIXED CHIMERISM; RENAL-TRANSPLANTATION; ALLOGRAFT TOLERANCE; INDUCTION C1 Massachusetts Gen Hosp, Dept Hemodialysis, Boston, MA 02114 USA. RP Tolkoff-Rubin, NE (reprint author), Massachusetts Gen Hosp, Dept Hemodialysis, GRB 130,55 Fruit St, Boston, MA 02114 USA. NR 12 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 1062-4821 J9 CURR OPIN NEPHROL HY JI Curr. Opin. Nephrol. Hypertens. PD NOV PY 2002 VL 11 IS 6 BP 579 EP 581 DI 10.1097/01.mnh.0000040040.55337.cb PG 3 WC Urology & Nephrology; Peripheral Vascular Disease SC Urology & Nephrology; Cardiovascular System & Cardiology GA 613JD UT WOS:000179128400001 PM 12394600 ER PT J AU Mauiyyedi, S Colvin, RB AF Mauiyyedi, S Colvin, RB TI Humoral rejection in kidney transplantation: new concepts in diagnosis and treatment SO CURRENT OPINION IN NEPHROLOGY AND HYPERTENSION LA English DT Review DE humoral rejection; antibodies; transplantation; kidney; C4d ID RENAL-ALLOGRAFT REJECTION; C4D COMPLEMENT FRAGMENT; PERITUBULAR CAPILLARIES; PATHOLOGICAL FEATURES; GRAFT LOSS; MEDIATED REJECTION; VASCULAR REJECTION; ENDOTHELIAL-CELLS; ANTIBODY; DEPOSITION AB Purpose of review Evidence from several transplant centers indicates that a substantial proportion of acute and chronic renal allograft rejection is caused by antibodies to donor antigens. Antibody-mediated injury arises despite potent anti-T cell pharmacological agents, and probably requires different therapy. Recent findings Acute humoral rejection occurs in 20-30% of acute rejection cases, has a poorer prognosis than cellular rejection, and is refractory to conventional immunosuppressive therapy. C4d deposition in peritubular capillaries of renal allografts has been demonstrated to be a sensitive and diagnostic in-situ marker of acute humoral rejection that correlates strongly with the presence of circulating donor-specific antibodies. Biopsies with chronic allograft arteriopathy or glomerulopathy also have a high frequency of C4d deposition and donor-specific antibodies. The vessels of other organs, notably the heart, can also be targets of humoral rejection. New polyclonal C4d antibodies work in paraffin sections. Pitfalls in C4d staining have been identified and must be considered in the valid interpretation of results. Summary As the histology is variable, the current diagnosis of humoral rejection in biopsies relies on the demonstration of C4d, a component of the classical complement pathway, in peritubular capillaries. The new classification of renal allograft rejection incorporates humoral and cellular mechanisms of injury, with the diagnostic criteria of each. This should prove useful in guiding clinical treatment, and stratifying drug trials, replacing obsolete terms such as 'vascular rejection'. Specific therapeutic strategies for humoral rejection with controlled trials targeting the humoral limb of immunosuppression are needed. C1 Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Pathol, Boston, MA 02114 USA. Univ Texas, Hlth Sci Ctr, Dept Pathol, Houston, TX USA. RP Colvin, RB (reprint author), Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Pathol, 55 Fruit St,Warren 225, Boston, MA 02114 USA. NR 47 TC 130 Z9 141 U1 0 U2 2 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 1062-4821 J9 CURR OPIN NEPHROL HY JI Curr. Opin. Nephrol. Hypertens. PD NOV PY 2002 VL 11 IS 6 BP 609 EP 618 DI 10.1097/01.mnh.0000040046.33359.cf PG 10 WC Urology & Nephrology; Peripheral Vascular Disease SC Urology & Nephrology; Cardiovascular System & Cardiology GA 613JD UT WOS:000179128400007 PM 12394606 ER PT J AU Raje, N Anderson, KC AF Raje, N Anderson, KC TI Thalidomide and immunomodulatory drugs as cancer therapy SO CURRENT OPINION IN ONCOLOGY LA English DT Review ID REFRACTORY MULTIPLE-MYELOMA; PHASE-II; AGENT THALIDOMIDE; CELL; CHEMOTHERAPY; RECURRENT; ANALOGS; GROWTH AB The demonstration of increased angiogenesis in cancer pathogenesis prompted the use of thalidomide in both solid tumors and hematologic malignancies. Its broad spectrum of actions besides its antiangiogenic potential, specifically, its immunomodulatory properties, antiinflammatory actions, and direct effect on tumor cells and their microenvironment, provides an alternative strategy in the armamentarium against cancer. Thalidomide is being evaluated for treatment of hematologic cancers like multiple myeloma and myelodysplasia, and solid tumors like lung, breast, renal, and colon cancer. Thalidomide analogues, the immunomodulatory drugs have increased potency and have demonstrated efficacy and reduced toxicity in phase I and II clinical studies. This article reviews both laboratory-based and clinical studies with thalidomide and the immunomodulatory drugs and their application in different cancers. (C) 2002 Lippincott Williams Wilkins, Inc. C1 Dana Farber Canc Inst, Jerome Lipper Multiple Myeloma Ctr, Dept Adult Oncol, Boston, MA 02115 USA. RP Anderson, KC (reprint author), Dana Farber Canc Inst, Jerome Lipper Multiple Myeloma Ctr, Dept Adult Oncol, 44 Binney St, Boston, MA 02115 USA. NR 53 TC 48 Z9 50 U1 0 U2 3 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 1040-8746 J9 CURR OPIN ONCOL JI Curr. Opin. Oncol. PD NOV PY 2002 VL 14 IS 6 BP 635 EP 640 DI 10.1097/00001622-200211000-00008 PG 6 WC Oncology SC Oncology GA 620LA UT WOS:000179533800008 PM 12409654 ER PT J AU Ng, JK Kawakami, Y Buscher, D Raya, A Itoh, T Koth, CM Esteban, CR Rodriguez-Leon, J Garrity, DM Fishman, MC Belmonte, JCI AF Ng, JK Kawakami, Y Buscher, D Raya, A Itoh, T Koth, CM Esteban, CR Rodriguez-Leon, J Garrity, DM Fishman, MC Belmonte, JCI TI The limb identity gene Tbx5 promotes limb initiation by interacting with Wnt2b and Fgf10 SO DEVELOPMENT LA English DT Article DE T-box; Tbx5; Wnt2b; Fgf10; pectoral fin; limb; zebrafish; chick; heartstrings ID T-BOX GENES; VERTEBRATE LIMB; CHICK-EMBRYO; TRANSCRIPTION FACTORS; DIFFERENTIAL EXPRESSION; ADDITIONAL LIMB; DEVELOPING EYE; SPECIFICATION; ROLES; INDUCTION AB A major gap in our knowledge of development is how the growth and identity of tissues and organs are linked during embryogenesis. The vertebrate limb is one of the best models to study these processes. Combining mutant analyses with gain- and loss-of-function approaches in zebrafish and chick embryos, we show that Tbx5, in addition to its role governing forelimb identity, is both necessary and sufficient for limb outgrowth. We find that Tbx5 functions downstream of WNT signaling to regulate Fgf10, which, in turn, maintains Tbx5 expression during limb outgrowth. Furthermore, our results indicate that Tbx5 and Wnt2b function together to initiate and specify forelimb outgrowth and identity. The molecular interactions governed by members of the T-box, Wnt and Fgf gene families uncovered in this study provide a framework for understanding not only limb development, but how outgrowth and identity of other tissues and organs of the embryo may be regulated. C1 Salk Inst Biol Studies, Gene Express Lab, La Jolla, CA 92037 USA. Inst Gulbenkian Ciencias, P-2780901 Oeiras, Portugal. Massachusetts Gen Hosp, Cardiovasc Res Ctr, Charlestown, MA 02129 USA. RP Belmonte, JCI (reprint author), Salk Inst Biol Studies, Gene Express Lab, 10010 N Torrey Pines Rd, La Jolla, CA 92037 USA. RI Raya, Angel/E-6205-2010; Rodriguez Leon, Joaquin Maria/C-6957-2013 OI Raya, Angel/0000-0003-2189-9775; Rodriguez Leon, Joaquin Maria/0000-0002-9582-5480 NR 47 TC 130 Z9 134 U1 1 U2 9 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 NOV PY 2002 VL 129 IS 22 BP 5161 EP 5170 PG 10 WC Developmental Biology SC Developmental Biology GA 623FT UT WOS:000179693200006 PM 12399308 ER PT J AU Datta, SR Ranger, AM Lin, MZ Sturgill, JF Ma, YC Cowan, CW Dikkes, P Korsmeyer, SJ Greenberg, ME AF Datta, SR Ranger, AM Lin, MZ Sturgill, JF Ma, YC Cowan, CW Dikkes, P Korsmeyer, SJ Greenberg, ME TI Survival factor-mediated BAD phosphorylation raises the mitochondrial threshold for apoptosis SO DEVELOPMENTAL CELL LA English DT Article ID DEATH AGONIST BAD; CELL-SURVIVAL; PROTEIN-KINASE; SIGNALING PATHWAYS; NEURONAL SURVIVAL; DEFICIENT MICE; GROWTH; INHIBITION; AKT; INDUCTION AB Growth factor suppression of apoptosis correlates with the phosphorylation and inactivation of multiple proapoptotic proteins, including the BCL-2 family member BAD. However, the physiological events required for growth factors to block cell death are not well characterized. To assess the contribution of BAD inactivation to cell survival, we generated mice with point mutations in the BAD gene that abolish BAD phosphorylation at specific sites. We show that BAD phosphorylation protects cells from the deleterious effects of apoptotic stimuli and attenuates death pathway signaling by raising the threshold at which mitochondria release cytochrome c to induce cell death. These findings establish a function for endogenous BAD phosphorylation, and elucidate a mechanism by which survival kinases block apoptosis in vivo. C1 Childrens Hosp, Div Neurosci, Boston, MA 02115 USA. Harvard Univ, Sch Med, Dept Neurobiol, Boston, MA 02115 USA. Harvard Univ, Sch Med, Howard Hughes Med Inst, Dana Farber Canc Inst,Dept Pathol, Boston, MA 02115 USA. Harvard Univ, Sch Med, Howard Hughes Med Inst, Dana Farber Canc Inst,Dept Med, Boston, MA 02115 USA. RP Greenberg, ME (reprint author), Childrens Hosp, Div Neurosci, Boston, MA 02115 USA. FU NCI NIH HHS [R37CA50239]; NICHD NIH HHS [P01 HD24926, P30-HD18655] NR 46 TC 188 Z9 195 U1 0 U2 4 PU CELL PRESS PI CAMBRIDGE PA 1100 MASSACHUSETTS AVE, CAMBRIDGE, MA 02138 USA SN 1534-5807 J9 DEV CELL JI Dev. Cell PD NOV PY 2002 VL 3 IS 5 BP 631 EP 643 DI 10.1016/S1534-5807(02)00326-X PG 13 WC Cell Biology; Developmental Biology SC Cell Biology; Developmental Biology GA 615DQ UT WOS:000179230900007 PM 12431371 ER PT J AU Hong, YK Harvey, N Noh, YH Schacht, V Hirakawa, S Detmar, M Oliver, G AF Hong, YK Harvey, N Noh, YH Schacht, V Hirakawa, S Detmar, M Oliver, G TI Prox1 is a master control gene in the program specifying lymphatic endothelial cell fate SO DEVELOPMENTAL DYNAMICS LA English DT Article DE Prox1; lymphatic vasculature; cell fate; endothelial cell; LYVE-1 ID RECEPTOR; SYSTEM; LYMPHANGIOGENESIS; GLYCOPROTEIN; CAPILLARIES; HYALURONAN; MECHANISMS; EXPRESSION; INDUCTION; PROSPERO AB Early during development, one of the first indications that lymphangiogenesis has begun is the polarized expression of the homeobox gene Prox1 in a subpopulation of venous endothelial cells. It has been shown previously that Prox1 expression in the cardinal vein promotes and maintains the budding of endothelial cells that will form the lymphatic vascular system. Prox1-deficient mice are devoid of lymphatic vasculature, and in these animals endothelial cells fail to acquire the lymphatic phenotype; instead, they remain as blood vascular endothelium. To investigate whether Prox1 is sufficient to induce a lymphatic fate in blood vascular endothelium, Prox1 cDNA was ectopically expressed by adenoviral. gene transfer in primary human blood vascular endothelial cells and by transient plasmid cDNA transfection in immortalized microvascular endothelial cells. Transcriptional profiling combined with quantitative real-time reverse transcription-polymerase chain reaction and Western blotting analyses revealed that Prox1 expression up-regulated the lymphatic endothelial cell markers podoplanin and vascular endothelial growth factor receptor-3. Conversely, genes such as laminin, vascular endothelial growth factor-C, neuropilin-1, and intercellular adhesion molecule-1, whose expression has been associated with the blood vascular endothelial cell phenotype, were down-regulated. These results were confirmed by the use of specific antibodies against some of these markers in sections of embryonic and adult tissues. These findings validate our previous proposal that Prox1 is a key player in the molecular pathway leading to the formation of lymphatic vasculature and identify Prox1 as a master switch in the program specifying lymphatic endothelial cell fate. That a single gene product was sufficient to re-program the blood vascular endothelium toward a lymphatic phenotype corroborates the close relationship between these two vascular systems and also suggests that during evolution, the lymphatic vasculature originated from the blood vasculature by the additional expression of only a few gene products such as Prox1. (C) 2002 Wiley-Liss, Inc. C1 Harvard Univ, Sch Med, Cutaneous Biol Res Ctr, Charlestown, MA 02129 USA. Massachusetts Gen Hosp, Cutaneous Biol Res Ctr, Charlestown, MA USA. St Jude Childrens Res Hosp, Dept Genet, Memphis, TN 38105 USA. RP Detmar, M (reprint author), Harvard Univ, Sch Med, Cutaneous Biol Res Ctr, Charlestown, MA 02129 USA. EM michael.detmar@cbrc2.mgh.harvard.edu; guillermo.oliver@stjude.org FU NCI NIH HHS [CA69184, CA86410, CA21765, CA91861]; NEI NIH HHS [EY12162]; NIGMS NIH HHS [GM58462] NR 24 TC 283 Z9 303 U1 1 U2 7 PU WILEY-BLACKWELL PI HOBOKEN PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA SN 1058-8388 J9 DEV DYNAM JI Dev. Dyn. PD NOV PY 2002 VL 225 IS 3 BP 351 EP 357 DI 10.1002/dvdy.10163 PG 7 WC Anatomy & Morphology; Developmental Biology SC Anatomy & Morphology; Developmental Biology GA 611GW UT WOS:000179008900017 PM 12412020 ER PT J AU Ruan, H Miles, PDG Ladd, CM Ross, K Golub, TR Olefsky, JM Lodish, HF AF Ruan, H Miles, PDG Ladd, CM Ross, K Golub, TR Olefsky, JM Lodish, HF TI Profiling gene transcription in vivo reveals adipose tissue as an immediate target of tumor necrosis factor-alpha - Implications for insulin resistance SO DIABETES LA English DT Article ID 3T3-L1 ADIPOCYTES; TRIACYLGLYCEROL HYDROLASE; EXPRESSION; OBESITY; LEPTIN; PROTEIN; LIPASE; OVEREXPRESSION; LIPOLYSIS; RECEPTOR AB Despite extensive studies implicating tumor necrosis factor (TNF)-alpha as a contributing cause of insulin resistance, the mechanism(s) by which TNF-alpha alters energy metabolism in vivo and the tissue specificity of TNF-alpha action are unclear. Here, we investigated the effects of TNF-alpha infusion on gene expression and energy metabolism in adult rats. A 1-day TNF-alpha treatment decreased overall insulin sensitivity and caused a 70% increase (P = 0.005) in plasma levels of free fatty acids (FFAs) and a 46% decrease (P = 0.01) in ACRP30. A 4-day TNF-a infusion caused insulin resistance and significant elevation of plasma levels of FFAs and triglycerides and reduction of ACRP30. Plasma glucose concentration was not altered following TNF-alpha infusion for up to 4 days. As revealed by oligonucleotide microarrays, TNF-alpha evoked major and rapid changes in adipocyte gene expression, favoring FFA release and cytokine production, and fewer changes in liver gene expression, but favoring FFA and cholesterol synthesis and VLDL production. There was only a moderate repressive effect on skeletal muscle gene expression. We demonstrate that TNF-alpha antagonizes the actions of insulin, at least in part, through regulation of adipocyte gene expression including reduction in ACRP30 mRNA and induction of lipolysis resulting in increased plasma FFAs. TNF-alpha later alters systemic energy homeostasis that closely resembles the insulin resistance phenotype. Our data suggest that blockade of TNF-alpha action in adipose tissue may prevent TNF-alpha-induced insulin resistance in vivo. C1 MIT, Whitehead Inst Biomed Res, Cambridge Ctr 9, Cambridge, MA 02142 USA. Harvard Univ, Sch Med, Dept Pediat, Boston, MA USA. Dana Farber Canc Inst, Boston, MA 02115 USA. MIT, Dept Biol, Cambridge, MA USA. Whittier Inst Diabet, La Jolla, CA USA. Vet Adm Med Ctr, La Jolla, CA 90034 USA. Univ Calif San Diego, Dept Med, San Diego, CA 92103 USA. MIT, Whitehead Inst Biomed Res, Genome Ctr, Cambridge, MA 02142 USA. Univ Calif San Diego, Dept Surg, San Diego, CA 92103 USA. RP Lodish, HF (reprint author), MIT, Whitehead Inst Biomed Res, Cambridge Ctr 9, Room 601, Cambridge, MA 02142 USA. FU NIDDK NIH HHS [DK33651, R37DK47618] NR 41 TC 147 Z9 161 U1 1 U2 3 PU AMER DIABETES ASSOC PI ALEXANDRIA PA 1660 DUKE ST, ALEXANDRIA, VA 22314 USA SN 0012-1797 J9 DIABETES JI Diabetes PD NOV PY 2002 VL 51 IS 11 BP 3176 EP 3188 DI 10.2337/diabetes.51.11.3176 PG 13 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA 609PV UT WOS:000178914900005 PM 12401708 ER PT J AU Makhlouf, L Kishimoto, K Smith, RN Abdi, R Koulmanda, M Winn, HJ Auchincloss, H Sayegh, MH AF Makhlouf, L Kishimoto, K Smith, RN Abdi, R Koulmanda, M Winn, HJ Auchincloss, H Sayegh, MH TI The role of autoimmunity in islet allograft destruction - Major histocompatibility complex class II matching is necessary for autoimmune destruction of allogeneic islet transplants after T-cell costimulatory blockade SO DIABETES LA English DT Article ID DIABETES-MELLITUS; NOD MICE; BB RATS; REJECTION; GRAFTS; MOUSE; EXPERIENCE; RESPONSES; RESISTANT; PATHWAYS AB Although it has often been assumed that transplanted allogeneic islets can be destroyed by recurrent autoimmunity in recipients with type 1 diabetes, definitive evidence is lacking and the settings in which this may occur have not been defined. To address these issues, we compared the survival of islet transplants (subject to tissue-specific autoimmunity) with cardiac transplants (not subject to tissue-specific autoimmunity) from various major histocompatibility complex (MHC)-matched and -mismatched donors transplanted into autoimmune NOD recipients. We found that when recipients were treated with combined B7 and CD154 T-cell costimulatory blockade, hearts survived best with better MHC matching, whereas islets survived worst when the donor and recipient shared MHC class II antigens. In the absence of full or MHC class II matching, there was no difference in the survival of islet and cardiac allografts. We also found that the tendency of NOD mice to resist tolerance induction by costimulation blockade is mediated by both CD4+ and CD8+ T-cells, not directly linked to the presence of autoimmunity, and conferred by non-MHC background genes. These findings have clinical importance because they suggest that under some circumstances, avoiding MHC class II sharing may provide better islet allograft survival in recipients with autoimmune diabetes, since mismatched allogeneic islets may be resistant to recurrent autoimmunity. Our results may have implications for the design of future clinical trials in islet transplantation. C1 Harvard Univ, Sch Med, Brigham & Womens Hosp, Dept Med,Lab Immunogenet & Transplantat,Renal Div, Boston, MA 02115 USA. Harvard Univ, Sch Med, Childrens Hosp, Div Nephrol, Boston, MA 02115 USA. Harvard Univ, Sch Med, Massachusetts Gen Hosp, Dept Surg, Boston, MA 02115 USA. Harvard Univ, Sch Med, Massachusetts Gen Hosp, Dept Pathol, Boston, MA 02115 USA. RP Sayegh, MH (reprint author), Harvard Univ, Sch Med, Brigham & Womens Hosp, Dept Med,Lab Immunogenet & Transplantat,Renal Div, Boston, MA 02115 USA. NR 26 TC 45 Z9 46 U1 1 U2 3 PU AMER DIABETES ASSOC PI ALEXANDRIA PA 1660 DUKE ST, ALEXANDRIA, VA 22314 USA SN 0012-1797 J9 DIABETES JI Diabetes PD NOV PY 2002 VL 51 IS 11 BP 3202 EP 3210 DI 10.2337/diabetes.51.11.3202 PG 9 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA 609PV UT WOS:000178914900008 PM 12401711 ER PT J AU Kumagai, N LaMattina, JC Kamano, C Vagefi, PA Barth, RN O'Neil, JJ Yamamoto, S Moran, SG Utsugi, R Sachs, DH Yamada, K AF Kumagai, N LaMattina, JC Kamano, C Vagefi, PA Barth, RN O'Neil, JJ Yamamoto, S Moran, SG Utsugi, R Sachs, DH Yamada, K TI Vascularized islet cell transplantation in miniature swine - Islet-kidney allografts correct the diabetic hyperglycemia induced by total pancreatectomy SO DIABETES LA English DT Article ID RENAL-ALLOGRAFTS; PANCREAS TRANSPLANTATION; LONG-TERM; CLASS-I; TOLERANCE; INDUCTION; TACROLIMUS; CHIMERISM; FK506; CYCLOSPORINE AB We have previously reported the preparation of vascularized islet-kidneys (IKs) by transplantation of islets under the autologous kidney capsule. Here, we compare the efficacy of transplanting vascularized versus non-vascularized islets into diabetic allogeneic swine recipients. In the vascularized islet transplantation (5,000 islet equivalents [IE]/kg), recipients received minor-mismatched (n = 4) or fully-mismatched (n = 2) IKs after pancreatectomy, with a 12-day course of cyclosporine A (CyA) or FK506, respectively. For the non-vascularized islet transplantation (7,000 IE/kg), three recipients received minor-mismatched islets alone and two recipients received minor-mismatched donor islets placed in a donor kidney on the day of transplantation. All recipients of nonvascularized islets were treated with a 12-day course of CyA. With vascularized islet transplantation, pancreatectomized recipients were markedly hyperglycemic pretransplant (fasting blood glucose >300 mg/dl). After composite IK transplantation, all recipients developed and maintained normoglycemia (<120 mg/dl) and stable renal function indefinitely (>3 months), and insulin therapy was not required. Major histocompatibility complex-mismatched recipients demonstrated in vitro donor-specific unresponsiveness. In contrast, recipients of nonvascularized islets remained hyperglycemic. In conclusion, IK allografts cured surgically induced diabetes across allogeneic barriers, whereas nonvascularized islet transplants did not. These data indicate that prevascularization of islet allografts is crucial for their subsequent engraftment and that composite IKs may provide a strategy for successful islet transplantation. C1 Massachusetts Gen Hosp, Transplantat Biol Res Ctr, Boston, MA 02129 USA. Niigata Univ, Sch Med, Dept Urol, Niigata, Japan. Joslin Diabet Ctr, Dept Islet Transplantat & Cell Biol, Boston, MA 02215 USA. RP Yamada, K (reprint author), Massachusetts Gen Hosp, Transplantat Biol Res Ctr, MGH-E,Bldg 149-9019,13th St, Boston, MA 02129 USA. RI Barth, Rolf/B-2542-2014; LaMattina, John/B-2976-2014 OI LaMattina, John/0000-0001-7016-0382 FU NIAID NIH HHS [R01AI 31046] NR 31 TC 19 Z9 20 U1 0 U2 2 PU AMER DIABETES ASSOC PI ALEXANDRIA PA 1660 DUKE ST, ALEXANDRIA, VA 22314 USA SN 0012-1797 J9 DIABETES JI Diabetes PD NOV PY 2002 VL 51 IS 11 BP 3220 EP 3228 DI 10.2337/diabetes.51.11.3220 PG 9 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA 609PV UT WOS:000178914900010 PM 12401713 ER PT J AU Feliers, D Frank, MA Riley, DJ AF Feliers, D Frank, MA Riley, DJ TI Activation of cyclin D1-Cdk4 and Cdk4-directed phosphorylation of RB protein in diabetic mesangial hypertrophy SO DIABETES LA English DT Article ID GROWTH-FACTOR-BETA; EPITHELIAL-CELL HYPERTROPHY; RETINOBLASTOMA GENE-PRODUCT; HIGH GLUCOSE; TGF-BETA; FUNCTIONAL INACTIVATION; GLOMERULAR VOLUME; RESTRICTION POINT; DEPENDENT KINASES; IN-VIVO AB To determine the role of cell-cycle proteins in regulating pathological renal hypertrophy, diabetes was induced in mice expressing a human retinoblastoma (RB) transgene and in wild-type littermates. Whole-kidney and glomerular hypertrophy caused by hyperglycemia was associated with specific G1 phase cell-cycle events: early and sustained increase in expression of cyclin D1 and activation of cyclin D1-cdk4 complexes, but no change in expression of cyclin E or cdk2 activity. Overexpression of RB alone likewise caused hypertrophy and increased only cyclin D1-cdk4 activity; these effects were not further augmented by high glucose. Identical observations were made when isolated mesangial cells conditionally overexpressing RB from a tetracycline-repressible system hypertrophied in response to high glucose. A mitogenic signal in the same cell-culture system, in contrast, transiently and sequentially activated both cyclin D1-cdk4 and cyclin E-cdk2. In vivo and in cultured mesangial cells, high glucose resulted in persistent partial phosphorylation of RB, an event catalyzed specifically by cyclin D1-cdk4. These data indicate that mesangial hypertrophy caused by hyperglycemia in diabetes results in sustained cyclin D1-cdk4-dependent phosphorylation of RB and maintenance of mesangial cells in the early-to-middle G1 phase of the cell cycle. C1 Univ Texas, Hlth Sci Ctr, San Antonio, TX 78229 USA. S Texas Vet Hlth Care Syst, Dept Med, Div Nephrol, San Antonio, TX USA. RP Riley, DJ (reprint author), Univ Texas, Hlth Sci Ctr, MC 7882,7703 Floyd Curl Dr, San Antonio, TX 78229 USA. NR 45 TC 24 Z9 26 U1 0 U2 1 PU AMER DIABETES ASSOC PI ALEXANDRIA PA 1660 DUKE ST, ALEXANDRIA, VA 22314 USA SN 0012-1797 J9 DIABETES JI Diabetes PD NOV PY 2002 VL 51 IS 11 BP 3290 EP 3299 DI 10.2337/diabetes.51.11.3290 PG 10 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA 609PV UT WOS:000178914900018 PM 12401721 ER PT J AU Wallace, C Reiber, GE LeMaster, J Smith, DG Sullivan, K Hayes, S Vath, C AF Wallace, C Reiber, GE LeMaster, J Smith, DG Sullivan, K Hayes, S Vath, C TI Incidence of falls, risk factors for falls, and fall-related fractures in individuals with diabetes and a prior foot ulcer SO DIABETES CARE LA English DT Article AB OBJECTIVE - To describe the incidence of falls, risk factors for falls, and the frequency of fall-related fractures in a cohort of individuals with diabetes and a prior foot ulcer. RESEARCH DESIGN AND METHODS - A total of 400 individuals with diabetes and a prior foot ulcer were recruited from two western Washington State health care organizations and followed prospectively for 2 years. Diabetes, demographic, and health information was collected at baseline, 1 year, and 2 years. Data on falls were collected at baseline, 4 weeks, and every 17 weeks thereafter. Medical records were abstracted to confirm fall-related morbidity. RESULTS - The average age of the study population was 62 years, with 77% male and 23% female. Approximately 32% had fixed foot deformities, 58% had insensate feet, and 76% had comorbid conditions. Of the participants, 252 (64%) reported at least one fall during the 2-year study period. The overall incidence of falls in this cohort was 1.25 falls/person-year (95% CI 1.17-1.33). For the 164 participants (41%) who reported two or more falls, a BMI greater than or equal to30 kg/m(2), the presence of one or more comorbid conditions, and insensate feet increased the risk. Two or more falls of any type were associated with a higher fracture risk. Although women were not at significantly greater risk for falls than men, their fracture incidence was 3.6 times higher. CONCLUSIONS - Falls are very common in individuals with diabetes and prior foot ulcers. A small percentage of falls resulted in fractures. The risk of a fall-related fracture was significantly higher in women than in men. Increased attention to falls and fall prevention is indicated for diabetes care providers. C1 VA Puget Sound Hlth Care Syst, Dept Vet Affairs, Seattle, WA 98108 USA. Univ Washington, Dept Hlth Serv, Seattle, WA 98195 USA. Univ Washington, Dept Epidemiol, Seattle, WA 98195 USA. Univ Washington, Dept Family Med, Seattle, WA 98195 USA. Univ Washington, Dept Orthoped Surg, Seattle, WA 98195 USA. Swedish Med Ctr, Joslin Diabet Ctr, Seattle, WA USA. RP Wallace, C (reprint author), VA Puget Sound Hlth Care Syst 152, 1660 S Columbian Way, Seattle, WA 98108 USA. NR 10 TC 87 Z9 92 U1 1 U2 3 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 NOV PY 2002 VL 25 IS 11 BP 1983 EP 1986 DI 10.2337/diacare.25.11.1983 PG 4 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA 724UG UT WOS:000185504600013 PM 12401743 ER PT J AU Delahanty, L Meigs, JB Hayden, D Williamson, DA Nathan, DM AF Delahanty, L Meigs, JB Hayden, D Williamson, DA Nathan, DM CA DPP Res Grp TI Psychological and behavioral correlates of baseline BMI in the Diabetes Prevention Program (DPP) SO DIABETES CARE LA English DT Article ID BINGE-EATING DISORDER; WEIGHT CONTROL PROGRAM; SELF-EFFICACY; WOMEN; OBESITY; QUESTIONNAIRE; VALIDATION; DEPRESSION; STRESS; EATERS AB OBJECTIVE - To determine psychological and behavioral correlates of baseline BMI in the Diabetes Prevention Program (DPP). RESEARCH DESIGN AND METHODS - Of 1,079 DPP lifestyle intervention participants, 274 completed validated questionnaires at baseline assessing weight loss history, stage of change, self-efficacy, dietary restraint, emotional eating, binge eating, perceived stress, depression, and anxiety. RESULTS - The mean age of subjects was 52.5 years, 65% were women, and their mean BMI was 33.9 kg/m(2). Higher BMI correlated with more frequent weight cycling (r = 0.50, P < 0.0001) and efforts at weight loss (r = 0.34, P < 0.0001); younger age when first overweight (r = -0.42, P < 0.0001); lower exercise efficacy (r = -0.15, P = 0.015); lower weight loss efficacy (r = -0.21, P < 0.001); a less advanced stage of change for weight loss (r = -0.12, P = 0.04); more perceived stress (r = 0.14, P = 0.02); emotional eating (r = 0.19, P = 0.001); poor dietary restraint (r = -0.14, P = 0.02); binge eating frequency (r = 0.18, P = 0.004) and severity (r = 0.30, P < 0.0001); feeling deprived, angry, or upset while dieting (r = 0.27, P &LE; 0.0001); and food cravings while dieting (r = 0.31, P < 0.0001). Correlations did not differ as a function of sex; however, correlations of BMI with anxiety and low-fat diet and weight loss self-efficacy differed as a function of ethnicity. In multivariate models, binge eating severity, poor dietary restraint, and food craving were independent correlates of baseline BMI. CONCLUSIONS - Many psychological and behavioral factors are associated with higher BMI in this ethnically diverse group of men and women. Whether strategies that help patients increase levels of dietary restraint and reduce binge eating and food craving lead to long-term weight loss maintenance needs longitudinal study. C1 Massachusetts Gen Hosp, Ctr Diabet, Boston, MA 02114 USA. Massachusetts Gen Hosp, Div Gen Med, Boston, MA 02114 USA. Massachusetts Gen Hosp, Ctr Biostat, Boston, MA 02114 USA. Pennington Biomed Res Ctr, Baton Rouge, LA USA. RP Delahanty, L (reprint author), Massachusetts Gen Hosp, Ctr Diabet, 50 Staniford St,Suite 340, Boston, MA 02114 USA. FU NCRR NIH HHS [M01 RR001066, M01RR01066]; NIDDK NIH HHS [U01 DK048397, U01 DK048397-06, U01 DK048397-07, U01 DK048397-08, U01 DK048397-09] NR 49 TC 89 Z9 93 U1 6 U2 15 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 NOV PY 2002 VL 25 IS 11 BP 1992 EP 1998 DI 10.2337/diacare.25.11.1992 PG 7 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA 724UG UT WOS:000185504600015 PM 12401745 ER PT J AU Bril, V Perkins, BA AF Bril, V Perkins, BA TI Validation of the Toronto Clinical Scoring System for diabetic polyneuropathy SO DIABETES CARE LA English DT Article ID PERIPHERAL-NERVE FUNCTION; GLYCEMIC CONTROL; RISK-FACTORS; SENSORIMOTOR POLYNEUROPATHY; FOOT ULCERATION; SURAL NERVE; NEUROPATHY; COMPLICATIONS; CONDUCTION; SEVERITY AB OBJECTIVE - The aim of the current study was to determine the validity of the Toronto Clinical Scoring System (CSS) in reflecting the presence and severity of diabetic peripheral sensorimotor polyneneuropathy (DSP) as determined by myelinated fiber density (FD) on sural nerve biopsy. RESEARCH DESIGN AND METHODS - Eighty-nine patients with both type 1 and type 2 diabetes, ascertained from a large therapeutic randomized controlled trial, were included this cross-sectional, observational cohort study. Morphological severity of DSP was expressed the FD in the sural nerve biopsy. The Toronto CSS was applied to all patients to determine a clinical neuropathy score. General linear regression models were used to assess the relationship between the morphological severity of DSP and the Toronto CSS. RESULTS - The Toronto CSS showed a significant negative correlation with sural nerve FD (R-2 = 0.256 P < 0.0001). The Toronto CSS was lower in those with better glycemic control (HbA(1c) &LE;8%). Sural nerve FD and the Toronto CSS showed strong correlations with electro-physiology, by both summed amplitude and summed conduction velocity values. CONCLUSIONS - The Toronto CSS is a valid instrument to reflect the presence and severity of DSP as measured by sural nerve morphology and electrophysiology. The results of the current study underscore the interrelationships between clinical deficits, electrophysiological findings, and morphological changes in USP. This evidence suggests that the Toronto CSS may prove useful in documenting and monitoring DSP in the clinic and in clinical research trials. C1 Univ Toronto, Toronto Gen Hosp, Univ Hlth Network, Toronto, ON M5G 2C4, Canada. Harvard Univ, Joslin Diabet Ctr, Boston, MA 02115 USA. RP Bril, V (reprint author), Univ Toronto, Toronto Gen Hosp, Univ Hlth Network, EN 11-209,200 Elizabeth St, Toronto, ON M5G 2C4, Canada. NR 26 TC 122 Z9 133 U1 0 U2 4 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 NOV PY 2002 VL 25 IS 11 BP 2048 EP 2052 DI 10.2337/diacare.25.11.2048 PG 5 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA 724UG UT WOS:000185504600025 PM 12401755 ER PT J AU Willi, SM Kennedy, A Brant, BP Wallace, P Rogers, NL Garvey, WT AF Willi, SM Kennedy, A Brant, BP Wallace, P Rogers, NL Garvey, WT TI Effective use of thiazolidinediones for the treatment of glucocorticoid-induced diabetes SO DIABETES RESEARCH AND CLINICAL PRACTICE LA English DT Article DE type 2 diabetes mellitus; glucocorticoids; thiazolidinedione; troglitazone; glucose tolerance; free fatty acids; leptin ID INDUCED INSULIN-RESISTANCE; RAT SKELETAL-MUSCLE; OB GENE-EXPRESSION; GLUCOSE-TOLERANCE; ADIPOSE-TISSUE; FATTY-ACIDS; TROGLITAZONE; SENSITIVITY; METABOLISM; MELLITUS AB We evaluated the efficacy of a thiazolidinedione in the treatment of diabetes induced by glucocorticoids. We examined the effectiveness of troglitazone in seven patients with long-standing steroid-induced diabetes. Five of the seven subjects were treated with insulin alone, one was treated with both insulin and oral therapy and one was treated with oral therapy alone. The mean insulin dose in six of the seven subjects was 0.66 +/- 0.09 units/kg per day. Diabetes status was assessed by measuring serum fructosamine, HgbAlc, oral glucose and meal tolerance tests (OGTT and MTT) at baseline and after treatment for 5-8 weeks with troglitazone 400 mg/day. Troglitazone caused a significant decrease in fructosamine (274 +/- 32 vs. 217 +/- 22 mmol/l; P < 0.01) and HgbA1C (7.8 +/- 0.4 vs. 7.2 +/- 0.4%; P < 0.01) as well as decrements in the areas under the OGTT 2,308 +/- 156 vs. 1,937 +/- 127 mmol/l; P < 0.05) and MTT glucose curves (4694 +/- 449 vs. 4057 +/- 437 mmol/l; P < 0.05). In addition, the area under the insulin curve for the oral glucose tolerance test showed a significant increase from 27,438 +/- 4,488 to 41,946 +/- 6,048 pmol/l (P < 0.05). Total and LDL cholesterol were also significantly decreased (6.4 +/- 0.9 vs. 5.0 +/- 0.6 mmol/1 and 3.8 +/- 0.7 vs. 2.7 +/- 0.4 mmol/l, respectively, P < 0.05). Fasting leptin values decreased by 23% despite an increase in body weight. Troglitazone is effective in the treatment of glucocorticoid-induced diabetes as manifested by lower measures of glycemia, HgbAlc, and post-prandial glucose values, while the doses of other diabetes medications remained unchanged or were reduced. The insulin-sensitizing drug also produced a marked increase in endogenous insulin secretion in response to glucose, lower total and LDL cholesterol, and decreased fasting leptin despite weight gain. Thiazolidinediones may improve diabetes-related parameters by antagonizing pathways of glucocorticoid-induced insulin resistance and by reversing adverse effects of glucocorticoids on beta cell function. (C) 2002 Elsevier Science Ireland Ltd. All rights reserved. C1 Med Univ S Carolina, Dept Pediat, Charleston, SC 29425 USA. Med Univ S Carolina, Gen Clin Res Ctr, Charleston, SC 29425 USA. Med Univ S Carolina, Dept Med, Charleston, SC 29425 USA. Ralph H Johnson Vet Affairs Med Ctr, Charleston, SC USA. RP Willi, SM (reprint author), Med Univ S Carolina, Dept Pediat, 171 Ashley Ave, Charleston, SC 29425 USA. FU NCRR NIH HHS [M01 RR-01070-20S3]; NIDDK NIH HHS [DK-38764] NR 45 TC 30 Z9 33 U1 1 U2 1 PU ELSEVIER SCI IRELAND LTD PI CLARE PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE, IRELAND SN 0168-8227 J9 DIABETES RES CLIN PR JI Diabetes Res. Clin. Pract. PD NOV PY 2002 VL 58 IS 2 BP 87 EP 96 AR PII S0168-8227(02)00127-4 DI 10.1016/S0168-8227(02)00127-4 PG 10 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA 608YJ UT WOS:000178875200002 PM 12213349 ER PT J AU Wheeler, SG Ahroni, JH Boyko, EJ AF Wheeler, SG Ahroni, JH Boyko, EJ TI Prospective study of autonomic neuropathy as a predictor of mortality in patients with diabetes SO DIABETES RESEARCH AND CLINICAL PRACTICE LA English DT Article DE type 2 diabetes; autonomic neuropathy; heart rate variability; mortality; prospective study ID HEART-RATE-VARIABILITY; INFARCTION; RISK AB Objective: The objective of this study is to evaluate whether autonomic neuropathy predicts short term all-cause mortality in an elderly cohort of veteran patients with diabetes; Research design and methods: All of the diabetic patients receiving primary care at one VA medical center were eligible for participation, between 1990 and 1997. One thousand and fifteen patients were identified, of whom 14% declined to participate, so that a total of 843 diabetic patients were enrolled. Autonomic neuropathy was evaluated by heart rate response to timed deep breathing. One hundred and fifty one patients have died since the onset of the study. Results: Mean follow-up was 42.4 months. Subjects who died had greater diabetes duration compared with survivors (13.1 vs. 11.4 years, P=0.04) but were comparable with regards to type of diabetes and mean glycosylated hemoglobin level. The Cox proportional hazards analysis, adjusting for age, smoking status, creatinine, pack-years of cigarettes smoked, diabetes duration, race, history of ischemic heart disease and hypertension showed that those patients with the lowest quintile of heart rate variability had a significantly increased risk of mortality (hazard ratio = 1.49, 95% confidence limits 1.01-2.19). Conclusions: This study supports the hypothesis that decreased heart rate variability is an independent risk factor for mortality in diabetic patients followed in a primary care setting. (C) 2002 Published by Elsevier Science Ireland Ltd. C1 Vet Affairs Puget Sound Hlth Care Syst, Primary & Specialty Care Serv, Seattle, WA 98108 USA. Vet Affairs Puget Sound Hlth Care Syst, ERIC, Seattle Div, Seattle, WA USA. Vet Affairs Puget Sound Hlth Care Syst, Res & Dev Serv, Seattle, WA USA. RP Wheeler, SG (reprint author), Vet Affairs Puget Sound Hlth Care Syst, Primary & Specialty Care Serv, 1660 S Columbian Way, Seattle, WA 98108 USA. NR 22 TC 50 Z9 52 U1 0 U2 1 PU ELSEVIER SCI IRELAND LTD PI CLARE PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE, IRELAND SN 0168-8227 J9 DIABETES RES CLIN PR JI Diabetes Res. Clin. Pract. PD NOV PY 2002 VL 58 IS 2 BP 131 EP 138 AR PII S0168-8227(02)00128-6 DI 10.1016/S0168-8227(02)00128-6 PG 8 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA 608YJ UT WOS:000178875200008 PM 12213355 ER PT J AU Paoletta, M Kahn, SE Halban, PA AF Paoletta, M Kahn, SE Halban, PA TI Truncated (des-[27-31]) C-peptide is not a major secretory product of human islets SO DIABETOLOGIA LA English DT Article DE Type II diabetes; insulinoma; proinsulin; insulin; newborn ID HUMAN CELL-MEMBRANES; K+-ATPASE ACTIVITY; PROINSULIN; BINDING; RAT; NA+ AB Aims/hypothesis. It has been suggested that C-peptide is bioactive and that such bioactivity is lost when the last five amino acids are removed. In rats, C-peptide is truncated in beta-cell granules leading to the loss of these last five residues and secretion of des-[27-31]-C-peptide. The aim of this study was to determine whether this truncated form of C-peptide was also a secretory product of human islets. Methods. Plasma from healthy subjects, patients with Type II (non-insulin-dependent) diabetes mellitus or insulinoma and cord blood was analysed by HPLC and ELISA. This method allows for separation and quantification of intact C-peptide and des-[27-31]-C-peptide. Human islets were pulse-chased and secretion stimulated by a mixture of secretagogues. Radioactive products secreted to the medium were analysed by HPLC and the relative amount of intact and truncated C-peptide measured. Results. The proportion of total C-peptide immunoreactivity comprised of des-[27-31]-C-peptide was 1.5% or less in all plasma samples, except for that from one patient with insulinoma where it was 4.2%. The proportion of radiolabelled des-[27-31]-C-peptide released from isolated islets was less than 1%. Conclusion/interpretation. In contrast to the situation in rats, des-[27-31]-C-peptide is not a major secretory product of human islets and its contribution to total circulating C-peptide is not increased in Type II diabetes or in patients with insulinoma: C1 Univ Geneva, Med Ctr, Louis Jeantet Res Labs, CH-1211 Geneva 4, Switzerland. Vet Affairs Puget Sound Hlth Care Syst, Div Metab Endocrinol & Nutr, Dept Med, Seattle, WA USA. Univ Washington, Seattle, WA 98195 USA. RP Halban, PA (reprint author), Univ Geneva, Med Ctr, Louis Jeantet Res Labs, 1 Rue Michel Servet, CH-1211 Geneva 4, Switzerland. OI Kahn, Steven/0000-0001-7307-9002 FU NIDDK NIH HHS [DK-02654, DK-17047] NR 16 TC 5 Z9 5 U1 0 U2 1 PU SPRINGER-VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 USA SN 0012-186X J9 DIABETOLOGIA JI Diabetologia PD NOV PY 2002 VL 45 IS 11 BP 1523 EP 1527 DI 10.1007/s00125-002-0938-y PG 5 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA 624ZV UT WOS:000179792900007 PM 12436335 ER PT J AU Atchley, DH Lopes-Virella, MF Zheng, D Kenny, D Virella, G AF Atchley, DH Lopes-Virella, MF Zheng, D Kenny, D Virella, G TI Oxidized LDL-anti-oxidized LDL immune complexes and diabetic nephropathy SO DIABETOLOGIA LA English DT Article DE Type I diabetes; autoimmunity oxidized; LDL; oxidized LDL antibodies; immune complexes ID LOW-DENSITY-LIPOPROTEIN; CORONARY-ARTERY DISEASE; MALONDIALDEHYDE-MODIFIED LDL; HEART-DISEASE; RISK-FACTORS; PITTSBURGH EPIDEMIOLOGY; IDDM PATIENTS; CAROTID ATHEROSCLEROSIS; CARDIOVASCULAR-DISEASE; MYOCARDIAL-INFARCTION AB Aims/hypothesis. Oxidized LDL is immunogenic and immune complexes formed by oxidized LDL and corresponding antibodies are pro-atherogenic and pro-inflammatory. Considering that macroalbuminuria is a risk factor for coronary heart disease and that common pathogenic factors for atherosclerosis and glomerulosclerosis exist, our aim was to determine whether the amount and/or characteristics of oxidized LDL- anti-oxidized LDL complexes correlated with the degree of albuminuria patients with Type I (insulin-dependent) diabetes mellitus. Methods. We studied 33 macroalbuminuric patients (albumin excretion rate >300 mg/24 h) and 29 microalbuminuric patients (albumin excretion rate greater than or equal to30 mg/24 h and less than or equal to300 mg/24 h) who were matched for age, sex and HbA(1C) concentrations with 43 patients with normal albuminuria. In all patients we isolated. and characterized oxidized LDL-anti-oxidized LDL complexes. A subgroup of 47 patients (22 with normal albuminuria, 11 with microalbuminuria, and 14 with macroalbuminuria) was randomly selected from the. larger group for characterization of the antibody moiety of oxidized LDL immune complexes. Results. The concentrations of oxidized LDL immune complexes were increased in patients with macroalbuminuria (total cholesterol in immune complexes isolated from patients with macroalbuminuria was 272 +/- 20 vs 204 +/- 18 mug/ml in patients with normoalbuminuria, p<0.03). Also, the Kd of oxLDL antibodies isolated from the immune complexes was looter in patients with abnormal albuminuria than in patients with normoalbuminuria (0.86 +/- 0.1x10(-8) vs 1.13+0.1x10(-8) mol/l, p<0.005). Conclusion/interpretation. The data indicate that high concentrations of oxidized LDL-anti-oxidized LDL complexes, particularly when formed with antibodies of higher avidity, are associated with abnormal proteinuria. C1 Med Univ S Carolina, Div Endocrinol Diabet & Med Genet, Dept Med, Charleston, SC 29425 USA. Med Univ S Carolina, Dept Microbiol & Immunol, Charleston, SC 29425 USA. Med Univ S Carolina, Dept Biometry & Epidemiol, Charleston, SC 29425 USA. Ralph H Johnson Vet Adm Med Ctr, Charleston, SC 29425 USA. George Washington Univ, DCCT EDIC, Ctr Biostat, Washington, DC USA. RP Lopes-Virella, MF (reprint author), Med Univ S Carolina, Div Endocrinol Diabet & Med Genet, Dept Med, 114 Doughty St,Room 529, Charleston, SC 29425 USA. FU NCRR NIH HHS [M01-RR-1070]; NHLBI NIH HHS [P01-HL55782] NR 71 TC 40 Z9 44 U1 0 U2 0 PU SPRINGER-VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 USA SN 0012-186X J9 DIABETOLOGIA JI Diabetologia PD NOV PY 2002 VL 45 IS 11 BP 1562 EP 1571 DI 10.1007/s00125-002-0962-y PG 10 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA 624ZV UT WOS:000179792900012 PM 12436340 ER PT J AU Kearney, DJ Hubbard, T Putnam, D AF Kearney, DJ Hubbard, T Putnam, D TI Breath ammonia measurement in Helicobacter pylori infection SO DIGESTIVE DISEASES AND SCIENCES LA English DT Article DE Helicobacter pylori; ammonia ID GASTRIC-JUICE AMMONIA; PERFUSED-RAT-LIVER; CAMPYLOBACTER-PYLORI; GLUTAMINE-METABOLISM; UREA; DIAGNOSIS; CIRRHOSIS; HYPERAMMONEMIA; ERADICATION AB Our aim was to define the utility of breath ammonia measurement in assessing Helicobacter pylori infection. Volunteers breathed into a device containing three fiberoptic NH3 sensors at baseline and after ingesting 300 mg of urea. Breath ammonia levels were compared to the [C-14] urea breath test. Thirteen subjects were tested. Before urea ingestion, H. pylori-positive subjects had significantly lower breath ammonia levels than negative subjects (mean +/- SD, 0.04 ppm +/- 0.09 vs 0.49 ppm +/- 0.24, P = 0.002) and had a significantly greater increases in breath ammonia after urea ingestion (range 198-1494% vs 6-98%). One H. pylori-positive subject underwent treatment and breath ammonia levels shifted from the pattern seen in positive subjects to that seen in negative subjects. In conclusion, breath ammonia measurement for H. Pylori-positive and negative subjects showed distinct patterns. Breath ammonia measurement may be feasible as a diagnostic test for H. pylori. C1 VA Puget Sound Hlth Care Syst, Primary & Specialty Med Care Serv, Seattle, WA USA. Univ Washington, Sch Med, Dept Med, Seattle, WA 98195 USA. Pacific Technol, Kirkland, WA USA. RP Kearney, DJ (reprint author), Vet Affairs Med Ctr, 111GI,1660 S Columbian Way, Seattle, WA 98108 USA. NR 26 TC 52 Z9 52 U1 1 U2 20 PU KLUWER ACADEMIC/PLENUM PUBL PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA SN 0163-2116 J9 DIGEST DIS SCI JI Dig. Dis. Sci. PD NOV PY 2002 VL 47 IS 11 BP 2523 EP 2530 DI 10.1023/A:1020568227868 PG 8 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA 602XE UT WOS:000178529100025 PM 12452390 ER PT J AU Schlozman, SC AF Schlozman, SC TI The shrink in the classroom - An explosive debate: The bipolar child SO EDUCATIONAL LEADERSHIP LA English DT Editorial Material C1 Harvard Univ, Massachusetts Gen Hosp, Sch Med, Boston, MA USA. Harvard Univ, Grad Sch Educ, Cambridge, MA 02138 USA. RP Schlozman, SC (reprint author), Harvard Univ, Massachusetts Gen Hosp, Sch Med, Boston, MA USA. NR 2 TC 1 Z9 1 U1 0 U2 0 PU ASSOC SUPERVISION CURRICULUM DEVELOPMENT PI ALEXANDRIA PA 1703 N BEAUREGARD ST, ALEXANDRIA, VA 22311-1717 USA SN 0013-1784 J9 EDUC LEADERSHIP JI Educ. Leadership PD NOV PY 2002 VL 60 IS 3 BP 89 EP 90 PG 2 WC Education & Educational Research SC Education & Educational Research GA 612CY UT WOS:000179058000021 ER PT J AU Chon, BH Loeffler, JS AF Chon, BH Loeffler, JS TI Efficacy and risk for radiotherapy for pituitary tumors SO ENDOCRINOLOGIST LA English DT Article ID STEREOTAXIC RADIOSURGERY; CONFORMAL RADIOTHERAPY; RADIATION; IRRADIATION; DYSFUNCTION; TOLERANCE; SURGERY; ADENOMA; DISEASE; SKULL AB The management of pituitary adenomas requires a multidisciplinary approach. The role of radiation therapy is well established for medically inoperable patients, subtotally resected lesions, and patients with persistent pituitary hypersecretion. In the magnetic resonance imaging/computed tomography (CT) scan era, radiation therapy can be elegantly delivered with minimal morbidity. With the advent of three-dimensional CT planning plat, forms and stereotactic radiosurgery/radiotherapy, local tumor control and endocrine normalization is realized in most patients who undergo radiotherapy. Well,established radiation tolerance of normal structures, including the brain and the optic structures, allow safe dose delivery to the tumor with minimal risk for optic neuropathy and brain injury. Despite the recent technological progress in radiation delivery, late hypopituitarism. following radiation therapy occurs in about 20-50% of the patients at 5 years. Consequently, proper pretreatment and posttreatment evaluation by a neuroendocrinologist is essential for these patients. Because pituitary adenoma patients are likely to be long-term survivors, the risk for radiation induced malignancies and neurocognitive defects must also be considered. A review of the literature quantitates the risk for radiation associated secondary tumors as < 1% at 20 years. The published literature, although noting higher neurocognitive defects for pituitary adenoma patients, cites multiple variables for this finding-including underlying hormonal imbalance, multiple intracranial surgeries, and radiation therapy. Overall, radiation therapy remains a safe and effective treatment option for select patients. C1 Massachusetts Gen Hosp, Dept Radiat Oncol, Boston, MA 02114 USA. Harvard Univ, Sch Med, Boston, MA USA. RP Loeffler, JS (reprint author), Massachusetts Gen Hosp, Dept Radiat Oncol, 100 Blossom St, Boston, MA 02114 USA. NR 31 TC 1 Z9 1 U1 1 U2 1 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 1051-2144 J9 ENDOCRINOLOGIST JI Endocrinologist PD NOV-DEC PY 2002 VL 12 IS 6 BP 525 EP 530 PG 6 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA 619BY UT WOS:000179454500007 ER PT J AU Pru, JK Hendry, IR Davis, JS Rueda, BR AF Pru, JK Hendry, IR Davis, JS Rueda, BR TI Soluble fas ligand activates the sphingomyelin pathway and induces apoptosis in luteal steroidogenic cells independently of stress-activated p38(MAPK) SO ENDOCRINOLOGY LA English DT Article ID MESSENGER-RIBONUCLEIC-ACID; BOVINE CORPUS-LUTEUM; TUMOR-NECROSIS-FACTOR; GRANULOSA-CELLS; PROTEIN-KINASE; CERAMIDE SYNTHASE; AKT KINASE; IN-VIVO; ANTIGEN; EXPRESSION AB Fas ligand (FasL) is implicated as a mediator of luteolysis. However, a gap exists in our understanding of the Fas-mediated signaling mechanisms that are involved in either the loss of progesterone production or the structural regression of the corpus luteum. In the present study we investigated the acute and chronic effects of FasL, with respect to activation of cytokine/stress-induced signaling pathways and apoptosis in bovine steroidogenic cells. More specifically, we investigated soluble Fasl, (sFasL)-activated production of ceramide, a second messenger of the sphingomyelin pathway, and activation of p38(MAPK), a member of the MAPK family. sFasL activated the sphingomyelin pathway, as evidenced by a 2-fold increase (P < 0.05) in the production of ceramide. Pretreatment with imipramine (50 mum), an inhibitor of acid sphingomyelinase activity, attenuated (75%; P < 0.05) sFasL-induced ceramide production, suggesting that the increase in ceramide was par- tially the result of acid sphingomyelinase-mediated hydrolysis of sphingomyelin. Treatment of luteal cells with sFasL or a cell-permeable ceramide analog (C8) for 24-48 h resulted in a significant increase (P < 0.05) in apoptosis. Western blot analysis revealed that sFasL had little effect on the activation of p38(MAPK) in primary bovine luteal steroidogenic cells. Furthermore, pretreatment with the p38(MAPK) inhibitor SB203590 failed (P > 0.05) to inhibit sFasL- or C8-induced death. Although sFasL did not alter basal progesterone levels detected in the culture medium, C8 caused a significant increase (P < 0.05) in progesterone concentrations within the medium. Collectively, these data suggest that the role of FasL, in luteolysis may be to activate the stress-induced sphingomyelin pathway that, in turn, serves as a mediator of apoptosis. C1 Massachusetts Gen Hosp, Vincent Ctr Reprod Biol, Boston, MA 02114 USA. Univ Nebraska, Med Ctr, Dept Obstet & Gynecol, Olson Ctr Womens Hlth, Omaha, NE 68105 USA. Vet Affairs Med Ctr, Omaha, NE 68105 USA. Univ Kansas, Sch Med, Dept Obstet & Gynecol, Wichita, KS 67214 USA. Womens Res Inst, Wichita, KS 67214 USA. RP Rueda, BR (reprint author), Massachusetts Gen Hosp, Vincent Ctr Reprod Biol, VBK137E-GYN,55 Fruit St, Boston, MA 02114 USA. FU NICHD NIH HHS [R01-HD-35934] NR 60 TC 18 Z9 20 U1 0 U2 0 PU ENDOCRINE SOC PI BETHESDA PA 4350 EAST WEST HIGHWAY SUITE 500, BETHESDA, MD 20814-4110 USA SN 0013-7227 J9 ENDOCRINOLOGY JI Endocrinology PD NOV PY 2002 VL 143 IS 11 BP 4350 EP 4357 DI 10.1210/en.2002-220229 PG 8 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA 608YV UT WOS:000178876700026 PM 12399431 ER PT J AU Asakawa, JI Kodaira, M Ishikawa, N Hirai, Y Nagataki, S Moatamed, F Sugawara, M AF Asakawa, JI Kodaira, M Ishikawa, N Hirai, Y Nagataki, S Moatamed, F Sugawara, M TI Two-dimensional complementary deoxyribonucleic acid electrophoresis revealing up-regulated human epididymal protein-1 and down-regulated CL-100 in thyroid papillary carcinoma SO ENDOCRINOLOGY LA English DT Article ID MAJOR SECRETORY PROTEIN; GENE-EXPRESSION; HE-1; DISPLAY; CANCER AB Two-dimensional cDNA electrophoresis was used to analyze gene expressions in papillary carcinoma and normal tissue of thyroid glands. Pooled thyroid tissues were used to extract mRNA. Complementary DNAs, synthesized with NotI anchor primers, were digested with three restriction enzymes, NotI, EcoRV, and PvuII. The protruding NotI ends were filled in with P-32 deoxynucleotide triphosphates, and the radiolabeled cDNA fragments were separated in two dimensions. Approximately 500 cDNA fragments were visualized as discrete spots without probes. A total of 20 spots, 9 up-regulated and 11 down-regulated cDNAs in papillary carcinoma, were selected and cloned for sequencing. This experiment lent itself to a novel discovery of up-regulated human epididymal protein 1 (HE-1) and down-regulated CL-100 genes in thyroid papillary carcinomas confirmed by Northern blot analysis. Immunohistochemical stains showed abundant HE-1 protein in the papillary carcinoma, whereas little or no HE-1 protein was detected in other types of thyroid cancers and normal thyroid tissues. The restricted localization of HE-1-protein to the portions of papillary projections suggests an involvement of HE-1 protein for forming papillary shape. Our study showed that two-dimensional cDNA electrophoresis is a useful method of detecting differentially expressed genes in human diseases as demonstrated for HE-1 and CL-100 in papillary carcinoma. C1 Univ Calif Los Angeles, Sch Med, Los Angeles, CA 90073 USA. Los Angeles VA Hlth Care Syst, Div Endocrinol & Metab, Dept Med, Los Angeles, CA 90073 USA. Los Angeles VA Hlth Care Syst, Mol Pathol Div, Dept Pathol & Lab Med, Los Angeles, CA 90073 USA. RP Asakawa, JI (reprint author), Radiat Effects Res Fdn, Minami Ku, 5-2 Hijiyama Pk, Hiroshima 7320815, Japan. OI nagataki, shigenobu/0000-0002-9974-3554 NR 23 TC 3 Z9 3 U1 0 U2 0 PU ENDOCRINE SOC PI BETHESDA PA 4350 EAST WEST HIGHWAY SUITE 500, BETHESDA, MD 20814-4110 USA SN 0013-7227 J9 ENDOCRINOLOGY JI Endocrinology PD NOV PY 2002 VL 143 IS 11 BP 4422 EP 4428 DI 10.1210/en.2002-220550 PG 7 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA 608YV UT WOS:000178876700034 PM 12399439 ER PT J AU Cornford, EM Shamsa, K Zeitzer, JM Enriquez, CM Wilson, CL Behnke, EJ Fried, I Engel, J AF Cornford, EM Shamsa, K Zeitzer, JM Enriquez, CM Wilson, CL Behnke, EJ Fried, I Engel, J TI Regional analyses of CNS microdialysate glucose and lactate in seizure patients SO EPILEPSIA LA English DT Article DE brain microdialysate; regional variations; complex partial seizures; glucose; lactate; lactate/lucose ratio ID BLOOD-BRAIN-BARRIER; POSITRON-EMISSION-TOMOGRAPHY; GLUT-1 DEFICIENCY SYNDROME; CEREBRAL METABOLIC-RATE; TEMPORAL-LOBE EPILEPSY; INTRACEREBRAL MICRODIALYSIS; QUANTITATIVE MICRODIALYSIS; EXTRACELLULAR LACTATE; INTENSIVE-CARE; NORMAL VALUES AB Purpose: To correlate glucose (and lactate) results obtained from microdialysate to recent studies suggesting that glucose transporter activity may be significantly altered in seizures. Methods: We used a fluorometric technique to quantify glucose and lactate levels in microdialysates collected from two to four depth electrodes implanted per patient in the temporal and frontal lobes of a series of four patients. Hour-by-hour and day-to-day changes in brain glucose and lactate levels at the same site were recorded. Additionally we compared regional variations in lactate/glucose ratios around the predicted epileptogenic region. Results: Lactate/glucose ratios in the range of 1-2:1 were the most commonly seen. When the lactate/glucose ratio was <1: 1, we typically observed a relative increase in local glucose concentration (rather than decreased lactate), suggesting increased transport, perhaps without increased glycolysis. In some sites, lactate/glucose ratios of 3:1-15: 1 were seen, suggesting that a circumscribed zone of inhibition of tricarboxylic acid cycle activity may have been locally induced. In these dialysates, collected from probes closer to the epileptogenic region, the large increase in lactate/glucose ratios was a result of both increased lactate and reduced glucose levels. Conclusions: We conclude that regional variations in brain extracellular glucose concentrations may be of greater magnitude than previously believed and become even more accentuated in partial seizure patients. Data from concomitant assays of microdialysate lactate and glucose may aid in understanding cerebral metabolism. C1 VA Greater Los Angeles Healthcare Syst, Serv Neurol, Los Angeles, CA 90073 USA. VA Greater Los Angeles Healthcare Syst, Res Serv, Los Angeles, CA 90073 USA. Univ Calif Los Angeles, Sch Med, Dept Neurol, Los Angeles, CA 90024 USA. Univ Calif Los Angeles, Sch Med, Dept Neurosurg, Los Angeles, CA 90024 USA. Univ Calif Los Angeles, Sch Med, Dept Neurobiol, Los Angeles, CA 90024 USA. Univ Calif Los Angeles, Sch Med, Dept Psychiat & Biobehav Sci, Los Angeles, CA 90024 USA. Univ Calif Los Angeles, Inst Brain Res, Los Angeles, CA 90024 USA. RP Cornford, EM (reprint author), VA Greater Los Angeles Healthcare Syst, Serv Neurol, W127,11301 Wilshire Blvd, Los Angeles, CA 90073 USA. OI Zeitzer, Jamie/0000-0001-6174-5282 FU NINDS NIH HHS [NS 02808, NS 33310, NS 37360, NS 45292] NR 42 TC 10 Z9 12 U1 0 U2 2 PU BLACKWELL PUBLISHING INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 USA SN 0013-9580 J9 EPILEPSIA JI Epilepsia PD NOV PY 2002 VL 43 IS 11 BP 1360 EP 1371 DI 10.1046/j.1528-1157.2002.01602.x PG 12 WC Clinical Neurology SC Neurosciences & Neurology GA 616MQ UT WOS:000179307900011 PM 12423386 ER PT J AU Houston, HR Harada, N Makinodan, T AF Houston, HR Harada, N Makinodan, T TI Development of a culturally sensitive educational intervention program to reduce the high incidence of tuberculosis among foreign-born Vietnamese SO ETHNICITY & HEALTH LA English DT Article DE tuberculosis (TB); Vietnamese; cultural beliefs; barriers; immigrants ID PACIFIC ISLANDERS; ASIAN-AMERICANS AB Objective. In Los Angeles County and Orange County, 98% of Asians with tuberculosis (TB) were foreign born; newly arrived Vietnamese immigrants had the highest TB risk: i.e.>100 times higher than that of the USA. The study objective was to find ways to reduce the high incidence of tuberculosis among the Vietnamese by: (1) identifying and understanding the cultural health beliefs and barriers among the Vietnamese population of Orange County, California; and (2) developing a partnership between UCLAA/VA/RAND MEDTEP, key Vietnamese community-based organizations, and community leaders in Orange County to develop and implement a comprehensive, culturally sensitive educational intervention program. Design. Vietnamese residing in Orange County were recruited to obtain qualitative and quantitative data in 1998 and 1999, respectively. The study design included focus groups, in-depth interviews, and community surveys. Data were collected via qualitative reports, computer-assisted random telephone interviews, and self-administered questionnaires. Results. A conceptual schema was identified within the Vietnamese health belief system that recognized two different forms of tuberculosis: non-infectious psychological and infectious physical tuberculosis. It was possible to engage community organizations in developing programs to combat TB in the Vietnamese population. Conclusion. The Health beliefs of Vietnamese will be important considerations in developing a culturally sensitive educational intervention program to service this at-risk population. C1 Calif State Univ Los Angeles, COBAE, Dept Mkt, Los Angeles, CA 90032 USA. Univ Calif Los Angeles, Dept Med, UCLA VA RAND MEDTEP Ctr Asians & Pacific Isl, Los Angeles, CA 90024 USA. Vet Adm Greater Los Angeles Healthcare Syst, Los Angeles, CA 90073 USA. RP Houston, HR (reprint author), Calif State Univ Los Angeles, COBAE, Dept Mkt, 5151 State Univ Dr, Los Angeles, CA 90032 USA. EM hhousto@calstatela.edu FU AHRQ HHS [HS-07370] NR 20 TC 16 Z9 16 U1 0 U2 5 PU CARFAX PUBLISHING PI BASINGSTOKE PA RANKINE RD, BASINGSTOKE RG24 8PR, HANTS, ENGLAND SN 1355-7858 J9 ETHNIC HEALTH JI Ethn. Health PD NOV PY 2002 VL 7 IS 4 BP 255 EP 265 DI 10.1080/1355785022000060718 PG 11 WC Ethnic Studies; Public, Environmental & Occupational Health SC Ethnic Studies; Public, Environmental & Occupational Health GA 659FP UT WOS:000181766900004 PM 12772545 ER PT J AU Cox, ID Thompson, CA Oesterle, SN AF Cox, ID Thompson, CA Oesterle, SN TI Biointerventional cardiovascular therapy SO EUROPEAN HEART JOURNAL LA English DT Review ID MYOCARDIAL GENE-TRANSFER; SKELETAL MYOBLAST TRANSPLANTATION; REPLICATION-DEFECTIVE ADENOVIRUS; IN-VIVO; INFARCTED MYOCARDIUM; HEART; ANGIOGENESIS; DELIVERY; FAILURE C1 Massachusetts Gen Hosp, Div Cardiol, Boston, MA 02114 USA. RP Cox, ID (reprint author), Massachusetts Gen Hosp, Div Cardiol, Bulfinch 105,55 Fruit St, Boston, MA 02114 USA. NR 29 TC 1 Z9 1 U1 0 U2 0 PU W B SAUNDERS CO LTD PI LONDON PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND SN 0195-668X J9 EUR HEART J JI Eur. Heart J. PD NOV PY 2002 VL 23 IS 22 BP 1753 EP 1756 DI 10.1053/euhj.2002.3321 PG 4 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA 617UE UT WOS:000179378600007 PM 12419294 ER PT J AU Douillard, JY Natale, R Giaccone, G Lynch, T Nakagawa, K Brahmer, J Averbuch, S Kay, A AF Douillard, JY Natale, R Giaccone, G Lynch, T Nakagawa, K Brahmer, J Averbuch, S Kay, A TI ZD1839 ('Iressa') provides clinically significant antitumor activity and improves disease-related symptoms in pretreated patients with advanced non-small-cell lung cancer (NSCLC): results of two Phase II trials (IDEAL 1 and IDEAL 2) SO EUROPEAN JOURNAL OF CANCER LA English DT Meeting Abstract CT 14th EORTC/NCI/AACR Symposium on Molecular Targets and Cancer Therapeutics CY NOV 19-22, 2002 CL FRANKFURT, GERMANY C1 CRLCC Rene Gauducheau, St Herblain, France. Cedars Sinai Comprehens Canc Ctr, Los Angeles, CA USA. Free Univ Amsterdam Hosp, Amsterdam, Netherlands. Massachusetts Gen Hosp, Ctr Canc, Boston, MA USA. Kinki Univ, Sch Med, Osaka 589, Japan. Johns Hopkins Univ Hosp, Baltimore, MD 21205 USA. AstraZeneca, Wilmington, DE USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND SN 0959-8049 J9 EUR J CANCER JI Eur. J. Cancer PD NOV PY 2002 VL 38 SU 7 MA 177 BP S56 EP S57 PG 2 WC Oncology SC Oncology GA 626VZ UT WOS:000179895700179 ER PT J AU Gries, J Kasimis, B Schwarzenberger, P Shapiro, G Fidias, P Rodrigues, L Cogswell, J Bukowski, R AF Gries, J Kasimis, B Schwarzenberger, P Shapiro, G Fidias, P Rodrigues, L Cogswell, J Bukowski, R TI Phase I study of flavopiridol (HMR1275) in combination with paclitaxel and carboplatin in non-small cell lung cancer (NCSLC) patients SO EUROPEAN JOURNAL OF CANCER LA English DT Meeting Abstract CT 14th EORTC/NCI/AACR Symposium on Molecular Targets and Cancer Therapeutics CY NOV 19-22, 2002 CL FRANKFURT, GERMANY C1 Aventis Pharmaceut, Clin Pharmacol, Bridgewater, MA USA. VA Med Ctr, Dept Oncol, E Orange, NJ USA. Louisiana State Med Ctr, Dept Oncol, New Orleans, LA USA. Massachusetts Gen Hosp, Boston, MA 02114 USA. Cleveland Clin Fdn, Cleveland, OH 44195 USA. Dana Farber Canc Inst, Boston, MA 02115 USA. NR 0 TC 3 Z9 3 U1 0 U2 0 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 NOV PY 2002 VL 38 SU 7 MA 152 BP S49 EP S50 PG 2 WC Oncology SC Oncology GA 626VZ UT WOS:000179895700154 ER PT J AU Kroning, R Carter, EA Srivatsan, E Lichtenstein, A Nagami, GT AF Kroning, R Carter, EA Srivatsan, E Lichtenstein, A Nagami, GT TI Cellular accumulation of cisplatin is mediated by the ubiquitously expressed sodium-dependent human ASCT1-amino acid transporter SO EUROPEAN JOURNAL OF CANCER LA English DT Meeting Abstract CT 14th EORTC/NCI/AACR Symposium on Molecular Targets and Cancer Therapeutics CY NOV 19-22, 2002 CL FRANKFURT, GERMANY C1 Univ Calif Los Angeles, Dept Med, Los Angeles, CA 90024 USA. Univ Calif Los Angeles, Dept Chem & Biochem, Los Angeles, CA 90024 USA. VA Greater Los Angeles Healthcare Syst, Dept Surg, Los Angeles, CA USA. VA Greater Los Angeles Healthcare Syst, Dept Hematol & Oncol, Los Angeles, CA USA. VA Greater Los Angeles Healthcare Syst, Dept Nephrol, Los Angeles, CA USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND SN 0959-8049 J9 EUR J CANCER JI Eur. J. Cancer PD NOV PY 2002 VL 38 SU 7 MA 315 BP S96 EP S96 PG 1 WC Oncology SC Oncology GA 626VZ UT WOS:000179895700317 ER PT J AU Schwartz, C Ryan, L Nwangwu, J Blum, R AF Schwartz, C Ryan, L Nwangwu, J Blum, R TI Phase II trial of edatrexate in adult patients with metastatic soft tissue sarcomas, an Eastern Cooperative Oncology Group (ECOG) final report SO EUROPEAN JOURNAL OF CANCER LA English DT Meeting Abstract CT 14th EORTC/NCI/AACR Symposium on Molecular Targets and Cancer Therapeutics CY NOV 19-22, 2002 CL FRANKFURT, GERMANY C1 Columbia Univ, St Lukes Roosevelt Hosp Ctr, Dept Hematol & Oncol, New York, NY USA. Beth Israel Med Ctr, Dept Hematol & Oncol, New York, NY 10003 USA. Dana Farber Canc Inst, Dept Biostat Sci, Boston, MA 02115 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND SN 0959-8049 J9 EUR J CANCER JI Eur. J. Cancer PD NOV PY 2002 VL 38 SU 7 MA 63 BP S24 EP S24 PG 1 WC Oncology SC Oncology GA 626VZ UT WOS:000179895700062 ER PT J AU Screpanti, I Bellavia, D Campese, A Checquolo, S Balestri, A Biondi, A Cazzaniga, G von Boehmer, H Frati, L Gulino, A AF Screpanti, I Bellavia, D Campese, A Checquolo, S Balestri, A Biondi, A Cazzaniga, G von Boehmer, H Frati, L Gulino, A TI Combined expression of pTa and Notch3 in T cell leukemia identifies the requirement of preTCR for leukemogenesis SO EUROPEAN JOURNAL OF CANCER LA English DT Meeting Abstract CT 14th EORTC/NCI/AACR Symposium on Molecular Targets and Cancer Therapeutics CY NOV 19-22, 2002 CL FRANKFURT, GERMANY C1 Univ Roma La Sapienza, Dept Expt Med & Pathol, I-00185 Rome, Italy. Univ Aquila, Dept Expt Med, I-67100 Laquila, Italy. Univ Milan Bicocca, Tettamanti Res Ctr, Monza, Italy. Dana Farber Canc Inst, Dept Pathol, Boston, MA 02115 USA. RI Campese, Antonio /A-9783-2015 NR 0 TC 0 Z9 0 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND SN 0959-8049 J9 EUR J CANCER JI Eur. J. Cancer PD NOV PY 2002 VL 38 SU 7 MA 357 BP S106 EP S106 PG 1 WC Oncology SC Oncology GA 626VZ UT WOS:000179895700359 ER PT J AU Yang, X Stone, R AF Yang, X Stone, R TI Inhibition of MEK/ERK and PI3K/Akt pathways blocks apoptosis suppression signaling of FLT3/ITD SO EUROPEAN JOURNAL OF CANCER LA English DT Meeting Abstract CT 14th EORTC/NCI/AACR Symposium on Molecular Targets and Cancer Therapeutics CY NOV 19-22, 2002 CL FRANKFURT, GERMANY C1 Dana Farber Canc Inst, Dept Adult Oncol, Boston, MA 02115 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND SN 0959-8049 J9 EUR J CANCER JI Eur. J. Cancer PD NOV PY 2002 VL 38 SU 7 MA 557 BP S166 EP S166 PG 1 WC Oncology SC Oncology GA 626VZ UT WOS:000179895700562 ER PT J AU Schenten, D Gerlach, VL Guo, CX Velasco-Miguel, S Hladilk, CL White, CL Friedberg, EC Rajewsky, K Esposito, G AF Schenten, D Gerlach, VL Guo, CX Velasco-Miguel, S Hladilk, CL White, CL Friedberg, EC Rajewsky, K Esposito, G TI DNA polymerase kappa deficiency does not affect somatic hypermutation in mice SO EUROPEAN JOURNAL OF IMMUNOLOGY LA English DT Article DE B cell; somatic hypermutation; DNA polymerase kappa ID HUMAN DINB1 GENE; CLASS-SWITCH RECOMBINATION; CYTIDINE DEAMINASE AID; DOUBLE-STRAND BREAKS; IMMUNOGLOBULIN GENES; EMBRYONIC LETHALITY; IG GENES; MONOCLONAL-ANTIBODIES; IMMUNE-RESPONSE; MOUSE HOMOLOGS AB Somatic hypermutation (SH) in B cells undergoing T cell-dependent immune responses generates high-affinity antibodies that provide protective immunity. Most current models of SH postulate the introduction of a nick into the DNA and subsequent replication-independent, error-prone short-patch synthesis by one or more DNA polymerases. The PolK (DinB1) gene encodes a specialized mammalian DNA polymerase called DNA polymerase kappa (polkappa), a member of the recently discovered Y family of DNA polymerases. The mouse PolK gene is expressed at high levels in the seminiferous tubules of the testis and in the adrenal cortex, and at lower levels in most other cells of the body including B lymphocytes. In vitro studies showed that polkappa can act as an error-prone polymerase, although they failed to ascribe a clear function to this enzyme. The ability of polkappa to generate mutations when extending primers on undamaged DNA templates identifies this enzyme as a potential candidate for the introduction of nucleotide changes in the immunoglobulin (Ig) genes during the process of SH. Here we show that polkappa-deficient mice are viable, fertile and able to mount a normal immune response to the antigen (4-hydroxy-3-nitrophenyl)acetyl-chicken gamma-globulin (NP-GC). They also mutate their Ig genes normally. However, polkappa-deficient embryonic fibroblasts are abnormally sensitive to killing following exposure to ultraviolet (UV) radiation, suggesting a role of polkappa in translesion DNA synthesis. C1 Univ Cologne, Inst Genet, D-50931 Cologne, Germany. Univ Texas, SW Med Ctr, Dept Pathol, Lab Mol Pathol, Dallas, TX USA. Ctr Blood Res, Boston, MA 02115 USA. RP Esposito, G (reprint author), Univ Cologne, Inst Genet, Weyertal 121, D-50931 Cologne, Germany. FU NIEHS NIH HHS [ES-11344] NR 49 TC 108 Z9 108 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 NOV PY 2002 VL 32 IS 11 BP 3152 EP 3160 DI 10.1002/1521-4141(200211)32:11<3152::AID-IMMU3152>3.0.CO;2-2 PG 9 WC Immunology SC Immunology GA 615YZ UT WOS:000179276100015 PM 12555660 ER PT J AU Nanthakumar, NN Dai, DW Newburg, DS Walker, WA AF Nanthakumar, NN Dai, DW Newburg, DS Walker, WA TI The role of indigenous microflora in the development of murine intestinal fucosyl- and sialyltransferases SO FASEB JOURNAL LA English DT Article DE luminal bacteria; germ-free mice; postnatal development; brush border membrane glycoconjugates; extrinsic regulation ID BETA-GALACTOSIDE ALPHA-2,6-SIALYLTRANSFERASE; RAT SMALL-INTESTINE; EPITHELIAL-CELLS; BACTERIAL-COLONIZATION; ECOSYSTEM; EXPRESSION; ADULT; FETAL; MICE; GLYCOSYLATION AB Most enteric bacteria use intestinal brushborder glycoconjugates as their target host cell receptors. It has been postulated that resident microbes regulate specific glycosyltransferases that are responsible for synthesizing brushborder glycoconjugates. To investigate this hypothesis, we measured glycosyltransferase enzyme activities in intestine from different regions of maturing conventional (CONV), germ-free (GF), and ex-germ-free (XGF) mice and compared them to general enzyme markers of gut development, for example, disaccharidases. High alpha2,3/6-Sialyltransferase (ST) activity and low alpha1,2-fucosyltransferase (FT) activities were detected from duodenum to colon in suckling CONV mice, but the relative levels of these activities reversed during the third postnatal wk, rapidly reaching adult levels by the fourth wk. These age-related enzyme changes were significantly attenuated in GF mice, maintaining an immature pattern well past 3 wk. Introduction of gut microflora in GF mice rapidly initiated maturation of glycosyltransferase activity but had no significant affect on developmental programming of dissacharidases. Therefore, in mice, intestinal glycosyltransferase activities are under tissue and developmental control and microflora play a major role in their specific ontogeny but not in overall development. These findings may help explain the regional specificity of commensal bacteria and of enteric pathogens and may also relate age-related changes in microflora to susceptibility to enteropathogens. C1 Massachusetts Gen Hosp, Dev Gastroenterol Lab, Combined Program Pediat Gastroenterol & Nutr, Charlestown, MA 02129 USA. Harvard Univ, Sch Med, Boston, MA 02115 USA. Xinhua Hosp, Shanghai Inst Pediat Res, Shanghai, Peoples R China. Shanghai Med Univ 2, Shanghai, Peoples R China. Eunice Kennedy Shriver Ctr Mental Retardat Inc, Program Glycobiol, Waltham, MA 02254 USA. RP Walker, WA (reprint author), Massachusetts Gen Hosp, Dev Gastroenterol Lab, Combined Program Pediat Gastroenterol & Nutr, 114 16th St 114-3503, Charlestown, MA 02129 USA. EM wwalker@partners.org NR 40 TC 1 Z9 1 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 NOV PY 2002 VL 16 IS 13 BP 44 EP + DI 10.1096/fj.02-0031fje PG 18 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 632HU UT WOS:000180218500024 ER PT J AU Issa, R Zhou, XY Trim, N Millward-Sadler, H Krane, S Benyon, C Iredale, J AF Issa, R Zhou, XY Trim, N Millward-Sadler, H Krane, S Benyon, C Iredale, J TI Mutation in collagen-I that confers resistance to the action of collagenase results in failure of recovery from CCl4-induced liver fibrosis, persistence of activated hepatic stellate cells, and diminished hepatocyte regeneration SO FASEB JOURNAL LA English DT Article DE apoptosis; metalloproteinase (MMP); tissue inhibitor of metalloproteinase (TIMP); hepatic regeneration ID NORMAL RAT-LIVER; TISSUE INHIBITOR; INTERSTITIAL COLLAGENASE; MATRIX METALLOPROTEINASE-2; LIPOCYTES SYNTHESIZE; GENE-EXPRESSION; APOPTOSIS; CLEAVAGE; ANGIOGENESIS; MECHANISMS AB Collagen-I, which predominates in the neomatrix of fibrotic liver, regulates hepatocyte and hepatic stellate cell (HSC) phenotypes. Recovery from liver fibrosis is accompanied by hepatocyte regeneration, matrix degradation, and HSC apoptosis. Using mice bearing a mutated collagen-I gene (r/r mice), which confers resistance to collagenase degradation, we have investigated the hypothesis that collagen-I degradation is critical to HSC apoptosis and hepatocyte regeneration during recovery from liver fibrosis. During a 28-day recovery period after 8 wk of CCl4 treatment, wild-type (WT) livers had significantly (43%) decreased hydroxyproline (OHP) content. In r/r livers, however, OHP content remained elevated at peak fibrosis levels. Expressed markers of activated HSC (alpha-smooth muscle actin, collagen-I), elevated at peak fibrosis, dropped to control levels in WT livers after 28 days but remained raised in the r/r livers. Moreover, relative to WT livers, r/r livers had significantly reduced stellate cell apoptosis and hepatocyte regeneration during the recovery period. Using extracted collagen-I from each genotype as culture substrata, relative to r/r, we show that WT collagen-I promotes hepatocyte proliferation via stimulation of integrin alphavbeta(3). Failure to degrade collagen-I critically impairs HSC apoptosis and may prevent the effective restoration of hepatocyte mass in liver fibrosis. C1 Univ Southampton, Southampton Gen Hosp, Liver Res Grp, Southampton SO19 6YD, Hants, England. Univ Southampton, Southampton Gen Hosp, Dept Histopathol Infect Inflammat & Repair, Southampton SO19 6YD, Hants, England. Harvard Univ, Sch Med, Massachusetts Gen Hosp, Boston, MA 02114 USA. RP Iredale, J (reprint author), Univ Southampton, Southampton Gen Hosp, Mail Point 811,Level D,S Block, Southampton SO19 6YD, Hants, England. EM jpi@soton.ac.uk NR 45 TC 5 Z9 5 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 NOV PY 2002 VL 16 IS 13 BP 47 EP + DI 10.1096/fj.02-0494fje PG 24 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 632HU UT WOS:000180218500026 ER PT J AU Lu, SC Gukovsky I Lugea, A Reyes, CN Huang, ZZ Chen, LX Mato, JM Bottiglieri, T Pandol, SJ AF Lu, SC Gukovsky, I Lugea, A Reyes, CN Huang, ZZ Chen, LX Mato, JM Bottiglieri, T Pandol, SJ TI Role of S-adenosylmethionine in two experimental models of pancreatitis SO FASEB JOURNAL LA English DT Article DE methionine adenosyltransferase 1A; methionine adenosyltransferase 2A; CDE diet; cerulein ID ADENOSYL-L-METHIONINE; KAPPA-B ACTIVATION; RAT-LIVER; ADENOSYLTRANSFERASE GENES; DIFFERENTIAL EXPRESSION; CHOLINE-DEFICIENT; SYNTHETASE; CELLS; HEPATOCYTES; ETHIONINE AB Severe necrotizing pancreatitis occurs in young female mice fed a choline-deficient and ethionine-supplemented (CDE) diet. Although the mechanism of the pancreatitis is unknown, one consequence of this diet is depletion of hepatic S-adenosylmethionine (SAM). SAM formation is catalyzed by methionine adenosyltransferases (MATs), which are encoded by liver-specific (MAT1A) and non-liver-specific (MAT2A) genes. In this work, we examined changes in pancreatic SAM homeostasis in mice receiving the CDE diet and the effect of SAM treatment. We found that both MAT forms are expressed in normal pancreas and pancreatic acini. After 48 h of the CDE diet, SAM levels decreased 50% and MAT1A-encoded protein disappeared via post-translational mechanisms, whereas MAT2A-encoded protein increased via pretranslational mechanisms. CDE-fed mice exhibited extensive necrosis, edema, and acute pancreatic inflammatory infiltration, which were prevented by SAM treatment. However, old female mice consuming the CDE diet that do not develop pancreatitis showed a similar fall in pancreatic SAM level. SAM was also protective in cerulein-induced pancreatitis in the rat, but the protection was limited. Although the pancreatic SAM level fell by more than 80% in the MAT1A knockout mice, no pancreatitis developed. This study thus provides several novel findings. First, the so-called liver-specific MAT1A is highly expressed in the normal pancreas and pancreatic acini. Second, the CDE diet causes dramatic changes in the expression of MAT isozymes by different mechanisms. Third, in contrast to the situation in the liver, where absence of MAT1A and decreased hepatic SAM level can lead to spontaneous tissue injury, in the pancreas the roles of SAM and MAT1A appear more complex and remain to be defined. C1 Univ So Calif, Dept Med, Div Gastrointestinal & Liver Dis, Keck Sch Med,Liver Dis Res Ctr, Los Angeles, CA 90033 USA. Univ Calif Los Angeles, Res Ctr Alcohol Liver & Pancreat Dis, VA Greater Los Angeles Healthcare Syst, Los Angeles, CA 90073 USA. Univ Navarra, Sch Med, Div Hepatol & Gene Therapy, E-31080 Pamplona, Spain. Baylor Univ, Med Ctr, Inst Metab Dis, Dallas, TX 75226 USA. RP Lu, SC (reprint author), Univ So Calif, Dept Med, Div Gastrointestinal & Liver Dis, Keck Sch Med,Liver Dis Res Ctr, HMR Bldg,415,2011 Zonal Ave, Los Angeles, CA 90033 USA. EM Stephen.Pandol@med.va.gov RI MATO, JOSE/A-5187-2011 NR 40 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 NOV PY 2002 VL 16 IS 13 BP 56 EP + DI 10.1096/fj.01-0752fje PG 17 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 632HU UT WOS:000180218500034 ER PT J AU Joussen, AM Poulaki V Mitsiades, N Cai, WY Suzuma I Pak, J Ju, ST Rook, SL Esser, P Mitsiades, C Kirchhof, B Adamis, AP Aiello, LP AF Joussen, AM Poulaki, V Mitsiades, N Cai, WY Suzuma, I Pak, J Ju, ST Rook, SL Esser, P Mitsiades, C Kirchhof, B Adamis, AP Aiello, LP TI Suppression of Fas-FasL-induced endothelial cell apoptosis prevents diabetic blood-retinal barrier breakdown in a model of streptozotocin-induced diabetes SO FASEB JOURNAL LA English DT Article DE diabetic retinopathy; apoptosis; leukocyte adhesion ID ADHESION MOLECULE-1; VASCULAR-PERMEABILITY; DOWN-REGULATION; LIGAND; EXPRESSION; RETINOPATHY; GROWTH; DEATH; LEUKOSTASIS; MECHANISM AB Diabetic macular edema, resulting from increased microvascular permeability, is the most prevalent cause of vision loss in diabetes. The mechanisms underlying this complication remain poorly understood. In the current study, diabetic vascular permeability (blood-retinal barrier breakdown) is demonstrated to result from a leukocyte-mediated Fas-FasL-dependent apoptosis of the retinal vasculature. Following the onset of streptozotocin-induced diabetes, FasL expression was increased in rat neutrophils (P<0.005) and was accompanied by a simultaneous increase in Fas expression in the retinal vasculature. Static adhesion assays demonstrated that neutrophils from diabetic, but not control, rats induced endothelial cell apoptosis in vitro (P<0.005). The latter was inhibited via an antibody-based FasL blockade (P<0.005). In vivo, the inhibition of FasL potently reduced retinal vascular endothelial cell injury, apoptosis, and blood-retinal barrier breakdown (P<0.0001) but did not diminish leukocyte adhesion to the diabetic retinal vasculature. Taken together, these data are the first to identify leukocyte-mediated Fas-FasL-dependent retinal endothelial cell apoptosis as a major cause of blood-retinal barrier breakdown in early diabetes. These data imply that the targeting of the Fas-FasL pathway may prove beneficial in the treatment of diabetic retinopathy. C1 Univ Cologne, Ctr Ophthalmol, Dept Vitreoretinal Surg, D-50931 Cologne, Germany. Univ Cologne, Ctr Mol Med ZMMK, D-50931 Cologne, Germany. Harvard Univ, Massachusetts Eye & Ear Infirm, Sch Med, Retina Res Inst, Boston, MA 02114 USA. Joslin Diabet Ctr, Beetham Eye Inst, Boston, MA 02115 USA. Harvard Univ, Sch Med, Childrens Hosp, Surg Res Labs, Boston, MA 02115 USA. Harvard Univ, Sch Med, Dana Farber Canc Inst, Boston, MA 02115 USA. Harvard Univ, Sch Med, Dept Ophthalmol, Boston, MA 02215 USA. RP Joussen, AM (reprint author), Univ Cologne, Ctr Ophthalmol, Dept Vitreoretinal Surg, Joseph Stelzmann Str 9, D-50931 Cologne, Germany. EM JoussenA@aol.com; tony_adamis@meei.harvard.edu NR 29 TC 8 Z9 8 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 NOV PY 2002 VL 16 IS 13 BP 76 EP + DI 10.1096/fj.02-0157fje PG 20 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 632HU UT WOS:000180218500021 ER PT J AU Micchelli, CA Esler, WP Kimberly, WT Jack, C Berezovska, O Kornilova, A Hyman, BT Perrimon, N Wolfe, MS AF Micchelli, CA Esler, WP Kimberly, WT Jack, C Berezovska, O Kornilova, A Hyman, BT Perrimon, N Wolfe, MS TI gamma-secretase/presenilin inhibitors for Alzheimer's disease phenocopy Notch mutations in Drosophila SO FASEB JOURNAL LA English DT Article DE protease; developmental biology; drug screening ID SECRETASE INHIBITORS; TRANSMEMBRANE ASPARTATES; THYMOCYTE DEVELOPMENT; INTRACELLULAR DOMAIN; WINGLESS EXPRESSION; PRESENILIN-1; GENE; PROTEASE; SIGNAL; INTEGRATION AB Signaling from the Notch (N) receptor is essential for proper cell-fate determinations and tissue patterning in all metazoans. N signaling requires a presenilin (PS)-dependent transmembrane-cleaving activity that is closely related or identical to the gamma-secretase proteolysis of the amyloid-beta precursor protein (APP) involved in Alzheimer's disease pathogenesis. Here, we show that N-[N-(3,5-difluorophenacetyl)-L-alanyl]-(S)-phenylglycine t-butyl ester, a potent gamma-secretase inhibitor reported to reduce amyloid-beta levels in transgenic mice, prevents N processing, translocation, and signaling in cell culture. This compound also induces developmental defects in Drosophila remarkably similar to those caused by genetic reduction of N. The appearance of this phenocopy depends on the timing and dose of compound exposure, and effects on N-dependent signaling molecules established its biochemical mechanism of action in vivo. Other gamma-secretase inhibitors caused similar effects. Thus, the three-dimensional structure of the drug-binding site(s) in Drosophila gamma-secretase is remarkably conserved vis-a-vis the same site(s) in the mammalian enzyme. These results show that genetics and developmental biology can help elucidate the in vivo site of action of pharmacological agents and suggest that organisms such as Drosophila may be used as simple models for in vivo prescreening of drug candidates. C1 Harvard Univ, Ctr Neurol Dis, Brigham & Womens Hosp, Sch Med, Boston, MA 02115 USA. Harvard Univ, Dept Genet, Howard Hughes Med Inst, Sch Med, Boston, MA 02115 USA. Harvard Univ, Dept Neurol, Massachusetts Gen Hosp, Alzheimers Dis Res Lab,Sch Med, Charlestown, MA 02129 USA. RP Wolfe, MS (reprint author), Harvard Univ, Ctr Neurol Dis, Brigham & Womens Hosp, Sch Med, 77 Ave Louis Pasteur,HIM 626, Boston, MA 02115 USA. EM mwolfe@rics.bwh.harvard.edu NR 44 TC 5 Z9 5 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 NOV PY 2002 VL 16 IS 13 BP 79 EP + DI 10.1096/fj.02-0394fje PG 17 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 632HU UT WOS:000180218500042 ER PT J AU Schiff, I Frigoletto, F AF Schiff, I Frigoletto, F TI Obituary for Kenneth J. Ryan, MD SO FERTILITY AND STERILITY LA English DT Biographical-Item C1 Massachusetts Gen Hosp, Vincent Obstet & Gynecol Serv, Boston, MA 02114 USA. Harvard Univ, Sch Med, Dept Obstet Gynecol & Reprod Biol, Boston, MA USA. RP Schiff, I (reprint author), Massachusetts Gen Hosp, Vincent Obstet & Gynecol Serv, 55 Fruit St, Boston, MA 02114 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0015-0282 J9 FERTIL STERIL JI Fertil. Steril. PD NOV PY 2002 VL 78 IS 5 BP 1136 EP 1137 AR PII S0015-0282(02)04235-8 DI 10.1016/S0015-0282(02)04235-8 PG 2 WC Obstetrics & Gynecology; Reproductive Biology SC Obstetrics & Gynecology; Reproductive Biology GA 611PP UT WOS:000179027200038 ER PT J AU Shin, JM Sachs, G AF Shin, JM Sachs, G TI Restoration of acid secretion following treatment with proton pump inhibitors SO GASTROENTEROLOGY LA English DT Article ID GASTRIC H+,K+-ATPASE ACTIVITY; REFLUX DISEASE; H+/K+-ATPASE; K+-ATPASE; OMEPRAZOLE; LANSOPRAZOLE; PANTOPRAZOLE; SITE; RABEPRAZOLE; H,K-ATPASE AB Background & Aims: Proton pump inhibitors (PPIs) are covalent inhibitors of the gastric H+,K+-adenosine triphosphatase (ATPase) forming disulfide bonds. Recovery of acid secretion after PPI inhibition may be due to de novo synthesis of pump protein and/or disulfide reduction and reactivation of inhibited pump. The half-time of recovery of acid secretion in rats following omeprazole treatment is similar to15 hours, whereas pump protein half-life is 54 hours. In humans, the half-life of the inhibitory effect on acid secretion is similar to28 hours for omeprazole and similar to46 hours for pantoprazole. Whereas all PPIs bind to cysteine 813, pantoprazole additionally binds to cysteine 822, deeper in the membrane domain of TM6. Their different durations of action may reflect different rates of pump reactivation due to differing accessibility of the disulfides to glutathione. Methods: Rats were stimulated and treated with 30 mg/kg of each PPI. Gastric ATPase was prepared and reversal of inhibition of the H+,K+-ATPase was measured as the time-dependent restoration of activity by incubation with dithiothreitol or glutathione. Results: One hundred percent reactivation of ATPase following inhibition in vivo by omeprazole or its enantiomers was seen with dithiothreitol and 89% with glutathione. Similar data were found for lansoprazole or rabeprazole. No reactivation by either reducing agent was seen following inhibition by pantoprazole. Conclusions: Recovery of acid secretion following inhibition by all PPIs, other than pantoprazole, may depend on both protein turnover and reversal of the inhibitory disulfide bond. In contrast, recovery of acid secretion after pantoprazole may depend entirely on new protein synthesis. C1 VA Greater Los Andeles Healthcare Syst, Los Angeles, CA USA. Univ Calif Los Angeles, Dept Physiol & Med, Los Angeles, CA USA. RP W Los Angeles Vet Affairs Med Ctr, Membrane Biol Lab, 11301 Wilshire Blvd,Bldg 113,Room 324, Los Angeles, CA 90073 USA. EM gsachs@ucla.edu FU NIDDK NIH HHS [DK46917]; PHS HHS [53462, 17294, 41301] NR 40 TC 51 Z9 55 U1 0 U2 4 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 EI 1528-0012 J9 GASTROENTEROLOGY JI Gastroenterology PD NOV PY 2002 VL 123 IS 5 BP 1588 EP 1597 DI 10.1053/gast.2002.36593 PG 10 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA 609UN UT WOS:000178923100023 PM 12404233 ER PT J AU Contreras, AM Chung, RT AF Contreras, AM Chung, RT TI Hepatitis C virus in solid organ transplantation: not always a bad thing? SO GASTROENTEROLOGY LA English DT Editorial Material ID LIVER FIBROSIS PROGRESSION; HYPERVARIABLE REGION-1; KIDNEY-TRANSPLANTATION; CHOLESTATIC HEPATITIS; LONGITUDINAL ANALYSIS; VIRAL-HEPATITIS; RECIPIENTS; INFECTION; RECURRENCE; IMPACT C1 Massachusetts Gen Hosp, Gastrointestinal Unit, Boston, MA 02114 USA. Harvard Univ, Sch Med, Boston, MA USA. RP Chung, RT (reprint author), Massachusetts Gen Hosp, Gastrointestinal Unit, Boston, MA 02114 USA. NR 36 TC 2 Z9 3 U1 0 U2 1 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD NOV PY 2002 VL 123 IS 5 BP 1729 EP 1733 DI 10.1053/gast.2002.36852 PG 5 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA 609UN UT WOS:000178923100035 PM 12404247 ER PT J AU Dobie, DJ Kivlahan, DR Maynard, C Bush, KR McFall, M Epler, AJ Bradley, KA AF Dobie, DJ Kivlahan, DR Maynard, C Bush, KR McFall, M Epler, AJ Bradley, KA TI Screening for post-traumatic stress disorder in female Veteran's Affairs patients: validation of the PTSD checklist SO GENERAL HOSPITAL PSYCHIATRY LA English DT Article DE stress disorders; post-traumatic; women; veterans; psychiatric status rating scales; quality of life ID QUALITY-OF-LIFE; PSYCHOMETRIC PROPERTIES; CIVILIAN VERSION; VIETNAM VETERANS; SCORING RULES; SEXUAL ABUSE; PRIMARY-CARE; HEALTH; WOMEN; SCALE AB We evaluated the screening validity of a self-report measure for post traumatic stress disorder (PTSD), the PTSD Checklist (PCL), in female Veterans Affairs (VA) patients. All women seen for care at the VA Puget Sound Health Care system from October 1996-January 1999 (n=2,545) were invited to participate in a research interview. Participants (n=282) completed the 17-item PCL, followed by a gold standard diagnostic interview for PTSD, the Clinician Administered PTSD Scale (CAPS). Thirty-six percent of the participants (n=100) met CAPS diagnostic criteria for current PTSD. Receiver Operating Characteristic (ROC) analysis was used to evaluate the screening performance of the PCL. The area under the ROC curve was 0.86 (95% CI 0.82-0.90). A PCL score of 38 optimized the performance of the PCL as a screening test (sensitivity 0.79, specificity 0.79). The PCL performed well as a screening measure for the detection of PTSD in female VA patients. (C) 2002 Elsevier Science Inc. All rights reserved. C1 VA Puget Sound Hlth Care Syst, Mental Illness Res Educ & Clin Ctr, Seattle, WA 98108 USA. VA Puget Sound Hlth Care Syst, Ctr Excellence Substance Abuse Treatment & Educ, Seattle, WA 98108 USA. VA Puget Sound Hlth Care Syst, Hlth Serv Res & Dev, Seattle, WA 98108 USA. VA Puget Sound Hlth Care Syst, Epidemiol Res & Informat Ctr, Seattle, WA 98108 USA. Univ Washington, Dept Psychiat, Seattle, WA 98195 USA. Univ Washington, Dept Behav Sci, Seattle, WA 98195 USA. Univ Washington, Dept Med, Seattle, WA 98195 USA. Univ Washington, Sch Publ Hlth, Seattle, WA 98195 USA. RP Dobie, DJ (reprint author), VA Puget Sound Hlth Care Syst, Mental Illness Res Educ & Clin Ctr, Seattle, WA 98108 USA. RI Maynard, Charles/N-3906-2015 OI Maynard, Charles/0000-0002-1644-7814 FU NIAAA NIH HHS [K23AA00313] NR 57 TC 111 Z9 130 U1 0 U2 1 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0163-8343 J9 GEN HOSP PSYCHIAT JI Gen. Hosp. Psych. PD NOV-DEC PY 2002 VL 24 IS 6 BP 367 EP 374 AR PII S0163-8343(02)00207-4 DI 10.1016/S0163-8343(02)00207-4 PG 8 WC Psychiatry SC Psychiatry GA 632FA UT WOS:000180212100002 PM 12490337 ER PT J AU Oh, SP Yeo, CY Lee, Y Schrewe, H Whitman, M Li, E AF Oh, SP Yeo, CY Lee, Y Schrewe, H Whitman, M Li, E TI Activin type IIA and IIB receptors mediate Gdf11 signaling in axial vertebral patterning SO GENES & DEVELOPMENT LA English DT Article DE activin receptor; nodal; Gdf11; vertebrae; left-right asymmetry ID BETA SUPERFAMILY; MOUSE; EXPRESSION; GENES; GASTRULATION; REQUIREMENT; FACTOR-11; PATHWAY; KINASE; MEMBER AB Vertebral bodies are segmented along the anteroposterior (AP) body axis, and the segmental identity of the vertebrae is determined by the unique expression pattern of multiple Hox genes. Recent studies have demonstrated that a transforming growth factor beta (TGF-beta) family protein, Gdf11 (growth and differentiation factor 11), and the activin type II receptor, ActRIIB, are involved in controlling the spatiotemporal expression of multiple Hox genes along the AP axis, and that the disruption of each of these genes causes anterior transformation of the vertebrae. Skeletal defects are more severe in Gdf11-null mice than in ActRIIB-null mice, however, leaving it uncertain whether Gdf11 signals via ActRIIB. Here we demonstrate using genetic and biochemical studies that ActRIIB and its subfamily receptor, ActRIIA, cooperatively mediate the Gdf11 signal in patterning the axial vertebrae, and that Gdf11 hinds to both ActRIIA and ActRIIB, and induces phosphorylation of Smad2. In addition, we also show that these two receptors can functionally compensate for one another to mediate signaling of another TGF-beta ligand, nodal, during left-right patterning and the development of anterior head structure. C1 Univ Florida, Coll Med, Dept Physiol & Funct Genom, Gainesville, FL 32610 USA. Harvard Univ, Sch Med, Dept Cell Biol, Boston, MA 02115 USA. Max Planck Inst Immunbiol, Dept Dev Biol, D-7800 Freiburg, Germany. Harvard Univ, Massachusetts Gen Hosp, Sch Med, Cutaneous Biol Res Ctr, Charlestown, MA 02129 USA. Harvard Univ, Massachusetts Gen Hosp, Sch Med, Cardiovasc Res Ctr, Charlestown, MA 02129 USA. RP Oh, SP (reprint author), Univ Florida, Coll Med, Dept Physiol & Funct Genom, Gainesville, FL 32610 USA. OI Yeo, Chang-Yeol/0000-0002-4440-1215 FU NHLBI NIH HHS [HL64024, R01 HL064024]; NICHD NIH HHS [HD35286, R01 HD035286, HD24926] NR 33 TC 97 Z9 106 U1 2 U2 10 PU COLD SPRING HARBOR LAB PRESS PI PLAINVIEW PA 1 BUNGTOWN RD, PLAINVIEW, NY 11724 USA SN 0890-9369 J9 GENE DEV JI Genes Dev. PD NOV 1 PY 2002 VL 16 IS 21 BP 2749 EP 2754 DI 10.1101/gad.1021802 PG 6 WC Cell Biology; Developmental Biology; Genetics & Heredity SC Cell Biology; Developmental Biology; Genetics & Heredity GA 611PX UT WOS:000179027900003 PM 12414726 ER PT J AU Lei, EP Silver, PA AF Lei, EP Silver, PA TI Intron status and 3 '-end formation control cotranscriptional export of mRNA SO GENES & DEVELOPMENT LA English DT Article DE Yra1; Npl3; mRNA export; transcription; splicing; chromatin IP ID MESSENGER-RNA EXPORT; SACCHAROMYCES-CEREVISIAE; BINDING PROTEIN; NUCLEAR EXPORT; NUCLEOCYTOPLASMIC TRANSPORT; YEAST HOMOLOG; TRANSCRIPTION; CYTOPLASM; SHUTTLES; GENE AB Messenger RNA export factors are recruited to genes in a transcription-dependent manner. To ascertain the mechanism of this process, we show that RNA polymerase II transcription is sufficient to recruit the Saccharomyces cerevisiae hnRNP protein Npl3 to a gene independent of RNA sequence. In contrast, the cotranscriptional recruitment of the RNA-binding protein Yra1 is dependent on pre-mRNA processing. Yra1 associates with introns of intron-containing genes in a splicing-dependent manner. Conversely, Yra1 recruitment to genes without introns is not dependent on splicing. Finally, T-end formation is required for Yra1 recruitment to genes regardless of intron status. C1 Harvard Univ, Sch Med, Dept Biol Chem & Mol Pharmacol, Boston, MA 02115 USA. Dana Farber Canc Inst, Boston, MA 02115 USA. RP Silver, PA (reprint author), Harvard Univ, Sch Med, Dept Biol Chem & Mol Pharmacol, Boston, MA 02115 USA. NR 39 TC 90 Z9 91 U1 1 U2 4 PU COLD SPRING HARBOR LAB PRESS PI PLAINVIEW PA 1 BUNGTOWN RD, PLAINVIEW, NY 11724 USA SN 0890-9369 J9 GENE DEV JI Genes Dev. PD NOV 1 PY 2002 VL 16 IS 21 BP 2761 EP 2766 DI 10.1101/gad.1032902 PG 6 WC Cell Biology; Developmental Biology; Genetics & Heredity SC Cell Biology; Developmental Biology; Genetics & Heredity GA 611PX UT WOS:000179027900005 PM 12414728 ER PT J AU Serebriiskii, IG Mitina, O Pugacheva, EN Benevolenskaya, E Kotova, E Toby, GG Khazak, V Kaelin, WG Chernoff, J Golemis, EA AF Serebriiskii, IG Mitina, O Pugacheva, EN Benevolenskaya, E Kotova, E Toby, GG Khazak, V Kaelin, WG Chernoff, J Golemis, EA TI Detection of peptides, proteins, and drugs that selectively interact with protein targets SO GENOME RESEARCH LA English DT Article ID 2-HYBRID SYSTEM; BINDING; YEAST; CDC42 AB Genome sequencing has been completed for multiple organisms, and pilot proteomic analyses reported for yeast and higher eukaryotes. This work has emphasized the facts that proteins are frequently engaged in multiple interactions, and that governance of protein interaction specificity is a primary means of regulating biological systems. In particular, the ability to deconvolute complex protein interaction networks to identify which interactions govern specific signaling pathways requires the generation of biological tools that allow the distinction of critical from noncritical interactions. We report the application of an enhanced Dual Bait two-hybrid system to allow detection and manipulation of highly specific protein-protein interactions. We summarize the use of this system to detect proteins and peptides that target well-defined specific motifs in larger protein structures, to facilitate rapid identification of specific interactors from a pool of putative interacting proteins obtained in a library screen, and to score specific drug-mediated disruption of protein-protein interaction. C1 Fox Chase Canc Ctr, Div Basic Sci, Philadelphia, PA 19111 USA. Russian State Med Univ, Dept Mol Biol & Med Biotechnol, Moscow 117437, Russia. Dana Farber Canc Inst, Boston, MA 02115 USA. Univ Penn, Sch Med, Cell & Mol Biol Grp, Philadelphia, PA 19104 USA. Morphochem Inc, Monmouth Jct, NJ 08852 USA. RP Golemis, EA (reprint author), Fox Chase Canc Ctr, Div Basic Sci, 7701 Burholme Ave, Philadelphia, PA 19111 USA. RI Chernoff, Jonathan/I-7631-2014 OI Chernoff, Jonathan/0000-0002-4803-7836 FU NCI NIH HHS [CA06927, CA63366, P30 CA006927, R01 CA063366]; NIGMS NIH HHS [GM54168, R01 GM054168] NR 24 TC 27 Z9 28 U1 0 U2 3 PU COLD SPRING HARBOR LAB PRESS PI PLAINVIEW PA 1 BUNGTOWN RD, PLAINVIEW, NY 11724 USA SN 1088-9051 J9 GENOME RES JI Genome Res. PD NOV PY 2002 VL 12 IS 11 BP 1785 EP 1791 DI 10.1101/gr.450702 PG 7 WC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Genetics & Heredity SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Genetics & Heredity GA 612DB UT WOS:000179058300018 PM 12421766 ER PT J AU van den Brink, GR Hardwick, JCH Nielsen, C Xu, C ten Kate, FJ Glickman, J van Deventer, SJH Roberts, DJ Peppelenbosch, MP AF van den Brink, GR Hardwick, JCH Nielsen, C Xu, C ten Kate, FJ Glickman, J van Deventer, SJH Roberts, DJ Peppelenbosch, MP TI Sonic hedgehog expression correlates with fundic gland differentiation in the adult gastrointestinal tract SO GUT LA English DT Article ID LEFT-RIGHT ASYMMETRY; GROWTH-FACTOR-ALPHA; MENETRIERS-DISEASE; TRANSGENIC MICE; INTESTINAL METAPLASIA; HUMAN STOMACH; MOUSE; EPITHELIUM; MORPHOGENESIS; PATHOGENESIS AB Background: Sonic hedgehog (Shh) is an important endodermal morphogenetic signal during the development of the vertebrate gut. It controls gastrointestinal patterning in general, and gastric gland formation in particular. We have previously shown that Shh regulates gastric gland proliferation in the adult but detailed analysis of its expression along the adult gastrointestinal tract has never been undertaken. We therefore studied Shh expression along the normal human and rodent adult gastrointestinal tract as well as in intestinal metaplasia of the stomach, gastric and intestinal metaplasia of the oesophagus, and gastric heterotopia in Meckel's diverticulum. Methods: The studies were performed with in situ hybridisation and by immunohistochemistry using an antibody that recognises the Shh precursor form. Results: We found that in the normal gastrointestinal tract, high levels of Shh were expressed in the fundic glands of the stomach. Shh expression was also found in fundic gland metaplasia and heterotopia. However, Shh expression was lost in intestinal metaplasia of the stomach. Conclusion: We found a strong correlation between Shh expression and fundic gland differentiation. Our current study therefore provides evidence that in addition to its role in gastric epithelial development, Shh plays a unique role in gastric epithelial differentiation in adults. C1 Acad Med Ctr, Lab Exp Internal Med, Dept Expt Internal Med, NL-1105 AZ Amsterdam, Netherlands. Brigham & Womens Hosp, Dept Pediat Surg, Massachusetts Gen Hosp, Boston, MA 02115 USA. Acad Med Ctr, Dept Pathol, Amsterdam, Netherlands. Acad Med Ctr, Dept Gastroenterol, Amsterdam, Netherlands. RP van den Brink, GR (reprint author), Acad Med Ctr, Lab Exp Internal Med, Dept Expt Internal Med, Room G2-130,Meibergdreef 9, NL-1105 AZ Amsterdam, Netherlands. NR 35 TC 113 Z9 114 U1 0 U2 0 PU BRITISH MED JOURNAL PUBL GROUP PI LONDON PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND SN 0017-5749 J9 GUT JI Gut PD NOV PY 2002 VL 51 IS 5 BP 628 EP 633 DI 10.1136/gut.51.5.628 PG 6 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA 607TA UT WOS:000178805800007 PM 12377798 ER PT J AU Kubicki, M Westin, CF Maier, SE Mamata, H Frumin, M Ersner-Hershfield, H Kikinis, R Jolesz, FA McCarley, R Shenton, ME AF Kubicki, M Westin, CF Maier, SE Mamata, H Frumin, M Ersner-Hershfield, H Kikinis, R Jolesz, FA McCarley, R Shenton, ME TI Diffusion tensor imaging and its application to neuropsychiatric disorders SO HARVARD REVIEW OF PSYCHIATRY LA English DT Review ID APPEARING WHITE-MATTER; ACUTE HUMAN STROKE; MAGNETIC-RESONANCE; MULTIPLE-SCLEROSIS; WATER-DIFFUSION; IN-VIVO; ALZHEIMERS-DISEASE; HUMAN BRAIN; CORPUS-CALLOSUM; CEREBRAL-ISCHEMIA AB Magnetic resonance diffusion tensor imaging (DTI) is a new technique that can be used to visualize and measure the diffusion of water in brain tissue; it is particularly useful for evaluating white matter abnormalities. In this paper, we review research studies that have applied DTI for the purpose of understanding neuropsychiatric disorders. We begin with a discussion of the principles involved in DTI, followed by a historical overview of magnetic resonance diffusion-weighted imaging and DTI and a brief description of several different methods of image acquisition and quantitative analysis. We then review the application of this technique to clinical populations. We include all studies published in English from January 1996 through March 2002 on this topic, located by searching PubMed and Medline on the key words "diffusion tensor imaging" and "MRI." Finally, we consider potential future uses of DTI, including fiber tracking and surgical planning and follow-up. C1 VA Boston Healthcare Syst, Brockton Div, Dept Psychiat, Lab Neurosci,Clin Neurosci Div, Brockton, MA 02301 USA. Brigham & Womens Hosp, Dept Radiol, Boston, MA 02115 USA. Harvard Univ, Sch Med, Dept Psychiat, Boston, MA 02115 USA. Harvard Univ, Sch Med, Dept Radiol, Boston, MA 02115 USA. RP Shenton, ME (reprint author), VA Boston Healthcare Syst, Brockton Div, Dept Psychiat, Lab Neurosci,Clin Neurosci Div, 116A,940 Belmont St, Brockton, MA 02301 USA. RI Hershfield, Hal/J-2919-2016 OI Hershfield, Hal/0000-0002-1507-7022 FU NCRR NIH HHS [P41 RR 13218, P41 RR013218, P41 RR013218-02, R01 RR 11747, R01 RR011747, R01 RR011747-02]; NIMH NIH HHS [K02 MH001110-06, K02 MH 01110, K02 MH001110, R01 MH 40799, R01 MH 50747, R01 MH040799, R01 MH040799-13, R01 MH050740, R01 MH050740-06]; NINDS NIH HHS [R01 NS 39335, R01 NS039335, R01 NS039335-01A1] NR 92 TC 85 Z9 91 U1 1 U2 4 PU MOSBY, INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 USA SN 1067-3229 J9 HARVARD REV PSYCHIAT JI Harv. Rev. Psychiatr. PD NOV-DEC PY 2002 VL 10 IS 6 BP 324 EP 336 DI 10.1093/hrp/10.6.324 PG 13 WC Psychiatry SC Psychiatry GA 632DL UT WOS:000180208400002 PM 12485979 ER PT J AU Dienstag, JL AF Dienstag, JL TI The role of liver biopsy in chronic hepatitis C SO HEPATOLOGY LA English DT Article ID INTERFERON-ALPHA-2B PLUS RIBAVIRIN; VIRUS-INFECTION; NATURAL-HISTORY; ALANINE AMINOTRANSFERASE; AST/ALT RATIO; BIOCHEMICAL MARKERS; RANDOMIZED TRIAL; USEFUL PREDICTOR; SERUM ASPARTATE; ACTIVITY INDEX AB The report of the 1997 National Institutes of Health Consensus Development Conference on hepatitis C endorsed pretreatment liver biopsy. We revisit the following questions: Does liver histology help determine the urgency of, and predict the likelihood of response to, antiviral therapy, and can surrogate markers supplant histological assessment? Because the rate of progression of chronic hepatitis C is influenced by baseline histological grade/stage, patients can be stratified into those with moderate to severe hepatitis, who merit imminent therapy, and those with mild hepatitis, in whom therapy can be postponed until more effective/tolerable treatments become available. Less advanced baseline histology has been shown to be an independent predictor of responsiveness to antiviral therapy. Although the predictive value of biopsy is insufficient to withhold therapy from patients with advanced fibrosis, baseline biopsy helps gauge expectations for the outcome of therapy. Reports have been published recently suggesting that laboratory markers can predict distinctions between low-grade fibrosis and therapy-indicating septal fibrosis/cirrhosis. These indices, however, are insufficiently reliable to predict histological distinctions in populations with varying prevalences of fibrosis/cirrhosis or to provide anything more than broad qualitative distinctions, far short of the potential information in a liver biopsy. For most patients, the value of pretreatment liver biopsy outweighs its risks, provides information about the urgency of treatment, and should be retained. Studies to identify noninvasive laboratory markers of histological activity and stage, especially genetic predictors of accelerated disease progression, command a high priority. C1 Massachusetts Gen Hosp, Gastrointestinal Unit, Med Serv, Boston, MA 02114 USA. Harvard Univ, Sch Med, Dept Med, Boston, MA 02115 USA. RP Dienstag, JL (reprint author), Massachusetts Gen Hosp, Gastrointestinal Unit, Med Serv, Jackson 7,55 Fruit St, Boston, MA 02114 USA. FU NCRR NIH HHS [M01RR01066]; NIDDK NIH HHS [N01-DK-9-2319] NR 59 TC 151 Z9 162 U1 1 U2 4 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 USA SN 0270-9139 J9 HEPATOLOGY JI Hepatology PD NOV PY 2002 VL 36 IS 5 SU 1 BP S152 EP S160 DI 10.1053/jhep.2002.36381 PG 9 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA 611VT UT WOS:000179039000019 PM 12407589 ER PT J AU El-Serag, HB AF El-Serag, HB TI Hepatocellular carcinoma and hepatitis C in the United States SO HEPATOLOGY LA English DT Article ID VIRUS-RELATED CIRRHOSIS; PRIMARY LIVER-CANCER; RISK-FACTORS; INTERFERON THERAPY; DIABETES-MELLITUS; SPANISH PATIENTS; NATURAL-HISTORY; HCV INFECTION; PREVALENCE; PROGRESSION AB Chronic infection with hepatitis C virus (HCV) is a major risk factor for development of hepatocellular carcinoma (HCC). In general, HCC develops only after 2 or more decades of HCV infection and the increased risk is restricted largely to patients with cirrhosis or advanced fibrosis. Factors that predispose to HCC among HCV-infected persons include mate sex, older age, hepatitis B virus (HBV) coinfection, heavy alcohol intake, and possibly diabetes and a transfusion-related source of HCV infection. Viral factors play a minor role. The likelihood of development of HCC among HCV-infected persons is difficult to determine because of the paucity of adequate long-term cohort studies; the best estimate is 1% to 3% after 30 years. Once cirrhosis is established, however, HCC develops at an annual rate of 1% to 4%. Successful antiviral therapy of patients with HCV-related cirrhosis may reduce the future risk for HCC. The incidence of and mortality caused by all HCC has doubled in the United States over the past 25 years, an increase that has affected all ethnic groups, both sexes, and younger age groups. Given the current prevalence of HCV infection among persons 30 to 50 years of age, the incidence and mortality rates of HCC are likely to double in the United States over the next 10 to 20 years. Future research should focus on improving understanding of the incidence and risk factors for HCC, causes of HCV-related carcinogenesis, means of early detection, and better treatment for HCC. C1 Houston Dept Vet Affairs Med Ctr, Gastroenterol Sect, Houston, TX USA. Houston Dept Vet Affairs Med Ctr, Sect Hlth Serv Res, Houston, TX USA. Baylor Coll Med, Houston, TX 77030 USA. RP El-Serag, HB (reprint author), Houston Vet Adm Med Ctr, 152,2002 Holcombe Blvd, Houston, TX 77030 USA. NR 88 TC 281 Z9 284 U1 1 U2 6 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 USA SN 0270-9139 J9 HEPATOLOGY JI Hepatology PD NOV PY 2002 VL 36 IS 5 SU 1 BP S74 EP S83 DI 10.1053/jhep.2002.36807 PG 10 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA 611VT UT WOS:000179039000009 PM 12407579 ER PT J AU Zhang, Y Yu, J Unni, E Shao, TC Nan, BC Snabboon, T Kasper, S Andriani, F Denner, L Marcelli, M AF Zhang, Y Yu, J Unni, E Shao, TC Nan, BC Snabboon, T Kasper, S Andriani, F Denner, L Marcelli, M TI Monogene and polygene therapy for the treatment of experimental prostate cancers by use of apoptotic genes bax and bad driven by the prostate-specific promoter ARR(2)PB SO HUMAN GENE THERAPY LA English DT Article ID STAUROSPORINE-INDUCED APOPTOSIS; CHRONIC MYELOID-LEUKEMIA; HUMAN ADENOVIRUS TYPE-5; BCL-2 FAMILY-MEMBERS; CELL-LINE LNCAP; SURVIVAL; OVEREXPRESSION; PHOSPHORYLATION; CASPASE-7; PROTEIN AB We have shown that adenovirus-mediated manipulation of apoptotic genes such as bax could be a therapeutic option for prostate cancer. Unfortunately, the response of experimental prostate tumors to a single therapeutic gene of the apoptotic pathway is short-lived, and most of these tumors relapse after a short period of time. In this investigation we present data generated with adenovirus AvARR(2)PB-Bad, in which the apoptotic gene bad was placed under the control of the dihydrotestosterone (DHT)-inducible third-generation probasin-derived promoter ARR(2)PB. This therapeutic virus was given alone or in combination with other therapeutic viruses to a variety of in vitro and in vivo experimental models of prostate cancer. On infection with AvARR(2)PB-Bad, DHT-induced Bad overexpression occurred specifically in androgen receptor-positive (AR(+)) cells of prostatic derivation. The apoptotic effect of AvARR(2)PB-Bad ( group 1) was compared with that of AvARR(2)PB-Bax ( which overexpresses the apoptotic protein Bax) ( group 2), with that of the combination AvARR(2)PB-Bad plus AvARR(2)PB-Bax ( group 3), and with that of the control virus AvARR(2)PB-CAT ( group 4) in the cell line LNCaP. In addition to identifying the modality of apoptosis induction by overexpressed Bad, the results suggested that group 3 contained more apoptotic cells than any other group. In additional studies, AR1 androgen-dependent LNCaP cells or AR1 and androgen-independent C4-2 cells were injected subcutaneously into nude mice. Four groups of six LNCaP or C4-2 tumors were treated with the same combinations of viruses discussed above for groups 1, 2, 3, and 4. Treatment resulted in decreased tumor size in groups 1, 2, and 3 compared with group 4. There was a better response in group 3 compared with group 2, and in group 2 compared with group 1. A better response in group 3 was confirmed during a 8-week follow-up period, in which no treatment was administered. Two LNCaP and C4-2 tumors of group 3 disappeared at the end of treatment and did not recur after an 8-week follow-up period. The data suggest that polygene therapy with apoptotic molecules is more effective in experimental models of androgen-dependent or - independent prostate cancer than monogene therapy. C1 Baylor Coll Med, VA Med Ctr, Dept Med Mol & Cellular Biol, Houston, TX 77030 USA. Baylor Coll Med, Dept Med, Houston, TX 77030 USA. Vanderbilt Univ, Med Ctr, Dept Urol Surg, Nashville, TN 37232 USA. Texas Biotechnol Corp, Apoptosis Program, Houston, TX 77030 USA. RP Marcelli, M (reprint author), Baylor Coll Med, VA Med Ctr, Dept Med Mol & Cellular Biol, 2002 Holcombe Blvd,Bldg 109,Room 217, Houston, TX 77030 USA. EM marcelli@bcm.tmc.edu RI Andriani, Francesca/D-4898-2017 OI Andriani, Francesca/0000-0002-6178-7789 NR 35 TC 17 Z9 18 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 USA SN 1043-0342 J9 HUM GENE THER JI Hum. Gene Ther. PD NOV PY 2002 VL 13 IS 17 BP 2051 EP 2064 DI 10.1089/10430340260395901 PG 14 WC Biotechnology & Applied Microbiology; Genetics & Heredity; Medicine, Research & Experimental SC Biotechnology & Applied Microbiology; Genetics & Heredity; Research & Experimental Medicine GA 766CM UT WOS:000188327900005 PM 12490000 ER PT J AU Lloyd-Jones, DM Evans, JC Larson, MG Levy, D AF Lloyd-Jones, DM Evans, JC Larson, MG Levy, D TI Treatment and control of hypertension in the community - A prospective analysis SO HYPERTENSION LA English DT Article DE blood pressure; hypertension, detection and control antihypertensive therapy; epidemiology; population ID ISOLATED SYSTOLIC HYPERTENSION; NUTRITION EXAMINATION SURVEY; DIASTOLIC BLOOD-PRESSURE; CORONARY HEART-DISEASE; NATIONAL-HEALTH; MORTALITY; MORBIDITY; LEVEL; AGE AB Cross-sectional national data indicate poor levels of treatment and control of hypertension. We identified factors that prospectively predict initiation of antihypertensive therapy and attainment of blood pressure control in the community. We included all Framingham Heart Study subjects examined between 1987 and 1999 whoa had untreated or uncontrolled hypertension (systolic greater than or equal to140 or diastolic greater than or equal to90 mm Hg) at a baseline examination and presented for follow-up examination 4 years later. Clinical covariates were examined for their association with initiation or control at follow-up. Among 1103 hypertensive participants who were untreated at baseline, 350 (31.7%) subjects were receiving therapy at follow-up, including 25.7% of subjects with stage 1 and 51.2% of those with stage greater than or equal to2 hypertension at baseline. Multivariate predictors of initiation of therapy included higher systolic and diastolic pressure, prevalent and interim cardiovascular disease, and left ventricular hypertrophy. Other cardiovascular risk factors did not predict initiation of treatment. Among 2475 hypertensive participants who were uncontrolled (treated or untreated) at baseline, 988 (39.9%) were controlled at follow-up. Prevalent cardiovascular disease and interim initiation of therapy predicted control; older age and higher baseline systolic levels predicted lack of control. These data provide estimates of longitudinal rates of treatment and control of hypertension in the community. It appears that global risk was not taken into consideration when making decisions for initiation of therapy. Greater emphasis is needed on achieving blood pressure control in all patients but particularly among older subjects and those with systolic hypertension. C1 NHLBI, Framingham Heart Study, Framingham, MA 01702 USA. Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Med,Cardiol Div, Boston, MA USA. Boston Univ, Sch Med, Div Epidemiol & Prevent Med, Boston, MA 02118 USA. NHLBI, Bethesda, MD 20892 USA. RP Lloyd-Jones, DM (reprint author), NHLBI, Framingham Heart Study, 73 Mt Wayte Ave, Framingham, MA 01702 USA. RI Lloyd-Jones, Donald/C-5899-2009; OI Larson, Martin/0000-0002-9631-1254 FU NHLBI NIH HHS [K23 HL04253, N01-HC-25195] NR 24 TC 63 Z9 70 U1 0 U2 2 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0194-911X J9 HYPERTENSION JI Hypertension PD NOV PY 2002 VL 40 IS 5 BP 640 EP 646 DI 10.1161/01.HYP.0000035855.44620.DA PG 7 WC Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 612QU UT WOS:000179087600009 PM 12411456 ER PT J AU Corey, V Peterman, C Shearin, S Greenberg, MS Van Bokkelen, J AF Corey, V Peterman, C Shearin, S Greenberg, MS Van Bokkelen, J TI Network forensics analysis SO IEEE INTERNET COMPUTING LA English DT Article C1 Massachusetts Gen Hosp, Boston, MA 02114 USA. NR 9 TC 33 Z9 34 U1 0 U2 2 PU IEEE COMPUTER SOC PI LOS ALAMITOS PA 10662 LOS VAQUEROS CIRCLE, PO BOX 3014, LOS ALAMITOS, CA 90720-1314 USA SN 1089-7801 J9 IEEE INTERNET COMPUT JI IEEE Internet Comput. PD NOV-DEC PY 2002 VL 6 IS 6 BP 60 EP 66 DI 10.1109/MIC.2002.1067738 PG 7 WC Computer Science, Software Engineering SC Computer Science GA 615ZR UT WOS:000179277700012 ER PT J AU Desai, M Mangoubi, R Shah, J Karl, W Pien, H Worth, A Kennedy, D AF Desai, M Mangoubi, R Shah, J Karl, W Pien, H Worth, A Kennedy, D TI Functional MRI activity characterization using response time shift estimates from curve evolution SO IEEE TRANSACTIONS ON MEDICAL IMAGING LA English DT Article DE curve evolution; delay; functional magnetic resonance imaging (fMRI); hypothesis test; matched filter; non-Gaussian detection; response time shift; robust detection ID HUMAN BRAIN; RETROSPECTIVE ESTIMATION; SENSORY STIMULATION; FMRI DATA; SEGMENTATION; ACTIVATION; IMAGES AB Characterizing the response of the brain to a stimulus based on functional magnetic resonance imaging data is a major challenge due to the fact that the response time delay of the brain may be different from one stimulus phase to the next and from pixel to pixel. To enhance delectability, this work introduces the use of a curve evolution approach that provides separate estimates of the response time shifts at each phase of the stimulus on a pixel-by-pixel basis. The approach relies on a parsimonious but simple model that is nonlinear in the time shifts of the response relative to the stimulus and linear in the gains. To effectively use the response time shift estimates in a subspace detection framework, we implement a robust hypothesis test based on a Laplacian noise model. The algorithm provides a pixel-by-pixel functional characterization of the brain's response. The results based on experimental data show that response time shift estimates, when properly implemented, enhance delectability without sacrificing robustness. C1 Charles Stark Draper Lab Inc, Cambridge, MA 02139 USA. Boston Univ, Dept Elect & Comp Engn, Boston, MA 02115 USA. Massachusetts Gen Hosp, Boston, MA 02214 USA. RP Charles Stark Draper Lab Inc, M53F,555 Technol Sq, Cambridge, MA 02139 USA. EM mdesai@draper.com RI Kennedy, David/H-3627-2012 FU NINDS NIH HHS [2 R01 NS34189-04] NR 43 TC 12 Z9 12 U1 0 U2 0 PU IEEE-INST ELECTRICAL ELECTRONICS ENGINEERS INC PI PISCATAWAY PA 445 HOES LANE, PISCATAWAY, NJ 08855-4141 USA SN 0278-0062 EI 1558-254X J9 IEEE T MED IMAGING JI IEEE Trans. Med. Imaging PD NOV PY 2002 VL 21 IS 11 BP 1402 EP 1412 DI 10.1109/TMI.2002.806419 PG 11 WC Computer Science, Interdisciplinary Applications; Engineering, Biomedical; Engineering, Electrical & Electronic; Imaging Science & Photographic Technology; Radiology, Nuclear Medicine & Medical Imaging SC Computer Science; Engineering; Imaging Science & Photographic Technology; Radiology, Nuclear Medicine & Medical Imaging GA 642FW UT WOS:000180794400008 PM 12575877 ER PT J AU Sama, SR Christiani, DC Milton, DK AF Sama, SR Christiani, DC Milton, DK TI Diagnosis and management of occupational asthma SO IMMUNOLOGY AND ALLERGY CLINICS OF NORTH AMERICA LA English DT Article ID AIRWAYS DYSFUNCTION SYNDROME; EXPIRATORY FLOW MEASUREMENTS; PERSISTENT ASTHMA; LUNG-DISEASE; PEAK FLOW; DISABILITY; ADULTS; SYSTEM; WORKPLACE; EXPOSURE AB Occupational asthma (OA) remains the most prevalent occupational lung disease in developed countries. Nonsensitizing toxins can induce irritant asthma and reactive airways dysfunction syndrome and are in widespread use in many occupational settings. The pathophysiology and natural history of the disease are better understood. Although knowledge of OA has increased dramatically over the past several years and continues to improve, much remains to be learned. Efforts must be focused on the ability to quickly recognize OA and the ever-increasing list of causal agents because this informs individual prognosis and requirements for general prevention. C1 Harvard Univ, Sch Publ Hlth, Harvard Occupat Hlth Program, Boston, MA 02115 USA. Harvard Univ, Massachusetts Gen Hosp, Sch Med,Dept Med, Pulm & Crit Care Unit, Boston, MA 02114 USA. RP Christiani, DC (reprint author), Harvard Univ, Sch Publ Hlth, Harvard Occupat Hlth Program, Bldg 1,Room 1402,665 Huntington Ave, Boston, MA 02115 USA. RI Milton, Donald/G-3286-2010 OI Milton, Donald/0000-0002-0550-7834 NR 45 TC 2 Z9 2 U1 0 U2 1 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 USA SN 0889-8561 J9 IMMUNOL ALLERGY CLIN JI Immunol. Allerg. Clin. North Am. PD NOV PY 2002 VL 22 IS 4 BP 791 EP + AR PII S0889-8561(02)00025-5 DI 10.1016/S0889-8561(02)00025-5 PG 17 WC Allergy; Immunology SC Allergy; Immunology GA 607JL UT WOS:000178788400006 ER PT J AU Gruber, A Chalmers, AS Popov, S Ruprecht, RM AF Gruber, A Chalmers, AS Popov, S Ruprecht, RM TI Functional aspects of binding of monoclonal antibody DCN46 to DC-SIGN on dendritic cells SO IMMUNOLOGY LETTERS LA English DT Article DE dendritic cell; DC-SIGN; positive selection by flow cytometry ID HIV; EXPRESSION; MONOCYTES; RECEPTOR AB Dendritic cell (DC)-specific ICAM-3 grabbing nonintegrin (DC-SIGN) is a DC-specific antigen that plays an important role in the induction of primary immune responses as well as during HIV infection. In the present study, we analyzed the effect of binding of monoclonal antibody DCN46 to DC surface, expressed DC-SIGN on DC function. DC-SIGN antibody treated, immature DC were able to differentiate into mature DC and had the same capacity as untreated DC to induce primary and secondary immune responses. In combination with flow cytometric cell sorting, DC-SIGN antibody treatment of DC yielded highly pure and functional DC. Given the apparent lack of functional effect of monoclonal antibody DCN46 on DC, the latter antibody may prove useful for research on and clinical use of highly pure and functional DC. (C) 2002 Elsevier Science B.V. All rights reserved. C1 Dana Farber Canc Inst, Dept Canc Immunol & AIDS, Boston, MA 02115 USA. Harvard Univ, Sch Med, Dept Med, Boston, MA USA. RP Gruber, A (reprint author), Dana Farber Canc Inst, Dept Canc Immunol & AIDS, 44 Binney St,JFB-809, Boston, MA 02115 USA. FU NIAID NIH HHS [R01 AI 43839] NR 17 TC 3 Z9 4 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0165-2478 J9 IMMUNOL LETT JI Immunol. Lett. PD NOV 1 PY 2002 VL 84 IS 2 BP 103 EP 108 AR PII S0165-2478(02)00144-X DI 10.1016/S0165-2478(02)00144-X PG 6 WC Immunology SC Immunology GA 618MB UT WOS:000179420900004 PM 12270546 ER PT J AU Worthington, JJ Simon, NM Korbly, NB Perlis, RH Pollack, MH AF Worthington, JJ Simon, NM Korbly, NB Perlis, RH Pollack, MH CA Anxiety Disorders Res Program TI Ropinirole for antidepressant-induced sexual dysfunction SO INTERNATIONAL CLINICAL PSYCHOPHARMACOLOGY LA English DT Article DE ropinirole; sexual dysfunction; antidepressants; SSRIs; dopamine; side effects; depression; anxiety ID SEROTONIN REUPTAKE INHIBITORS; FLUOXETINE-INDUCED ANORGASMIA; GINKGO-BILOBA; BUPROPION; CYPROHEPTADINE; OUTPATIENTS; GRANISETRON; AMANTADINE; SECONDARY; TRIAL AB Sexual dysfunction is a relatively common side-effect of antidepressants, occurring in approximately one-half of patients, and is associated with significant distress and treatment non-compliance. Dopaminergic agents have been reported to be helpful for the treatment of antidepressant-induced sexual dysfunction and, in this report, we examined the efficacy of the dopamine agonist ropinirole for this indication. Thirteen patients (three women, 10 men), aged 42.6 +/- 7.7 years, who reported sexual dysfunction on a stable dose of antidepressant, were treated openly with ropinirole initiated at 0.25 mg/day and titrated up to 2-4 mg/day over 4 weeks, as tolerated. Ten of the 13 took ropinirole for at least 4 weeks, one discontinued due to an adverse event and two because of lack of response. Sexual dysfunction, as assessed by the Arizona Sexual Experience Scale scores, was reduced from 18.8 +/- 3.6 to 13.8 +/- 4.3 after 4 weeks on ropinirole at a mean dose of 2.1 mg/day. Overall, seven of 13 patients (54%) were rated as responders on the Clinical Global Impression of Improvement Scale. The addition of ropinirole may represent a potentially useful treatment strategy for antidepressant-induced sexual dysfunction. Int Clin Psychopharmacol 17:307-310 (C) 2002 Lippincott Williams Wilkins. C1 Massachusetts Gen Hosp, WAC815, Boston, MA 02114 USA. Harvard Univ, Sch Med, Boston, MA 02215 USA. RP Worthington, JJ (reprint author), Massachusetts Gen Hosp, WAC815, 15 Parkman St, Boston, MA 02114 USA. NR 37 TC 20 Z9 21 U1 2 U2 4 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0268-1315 J9 INT CLIN PSYCHOPHARM JI Int. Clin. Psychopharmacol. PD NOV PY 2002 VL 17 IS 6 BP 307 EP 310 DI 10.1097/00004850-200211000-00006 PG 4 WC Pharmacology & Pharmacy; Psychiatry SC Pharmacology & Pharmacy; Psychiatry GA 613BZ UT WOS:000179112400006 PM 12409684 ER PT J AU Xu, GL Meyer, JS Thornby, J Chowdhury, M Quach, M AF Xu, GL Meyer, JS Thornby, J Chowdhury, M Quach, M TI Screening for mild cognitive impairment (MCI) utilizing combined mini-mental-cognitive capacity examinations for identifying dementia prodromes SO INTERNATIONAL JOURNAL OF GERIATRIC PSYCHIATRY LA English DT Article DE MCI screening for dementia prodromes by combined MMSE-CCSE ID AMERICAN-NEUROPSYCHIATRIC-ASSOCIATION; STATE-EXAMINATION; ALZHEIMERS-DISEASE; INTERNATIONAL WORKSHOP; VASCULAR DEMENTIA; DIAGNOSIS; INSTRUMENTS; POPULATION; MMSE; INDIVIDUALS AB Objective To test correctness of results when combining Mini-Mental State Examination (MMSE) and Cognitive Capacity Screening Examination (CCSE) for identifying mild cognitive impairment (MCI) among non-demented elderly subjects at risk for developing dementia. Methods A retrospective study was conducted among consecutively referred volunteers with memory complaints to a research out-patient clinic. Two cognitive screening tests (MMSE and CCSE) were performed according to established protocol. Resulting combined screening test (termed by acronym as CMC) combined the non-overlapping test items derived from both MMSE and CCSE. Conversion to dementia at follow-up served as the 'gold-standard' for evaluating correctness of CMC for identifying MCI. Results Of 351 subjects completing cognitive assessments and meeting requirements for study protocol, 84 (23.9%) developed dementia of different types within 3-6 years (3.89 +/- 2.17) of follow-up. Among these, 47 met criteria for probable Alzheimer disease (AD), 22 for probable vascular dementia (VaD), 12 for mixed AD/VaD and three for probable frontotemporal dementia. When final diagnosis of AD was used as the 'gold standard' for testing correctness of MCI identified by cognitive screening tests, sensitivities of MMSE, CCSE and CMC for identifying MCI were relatively 61.0%, 74.3% and 83.1% with minimum specificity set at 80%. When diagnosis of all types of dementia was used as the standard for testing predictive correctness of MCI, CCSE emerged as an optimal MCI screening test. Conclusion Combining the CCSE and MMSE screening tests resulted in higher sensitivity than was achieved by MMSE alone and maintained specificity at comparable levels for identifying MCI. The results confirmed that CMC has optimal correctness and utility as a brief cognitive test for screening MCI as a prodrome for dementia among non-demented elderly populations. Published in 2002 by John Wiley Sons, Ltd. C1 VA Med Ctr, Cerebrovasc Res Lab, Houston, TX 77030 USA. VA Med Ctr, Biostat Labs, Houston, TX 77030 USA. Baylor Coll Med, Dept Neurol, Houston, TX 77030 USA. Baylor Coll Med, Dept Family & Community Med, Houston, TX 77030 USA. RP Meyer, JS (reprint author), VA Med Ctr, Cerebrovasc Res Lab, Bldg 110 Room 225,2002 Holcombe Blvd, Houston, TX 77030 USA. OI Xu, Gelin/0000-0002-6194-0341 NR 52 TC 56 Z9 61 U1 0 U2 4 PU JOHN WILEY & SONS LTD PI W SUSSEX PA BAFFINS LANE CHICHESTER, W SUSSEX PO19 1UD, ENGLAND SN 0885-6230 J9 INT J GERIATR PSYCH JI Int. J. Geriatr. Psychiatr. PD NOV PY 2002 VL 17 IS 11 BP 1027 EP 1033 DI 10.1002/gps.744 PG 7 WC Geriatrics & Gerontology; Gerontology; Psychiatry SC Geriatrics & Gerontology; Psychiatry GA 614YD UT WOS:000179218300006 PM 12404652 ER PT J AU Farag, SS Archer, KJ Mrozek, K Vardiman, JW Carroll, AJ Pettenati, MJ Moore, JO Kolitz, JE Mayer, RJ Stone, RM Larson, RA Bloomfield, CD AF Farag, SS Archer, KJ Mrozek, K Vardiman, JW Carroll, AJ Pettenati, MJ Moore, JO Kolitz, JE Mayer, RJ Stone, RM Larson, RA Bloomfield, CD TI Isolated trisomy of chromosomes 8, 11, 13 and 21 is an adverse prognostic factor in adults with de novo acute myeloid leukemia: Results from Cancer and Leukemia Group B 8461 SO INTERNATIONAL JOURNAL OF ONCOLOGY LA English DT Article DE chromosome aberrations; human; karyotyping; prognosis ID ACUTE PROMYELOCYTIC LEUKEMIA; INTENSIVE POSTREMISSION CHEMOTHERAPY; ACQUIRED KARYOTYPIC ABNORMALITY; ACUTE NONLYMPHOCYTIC LEUKEMIA; ACUTE MYELOGENOUS LEUKEMIA; COLONY-STIMULATING FACTOR; HIGH-DOSE CYTARABINE; TRANS-RETINOIC ACID; FIRST REMISSION; CYTOGENETICS AB Isolated trisomy is a relatively common cytogenetic abnormality in acute myeloid leukemia (AML), but with uncertain prognostic significance. We studied a large cohort of newly diagnosed de novo AML patients karyotyped on CALGB 8461 from 1984-1999, where trisomy was the sole abnormality. The common isolated trisomies (ITC), +8, +11, +13 and +21, comprised 90% of all sole trisomies. The outcome of 101 ITC patients was compared to that of 976 with normal and 'poor risk' cytogenetics. The overall survival (OS) for ITC patients was unsatisfactory with 10% [95% confidence interval (CI), 3-17%] alive at 5 years. Repeated cycles of I/HDAC intensification did not improve outcome. However, SCT significantly improved relapse-free survival (RFS). Among ITC patients <60 years in first remission, only I of 7 receiving SCT relapsed, compared to 16 of 19 patients treated with chemotherapy only. The prognosis of ITC was dependent on SCT. For non-transplanted patients, the 5-year OS for ITC was 5% (95% CI, 0-11%), compared to 20% (95% CI, 16-23%) for 640 normal cytogenetics patients. ITC was an independent adverse prognostic factor for OS in non-transplanted patients. In those receiving SCT, however, the 5-year OS for CTC patients (69%, 95% CI, 32-100%) was not different to that of transplanted normal cytogenetics patients (60%, 95% CI, 38-81%). We conclude that in de novo adult AML patients not receiving SCT, ITC appears to independently predict a poor outcome that may be improved with SCT in first remission. Prospective studies are required to confirm this hypothesis. C1 Ohio State Univ, Div Hematol & Oncol, Dept Internal Med, Columbus, OH 43210 USA. CALGB Stat Ctr, Durham, NC USA. Univ Chicago, Chicago, IL 60637 USA. Univ Alabama, Birmingham, AL USA. Wake Forest Univ, Winston Salem, NC 27109 USA. Duke Univ, Durham, NC USA. N Shore Univ, Manhasset, NY USA. Dana Farber Canc Inst, Boston, MA 02115 USA. RP Farag, SS (reprint author), Ohio State Univ, Div Hematol & Oncol, Dept Internal Med, A433A Starling Loving Hall,320 W 10th Ave, Columbus, OH 43210 USA. RI Mrozek, Krzysztof/A-3142-2008; OI Larson, Richard/0000-0001-9168-3203 FU NCI NIH HHS [CA 12046, CA 02599, CA 03927, CA 04326, CA 04457, CA 07968, CA 08025, CA 11028, CA 11789, CA 16058, CA 31946, CA 31983, CA 32291, CA 33601, CA 35279, CA 35406, CA 35421, CA 37135, CA 41287, CA 45418, CA 45808, CA 47545, CA 47555, CA 47577, CA 47599, CA 47642, CA 52784, CA 71323, CA 74811, CA 77298, CA 77406, CA 77440, CA 77658] NR 36 TC 33 Z9 37 U1 0 U2 1 PU PROFESSOR D A SPANDIDOS PI ATHENS PA 1, S MERKOURI ST, EDITORIAL OFFICE,, ATHENS 116 35, GREECE SN 1019-6439 J9 INT J ONCOL JI Int. J. Oncol. PD NOV PY 2002 VL 21 IS 5 BP 1041 EP 1051 PG 11 WC Oncology SC Oncology GA 603RX UT WOS:000178574600017 PM 12370753 ER PT J AU Zietman, AL AF Zietman, AL TI Dose escalation in localized prostate cancer: Make no assumptions SO INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS LA English DT Editorial Material ID CONFORMAL PROTONS; RADIOTHERAPY; IRRADIATION; PHOTONS C1 Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Radiat Oncol, Boston, MA 02114 USA. RP Zietman, AL (reprint author), Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Radiat Oncol, 100 Blossom St, Boston, MA 02114 USA. NR 6 TC 9 Z9 9 U1 0 U2 2 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 NOV 1 PY 2002 VL 54 IS 3 BP 635 EP 636 AR PII S0360-3016(02)02978-4 DI 10.1016/S0360-3016(02)02978-4 PG 2 WC Oncology; Radiology, Nuclear Medicine & Medical Imaging SC Oncology; Radiology, Nuclear Medicine & Medical Imaging GA 606CG UT WOS:000178715200002 PM 12377310 ER PT J AU Das, P Chen, MH Valentine, K Lopes, L Cormack, RA Renshaw, AA Tempany, CM Kumar, S D'Amico, AV AF Das, P Chen, MH Valentine, K Lopes, L Cormack, RA Renshaw, AA Tempany, CM Kumar, S D'Amico, AV TI Using the magnitude of PSA bounce after MRI-guided prostate brachytherapy to distinguish recurrence, benign precipitating factors, and idiopathic bounce SO INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS LA English DT Article DE prostate cancer; prostate-specific antigen; brachytherapy; PSA bounce; recurrence ID EXTERNAL-BEAM RADIATION; RADICAL PROSTATECTOMY; ANTIGEN CONCENTRATION; CANCER; THERAPY AB Purpose: To identify events that precipitated a prostate-specific antigen (PSA) bounce and characterize the magnitude, duration, and time to PSA bounce after MRI-guided prostate brachytherapy. Methods and Materials: Between 1997 and 2001, 186 patients with low-risk prostate cancer underwent MRI-guided permanent 1251 source implantation, with or without external beam radiotherapy. A PSA bounce was defined as a greater than or equal to 15% elevation in PSA compared with the most recent value, followed by a decline to a level at or less than the prebounce value. At the time of PSA measurement, data were prospectively collected on whether the patient had recent ejaculation, ongoing radiation proctitis, or recent instrumentation. Results: A total of 115 patients (61.8%) had a total of 156 PSA bounces. Of these, 36 patients had PSA bounces associated with ejaculation, proctitis, or instrumentation, and 79 experienced idiopathic PSA bounces (not associated with a precipitating event). The magnitude of the PSA bounce was significantly lower for the idiopathic PSA bounce (0.6 ng/mL) compared with that associated with ejaculation (p = 0.003), proctitis (p < 0.0001), or instrumentation (p = 0.007). Patients with biopsy-proven local recurrence had a median PSA elevation of 1.2 ng/mL, significantly higher (p = 0.006) than the magnitude of the idiopathic PSA bounce, but not significantly different from the magnitude of the PSA bounce due to ejaculation, proctitis, or instrumentation. Conclusion: In patients treated with MRI-guided prostate brachytherapy, recent ejaculation, instrumentation, or ongoing radiation proctitis can cause a transient increase in PSA, the magnitude of which is significantly higher than that for idiopathic PSA bounce, but is similar to that in patients with recurrent disease. (C) 2002 Elsevier Science Inc. C1 Harvard Univ, Sch Med, Joint Ctr Radiat Therapy, Boston, MA 02115 USA. Univ Connecticut, Dept Stat, Storrs, CT 06269 USA. Dana Farber Canc Inst, Brigham & Womens Hosp, Dept Radiat Oncol, Boston, MA 02115 USA. Dana Farber Canc Inst, Brigham & Womens Hosp, Dept Pathol, Boston, MA 02115 USA. Dana Farber Canc Inst, Brigham & Womens Hosp, Dept Radiol, Boston, MA 02115 USA. Dana Farber Canc Inst, Brigham & Womens Hosp, Dept Urol, Boston, MA 02115 USA. RP Das, P (reprint author), Brigham & Womens Hosp, Dept Radiat Oncol, Joint Ctr Radiat Therapy, 75 Francis St, Boston, MA 02115 USA. OI Cormack, Robert/0000-0001-5553-9984 NR 14 TC 47 Z9 48 U1 0 U2 0 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 NOV 1 PY 2002 VL 54 IS 3 BP 698 EP 702 AR PII S0360-3016(02)03036-5 DI 10.1016/S0360-3016(02)03036-5 PG 5 WC Oncology; Radiology, Nuclear Medicine & Medical Imaging SC Oncology; Radiology, Nuclear Medicine & Medical Imaging GA 606CG UT WOS:000178715200012 PM 12377320 ER PT J AU Su, CK Wang, CC AF Su, CK Wang, CC TI Prognostic value of Chinese race in nasopharyngeal cancer SO INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS LA English DT Article DE nasopharyngeal neoplasms; lymphoepithelioma; epidemiology; Chinese race; radiation therapy ID LOCAL-CONTROL; CARCINOMA; CHEMOTHERAPY; RADIOTHERAPY; CHEMORADIOTHERAPY; HISTOLOGY; GOODNESS; MODEL; TESTS; FIT AB Purpose: Nasopharyngeal carcinoma is rare in the United States and common in southern China. Evaluating American patients treated using a uniform technique and staged with CT scanning, we determined whether Chinese and non-Chinese patients differ in presentation and outcome. Methods and Materials: Between 1979 and 1996, 172 patients treated at Massachusetts General Hospital received primary radiotherapy with curative intent for nasopharyngeal carcinoma. Forty-one patients (24%) were of Chinese descent, and 41% of cancers were classified as having lymphoepithelioma histologic features. Most patients received twice-daily radiotherapy and a brachytherapy boost, receiving a median dose of 72 Gy to the nasopharynx. Results: At the initial presentation, the Chinese patients were significantly younger, less likely to smoke, more likely to have Stage IV disease, and more likely to have cancer with lymphoepithelioma histologic features. After controlling for stage, age, histologic type, and treatment variables, Chinese patients were significantly more likely to develop distant metastases (p < 0.05). Although Chinese race does not predict for local control or overall survival, a younger age, continued tobacco use, total radiation dose, and lymphoepithelioma histologic features do. Conclusion: In a large retrospective analysis of nasopharyngeal carcinoma, Chinese and non-Chinese patients differed significantly in presentation-age, stage, and histologic features-and outcome. We suggest as an explanation differences in intrinsic tumor biology rather than differences in treatment techniques or staging systems. Additional trials in endemic countries are needed to confirm the optimal treatment of Chinese and Chinese-American patients. (C) 2002 Elsevier Science Inc. C1 Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Radiat Oncol, Boston, MA USA. RP Su, CK (reprint author), Stanford Univ, Med Ctr, Dept Radiat Oncol, 300 Pasteur Dr, Stanford, CA 94305 USA. NR 35 TC 24 Z9 26 U1 0 U2 1 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 NOV 1 PY 2002 VL 54 IS 3 BP 752 EP 758 AR PII S0360-3016(02)02969-3 DI 10.1016/S0360-3016(02)02969-3 PG 7 WC Oncology; Radiology, Nuclear Medicine & Medical Imaging SC Oncology; Radiology, Nuclear Medicine & Medical Imaging GA 606CG UT WOS:000178715200019 PM 12377327 ER PT J AU Roth, BJ Manola, J Dreicer, R Graham, D Wilding, G AF Roth, BJ Manola, J Dreicer, R Graham, D Wilding, G TI Piritrexim in advanced, refractory carcinoma of the urothelium (E3896): A phase II trial of the Eastern Cooperative Oncology Group SO INVESTIGATIONAL NEW DRUGS LA English DT Article DE bladder cancer; piritrexim; refractory disease; transitional cell carcinoma; urothelial cancer ID TRANSITIONAL-CELL-CARCINOMA; GEMCITABINE PLUS CISPLATIN; ADVANCED BLADDER-CANCER; ORAL PIRITREXIM; DIHYDROFOLATE-REDUCTASE; PACLITAXEL; METHOTREXATE; CARBOPLATIN; VINBLASTINE; DOXORUBICIN AB This was a single-agent phase II clinical trial of the antifol piritrexim in patients with advanced transitional cell carcinoma of the bladder. Methods: Patients with previously-treated, advanced urothelial carcinoma were treated with oral piritrexim at a dose of 25 mg three times daily for 5 consecutive days each week for 3 consecutive weeks followed by a 1-week rest period. Courses were repeated every 28 days. Results: Thirty-five patients were enrolled in the study, with 28 patients evaluable for survival and toxicity and 27 evaluable for response. Toxicity: Myelosuppression was the major dose-limiting toxicity, with WHO grade 3/4 thrombocytopenia in 4 patients, granulocytopenia in 1 patient, and anemia in 3 patients. Grade 3 nonhematologic toxicity consisted of neuropathy in 5 patients, hepatotoxicity in 2, nausea in 2, and 1 each with pulmonary toxicity and rash. Efficacy: Of the 27 patients evaluable for response, 2 (7%) achieved an objective response, lasting 112 and 142 days, respectively. Conclusion: Piritrexim has minimal activity in patients with previously treated transitional cell carcinoma of the bladder, regardless of prior exposure to methotrexate, and further evaluation of this compound in this clinical setting is not warranted. C1 Vanderbilt Ingram Canc Ctr, Nashville, TN USA. Dana Farber Canc Inst, Boston, MA 02115 USA. Cleveland Clin Fdn, Cleveland, OH 44195 USA. Carle Clin Assoc, Urbana, IL USA. Univ Wisconsin, Madison, WI USA. RP Roth, BJ (reprint author), 777 Preston Res Bldg, Nashville, TN 37232 USA. FU NCI NIH HHS [CA23318, CA66636, CA49957, CA21076, CA13650, CA21115] NR 20 TC 23 Z9 23 U1 0 U2 0 PU KLUWER ACADEMIC PUBL PI DORDRECHT PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS SN 0167-6997 J9 INVEST NEW DRUG JI Invest. New Drugs PD NOV PY 2002 VL 20 IS 4 BP 425 EP 429 DI 10.1023/A:1020675017737 PG 5 WC Oncology; Pharmacology & Pharmacy SC Oncology; Pharmacology & Pharmacy GA 604BM UT WOS:000178595800009 PM 12448661 ER PT J AU Hong, DH Li, TS AF Hong, DH Li, TS TI Complex expression pattern of RPGR reveals a role for purine-rich exonic splicing enhancers SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Article ID LINKED RETINITIS-PIGMENTOSA; NUCLEOTIDE-EXCHANGE FACTOR; T ALTERNATIVE EXON; SITE SELECTION; SR-PROTEINS; MOUSE; GENE; PHOTORECEPTOR; TERMINATION; TRANSPORT AB PURPOSE. To examine the mechanism underlying transcript heterogeneity in the gene for the retinitis pigmentosa GTPase regulator (RPGR). METHODS. Transcript heterogeneity was analyzed by reverse transcription-polymerase chain reactions (RT-PCR), rapid amplification of cDNA ends (RACE), and transient expression of minigene constructs. Protein variants were identified by immunoblot analysis and by immunocytochemistry. RESULTS. RPGR transcripts terminated either uniformly at the end of exon 19, producing the constitutive transcript with few variants, or at variable sites downstream from exon 15. The latter transcripts resembled the previously described open reading frame (ORF)14/15 variant, but the ORF14/15 exon was not found in full length. Instead, various portions of a purine-rich region were removed as introns. Numerous splice site combinations were used, giving rise to innumerable variants. Analysis of the purine-rich region found multiple exonic splicing enhancers (ESEs) known to promote splicing through interaction with serine-arginine repeat (SR) proteins. Antibodies targeting different regions of RPGR detected a multitude of RPGR proteins in photoreceptors, concentrated in the connecting cilium. Predominant ORF14/15-encoded RPGR polypeptides migrated at approximately 200 kDa and were photoreceptor specific. CONCLUSIONS. The exceptional heterogeneity in RPGR transcript processing results primarily from a novel form of alternative RNA splicing mediated by multiple exonic splicing enhancers. RPGR is composed of a population of proteins with a constant N-terminal core encompassing the RCC1 homology domain followed by a C-terminal portion of variable lengths and sequences. C1 Harvard Univ, Berman Gund Lab, Massachusetts Eye & Ear Infirm, Sch Med, Boston, MA 02114 USA. RP Li, TS (reprint author), Harvard Univ, Berman Gund Lab, Massachusetts Eye & Ear Infirm, Sch Med, 243 Charles St, Boston, MA 02114 USA. FU NEI NIH HHS [EY10309] NR 30 TC 44 Z9 44 U1 0 U2 1 PU ASSOC RESEARCH VISION OPHTHALMOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD NOV PY 2002 VL 43 IS 11 BP 3373 EP 3382 PG 10 WC Ophthalmology SC Ophthalmology GA 609AB UT WOS:000178879500004 PM 12407146 ER PT J AU Schambelan, M Benson, CA Carr, A Currier, JS Dube, MP Gerber, JG Grinspoon, SK Grunfeld, C Kotler, DP Mulligan, K Powderly, WG Saag, MS AF Schambelan, M Benson, CA Carr, A Currier, JS Dube, MP Gerber, JG Grinspoon, SK Grunfeld, C Kotler, DP Mulligan, K Powderly, WG Saag, MS TI Management of metabolic complications associated with antiretroviral therapy for HIV-1 infection: Recommendations of an International AIDS Society-USA panel SO JAIDS-JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES LA English DT Review DE HIV; antiretroviral; insulin resistance; hyperlipidemia; lipodystrophy; lactic anemia; osteoporosis; AIDS; guidelines; metabolic complications ID HUMAN-IMMUNODEFICIENCY-VIRUS; PROTEASE INHIBITOR THERAPY; VISCERAL ADIPOSE-TISSUE; HUMAN GROWTH-HORMONE; REVERSE-TRANSCRIPTASE INHIBITORS; ABDOMINAL-FAT ACCUMULATION; INSULIN-RESISTANCE; BODY-COMPOSITION; LIPID ABNORMALITIES; MAGNETIC-RESONANCE AB Objective: Alterations in glucose and lipid metabolism, lactic acidemia, bone disorders, and abnormal body fat distribution have been recognized recently as frequent complications associated with HIV-1 infection and potent antiretroviral therapy, but limited data are available regarding the appropriate management of these disorders. These recommendations were developed to guide physicians actively involved in HIV care in the management of metabolic complications that occur primarily within the context of potent antiretroviral therapy. Participants: A 12-member panel representing international expertise in HIV-1 patient care, antiretroviral therapy, and endocrine and metabolic disorders was selected in the spring of 2000 by the International AIDS Society-USA, a not-for-profit physician education organization. Panel members met in closed meetings beginning in May 2000. All work was funded by the International AIDS Society-USA; the panel members are not compensated for their participation. Evidence: The panel reviewed published results of clinical, epidemiologic, and basic science studies and data and abstracts presented at research conferences, primarily from 1997 to 2002. The panel also considered studies of the pathophysiology and treatment of similar metabolic abnormalities in noninfected persons. Emphasis was placed on results from prospective, randomized, controlled clinical trials when available. Process: For each metabolic complication, I or more member(s) reviewed and presented all available evidence to the panel, and then wrote a summary of the evidence and preliminary recommendations. Final recommendations were determined by full group consensus. The summaries were combined into a single working document and all panel members edited and approved all subsequent drafts. Conclusions: Carefully controlled studies to determine the incidence, etiology, risk factors, and most appropriate treatments for metabolic complications in HIV-1 infection are urgently needed. In the absence of these data, and to prevent acute illness and mitigate long-term risks, the panel recommends routine assessment and monitoring of glucose and lipid levels and assessment and monitoring of lactic acidemia and bone abnormalities if clinical signs or symptoms are detected. With the exception of body fat distribution abnormalities, specific treatments for these complications are also recommended. Successful long-term antiretroviral therapy will require diligent monitoring and preemptive treatment of metabolic complications to optimize the risk-benefit ratio of antiretroviral therapies. C1 Int AIDS Soc USA, San Francisco, CA 94129 USA. Univ Calif San Francisco, San Francisco Gen Hosp, San Francisco, CA 94143 USA. Univ Colorado, Hlth Sci Ctr, Denver, CO 80262 USA. St Vincents Hosp, Sydney, NSW 2010, Australia. Univ Calif Los Angeles, Los Angeles, CA 90024 USA. Indiana Univ, Sch Med, Indianapolis, IN 46223 USA. Harvard Univ, Massachusetts Gen Hosp, Sch Med, Boston, MA 02129 USA. San Francisco Vet Affairs Med Ctr, San Francisco, CA USA. Columbia Univ, St Lukes Roosevelt Hosp, New York, NY 10027 USA. Washington Univ, Sch Med, St Louis, MO 63130 USA. Univ Alabama, Birmingham, AL 35294 USA. RP Schambelan, M (reprint author), Int AIDS Soc USA, 1001 B Oreilly Ave, San Francisco, CA 94129 USA. NR 208 TC 229 Z9 234 U1 0 U2 5 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 1525-4135 J9 JAIDS JI JAIDS PD NOV 1 PY 2002 VL 31 IS 3 BP 257 EP 275 PG 19 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA 612NR UT WOS:000179082800001 PM 12439201 ER PT J AU Litonjua, AA Milton, DK Celedon, JC Ryan, L Weiss, ST Gold, DR AF Litonjua, AA Milton, DK Celedon, JC Ryan, L Weiss, ST Gold, DR TI A longitudinal analysis of wheezing in young children: The independent effects of early life exposure to house dust endotoxin, allergens, and pets SO JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY LA English DT Article DE endotoxin; allergens; domestic animals; wheeze; asthma ID HAY-FEVER; ASTHMA; RISK; SENSITIZATION; ATOPY; INHALATION; COMMUNITY; DECREASES; COCKROACH; RESPONSES AB Background: It has been postulated that exposure to bacterial endotoxins and animals early in life might confer protection against the development of asthma and allergies. Objective: We investigated the longitudinal effects of exposure to house dust endotoxin (HDE), allergen levels, and the presence of a dog in the home on wheezing in young children over a 4-year period. Methods: Two hundred twenty-six children younger than 5 years were followed for 4 years. Endotoxin and allergen levels were measured from house dust collected at baseline. Longitudinal associations were investigated by using a proportional hazards technique that allowed for multiple outcomes per subject. Results: Exposure to high concentrations of HDE of greater than the median level was associated with an increased risk for wheezing over the period of observation (multivariate relative risk, 1.52; 95% CI, 1.07-2.14), but this risk rapidly decreased over time (P for trend = .005). Exposure to cockroach allergen was associated with increased risk for wheezing, whereas exposure to cat allergen and the presence of a dog in the home were both associated with decreased risk for wheezing. The risks associated with cockroach allergen, cat allergen, and dog did not change over the period of observation. Conclusion: The negative associations between exposures to dogs and cat allergen and wheeze appear to be independent of the effects of endotoxin and suggest that separate mechanisms might mediate the effects of HDE exposure and pet exposure on the developing immune system. C1 Brigham & Womens Hosp, Dept Med, Channing Lab, Boston, MA 02115 USA. Beth Israel Deaconess Med Ctr, Div Pulm & Crit Care Med, Boston, MA 02215 USA. Harvard Univ, Sch Med, Boston, MA 02115 USA. Harvard Univ, Sch Publ Hlth, Boston, MA 02115 USA. Dana Farber Canc Inst, Boston, MA 02115 USA. RP Litonjua, AA (reprint author), Channing Labs, 181 Longwood Ave, Boston, MA 02115 USA. RI Milton, Donald/G-3286-2010; Ryan, Louise/A-4562-2009; OI Milton, Donald/0000-0002-0550-7834; Ryan, Louise/0000-0001-5957-2490; Litonjua, Augusto/0000-0003-0422-5875 FU NHLBI NIH HHS [K08 HL-03870]; NIAID NIH HHS [R01 AI/EHS-35786]; NIEHS NIH HHS [R01 ES-07036] NR 33 TC 118 Z9 118 U1 0 U2 4 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 NOV PY 2002 VL 110 IS 5 BP 736 EP 742 DI 10.1067/mai.2002.128948 PG 7 WC Allergy; Immunology SC Allergy; Immunology GA 612NN UT WOS:000179082500008 PM 12417882 ER PT J AU Musch, G Layfield, JDH Harris, RS Melo, MFV Winkler, T Callahan, RJ Fischman, AJ Venegas, JG AF Musch, G Layfield, JDH Harris, RS Melo, MFV Winkler, T Callahan, RJ Fischman, AJ Venegas, JG TI Topographical distribution of pulmonary perfusion and ventilation, assessed by PET in supine and prone humans SO JOURNAL OF APPLIED PHYSIOLOGY LA English DT Article DE functional lung imaging; positron emission tomography; gas exchange; heterogeneity; prone position ID INTER-REGIONAL DISTRIBUTION; ANESTHETIZED-PARALYZED MAN; BLOOD-FLOW DISTRIBUTION; GAS-DISTRIBUTION; V/Q RATIOS; POSITION; GRAVITY; AWAKE; QUANTIFICATION; HETEROGENEITY AB Using positron emission tomography (PET) and intravenously injected N-13(2), we assessed the topographical distribution of pulmonary perfusion ((Q) over dot) and ventilation ((V) over dot) in six healthy, spontaneously breathing subjects in the supine and prone position. In this technique, the intrapulmonary distribution of N-13(2), measured during a short apnea, is proportional to regional (Q) over dot. After resumption of breathing, regional specific alveolar (V) over dot (s(V) over dot A, ventilation per unit of alveolar gas volume) can be calculated from the tracer washout rate. The PET scanner imaged 15 contiguous, 6-mm-thick, slices of lung. Vertical gradients of (Q) over dot and s(V) over dot A were computed by linear regression, and spatial heterogeneity was assessed from the squared coefficient of variation 2). Both C (V) over dot (2)(Q) and CVs(s(V) over dot)(2) (A) were corrected for the estimated contribution of random imaging noise. We found that 1) both (Q) over dot and (V) over dot had vertical gradients favoring dependent lung regions, 2) vertical gradients were similar in the supine and prone position and explained, on average, 24% of (Q) over dot heterogeneity and 8% of (V) over dot heterogeneity, 3) CV(Q) over dot2 was similar in the supine and prone position, and 4) CVs(V) over dot A2 was lower in the prone position. We conclude that, in recumbent, spontaneously breathing humans, 1) vertical gradients favoring dependent lung regions explain a significant fraction of heterogeneity, especially of (Q) over dot , and 2) although (Q) does not seem to be atically more homogeneous in the prone position, differences in individual behaviors may make the prone position advantageous, in terms of (V) over dot -to-(Q) over dot matching, in selected subjects. C1 Massachusetts Gen Hosp, Dept Anesthesia & Crit Care, CLN 309, Boston, MA 02114 USA. Massachusetts Gen Hosp, Dept Med, Pulm & Crit Care Unit, Boston, MA 02114 USA. Massachusetts Gen Hosp, Dept Radiol, Div Nucl Med, Boston, MA 02114 USA. Harvard Univ, Sch Med, Boston, MA 02114 USA. MIT, Cambridge, MA 02139 USA. Dresden Univ Technol, Univ Clin Carl Gustav Carus, Clin Anesthesiol & Intens Care Med, D-01307 Dresden, Germany. RP Musch, G (reprint author), Massachusetts Gen Hosp, Dept Anesthesia & Crit Care, CLN 309, 32 Fruit St, Boston, MA 02114 USA. RI Winkler, Tilo/B-5337-2009 OI Winkler, Tilo/0000-0002-7276-5550 FU NHLBI NIH HHS [HL-38267, HL-68011]; NIGMS NIH HHS [GM-07592] NR 34 TC 114 Z9 114 U1 1 U2 3 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA SN 8750-7587 J9 J APPL PHYSIOL JI J. Appl. Physiol. PD NOV PY 2002 VL 93 IS 5 BP 1841 EP 1851 DI 10.1152/japplphysiol.00223.2002 PG 11 WC Physiology; Sport Sciences SC Physiology; Sport Sciences GA 606QJ UT WOS:000178744400034 PM 12381773 ER PT J AU Kim, N Weeks, DL Shin, JM Scott, DR Young, MK Sachs, G AF Kim, N Weeks, DL Shin, JM Scott, DR Young, MK Sachs, G TI Proteins released by Helicobacter pylori in vitro SO JOURNAL OF BACTERIOLOGY LA English DT Article ID GASTRIC EPITHELIAL-CELLS; NECROSIS-FACTOR-ALPHA; VACUOLATING CYTOTOXIN; IV SECRETION; INFECTION; CAGA; INTERLEUKIN-8; TRANSLOCATION; PATHOGENICITY; PATHOGENESIS AB Secretion of proteins by Helicobacter pylori may contribute to gastric inflammation and epithelial damage. An in vitro analysis was designed to identify proteins released by mechanisms other than nonspecific lysis. The radioactivity of proteins in the supernatant was compared with that of the intact organism by two-dimensional gel phosphorimaging following a 4-h pulse-chase. The ratio of the amount of UreB, a known cytoplasmic protein, in the supernatant to that in the pellet was found to be 0.25, and this was taken as an index of lysis during the experiments (n = 6). Ratios greater than that of UreB were used to distinguish proteins that were selectively released into the medium. Thus, proteins enriched more than 10-fold in the supernatant compared to UreB were identified by mass spectrometry. Sixteen such proteins were present in the supernatant: VacA; a conserved secreted protein (HP1286); putative peptidyl cis-trans isomerase (HP0175); six proteins encoded by HP0305, HP0231, HP0973, HP0721, HP0129, and HP0902; thioredoxin (HP1458); single-stranded-DNA-binding 12RNP2 precursor (HP0827); histone-like DNA-binding protein HU (HP0835); ribosomal protein L11 (HP1202); a putative outer membrane protein (HP1564); and outer membrane proteins Omp21 (HP0913) and Omp20 (HP0912). All except HP0902, thioredoxin, HP0827, HP0835, and HP1202 had a signal peptide. When nalidixic acid, a DNA synthesis inhibitor, was added to inhibit cell division but not protein synthesis, to decrease possible contamination due to outer membrane shedding, two outer membrane proteins (Omp21 and Omp20) disappeared from the supernatant, and the amount of VacA also decreased. Thus, 13 proteins were still enriched greater than 10-fold in the medium after nalidixic acid treatment, suggesting these were released specifically, possibly by secretion. These proteins may be implicated in H. pylori-induced effects on the gastric epithelium. C1 Univ Calif Los Angeles, Digest Dis Ctr, Dept Physiol & Med, Los Angeles, CA 90073 USA. VA Greater Los Angeles Hlth Care Syst, Los Angeles, CA 90073 USA. City Hope Natl Med Ctr, Beckman Res Inst, Div Immunol, Spectrometry & Microsequencing Core Facil, Duarte, CA 91010 USA. RP Sachs, G (reprint author), VA Greater Los Angeles Hlth Care Syst, Bldg 113,Room 324,11301 Wilshore Blvd, Los Angeles, CA 90073 USA. EM gsachs@ucla.edu RI Kim, Nayoung/J-5387-2012 FU NIDDK NIH HHS [DK46917, R01 DK046917]; PHS HHS [41301, 17294, 53462] NR 53 TC 52 Z9 58 U1 0 U2 2 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA SN 0021-9193 J9 J BACTERIOL JI J. Bacteriol. PD NOV PY 2002 VL 184 IS 22 BP 6155 EP 6162 DI 10.1128/JB.184.22.6155-6162.2002 PG 8 WC Microbiology SC Microbiology GA 609QU UT WOS:000178916700009 PM 12399485 ER PT J AU Kloek, C Haq, AK Dunn, SL Lavery, HJ Banks, AS Myers, MG AF Kloek, C Haq, AK Dunn, SL Lavery, HJ Banks, AS Myers, MG TI Regulation of Jak kinases by intracellular leptin receptor sequences SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID SIGNAL TRANSDUCER GP130; OB-R; ERYTHROPOIETIN RECEPTOR; CYTOPLASMIC DOMAINS; CYTOKINE RECEPTORS; ALPHA-INTERFERON; ACTIVATION; INTERLEUKIN-6; EXPRESSION; NEURONS AB Leptin signals the status of body energy stores via the leptin receptor (LR), a member of the Type I cytokine receptor family. Type I cytokine receptors mediate intracellular signaling via the activation of associated Jak family tyrosine kinases. Although their COOH-terminal sequences vary, alternatively spliced LR isoforms (LRa-LRd) share common NH2-terminal sequences, including the first 29 intracellular amino acids. The so-called long form LR (LRb) activates Jak-dependent signaling and is required for the physiologic actions of leptin. In this study, we have analyzed Jak activation by intracellular LR sequences under the control of the extracellular erythropoeitin (Epo) (Epo receptor/LRb chimeras). We show that Jak2 is the requisite Jak kinase for signaling by the LRb intracellular domain and confirm the requirement for the Box 1 motif for Jak2 activation. A minimal LRb intracellular domain for Jak2 activation includes intracellular amino acids 31-48. Although the sequence requirements for intracellular amino acids 37-48 are flexible, intracellular amino acids 31-36 of LRb play a critical role in Jak2 activation and contain a loose homology motif found in other Jak2-activating cytokine receptors. The failure of short form sequences to function in Jak2 activation reflects the absence of this motif. C1 Joslin Diabet Ctr, Div Res, Sect Obes, Boston, MA 02215 USA. Harvard Univ, Sch Med, Dept Med, Boston, MA 02215 USA. RP Myers, MG (reprint author), Joslin Diabet Ctr, Div Res, Sect Obes, 1 Joslin Pl, Boston, MA 02215 USA. RI Banks, Alexander/B-4832-2012 OI Banks, Alexander/0000-0003-1787-6925 FU NIDDK NIH HHS [DK56731] NR 33 TC 141 Z9 153 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 NOV 1 PY 2002 VL 277 IS 44 BP 41547 EP 41555 DI 10.1074/jbc.M205148200 PG 9 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA 610WR UT WOS:000178985300033 PM 12196522 ER PT J AU Mueller, E Drori, S Aiyer, A Yie, J Sarraf, P Chen, H Hauser, S Rosen, ED Ge, K Roeder, RG Spiegelman, BM AF Mueller, E Drori, S Aiyer, A Yie, J Sarraf, P Chen, H Hauser, S Rosen, ED Ge, K Roeder, RG Spiegelman, BM TI Genetic analysis of adipogenesis through peroxisome proliferator-activated receptor gamma isoforms SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID PPAR-GAMMA; NUCLEAR RECEPTORS; C/EBP-ALPHA; DIFFERENTIATION; EXPRESSION; COACTIVATOR; INTERACTS; PROTEIN; COMPLEX; LIGAND AB dPeroxisome proliferator-activated receptor (PPAR) gamma is a nuclear receptor that is a key regulator of adipogenesis and is present in two isoforms generated by alternative splicing, PPARgamma1 and PPARgamma2. Studies of the ability of each isoform to stimulate fat differentiation have yielded ambiguous results, in part because PPARgamma stimulates its own expression. We have thus undertaken a formal genetic analysis using PPARgamma-null fibroblast cell lines to assess the specific role of each individual isoform in adipogenesis. We show here that both PPARgamma1 and PPARgamma2 have the intrinsic ability to stimulate robust adipogenesis. Adipose cells stimulated by either PPARgamma1 or PPARgamma2 express a similar gene profile and show similar responses to insulin. However, in response to low ligand concentrations, PPARgamma2 shows a quantitatively greater ability to induce adipogenesis. Analyses involving coactivator binding and transcriptional assays indicate that PPARgamma2 has an enhanced ability to bind components of the DRIP/TRAP complex, coactivators required for fat differentiation. C1 Harvard Univ, Sch Med, Dana Farber Canc Inst, Boston, MA 02115 USA. Harvard Univ, Sch Med, Dept Cell Biol, Boston, MA 02115 USA. Millenium Pharmaceut Inc, Cambridge, MA 02139 USA. Rockefeller Univ, Biochem & Mol Biol Lab, New York, NY 10021 USA. RP Spiegelman, BM (reprint author), Harvard Univ, Sch Med, Dana Farber Canc Inst, 1 Jimmy Fund Way, Boston, MA 02115 USA. OI Ge, Kai/0000-0002-7442-5138 FU NIDDK NIH HHS [2R37DK31405] NR 26 TC 151 Z9 164 U1 0 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 NOV 1 PY 2002 VL 277 IS 44 BP 41925 EP 41930 DI 10.1074/jbc.M206950200 PG 6 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA 610WR UT WOS:000178985300080 PM 12200443 ER PT J AU Benarafa, C Cooley, J Zeng, WL Bird, PI Remold-O'Donnell, E AF Benarafa, C Cooley, J Zeng, WL Bird, PI Remold-O'Donnell, E TI Characterization of four murine homologs of the human ov-serpin monocyte neutrophil elastase inhibitor MNEI (SERPINB1) SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID REACTIVE CENTER LOOP; ENDOGENOUS RETROVIRUS; CHROMOSOMAL LOCALIZATION; PROTEINASE COMPLEX; CYSTIC-FIBROSIS; GENE; SEQUENCE; FAMILY; SUPERFAMILY; EXPRESSION AB The human ov-serpin monocyte neutrophil elastase inhibitor (MNEI) is encoded by a single gene SERPINB1. It is a highly efficient inhibitor of neutrophil granule proteases. Four murine genes with high sequence identity with MNEI were identified and fully sequenced, and these were named EIA, EIB, EIC, and EID. EIA, EIB and EIC showed the same seven-exon gene structure as SERPINB1. However, EIC included an additional, alternatively spliced, exon due to the insertion of an endogenous retrovirus-like sequence. EID lacked several exons and is a pseudogene. Reverse transcriptase-PCR showed that EIA, like MNEI, is expressed at high levels in many tissues. EIB is mainly expressed in brain, and EIC was only expressed as splicing variants unlikely to encode a functional serpin. Upon incubation with serine proteases, EIA formed inhibitory covalent complexes with pancreatic and neutrophil elastases, cathepsin G, proteinase-3, and chymotrypsin, as previously shown for MNEI, whereas EIB was only able to do so with cathepsin G. According to the new serpin nomenclature, the genes encoding EIIA, EIB, EIC, and EID will be called Serpinb1, Serpinb1b, Serpinb1c, and Serpinb1-ps1. These data demonstrate that the four murine homologs of MNEI have met different evolutionary fates, and that EIA is the mouse ortholog of MNEI. C1 Harvard Univ, Sch Med, Ctr Blood Res, Boston, MA 02115 USA. Harvard Univ, Sch Med, Dept Pediat, Boston, MA 02115 USA. Monash Univ, Dept Biochem & Mol Biol, Clayton, Vic 3800, Australia. RP Benarafa, C (reprint author), Harvard Univ, Sch Med, Ctr Blood Res, 800 Huntington Ave, Boston, MA 02115 USA. OI Benarafa, Charaf/0000-0002-2049-7769; Bird, Phillip/0000-0002-6695-606X FU NHLBI NIH HHS [HL66548-02, R01 HL066548] NR 40 TC 40 Z9 43 U1 1 U2 5 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 NOV 1 PY 2002 VL 277 IS 44 BP 42028 EP 42033 DI 10.1074/jbc.M207080200 PG 6 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA 610WR UT WOS:000178985300092 PM 12189154 ER PT J AU Geiben-Lynn, R Brown, N Walker, BD Luster, AD AF Geiben-Lynn, R Brown, N Walker, BD Luster, AD TI Purification of a modified form of bovine antithrombin III as an HIV-1CD8(+) T-cell antiviral factor SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID IMMUNODEFICIENCY-VIRUS TYPE-1; MACROPHAGE-DERIVED CHEMOKINE; REVERSE TRANSCRIPTION; HEPARIN-BINDING; HIV-1 INFECTION; MEDIATED SUPPRESSION; SERPIN ANTITHROMBIN; BETA-CHEMOKINES; GENE-EXPRESSION; CD8(+) CELLS AB CD8(+) T-cells secrete soluble factor(s) capable of inhibiting both R5- and X4-tropic strains of human immunodeficiency virus type 1 (HIV-1). CCR5 chemokine ligands, released from activated CD8(+) T-cells, contribute to the antiviral activity of these cells. These CC-chemokines, however, do not account for all CD8(+) T-cell antiviral factor(s) (CAF) released from these cells, particularly because the elusive CAF can inhibit the replication of X4 HIV-1 strains that use CXCR4 and not CCR5 as a coreceptor. Here we demonstrate that activated CD8(+) T-cells of HIV-1-seropositive individuals modify serum bovine antithrombin III into an HIV-1 inhibitory factor capable of suppressing the replication of X4 HIV-1. These data indicate that antithrombin III may play a role in the progression of HIV-1 disease. C1 Massachusetts Gen Hosp, Div Rheumatol Allergy & Immunol, Boston, MA 02129 USA. Massachusetts Gen Hosp, Ctr Immunol & Inflammatory Dis, Partners AIDS Res Ctr, Boston, MA 02129 USA. Harvard Univ, Sch Med, Boston, MA 02115 USA. RP Luster, AD (reprint author), Massachusetts Gen Hosp, Bldg 149,13th St, Charlestown, MA 02129 USA. FU NIAID NIH HHS [AI46999, AI30914, AI28568] NR 44 TC 26 Z9 29 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 NOV 1 PY 2002 VL 277 IS 44 BP 42352 EP 42357 DI 10.1074/jbc.M207079200 PG 6 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA 610WR UT WOS:000178985300131 PM 12192009 ER PT J AU Rui, LY Yuan, MS Frantz, D Shoelson, S White, MF AF Rui, LY Yuan, MS Frantz, D Shoelson, S White, MF TI SOCS-1 and SOCS-3 block insulin signaling by ubiquitin-mediated degradation of IRS1 and IRS2 SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID RECEPTOR SUBSTRATE-1; PHOSPHATIDYLINOSITOL 3-KINASE; BOX MOTIF; IFN-GAMMA; RESISTANCE; SUPPRESSORS; MICE; PROTEINS; LIVER; GENE AB Inflammation associates with peripheral insulin resistance, which dysregulates nutrient homeostasis and leads to diabetes. Inflammation induces the expression of SOCS proteins. We show that SOCS1 or SOCS3 targeted IRS1 and IRS2, two critical signaling molecules for insulin action, for ubiquitin-mediated degradation. SOCS1 or SOCS3 bound both recombinant and endogenous IRS1 and IRS2 and promoted their ubiquitination and subsequent degradation in multiple cell types. Mutations in the conserved SOCS box of SOCS1 abrogated its interaction with the elongin BC ubiquitin-ligase complex without affecting its binding to IRS1 or IRS2. The SOCS1 mutants also failed to promote the ubiquitination and degradation of either IRS1 or IRS2. Adenoviral-mediated expression of SOCS1 in mouse liver dramatically reduced hepatic IRS1 and IRS2 protein levels and caused glucose intolerance; by contrast, expression of the SOCS1 mutants had no effect. Thus, SOCS-mediated degradation of IRS proteins, presumably via the elongin BC ubiquitin-ligase, might be a general mechanism of inflammation-induced insulin resistance, providing a target for therapy. C1 Harvard Univ, Sch Med, Joslin Diabet Ctr, Howard Hughes Med Inst, Boston, MA 02215 USA. RP White, MF (reprint author), Harvard Univ, Sch Med, Joslin Diabet Ctr, Howard Hughes Med Inst, 1 Joslin Pl, Boston, MA 02215 USA. NR 45 TC 482 Z9 512 U1 6 U2 32 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 NOV 1 PY 2002 VL 277 IS 44 BP 42394 EP 42398 DI 10.1074/jbc.C200444200 PG 5 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA 610WR UT WOS:000178985300137 PM 12228220 ER PT J AU Saltzman, CL AF Saltzman, CL TI Two types of therapeutic shoes were no better than usual footwear for preventing foot reulceration SO JOURNAL OF BONE AND JOINT SURGERY-AMERICAN VOLUME LA English DT Editorial Material C1 VA Puget Sound Hlth Care Syst, Seattle, WA 98108 USA. RP Saltzman, CL (reprint author), VA Puget Sound Hlth Care Syst, 1660 S Columbian Way, Seattle, WA 98108 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU JOURNAL BONE JOINT SURGERY INC PI NEEDHAM PA 20 PICKERING ST, NEEDHAM, MA 02192 USA SN 0021-9355 J9 J BONE JOINT SURG AM JI J. Bone Joint Surg.-Am. Vol. PD NOV PY 2002 VL 84A IS 11 BP 2107 EP 2107 PG 1 WC Orthopedics; Surgery SC Orthopedics; Surgery GA 612NJ UT WOS:000179082100038 PM 12429781 ER EF