FN Thomson Reuters Web of Science™ VR 1.0 PT J AU Bischoff, TA Kelley, CJ Karchesy, Y Laurantos, M Nguyen-Dinh, P Arefi, AG AF Bischoff, TA Kelley, CJ Karchesy, Y Laurantos, M Nguyen-Dinh, P Arefi, AG TI Antimalarial activity of Lactucin and Lactucopicrin: sesquiterpene lactones isolated from Cichorium intybus L. SO JOURNAL OF ETHNOPHARMACOLOGY LA English DT Article DE Cichorium intybus; lactucin; lactucopicrin; antimalarial; plasmodium ID VACUUM LIQUID-CHROMATOGRAPHY; SEPARATION; MIXTURES AB Folklore reports from Afghanistan prior to the wars described the use of aqueous root extracts of Cichorium intybus (L.) as a light-sensitive plant remedy for malaria. Preparative isolation and bioassay against HB3 clone of strain Honduras-1 of Plasmodiumfalciparum identified the previously known light-sensitive sesquiterpene lactones Lactucin and Lactueopicrin to be antimalarial compounds. (C) 2004 Elsevier Ireland Ltd. All rights reserved. C1 Massachusetts Gen Hosp, Dept Pharm, Boston, MA 02114 USA. Massachusetts Coll Pharm & Allied Hlth Sci, Heber Younken Pharmacognosy Lab, Boston, MA 02115 USA. Ctr Dis Control & Prevent, Div Parasit Dis, Biol & Diagnost Branch, Atlanta, GA 30333 USA. RP Bischoff, TA (reprint author), Massachusetts Gen Hosp, Dept Pharm, Boston, MA 02114 USA. EM Bischoff.Theodore@MGH.Harvard.edu NR 9 TC 38 Z9 45 U1 2 U2 11 PU ELSEVIER SCI IRELAND LTD PI CLARE PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE, IRELAND SN 0378-8741 J9 J ETHNOPHARMACOL JI J. Ethnopharmacol. PD DEC PY 2004 VL 95 IS 2-3 BP 455 EP 457 DI 10.1016/j.jep.2004.06.031 PG 3 WC Plant Sciences; Chemistry, Medicinal; Integrative & Complementary Medicine; Pharmacology & Pharmacy SC Plant Sciences; Pharmacology & Pharmacy; Integrative & Complementary Medicine GA 871SU UT WOS:000225154500053 PM 15507374 ER PT J AU Chandler, NM Canete, JJ Callery, MP AF Chandler, NM Canete, JJ Callery, MP TI Caspase-3 drives apoptosis in pancreatic cancer cells after treatment with gemcitabine SO JOURNAL OF GASTROINTESTINAL SURGERY LA English DT Article; Proceedings Paper CT 4th Biennial Congress of the American-Hepato-Pancreato-Biliary-Association CY FEB 28-MAR 02, 2003 CL MIAMI BEACH, FL SP Amer Hepato Pancreato Biliary Assoc DE caspase; pancreatic cancer; apoptosis; gemcitabine ID MULTIPLE-MYELOMA; INHIBITION; ACTIVATION AB Pancreatic cancer remains a highly chemoresistant malignancy. Gemcitabine, the most effective first-line agent available, acts by disrupting cellular replication. Caspases belong to a family of proteases that function as key components of the apoptotic death machinery. We investigated the mechanisms by which gemcitabine blocks proliferation and whether it can induce apoptosis in pancreatic cancer cells. Quiescent pancreatic cancer cells (BxPC-3) were stimulated to proliferate (10% fetal calf serum) with or without gemcitabine, PS-341 (26S proteasome inhibitor), or both. Proliferation was measured by MTT assay and apoptosis by propidium iodine staining. To determine activation of the apoptotic regulatory cell proteins, caspase-3 and cleavage of poly(ADP-ribose)polymerase (PARP) into its 85-kDa fragment were assessed by Western blotting. Gemcitabine at even low doses (10 mumol/L) significantly inhibited cellular proliferation, whereas PS-341 (10 nmol/L) had no effect. With combined treatment, PS-341 potentiated the antiproliferative effects of gemcitabine (P = 0.001). At 48 hours, the apoptotic fraction was greatly enhanced by the presence of PS-341 compared with gemcitabine alone. Caspase-3 accumulated as early as 30 minutes and was associated with cleavage of PARP to its apoptotic fragment. Gemcitabine, a nucleoside analogue, may in part exert its anti proliferative effects by directing pancreatic cancer cells to a default pathway of apoptosis. 26S proteasome inhibition potentiates this effect, suggesting its potential clinical value against chemoresistance in pancreatic cancer. (C) 2004 The Society for Surgery of the Alimentary Tract. C1 Harvard Univ, Sch Med, Beth Israel Deaconess Med Ctr, Div Gen Surg,Dept Surg, Boston, MA 02215 USA. Univ Massachusetts, Sch Med, Dept Surg, Worcester, MA USA. RP Callery, MP (reprint author), Harvard Univ, Sch Med, Beth Israel Deaconess Med Ctr, Div Gen Surg,Dept Surg, 330 Brookline Ave,Stoneman 920, Boston, MA 02215 USA. EM mcallery@caregroup.harvard.edu NR 16 TC 25 Z9 26 U1 5 U2 9 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 1091-255X J9 J GASTROINTEST SURG JI J. Gastrointest. Surg. PD DEC PY 2004 VL 8 IS 8 BP 1072 EP 1078 DI 10.1016/j.gassur.2004.09.054 PG 7 WC Gastroenterology & Hepatology; Surgery SC Gastroenterology & Hepatology; Surgery GA 883TR UT WOS:000226039100030 PM 15585396 ER PT J AU Farwell, WR Stump, TE Wang, J Tafesse, E L'Italien, G Tierney, WM AF Farwell, WR Stump, TE Wang, J Tafesse, E L'Italien, G Tierney, WM TI Weight gain and new onset diabetes associated with olanzapine and risperidone SO JOURNAL OF GENERAL INTERNAL MEDICINE LA English DT Article; Proceedings Paper CT 156th Annual Meeting of the American-Psychiatric-Association CY MAY 17-22, 2003 CL SAN FRANCISCO, CA SP Amer Psychiat Assoc DE olanzapine; risperidone; diabetes; weight gain; schizophrenia ID ATYPICAL ANTIPSYCHOTICS; UNITED-STATES; BODY-WEIGHT; SCHIZOPHRENIA; MELLITUS; TRENDS; DRUGS AB OBJECTIVE: To assess whether newer antipsychotic medications are associated with weight gain and development of diabetes. DESIGN: Retrospective cohort study. SETTING: Data from a comprehensive electronic medical record serving an urban public hospital and a citywide network of mental health clinics. PATIENTS/PARTICIPANTS; Three thousand one hundred fifteen patients at least 18 years old who were prescribed a single antipsychotic drug for at least 1 year. METHODS: We identified independent predictors of significant weight gain (greater than or equal to7%) and new onset of diabetes mellitus in the first year of antipsychotic drug treatment, using logistic regression adjusted for demographic characteristics, obesity, preexisting psychiatric diagnoses, alcohol and drug abuse, number of primary care, psychiatric clinic, and emergency department visits, and pretreatment weight. MEASUREMENTS AND MAIN RESULTS: Twenty-five percent of patients taking older phenothiazines developed significant weight gain in the first year of treatment compared to 40% of the patients taking olanzapine (adjusted odds ratio [OR], 2.8; 95% confidence interval [CI], 1.7 to 4.6; P <.0001) and 37% of patients taking risperidone (adjusted OR, 2.3; 95% CI, 1.5 to 3.4; P <.0001). New diabetes developed in 3% of patients taking older phenothiazines was new onset diabetes compared to 8.0% of patients taking olanzapine (adjusted OR, 1.9; 95% Cl, 1.1 to 3.3; P =.03) and 3.5% of patients taking risperidone (adjusted OR, 0.7; 95% Cl, 0.4 to 1.4; P =.3). No association was found between significant weight gain and developing diabetes (adjusted OR, 0.7; 95% CI, 0.4 to 1.4; P =.4). CONCLUSIONS: Olanzapine and risperidone use was associated with gaining weight in the first year, but only olanzapine was associated with developing diabetes mellitus. C1 VA Boston Healthcare Syst, Dept Med, Boston, MA USA. Indiana Univ, Sch Med, Dept Med, Indianapolis, IN USA. Bristol Myers Squibb Co, Pharmaceut Res Inst, Wallingford, CT USA. RP Tierney, WM (reprint author), Wishard Mem Hosp, OPW, M200,1001 W 10th St, Indianapolis, IN 46202 USA. EM wtierney@iupui.edu NR 34 TC 37 Z9 39 U1 0 U2 1 PU BLACKWELL PUBLISHING INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 USA SN 0884-8734 J9 J GEN INTERN MED JI J. Gen. Intern. Med. PD DEC PY 2004 VL 19 IS 12 BP 1200 EP 1205 DI 10.1111/j.1525-1497.2004.40126.x PG 6 WC Health Care Sciences & Services; Medicine, General & Internal SC Health Care Sciences & Services; General & Internal Medicine GA 882XF UT WOS:000225973000005 PM 15610330 ER PT J AU Montori, VM Saha, S Clarke, M AF Montori, VM Saha, S Clarke, M TI A call for systematic reviews SO JOURNAL OF GENERAL INTERNAL MEDICINE LA English DT Editorial Material ID RANDOMIZED CONTROLLED-TRIALS; HEALTH-CARE; QUALITY; METAANALYSES; ARTICLE; SCIENCE C1 Mayo Clin, Coll Med, Rochester, MN 55905 USA. Portland VA Med Ctr, Portland, OR USA. Oregon Hlth & Sci Univ, Portland, OR USA. UK Cochrane Ctr, Oxford, England. RP Montori, VM (reprint author), Mayo Clin, Coll Med, Rochester, MN 55905 USA. OI Montori, Victor/0000-0003-0595-2898 NR 16 TC 5 Z9 5 U1 0 U2 0 PU BLACKWELL PUBLISHING INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 USA SN 0884-8734 J9 J GEN INTERN MED JI J. Gen. Intern. Med. PD DEC PY 2004 VL 19 IS 12 BP 1240 EP 1241 DI 10.1111/j.1525-1497.2004.41001.x PG 2 WC Health Care Sciences & Services; Medicine, General & Internal SC Health Care Sciences & Services; General & Internal Medicine GA 882XF UT WOS:000225973000010 PM 15610335 ER PT J AU Ho, CL Walton, DS AF Ho, CL Walton, DS TI Goniosurgery for glaucoma secondary to chronic anterior uveitis - Prognostic factors and surgical technique SO JOURNAL OF GLAUCOMA LA English DT Article; Proceedings Paper CT 14th Annual Meeting of the American-Glaucoma-Society CY MAR 05, 2004 CL Sarasota, FL SP Amer Glaucoma Soc DE goniotomy; uveitis; glaucoma ID JUVENILE RHEUMATOID-ARTHRITIS; CHRONIC CHILDHOOD UVEITIS; INFLAMMATORY GLAUCOMA; GONIOTOMY AB Purpose: To describe the preoperative prognostic factors that correlate with the surgical success of goniosurgery for glaucoma complicating chronic anterior uveitis and to describe the surgical technique. Methods: The medical records of 31 patients with 31 eyes with glaucoma secondary to chronic anterior uveitis for which 38 goniotomy procedures were performed were reviewed. Uveitis etiology, gender, age of onset of iritis, duration of iritis before recognition of glaucoma, duration of iritis and duration of glaucoma until initial goniosurgery, preoperative gonioscopic findings, lens status, surgical outcome, age at initial goniosurgery, duration of postoperative observation, lens status, preoperative and postoperative intraocular pressures, topical steroid, and glaucoma medication use were reviewed. Complete success was defined by an intraocular pressure (IOP) less than or equal to 21 mm Hg, and qualified success as IOP less than or equal to 21 mm Hg with use of glaucoma medications. The surgical technique used to perform the goniosurgery was reviewed. Results: Overall surgical success was achieved in 22 (71%) of 31 eyes. The mean age at surgery was 10.2 +/- 4.2 years (range, 4-21 years). All but 8 patients were female. Mean follow-up interval was 10.3 +/- 6.4 years (range, 1.5-22 years). Significant correlation was found between outcome and age at initial surgery, lens status, duration of glaucoma before goniosurgery, duration of iritis before glaucoma surgery, and hours of peripheral anterior synechia (PAS). The mean number of clock hours of preoperative (PAS) was 0.5 hours in eyes with success versus 2.5 hours in eyes with failure. Age of onset of iritis, duration of iritis before recognition of glaucoma, trabecular meshwork pigmentation (TM), TM opacification, and circumferential ciliary body band narrowing did not correlate with surgical outcome. Conclusion: Goniosurgery is an effective treatment of glaucoma secondary to chronic anterior uveitis. The outcome of surgery was unfavorably influenced by older age, longer duration of glaucoma, and evidence of more advanced preoperative filtration angle abnormalities secondary to uveitis. Goniosurgery for this secondary glaucoma can be successfully performed utilizing the standard goniotomy technique. C1 Harvard Univ, Sch Med, Massachusetts Eye & Ear Infirm, Boston, MA 02114 USA. Singapore Natl Eye Ctr, Singapore, Singapore. RP Walton, DS (reprint author), Harvard Univ, Sch Med, Massachusetts Eye & Ear Infirm, 2 Longfellow Pl,Suite 201, Boston, MA 02114 USA. EM blacki@att.net NR 13 TC 14 Z9 14 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 1057-0829 J9 J GLAUCOMA JI J. Glaucoma PD DEC PY 2004 VL 13 IS 6 BP 445 EP 449 DI 10.1097/01.ijg.0000141368.96950.3c PG 5 WC Ophthalmology SC Ophthalmology GA 873IO UT WOS:000225273300003 PM 15534467 ER PT J AU Zhu, AX Lauwers, GY Tanabe, KK AF Zhu, Andrew X. Lauwers, Gregory Y. Tanabe, Kenneth K. TI Cholangiocarcinoma in association with Thorotrast exposure SO JOURNAL OF HEPATO-BILIARY-PANCREATIC SURGERY LA English DT Article DE Thorotrast; Cholangiocarcinoma AB Thorotrast is a colloidal suspension of thorium dioxide that was used as an intravascular contrast agent until the 1950's. It is retained by the reticuloendothelial system, and because it emits densely ionizing radioactivity thorium dioxide it is carcinogenic. Two patients with prior thorium dioxide exposure diagnosed with cholangiocarcinoma and recently treated at the Massachusetts General Hospital are presented. Radiology, treatment, pathologic findings, and relevant literature are discussed. C1 [Zhu, Andrew X.] Massachusetts Gen Hosp, Dept Hematol Oncol, Boston, MA 02114 USA. [Lauwers, Gregory Y.] Massachusetts Gen Hosp, Dept Pathol, Boston, MA 02114 USA. [Tanabe, Kenneth K.] Massachusetts Gen Hosp, Dept Surg Oncol, Boston, MA 02114 USA. [Zhu, Andrew X.; Lauwers, Gregory Y.; Tanabe, Kenneth K.] Harvard Univ, Sch Med, Boston, MA USA. RP Zhu, AX (reprint author), Massachusetts Gen Hosp, Dept Hematol Oncol, 55 Fruit St, Boston, MA 02114 USA. NR 13 TC 10 Z9 10 U1 1 U2 1 PU SPRINGER TOKYO PI TOKYO PA 1-11-11 KUDAN-KITA, CHIYODA-KU, TOKYO, 102-0073, JAPAN SN 0944-1166 J9 J HEPATO-BILIARY-PAN JI J. Hepato-Biliary-Pancreatic Surg. PD DEC PY 2004 VL 11 IS 6 BP 430 EP 433 DI 10.1007/s00534-004-0924-5 PG 4 WC Gastroenterology & Hepatology; Surgery SC Gastroenterology & Hepatology; Surgery GA V06EW UT WOS:000207177900009 PM 15619021 ER PT J AU Appel, H Kuon, W Kuhne, M Hulsmeyer, M Kollnberger, S Kuhlmann, S Weiss, E Zeitz, M Wucherpfennig, K Bowness, P Sieper, J AF Appel, H Kuon, W Kuhne, M Hulsmeyer, M Kollnberger, S Kuhlmann, S Weiss, E Zeitz, M Wucherpfennig, K Bowness, P Sieper, J TI The solvent-inaccessible Cys(67) residue of HLA-B27 contributes to T cell recognition of HLA-B27/peptide complexes SO JOURNAL OF IMMUNOLOGY LA English DT Article ID PEPTIDE-MHC COMPLEXES; CLASS-I MOLECULES; ANKYLOSING-SPONDYLITIS; REACTIVE ARTHRITIS; 3-DIMENSIONAL STRUCTURE; INVITRO MUTAGENESIS; ANCHOR POSITIONS; HLA-B; BINDING; IDENTIFICATION AB Crystallographic studies have suggested that the cysteine at position 67 (Cys(67)) in the B pocket of the MHC molecule HLA-B*2705 is of importance for peptide binding, and biophysical studies have documented altered thermodynamic stability of the molecule when Cys(67) was mutated to serine (Serb(67)). In this study, we used HLA-B27. Cys(67) and HLA-B27.Ser(67) tetramers with defined T cell epitopes to determine the contribution of this polymorphic, solvent-inaccessible MHC residue to T cell recognition. We generated these HLA-B27 tetramers using immunodominant viral peptides with high binding affinity to HLA-B27 and cartilage-derived peptides with lower affinity. We demonstrate that the yield of refolding of HLA-B27.Ser(67) molecules was higher than for HLA-B27.Cys(67) molecules and strongly dependent on the affinity of the peptide. T cell recognition did not differ between HLAB27.Cys(67) and HLA.B27.Ser(67) tetramers for the viral peptides that were investigated. However, an aggrecan peptide-specific T cell line derived from an HLA-B27 transgenic BALB/c mouse bound significantly stronger to the HLA-B27.Cys(67) tetramer than to the HLA-B27.Ser(67) tetramer. Modeling studies of the molecular structure suggest the loss of a SH...pi hydrogen bond with the Cys-->Ser substitution in the HLA-B27 H chain which reduces the stability of the HLA-B27/peptide complex. These results demonstrate that a solvent-inaccessible residue in the B pocket of HLA-B27 can affect TCR binding in a peptide-dependent fashion. C1 Free Univ Berlin, Charite Berlin, Dept Gastroenterol Infectiol & Rheumatol, Div Gastroenterol Infectiol & Rheumatol, D-1000 Berlin, Germany. Free Univ Berlin, Inst Chem Crystallog, D-1000 Berlin, Germany. Deutsch Rheumaforschungszentrum, Berlin, Germany. John Radcliffe Hosp, Weatherall Inst Mol Med, Med Res Council Human Immunol Unit, Oxford OX3 9DU, England. Univ Munich, Inst Anthropol & Human Genet, D-80539 Munich, Germany. Harvard Univ, Sch Med, Dana Farber Canc Inst, Dept Canc Immunol, Boston, MA 02115 USA. Harvard Univ, Sch Med, Dept Neurol, Boston, MA 02115 USA. RP Appel, H (reprint author), Free Univ Berlin, Charite Berlin, Dept Gastroenterol Infectiol & Rheumatol, Div Gastroenterol Infectiol & Rheumatol, Campus Benjamin Franklin, D-1000 Berlin, Germany. EM heiner.appel@charite.de RI Kuhne, Maren/B-9844-2009 NR 52 TC 12 Z9 12 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 DEC 1 PY 2004 VL 173 IS 11 BP 6564 EP 6573 PG 10 WC Immunology SC Immunology GA 873UV UT WOS:000225307500010 PM 15557146 ER PT J AU Nichols, FC Riep, B Mun, JY Morton, MD Bojarski, MT Dewhirst, FE Smith, MB AF Nichols, FC Riep, B Mun, JY Morton, MD Bojarski, MT Dewhirst, FE Smith, MB TI Structures and biological activity of phosphorylated dihydroceramides of Porphyromonas gingivalis SO JOURNAL OF LIPID RESEARCH LA English DT Article DE phosphoethanolamine ceramide; phosphoglycerol dihydroceramide; interleukin-1 beta; prostaglandin E-2; gival fibroblast; long-chain base; gas chromatography-mass spectrometry; electrospray MS/MS ID ADULT PERIODONTITIS; CERAMIDE; INTERLEUKIN-1-BETA; PHOSPHOLIPIDS; SPHINGOSINE; METABOLISM; EXTRACTION; SECRETION; CELLS AB Porphyromonas gingivalis, a recognized periodontal pathogen, synthesizes free ceramides as well as other phosphorylated ceramide lipids. The purpose of this study was to separate complex lipids of P gingivalis by high-performance liquid chromatography (HPLC) and determine the structures and biological activities of the major ceramide classes. Using gas chromatography-mass spectrometry, electrospray tandem mass spectrometry (ESI-MS/MS) and NMR analyses, three major classes of dihydroceramides were identified in specific HPLC fractions, with all classes containing the same dihydroceramide base structures (3-OH isoC(17:0) in amide linkage to saturated long-chain bases of 17, 18, or 19 carbons). The free dihydroceramide class recovered in HPLC fractions 7-8 revealed little biological activity. HPLC fraction 20 dihydroceramides, substituted with 1-O-phosphoglycerol and isoC(15:0) linked to the hydroxyl of 3-OH isoC(17:0), significantly potentiated interleukin-1beta (IL-1beta)-mediated prostaglandin secretion and produced marked alterations in fibroblast morphology. HPLC fraction 28 dihydroceramides, substituted with 1-O-phosphoethanolamine, demonstrated little capacity to potentiate IL-1beta-mediated prostaglandin secretion. The novel phosphorylated dihydroceramides synthesized by P. gingivalis demonstrate varying biological activities based on the phosphorylated head group substitution and/or the addition of esterified fatty acid. These results also demonstrate the strong virulence capacity of phosphoglycerol dihydroceramides of P gingivalis to promote inflammatory factor secretion from IL-1beta-treated fibroblasts and to produce marked alterations in cell morphology in culture.-Nichols, E C., B. Riep, J. Mun, M. D. Morton, M. T. Bojarski, E E. Dewhirst, and M. B. Smith. Structures and biological activity of phosphorylated dihydroceramides of Porphyromonas gingivalis. C1 Univ Connecticut, Sch Dent Med, Dept Periodontol, Farmington, CT 06032 USA. Univ Med Berlin, Charite, Dept Periodontol & Synopt Dent, Berlin, Germany. Univ Connecticut, Dept Chem, Storrs, CT USA. Forsyth Inst, Dept Mol Genet, Boston, MA USA. RP Nichols, FC (reprint author), Univ Connecticut, Sch Dent Med, Dept Periodontol, 263 Farmington Ave, Farmington, CT 06032 USA. EM nicliols@nso.uchc.edu NR 26 TC 29 Z9 30 U1 0 U2 3 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA SN 0022-2275 J9 J LIPID RES JI J. Lipid Res. PD DEC PY 2004 VL 45 IS 12 BP 2317 EP 2330 DI 10.1194/jlr.M400278-JLR200 PG 14 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA 877VM UT WOS:000225602100017 PM 15466368 ER PT J AU Akella, NS Twieg, DB Mikkelsen, T Hochberg, FH Grossman, S Cloud, GA Nabors, LB AF Akella, NS Twieg, DB Mikkelsen, T Hochberg, FH Grossman, S Cloud, GA Nabors, LB TI Assessment of brain tumor angiogenesis inhibitors using perfusion magnetic resonance imaging: Quality and analysis results of a phase I trial SO JOURNAL OF MAGNETIC RESONANCE IMAGING LA English DT Article DE brain tumors; angiogenesis; dynamic susceptibility contrast enhanced MRI (DSC-MRI); cilengitide; cerebral blood flow (CBF); cerebral blood volume (CBV) ID CEREBRAL BLOOD-FLOW; CONTRAST-ENHANCED MRI; GAMMA-VARIATE; VOLUME MAPS; GD-DTPA; GLIOMAS; GRADE; ECHO; CONSEQUENCES; PERMEABILITY AB Purpose: To determine thresholds of quality for a T2*-weighted perfusion magnetic resonance imaging (MRI) study and evaluate the effects of an angiogenesis inhibitor on relative blood low and volume changes in brain tumor patients in a multi-institution setting. Materials and Methods: A total of 36 volunteers from four participating institutions with clinically diagnosed malignant gliomas were studied using perfusion MRI protocols. These included a baseline study, and follow-up studies every eight weeks to evaluate the effect of an anti-angiogenic agent on tumor perfusion. Quality tests were performed on the perfusion imaging data by defining statistical thresholds of acceptance. Region of interest (ROI) analysis was performed on tumors and kinetic parameters were normalized with respect to normal tissue. Results: Statistical thresholds for goodness of the gamma variate fit, T2* recovery, and mean signal full-width half-minimum (FWHMin) were computed for our data sets with a 99% one-sided confidence interval; these were 6.91%, 79.48%, and 23.35 seconds, respectively. Decreases in-blood volume and flow measurements were observed in patients with documented clinical response. Conclusion: Malignant brain tumors have altered perfusion parameters that may be used to understand and monitor neovascularization. This permits non-invasive assessment of the efficacy of angiogenesis inhibiting drugs. (C) 2004 Wiley-Liss, Inc. C1 Univ Alabama, Dept Neurol, Brain Tumor Treatment & Res Program, Dept Biomed Engn, Birmingham, AL USA. Henry Ford Hosp, Dept Neurol, Hermelin Brain Tumor Ctr, Detroit, MI 48202 USA. CNS, New Approaches Brain Tumor Therapy, Baltimore, MD USA. Harvard Univ, Massachusetts Gen Hosp, Dept Neurol, Boston, MA 02115 USA. Johns Hopkins Univ, Dept Oncol, Baltimore, MD USA. Univ Alabama, Med Stat Sect, Div Hematol Oncol, Birmingham, AL USA. RP Nabors, LB (reprint author), Univ Alabama, Dept Neurol, Brain Tumor Treatment & Res Program, Dept Biomed Engn, 510 20th St S,FOT 1020, Birmingham, AL USA. EM bnabors@uab.edu FU NCI NIH HHS [R21 CA091560]; NCRR NIH HHS [RR00032UABGCRC] NR 36 TC 59 Z9 62 U1 1 U2 3 PU JOHN WILEY & SONS INC PI HOBOKEN PA 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 1053-1807 J9 J MAGN RESON IMAGING JI J. Magn. Reson. Imaging PD DEC PY 2004 VL 20 IS 6 BP 913 EP 922 DI 10.1002/jmri.20202 PG 10 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA 874CJ UT WOS:000225328200002 PM 15558578 ER PT J AU Steffens, S Tebbets, J Kramm, CM Lindemann, D Flake, A Sena-Esteves, M AF Steffens, S Tebbets, J Kramm, CM Lindemann, D Flake, A Sena-Esteves, M TI Transduction of human glial and neuronal tumor cells with different lentivirus vector pseudotypes SO JOURNAL OF NEURO-ONCOLOGY LA English DT Article DE 10A1; gene therapy; glial; human foamy virus; LCMV; lentivirus; Mokola; murine leukemia virus; neuronal; pseudotyping; rabies; VSV-G ID EFFICIENT GENE-TRANSFER; IN-VIVO; RETROVIRAL VECTORS; NONDIVIDING CELLS; HIGH-TITER; EXPRESSION; GLYCOPROTEIN; DELIVERY; LYMPHOCYTES; INJECTION AB Lentiviral vectors have proven to be valuable tools for in vitroand in vivo gene delivery because they can transduce dividing and non-dividing cells efficiently, and mediate long-term gene expression. Pseudotyping of lentiviral vectors with envelope proteins other than VSV-G has resulted in enhanced transduction of certain cell types and tissues. In order to improve lentiviral vector-based gene therapy for peripheral neuroectodermal and brain tumors, we compared the efficiency of eight different lentivirus pseudotypes in transducing neuronal and glial tumor cell lines. Here, lentiviral vectors pseudotyped with the envelopes from human foamy virus, rabies, Mokola or amphotropic murine leukemia virus displayed the highest transduction efficiency in neuroblastomas, whereas pseudotyping with the lymphocytic choriomeningitis virus glycoprotein from strain Armstrong 53b resulted in the highest transduction efficiency in gliomas. C1 Childrens Hosp Philadelphia, Abramson Res Ctr, Dept Surg, Philadelphia, PA 19104 USA. Univ Dusseldorf, Univ Childrens Hosp, Dept Pediat Oncol, D-4000 Dusseldorf, Germany. Tech Univ Dresden, Inst Virol, D-8027 Dresden, Germany. RP Sena-Esteves, M (reprint author), Massachusetts Gen Hosp, Dept Neurol, Blgd 149,13th St,Room 6309, Charlestown, MA 02129 USA. EM msesteves@partners.org RI Lindemann, Dirk/H-5857-2013 OI Lindemann, Dirk/0000-0002-0320-4223 NR 27 TC 18 Z9 18 U1 0 U2 3 PU KLUWER ACADEMIC PUBL PI DORDRECHT PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS SN 0167-594X J9 J NEURO-ONCOL JI J. Neuro-Oncol. PD DEC PY 2004 VL 70 IS 3 BP 281 EP 288 DI 10.1007/s11060-004-6046-8 PG 8 WC Oncology; Clinical Neurology SC Oncology; Neurosciences & Neurology GA 882UC UT WOS:000225963000002 PM 15662969 ER PT J AU Manoach, DS Lindgren, KA Barton, JJS AF Manoach, DS Lindgren, KA Barton, JJS TI Deficient saccadic inhibition in Asperger's disorder and the social-emotional processing disorder SO JOURNAL OF NEUROLOGY NEUROSURGERY AND PSYCHIATRY LA English DT Article ID POSITRON-EMISSION-TOMOGRAPHY; NONVERBAL LEARNING-DISABILITIES; HIGH-FUNCTIONING AUTISM; SPATIAL WORKING-MEMORY; RIGHT-HEMISPHERE; EYE-MOVEMENTS; LOBE LESIONS; FRONTAL-LOBE; ANTISACCADES; DYSFUNCTION AB Background: Both Asperger's disorder and the social-emotional processing disorder (SEPD), a form of non-verbal learning disability, are associated with executive function deficits. SEPD has been shown to be associated with deficient saccadic inhibition. Objective: To study two executive functions in Asperger's disorder and SEPD, inhibition and task switching, using a single saccadic paradigm. Methods: 22 control subjects and 27 subjects with developmental social processing disorders-SEPD, Asperger's disorder, or both syndromes-performed random sequences of prosaccades and anti-saccades. This design resulted in four trial types, prosaccades and antisaccades, that were either repeated or switched. The design allowed the performance costs of inhibition and task switching to be isolated. Results: Subjects with both Asperger's disorder and SEPD showed deficient inhibition, as indicated by increased antisaccade errors and a disproportionate increase in latency for antisaccades relative to prosaccades. In contrast, task switching error and latency costs were normal and unrelated to the costs of inhibition. Conclusions: This study replicates the finding of deficient saccadic inhibition in SEPD, extends it to Asperger's disorder, and implicates prefrontal cortex dysfunction in these syndromes. The finding of intact task switching shows that executive function deficits in Asperger's disorder and SEPD are selective and suggests that inhibition and task switching are mediated by distinct neural networks. C1 Harvard Univ, Sch Med, Massachusetts Gen Hosp, Dept Psychiat, Boston, MA 02129 USA. Harvard Univ, Sch Med, Massachusetts Gen Hosp, Athinoula A Martinos Ctr Biomed Imaging, Boston, MA 02129 USA. Beth Israel Deaconess Med Ctr, Dept Neurol, Boston, MA 02215 USA. RP Manoach, DS (reprint author), Harvard Univ, Sch Med, Massachusetts Gen Hosp, Dept Psychiat, Charlestown Navy Yard,36 1st Ave,Room 420, Boston, MA 02129 USA. EM dara@nmr.mgh.harvard.edu RI Barton, Jason/A-6362-2012 FU NIMH NIH HHS [K23MH01829]; NINDS NIH HHS [K08NS01920-01A1] NR 60 TC 14 Z9 14 U1 1 U2 4 PU B M J PUBLISHING GROUP PI LONDON PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND SN 0022-3050 J9 J NEUROL NEUROSUR PS JI J. Neurol. Neurosurg. Psychiatry PD DEC PY 2004 VL 75 IS 12 BP 1719 EP 1726 DI 10.1136/jnnp.2003.025981 PG 8 WC Clinical Neurology; Psychiatry; Surgery SC Neurosciences & Neurology; Psychiatry; Surgery GA 871UZ UT WOS:000225162400018 PM 15548490 ER PT J AU Mendez, ME O'Connor, SM Lim, GTH AF Mendez, ME O'Connor, SM Lim, GTH TI Hypersexuality after right pallidotomy for Parkinson's disease SO JOURNAL OF NEUROPSYCHIATRY AND CLINICAL NEUROSCIENCES LA English DT Article ID SEXUAL-BEHAVIOR; DOPAMINE AB The authors describe hypersexuality following atypical right pallidotomy for intractable Parkinson's disease (PD). This patient and literature review suggest important roles for the pallidum in sexual behavior and dopamine in sexual arousal. C1 Univ Calif Los Angeles, Dept Neurol, Los Angeles, CA 90024 USA. Univ Calif Los Angeles, Dept Psychiat & Biobehav Sci, Los Angeles, CA 90024 USA. RP Mendez, ME (reprint author), VA Greater LA Healthcare Syst, Neurobehav Unit 116AF, 11301 Wilshire Blvd, Los Angeles, CA 90073 USA. EM mmendez@UCLA.edu NR 16 TC 29 Z9 29 U1 0 U2 3 PU AMER PSYCHIATRIC PRESS, INC PI ARLINGTON PA 1000 WILSON BOULEVARD, STE 1825, ARLINGTON, VA 22209-3901 USA SN 0895-0172 J9 J NEUROPSYCH CLIN N JI J. Neuropsychiatr. Clin. Neurosci. PD WIN PY 2004 VL 16 IS 1 BP 37 EP 40 DI 10.1176/appi.neuropsych.16.1.37 PG 4 WC Clinical Neurology; Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA 777PM UT WOS:000189186800005 PM 14990757 ER PT J AU Kimble, M Ruddy, K Deldin, P Kaufman, M AF Kimble, M Ruddy, K Deldin, P Kaufman, M TI A CNV-distraction paradigm in combat veterans with posttraumatic stress disorder SO JOURNAL OF NEUROPSYCHIATRY AND CLINICAL NEUROSCIENCES LA English DT Article ID CONTINGENT NEGATIVE-VARIATION; HUMAN BRAIN; SCHIZOPHRENICS; ASSOCIATION; POTENTIALS; ATTENTION; RESPONSES AB Fourteen veterans with posttraumatic stress disorder (PTSD) and 14 without PTSD participated in a contingent negative variation (CNV)-distraction paradigm. Subjects were instructed to press a button after hearing a high-pitched tone (S2) preceded by a low-pitched tone (S1). One-half of the trials included a white-noise distracter placed in the S1-S2 interval. Posttraumatic stress disorder subjects had larger frontal, but smaller central and parietal CNVs, regardless of condition (distracter, no distracter) or epoch (early CNV, late, CNV). In PTSD subjects, the N1/P2 complex was smaller to warning (S1) and distracter stimuli and did not show the extent of facilitation present in non-PTSD subjects. Findings highlight PTSD-related differences in phasic cortical excitability and attention. C1 Univ Wales, Sch Psychol, Bangor LL57 2AS, Gwynedd, Wales. Boston Univ, Sch Med, Natl Ctr PTSD, VA Boston Healthcare Syst Behav Sci Div, Boston, MA 02118 USA. Harvard Univ, Dept Psychol, Boston, MA 02115 USA. RP Kimble, M (reprint author), Univ Wales, Sch Psychol, Bangor LL57 2AS, Gwynedd, Wales. EM M.Kimble@bangor.ac.uk FU NIMH NIH HHS [R29 MH58215] NR 23 TC 6 Z9 6 U1 1 U2 3 PU AMER PSYCHIATRIC PRESS, INC PI ARLINGTON PA 1000 WILSON BOULEVARD, STE 1825, ARLINGTON, VA 22209-3901 USA SN 0895-0172 J9 J NEUROPSYCH CLIN N JI J. Neuropsychiatr. Clin. Neurosci. PD WIN PY 2004 VL 16 IS 1 BP 102 EP 108 DI 10.1176/appi.neuropsych.16.1.102 PG 7 WC Clinical Neurology; Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA 777PM UT WOS:000189186800013 PM 14990765 ER PT J AU Offner, H AF Offner, H TI Neuroimmunoprotective effects of estrogen and derivatives in experimental autoimmune encephalomyelitis: Therapeutic implications for multiple sclerosis SO JOURNAL OF NEUROSCIENCE RESEARCH LA English DT Review DE estrogen; estrogen receptors; immunoregulation; neuroprotection; EAE; multiple sclerosis ID REGULATORY T-CELLS; EXPERIMENTAL ALLERGIC ENCEPHALOMYELITIS; CENTRAL-NERVOUS-SYSTEM; IMMUNOLOGICAL SELF-TOLERANCE; MYELIN PROTEOLIPID PROTEIN; CD4(+)CD25(+) TREG CELLS; RECEPTOR-ALPHA; ER-BETA; CYTOKINE PRODUCTION; GENE-EXPRESSION AB The extensive literature and the work from our laboratory illustrate the large number of complex processes affected by estrogen that might contribute to the striking ability of 17beta-estradiol (E2) and its derivatives to inhibit clinical and histological signs of experimental autoimmune encephalomyelitis (EAE) in mice. These effects require sustained exposure to relatively low doses of exogenous hormone and offer better protection when initiated prior to induction of EAE. However, oral ethinyl estradiol (EE) and fluasterone, which lacks estrogenic side effects, could partially reverse clinical EAE when given after the onset of disease. The three main areas discussed in this review include E2-mediated inhibition of encephalitogenic T cells, inhibition of cell migration into central nervous system tissue, and neuroprotective effects that promote axon and myelin survival. E2 effects on EAE were mediated through Esrl (alpha receptor for E2) but not Esr2 (beta receptor for E2), as were its antiinflammatory and neuroprotective effects. A novel finding is that E2 up-regulated the expression of Foxp3 and CTLA-4 that contribute to the activity of CD4(+)CD25(+) Treg cells. The protective effects of E2 in EAE suggest its use as therapy for MS, although the risk of cardiovascular disease may complicate treatment in postmenopausal women. This risk could be minimized by using subpregnancy levels of exogenous E2 that produced synergistic effects when used in combination another immunoregulatory therapy. Alternatively, one might envision using EE or fluasterone metabolites alone or in combination therapies in both male and female MS patients. (C) 2004 Wiley-Liss, Inc. C1 Portland VA Med Ctr, Neuroimmunol Res R&D 31, Portland, OR 97239 USA. Oregon Hlth Sci Univ, Dept Neurol, Portland, OR 97201 USA. RP Offner, H (reprint author), Portland VA Med Ctr, Neuroimmunol Res R&D 31, 3710 SW US Vet Hosp Rd, Portland, OR 97239 USA. EM offnerva@ohsu.edu FU NIAID NIH HHS [AI42376]; NINDS NIH HHS [NS23444] NR 162 TC 58 Z9 61 U1 0 U2 2 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 0360-4012 J9 J NEUROSCI RES JI J. Neurosci. Res. PD DEC 1 PY 2004 VL 78 IS 5 BP 603 EP 624 DI 10.1002/jnr.20330 PG 22 WC Neurosciences SC Neurosciences & Neurology GA 875JS UT WOS:000225417000001 PM 15515048 ER PT J AU El Fakhri, G Kijewski, MF Albert, MS Johnson, KA Moore, SC AF El Fakhri, G Kijewski, MF Albert, MS Johnson, KA Moore, SC TI Quantitative SPECT leads to improved performance in discrimination tasks related to prodromal Alzheimer's disease SO JOURNAL OF NUCLEAR MEDICINE LA English DT Article DE quantitative brain SPECT; prodromal Alzheimer's disease; iterative reconstruction; attenuation correction; scatter correction; resolution recovery ID MAXIMUM-LIKELIHOOD-ESTIMATION; EMISSION COMPUTED-TOMOGRAPHY; MAGNETIC-RESONANCE; ATTENUATION CORRECTION; ENTORHINAL CORTEX; TEMPORAL-LOBE; SCATTER; BRAIN; COMPENSATION; HIPPOCAMPUS AB We investigated the impact of the quantitation and reconstruction protocol on clinical tasks. The performance of standard clinical reconstruction procedures in discrimination tasks related to the diagnosis of prodromal Alzheimer's disease (AD) was compared with the performance of a quantitative approach incorporating improved corrections for scatter, attenuation, intrinsic spatial resolution, and distance-dependent spatial resolution. Methods: Seventeen normal controls (normal group), 56 subjects who did not have dementia, who did have memory problems, but who did not develop AD within 5 y of follow-up (questionable group), and 27 subjects who did not have dementia, who did have memory problems, and who did develop AD over the follow-up period (converter group) were considered in this study. Tc-99m-hexamethylpropyleneamine oxime SPECT and MRI studies were performed for each subject at baseline. The standard quantitation protocol (STD), routinely used in our clinic, consisted of Compton window scatter correction followed by filtered backprojection with attenuation correction using a uniform attenuation map. In the improved quantitative approach (QUAN), projections were corrected for scatter by use of a general spectral method and reconstructed by use of ordered-subset(s) expectation maximization, incorporating corrections for collimator response and attenuation using both a uniform attenuation map (QUANunif) and a nonuniform attenuation map (QUANnonunif). Mean SPECT activity concentration and MRI volume were estimated for 7 structures: rostral anterior cingulate gyrus, caudal anterior cingulate gyrus, posterior cingulate gyrus, hippocampus, basal forebrain, amygdala, and the banks of the superior temporal sulcus. Data were analyzed by pairwise discriminant analysis, and performance in binary group discrimination was measured by correlated receiver-operating-characteristic analysis. Results: The use of QUANnonunif yielded a small but systematic improvement in discrimination accuracy for normal versus converter groups (accuracy or area under the receiver-operating-characteristic curve [Az], 0.965), normal versus questionable groups (Az, 0.973), and questionable versus converter groups (Az, 0.881) compared with the results obtained with QUANunif (Az, 0.955, 0.962, and 0.866, respectively). Discrimination performance was significantly lower (P < 0.05) with STD than with QUAN in all 3 tasks (Az with STD, 0.906, 0.878, and 0.768, respectively). MRI volume estimation led to a lower overall performance in all 3 tasks than did QUANnonunif (Az with MRI, 0.947, 0.917, and 0.872, respectively). Conclusion: Improved quantitative image reconstruction with accurate compensation for scatter, attenuation, and variable collimator response led to significantly better performance in discrimination tasks related to the diagnosis of prodromal AD than did standard clinical reconstruction procedures. The use of a nonuniform brain attenuation map yields a small improvement in discrimination accuracy. C1 Brigham & Womens Hosp, Dept Radiol, Boston, MA 02115 USA. Harvard Univ, Sch Med, Dept Radiol, Boston, MA 02115 USA. Johns Hopkins Univ, Sch Med, Div Cognit Neurosci, Baltimore, MD 21218 USA. Massachusetts Gen Hosp, Dept Radiol, Boston, MA 02114 USA. RP El Fakhri, G (reprint author), Brigham & Womens Hosp, Dept Radiol, 75 Francis St, Boston, MA 02115 USA. EM elfakhri@bwh.harvard.edu FU NIA NIH HHS [P01-AG4953]; NIBIB NIH HHS [R01-EB001989, R01 EB000802, R01-EB000802] NR 34 TC 10 Z9 11 U1 0 U2 5 PU SOC NUCLEAR MEDICINE INC PI RESTON PA 1850 SAMUEL MORSE DR, RESTON, VA 20190-5316 USA SN 0161-5505 J9 J NUCL MED JI J. Nucl. Med. PD DEC PY 2004 VL 45 IS 12 BP 2026 EP 2031 PG 6 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA 882GL UT WOS:000225927200011 PM 15585477 ER PT J AU Takesaka, J Crowley, R Casarett, D AF Takesaka, J Crowley, R Casarett, D TI What is the risk of distress in palliative care survey research? SO JOURNAL OF PAIN AND SYMPTOM MANAGEMENT LA English DT Article DE distress; end-of-life care; research methods ID GOOD DEATH; FAMILY MEMBERS; PERCEPTIONS; EXPERIENCE; QUALITY; HOSPICE; LIFE AB To determine whether caregivers believe that interviews about end-of-life care are distressing and to identify patient and respondent characteristics associated with an increased risk of distress, distress was assessed in four studies that used family interviews. The setting was four rhledicare certified hospice organizations, the University of Pennsylvania Memory Disorders Clinic, and two nursing homes, and participants included 296 family members of seriously ill or recently deceased patients. For three of the studies, respondents described their distress on, a 5-point scale. Distress was reported as either present or absent in the fourth study. Sixty-four respondents (22%) reported experiencing distress. Intensity of distress was higher for younger respondents (Spearman rho -0.16; P = 0.013), younger patients (Spearman rho -0.28; P < 0.001), and family members of patients with cancer (mean. 0.55 vs. 0.24; Rank sum test P < 0.001). In a multivariable model, after adjusting for study population, younger patient age and cancer diagnosis were independently associated with the severity of distress. Sensitive questions about death and dying are unlikely to cause distress for family members. Although the likelihood of distress is low overall, investigators recruiting from these populations may improve the research by incorporating methods to assess and manage distress. (C) 2004 U.S. Cancer Pain Relief Committee. Published by Elsevier Inc. All rights reserved. C1 Univ Penn, Div Geriatr Med, Philadelphia, PA 19104 USA. Univ Penn, VA Ctr Hlth Equ Res & Promot, Philadelphia, PA 19104 USA. Univ Penn, Ctr Bioeth, Philadelphia, PA 19104 USA. Univ Penn, Leonard Davis Inst Hlth Econ, Philadelphia, PA 19104 USA. RP Casarett, D (reprint author), 3615 Chestnut St, Philadelphia, PA 19104 USA. NR 25 TC 21 Z9 21 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0885-3924 J9 J PAIN SYMPTOM MANAG JI J. Pain Symptom Manage. PD DEC PY 2004 VL 28 IS 6 BP 593 EP 598 DI 10.1016/j.jpainsymman.2004.03.006 PG 6 WC Health Care Sciences & Services; Medicine, General & Internal; Clinical Neurology SC Health Care Sciences & Services; General & Internal Medicine; Neurosciences & Neurology GA 885IJ UT WOS:000226150000012 PM 15589084 ER PT J AU Maldonado, A He, L Game, BA Nareika, A Sanders, JJ London, SD Lopes-Virella, MF Huang, Y AF Maldonado, A He, L Game, BA Nareika, A Sanders, JJ London, SD Lopes-Virella, MF Huang, Y TI Pre-exposure to high glucose augments lipopolysaccharide-stimulated matrix metalloproteinase-1 expression by human U937 histiocytes SO JOURNAL OF PERIODONTAL RESEARCH LA English DT Article DE diabetes mellitus; gene expression; glucose; lipopolysaccharide; macrophages; matrix metalloproteinases; periodontal diseases; signal transduction ID ACTIVATED PROTEIN-KINASES; DIABETES-MELLITUS; GENE-EXPRESSION; P38; PERIODONTITIS; INDUCTION; COMPLICATIONS; COLLAGENASE; INHIBITOR; CYTOKINE AB Background and objectives: It has been well established that patients with diabetes have increased prevalence and severity of periodontal diseases. However, the underlying mechanisms are not well understood. Given that bacterial infection is the primary cause of periodontal disease, we postulated that hyperglycemia may interplay with bacterial virulence factors such as lipopolysaccharide to up-regulate matrix metalloproteinase (MMP), leading to increased periodontal tissue destruction. Methods and results: We showed that prolonged pre-exposure of U937 histiocytes to high glucose markedly increased lipopolysaccharide-stimulated MMP-1 secretion and mRNA expression. Our results also showed that the effect of high glucose on lipopolysaccharide-induced MMP-1 expression is cell type-specific because no similar response was observed in human gingival fibroblasts. In addition to MMP-1, high glucose also augments lipopolysaccharide-stimulated MMP-7, -8, and -9 mRNA expression. In the investigation of the signaling pathways involved in the enhancement of lipopolysaccharide-induced MMP-1 expression by high glucose, we found that both high glucose and lipopolysaccharide regulate MMP-1 expression through the nuclear factor kappaB (NFkappaB) and mitogen-activated protein kinase (MAPK) cascades. Conclusions: The present study has shown that pre-exposure to high glucose and subsequent lipopolysaccharide treatment synergistically stimulates MMP-1 expression by mononuclear phagocytes through the NFkappaB and MAPK signaling pathways. This study has thus delineated a pathogenic mechanism that may be involved in the exacerbated periodontal disease in diabetic patients. C1 Med Univ S Carolina, Dept Med, Div Endocrinol Diabet & Med Genet, Charleston, SC 29425 USA. Med Univ S Carolina, Coll Dent Med, Charleston, SC 29425 USA. Ralph H Johnson Vet AFfairs Med Ctr, Charleston, SC 29401 USA. RP Huang, Y (reprint author), Ralph H Johnson Vet Affairs Med Ctr, 114 Doughty St, Charleston, SC 29403 USA. EM huangyan@musc.edu NR 29 TC 20 Z9 23 U1 0 U2 4 PU BLACKWELL MUNKSGAARD PI COPENHAGEN PA 35 NORRE SOGADE, PO BOX 2148, DK-1016 COPENHAGEN, DENMARK SN 0022-3484 J9 J PERIODONTAL RES JI J. Periodont. Res. PD DEC PY 2004 VL 39 IS 6 BP 415 EP 423 DI 10.1111/j.1600-0765.2004.00756.x PG 9 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA 871VK UT WOS:000225164500007 PM 15491346 ER PT J AU Sasaki, H Okamatsu, Y Kawai, T Kent, R Taubman, M Stashenko, P AF Sasaki, H Okamatsu, Y Kawai, T Kent, R Taubman, M Stashenko, P TI The interleukin-10 knockout mouse is highly susceptible to Porphyromonas gingivalis-induced alveolar bone loss SO JOURNAL OF PERIODONTAL RESEARCH LA English DT Article DE alveolar bone loss; animal model; interleukin-10; Porphyromonas gingivalis ID NITRIC-OXIDE SYNTHASE; TUMOR-NECROSIS-FACTOR; RESORPTION IN-VIVO; CD4(+) T-CELLS; CHRONIC ENTEROCOLITIS; EXPERIMENTAL PERIODONTITIS; RHEUMATOID-ARTHRITIS; ESTROGEN DEFICIENCY; GAMMA-INTERFERON; IFN-GAMMA AB Objective: Interleukin-10 is an anti-inflammatory cytokine that reduces periapical bone loss, but its role in periodontal bone loss is unclear. In the present study, we tested the hypothesis that endogenous interleukin-10 is a potent suppressor of Porphyromonas gingivalis-induced alveolar bone loss in vivo. Methods: Interleukin-10 knockout (-/-) and wild-type mice were inoculated intraorally with P. gingivalis. Non-infected animals served as negative controls. Alveolar bone loss, gingival cytokine levels, and gingival gene expression were assessed using morphometric analysis, enzyme-linked immunosorbent assay (ELISA), and semiquantitative reverse transcription polymerase chain reaction (RT-PCR), respectively. Results: P. gingivalis-infected interleukin-10(-/-) mice exhibited severe alveolar bone loss compared to non-infected interleukin-10(-/-) and wild-type mice by day 42. Surprisingly, bone resorptive cytokines interleukin-lot and tumor necrosis factor alpha (TNF-alpha) were not up-regulated in gingival tissues by P. gingivalis-infection. Although interleukin-1beta was marginally increased, blockade of both interleukin-1 isoforms or interleukin-1 receptor type I with neutralizing antisera failed to reduce alveolar bone loss in interleukin-10(-/-) mice, indicating the operation of an interleukin-1-independent mechanism. No strong correlations between bone loss and other cytokines was observed, although interferon gamma (IFNgamma), interleukin-6, interleukin-4, and prostaglandin E-2 were modestly up-regulated in infected interleukin-10(-/-) mice. P. gingivalis infection reduced the expression of cell markers in gingival tissue on days 7 and 14 in both interleukin-10(-/-) and wild-type animals, suggestive of bacteria-induced cytotoxicity or apoptosis. This was followed by up-regulated expression of receptor activator of nuclear factor kappa B ligand (RANKL) and CD40 ligand (CD40L on days 28 and 70 in infected interleukin-10(-/-) mice only. Conclusion: The interleukin-10(-/-) mouse is highly susceptible to bone loss induced by the periodontal pathogen P. gingivalis, which is mediated via an interleukin-1-independent pathway. C1 Forsyth Inst, Dept Cytokine Biol, Boston, MA 02115 USA. Forsyth Inst, Dept Immunol, Boston, MA 02115 USA. Forsyth Inst, Dept Biostat, Boston, MA 02115 USA. Showa Univ, Sch Dent, Dept Periodontol, Tokyo 142, Japan. RP Stashenko, P (reprint author), Forsyth Inst, Dept Cytokine Biol, 140 The Fenway, Boston, MA 02115 USA. EM pstashenko@forsyth.org FU NIDCR NIH HHS [DE-09018, DE-014551, DE-015888, DE-03420, DE-13747] NR 51 TC 77 Z9 79 U1 0 U2 4 PU BLACKWELL MUNKSGAARD PI COPENHAGEN PA 35 NORRE SOGADE, PO BOX 2148, DK-1016 COPENHAGEN, DENMARK SN 0022-3484 J9 J PERIODONTAL RES JI J. Periodont. Res. PD DEC PY 2004 VL 39 IS 6 BP 432 EP 441 DI 10.1111/j.1600-0765.2004.00760.x PG 10 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA 871VK UT WOS:000225164500009 PM 15491348 ER PT J AU Copeland, LB Krall, EA Brown, LJ Garcia, RI Streckfus, CF AF Copeland, LB Krall, EA Brown, LJ Garcia, RI Streckfus, CF TI Predictors of tooth loss in two US adult populations SO JOURNAL OF PUBLIC HEALTH DENTISTRY LA English DT Article DE tooth loss; epidemiology; aging; dental caries; periodontal disease; longitudinal studies; cohort studies ID UNITED-STATES; RISK-FACTORS; BONE LOSS; DISEASE; OLDER AB Objectives: This study determines tooth loss rate over a 10-year period and identifies predictors of tooth loss in two separate US adult longitudinal study populations. Methods: Subjects from the Baltimore Longitudinal Study of Aging (BLSA), consisting of 4 7 men and 4 7 women, ages ranging from 30 to 69 years, were compared to subjects from the VA Dental Longitudinal Study (VADLS) in Boston, MA, consisting of 481 men in the same age range. Baseline and follow-up examinations were performed on each cohort over a 10-year period. Using multivariate regression models, significant predictors of tooth loss were identified. Results: A mean rate of tooth loss of 1.5 teeth lost per 10 years was noted in the VADLS cohort compared to 0.6 teeth lost per 10 years in the BLSA (P < .001). Combining subjects from both populations, significant predictors of tooth loss were baseline values of., percent of teeth with restorations, mean probing pocket depth score, age, tobacco use, alcohol consumption, number of teeth present, and male sex. However, the set of significant predictor variables differed between the two populations and sexes. In BLSA men, number of teeth present, percent of teeth with restorations, mean probing pocket depth score, and alcohol consumption, but not age, were significant, while in BLSA women, only age was a significant predictor. Conclusions: Over a 10-year period, the incidence of tooth loss, the rates of tooth loss, and the predictors of tooth loss were found to vary by population and by sex. These results illustrate the limits of generalizing tooth loss findings across different study cohorts and indicate that there may exist important differences in risk factors for tooth loss among US adult populations. C1 Boston Univ, Goldman Sch Dent Med, Boston, MA 02118 USA. Univ Mississippi, Med Ctr, Sch Dent, University, MS 38677 USA. VA Boston Healthcare Syst, Massachusetts Vet Epidemiol Res & Informat Ctr, Boston, MA USA. Amer Dent Assoc, Hlth Policy Resources Ctr, Chicago, IL USA. RP Garcia, RI (reprint author), Boston Univ, Goldman Sch Dent Med, 715 Albany St,560,3rd Floor, Boston, MA 02118 USA. EM rig@bu.edu FU NIDCR NIH HHS [K24 DE00419] NR 23 TC 56 Z9 57 U1 3 U2 3 PU AAPHD NATIONAL OFFICE PI PORTLAND PA 3760 SW LYLE COURT, PORTLAND, OR 97221 USA SN 0022-4006 J9 J PUBLIC HEALTH DENT JI J. Public Health Dent. PD WIN PY 2004 VL 64 IS 1 BP 31 EP 37 DI 10.1111/j.1752-7325.2004.tb02723.x PG 7 WC Dentistry, Oral Surgery & Medicine; Public, Environmental & Occupational Health SC Dentistry, Oral Surgery & Medicine; Public, Environmental & Occupational Health GA 804HT UT WOS:000220290500006 PM 15078059 ER PT J AU Wood, KB Mehbod, AA AF Wood, KB Mehbod, AA TI Operative treatment for coccygodynia SO JOURNAL OF SPINAL DISORDERS & TECHNIQUES LA English DT Article DE coccyx; coccygodynia; coccygectomy; injection ID COCCYDYNIA; COCCYGECTOMY; ETIOLOGY; COCCYX AB Objective: Few data exist comparing the surgical and nonsurgical treatment of coccygodynia. We sought to retrospectively review our experience with coccygectomy compared with injections for the relief of coccygodynia to determine rates of success and patient satisfaction and identify complications. Methods: From March 1993 to January 2002, 51 consecutive patients with the diagnosis of coccygodynia were evaluated. All of the patients complained of pain while sitting and had localized pain to external and internal palpation of the coccyx on physical examination. Nonoperative treatment (medications, cushions, therapy) had failed to relieve the patients' symptoms. All patients were seen in follow-up for physical examination and completed a questionnaire by an independent examiner. Follow-up of the patients was 26 months (range 12-59 months). Follow-up data were available on 45 of the 51 enrolled. The patients were divided as follows: 20 patients were treated with total coccygectomy and 25 patients were treated with injection therapy. Results: Of those treated operatively, 18 patients (90%) felt improved and were satisfied with the procedure. Two patients felt their symptoms to be unchanged and were dissatisfied. Postoperative complications included seven wound problems: four superficial infections and three patients with persistent drainage. All resolved with local wound care and oral antibiotics. No further surgery was necessary. There were no bowel injuries and no reports of sphincter problems. Of those treated with injections, 5 of the 25 (20%) felt improvement and were satisfied. Sixteen (64%) were not improved, and four (16%) felt worse. Five (20%) eventually were treated with coccygectomy, four with satisfactory relief in symptoms. Conclusions: Despite the potential for wound problems, coccygectomy for relief of coccygodynia can be a safe and effective treatment option with a high patient satisfaction rate. Wound closure and postoperative wound care are of utmost importance. C1 Massachusetts Gen Hosp, Dept Orthopaed Surg, Wang Ambulatory Care Ctr, Boston, MA 02114 USA. Twin Cities Spine Ctr, Minneapolis, MN USA. RP Wood, KB (reprint author), Massachusetts Gen Hosp, Dept Orthopaed Surg, Wang Ambulatory Care Ctr, 15 Parkman St,Suite 503, Boston, MA 02114 USA. EM kbwood@partners.org NR 22 TC 14 Z9 15 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 1536-0652 J9 J SPINAL DISORD TECH JI J. Spinal Disord. Tech. PD DEC PY 2004 VL 17 IS 6 BP 511 EP 515 DI 10.1097/01.bsd.0000128691.36652.16 PG 5 WC Clinical Neurology; Orthopedics SC Neurosciences & Neurology; Orthopedics GA 878UY UT WOS:000225673800008 PM 15570123 ER PT J AU Chang, ALS Agredano, YZ Kimball, AB AF Chang, ALS Agredano, YZ Kimball, AB TI Risk factors associated with striae gravidarum SO JOURNAL OF THE AMERICAN ACADEMY OF DERMATOLOGY LA English DT Article; Proceedings Paper CT 65th Annual Meeting of the Society-for-Investigative-Dermatology CY APR 28-MAY 01, 2004 CL Providence, RI SP Soc Investigat Dermatol ID STRETCH MARKS; LASER AB Background: Striae gravidarum (SG) is a poorly characterized but common disfiguring condition of pregnancy. Objective: To better characterize the epidemiological factors associated with SG. Methods: An anonymous survey administered at Stanford Ambulatory Clinics sampled 161 women who had given birth. Results: Forty-eight-point-three percent of women with SG (43/89) versus 19.4% without SG (14/72) reported mothers with SG (odds ratio = 7.0, 95% confidence interval [CI] 2.7, 18.6). Forty-seven percent of women with SG (42/89 women) versus 18.1% without SG (13/72) reported additional relatives with SG (odds ratio = 7.2, 95% CI 2.9, 18.2). Eighty-one percent of women with SG (68/84) versus 30.5% without SG (18/59) reported a history of breast or thigh striae (odds ratio = 8.6, 95% CI 3.8, 19.9). Forty-seven percent of women with SG versus 17% without SG were non-white (odds ratio = 4.2, 95% CI 1.9, 9.6). Conclusion: This study suggests that a history of breast or thigh striae, family history, and race is significantly predictive of SG development. C1 Massachusetts Gen Hosp, Dermatol Clin Studies Unit, Boston, MA 02115 USA. Brigham & Womens Hosp, Dermatol Clin Studies Unit, Boston, MA 02115 USA. Stanford Univ, Sch Med, Dept Dermatol, Stanford, CA 94305 USA. RP Kimball, AB (reprint author), Massachusetts Gen Hosp, Dermatol Clin Studies Unit, 221 Longwood Ave,1st Floor, Boston, MA 02115 USA. EM harvardskinstudies@partners.org NR 14 TC 47 Z9 48 U1 0 U2 1 PU MOSBY, INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 USA SN 0190-9622 J9 J AM ACAD DERMATOL JI J. Am. Acad. Dermatol. PD DEC PY 2004 VL 51 IS 6 BP 881 EP 885 DI 10.1016/j.jaad.2004.05.030 PG 5 WC Dermatology SC Dermatology GA 879UV UT WOS:000225745300002 PM 15583577 ER PT J AU Middelkamp-Hup, MA Pathak, MA Parrado, C Goukassian, D Rius-Diaz, F Mihm, MC Fitzpatrick, TB Gonzalez, S AF Middelkamp-Hup, MA Pathak, MA Parrado, C Goukassian, D Rius-Diaz, F Mihm, MC Fitzpatrick, TB Gonzalez, S TI Oral Polypodium leucotomos extract decreases ultraviolet-induced damage of human skin SO JOURNAL OF THE AMERICAN ACADEMY OF DERMATOLOGY LA English DT Article; Proceedings Paper CT 20th World Congress of Dermatology CY JUL 03-05, 2002 CL PARIS, FRANCE ID RANDOMIZED CONTROLLED-TRIAL; D-ALPHA-TOCOPHEROL; BETA-CAROTENE; ASCORBIC-ACID; MAST-CELLS; VITAMIN-E; XERODERMA-PIGMENTOSUM; PYRIMIDINE DIMERS; CLINICAL-TRIAL; IN-VITRO AB Background: UV radiation induces damage to human skin. Protection of skin by an oral photoprotective agent would have substantial benefits. Objective: We investigated the photoprotective effect of oral administration of an extract of the natural antioxidant Polypodium leucotomos (PL). Methods: A total of 9 healthy participants of skin types II to III were exposed to varying closes of artificial UV radiation without and after oral administration of PL (7.5 mg/kg). At 24 hours after exposure the erythema reaction was assessed and paired biopsy specimens were obtained from PL-treated and untreated skin. Results: A significant decrease in erythema was found in PL-treated skin (P <.01). Histologically, PL-treated biopsy specimens showed less sunburn cells (P <.05), cyclobutane pyrimidine dimers (P <.001), proliferating epidermal cells (P <.001), and dermal mast cell infiltration (P <.05). A trend toward Langerhans cell preservation was seen. Conclusion: Oral administration of PL is an effective systemic chemophotoprotective agent leading to significant protection of skin against UV radiation. C1 Harvard Univ, Massachusetts Gen Hosp, Sch Med, Wellman Labs Photomed,Dept Dermatol, Boston, MA 02114 USA. Harvard Univ, Massachusetts Gen Hosp, Sch Med, Wellman Labs Photomed,Dept Pathol Dermapathol, Boston, MA 02114 USA. Univ Malaga, Fac Med, Dept Morphol Sci, E-29071 Malaga, Spain. Boston Univ, Sch Med, Dept Dermatol, Boston, MA 02215 USA. RP Gonzalez, S (reprint author), Harvard Univ, Massachusetts Gen Hosp, Sch Med, Wellman Labs Photomed,Dept Dermatol, BHX 630, Boston, MA 02114 USA. EM sgonzalez3@partners.org RI Parrado, Concepcion/K-9270-2014 OI Parrado, Concepcion/0000-0002-7627-4310 NR 57 TC 60 Z9 63 U1 0 U2 2 PU MOSBY, INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 USA SN 0190-9622 J9 J AM ACAD DERMATOL JI J. Am. Acad. Dermatol. PD DEC PY 2004 VL 51 IS 6 BP 910 EP 918 DI 10.1016/j.jaad.2004.06.027 PG 9 WC Dermatology SC Dermatology GA 879UV UT WOS:000225745300007 PM 15583582 ER PT J AU Nori, S Rius-Diaz, F Cuevas, J Goldgeier, M Jaen, P Torres, A Gonzalez, S AF Nori, S Rius-Diaz, F Cuevas, J Goldgeier, M Jaen, P Torres, A Gonzalez, S TI Sensitivity and specificity of reflectance-mode confocal microscopy for in vivo diagnosis of basal cell carcinoma: A multicenter study SO JOURNAL OF THE AMERICAN ACADEMY OF DERMATOLOGY LA English DT Article ID SCANNING LASER MICROSCOPY; MALIGNANT-MELANOMA; ROUTINE HISTOLOGY; HUMAN SKIN; TIME; AGE AB Background: The Current standard diagnostic procedure for basal cell carcinoma (BCC) is histologic examination after invasive biopsy. Reflectance-mode confocal microscopy (RCM) offers noninvasive high-resolution imaging of human skin in vivo. Objective: The objective Of this Study was to explore the sensitivity and specificity of RCM for diagnosis of BCC. Methods: This was a retrospective study of RCM images from 4 institutions of 152 skin lesions representing a variety of benign and malignant diagnoses. These 152 lesions were examined clinically, with biopsies recorded for all the 83 BCCs detected. Based on a previous study, a set of 5 histologically correlated confocal imaging criteria for diagnosing BCC was established, eg, the presence of elongated monomorphic nuclei. Blinded retrospective analysis of the images from the 152 lesions was carried Out by a single novice reviewer to determine the sensitivity and specificity of these 5 RCM criteria for diagnosing BCC. The accuracy of combining the probability of BCC based on examination of clinical photographs with the predicted probability of BCC based on confocal criteria was also evaluated. Results: The presence of two or more criteria is 100% sensitive for the diagnosis of BCC, and with 4 or more RCM criteria present the specificity was 95.7% and sensitivity was 82.9%. These results were found to have little variability across study sites and across BCC subtypes. The combination of RCM with photography-based predictions of clinical probability of BCC significantly improved the accuracy for noninvasive diagnosis of BCC. Conclusion: RCM offers a sensitive and specific tool for the noninvasive diagnosis of BCC in vivo. C1 Massachusetts Gen Hosp, Wellman Labs Photomed, Dept Dermatol, Boston, MA 02114 USA. Univ Alcala de Henares, Hosp Guadalajara, Pathol Serv, Madrid, Spain. Univ Alcala de Henares, Hosp Guadalajara, Dermatol Serv, Madrid, Spain. Loma Linda Univ, Div Dermatol, Sch Med, Loma Linda, CA 92350 USA. RP Gonzalez, S (reprint author), Massachusetts Gen Hosp, Wellman Labs Photomed, Dept Dermatol, 50 Blossom St,Bartlett 3, Boston, MA 02114 USA. EM sgonzalez3@partners.org FU NIOSH CDC HHS [R01 OH04029] NR 24 TC 158 Z9 164 U1 1 U2 3 PU MOSBY, INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 USA SN 0190-9622 J9 J AM ACAD DERMATOL JI J. Am. Acad. Dermatol. PD DEC PY 2004 VL 51 IS 6 BP 923 EP 930 DI 10.1016/j.jaad.2004.06.028 PG 8 WC Dermatology SC Dermatology GA 879UV UT WOS:000225745300009 PM 15583584 ER PT J AU Delahanty, LM Nathan, DM AF Delahanty, LM Nathan, DM TI Research navigating the course of clinical practice in diabetes SO JOURNAL OF THE AMERICAN DIETETIC ASSOCIATION LA English DT Review ID COMPLICATIONS TRIAL; INTENSIVE THERAPY; PREVENTION PROGRAM; WEIGHT-LOSS; MELLITUS; INSULIN; INTERVENTIONS; DESIGN; IMPLEMENTATION; EPIDEMIOLOGY AB Three of the four largest and, arguably, most important long-term clinical trials focusing on diabetes in the past 2 decades have had medical nutrition therapy (MNT) as a major element of their experimental therapies: the Diabetes Control and Complications Trial and its follow-up study the Epidemiology of Diabetes Interventions and Complications Study, the Diabetes Prevention Program, and the Look AHEAD (Action for Health in Diabetes) study. The important features of these studies, their major results, and implications for current and future practice of MNT in the prevention and treatment of diabetes are delineated. The evidence suggests that dietetics professionals have an increasingly important role in the early initiation of MNT in the treatment and prevention of diabetes and in establishing the long-term relationships required to shape behavior and sustain the lifestyle habits that translate into significant reductions in the incidence of diabetes-related health outcomes and improved cost-effectiveness over time. C1 Massachusetts Gen Hosp, Ctr Diabet, Boston, MA 02114 USA. RP Delahanty, LM (reprint author), Massachusetts Gen Hosp, Ctr Diabet, 50 Staniford St,Suite 340, Boston, MA 02114 USA. EM ldelahanty@partners.org NR 44 TC 6 Z9 6 U1 0 U2 2 PU AMER DIETETIC ASSOC PI CHICAGO PA 120 S RIVERSIDE PLZ, STE 2000, CHICAGO, IL 60606-6995 USA SN 0002-8223 J9 J AM DIET ASSOC JI J. Am. Diet. Assoc. PD DEC PY 2004 VL 104 IS 12 BP 1846 EP 1853 DI 10.1016/j.jada.2004.09.028 PG 8 WC Nutrition & Dietetics SC Nutrition & Dietetics GA 877DX UT WOS:000225549100016 PM 15565079 ER PT J AU Shores, MM Moceri, VM Gruenewald, DA Brodkin, KI Matsumoto, AM Kivlahan, DR AF Shores, MM Moceri, VM Gruenewald, DA Brodkin, KI Matsumoto, AM Kivlahan, DR TI Low testosterone is associated with decreased function and increased mortality risk: A preliminary study of men in a geriatric rehabilitation unit SO JOURNAL OF THE AMERICAN GERIATRICS SOCIETY LA English DT Article DE testosterone; elderly; function; mortality; rehabilitation ID SEX-HORMONE LEVELS; OLDER MEN; CRITICAL ILLNESS; HYPOGONADAL MEN; NURSING-HOMES; ELDERLY MEN; REPLACEMENT; HYPOPITUITARISM; MOOD; AGE AB OBJECTIVES: To evaluate whether low testosterone levels are associated with greater depression or poorer function in a geriatric rehabilitation unit. DESIGN: Retrospective review. SETTING: Geriatric rehabilitation unit. MEASUREMENTS: Low testosterone levels were defined as total testosterone of 3.0 ng/mL or less or free testosterone of 9.0 pg/mL or less. Age, ethnicity, weight, depression, ambulation, length of rehabilitation, and 6-month rehospitalization and mortality rates were obtained. Overall illness severity was determined using the Cumulative Illness Rating Scale for Geriatrics. RESULTS: Low testosterone levels were present in 29 of 44 (65.9%) men. There were no significant differences between men with low and normal testosterone levels in ethnicity, age, weight, depression, and overall illness severity. Lower testosterone levels were correlated with decreased ability to ambulate and transfer (Spearman P>.34; P<.05). There were no significant differences between men with low and normal testosterone in length of stay on the rehabilitation unit (mean+/-standard deviation= 19.6+/-11.6 vs 17.7+/-17.5 days, P=.68) or rehospitalization rates (41.4% vs 26.7%; P=.34). Men with low testosterone had a trend toward increased 6-month mortality (31.0% vs 6.7%; chi(2)=3.3, P=.07) and shorter survival time (log rank=3.2; df 1, P=.07). After entering testosterone and variables with potential prognostic significance for mortality in a stepwise manner in a Cox regression analysis, there was a significant mortality risk associated with low testosterone (hazard ratio=27.9, 95% confidence interval=2.0-384.0; P=.01). CONCLUSION: Low testosterone levels were correlated with decreased physical function and increased risk for 6-month mortality. Prospective studies with larger sample sizes and better standardized testosterone measures are needed to confirm these findings. C1 Univ Washington, VA Puget Sound Hlth Care Syst, Seattle, WA 98108 USA. Univ Washington, Dept Psychiat & Behav Sci, Seattle, WA 98195 USA. Univ Washington, Dept Med, Seattle, WA 98195 USA. Univ Washington, Dept Epidemiol, Seattle, WA 98195 USA. RP Shores, MM (reprint author), Univ Washington, VA Puget Sound Hlth Care Syst, 1660 S Columbian Way,S-182 GRECC, Seattle, WA 98108 USA. EM molly.shores@med.va.gov NR 30 TC 40 Z9 42 U1 1 U2 3 PU BLACKWELL PUBLISHING INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 USA SN 0002-8614 J9 J AM GERIATR SOC JI J. Am. Geriatr. Soc. PD DEC PY 2004 VL 52 IS 12 BP 2077 EP 2081 DI 10.1111/j.1532-5415.2004.52562.x PG 5 WC Geriatrics & Gerontology; Gerontology SC Geriatrics & Gerontology GA 872DT UT WOS:000225188300017 PM 15571546 ER PT J AU Katz, IR AF Katz, IR TI Optimizing atypical antipsychotic treatment strategies in the elderly SO JOURNAL OF THE AMERICAN GERIATRICS SOCIETY LA English DT Article ID PLACEBO-CONTROLLED-TRIAL; DRUG-INDUCED PSYCHOSIS; HEALTH PLAN DATABASE; PARKINSONS-DISEASE; BEHAVIORAL DISTURBANCES; TARDIVE-DYSKINESIA; DIABETES-MELLITUS; OLDER PATIENTS; DOUBLE-BLIND; FOLLOW-UP C1 Univ Penn, Dept Psychiat, Philadelphia, PA 19104 USA. Vet Affairs Med Ctr, Philadelphia, PA USA. RP Katz, IR (reprint author), Univ Penn, Dept Psychiat, VISN 4 MIRECC Med Ctr,3535 Market St,Room 3001, Philadelphia, PA 19104 USA. EM katzi@mail.med.upenn.edu NR 35 TC 11 Z9 11 U1 2 U2 2 PU BLACKWELL PUBLISHING INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 USA SN 0002-8614 J9 J AM GERIATR SOC JI J. Am. Geriatr. Soc. PD DEC PY 2004 VL 52 IS 12 SU S BP S272 EP S277 DI 10.1111/j.1532-5415.2004.52604.x PG 6 WC Geriatrics & Gerontology; Gerontology SC Geriatrics & Gerontology GA 870MH UT WOS:000225060700005 PM 15541168 ER PT J AU Fried, L Solomon, C Shlipak, M Seliger, S Stehman-Breen, C Bleyer, AJ Chaves, P Furberg, C Kuller, L Newman, A AF Fried, L Solomon, C Shlipak, M Seliger, S Stehman-Breen, C Bleyer, AJ Chaves, P Furberg, C Kuller, L Newman, A TI Inflammatory and prothrombotic markers and the progression of renal disease in elderly individuals SO JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY LA English DT Article ID CHRONIC KIDNEY-DISEASE; C-REACTIVE PROTEIN; CARDIOVASCULAR HEALTH; VASCULAR-DISEASE; RISK-FACTORS; ATHEROSCLEROSIS; INSUFFICIENCY; FAILURE; POPULATION; PREVALENCE AB Inflammatory and prothrombotic markers are elevated in individuals with mild to moderate renal disease. It was hypothesized that these markers may also be determinants of the progression of renal disease. The association of six markers-serum C-reactive protein (CRP), white blood cell (WBC) count, fibrinogen, factor VII, albumin, and hemoglobin-with subsequent elevations of creatinine and decline in estimated GFR in the Cardiovascular Health Study, a community-based cohort of elderly individuals, was analyzed. Linear regression was used to determine predictors of an annualized change in serum creatinine as the main outcome. Duration of follow-up was 7 yr for the original cohort and 4 yr for the more recently recruited black cohort. A total of 588 (12.7%) individuals had a decline in estimated GFR of at least 3 ml/min per yr per 1.73 m(2). Higher CRP (P < 0.001), WBC count (P < 0.001), fibrinogen (P < 0.001), and factor VII (P < 0.001) levels and lower albumin (P < 0.001) and hemoglobin levels (P < 0.001) were associated with a rise in creatinine, after adjusting for age. With additional adjustments for race, gender, baseline creatinine, systolic and diastolic BP, lipid levels, weight, and packyears smoking, higher CRP, factor VII, fibrinogen, WBC count, and lower albumin and hemoglobin levels remained associated with a rise in creatinine. Similar results were found for decline in estimated GFR. The decline in GFR was greater with increasing number of inflammatory or prothrombotic markers that were above the median (below for hemoglobin and albumin). Inflammatory and prothrombotic markers are predictors for a change in kidney function in elderly individuals. Interventions that reduce inflammation might confer significant cardiovascular and renal benefits. C1 Univ Pittsburgh, Sch Med, VA Pittsburgh Healthcare Syst, Renal Sect, Pittsburgh, PA 15240 USA. Univ Pittsburgh, Sch Med, Dept Med, Renal Electrolyte Div, Pittsburgh, PA 15240 USA. Univ Washington, Dept Biostat, Seattle, WA 98195 USA. Univ Calif San Francisco, Med Serv, Vet Affairs Med Ctr, San Francisco, CA 94143 USA. Univ Calif San Francisco, Dept Med, San Francisco, CA 94143 USA. Univ Calif San Francisco, Dept Epidemiol & Biostat, San Francisco, CA 94143 USA. Univ Washington, Div Nephrol, Seattle, WA 98195 USA. VA Puget Sound Hlth Care Syst, Renal Sect, Seattle, WA USA. Wake Forest Univ, Nephrol Sect, Sch Med, Winston Salem, NC 27109 USA. Johns Hopkins Univ, Dept Med, Baltimore, MD USA. Johns Hopkins Univ, Dept Epidemiol, Baltimore, MD USA. Wake Forest Univ, Sch Med, Dept Publ Hlth Sci, Winston Salem, NC 27109 USA. Univ Pittsburgh, Sch Publ Hlth, Dept Epidemiol, Pittsburgh, PA 15260 USA. Univ Pittsburgh, Sch Med, Div Geriatr Med, Pittsburgh, PA 15260 USA. RP Fried, L (reprint author), Univ Pittsburgh, Sch Med, VA Pittsburgh Healthcare Syst, Renal Sect, Univ Dr C,Mailstop 111F-U, Pittsburgh, PA 15240 USA. EM Linda.Fried@med.va.gov RI Newman, Anne/C-6408-2013 OI Newman, Anne/0000-0002-0106-1150 FU NHLBI NIH HHS [N01 HC 35129, N01 HC 15103, N01 HC 85079, N01 HC 85086] NR 28 TC 128 Z9 129 U1 0 U2 3 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 1046-6673 J9 J AM SOC NEPHROL JI J. Am. Soc. Nephrol. PD DEC PY 2004 VL 15 IS 12 BP 3184 EP 3191 DI 10.1097/01.ASN.0000146422.45434.35 PG 8 WC Urology & Nephrology SC Urology & Nephrology GA 876NW UT WOS:000225504800027 PM 15579522 ER PT J AU Forman, JL Tolkoff-Rubin, N Pascual, M Lin, J AF Forman, JL Tolkoff-Rubin, N Pascual, M Lin, J TI Hepatitis C, acute humoral rejection, and renal allograft survival SO JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY LA English DT Article; Proceedings Paper CT 36th Annual Meeting of the American-Society-of-Nephrology CY NOV 12-17, 2003 CL SAN DIEGO, CA SP Amer Soc Nephrol ID KIDNEY-TRANSPLANT RECIPIENTS; VIRUS-INFECTION; IMPACT; CLASSIFICATION; PATHOLOGY AB The effect of recipient hepatitis C virus (HCV) infection on renal allograft loss and acute rejection in kidney transplantation remains controversial. We studied 354 renal allograft recipients transplanted during 1996 to 2001 who had HCV antibodies (Ab) measured before transplantation. The primary outcome was death-censored allograft loss and the secondary outcome was acute Immoral rejection (AHR). Compared with HCV Ab-negative patients, those with positive HCV Ab had longer time on dialysis before transplantation, higher percentage of panel-reactive antibodies (PRA), were more likely to receive a. cadaveric transplant, and were more likely to develop delayed graft function (DGF). In univariate analyses, predictors of renal allograft loss included HCV, ca- daveric graft, PRA >20%, HLA mismatch greater than or equal to5, retransplantation, DGF, induction therapy, and AHR. When adjusted for PRA >20%, HLA mismatch greater than or equal to5, and multiple transplant status, HCV was not a statistically significant predictor of allograft loss. HCV was also associated with AHR but lost significance when adjusted for PRA >20%. HCV Ab-positive patients were more likely to have longer duration of dialysis before transplantation prior to kidney transplants, higher PRA, and to receive cadaveric transplants. These characteristics likely resulted in more DGF and AHR after transplantation. After adjusting for these confounding factors, the association between HCV Ab positivity and renal allograft loss was notably attenuated and no longer statistically significant. C1 Brigham & Womens Hosp, Div Renal, Dept Med, Boston, MA 02115 USA. Massachusetts Gen Hosp, Dept Med, Renal Unit, Boston, MA 02114 USA. Harvard Univ, Sch Med, Boston, MA 02115 USA. CHU Vaudois, Transplant Ctr, CH-1011 Lausanne, Switzerland. Fac Med, CH-1011 Lausanne, Switzerland. RP Lin, J (reprint author), Brigham & Womens Hosp, Div Renal, Dept Med, 75 Francis St,MRB-4, Boston, MA 02115 USA. EM jlin11@partners.org FU NIDDK NIH HHS [K08 DK 066246] NR 25 TC 36 Z9 37 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 1046-6673 J9 J AM SOC NEPHROL JI J. Am. Soc. Nephrol. PD DEC PY 2004 VL 15 IS 12 BP 3249 EP 3255 DI 10.1097/01.ASN.0000145896.16153.43 PG 7 WC Urology & Nephrology SC Urology & Nephrology GA 876NW UT WOS:000225504800034 PM 15579529 ER PT J AU Wu, ZJ Irizarry, RA Gentleman, R Martinez-Murillo, F Spencer, F AF Wu, ZJ Irizarry, RA Gentleman, R Martinez-Murillo, F Spencer, F TI A model-based background adjustment for oligonucleotide expression arrays SO JOURNAL OF THE AMERICAN STATISTICAL ASSOCIATION LA English DT Article DE affymetrix GeneChip; background adjustment; expression measure; high density oligonucleotide microarrays ID PROBE LEVEL DATA; MICROARRAY DATA; NORMALIZATION; SUMMARIES; VARIANCE AB High-density oligonucleotide expression arrays are widely used in many areas of biomedical research. Affymetrix GeneChip arrays are the most popular, In the Affymetrix system. a fair amount of further preprocessing and data reduction occurs after the image-processing step. Statistical procedures developed by academic groups have been successful in improving the default algorithms provided by the Affymetrix system. In this article we present a solution to one of the preprocessing steps-background adjustment-based on a formal statistical framework. Our Solution greatly improves the performance of the technology in various practical applications. These arrays use short oligonucleotides to probe for genes in an RNA sample. Typically, each gene is represented by 11-20 pairs of oligonucleotide probes. The first component of these pairs is referred to as a perfect match probe and is designed to hybridize only with transcripts from the intended gene (i.e.. specific hybridization). However, hybridization by other sequences (i.e., nonspecific hybridization) is unavoidable. Furthermore. hybridization strengths are measured by a scanner that introduces optical noise. Therefore, the observed intensities need to be adjusted to give accurate measurements of specific hybridization. We have found that the default ad hoc adjustment, provided as part of the Affymetrix system can be improved through the use of estimators derived from a statistical model that uses probe sequence information. A final step in preprocessing is to summarize the probe-level data for each gene to define a measure of expression that represents the amount of the corresponding mRNA species. In this article we illustrate the practical consequences of not adjusting appropriately for the presence of nonspecific hybridization and provide a solution based on our background adjustment procedure. Software that computes our adjustment is available as part of the Bioconductor Project (http://bioconductor.org). C1 Johns Hopkins Univ, Dept Biostat, Baltimore, MD 21205 USA. Johns Hopkins Univ, JHMI Microarray Core, Baltimore, MD 21205 USA. Johns Hopkins Univ, Dept Med & Mol Biol & Genet, Baltimore, MD 21205 USA. Dana Farber Canc Inst, Dept Biostat, Boston, MA 02115 USA. RP Johns Hopkins Univ, Dept Biostat, Baltimore, MD 21205 USA. EM rafa@jhu.edu RI wu, zhijin/J-2282-2014; wu, zhijin/J-4995-2016 OI wu, zhijin/0000-0002-9596-9134 NR 18 TC 990 Z9 1013 U1 0 U2 29 PU AMER STATISTICAL ASSOC PI ALEXANDRIA PA 732 N WASHINGTON ST, ALEXANDRIA, VA 22314-1943 USA SN 0162-1459 EI 1537-274X J9 J AM STAT ASSOC JI J. Am. Stat. Assoc. PD DEC PY 2004 VL 99 IS 468 BP 909 EP 917 DI 10.1198/016214504000000683 PG 9 WC Statistics & Probability SC Mathematics GA 874FX UT WOS:000225337400001 ER PT J AU Sarkar-Agrawal, P Vergilis, I Sharpless, NE DePinho, RA Runger, TM AF Sarkar-Agrawal, P Vergilis, I Sharpless, NE DePinho, RA Runger, TM TI Impaired processing of DNA photoproducts and ultraviolet hypermutability with loss of p16(INK4a) or p19(ARF) SO JOURNAL OF THE NATIONAL CANCER INSTITUTE LA English DT Article ID CUTANEOUS MALIGNANT-MELANOMA; DYSPLASTIC NEVUS SYNDROME; SHUTTLE VECTOR PLASMID; XERODERMA-PIGMENTOSUM; FAMILIAL MELANOMA; TUMOR SUPPRESSION; EXCISION-REPAIR; HUMAN-CELLS; P53; MUTATIONS AB Reduced DNA repair has been linked to an increased risk of cutaneous malignant melanoma, but insights into the molecular mechanisms of that link are scarce. The INK4a/ARF (CDKN2a) locus, which codes for the p16(INK4a) and P19(ARF) proteins, is often mutated in sporadic and familial malignant melanoma, but it has not been directly associated with reduced DNA repair. We transfected unirradiated mouse fibroblast cells with UV-treated DNA to measure DNA repair in normal, p16(INK4a) mutant, P19(ARF) mutant, or double mutant mouse host cells. Loss of either p16(INK4a) or P19(ARF) reduced the ability of the cells to process UVinduced DNA damage, independent of cell cycle effects incurred by the loss. These results may further explain why INK4a/ARF mutations predispose to malignant melanoma, a UVinduced tumor. C1 Boston Univ, Sch Med, Dept Dermatol, Boston, MA 02118 USA. Univ N Carolina, Lineberger Canc Res Ctr, Chapel Hill, NC 27599 USA. Harvard Univ, Sch Med, Dana Farber Canc Inst, Dept Adult Oncol, Boston, MA 02115 USA. RP Runger, TM (reprint author), Boston Univ, Sch Med, Dept Dermatol, 609 Albany St, Boston, MA 02118 USA. EM truenger@bu.edu OI Ruenger, Thomas/0000-0001-8453-0276 FU NCI NIH HHS [5 U01 CA84313-04] NR 31 TC 30 Z9 30 U1 0 U2 2 PU OXFORD UNIV PRESS INC PI CARY PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA SN 0027-8874 J9 J NATL CANCER I JI J. Natl. Cancer Inst. PD DEC 1 PY 2004 VL 96 IS 23 BP 1790 EP 1793 DI 10.1093/jnci/djh307 PG 4 WC Oncology SC Oncology GA 876FB UT WOS:000225480800012 PM 15572761 ER PT J AU Zwicker, JI Uhl, L Huang, WY Shaz, BH Bauer, KA AF Zwicker, JI Uhl, L Huang, WY Shaz, BH Bauer, KA TI Thrombosis and ELISA optical density values in hospitalized patients with heparin-induced thrombocytopenia SO JOURNAL OF THROMBOSIS AND HAEMOSTASIS LA English DT Article DE ELISA; heparin-induced thrombocytopenia; heparin-PF4 antibodies; HIT; thrombosis ID LINKED-IMMUNOSORBENT-ASSAY; PLATELET-AGGREGATION TEST; INDUCED SKIN NECROSIS; RELEASE ASSAY; DIAGNOSIS; ANTIBODIES; ACTIVATION; LEPIRUDIN; RISK AB The natural history of heparin-induced thrombocytopenia (HIT) in the absence of thrombosis was previously established using functional assays for confirmation of diagnosis (e.g. C-14 serotonin release assay). An enzyme-linked immunosorbent assay (ELISA) that detects the presence of antibodies directed against the heparin-platelet factor-4 (PF4) complex has largely replaced functional assays in many medical centers. Although the ELISA is highly sensitive for detecting HIT antibodies, its usefulness for predicting thrombotic outcomes has not been clearly established. We performed a retrospective chart review of all hospitalized patients at a University hospital who tested seropositive for HIT by a commercial ELISA during 2001 and 2002. A total of 63 inpatients were identified as HIT positive by ELISA. Forty-eight patients had no apparent HIT-associated thrombosis at the time of HIT seropositivity (i.e. isolated HIT) and only one was treated prophylactically with a direct thrombin inhibitor. The 30-day thrombosis rate for patients with isolated HIT was 17% (eight of 48). Higher ELISA optical density (OD) measurements correlated significantly with thrombosis (1.41 +/- 0.87 vs. 0.79 +/- 0.46, P < 0.001). Patients with isolated HIT and an OD measurement of greater than or equal to 1.0 demonstrated nearly a 6-fold increased risk of thrombosis compared with those with OD values between 0.4 and 0.99 (odds ratio 5.74, 95% confidence interval 1.73, 19.0; absolute rate of thrombosis, 36/,, vs. 9%, respectively, P = 0.07). We conclude that in hospitalized patients with isolated HIT, the presence of heparin-PF4 antibodies detected by ELISA was associated with a significant risk of subsequent thrombosis and higher ELISA values were observed among patients suffering thrombotic events. C1 Harvard Univ, Sch Med, Beth Israel Deaconess Med Ctr, Div Hematol Oncol, Boston, MA 02215 USA. Harvard Univ, Sch Med, Beth Israel Deaconess Med Ctr, Dept Pathol, Boston, MA 02215 USA. VA Boston Healthcare Syst, Hematol Sect, Boston, MA USA. RP Zwicker, JI (reprint author), Harvard Univ, Sch Med, Beth Israel Deaconess Med Ctr, Div Hematol Oncol, 330 Brookline Ave, Boston, MA 02215 USA. EM jzwicker@bidmc.harvard.edu NR 23 TC 160 Z9 162 U1 1 U2 3 PU BLACKWELL PUBL LTD PI OXFORD PA 108 COWLEY RD, OXFORD OX4 1JF, OXON, ENGLAND SN 1538-7933 J9 J THROMB HAEMOST JI J. Thromb. Haemost. PD DEC PY 2004 VL 2 IS 12 BP 2133 EP 2137 DI 10.1111/j.1538-7836.2004.01039.x PG 5 WC Hematology; Peripheral Vascular Disease SC Hematology; Cardiovascular System & Cardiology GA 880GB UT WOS:000225775900010 PM 15613017 ER PT J AU Briggs, SM AF Briggs, SM TI Paradoxical missile embolus to the right superficial femoral artery following gunshot wound to the liver: A case report - Editorial comment SO JOURNAL OF TRAUMA-INJURY INFECTION AND CRITICAL CARE LA English DT Editorial Material C1 Massachusetts Gen Hosp, Boston, MA 02114 USA. RP Briggs, SM (reprint author), 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 0022-5282 J9 J TRAUMA JI J. Trauma-Injury Infect. Crit. Care PD DEC PY 2004 VL 57 IS 6 BP 1339 EP 1340 PG 2 WC Critical Care Medicine; Surgery SC General & Internal Medicine; Surgery GA 884FB UT WOS:000226069100037 ER PT J AU O'Toole, TP Conde-Martel, A Gibbon, JL Hanusa, BH Freyder, PJ Fine, MJ AF O'Toole, TP Conde-Martel, A Gibbon, JL Hanusa, BH Freyder, PJ Fine, MJ TI Substance-abusing urban homeless in the late 1990s: How do they differ from non-substance-abusing homeless persons? SO JOURNAL OF URBAN HEALTH-BULLETIN OF THE NEW YORK ACADEMY OF MEDICINE LA English DT Article DE comorbidities; homelessness; needs; substance abuse ID DRUG-ABUSE; HEALTH; CARE; DISORDERS; ALCOHOL; POVERTY; ADULTS AB Much of our understanding of substance abuse and homelessness comes from data from the 1980s and may not necessarily reflect issues or trends prevalent during the 1990s. We report data from a two-city, community-based, populations-proportionate sample of 531 randomly selected homeless adults; the study was conducted in 1997 and compared substance-abusing to non-substance-abusing respondents. Most (78.3%) met criteria for substance abuse/dependence and were abusing either cocaine or alcohol and cocaine (68.5%). In the multiple logistic regression model, male gender (odds ratio [OR] 2.94, 95% confidence interval [CI] 1.70-5.09), less than a 12th grade education (OR 1.96, 95% CI 1.11-3.46), bustling or stealing for sustenance (OR 3.14, 95% CI 1.15-8.55), and identifying a need to learn bow to manage one's money (OR 2.41, 95% CI 1.45-3.98) were independently associated with substance abuse/dependence. Drug abuse/dependence and polysubstance use among urban homeless persons became a more prevalent issue in the late 1990s. These individuals have unique needs that will require tailored interventions. C1 Georgetown Univ, Sch Med, Washington, DC 20007 USA. Univ Pittsburgh, Ctr Res Hlth Care, Pittsburgh, PA 15260 USA. Pittsburgh Salvat Army Publ Inebriate Program, Pittsburgh, PA USA. VA Pittsburgh Healthcare Syst, Ctr Hlth Equ Res & Promot, Pittsburgh, PA USA. RP O'Toole, TP (reprint author), Georgetown Univ, Sch Med, 1111 NE Med Dent Bldg,3900 Reservoir Rd NW, Washington, DC 20007 USA. EM Tpo6@georgetown.edu NR 21 TC 17 Z9 17 U1 1 U2 4 PU OXFORD UNIV PRESS INC PI CARY PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA SN 1099-3460 J9 J URBAN HEALTH JI J. Urban Health PD DEC PY 2004 VL 81 IS 4 BP 606 EP 617 DI 10.1093/jurban/jth144 PG 12 WC Public, Environmental & Occupational Health; Medicine, General & Internal SC Public, Environmental & Occupational Health; General & Internal Medicine GA 862PU UT WOS:000224504000007 PM 15466842 ER PT J AU Sylvestre, DL Loftis, JM Hauser, P Genser, S Cesari, H Borek, N Kresina, TF Seeff, L Francis, H AF Sylvestre, DL Loftis, JM Hauser, P Genser, S Cesari, H Borek, N Kresina, TF Seeff, L Francis, H TI Co-occurring hepatitis C, substance use, and psychiatric illness: Treatment issues and developing integrated models of care SO JOURNAL OF URBAN HEALTH-BULLETIN OF THE NEW YORK ACADEMY OF MEDICINE LA English DT Article DE comorbidities; HIV; HCV; psychiatric illness; treatment ID ALCOHOL-USE DISORDERS; IDENTIFICATION TEST AUDIT; SEVERE MENTAL-ILLNESS; METHADONE-MAINTENANCE PATIENTS; SEROTONIN REUPTAKE INHIBITORS; INJECTING DRUG-USERS; INTERFERON-ALPHA; SCREENING-TEST; RATING-SCALE; DEPRESSIVE DISORDER AB Hepatitis C virus (HCV) infection is transmitted by injection drug use and associated with psychiatric conditions. Patients with drug use or significant psychiatric illness have typically been excluded from HCV treatment trials noting the 1997 National Institutes of Health Consensus Statement on HCV that indicated active drug use and major depressive illness were contraindications to treatment of HCV infection. However, the 2002 NIH Consensus Statement recognized that these patients could be effectively treated for HCV infection and recommended that treatment be considered on a case-by-case basis. Treating HCV infection in these patients is challenging, with drug use relapse possibly leading to psychosocial instability, poor adherence, and HCV reinfection. Interferon therapy may exacerbate preexisting psychiatric symptoms. Co-occurring human immunodeficiency virus or hepatitis B virus provide additional challenges, and access to ancillary medical and psychiatric services may be limited. Patients with co-occurring HCV infection, substance use, and psychiatric illness can complete interferon treatment with careful monitoring and aggressive intervention. Clinicians must integrate early interventions for psychiatric conditions and drug use into their treatment algorithm. Few programs or treatment models are designed to manage co-occurring substance use, psychiatric illness, and HCV infection and therapy. The National Institute on Drug Abuse convened a panel of experts to address the current status and the long-range needs through a 2-day workshop, Co-occurring Hepatitis C, Substance Abuse, and Psychiatric Illness: Addressing the Issues and Developing Integrated Models of Care. This conference report summarizes current data, medical management issues, and strategies discussed. C1 Natl Inst Drug Abuse, Ctr AIDS & Other Med Consequences Drug Abuse, NIH, Bethesda, MD 20892 USA. Univ Calif San Francisco, Dept Med, San Francisco, CA 94143 USA. Oregon Hlth Sci Univ, Sch Med, Portland, OR 97201 USA. Portland VA Med Ctr, NW Hepatitis C Resource Ctr, Portland, OR USA. NIDDKD, NIH, Bethesda, MD 20892 USA. RP Hauser, P (reprint author), Natl Inst Drug Abuse, Ctr AIDS & Other Med Consequences Drug Abuse, NIH, 6001 Execut Blvd,MSC 9593, Bethesda, MD 20892 USA. EM peter.hauser2@med.va.gov NR 89 TC 61 Z9 61 U1 0 U2 5 PU OXFORD UNIV PRESS INC PI CARY PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA SN 1099-3460 J9 J URBAN HEALTH JI J. Urban Health PD DEC PY 2004 VL 81 IS 4 BP 719 EP 734 DI 10.1093/jurban/jth153 PG 16 WC Public, Environmental & Occupational Health; Medicine, General & Internal SC Public, Environmental & Occupational Health; General & Internal Medicine GA 862PU UT WOS:000224504000016 PM 15466851 ER PT J AU Spencer, BA Fung, CH Wang, MM Rubenstein, LV Litwin, MS AF Spencer, BA Fung, CH Wang, MM Rubenstein, LV Litwin, MS TI Geographic variation across veterans affairs medical centers in the treatment of early stage prostate cancer SO JOURNAL OF UROLOGY LA English DT Article DE prostatic neoplasms; cluster analysis; United States Department of Veterans Affairs ID DATA-BASE REPORT; RADICAL PROSTATECTOMY; DEMOGRAPHIC VARIATION; RADIATION-THERAPY; TIME TRENDS; NEW-HAVEN; RATES; AGE; BENEFICIARIES; CARCINOMA AB Purpose: We investigated geographic variation in the treatment of early stage prostate cancer in a national sample of veterans after widespread adoption of the prostate specific antigen test. Materials and Methods: Our sample consisted of 16,352 cases from the Veterans Affairs Central Cancer Registry that were diagnosed between January 1997 and December 1999 with stage I or II prostate cancer. We used a 2-stage nested logit model to compare surgery, radiation therapy and noncurative treatment among 4 geographic regions of the United States. Results: Multivariate analysis showed that patients in the West (referent group) had a higher OR of undergoing surgery than radiation compared with the Northeast, South or Midwest (OR 0.77, 95% CI 0.67 to 0.87, OR 0.86, 95% CI 0.76 to 0.98 and OR 0.75, 95% CI 0.64 to 0.87, respectively. Black men, men with lower grade and higher stage tumors, and unmarried men were less likely to undergo curative treatment and less likely to undergo surgery than radiation. Conclusions: Geographic variation persists in patterns of care in men with early stage prostate cancer. However, this variation is limited to the choice between surgery and radiation rather than to the choice between curative and noncurative treatment. C1 Univ Calif Los Angeles, Dept Urol, David Geffen Sch Med, Los Angeles, CA 90095 USA. Univ Calif Los Angeles, Robert Wood Johnson Clin Scholars Program, Los Angeles, CA 90095 USA. Univ Calif Los Angeles, Greater Los Angeles Vet Affairs Healthcare Syst, Los Angeles, CA 90095 USA. Univ Calif Los Angeles, Sch Publ Hlth, Dept Hlth Serv, Los Angeles, CA 90095 USA. RAND Hlth Sci Program, Santa Monica, CA USA. RP Spencer, BA (reprint author), Univ Calif Los Angeles, Dept Urol, David Geffen Sch Med, Box 951738, Los Angeles, CA 90095 USA. EM benjspencel@hotmail.com NR 18 TC 12 Z9 12 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0022-5347 J9 J UROLOGY JI J. Urol. PD DEC PY 2004 VL 172 IS 6 BP 2362 EP 2365 DI 10.1097/01.ju.0000144064.54670.7b PN 1 PG 4 WC Urology & Nephrology SC Urology & Nephrology GA 872GE UT WOS:000225194900055 PM 15538268 ER PT J AU McNaughton-Collins, M Barry, MJ Caubet, JF Bates, DW Lee, JM Hauser, A Fowler, FJ AF McNaughton-Collins, M Barry, MJ Caubet, JF Bates, DW Lee, JM Hauser, A Fowler, FJ TI Validity of primary care patient self-report of abnormal (but not cancer) prostate biopsy results SO JOURNAL OF UROLOGY LA English DT Article DE prostate; biopsy; questionnaires; prostatic neoplasms; mass screening ID NEEDLE BIOPSIES; INTRAEPITHELIAL NEOPLASIA; FOLLOW-UP; ACCURACY; MEN; ADENOCARCINOMA; POPULATION; DIAGNOSIS AB Purpose: We assessed the validity of patient self-report of abnormal (but not cancer) prostate biopsy results, ie, atypical cells or prostatic intraepithelial neoplasia. Materials and Methods: We compared survey responses and pathology records for 156 men from a multicenter, prospective cohort study, which was designed to evaluate the impact of a suspicious prostate cancer screening test followed by benign prostate biopsy. Results: Of the 156 subjects 45 (29%) reported having had atypical cells or prostatic intraepithelial neoplasia and 38 (24%) had a pathology report with atypia or prostate intraepithelial neoplasia. The sensitivity of the self-report was 87%, specificity was 90%, positive predictive value was 73% and negative predictive value was 95%. The K statistic was 0.7. Conclusions: Men in this study reported this complex result accurately. However, it was concerning that 5 men (13%) appeared unaware of an abnormal prostate biopsy result, especially given the substantial residual risk of prostate cancer conferred by this result. C1 Massachusetts Gen Hosp, Div Gen Med, Boston, MA 02114 USA. Univ Massachusetts, Survey Res Ctr, Amherst, MA 01003 USA. Brigham & Womens Hosp, Div Gen Med, Boston, MA 02115 USA. Boston Med Ctr, Div Gen Med, Boston, MA USA. RP McNaughton-Collins, M (reprint author), Massachusetts Gen Hosp, Div Gen Med, 50 Staniford St,9th Floor, Boston, MA 02114 USA. EM mmcnaughtoncollins@partners.org NR 18 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0022-5347 J9 J UROLOGY JI J. Urol. PD DEC PY 2004 VL 172 IS 6 BP 2366 EP 2368 DI 10.1097/01.ju.0000145178.29852.7b PN 1 PG 3 WC Urology & Nephrology SC Urology & Nephrology GA 872GE UT WOS:000225194900056 PM 15538269 ER PT J AU Lu, R Limon, A Devroe, E Silver, PA Cherepanov, P Engelman, A AF Lu, R Limon, A Devroe, E Silver, PA Cherepanov, P Engelman, A TI Class II integrase mutants with changes in putative nuclear localization signals are primarily blocked at a postnuclear entry step of human immunodeficiency virus type 1 replication SO JOURNAL OF VIROLOGY LA English DT Article ID STRUCTURE-BASED MUTAGENESIS; INFECTIOUS MOLECULAR CLONE; AMINO-ACID-RESIDUES; CENTRAL DNA FLAP; HIV-1 INTEGRASE; IN-VITRO; REVERSE-TRANSCRIPTASE; KARYOPHILIC PROPERTIES; CATALYTIC DOMAIN; GENE-EXPRESSION AB Integrase has been implicated in human immunodeficiency virus type 1 (HIV-1) nuclear import. Integrase analyses, however, can be complicated by the pleiotropic nature of mutations: whereas class I mutants are integration defective, class II mutants display additional assembly and/or reverse transcription defects. We previously determined that HIV-1(V165A),originally reported as defective for nuclear import, was a class II mutant. Here we analyzed mutants containing changes in other putative nuclear localization signals, including (186)KRK(188/211)KELQKQITK(219)and Cys-130. Previous work established HIV-1(K186Q), HIV-1(Q214L/Q216L,) and HIV-1(C130G), as replication defective, but phenotypic classification was unclear and nuclear import in nondividing cells was not addressed. Consistent with previous reports, most of the bipartite mutants studied here were replication defective. These mutants as well as HIV-1(V165A) synthesized reduced cDNA levels, but a normal fraction of mutant cDNA localized to dividing and nondividing cell nuclei. Somewhat surprisingly, recombinant class II mutant proteins were catalytically active, and class II Vpr-integrase fusion proteins efficiently complemented class I mutant virus. Since a class I Vpr-integrase mutant efficiently complemented class H mutant viruses under conditions in which class II Vpr-integrases failed to function, we conclude that classes I and H define two distinct complementation groups and suggest that class II mutants are primarily defective at a postnuclear entry step of HIV-1 replication. HIV-1(C130G) was also defective for reverse transcription, but Vpr-integrase(c130G) did not efficiently complement class I mutant HIV-1. Since HIV-1(C130A) grew like the wild type, we conclude that Cys-130 is not essential for replication and speculate that perturbation of integrase structure contributed to the pleiotropic HIV-1(C130G) phenotype. C1 Dana Farber Canc Inst, Dept Canc Immunol & AIDS, Boston, MA 02115 USA. Dana Farber Canc Inst, Dept Canc Biol, Boston, MA 02115 USA. Harvard Univ, Sch Med, Dept Pathol, Boston, MA 02115 USA. Harvard Univ, Sch Med, Dept Syst Biol, Boston, MA 02115 USA. RP Engelman, A (reprint author), Dana Farber Canc Inst, Dept Canc Immunol & AIDS, 44 Binney St, Boston, MA 02115 USA. EM alan_engelman@dfci.harvard.edu RI Cherepanov, Peter/F-6859-2010 OI Cherepanov, Peter/0000-0002-0634-538X FU NIAID NIH HHS [AI28691, AI52014, P30 AI028691, R01 AI052014] NR 68 TC 85 Z9 87 U1 0 U2 3 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA SN 0022-538X J9 J VIROL JI J. Virol. PD DEC PY 2004 VL 78 IS 23 BP 12735 EP 12746 DI 10.1128/JVI.78.23.12735-12746.2004 PG 12 WC Virology SC Virology GA 870VT UT WOS:000225087500002 PM 15542626 ER PT J AU Yang, XZ Tomov, V Kurteva, S Wang, LP Ren, XP Gorny, MK Zoa-Pazner, S Sodroski, J AF Yang, XZ Tomov, V Kurteva, S Wang, LP Ren, XP Gorny, MK Zoa-Pazner, S Sodroski, J TI Characterization of the outer domain of the gp120 glycoprotein from human immunodeficiency virus type 1 SO JOURNAL OF VIROLOGY LA English DT Article ID HUMAN MONOCLONAL-ANTIBODY; CD4 BINDING-SITE; ENVELOPE GLYCOPROTEIN; NEUTRALIZING ANTIBODIES; HIV-1 GP120; IMMUNE-RESPONSES; AIDS PATIENTS; HTLV-III; V3-SPECIFIC ANTIBODIES; CRYSTAL-STRUCTURE AB The core of the gp120 glycoprotein from human immunodeficiency virus type 1 (HIV-1) is comprised of three major structural domains: the outer domain, the inner domain, and the bridging sheet. The outer domain is exposed on the HIV-1 envelope glycoprotein trimer and contains binding surfaces for neutralizing antibodies such as 2G12, immunoglobulin G1b12, and anti-V3 antibodies. We expressed the outer domain of HIV-YU2 gp120 as an independent protein, termed OD1. OD1 efficiently bound 2G12 and a large number of anti-V3 antibodies, indicating its structural integrity. Immunochemical studies with OD1 indicated that antibody responses against the outer domain of the HIV-1 gp120 envelope glycoprotein are rare in HIV-1-infected human sera that potently neutralize the virus. Surprisingly, such outer-domain-directed antibody responses are commonly elicited by immunization with recombinant monomeric gp120. Immunization with soluble, stabilized HIV-1 envelope glycoprotein trimers elicited antibody responses that more closely resembled those in the sera of HIV-1-infected individuals. These results underscore the qualitatively different humoral immune responses elicited during natural infection and after gp120 vaccination and help to explain the failure of gp120 as an effective vaccine. C1 Dana Farber Canc Inst, Dept Canc Immunol & AIDS, Boston, MA 02115 USA. Harvard Univ, Sch Med, Dept Pathol, Div AIDS, Boston, MA USA. Harvard Univ, Sch Publ Hlth, Dept Immunol & Infect Dis, Boston, MA 02115 USA. NYU, Sch Med, Dept Pathol, New York, NY USA. Vet Affairs New York Harbor Syst, Res Enhancement Award Program, New York, NY USA. RP Sodroski, J (reprint author), Dana Farber Canc Inst, Dept Canc Immunol & AIDS, 44 Binney St,JFB 824, Boston, MA 02115 USA. EM joseph_sodroski@dfci.harvard.edu OI Gorny, Miroslaw/0000-0002-2714-8780 FU NIAID NIH HHS [R01 AI031783, AI39420, P30 AI042848, R01 AI039420, AI24755, AI40895, AI42848, AI31783, R37 AI024755, R01 AI040895] NR 84 TC 51 Z9 52 U1 0 U2 1 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA SN 0022-538X J9 J VIROL JI J. Virol. PD DEC PY 2004 VL 78 IS 23 BP 12975 EP 12986 DI 10.1128/JVI.78.23.12975-12986.2004 PG 12 WC Virology SC Virology GA 870VT UT WOS:000225087500025 PM 15542649 ER PT J AU Clarke, P Meintzer, SM Wang, YB Moffitt, LA Richardson-Burns, SM Johnson, GL Tyler, KL AF Clarke, P Meintzer, SM Wang, YB Moffitt, LA Richardson-Burns, SM Johnson, GL Tyler, KL TI JNK regulates the release of proapoptotic mitochondrial factors in reovirus-infected cells SO JOURNAL OF VIROLOGY LA English DT Article ID INDUCED APOPTOSIS REQUIRES; JUN NH2-TERMINAL KINASE; BAX-DEPENDENT APOPTOSIS; CYTOCHROME-C RELEASE; BCL-2 FAMILY-MEMBERS; VIRAL PROTEIN-R; SIGNAL-TRANSDUCTION; NEURONAL APOPTOSIS; INDUCE APOPTOSIS; VIRUS-INFECTION AB Reovirus-induced apoptosis is associated with activation of the proapoptotic mitogen-activated protein kinase c-Jun N-terminal kinase (JNK) and the JNK-associated transcription factor c-Jun. Here we show that reovirus-induced apoptosis and activation of caspase 3 are inhibited in cells deficient in MEK kinase 1, an upstream activator of JNK in reovirus-infected cells. Inhibition of JNK activity following reovirus infection delays the release of proapoptotic mitochondrial factors and the subsequent onset of apoptosis. In contrast, reovirus-induced apoptosis is not blocked by infection with adenovirus expressing dominant-negative c-Jun, and c-Jun activation does not correlate with apoptosis in reovirus-infected cells. This is the first report demonstrating that JNK is associated with regulation of mitochondrial pathways of apoptosis following viral infection. C1 Univ Colorado, Hlth Sci Ctr, Dept Neurol B182, Denver, CO 80262 USA. Univ Colorado, Hlth Sci Ctr, Dept Immunol, Denver, CO 80262 USA. Univ Colorado, Hlth Sci Ctr, Dept Neurosci, Denver, CO 80262 USA. Univ Colorado, Hlth Sci Ctr, Dept Med & Microbiol, Denver, CO 80262 USA. Denver Vet Affairs Med Ctr, Denver, CO USA. Univ N Carolina, Sch Med, Dept Pharmacol, Chapel Hill, NC USA. Univ N Carolina, Lineberger Comprehens Canc Ctr, Sch Med, Chapel Hill, NC 27599 USA. RP Clarke, P (reprint author), Univ Colorado, Hlth Sci Ctr, Dept Neurol B182, 4200 E 9th Ave, Denver, CO 80262 USA. EM penny.clarke@uchsc.edu OI Tyler, Kenneth/0000-0003-3294-5888 FU NIA NIH HHS [1R01AG14071] NR 44 TC 43 Z9 45 U1 0 U2 1 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA SN 0022-538X J9 J VIROL JI J. Virol. PD DEC PY 2004 VL 78 IS 23 BP 13132 EP 13138 DI 10.1128/JVI.78.23.13132-13138.2004 PG 7 WC Virology SC Virology GA 870VT UT WOS:000225087500041 PM 15542665 ER PT J AU Peyerl, FW Bazick, HS Newberg, MH Barouch, DH Sodroski, J Letvin, NL AF Peyerl, FW Bazick, HS Newberg, MH Barouch, DH Sodroski, J Letvin, NL TI Fitness costs limit viral escape from cytotoxic T lymphocytes at a structurally constrained epitope SO JOURNAL OF VIROLOGY LA English DT Article ID SIMIAN IMMUNODEFICIENCY VIRUS; MHC CLASS-I; RHESUS-MONKEYS; DISEASE PROGRESSION; PRIMARY INFECTION; IMMUNE-RESPONSES; REPLICATION; TYPE-1; AIDS; RECOGNITION AB The intense selection pressure exerted by virus-specific cytotoxic T lymphocytes (CTL) on replicating human immunodeficiency virus and simian immunodeficiency virus results in the accumulation of CTL epitope mutations. It has been assumed that fitness costs can limit the evolution of CTL epitope mutations. However, only a limited number of studies have carefully examined this possibility. To explore the fitness costs associated with viral escape from p11C, C-M-specific CTL, we constructed a panel of viruses encoding point mutations at each position of the entire p11C, C-M epitope. Amino acid substitutions at positions 3, 4, 5, 6, 7, and 9 of the epitope significantly impaired virus replication by altering virus production and Gag protein expression as well as by destabilizing mature cores. Amino acid substitutions at position 2 of the epitope were tolerated but required reversion or additional compensatory mutations to generate replication-competent viruses. Finally, while amino acid substitutions at positions 1 and 8 of the p11C, C-M epitope were functionally tolerated, these substitutions were recognized by p11C, C-M-specific CTL and therefore provided no selection advantage for the virus. Together, these data suggest that limited sequence variation is tolerated by the region of the capsid encoding the p11C, C-M epitope and therefore that only a very limited number of mutations can allow successful viral escape from the p11C, C-M-specific CTL response. C1 Harvard Univ, Sch Med, Beth Israel Deaconess Med Ctr, Div Viral Pathogenesis, Boston, MA 02215 USA. Harvard Univ, Sch Med, Dana Farber Canc Inst, Dept Pathol,Div AIDS,Dept Canc Immunol & AIDS, Boston, MA 02215 USA. Harvard Univ, Sch Publ Hlth, Dept Immunol & Infect Dis, Boston, MA 02215 USA. RP Letvin, NL (reprint author), Harvard Univ, Sch Med, Beth Israel Deaconess Med Ctr, Div Viral Pathogenesis, Res E Room 113,330 Brookline Ave, Boston, MA 02215 USA. EM nletvin@bidmc.harvard.edu FU NIAID NIH HHS [AI-20729, R01 AI020729, R37 AI020729, T32 AI007387, T32-AI07387] NR 53 TC 77 Z9 79 U1 1 U2 1 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA SN 0022-538X J9 J VIROL JI J. Virol. PD DEC PY 2004 VL 78 IS 24 BP 13901 EP 13910 DI 10.1128/JVI.78.24.13901-13910.2004 PG 10 WC Virology SC Virology GA 875HC UT WOS:000225409900049 PM 15564498 ER PT J AU Grisson, RD Chenine, AL Yeh, LY He, J Wood, C Bhat, GJ Xu, WD Kankasa, C Ruprecht, RM AF Grisson, RD Chenine, AL Yeh, LY He, J Wood, C Bhat, GJ Xu, WD Kankasa, C Ruprecht, RM TI Infectious molecular clone of a recently transmitted pediatric human immunodeficiency virus clade c isolate from Africa: Evidence of intraclade recombination SO JOURNAL OF VIROLOGY LA English DT Article ID TYPE-1 SUBTYPE-C; FULL-LENGTH CLONES; NF-KAPPA-B; HIV TYPE-1; DNA CLONE; BIOLOGICAL CHARACTERIZATION; REPLICATION-COMPETENT; CHEMOKINE RECEPTORS; REFERENCE SEQUENCES; CONSTRUCTION AB Although human immunodeficiency virus type 1 (HIV-1) clade C continues to dominate the pandemic, only two infectious clade C proviral DNA clones have been described (N. Mochizuki, N. Otsuka, K. Matsuo, T. Shiino, A. Kojima, T. Kurata, K. Sakai, N. Yamamoto, S. Isomura, T. N. Dhole, Y. Takebe, M. Matsuda, and M. Tatsumi, AIDS Res. Hum. Retrovir. 15:1321-1324, 1999; T. Ndung'u, B. Renjifo, and M. Essex, J. Virol. 75:4964-4972, 2001). We have generated an infectious molecular clone of a pediatric clade C strain, HIV1084i, which was isolated from a Zambian infant infected either intrapartum or through breastfeeding. HIV1084i is an R5, non-syncytium-inducing isolate that bears all known clade C signatures; gag, pol, and env consistently mapped within clade C. Interestingly, gag resembled Asian isolates, whereas pol and env resembled African isolates, indicating that HIIV1084i probably arose from an intraclade recombination. As a recently transmitted clade C strain, HIV1084i will be a useful vaccine development tool. C1 Dana Farber Canc Inst, Dept Canc Immunol & AIDS, Boston, MA 02115 USA. Harvard Univ, Med Ctr, Dept Med, Boston, MA 02115 USA. Univ Nebraska, Nebraska Ctr Virol, Lincoln, NE USA. Univ Nebraska, Sch Biol Sci, Lincoln, NE USA. Univ Teaching Hosp, Dept Pediat, Lusaka, Zambia. RP Ruprecht, RM (reprint author), Dana Farber Canc Inst, Dept Canc Immunol & AIDS, 44 Binney St, Boston, MA 02115 USA. EM ruth_ruprecht@dfci.harvard.edu FU NCI NIH HHS [R01 CA075903, R01 CA75903]; NCRR NIH HHS [P20 RR015635, P20 RR15635]; NIAID NIH HHS [P01 AI048240, P01 AI48240]; NICHD NIH HHS [R01 HD039620, R01 HD39620]; NIDCR NIH HHS [R01 DE012937, R01 DE016013, R01 DE12937] NR 25 TC 28 Z9 28 U1 1 U2 1 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA SN 0022-538X J9 J VIROL JI J. Virol. PD DEC PY 2004 VL 78 IS 24 BP 14066 EP 14069 DI 10.1128/JVI.78.24.14066-14069.2004 PG 4 WC Virology SC Virology GA 875HC UT WOS:000225409900068 PM 15564517 ER PT J AU Steinhauer, K Grayhack, JP Smiley-Oyen, AL Shaiman, S McNeil, MR AF Steinhauer, K Grayhack, JP Smiley-Oyen, AL Shaiman, S McNeil, MR TI The relationship among voice onset, voice quality, and fundamental frequency: A dynamical perspective SO JOURNAL OF VOICE LA English DT Article; Proceedings Paper CT 29th Annual Symposium: Care of the Professional Voice CY JUN, 2000 CL PHILADELPHIA, PA DE voice-register-dynamical systems; voice motor control; nonlinear dynamics ID INTRINSIC LARYNGEAL MUSCLES; COORDINATION DYNAMICS; REGISTERS; PHONATION AB In dynamical motor theory, skill acquisition occurs as a modification of preexisting coordination patterns or attractor states. The purpose of this study was to assess how different levels of voice onset, voice quality, and fundamental frequency (F-0) combine to form the attractor states common to voice motor control. Three levels of voice onset (glottal, simultaneous, and breathy), voice quality (modal speech, mixed, and falsetto), and fundamental frequency (low, mid, and high) were manipulated by vocally untrained, female subjects. Percent correct of acquisition trials and self-report of effort were used as measures of stable phonations indicative of an attractor state. Using intensity as a covariate, the results provided support for two of the three predicted triads representing attractor states in female speakers: (1) glottal onset/modal speech quality/low F-0; and (2) breathy onset/falsetto quality/high F-0. The results of this study suggest that certain parameters of voice motor control, such as onset, quality, and F-0, exist as part of a dynamical system that can be identified and manipulated in voice motor acquisition and learning. C1 Univ Pittsburgh, Voice Ctr, Pittsburgh, PA 15214 USA. VA Pittsburgh Healthcare Syst, Pittsburgh, PA USA. Univ Pittsburgh, Dept Commun Sci & Disorders, Pittsburgh, PA USA. Iowa State Univ, Dept Hlth & Human Performance, Ames, IA USA. RP Steinhauer, K (reprint author), Univ Pittsburgh, Voice Ctr, 200 Lothrop St, Pittsburgh, PA 15214 USA. EM tkstein@adelphia.net NR 30 TC 7 Z9 8 U1 2 U2 3 PU MOSBY, INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 USA SN 0892-1997 J9 J VOICE JI J. Voice PD DEC PY 2004 VL 18 IS 4 BP 432 EP 442 DI 10.1016/j.jvoice.2004.01.006 PG 11 WC Otorhinolaryngology SC Otorhinolaryngology GA 880VI UT WOS:000225817400002 PM 15567045 ER PT J AU Godfrey, JR Geller, SE Abrahamson, MJ AF Godfrey, JR Geller, SE Abrahamson, MJ TI Toward optimal health: The experts discuss important issues in hormone replacement and in diabetes SO JOURNAL OF WOMENS HEALTH LA English DT Editorial Material C1 Journal Womens Hlth, Montclair, NJ 07043 USA. Univ Illinois, Coll Med, UIC Natl Ctr Excellence Womens Hlth, Chicago, IL 60680 USA. Univ Illinois, Sch Publ Hlth, Chicago, IL 60680 USA. Harvard Univ, Sch Med, Boston, MA USA. Joslin Diabet Ctr, Boston, MA 02215 USA. RP Godfrey, JR (reprint author), Journal Womens Hlth, 31 Macopin Ave, Montclair, NJ 07043 USA. EM jgmeisler@comcast.net NR 2 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 USA SN 1540-9996 J9 J WOMENS HEALTH JI J. Womens Health PD DEC PY 2004 VL 13 IS 10 BP 1075 EP 1079 DI 10.1089/jwh.2004.13.1075 PG 5 WC Public, Environmental & Occupational Health; Medicine, General & Internal; Obstetrics & Gynecology; Women's Studies SC Public, Environmental & Occupational Health; General & Internal Medicine; Obstetrics & Gynecology; Women's Studies GA 885MJ UT WOS:000226160900001 ER PT J AU Ibrahim, SA Zhang, A Mercer, MB Baughman, M Kwoh, CK AF Ibrahim, SA Zhang, A Mercer, MB Baughman, M Kwoh, CK TI Inner city African-American elderly patients' perceptions and preferences for the care of chronic knee and hip pain: Findings from focus groups SO JOURNALS OF GERONTOLOGY SERIES A-BIOLOGICAL SCIENCES AND MEDICAL SCIENCES LA English DT Article ID HEALTH-CARE; ETHNIC-DIFFERENCES; DECISION-MAKING; CLINICAL CARE; OSTEOARTHRITIS; PHYSICIANS; CULTURE; COMMUNICATION; GENDER; ARTHROPLASTY AB Background. African Americans undergo joint replacement less often than do white persons. The authors studied African-Arnerican perceptions and preferences for the care of knee and hip pain. Methods. 10 focus groups Were conducted in an inner city community. Participants, older persons with chronic knee or hip pain, were asked to discuss their perceptions and preferences for the care of knee and hip pain. Transcripts were coded for thematic structure using NUD*ST software. Results. Cultural preferences and perceptions for care emerged as a major theme. Important subcategories of this theme included respect for the patient's faith and religiosity and perceptions of physician ethnicity, race, and sex. Conclusions. This sample of older inner city African Americans expressed unique cultural perceptions and preferences for the care of their knee and hip pain. Respect for patients' faith was important, whereas physicians' race, ethnicity, and religious background were not. C1 VA Pittsburgh Healthcare Syst, Ctr Hlth Equ Res & Promot, Pittsburgh, PA USA. Case Western Reserve Univ, Sch Med, Cleveland, OH USA. RP Ibrahim, SA (reprint author), VA Pittsburgh Healthcare Syst, Ctr Hlth Equ Res & Promot, Pittsburgh, PA USA. EM said.ibrahim2@med.va.gov NR 51 TC 17 Z9 17 U1 0 U2 0 PU GERONTOLOGICAL SOCIETY AMER PI WASHINGTON PA 1275 K STREET NW SUITE 350, WASHINGTON, DC 20005-4006 USA SN 1079-5006 J9 J GERONTOL A-BIOL JI J. Gerontol. Ser. A-Biol. Sci. Med. Sci. PD DEC PY 2004 VL 59 IS 12 BP 1318 EP 1322 PG 5 WC Geriatrics & Gerontology; Gerontology SC Geriatrics & Gerontology GA 896WF UT WOS:000226964200012 PM 15699532 ER PT J AU Zhang, SL Guo, J Moini, B Ingelfinger, JR AF Zhang, SL Guo, J Moini, B Ingelfinger, JR TI Angiotensin II stimulates Pax-2 in rat kidney proximal tubular cells: Impact on proliferation and apoptosis SO KIDNEY INTERNATIONAL LA English DT Article; Proceedings Paper CT 36th Annual Meeting of the American-Society-of-Nephrology CY NOV 12-17, 2003 CL SAN DIEGO, CA SP Amer Soc Nephrol DE Pax-2; angiotensin II; apoptosis; proximal tubular cells ID AT(2) RECEPTOR PROTEIN; HUMAN FETAL KIDNEY; TYPE-2 RECEPTOR; CONSCIOUS RATS; WILMS-TUMOR; JAK-STAT; EXPRESSION; GENE; SYSTEM; GROWTH AB Background. The intrarenal renin-angiotensin system (RAS) is intimately involved in the tubular cell proliferation, apoptosis and regeneration that occur following renal injury. Though tubular angiotensin II (Ang II) type 2 receptors (AT(2)R) decrease greatly after birth, their number increases after injury. Notably, during recovery from injury, renal tubular cells display a relatively immature phenotype expressing genes that are involved in nephron development, for example, the paired homeobox-2 gene (Pax-2). The present investigation hypothesized that AT2R activation would stimulate Pax-2 gene expression in immortalized rat renal proximal tubular cells (IRPTC), as we have found in fetal cells. Methods. Pax-2 gene expression in IRPTC was evaluated by immunofluorescence, Western blot, reverse transcription-polymerase chain reaction (RT-PCR) with or without Ang II treatment; apoptosis and proliferation were analyzed by terminal transferase-mediated deoxyuridine triphosphate (dUTP) nick end-labeling (TUNEL) assay and bromodeoxyuridine (BrdU) incorporation in stable IRPTC transformants with Pax-2 sense and antisense orientation, respectively. Results. Ang II up-regulated Pax-2 gene expression via AT2R in IRPTC. The stimulatory effect of both Ang II on Pax-2 gene expression was blocked by PD123319 (AT(2)R inhibitor), AG 490 (specific Janus kinase 2 (JAK2) inhibitor) and genistein (tyrosine kinase inhibitor), but not by losartan (AT(1)R inhibitor). Stable transfection of sense Pax-2 cDNA increased, whereas antisense Pax-2 cDNA down-regulated Pax-2 expression. Conclusion. Our studies suggest that Ang II stimulates Pax-2 gene expression in IRPTC via AT2R and the JAK2/signal transducers and activators of transcription (STAT) signaling transduction pathway, which may be important in renal repair following injury. Cells lacking Pax-2 gene expression appear to be prone toward apoptosis rather than proliferation. C1 Harvard Univ, Massachusetts Gen Hosp, Sch Med, Pediat Nephrol Unit, Boston, MA 02114 USA. Harvard Univ, Massachusetts Gen Hosp, Sch Med, Endocrinol Unit, Boston, MA 02114 USA. RP Ingelfinger, JR (reprint author), Harvard Univ, Massachusetts Gen Hosp, Sch Med, Pediat Nephrol Unit, 55 Fruit St,BHX-411, Boston, MA 02114 USA. EM jingelfinger@partners.org FU NHLBI NIH HHS [HL48455] NR 64 TC 28 Z9 33 U1 0 U2 0 PU BLACKWELL PUBLISHING INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 USA SN 0085-2538 J9 KIDNEY INT JI Kidney Int. PD DEC PY 2004 VL 66 IS 6 BP 2181 EP 2192 DI 10.1111/j.1523-1755.2004.66008.x PG 12 WC Urology & Nephrology SC Urology & Nephrology GA 870AK UT WOS:000225026200008 PM 15569307 ER PT J AU Kurella, M Luan, J Yaffe, K Chertow, GM AF Kurella, M Luan, J Yaffe, K Chertow, GM TI Validation of the kidney disease quality of life (KDQOL) cognitive function subscale SO KIDNEY INTERNATIONAL LA English DT Article DE chronic kidney disease; cognitive impairment; end-stage renal disease ID CHRONIC-HEMODIALYSIS; ELDERLY POPULATION; ALZHEIMERS-DISEASE; NORMATIVE DATA; IMPAIRMENT; HEALTH; DIALYSIS; PERFORMANCE; PREVALENCE; INSTRUMENT AB Background. Formal cognitive function testing is cumbersome, and no self- administered instruments for estimating cognitive function in persons with chronic kidney disease (CKD) and end- stage renal disease (ESRD) have been validated. The goal of this study was to determine the validity of the Kidney Disease Quality of Life Cognitive Function scale (KDQOL-CF) for the assessment of cognitive impairment in persons with kidney disease. Methods. We administered the KDQOL- CF to 157 subjects, 79 with ESRD and 78 with CKD participating in a cross-sectional study of cognitive function. Scores on the Modified Mini- Mental State Exam (3MS) were considered the gold standard measure of global cognitive function. Performance characteristics of the KDQOL- CF were assessed using correlation coefficients, Bland- Altman plots, and receiver operating characteristic curves. Results. Median scores on the KDQOL- CF were 73 (interquartile range 60- 87) for subjects with ESRD and 87 (interquartile range 73- 100) for subjects with CKD (P < 0.0001). Scores on the KDQOL- CF were directly correlated with scores on the 3MS (r = 0.31, P = 0.0001). Defining global cognitive impairment as a 3MS score < 80, a cut- point of 60 on the KDQOL- CF accurately classified 76% of subjects, with 52% sensitivity and 81% specificity. On multivariable analysis, cerebral and peripheral vascular disease, benzodiazepine use, and higher serum phosphorus concentrations were associated with lower KDQOL- CF scores, while beta blocker use, education, and higher serum albumin concentrations were associated with higher KDQOL- CF scores. Conclusion. The KDQOL- CF is a valid instrument for estimating cognitive function in patients with CKD and ESRD. KDQOL- CF screening followed by 3MS testing in selected individuals may prove to be an effective and efficient strategy for identifying cognitive impairment in patients with kidney disease. C1 Univ Calif San Francisco, Dept Med, Div Nephrol, San Francisco, CA USA. Univ Calif San Francisco, Dept Med, Div Psychiat, San Francisco, CA USA. Univ Calif San Francisco, Dept Med, Div Neurol, San Francisco, CA USA. Univ Calif San Francisco, Dept Med, Div Epidemiol, San Francisco, CA USA. Univ Calif San Francisco, Mt Zion Med Ctr, Moffitt Long Hosp, San Francisco, CA 94120 USA. San Francisco Vet Affairs Med Ctr, San Francisco, CA USA. RP Chertow, GM (reprint author), Univ Calif San Francisco, Dept Med Res, UCSF Laurel Hts Suite 430,3333 Calif St, San Francisco, CA 94118 USA. EM chertowg@medicine.ucsf.edu RI Kurella Tamura, Manjula/C-8284-2014 OI Kurella Tamura, Manjula/0000-0001-5227-2479 FU NIDDK NIH HHS [R01 DK01005, R01 DK58411] NR 25 TC 31 Z9 32 U1 2 U2 2 PU BLACKWELL PUBLISHING INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 USA SN 0085-2538 J9 KIDNEY INT JI Kidney Int. PD DEC PY 2004 VL 66 IS 6 BP 2361 EP 2367 DI 10.1111/j.1523-1755.2004.66024.x PG 7 WC Urology & Nephrology SC Urology & Nephrology GA 870AK UT WOS:000225026200028 PM 15569327 ER PT J AU Nielsen, CM Williams, J van den Brink, GR Lauwers, GY Roberts, DJ AF Nielsen, CM Williams, J van den Brink, GR Lauwers, GY Roberts, DJ TI Hh pathway expression in human gut tissues and in inflammatory gut diseases SO LABORATORY INVESTIGATION LA English DT Article DE SHH/SHH; PTCH1/PTCH1; inflammatory gut disease; epithelial-mesenchymal signaling; Hh pathway ID EPITHELIAL-MESENCHYMAL INTERACTIONS; SONIC-HEDGEHOG EXPRESSION; STEM-CELLS; INTESTINAL EPITHELIUM; SIGNALING PATHWAY; GENE-EXPRESSION; INDIAN HEDGEHOG; T-LYMPHOCYTES; DIFFERENTIATION; CANCER AB Sonic hedgehog (Shh) directs early gut patterning via epithelial-mesenchymal signaling and remains expressed in endoderm-derived tissues into the adult period. In human adult gut epithelium SHH/SHH expression is strongest in basal layers, which suggests that SHH may function in the maintenance of gut epithelial stem or progenitor cells. Recent publications suggest a role for aberrant SHH/SHH expression in gut epithelial neoplasias. We hypothesized that the regenerating gut epithelium in inflammatory gut disorders would show an upregulation of SHH/SHH signaling and this abnormal signal may explain the increased incidence of neoplasia in these diseases. Archived healthy gut and inflammatory gut diseased tissues were analyzed by RNA in situ hybridization and immunohistochemistry to describe location and levels of SHH signaling. We show that SHH/SHH and its receptor PTCH1/PTCH1 expression is restricted to the glandular epithelium of the gut, in an antiluminal pattern (strongest in basal layers and weak to absent in luminal epithelium). Inflammatory diseases of the gut show dramatic increases in epithelial SHH signaling. Expression increases in inflamed glandular epithelium (including metaplastic glandular epithelium), losing its radial (crypt-villous) polarity, and expression appears upregulated and present in all epithelial cells. We also describe strong SHH/SHH and PTCH1/PTCH1 expression in intraepithelial and mucosal inflammatory cells. We suggest that SHH signaling in inflammatory diseases of the gut acts to ensure stem cell restitution of damaged mucosal epithelium. However, such signaling may also present a risk for neoplastic transformation. C1 Massachusetts Gen Hosp, Dept Pathol, Boston, MA 02114 USA. Univ Amsterdam, Acad Med Ctr, Dept Expt Internal Med, NL-1105 AZ Amsterdam, Netherlands. RP Roberts, DJ (reprint author), Massachusetts Gen Hosp, Dept Pathol, 32 Fruit St, Boston, MA 02114 USA. EM djroberts@partners.org FU NICHD NIH HHS [HD34448-03] NR 53 TC 56 Z9 60 U1 0 U2 1 PU NATURE PUBLISHING GROUP PI NEW YORK PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA SN 0023-6837 J9 LAB INVEST JI Lab. Invest. PD DEC PY 2004 VL 84 IS 12 BP 1631 EP 1642 DI 10.1038/labinvest.3700197 PG 12 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA 874RD UT WOS:000225366600012 PM 15502857 ER PT J AU Jacobsen, E Freedman, A AF Jacobsen, E Freedman, A TI B-cell purging in autologous stem-cell transplantation for non-Hodgkin lymphoma SO LANCET ONCOLOGY LA English DT Review ID BONE-MARROW-TRANSPLANTATION; HIGH-DOSE THERAPY; PROGRESSION-FREE SURVIVAL; MINIMAL RESIDUAL DISEASE; TERM-FOLLOW-UP; MANTLE-CELL; FOLLICULAR LYMPHOMA; SEQUENTIAL CHEMOTHERAPY; PROGNOSTIC-FACTORS; INDOLENT LYMPHOMA AB Autologous stem-cell transplantation is a common therapy for B-cell non-Hodgkin lymphoma. However, a concern with the procedure is the potential of malignant cells to reinfuse with the stem-cell graft. Thus attempts have been made to purge, or eliminate, malignant cells from the graft. The oldest, and most well studied, method for prevention of reinfusion is in vitro use of antibodies against B cells that bind or lyse malignant B cells and healthy cells, while leaving T cells and stem cells to be reinfused. In the past 5 years, investigators have used rituximab, an antibody against CD20, to purge malignant cells in vivo without any manipulation in vitro. Both conventional and new techniques have shown promise, but their exact role remains to be defined. We analysed data on the purging of B cells by use of antibodies in the setting of autologous transplantation, with emphasis on the emerging technique of in vivo purging. C1 Harvard Univ, Sch Med, Dana Farber Canc Inst, Boston, MA 02115 USA. RP Freedman, A (reprint author), Harvard Univ, Sch Med, Dana Farber Canc Inst, 44 Binney St, Boston, MA 02115 USA. EM arnold_freedman@dfci.harvard.edu NR 37 TC 13 Z9 16 U1 0 U2 0 PU LANCET LTD PI LONDON PA 84 THEOBALDS RD, LONDON WC1X 8RR, ENGLAND SN 1470-2045 J9 LANCET ONCOL JI Lancet Oncol. PD DEC PY 2004 VL 5 IS 12 BP 711 EP 717 DI 10.1016/S1470-2045(04)01646-8 PG 7 WC Oncology SC Oncology GA 878TR UT WOS:000225670400014 PM 15581541 ER PT J AU Hirano, S Bless, DM del Rio, AM Connor, NP Ford, CN AF Hirano, S Bless, DM del Rio, AM Connor, NP Ford, CN TI Therapeutic potential of growth factors for aging voice SO LARYNGOSCOPE LA English DT Article; Proceedings Paper CT Meeting of the American-Laryngological-Association CY MAY 02-03, 2003 CL NASHVILLE, TN SP Amer Laryngol Assoc DE presbyphonia; basic fibroblast growth factor; hepatocyte growth factor; fibroblast; vocal fold; hyaluronic acid; collagen; age ID HUMAN VOCAL FOLD; AGE-RELATED-CHANGES; FIBROBLASTS; MANAGEMENT; EXPRESSION; COLLAGEN AB Objectives/Hypothesis: It has been reported that in aged vocal folds, dense collagen deposition takes place and hyaluronic acid decreases in the lamina propria, which are thought to contribute to the vocal problems occurring with age (presbyphonia). To restore aged vocal folds to their younger state, it seems crucial to address these age-related lamina propria changes. Intervention that might increase hyaluronic acid and decrease collagen would appear to be a potentially useful approach. The present study examined the effects of growth factors on aged fibroblasts in terms of the production of hyaluronic acid and collagen type I. Study Design: In vitro study using animal model. Methods: Fibroblasts were harvested from young and aged rat vocal folds and cultured with or without hepatocyte growth factor and/or basic fibroblast growth factor at different concentrations. Subsequently, the production of hyaluronic acid and collagen type I was examined in the supernatant culture media using enzyme-linked immunosorbent assay. Results: Aged fibroblasts produced less hyaluronic acid than younger fibroblasts. When aged and young fibroblasts were cultured with basic fibroblast growth factor, hyaluronic acid production increased and collagen type I production decreased regardless of the concentration, whereas the effects of hepatocyte growth factor appeared to vary with concentration. The basic fibroblast growth factor also was associated with stimulation of growth of aged fibroblasts. Conclusion: The present results suggest that growth factors, especially basic fibroblast growth factor, may have therapeutic potential in restoration of aged vocal fold. C1 Kyoto Natl Hosp, Dept Bronchoesophagol, Kyoto 6128555, Japan. Univ Wisconsin, Dept Surg, Div Otolaryngol Head & Neck Surg, Madison, WI USA. William S Middleton Mem Vet Adm Med Ctr, Dept Otolaryngol Head & Neck Surg, Madison, WI USA. RP Hirano, S (reprint author), Kyoto Natl Hosp, Dept Bronchoesophagol, 1-1 Fukakusa Mukaihata, Kyoto 6128555, Japan. EM chiraka@aol.com FU NIDCD NIH HHS [R01 DC 4428] NR 18 TC 52 Z9 57 U1 0 U2 4 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0023-852X J9 LARYNGOSCOPE JI Laryngoscope PD DEC PY 2004 VL 114 IS 12 BP 2161 EP 2167 DI 10.1097/01.mlg.0000149450.37640.db PG 7 WC Medicine, Research & Experimental; Otorhinolaryngology SC Research & Experimental Medicine; Otorhinolaryngology GA 878IE UT WOS:000225639300014 PM 15564837 ER PT J AU Kamil, SH Vacanti, MP Vacanti, CA Eavey, RD AF Kamil, SH Vacanti, MP Vacanti, CA Eavey, RD TI Microtia chondrocytes as a donor source for tissue-engineered cartilage SO LARYNGOSCOPE LA English DT Article DE tissue engineering; microtia; chondrocytes; tissue-engineered auricle ID GROWTH-FACTORS; AURICLE; SHAPE AB Objectives/Hypothesis. Current surgical techniques for the correction of microtia are challenging. Research in the field of tissue engineering is providing insight into chondrocyte behavior for a possible future treatment of microtia. The authors wished to evaluate the biological potential of chondrocytes isolated from microtia cartilage as compared with normal auricular cartilage as a source of tissue-engineered cartilage. Study Design: A comparative research design to study the potential of microtia cartilage chondrocytes with normal auricular chondrocytes as a source of tissue-engineered cartilage. Methods. Cartilage specimens from 12 pediatric patients (six normal auricular specimens and six auricular specimens with microtia) were obtained. The chondrocytes were isolated and cultured in vitro; chondrocyte number was increased by passaging. Each type of cell was implanted in nude mice to generate tissue-engineered cartilage. Eight weeks after implantation the specimens were dissected and removed. Results were compared between the normal auricular and microtia specimens in regard to cell number expansion in vitro and generation of tissue-engineered cartilage in vivo. Results. An initial mean cell number of 150,000 cells in each group (normal and microtia) increased to an average cell number of 120 million cells/mL in the normal and 130 million cells in the microtia subgroups, respectively, at the end of the second passage. histologically, both types of chondrocytes generated normal elastic cartilage. Conclusion: The study demonstrated the potential of cells isolated from microtia cartilage to generate tissue-engineered cartilage. Microtia cartilage represents an important additional donor source for the possible generation of a human tissue-engineered auricle. C1 Massachusetts Eye & Ear Infirm, Dept Otolaryngol, Boston, MA 02114 USA. Harvard Univ, Sch Med, Dept Otol & Laryngol, Boston, MA 02115 USA. Massachusetts Gen Hosp, Dept Pathol, Boston, MA 02114 USA. Brigham & Womens Hosp, Dept Anesthesiol Perioperat & Pain Med, Boston, MA USA. RP Eavey, RD (reprint author), Massachusetts Eye & Ear Infirm, Dept Otolaryngol, 243 Charles St, Boston, MA 02114 USA. EM roland_eavey@meei.harvard.edu NR 12 TC 14 Z9 16 U1 3 U2 5 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0023-852X J9 LARYNGOSCOPE JI Laryngoscope PD DEC PY 2004 VL 114 IS 12 BP 2187 EP 2190 DI 10.1097/01.mlg.0000149455.68135.de PG 4 WC Medicine, Research & Experimental; Otorhinolaryngology SC Research & Experimental Medicine; Otorhinolaryngology GA 878IE UT WOS:000225639300019 PM 15564842 ER PT J AU Weisberg, E Catley, L Kujawa, J Atadja, P Remiszewski, S Fuerst, P Cavazza, C Anderson, K Griffin, JD AF Weisberg, E Catley, L Kujawa, J Atadja, P Remiszewski, S Fuerst, P Cavazza, C Anderson, K Griffin, JD TI Histone deacetylase inhibitor NVP-LAQ824 has significant activity against myeloid leukemia cells in vitro and in vivo SO LEUKEMIA LA English DT Article DE myeloid leukemia; NVP-LAQ824; imatinib; STI571; Gleevec; chronic myeloid leukemia; acute myeloid leukemia; BCR/ABL ID ACUTE PROMYELOCYTIC LEUKEMIA; CHRONIC MYELOGENOUS LEUKEMIA; TYROSINE KINASE INHIBITOR; BREAST-CANCER CELLS; TRANS-RETINOIC ACID; ABL-POSITIVE CELLS; BCR-ABL; ANTITUMOR-ACTIVITY; SODIUM-BUTYRATE; PHASE-I AB NVP-LAQ824 is a novel potent hydroxamic acid-derived histone deacetylase inhibitor that induces apoptosis in nanomolar concentrations in myeloid leukemia cell lines and patient samples. Here we show the activity of NVP-LAQ824 in acute myeloid leukemia cells and BCR/ABL-expressing cells of mouse and human origin, both sensitive and resistant to imatinib mesylate ( Gleevec, STI-571). Whereas imatinib inhibited overall cellular tyrosine phosphorylation in Ba/F3.p210 cells, NVP-LAQ824 did not inhibit tyrosine phosphorylation, and did not affect BCR/ABL or ABL protein expression. Neither compound was able to inhibit cellular tyrosine phosphorylation in the imatinib-resistant Ba/F3.p210-T315I cell line. These data taken together suggest that BCR/ABL kinase activity is not a direct target of NVP-LAQ824. Synergy between NVP-LAQ824 and imatinib was demonstrated against BCR/ABL-expressing K562 myeloid leukemia cell lines. In addition, we show that NVP-LAQ824 was well tolerated in vivo in a pre-clinical murine leukemia model, with antileukemia activity resulting in significant prolongation of the survival of mice when treated with NVP-LAQ824 compared to control mice. Taken together, these findings provide the framework for NVP-LAQ824 as a novel therapeutic in myeloid malignancies. C1 Harvard Univ, Sch Med, Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02115 USA. Harvard Univ, Sch Med, Dept Med, Boston, MA 02115 USA. Novartis Inst Biomed Res, Oncol Res, E Hanover, NJ USA. RP Catley, L (reprint author), Harvard Univ, Sch Med, Dana Farber Canc Inst, Dept Med Oncol, 44 Binney St, Boston, MA 02115 USA. EM Laurence_Catley@dfci.harvard.edu RI Catley, Laurence/E-5313-2013 FU PHS HHS [R0120947, P0178378] NR 79 TC 43 Z9 43 U1 0 U2 1 PU NATURE PUBLISHING GROUP PI LONDON PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND SN 0887-6924 J9 LEUKEMIA JI Leukemia PD DEC PY 2004 VL 18 IS 12 BP 1951 EP 1963 DI 10.1038/sj.leu.2403519 PG 13 WC Oncology; Hematology SC Oncology; Hematology GA 872ZV UT WOS:000225249100006 PM 15496979 ER PT J AU Munoz, O Fend, F de Beaumont, R Husson, H Astier, A Freedman, AS AF Munoz, O Fend, F de Beaumont, R Husson, H Astier, A Freedman, AS TI TGF beta-mediated activation of Smad1 in B-cell non-Hodgkin's lymphoma and effect on cell proliferation SO LEUKEMIA LA English DT Article DE Smad1; TGF beta; follicular; lymphoma; microenvironment ID GROWTH-FACTOR-BETA; BONE MORPHOGENETIC PROTEIN; TRANSFORMED FOLLICULAR LYMPHOMA; MAD-RELATED PROTEIN; SIGNAL-TRANSDUCTION; I RECEPTORS; EXPRESSION; PATHWAYS; APOPTOSIS; SUPERFAMILY AB We have previously reported an overexpression of Smad1 in follicular lymphoma (FL) cells, which are characterized by the t(14; 18) bcl2/IgH translocation. Smad1 is commonly involved in bone morphogenetic protein but not in tumor-transforming growth factor beta (TGFbeta) signaling pathways. This study focuses on Smad1 signaling pathway in non-Hodgkin lymphoma cells including follicular or large-cell lymphoma cells. Our results support the notion that phosphorylation of Smad1 is mediated by TGFb present in the microenvironment and occurs in FL in vivo. Using an in vitro coculture system mimicking interactions between stroma cells and FL cells, we found that both the cell partners release TGFb at a sufficient concentration to activate Smad pathways in the malignant cells. This Smad1 activation involves TGFbetaRII but not ALK-1 receptors, and does not compete with the Smad2 pathway. Moreover, proliferation assays performed on lymphoma cells expressing wild-type or mutated Smad1, or in which endogenous Smad1 level was decreased by gene silencing, strongly supported that overexpression and activation of Smad1 modifies the biological response of lymphoma B cells to TGFb family members. This work opens new insights into aberrant Smad pathways and their pathophysiological role in FL and in other non-Hodgkin lymphomas. C1 Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02115 USA. Harvard Univ, Sch Med, Dept Med, Boston, MA USA. Tech Univ Munich, Inst Pathol, D-8000 Munich, Germany. RP Munoz, O (reprint author), Dana Farber Canc Inst, Dept Med Oncol, 44 Binney St, Boston, MA 02115 USA. EM omunoz@partners.org; Arnold_Freedman@dfci.harvard.edu RI Astier, Anne/A-1641-2008 OI Astier, Anne/0000-0002-0144-3431 NR 51 TC 21 Z9 22 U1 0 U2 0 PU NATURE PUBLISHING GROUP PI LONDON PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND SN 0887-6924 J9 LEUKEMIA JI Leukemia PD DEC PY 2004 VL 18 IS 12 BP 2015 EP 2025 DI 10.1038/sj.leu.2403485 PG 11 WC Oncology; Hematology SC Oncology; Hematology GA 872ZV UT WOS:000225249100014 PM 15470494 ER PT J AU McCarthy, PL Paltiel, O Maslova, E Kulikov, S Hahn, T Kopecky, KJ Drozdova, V Shmatina, N Tichonova, L Van Hoff, J Gavrilova, I Weinstein, H AF McCarthy, PL Paltiel, O Maslova, E Kulikov, S Hahn, T Kopecky, KJ Drozdova, V Shmatina, N Tichonova, L Van Hoff, J Gavrilova, I Weinstein, H TI Histopathologic verification of acute leukemia (AL) in a cohort of 463 post-Chernobyl patients from Belarus, Russia and Ukraine SO LEUKEMIA RESEARCH LA English DT Article DE leukemia diagnostic working group; histopathology; FAB classification ID ACUTE LYMPHOBLASTIC-LEUKEMIA; ACUTE MYELOID-LEUKEMIA; MORPHOLOGICAL CLASSIFICATION; FAB CLASSIFICATION; GROUP EXPERIENCE; CONCORDANCE; MORTALITY; CRITERIA AB Seven morphologists examined 382 slide and 82 non-slide, post-Chernobyl pediatric acute leukemia (AL) cases in radiation-exposed areas of Belarus, Russia and Ukraine; part of a case-control study by the International Consortium for Research on the Health Effects of Radiation. Among the slide cases, 99% were confirmed as AL: 92% acute lymphoid leukemia (ALL) and 86% acute myeloid leukemia (AMD demonstrating the utility of FAB classification for distinguishing ALL and AML. Among the non-slide cases, 79% were confirmed as AL: 84% ALL, and 71 % AML. This study affirms AL diagnostic accuracy during a time of social upheaval in the former Soviet Union. (C) 2004 Elsevier Ltd. All rights reserved. C1 Roswell Pk Canc Inst, Dept Med Blood & Marrow Transplant Sect, Buffalo, NY 14263 USA. Hadassah Med Org, Dept Social Med, IL-91120 Jerusalem, Israel. Int Consortium Res Hlth Effects Radiat, Data Coordinat Off, Moscow 12657, Russia. Natl Ctr Hematol, Moscow 125167, Russia. Fred Hutchinson Canc Res Ctr, SW Oncol Grp, Ctr Stat, Seattle, WA 98109 USA. Inst Haematol & Transfusiol, UA-01060 Kiev, Ukraine. Haematol & Transplantol Ctr, Minsk 220089, Byelarus. Yale Univ, Sch Med, Dept Pediat, Div Hematol & Oncol, New Haven, CT 06520 USA. Massachusetts Gen Hosp, Boston, MA 02114 USA. RP McCarthy, PL (reprint author), Roswell Pk Canc Inst, Dept Med Blood & Marrow Transplant Sect, Buffalo, NY 14263 USA. EM philip.mccarthy@roswellpark.org NR 14 TC 2 Z9 2 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND SN 0145-2126 J9 LEUKEMIA RES JI Leuk. Res. PD DEC PY 2004 VL 28 IS 12 BP 1273 EP 1280 DI 10.1016/j.leukres.2004.04.008 PG 8 WC Oncology; Hematology SC Oncology; Hematology GA 866NM UT WOS:000224780200006 PM 15475068 ER PT J AU Gong, JL Koido, S Kato, Y Tanaka, Y Chen, DS Jonas, A Galinsky, I DeAngelo, D Avigan, D Kufe, D Stone, R AF Gong, JL Koido, S Kato, Y Tanaka, Y Chen, DS Jonas, A Galinsky, I DeAngelo, D Avigan, D Kufe, D Stone, R TI Induction of anti-leukemic cytotoxic T lymphocytes by fusion of patient-derived dendritic cells with autologous myeloblasts SO LEUKEMIA RESEARCH LA English DT Article DE generation of dendritic cells; fusion of autologous DC and AML blasts; autologous T cell proliferation; anti-leukemia immunity ID ACUTE MYELOID-LEUKEMIA; THERAPEUTIC ANTITUMOR IMMUNITY; IN-VITRO; CARCINOMA-CELLS; CANCER-IMMUNOTHERAPY; CLINICAL-TRIAL; ANTIGEN; VACCINATION; RNA; IMMUNIZATION AB Presentation of AML antigens by dendritic cells DC could potentially induce a T cell-mediated anti-leukemic immune response. In the present study, we generated DC from adherent (AD-DC) and non-adherent (NAD-DC) myeloblasts obtained from bone marrows of AML patients. Both cell populations displayed morphological, phenotypic and functional properties of DC. The functions of NAD-DC were compared to AD-DC that had been fused with autologous AML blasts (FC/AML). The FC/AML induced greater T cell proliferation and CTL activity against autologous AML blasts (9/10 cases) as compared to NAD-DC. FC/AML may thus represent a promising strategy for DC-based immunotherapy of patients with AML. (C) 2004 Elsevier Ltd. All rights reserved. C1 Harvard Univ, Sch Med, Dana Farber Canc Inst, Boston, MA 02115 USA. Harvard Univ, Sch Med, Beth Israel Deaconess Med Ctr, Boston, MA 02115 USA. RP Gong, JL (reprint author), Harvard Univ, Sch Med, Dana Farber Canc Inst, Boston, MA 02115 USA. EM jgong@medicine.bu.edu FU NCI NIH HHS [R01CA87057] NR 45 TC 30 Z9 33 U1 1 U2 2 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND SN 0145-2126 J9 LEUKEMIA RES JI Leuk. Res. PD DEC PY 2004 VL 28 IS 12 BP 1303 EP 1312 DI 10.1016/j.leukres.2004.03.018 PG 10 WC Oncology; Hematology SC Oncology; Hematology GA 866NM UT WOS:000224780200010 PM 15475072 ER PT J AU Lagakos, S Harrington, D AF Lagakos, S Harrington, D TI Introduction to the Special Issue Dedicated to Marvin Zelen SO LIFETIME DATA ANALYSIS LA English DT Biographical-Item C1 Harvard Univ, Sch Publ Hlth, Dept Biostat, Cambridge, MA 02138 USA. Harvard Univ, Sch Publ Hlth, Dana Farber Canc Inst, Dept Biostat Sci, Cambridge, MA 02138 USA. RP Lagakos, S (reprint author), Harvard Univ, Sch Publ Hlth, Dept Biostat, Cambridge, MA 02138 USA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU SPRINGER PI DORDRECHT PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS SN 1380-7870 J9 LIFETIME DATA ANAL JI Lifetime Data Anal. PD DEC PY 2004 VL 10 IS 4 BP 321 EP 323 DI 10.1007/s10985-004-4769-7 PG 3 WC Mathematics, Interdisciplinary Applications; Statistics & Probability SC Mathematics GA 890OB UT WOS:000226519600001 ER PT J AU Zelen, M AF Zelen, M TI Forward and backward recurrence times and length biased sampling: Age specific models SO LIFETIME DATA ANALYSIS LA English DT Article DE recurrence times; backward recurrence times; forward recurrence times; length based biased sampling; disease modeling; early detection of disease AB Consider a chronic disease process which is beginning to be observed at a point in chronological time. The backward recurrence and forward recurrence times are defined for prevalent cases as the time with disease and the time to leave the disease state, respectively, where the reference point is the point in time at which the disease process is being observed. In this setting the incidence of disease affects the recurrence time distributions. In addition, the survival of prevalent cases will tend to be greater than the population with disease due to length biased sampling. A similar problem arises in models for the early detection of disease. In this case the backward recurrence time is how long an individual has had disease before detection and the forward recurrence time is the time gained by early diagnosis, i.e., until the disease becomes clinical by exhibiting signs or symptoms. In these examples the incidence of disease may be age related resulting in a non-stationary process. The resulting recurrence time distributions are derived as well as some generalization of length-biased sampling. C1 Harvard Univ, Sch Publ Hlth, Boston, MA 02115 USA. Dana Farber Canc Inst, Boston, MA 02115 USA. RP Zelen, M (reprint author), Harvard Univ, Sch Publ Hlth, Boston, MA 02115 USA. EM zelen@jimmy.harvard.edu FU NCI NIH HHS [CA-88270] NR 3 TC 23 Z9 23 U1 0 U2 4 PU SPRINGER PI DORDRECHT PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS SN 1380-7870 J9 LIFETIME DATA ANAL JI Lifetime Data Anal. PD DEC PY 2004 VL 10 IS 4 BP 325 EP 334 DI 10.1007/s10985-004-4770-1 PG 10 WC Mathematics, Interdisciplinary Applications; Statistics & Probability SC Mathematics GA 890OB UT WOS:000226519600002 PM 15690988 ER PT J AU Huang, J Harrington, D AF Huang, J Harrington, D TI Dimension reduction in the linear model for right-censored data: Predicting the change of HIV-1 RNA levels using clinical and protease gene mutation data SO LIFETIME DATA ANALYSIS LA English DT Article DE failure time model; cross-validation; dimension reduction; partial least squares ID PARTIAL LEAST-SQUARES; PRINCIPAL COMPONENTS REGRESSION; RESISTANCE; INHIBITOR; SAQUINAVIR; SHRINKAGE; INDINAVIR; SELECTION AB With rapid development in the technology of measuring disease characteristics at molecular or genetic level, it is possible to collect a large amount of data on various potential predictors of the clinical outcome of interest in medical research. It is often of interest to effectively use the information on a large number of predictors to make prediction of the interested outcome. Various statistical tools were developed to overcome the difficulties caused by the high-dimensionality of the covariate space in the setting of a linear regression model. This paper focuses on the situation, where the interested outcomes are subjected to right censoring. We implemented the extended partial least squares method along With other commonly used approaches for analyzing the high-dimensional covariates to the ACTG333 data set. Especially, we compared the prediction performance of different approaches with extensive cross-validation studies. The results show that the Buckley-James based partial least squares, stepwise subset model selection and principal components regression have similar promising predictive power and the partial least square method has several advantages in terms of interpretability and numerical computation. C1 Northwestern Univ, Feinberg Sch Med, Dept Prevent Med, Chicago, IL 60611 USA. Harvard Univ, Sch Publ Hlth, Dept Biostat, Boston, MA 02115 USA. Dana Farber Canc Inst, Dept Biostat Sci, Boston, MA 02115 USA. RP Huang, J (reprint author), Northwestern Univ, Feinberg Sch Med, Dept Prevent Med, 680 N Lake Shore,Suite 1102, Chicago, IL 60611 USA. EM jjhuang@northwestern.edu FU NIAID NIH HHS [AI24643, AI58217] NR 30 TC 0 Z9 0 U1 1 U2 2 PU SPRINGER PI DORDRECHT PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS SN 1380-7870 J9 LIFETIME DATA ANAL JI Lifetime Data Anal. PD DEC PY 2004 VL 10 IS 4 BP 425 EP 443 DI 10.1007/s10985-004-4776-8 PG 19 WC Mathematics, Interdisciplinary Applications; Statistics & Probability SC Mathematics GA 890OB UT WOS:000226519600008 PM 15690994 ER PT J AU Le Chevalier, T Lynch, T AF Le Chevalier, T Lynch, T TI Adjuvant treatment of lung cancer: current status and potential applications of new regimens SO LUNG CANCER LA English DT Article DE non-small-cell lung cancer; adjuvant; chemotherapy; docetaxel; cisplatin; IALT ID RESECTED STAGE-II; CHEMOTHERAPY; METAANALYSIS; CISPLATIN; THERAPY; TRIALS AB Non-small-cell. Lung cancer (NSCLC) accounts for approximately 80% of lung cancers diagnosed worldwide. Surgical resection offers the best chance for cure for those patients diagnosed with early-stage disease; however, the vast majority of patients will eventually relapse. Despite complete surgical resection, recurrences are likely due to undetectable microscopic disease at diagnosis, making these patients potential candidates for effective adjuvant therapy. Postoperative radiation therapy may actually have a detrimental effect in patients with N0-N1 disease and has been shown to possibly prevent local recurrences in patients with N2 disease. Although results from a large meta-analysis of data on adjuvant chemotherapy suggested an absolute benefit of 5% at 5 years from cisplatin-based chemotherapy, a rate similar to that seen in breast and colon cancers where adjuvant chemotherapy is a standard of care, the use of adjuvant therapy in NSCLC remained controversial. In addition, results of the International Adjuvant Lung Cancer Trial (IALT), which compared adjuvant cisplatin-based chemotherapy to observation in patients with resected stage-I-IIIA NSCLC, suggested that adjuvant therapy had the potential to prevent a substantial number of deaths each year. Two recently reported Landmark studies have demonstrated the survival advantages of adjuvant therapy for patients with early-stage NSCLC. Docetaxel, one of the most active agents for advanced NSCLC, is also regularly used for locally advanced disease as part of neoadjuvant or combined-modality regimens. As recent findings have established the value of adjuvant chemotherapy for early-stage NSCLC, agents such as docetaxel warrant rigorous evaluation in this setting. (C) 2004 Elsevier Science Ltd. C1 Inst Gustave Roussy, Dept Med, F-94800 Villejuif, France. Massachusetts Gen Hosp, Boston, MA 02114 USA. RP Le Chevalier, T (reprint author), Inst Gustave Roussy, Dept Med, F-94800 Villejuif, France. EM tle-che@igr.fr NR 18 TC 10 Z9 12 U1 0 U2 0 PU ELSEVIER SCI IRELAND LTD PI CLARE PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE, IRELAND SN 0169-5002 J9 LUNG CANCER-J IASLC JI Lung Cancer PD DEC PY 2004 VL 46 SU 2 BP S33 EP S39 DI 10.1016/S0169-5002(04)80039-4 PG 7 WC Oncology; Respiratory System SC Oncology; Respiratory System GA 888UZ UT WOS:000226401000005 PM 15698530 ER PT J AU Mandeville, JB Jenkins, BG Chen, YCI Choi, JK Kim, YR Belen, D Liu, C Kosofsky, BE Marota, JJA AF Mandeville, JB Jenkins, BG Chen, YCI Choi, JK Kim, YR Belen, D Liu, C Kosofsky, BE Marota, JJA TI Exogenous contrast agent improves sensitivity of gradient-echo functional magnetic resonance imaging at 9.4 T SO MAGNETIC RESONANCE IN MEDICINE LA English DT Article DE MRI; CBV; BOLD; brain ID CEREBRAL-BLOOD-FLOW; RAT FOREPAW STIMULATION; OXYGEN-CONSUMPTION; OXIDATIVE-METABOLISM; RELATIVE CMRO2; IRON-OXIDE; BRAIN; BOLD; FMRI; MRI AB Relative to common clinical magnetic field strengths, higher fields benefit functional brain imaging both by providing additional signal for high-resolution applications and by improving the sensitivity of endogenous contrast due to the blood oxygen level dependent (BOLD) mechanism, which has limited detection power at low magnetic fields relative to the use of exogenous contrast agent. This study evaluates the utility of iron oxide contrast agent for gradient echo functional MRI at 9.4 T in rodents using cocaine and methylphenidate as stimuli. Relative to the BOLD method, the use of high iron doses and short echo times provided a roughly twofold global increase in functional sensitivity, while also suppressing large vessel signal and reducing susceptibility artifacts. Furthermore, MRI measurements of the functional percentage change in cerebral blood volume (CBV) showed excellent agreement with results obtained at much lower magnetic field strengths, demonstrating that MRI estimates of this quantity are roughly independent of magnetic field when appropriate techniques are employed. The derived field dependencies for relative sensitivity and MRI estimates of the percentage change in CBV suggest that the benefits provided by exogenous agents will persist even at much higher magnetic fields than 9.4 T. (C) 2004 Wiley-Liss, Inc. C1 MIT, Massachusetts Gen Hosp, HMS Athinoula A Martinos Ctr Biomed Imaging, Boston, MA 02114 USA. Massachusetts Gen Hosp, Dept Radiol, Boston, MA 02114 USA. Massachusetts Gen Hosp, Dept Neurol, Boston, MA 02114 USA. Massachusetts Gen Hosp, Dept Anesthesia & Crit Care, Boston, MA 02114 USA. RP Mandeville, JB (reprint author), Massachusetts Gen Hosp, Bldg 149,Room 2301,13th St, Charlestown, MA 02129 USA. EM jbm@nmr.mgh.harvard.edu OI Liu, Christina/0000-0002-5723-177X FU NCRR NIH HHS [P41-RR14075, R01-RR14543A03]; NIBIB NIH HHS [R01-EB001782-01]; NIDA NIH HHS [P01-DA09467B10, K08-DA14665-01] NR 27 TC 54 Z9 56 U1 0 U2 0 PU JOHN WILEY & SONS INC PI HOBOKEN PA 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 0740-3194 J9 MAGNET RESON MED JI Magn. Reson. Med. PD DEC PY 2004 VL 52 IS 6 BP 1272 EP 1281 DI 10.1002/mrm.20278 PG 10 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA 876HA UT WOS:000225486200009 PM 15562489 ER PT J AU Tuch, DS AF Tuch, DS TI Q-Ball imaging SO MAGNETIC RESONANCE IN MEDICINE LA English DT Article DE diffusion MRI; diffusion tensor imaging; high angular; resolution diffusion imaging; tractography ID DIFFUSION-WEIGHTED MRI; HUMAN BRAIN; PROPAGATOR REPRESENTATION; FIELD-GRADIENT; ARCHITECTURE; NMR; SPECTROSCOPY; TISSUE AB Magnetic resonance diffusion tensor imaging (DTI) provides a powerful tool for mapping neural histoarchitecture in vivo. However, DTI can only resolve a single fiber orientation within each imaging voxel due to the constraints of the tensor model. For example, DTI cannot resolve fibers crossing, bending, or twisting within an individual voxel. Intravoxel fiber crossing can be resolved using q-space diffusion imaging, but q-space imaging requires large pulsed field gradients and time-intensive sampling. It is also possible to resolve intravoxel fiber crossing using mixture model decomposition of the high angular resolution diffusion imaging (HARDI) signal, but mixture modeling requires a model of the underlying diffusion process. Recently, it has been shown that the HARDI signal can be reconstructed model-independently using a spherical tomographic inversion called the Funk-Radon transform, also known as the spherical Radon transform. The resulting imaging method, termed q-ball imaging, can resolve multiple intravoxel fiber orientations and does not require any assumptions on the diffusion process such as Gaussianity or multi-Gaussianity. The present paper reviews the theory of q-ball imaging and describes a simple linear matrix formulation for the q-ball reconstruction based on spherical radial basis function interpolation. Open aspects of the q-ball reconstruction algorithm are discussed. (C) 2004 Wiley-Liss, Inc. C1 Massachusetts Gen Hosp, Athinoula A Martinos Ctr Biomed Imaging, NMR Ctr, Charlestown, MA USA. MIT, Harvard Mit Div Hlth Sci & Technol, Cambridge, MA 02139 USA. RP Tuch, DS (reprint author), MGH NMR Ctr, 149 13th St,Room 2301, Charlestown, MA 02129 USA. EM dtuch@nmr.mgh.harvard.edu FU NCRR NIH HHS [RR14075]; NINDS NIH HHS [NS46532] NR 40 TC 936 Z9 949 U1 2 U2 61 PU JOHN WILEY & SONS INC PI HOBOKEN PA 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 0740-3194 J9 MAGNET RESON MED JI Magn. Reson. Med. PD DEC PY 2004 VL 52 IS 6 BP 1358 EP 1372 DI 10.1002/mrm.20279 PG 15 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA 876HA UT WOS:000225486200019 PM 15562495 ER PT J AU Eisen, SV Normand, SL Belanger, AJ Spiro, A Esch, D AF Eisen, SV Normand, SL Belanger, AJ Spiro, A Esch, D TI The revised behavior and symptom identification scale (BASIS-R) - Reliability and validity SO MEDICAL CARE LA English DT Article; Proceedings Paper CT 20th Annual Research Meeting of the Academy-of-Health CY JUN 29, 2003 CL Nashville, TN SP Acad Hlth DE outcomes assessment; mental health research; patient surveys; measurement ID HEALTH OUTCOMES; ITEM; CARE; 21ST-CENTURY; INSTRUMENT; TESTS AB Background: To assess outcomes of health services, providers need brief, responsive, reliable, and valid measures that can be implemented in clinical settings with minimal cost and burden. The Behavior and Symptom Identification Scale (BASIS-32(R)) is a self-report measure developed in 1984 to assess mental health treatment outcomes. During the past 3 years, multiple methods were used to revise the instrument to improve reliability, validity, and applicability to diverse groups of mental health service recipients. Objective: The objective of this study was to field test the revised instrument, make further changes based on analysis of the field test data, and assess reliability and validity of the final version (BASIS-24). Methods: A field test was implemented at 27 treatment sites across the Untied States. A total of 2656 inpatients and 3222 outpatients participated. Factor analytic methods, classic test theory, and item response theory modeling were used to select the most discriminating, nonredundant items for inclusion in the final version of the instrument and to assess its reliability and validity. Item response theory modeling was used to score the instrument. Results: The final instrument includes 24 items assessing 6 domains: depression/ functioning, interpersonal relationships, self-harm, emotional lability, psychosis, and substance abuse. Test-retest and internal consistency reliability were acceptable. Tests of construct and discriminant validity supported the instrument's ability to discriminate groups expected to differ in mental health status, and its correlation with other measures of mental health. Conclusions: Analyses of the BASIS-24 supported its reliability and validity for assessing mental health status from the patient's perspective. C1 Edith Nourse Rogers Mem Vet Adm Hosp, Ctr Hlth Qual Outcomes & Econ Res, Bedford, MA 01730 USA. Boston Univ, Sch Publ Hlth, Dept Hlth Serv, Boston, MA 02215 USA. Boston Univ, Sch Med, Dept Hlth Care Policy, Boston, MA 02215 USA. Harvard Univ, Sch Publ Hlth, Dept Biostat, Boston, MA 02115 USA. VA Boston Healthcare Syst, MAVERIC, Boston, MA USA. Boston Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02215 USA. RP Eisen, SV (reprint author), Edith Nourse Rogers Mem Vet Adm Hosp, Ctr Hlth Qual Outcomes & Econ Res, 200 Springs Rd,152, Bedford, MA 01730 USA. EM seisen@bu.edu FU NIMH NIH HHS [R01 MH58240] NR 50 TC 113 Z9 114 U1 1 U2 5 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0025-7079 J9 MED CARE JI Med. Care PD DEC PY 2004 VL 42 IS 12 BP 1230 EP 1241 DI 10.1097/00005650-200412000-00010 PG 12 WC Health Care Sciences & Services; Health Policy & Services; Public, Environmental & Occupational Health SC Health Care Sciences & Services; Public, Environmental & Occupational Health GA 875US UT WOS:000225448000010 PM 15550803 ER PT J AU Cohen, T Becerra, MC Murray, MB AF Cohen, T Becerra, MC Murray, MB TI Isoniazid resistance and the future of drug-resistant tuberculosis SO MICROBIAL DRUG RESISTANCE-MECHANISMS EPIDEMIOLOGY AND DISEASE LA English DT Article ID NEW-YORK-CITY; MYCOBACTERIUM-TUBERCULOSIS; KATG GENE; SER315THR SUBSTITUTION; MOLECULAR ANALYSIS; GENOMIC MUTATIONS; S315T MUTATION; PREVALENCE; RIFAMPIN; INHA AB Bacterial chromosomal mutations that confer antibiotic resistance often have deleterious effects that impose costs on reproductive fitness. This observation has led to the generalization that in the absence of the selection pressure exerted through treatment, the frequency of resistance will decrease. This model implies that the prudent use of antibiotics will eventually result in a decline in the prevalence of drug resistance. Recent work, however, suggests that some resistance-conferring mutations may not significantly impair fitness and that others may be accompanied by compensatory mutations that restore the organisms' reproductive potential. Thus drug resistance, once introduced, may persist unless specific measures are implemented to target prevalent drug-resistant cases. Here we present ecological evidence to support the hypothesis that mutations at the 315 position of katG confer isoniazid resistance for Mycobacterium tuberculosis without diminishing virulence or transmissibility. C1 Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA. Harvard Univ, Sch Med, Dept Social Med, Boston, MA 02115 USA. Massachusetts Gen Hosp, Infect Dis Unit, Boston, MA 02115 USA. RP Murray, MB (reprint author), Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA. EM mmurray@hsph.harvard.edu RI Cohen, Ted/G-8101-2011 FU NIAID NIH HHS [R01 AI046669, K08 AI01930-01, K08 AI055985, K08 AI055985-02, R01 AI046669-02, T32 AI007433, T32 AI07433] NR 31 TC 32 Z9 36 U1 0 U2 3 PU MARY ANN LIEBERT INC PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 USA SN 1076-6294 J9 MICROB DRUG RESIST JI Microb. Drug Resist.-Mechan. Epidemiol. Dis. PD WIN PY 2004 VL 10 IS 4 BP 280 EP 285 DI 10.1089/mdr.2004.10.280 PG 6 WC Infectious Diseases; Microbiology; Pharmacology & Pharmacy SC Infectious Diseases; Microbiology; Pharmacology & Pharmacy GA 885PO UT WOS:000226169600002 PM 15650371 ER PT J AU Misdraji, J Burgart, LJ Lauwers, GY AF Misdraji, J Burgart, LJ Lauwers, GY TI Defective mismatch repair in the pathogenesis of low-grade appendiceal mucinous neoplasms and adenocarcinomas SO MODERN PATHOLOGY LA English DT Article DE appencliceal neoplasm; mucinous cystadenoma; mucinous adenocarcinoma; mismatch repair; microsatellite instability ID SPORADIC COLORECTAL-CANCER; DNA MICROSATELLITE INSTABILITY; NONPOLYPOSIS COLON-CANCER; HYPERPLASTIC POLYPS; CLINICOPATHOLOGICAL FEATURES; PSEUDOMYXOMA PERITONEI; REPLICATION ERRORS; HMLH1 PROMOTER; HEREDITARY; TUMORS AB Defective DNA mismatch repair has been proposed as a second pathway for colonic carcinogenesis, particularly in tumors arising in the right colon. We investigated whether tumors arising in the appendix are associated with defective DNA mismatch repair using immunohistochemistry for mismatch repair enzymes hMLH-1, hMSH-2, hMSH-6, and hPMS-2. These immunoassays have been shown to be highly sensitive and specific for defective DNA mismatch repair in sporadic and familial adenocarcinomas. Sporadic adenocarcinomas with defective DNA mismatch repair essentially always show loss of hMLH-1 while loss of hMSH-2, hMSH-6, or hPMS-2 is almost always due to germline mutation. In all, 35 cases of appendiceal epithelial neoplasms were evaluated, comprising 18 low-grade appendiceal mucinous neoplasms confined to the appendix; eight low-grade appendiceal mucinous neoplasms with extra-appendiceal spread (five peritoneum and ovaries, two peritoneum, one ovaries only); and nine invasive adenocarcinomas (three with metastatic disease). All immunohistochemical slides were reviewed by two pathologists. One (11%) invasive adenocarcinoma showed absent expression of hMSH-2 and hMSH-6, but preserved hMLH-1 and hPMS-2 expression. This case was a 26-year-old female with a history of synovial sarcoma who presented with acute appendicitis and appendiceal perforation (median age for other invasive carcinomas, 62 years; range 38-76 years). The appendiceal tumor was a moderately differentiated, colonic-type adenocarcinoma without significant extracellular mucin or tumor-infiltrating lymphocytes. The remaining invasive carcinomas and low-grade appendiceal mucinous neoplasms demonstrated preserved expression of all mismatch repair enzymes, including the seven cases in which extra-appendiceal tumor was also evaluated. We conclude that defective DNA mismatch repair does not play a role in the pathogenesis of low-grade appendiceal mucinous neoplasms. Defective DNA mismatch was found in 11% of invasive carcinomas, likely due to a germline mutation. These findings suggest that sporadic appendiceal neoplasia rarely arises through the defective DNA mismatch repair (mutator) pathway. C1 Harvard Univ, Massachusetts Gen Hosp, Sch Med, James Homer Wright Pathol Labs, Boston, MA 02114 USA. Mayo Clin & Mayo Fdn, Dept Pathol, Rochester, MN 55905 USA. RP Misdraji, J (reprint author), Harvard Univ, Massachusetts Gen Hosp, Sch Med, James Homer Wright Pathol Labs, Warren Bldg 831, Boston, MA 02114 USA. EM jmisdraji@partners.org NR 45 TC 13 Z9 13 U1 0 U2 1 PU NATURE PUBLISHING GROUP PI NEW YORK PA 345 PARK AVE SOUTH, NEW YORK, NY 10010-1707 USA SN 0893-3952 J9 MODERN PATHOL JI Mod. Pathol. PD DEC PY 2004 VL 17 IS 12 BP 1447 EP 1454 DI 10.1038/modpathol.3800212 PG 8 WC Pathology SC Pathology GA 875ET UT WOS:000225403800001 PM 15354187 ER PT J AU Wang, L Pitman, MB Fernandez-del Castillo, C Dal Cin, P Oliva, E AF Wang, L Pitman, MB Fernandez-del Castillo, C Dal Cin, P Oliva, E TI Choriocarcinoma involving the pancreas as first manifestation of a metastatic regressing mixed testicular germ cell tumor SO MODERN PATHOLOGY LA English DT Article DE choriocarcinoma; metastatic malignancy; pancreas; germ cell tumor; testis; regressing ID FINE-NEEDLE-ASPIRATION; ENDOSCOPIC ULTRASOUND; EXTRAGENITAL CHORIOCARCINOMA; RENAL PELVIS; CARCINOMA; DIFFERENTIATION; ADENOCARCINOMA; BIOPSY; DIAGNOSIS; CYTOLOGY AB We describe an unusual case of metastatic choriocarcinoma of the pancreas arising from a regressing testicular mixed germ cell tumor that clinically mimicked a primary pancreatic tumor. A 54-year-old male presented with a 2-month history of progressive upper abdominal pain, weight loss, and jaundice. He also had a history of recurrent epididymitis associated with the presence of a right testicular mass shown to be cystic by ultrasound and stable for at least 10 years. A computed tomography scan showed an isolated 6 cm mass in the head of the pancreas. A pancreaticoduodenectomy was performed. Upon histological examination, the pancreatic tumor showed extensive hemorrhage and necrosis. In the viable area, the tumor was composed of an intimate mixture of mononuclear cytotrophoblast cells and multinucleated syncytiotrophoblasts with vascular invasion. These characteristic features led to the correct diagnosis on frozen section. The cytology of the tumor was nonspecific and suggested undifferentiated carcinoma of the pancreas. The trophoblastic origin of the tumor cells was confirmed by immunohistochemistry staining. The testicular mass showed a regressed mixed germ cell tumor of predominantly seminoma with focal teratoma but without a choriocarcinoma component. In conclusion, we present a rare and unusual case of a regressing testicular mixed germ cell tumor that presented as a primary pancreatic tumor. Cytological features of the pancreatic mass were not specific and raised the possibility of a primary undifferentiated carcinoma of the pancreas. Characteristic histological features of choriocarcinoma led to the correct diagnosis on frozen section. Subsequent resection of the testicular mass confirmed the presence of a cystic and scarring (regressing) mixed germ cell tumor but without evidence of choriocarcinoma. C1 Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Pathol, Boston, MA 02114 USA. Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Surg, Boston, MA 02114 USA. Harvard Univ, Brigham & Womens Hosp, Sch Med, Dept Pathol, Boston, MA 02115 USA. RP Pitman, MB (reprint author), Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Pathol, 14 Fruit St, Boston, MA 02114 USA. EM mpitman@partners.org NR 47 TC 9 Z9 10 U1 0 U2 1 PU NATURE PUBLISHING GROUP PI NEW YORK PA 345 PARK AVE SOUTH, NEW YORK, NY 10010-1707 USA SN 0893-3952 J9 MODERN PATHOL JI Mod. Pathol. PD DEC PY 2004 VL 17 IS 12 BP 1573 EP 1580 DI 10.1038/modpathol.3800226 PG 8 WC Pathology SC Pathology GA 875ET UT WOS:000225403800016 PM 15545958 ER PT J AU Park, S Lee, YJ Lee, HJ Seki, T Hong, KH Park, J Beppu, H Lim, IK Yoon, JW Li, E Kim, SJ Oh, SP AF Park, S Lee, YJ Lee, HJ Seki, T Hong, KH Park, J Beppu, H Lim, IK Yoon, JW Li, E Kim, SJ Oh, SP TI B-cell translocation gene 2 (Btg2) regulates vertebral patterning by modulating bone morphogenetic protein/Smad signaling SO MOLECULAR AND CELLULAR BIOLOGY LA English DT Article ID TRANSLOCATION GENE-2 PROTEIN; CELLULAR-RESPONSE; AXIAL SKELETON; DNA-DAMAGE; EXPRESSION; DIFFERENTIATION; IDENTIFICATION; TRANSCRIPTION; COMPONENT; RECEPTOR AB Btg2 is a primary p53 transcriptional target gene which may function as a coactivator-corepressor and/or an adaptor molecule that modulates the activities of its interacting proteins. We have generated Btg2-null mice to elucidate the in vivo function of Btg2. Btg2-null mice are viable and fertile but exhibit posterior homeotic transformations of the axial vertebrae in a dose-dependent manner. Consistent with its role in vertebral patterning, Btg2 is expressed in the presomitic mesoderm, tail bud, and somites during somitogenesis. We further provide biochemical evidence that Btg2 interacts with bone morphogenetic protein (BMP)-activated Smads and enhances the transcriptional activity of BMP signaling. In view of the genetic evidence that reduced BMP signaling causes posteriorization of the vertebral pattern, we propose that the observed vertebral phenotype in Btg2-null mice is due to attenuated BMP signaling. C1 Univ Florida, Dept Physiol & Funct Genom, Coll Med, Gainesville, FL 32610 USA. Rosalind Franklin Univ Med & Sci, Dept Microbiol & Immunol, Immunol Res Ctr, Bligh Canc Res Labs, N Chicago, IL USA. NCI, Lab Cell Regulat & Carcinogenesis, Bethesda, MD 20892 USA. Massachusetts Gen Hosp, Cardiovasc Res Ctr, Charlestown, MA USA. Ajou Univ, Dept Biochem & Mol Biol, Sch Med, Suwon 441749, South Korea. RP Oh, SP (reprint author), Univ Florida, Dept Physiol & Funct Genom, Coll Med, 1600 SW Archer Rd,Room D533D, Gainesville, FL 32610 USA. EM ohp@phys.med.ufl.edu OI Park, Sean/0000-0003-3814-853X FU NHLBI NIH HHS [HL64024, R01 HL064024] NR 43 TC 44 Z9 46 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA SN 0270-7306 J9 MOL CELL BIOL JI Mol. Cell. Biol. PD DEC PY 2004 VL 24 IS 23 BP 10256 EP 10262 DI 10.1128/MCB.24.23.10256-10262.2004 PG 7 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA 871WR UT WOS:000225167800015 PM 15542835 ER PT J AU Takahashi, C Contreras, B Bronson, RT Loda, M Ewen, ME AF Takahashi, C Contreras, B Bronson, RT Loda, M Ewen, ME TI Genetic interaction between Rb and K-ras in the control of differentiation and tumor suppression SO MOLECULAR AND CELLULAR BIOLOGY LA English DT Article ID SKELETAL-MUSCLE CELLS; RETINOBLASTOMA PROTEIN; ADIPOCYTE DIFFERENTIATION; N-RAS; GLUCOCORTICOID RECEPTOR; MEDIATED TRANSCRIPTION; INCOMPLETE PENETRANCE; MOUSE; PRB; APOPTOSIS AB Although the retinoblastoma protein (pRb) has been implicated in the processes of cellular differentiation, there is no compelling genetic or in vivo evidence that such activities contribute to pRb-mediated tumor suppression. Motivated by cell culture studies suggesting that Ras is a downstream effector of pRb in the control of differentiation, we have examined the tumor and developmental phenotypes of Rb and K-ras double-knockout mice. We find that heterozygosity for K-ras (i) rescued a unique subset of developmental defects that characterize Rb-deficient embryos by affecting differentiation but not proliferation and (ii) significantly enhanced the degree of differentiation of pituitary adenocarcinomas arising in Rb heterozygotes, leading to their prolonged survival. These observations suggest that Rb and K-ras function together in vivo, in the contexts of both embryonic and tumor development, and that the ability to affect differentiation is a major facet of the tumor suppressor function of pRb. C1 Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02115 USA. Harvard Univ, Sch Med, Dept Med, Boston, MA USA. Harvard Univ, Sch Med, Dept Pathol, Boston, MA 02115 USA. Tufts Univ, Sch Med, Dept Pathol, Boston, MA 02111 USA. Tufts Univ, Sch Vet Med, Dept Pathol, Boston, MA USA. Kyoto Univ, Grad Sch Med, Dept Mol Oncol, Kyoto, Japan. Kyoto Univ, Grad Sch Med, Cent Ctr Excellence 21, Kyoto, Japan. RP Ewen, ME (reprint author), Dana Farber Canc Inst, Dept Med Oncol, 44 Binney St, Boston, MA 02115 USA. EM mark_ewen@dfci.harvard.edu FU NCI NIH HHS [R01 CA065842, R01CA65842, P01CA89021, P01 CA089021] NR 49 TC 29 Z9 29 U1 0 U2 2 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA SN 0270-7306 J9 MOL CELL BIOL JI Mol. Cell. Biol. PD DEC PY 2004 VL 24 IS 23 BP 10406 EP 10415 DI 10.1128/MCB.24.23.10406-10415.2004 PG 10 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA 871WR UT WOS:000225167800028 PM 15542848 ER PT J AU Bragg, DC Kaufman, CA Kock, N Breakefield, XO AF Bragg, DC Kaufman, CA Kock, N Breakefield, XO TI Inhibition of N-linked glycosylation prevents inclusion formation by the dystonia-related mutant form of torsinA SO MOLECULAR AND CELLULAR NEUROSCIENCE LA English DT Article ID ENDOPLASMIC-RETICULUM; NUCLEAR-ENVELOPE; HUMAN BRAIN; ALPHA-SYNUCLEIN; LEWY BODIES; GENE DYT1; PROTEIN; EXPRESSION; MEMBRANE; CELLS AB Most cases of early-onset torsion dystonia are associated with a mutation in the DYT1 gene that results in the loss of a glutamic acid residue in the carboxy terminus of the encoded protein, torsinA. When overexpressed in cultured cells, wild-type torsinA distributes diffusely throughout the endoplasmic reticulum (ER), while the dystonia-related mutant, torsinADeltaE, accumulates within multilamellar membrane inclusions. Here we show that inclusion formation requires the addition of an N-linked oligosaccharide to one of two asparagine residues within the ATP-binding domain of the mutant protein. In the absence of this modification, overexpressed torsinADeltaE was localized diffusely throughout the cell in a reticular pattern resembling that of wild-type torsinA. In contrast, the localization of wild-type torsinA did not appear to vary with its glycosylation state. These results thus indicate that torsinADeltaE must achieve a specific conformation to induce formation of intracellular membrane inclusions. (C) 2004 Elsevier Inc. All rights reserved. C1 Massachusetts Gen Hosp, Dept Neurol, Mol Neurogenet Unit, Boston, MA 02129 USA. Massachusetts Gen Hosp, Dept Radiol, Boston, MA 02129 USA. Harvard Univ, Sch Med, Neurosci Program, Boston, MA 02114 USA. RP Bragg, DC (reprint author), Massachusetts Gen Hosp, Dept Neurol, Mol Neurogenet Unit, 6th Floor,Bldg 149,13th St, Boston, MA 02129 USA. EM bragg@helix.mgh.harvard.edu FU NIA NIH HHS [5 T32 AG00222]; NINDS NIH HHS [NS37409, NS28384] NR 34 TC 19 Z9 19 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 1044-7431 J9 MOL CELL NEUROSCI JI Mol. Cell. Neurosci. PD DEC PY 2004 VL 27 IS 4 BP 417 EP 426 DI 10.1016/j.mcn.2004.07.009 PG 10 WC Neurosciences SC Neurosciences & Neurology GA 875UX UT WOS:000225448600006 PM 15555920 ER PT J AU Hunter, DD Zhang, ML Ferguson, JW Koch, M Brunken, WJ AF Hunter, DD Zhang, ML Ferguson, JW Koch, M Brunken, WJ TI The extracellular matrix component WIF-1 is expressed during, and can modulate, retinal development SO MOLECULAR AND CELLULAR NEUROSCIENCE LA English DT Article ID RAT RETINA; PHOTORECEPTOR DIFFERENTIATION; MULTIPOTENT PRECURSORS; CELL-DIFFERENTIATION; TARGETED DISRUPTION; INT-1 PROTOONCOGENE; LAMININ EXPRESSION; SECRETED PROTEIN; FROG RETINA; S-LAMININ AB We have shown previously that components of the extracellular matrix (ECM) modulate neuronal development. Here, we searched for additional ECM elements that might play roles in retinal histogenesis and identified a secreted glycoprotein that is heavily expressed in the retina. This molecule, named by others Wnt Inhibitory Factor-1 (WIF-1), is expressed during and after the period of rod photoreceptor morphogenesis in the mouse. We show that a potential WIF-1 ligand, Wnt4, as well as a potential Wnt4 receptor, fzd4, and a potential Wnt4 coreceptor, LRP6, are expressed in the region of, and at the time of, rod photoreceptor genesis. WIF-1 and Wnt4 are coexpressed during retinal development and bind to each other; therefore, they are likely to interact during rod production. WIF-1 protein inhibits rod production, and anti-WIF-1 antibodies increase rod production; in contrast, Wnt4 promotes rod production. Together, these data suggest that WIF-1 and Wnt4, both components of the ECM, regulate mammalian photoreceptor development. (C) 2004 Elsevier Inc. All rights reserved. C1 Tufts Univ, Sch Med, Dept Neurosci, Boston, MA 02111 USA. Tufts Univ, Sch Med, Dept Anat & Cellular Biol, Boston, MA 02111 USA. Tufts Univ, Sch Med, Dept Ophthalmol, Boston, MA 02111 USA. Tufts Univ, Sch Med, Tufts Ctr Vision Res, Boston, MA 02111 USA. Harvard Univ, Massachusetts Gen Hosp, Cutaneous Biol Res Ctr, Charlestown, MA USA. RP Hunter, DD (reprint author), Tufts Univ, Sch Med, Dept Neurosci, 136 Harrison Ave, Boston, MA 02111 USA. EM dale.hunter@tufts.edu OI Brunken, William J/0000-0001-7330-1814 FU NEI NIH HHS [EY12037, EY13078, P30 EY013078]; NINDS NIH HHS [R01 NS039502-03, NS39502, R01 NS039502, R01 NS039502-04] NR 55 TC 45 Z9 50 U1 0 U2 5 PU ACADEMIC PRESS INC ELSEVIER SCIENCE PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA SN 1044-7431 J9 MOL CELL NEUROSCI JI Mol. Cell. Neurosci. PD DEC PY 2004 VL 27 IS 4 BP 477 EP 488 DI 10.1016/j.mcn.2004.08.003 PG 12 WC Neurosciences SC Neurosciences & Neurology GA 875UX UT WOS:000225448600011 PM 15555925 ER PT J AU Didenko, VV Minchew, CL Shuman, S Baskin, DS AF Didenko, VV Minchew, CL Shuman, S Baskin, DS TI Semi-artificial fluorescent molecular machine for DNA damage detection SO NANO LETTERS LA English DT Article ID TOPOISOMERASE-I; LIVING ORGANISMS; RAT THYMOCYTES; APOPTOSIS; CLEAVAGE; FRAGMENTATION; DEGRADATION; SUBSTRATE; CELLS AB The design of artificial molecular machines is complicated because the mechanics used in macromachines is not readily adaptable for nano environments. We constructed a semi-artificial molecular device, which contains a naturally occurring molecular machine-a vaccinia virus encoded protein-linked with an artificial part. The self-assembled construct makes two fluorescently labeled detector units. It is the first sensor capable of selectively detecting different types of DNA breaks, exemplifying a practical approach to the design of molecular devices. C1 Baylor Coll Med, Houston, TX 77030 USA. Michael E DeBakey Vet Affairs Med Ctr, Houston, TX USA. Sloan Kettering Inst, New York, NY USA. RP Didenko, VV (reprint author), 2002 Holcombe Blvd,Bldg 109,Rm 204, Houston, TX 77030 USA. EM vdidenko@bcm.tmc.edu FU NIA NIH HHS [R03 AG022664-01, R03 AG022664-01, R03 AG022664] NR 41 TC 6 Z9 6 U1 1 U2 4 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA SN 1530-6984 J9 NANO LETT JI Nano Lett. PD DEC PY 2004 VL 4 IS 12 BP 2461 EP 2466 DI 10.1021/nl048357e PG 6 WC Chemistry, Multidisciplinary; Chemistry, Physical; Nanoscience & Nanotechnology; Materials Science, Multidisciplinary; Physics, Applied; Physics, Condensed Matter SC Chemistry; Science & Technology - Other Topics; Materials Science; Physics GA 878XS UT WOS:000225681300029 PM 17330146 ER PT J AU Temel, J AF Temel, Jennifer TI Can weight loss at presentation predict patient outcome in lung cancer? SO NATURE CLINICAL PRACTICE ONCOLOGY LA English DT Editorial Material DE chemotherapy; mesothelioma; non-small-cell lung cancer; small-cell lung cancer; weight C1 Massachusetts Gen Hosp, Boston, MA 02114 USA. RP Temel, J (reprint author), Harvard Univ, Sch Med, Ctr Thorac Canc, 55 Fruit St, Boston, MA 02114 USA. EM JTemel@partners.org NR 7 TC 1 Z9 1 U1 0 U2 0 PU NATURE PUBLISHING GROUP PI NEW YORK PA 75 VARICK STREET, 9TH FLOOR, NEW YORK, NY 10013-1917 USA SN 1743-4254 J9 NAT CLIN PRACT ONCOL JI Nat. Clin. Pract. Oncol. PD DEC PY 2004 VL 1 IS 2 BP 68 EP 69 DI 10.1038/ncponc0033 PG 2 WC Oncology SC Oncology GA V43JK UT WOS:000202931200005 PM 16264819 ER PT J AU Yock, TI Tarbell, NJ AF Yock, Torunn I. Tarbell, Nancy J. TI Technology Insight: proton beam radiotherapy for treatment in pediatric brain tumors SO NATURE CLINICAL PRACTICE ONCOLOGY LA English DT Review DE intensity-modulated radiation therapy; pediatric brain tumors; proton radidiotherapy; stereotactic radiotherapy; treatment AB Tumors of the central nervous system are the most common solid tumor in childhood. Treatment options for childhood brain tumors include radiation therapy, surgery and chemotherapy, often given in combination. Radiation therapy regularly has a pivotal role in treatment, and technological advancements during the past quarter of a century have dramatically improved the ability to deliver radiation in a more focused manner. Improvements in imaging and computing ability led to better targeting of tumor tissue using conventional X-ray therapy. These advances have been harnessed for proton radiation therapy. Proton radiotherapy has special physical characteristics that allow normal tissues to be spared better than even the most conformal photon radiation, and it will reduce the complications from treatment. This review discusses the characteristics of proton radiation, and describes examples of pediatric brain tumor patients who would benefit most from this form of treatment. C1 Massachusetts Gen Hosp, Dept Radiat Oncol, Boston, MA 02114 USA. Harvard Univ, Sch Med, Boston, MA USA. RP Yock, TI (reprint author), Massachusetts Gen Hosp, Dept Radiat Oncol, 55 Fruit St, Boston, MA 02114 USA. EM tyock@partners.org NR 46 TC 35 Z9 35 U1 1 U2 7 PU NATURE PUBLISHING GROUP PI NEW YORK PA 75 VARICK STREET, 9TH FLOOR, NEW YORK, NY 10013-1917 USA SN 1743-4254 J9 NAT CLIN PRACT ONCOL JI Nat. Clin. Pract. Oncol. PD DEC PY 2004 VL 1 IS 2 BP 97 EP 103 DI 10.1038/ncponc0090 PG 7 WC Oncology SC Oncology GA V43JK UT WOS:000202931200013 PM 16264827 ER PT J AU Ansel, KM Greenwald, RJ Agarwal, S Bassing, CH Monticelli, S Interlandi, J Djuretic, IM Lee, DU Sharpe, AH Walt, F Rao, A AF Ansel, KM Greenwald, RJ Agarwal, S Bassing, CH Monticelli, S Interlandi, J Djuretic, IM Lee, DU Sharpe, AH Walt, F Rao, A TI Deletion of a conserved Il4 silencer impairs T helper type 1-mediated immunity SO NATURE IMMUNOLOGY LA English DT Article ID SPECIES SEQUENCE COMPARISONS; CYTOKINE GENE-EXPRESSION; IL-4 GENE; CELL-DIFFERENTIATION; LEISHMANIA-MAJOR; MAST-CELLS; HYPERSENSITIVE SITES; COORDINATE REGULATOR; TRANSCRIPTION FACTOR; HISTONE ACETYLATION AB Helper T cell differentiation involves silencing as well as activation of gene expression. We have identified a conserved silencer of the gene encoding interleukin 4 (Il4) marked by DNase I hypersensitivity (HS IV) and permissive chromatin structure in all helper T cells. Deletion of HS IV increased Il4 and Il13 transcription by naive T cells and led to T helper type 2 skewing in vitro. HS IV controlled Il4 silencing during T helper type 1 differentiation, as HS IV-deficient T helper type 1 cells that expressed interferon-gamma also produced abundant interleukin 4 in vitro and in vivo. Despite mounting a vigorous interferon-gamma response, HS IV-deficient mice were more susceptible to Leishmania major infection than were wild-type littermate control mice, showing a critical function for Il4 silencing in T helper type 1-mediated immunity. C1 Harvard Univ, Sch Med, Dept Pathol, Boston, MA 02115 USA. CBR Inst Biomed Res, Boston, MA 02115 USA. Brigham & Womens Hosp, Dept Pathol, Boston, MA 02115 USA. Harvard Univ, Sch Med, Dept Genet, Boston, MA 02115 USA. Univ Milan, Div Biotechnol Appl Med Sci, I-20133 Milan, Italy. Howard Hughes Med Inst, Boston, MA 02115 USA. Childrens Hosp, Boston, MA 02115 USA. RP Rao, A (reprint author), Harvard Univ, Sch Med, Dept Pathol, Boston, MA 02115 USA. EM arao@cbr.med.harvard.edu FU NHLBI NIH HHS [HL67664]; NIAID NIH HHS [AI20047, AI35714, AI38310, AI44432] NR 50 TC 87 Z9 89 U1 0 U2 0 PU NATURE PUBLISHING GROUP PI NEW YORK PA 345 PARK AVE SOUTH, NEW YORK, NY 10010-1707 USA SN 1529-2908 J9 NAT IMMUNOL JI Nat. Immunol. PD DEC PY 2004 VL 5 IS 12 BP 1251 EP 1259 DI 10.1038/ni1135 PG 9 WC Immunology SC Immunology GA 874MC UT WOS:000225353500014 PM 15516924 ER PT J AU Zarrin, AA Alt, FW Chaudhuri, J Stokes, N Kaushal, D Du Pasquier, L Tian, M AF Zarrin, AA Alt, FW Chaudhuri, J Stokes, N Kaushal, D Du Pasquier, L Tian, M TI An evolutionarily conserved target motif for immunoglobulin class-switch recombination SO NATURE IMMUNOLOGY LA English DT Article ID SINGLE-STRANDED-DNA; CYTIDINE DEAMINASE AID; SOMATIC HYPERMUTATION; ANTIBODY DIVERSIFICATION; TANDEM REPEATS; IN-VITRO; REGION; TRANSCRIPTION; URACIL; REPAIR AB Immunoglobulin H class-switch recombination (CSR) occurs between switch regions and requires transcription and activation-induced cytidine deaminase (AID). Transcription through mammalian switch regions, because of their GC-rich composition, generates stable R-loops, which provide single-stranded DNA substrates for AID. However, we show here that the Xenopus laevis switch region S-mu, which is rich in AT and not prone to form R-loops, can functionally replace a mouse switch region to mediate CSR in vivo. X. laevis S-mu-mediated CSR occurred mostly in a region of AGCT repeats targeted by the AID-replication protein A complex when transcribed in vitro. We propose that AGCT is a primordial CSR motif that targets AID through a non-R-loop mechanism involving an AID-replication protein A complex. C1 Harvard Univ, Sch Med, Howard Hughes Med Inst, Childrens Hosp,CBR Inst Biomed Res, Boston, MA 02115 USA. Harvard Univ, Sch Med, Dept Genet, Boston, MA 02115 USA. Univ Basel, Inst Zool, CH-4051 Basel, Switzerland. RP Alt, FW (reprint author), Harvard Univ, Sch Med, Howard Hughes Med Inst, Childrens Hosp,CBR Inst Biomed Res, Boston, MA 02115 USA. EM alt@enders.tch.harvard.edu FU NIAID NIH HHS [AI31541, AI07512] NR 50 TC 108 Z9 112 U1 0 U2 0 PU NATURE PUBLISHING GROUP PI NEW YORK PA 345 PARK AVE SOUTH, NEW YORK, NY 10010-1707 USA SN 1529-2908 J9 NAT IMMUNOL JI Nat. Immunol. PD DEC PY 2004 VL 5 IS 12 BP 1275 EP 1281 DI 10.1038/ni1137 PG 7 WC Immunology SC Immunology GA 874MC UT WOS:000225353500017 PM 15531884 ER PT J AU Lo, EH AF Lo, EH TI Combination stroke therapy: easy as APC? SO NATURE MEDICINE LA English DT Editorial Material ID TISSUE-PLASMINOGEN ACTIVATOR; FOCAL CEREBRAL-ISCHEMIA; PROTEIN-C; NEURONAL DAMAGE; APOPTOSIS; INDUCTION C1 Massachusetts Gen Hosp, Dept Radiol, Neuroprotect Res Lab, Boston, MA 02114 USA. Massachusetts Gen Hosp, Dept Neurol, Neuroprotect Res Lab, Boston, MA 02114 USA. Harvard Univ, Sch Med, Program Neurosci, Boston, MA 02115 USA. RP Lo, EH (reprint author), Massachusetts Gen Hosp, Dept Radiol, Neuroprotect Res Lab, 32 Fruit St, Boston, MA 02114 USA. EM Lo@helix.mgh.harvard.edu NR 14 TC 9 Z9 9 U1 0 U2 0 PU NATURE PUBLISHING GROUP PI NEW YORK PA 345 PARK AVE SOUTH, NEW YORK, NY 10010-1707 USA SN 1078-8956 J9 NAT MED JI Nat. Med. PD DEC PY 2004 VL 10 IS 12 BP 1295 EP 1296 DI 10.1038/nm1204-1295 PG 3 WC Biochemistry & Molecular Biology; Cell Biology; Medicine, Research & Experimental SC Biochemistry & Molecular Biology; Cell Biology; Research & Experimental Medicine GA 876MK UT WOS:000225500900018 PM 15580249 ER PT J AU Nussenzweig, MC Alt, FW AF Nussenzweig, MC Alt, FW TI Antibody diversity: one enzyme to rule them all SO NATURE MEDICINE LA English DT Editorial Material ID CLASS-SWITCH RECOMBINATION; SINGLE-STRANDED-DNA; CYTIDINE DEAMINASE AID; SOMATIC HYPERMUTATION; B-CELLS; TRANSCRIPTION; MUTATION; REGION; DIVERSIFICATION; EXPRESSION C1 Rockefeller Univ, Lab Mol Immunol, New York, NY 10021 USA. Rockefeller Univ, Howard Hughes Med Inst, New York, NY 10021 USA. Childrens Hosp, Howard Hughes Med Inst, Boston, MA 02115 USA. Harvard Univ, Sch Med, Dept Genet, Boston, MA 02115 USA. Harvard Univ, Sch Med, Ctr Blood Res, Boston, MA 02115 USA. RP Nussenzweig, MC (reprint author), Rockefeller Univ, Lab Mol Immunol, 1230 York Ave, New York, NY 10021 USA. EM nussen@mail.rockefeller.edu; alt@enders.tch.harvard.edu NR 26 TC 26 Z9 27 U1 0 U2 0 PU NATURE PUBLISHING GROUP PI NEW YORK PA 345 PARK AVE SOUTH, NEW YORK, NY 10010-1707 USA SN 1078-8956 J9 NAT MED JI Nat. Med. PD DEC PY 2004 VL 10 IS 12 BP 1304 EP 1305 DI 10.1038/nm1204-1304 PG 2 WC Biochemistry & Molecular Biology; Cell Biology; Medicine, Research & Experimental SC Biochemistry & Molecular Biology; Cell Biology; Research & Experimental Medicine GA 876MK UT WOS:000225500900023 PM 15580255 ER PT J AU Williams, ZM Bush, G Rauch, SL Cosgrove, GR Eskandar, EN AF Williams, ZM Bush, G Rauch, SL Cosgrove, GR Eskandar, EN TI Human anterior cingulate neurons and the integration of monetary reward with motor responses SO NATURE NEUROSCIENCE LA English DT Article ID POSITRON-EMISSION-TOMOGRAPHY; DECISION-MAKING; CORTEX; CINGULOTOMY; SELECTION; STIMULUS AB The human dorsal anterior cingulate cortex (dACC) has been implicated in cognitive processes that have been proposed to play a role in integrating contextual information needed to select or modify appropriate motor responses. In humans, however, there has been little direct evidence tying the dACC to the integration of contextual information and behavioral response. We used single-neuron recordings from human subjects to evaluate the role of the dACC in reward-based decision making. Subjects undergoing planned surgical cingulotomy performed a task where they were instructed to make specific movements in response to changing monetary rewards. In many neurons, activity increased in response to a diminished reward, and was also predictive of the movement ultimately made. After dACC ablation, subjects made selectively more errors when they were required to change movement based on reward reduction. These findings suggest that the dACC in humans plays an important role in linking reward-related information with alternative actions. C1 Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Neurosurg, Boston, MA 02114 USA. Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Psychiat, Boston, MA 02114 USA. RP Eskandar, EN (reprint author), Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Neurosurg, Boston, MA 02114 USA. EM eeskandar@partners.org NR 31 TC 184 Z9 185 U1 1 U2 8 PU NATURE PUBLISHING GROUP PI NEW YORK PA 345 PARK AVE SOUTH, NEW YORK, NY 10010-1707 USA SN 1097-6256 J9 NAT NEUROSCI JI Nat. Neurosci. PD DEC PY 2004 VL 7 IS 12 BP 1370 EP 1375 DI 10.1038/nn1354 PG 6 WC Neurosciences SC Neurosciences & Neurology GA 874MG UT WOS:000225353900018 PM 15558064 ER PT J AU Guidetti, P Luthi-Carter, RE Augood, SJ Schwarcz, R AF Guidetti, P Luthi-Carter, RE Augood, SJ Schwarcz, R TI Neostriatal and cortical quinolinate levels are increased in early grade Huntington's disease SO NEUROBIOLOGY OF DISEASE LA English DT Article DE excitotoxins; excitotoxicity; free radicals; 3-hydroxykynurenine; kynurenines; kynurenic acid; neurodegeneration; neuroprotection ID ASPARTATE RECEPTOR ACTIVATION; RAT-BRAIN; KYNURENIC ACID; NMDA RECEPTORS; MOUSE MODELS; 3-HYDROXYKYNURENINE; STRIATUM; TOXICITY; PATHWAY; ASSOCIATION AB Huntington's disease (HD), an inherited neurodegenerative disorder, is caused by an abnormal polyglutamine expansion in the huntingtin protein. This genetic defect may result in heightened neuronal susceptibility to excitotoxic injury, a mechanism that has been postulated to play a critical role in HD. Quinolinate (QUIN) and kynurenate (KYNA), two endogenous neuroactive metabolites of the kynurenine pathway of tryptophan degradation, have been proposed to modulate excitotoxic neuronal death in HD. A third kynurenine pathway metabolite, the free radical generator 3-hydroxykynurenine (3-HK), has also been hypothesized to play a causal role in the pathogenesis of HD. We show here that the brain levels of both 3-HK and QUIN are increased three to four-fold in low-grade (grade 0/1) HD brain. These changes were seen in the neocortex and in the neostriatum, but not in the cerebellum. In contrast, brain 3-HK and QUIN levels were either unchanged or tended to decrease in grade 2 and advanced grade (grades 3-4) HD brain. Brain kynurenine and KYNA levels fluctuated only modestly as the illness progressed. These results support a possible involvement of 3-HK and QUIN in the early phases of HD pathophysiology and indicate novel therapeutic strategies against the disease. (C) 2004 Elsevier Inc. All rights reserved. C1 Univ Maryland, Maryland Psychiat Res Ctr, Sch Med, Baltimore, MD 21228 USA. Massachusetts Gen Hosp, MassGen Inst Neurodegenerat Dis, Boston, MA 02129 USA. RP Schwarcz, R (reprint author), Univ Maryland, Maryland Psychiat Res Ctr, Sch Med, POB 21247, Baltimore, MD 21228 USA. EM rschwarc@mprc.umaryland.edu NR 52 TC 124 Z9 128 U1 0 U2 2 PU ACADEMIC PRESS INC ELSEVIER SCIENCE PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA SN 0969-9961 J9 NEUROBIOL DIS JI Neurobiol. Dis. PD DEC PY 2004 VL 17 IS 3 BP 455 EP 461 DI 10.1016/j.ndb.2004.07.006 PG 7 WC Neurosciences SC Neurosciences & Neurology GA 878UD UT WOS:000225671600010 PM 15571981 ER PT J AU Li, YJ Pericak-Vance, MA Haines, JL Siddique, N McKenna-Yasek, D Hung, WY Sapp, P Allen, CI Chen, WJ Hosler, B Saunders, AM Dellefave, LM Brown, RH Siddique, T AF Li, YJ Pericak-Vance, MA Haines, JL Siddique, N McKenna-Yasek, D Hung, WY Sapp, P Allen, CI Chen, WJ Hosler, B Saunders, AM Dellefave, LM Brown, RH Siddique, T TI Apolipoprotein E is associated with age at onset of amyotrophic lateral sclerosis SO NEUROGENETICS LA English DT Article DE amyotrophic lateral sclerosis; apolipoprotein E; age at onset; association; quantitative trait ID PEDIGREE DISEQUILIBRIUM TEST; MOTOR-NEURON DISEASE; E EPSILON-4 ALLELE; QUANTITATIVE TRAITS; ALZHEIMERS-DISEASE; GENERAL PEDIGREES; LINKAGE ANALYSIS; LOCUS; GENOTYPE; FAMILIES AB Apolipoprotein E (APOE) is a confirmed risk factor for Alzheimer disease. APOE is also involved in several other neurodegenerative disorders, including Parkinson disease and multiple sclerosis. Previous studies of amyotrophic lateral sclerosis (Lou Gehrig disease, ALS) have investigated the effect of APOE on the risk of developing ALS. age at onset, site of onset, and duration of the disease. The results have been inconsistent, possibly due to small sample sizes and complete reliance on case-control data. No family-based association studies were performed. To address these limitations. we investigated the relationship between A-POE functional polymorphisms and age at onset of ALS in a large set of 508 families. We treated age at onset as a quantitative trait and performed family-based association analysis using the TDTQ5 method. APOE-2 is protective against earlier onset (P=0.001) with an average age at onset of APOE-2 carriers approximately 3 years later than that of non-APOE-2 carriers. Similar to our previous report. we did not find APOE associated with ALS risk. Our findings suggest that APOE may express its strongest effect through age at onset rather than on risk. C1 Duke Univ, Med Ctr, Ctr Human Genet, Dept Med, Durham, NC 27710 USA. Vanderbilt Univ, Med Ctr, Ctr Human Genet Res, Nashville, TN USA. Northwestern Univ, Feinberg Sch Med, Dept Neurol, Chicago, IL 60611 USA. Northwestern Univ, Inst Neurosci, Chicago, IL 60611 USA. Massachusetts Gen Hosp, Day Neuromuscular Lab, Charlestown, MA USA. MIT, Howard Hughes Med Inst, Dept Biol, Cambridge, MA 02139 USA. Duke Univ, Med Ctr, Dept Med, Div Neurol, Durham, NC 27710 USA. RP Li, YJ (reprint author), Duke Univ, Med Ctr, Ctr Human Genet, Dept Med, DUMC Box 3445, Durham, NC 27710 USA. EM yiju.li@duke.edu RI Haines, Jonathan/C-3374-2012 FU NINDS NIH HHS [NS 37912, NS021442] NR 37 TC 41 Z9 42 U1 0 U2 0 PU SPRINGER PI NEW YORK PA 233 SPRING STREET, NEW YORK, NY 10013 USA SN 1364-6745 J9 NEUROGENETICS JI Neurogenetics PD DEC PY 2004 VL 5 IS 4 BP 209 EP 213 DI 10.1007/s10048-004-0193-0 PG 5 WC Genetics & Heredity; Clinical Neurology SC Genetics & Heredity; Neurosciences & Neurology GA 887DI UT WOS:000226285100002 PM 15657798 ER PT J AU Chang, L Lee, PL Yiannoutsos, CT Ernst, T Marra, CM Richards, T Kolson, D Schifitto, G Jarvik, JG Miller, EN Lenkinski, R Gonzalez, G Navia, BA AF Chang, L Lee, PL Yiannoutsos, CT Ernst, T Marra, CM Richards, T Kolson, D Schifitto, G Jarvik, JG Miller, EN Lenkinski, R Gonzalez, G Navia, BA CA HIV MRS Consortium TI A multicenter in vivo proton-MRS study of HIV-associated dementia and its relationship to age SO NEUROIMAGE LA English DT Article DE HIV; spectroscopy; inflammation; dementia; neuroasymptomatic ID MAGNETIC-RESONANCE-SPECTROSCOPY; HUMAN-IMMUNODEFICIENCY-VIRUS; ANTIRETROVIRAL THERAPY; METABOLITE ABNORMALITIES; N-ACETYLASPARTATE; FRONTAL-LOBE; HUMAN BRAIN; SEROPOSITIVE INDIVIDUALS; CEREBROSPINAL-FLUID; NEOCORTICAL DAMAGE AB Objective: Differences in diagnostic criteria and methods have led to mixed results regarding the metabolite pattern of HIV-associated brain injury in relation to neurocognitive impairment. Therefore, a multicenter MRS consortium was formed to evaluate the neurometabolites in HIV patients with or without cognitive impairment. Methods: Proton magnetic resonance spectroscopy (MRS) at short-echo time (30 ms) was assessed in the frontal white matter, basal ganglia, and parietal cortex of 100 HIV patients [61 with AIDS dementia complex (ADC) and 39 neuroasymptomatic (NAS)] and 37 seronegative (SN) controls. Results: Compared to SN, NAS had higher glial marker myoinositol-to-creatine ratio (MI/Cr) in the white matter (multivariate analyses, adjusted P = 0.001), while ADC showed further increased MI/Cr in the white matter and basal ganglia (both P < 0.001), and increased choline compounds (Cho)/Cr in white matter (P = 0.04) and basal ganglia (P < 0.001). Compared to NAS, ADC showed a reduction in the neuronal marker N-acetyl compound (NA)/Cr in the frontal white matter (P = 0.007). CSF, but not plasma, viral load correlated with MI/Cr and Cho/Cr in white matter and NAA/Cr in parietal cortex. HIV infection and aging had additive effects on Cho/Cr and MI/Cr in the basal ganglia and white matter. Conclusions: The results suggest that glial activation occurs during the NAS stages of HIV infection, whereas further inflammatory activity, in the basal ganglia and neuronal injury in the white matter is associated with the development of cognitive impairment. Aging may further exacerbate brain metabolites associated with inflammation in HIV patient and thereby increase the risk for cognitive impairment. (C) 2004 Elsevier Inc. All rights reserved. C1 Tufts New England Med Ctr, Dept Neurol, Boston, MA 02111 USA. Tufts New England Med Ctr, Dept Psychiat, Boston, MA 02111 USA. Univ Hawaii, John A Burns Sch Med, Dept Med, Honolulu, HI USA. Harvard Univ, Sch Med, Massachusetts Gen Hosp, Dept Radiol, Charlestown, MA 02129 USA. Indiana Univ, Sch Med, Dept Med Biostat, Indianapolis, IN 46202 USA. Univ Washington, Sch Med, Dept Neurol, Seattle, WA 98101 USA. Univ Washington, Sch Med, Dept Radiol, Seattle, WA 98101 USA. Univ Washington, Sch Med, Dept Neurosurg, Seattle, WA 98101 USA. Univ Penn, Dept Neurol, Philadelphia, PA 19104 USA. Univ Rochester, Sch Med, Dept Neurol, Rochester, NY 14642 USA. Univ Calif Los Angeles, David Geffen Sch Med, Ctr Hlth Sci, Dept Psychiat, Los Angeles, CA 90095 USA. Harvard Univ, Sch Med, Beth Israel Deaconess Med Ctr, Dept Radiol, Boston, MA 02215 USA. RP Navia, BA (reprint author), Tufts New England Med Ctr, Dept Neurol, Boston, MA 02111 USA. EM Bnavia@tufts-nemc.org RI Lenkinski, Robert/F-9045-2014; OI Lenkinski, Robert/0000-0001-7371-5048 FU NCRR NIH HHS [MO1 RR00425, RR13213]; NIAID NIH HHS [R01 AI38855]; NIDA NIH HHS [K02 DA16991, K24 DA16170]; NIMH NIH HHS [R01 MH64409]; NINDS NIH HHS [R01 NS36524] NR 68 TC 102 Z9 105 U1 1 U2 3 PU ACADEMIC PRESS INC ELSEVIER SCIENCE PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA SN 1053-8119 J9 NEUROIMAGE JI Neuroimage PD DEC PY 2004 VL 23 IS 4 BP 1336 EP 1347 DI 10.1016/j.neuroimage.2004.07.067 PG 12 WC Neurosciences; Neuroimaging; Radiology, Nuclear Medicine & Medical Imaging SC Neurosciences & Neurology; Radiology, Nuclear Medicine & Medical Imaging GA 883US UT WOS:000226041800010 PM 15589098 ER PT J AU Kennedy, DN AF Kennedy, DN TI Barriers to the socialization of information SO NEUROINFORMATICS LA English DT Editorial Material C1 Harvard Univ, Sch Med, Massachusetts Gen Hosp, Dept Neurol, Boston, MA 02115 USA. Harvard Univ, Sch Med, Massachusetts Gen Hosp, Dept Radiol,Athinoula S Martinos Ctr Biomed Imagi, Boston, MA 02115 USA. RP Kennedy, DN (reprint author), Harvard Univ, Sch Med, Massachusetts Gen Hosp, Dept Neurol, Boston, MA 02115 USA. NR 0 TC 11 Z9 11 U1 0 U2 2 PU HUMANA PRESS INC PI TOTOWA PA 999 RIVERVIEW DRIVE SUITE 208, TOTOWA, NJ 07512 USA SN 1539-2791 J9 NEUROINFORMATICS JI Neuroinformatics PD WIN PY 2004 VL 2 IS 4 BP 367 EP 368 DI 10.1385/NI:2:4:367 PG 2 WC Computer Science, Interdisciplinary Applications; Neurosciences SC Computer Science; Neurosciences & Neurology GA 921VC UT WOS:000228792400001 PM 15800368 ER PT J AU Zhang, F Yin, W Chen, J AF Zhang, F Yin, W Chen, J TI Apoptosis in cerebral ischemia: executional and regulatory signaling mechanisms SO NEUROLOGICAL RESEARCH LA English DT Review DE apoptosis; cerebral ischemia; caspase; AIF; calpain; bcl-xL ID ENDOPLASMIC-RETICULUM STRESS; NEURONAL CELL-DEATH; CYTOCHROME-C RELEASE; MEDIATED HEPATOCYTE APOPTOSIS; TRANSIENT FOREBRAIN ISCHEMIA; PERMANENT FOCAL ISCHEMIA; BAX-DEPENDENT APOPTOSIS; TRAUMATIC BRAIN-INJURY; RAT-BRAIN; ARTERY OCCLUSION AB Programmed cell death, often in the form of apoptosis, is an important contributing mechanism in the pathogenesis of ischemic brain injury. Depending on the severity of the insult and the stage of the injury, the executional pathways that are directly responsible for cell death and the signaling mechanisms that participate in the regulation of these death pathways may vary. It is likely that molecular or pharmacological targeting of the upstream signaling mechanisms that control the death executional pathways may offer opportunities for more complete and longterm neuroprotection. This review summarizes the recent advancements in the understanding of the executional and regulatory signaling mechanisms in ischemic brain injury. C1 Univ Pittsburgh, Dept Neurol, Sch Med, Pittsburgh, PA 15213 USA. Univ Pittsburgh, Sch Med, Inst Neurodegenerat Disorders, Pittsburgh, PA 15213 USA. Vet Affairs Pittsburgh Hlth Care Syst, Educat & Clin Ctr, Pittsburgh, PA 15261 USA. RP Chen, J (reprint author), Univ Pittsburgh, Dept Neurol, Sch Med, S-507 Biomed Sci Tower, Pittsburgh, PA 15213 USA. EM chenj2@msx.upmc.edu FU NINDS NIH HHS [NS45048, NS43802, NS36736, NS38560] NR 135 TC 60 Z9 65 U1 0 U2 5 PU MANEY PUBLISHING PI LEEDS PA HUDSON RD, LEEDS LS9 7DL, ENGLAND SN 0161-6412 J9 NEUROL RES JI Neurol. Res. PD DEC PY 2004 VL 26 IS 8 BP 835 EP 845 DI 10.1179/016164104X3824 PG 11 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA 879NX UT WOS:000225725600006 PM 15727267 ER PT J AU Lee, SR Wang, XY Tsuji, K Lo, EH AF Lee, SR Wang, XY Tsuji, K Lo, EH TI Extracellular proteolytic pathophysiology in the neurovascular unit after stroke SO NEUROLOGICAL RESEARCH LA English DT Review DE neuroprotection; neurovascular unit; blood-brain barrier; matrix ID FOCAL CEREBRAL-ISCHEMIA; BLOOD-BRAIN-BARRIER; TISSUE-PLASMINOGEN ACTIVATOR; MATRIX-METALLOPROTEINASE EXPRESSION; MICROVESSEL ENDOTHELIAL-CELLS; ADHESION MOLECULE-1 ICAM-1; CENTRAL-NERVOUS-SYSTEM; NECROSIS-FACTOR-ALPHA; SMOOTH-MUSCLE-CELLS; HEMORRHAGIC TRANSFORMATION AB The NINDS Stroke Progress Review Group recommended a shift in emphasis from a purely neurocentric view of cell death towards a more integrative approach whereby responses in all brain cells and matrix are considered. The neurovascular unit (fundamentally comprising endothelium, astrocyte, and neuron) provides a conceptual framework where cell-cell and cell-matrix signaling underlies the overall tissue response to stroke and its treatments. Here, we briefly review recent data on extracellular proteolytic dysfunction in the neurovascular unit after a stroke. The breakdown of neurovascular matrix initiates blood-brain barrier disruption with edema and/or hemorrhage. Endothelial dysfunction amplifies inflammatory responses. Perturbation of cell-matrix homeostasis triggers multiple cell death pathways. Interactions between the major classes of extracellular proteases from the plasminogen and matrix metalloprotease families may underlie processes responsible for some of the hemorrhagic complications of thrombolytic stroke therapy. Targeting the proteolytic imbalance within the neurovascular unit may provide new approaches for improving the safety and efficacy of thrombolytic reperfusion therapy for stroke. C1 Massachusetts Gen Hosp, Dept Radiol, Neuroprotect Res Lab, Boston, MA 02129 USA. Massachusetts Gen Hosp, Dept Neurol, Neuroprotect Res Lab, Boston, MA 02129 USA. Harvard Univ, Sch Med, Program Neurosci, Charlestown, MA 02129 USA. RP Lo, EH (reprint author), Harvard Univ, Sch Med, Neuroprotect Res Lab, MGH E 149-2401, Charlestown, MA 02129 USA. EM lo@helix.mgh.harvard.edu FU NINDS NIH HHS [R01-NS38731, R01-NS40529, P50-NS10828, R01-NS37074] NR 131 TC 26 Z9 27 U1 1 U2 3 PU MANEY PUBLISHING PI LEEDS PA HUDSON RD, LEEDS LS9 7DL, ENGLAND SN 0161-6412 J9 NEUROL RES JI Neurol. Res. PD DEC PY 2004 VL 26 IS 8 BP 854 EP 861 DI 10.1179/016164101X3806 PG 8 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA 879NX UT WOS:000225725600008 PM 15727269 ER PT J AU Mazarati, AM AF Mazarati, AM TI Galanin and galanin receptors in epilepsy SO NEUROPEPTIDES LA English DT Review DE neuropeptides; galanin; G-protein coupled receptors; hippocampus; epilepsy; neuronal injury; neurogenesis; transgenic mice; antisense; viral vector ID SUSTAINING STATUS EPILEPTICUS; RAT VENTRAL HIPPOCAMPUS; GALR1 KNOCKOUT MICE; MESSENGER-RNA; PHOSPHOINOSITIDE TURNOVER; ACETYLCHOLINE-RELEASE; KAINATE RECEPTORS; PYRAMIDAL NEURONS; PERFORANT PATH; SPINAL-CORD AB The shift in the balance between the inhibition and the excitation in favor of the latter is a major mechanism of the evolvement of epileptic seizures. On the neurotransmitter level two major players contribute to such misbalance: an inhibitory transmitter gamma-aminobutyric acid, and an excitatory amino acid glutamate. Neuropeptides are powerful modulators of classical neurotransmitters, and thus represent an intriguing too] for restoring the balance between the inhibition and the excitation, through either blocking or activating peptide receptors depending on whether a peptide is pro- or anticonvulsant. Galanin, a 29-amino acid residues neuropeptide which inhibits glutamate release in the hippocampus, is a likely member of the anticonvulsant peptide family. During the past decade growing evidence has been suggesting that galanin is in fact a powerful inhibitor of seizure activity. This review summarizes the state of research of galanin in epilepsy, beginning with the first simple experiments which showed that central injection of galanin agonists inhibited seizures, and that seizures themselves affected galanin signaling in the hippocampus; exploring the impact of active manipulation with the expression of galanin and galanin receptors on seizures, using transgenic animals, antisense and pepticle-expressing vector approaches; and concluding with the recent advances in pharmacology, which led to the synthesis of non-peptide galanin receptor agonists with anticonvulsant properties. We also address recently established functions of galanin in seizure-associated neuronal degeneration and neuronal plasticity. (C) 2004 Elsevier Ltd. All rights reserved. C1 W Los Angeles Vet Affairs Med Ctr, Los Angeles, CA 90073 USA. Univ Calif Los Angeles, Dept Neurol, D Geffen Sch Med, Los Angeles, CA 90095 USA. RP Mazarati, AM (reprint author), W Los Angeles Vet Affairs Med Ctr, Res 151, Los Angeles, CA 90073 USA. EM mazarati@ucla.edu FU NINDS NIH HHS [NS 43409] NR 69 TC 52 Z9 54 U1 0 U2 5 PU CHURCHILL LIVINGSTONE PI EDINBURGH PA JOURNAL PRODUCTION DEPT, ROBERT STEVENSON HOUSE, 1-3 BAXTERS PLACE, LEITH WALK, EDINBURGH EH1 3AF, MIDLOTHIAN, SCOTLAND SN 0143-4179 J9 NEUROPEPTIDES JI Neuropeptides PD DEC PY 2004 VL 38 IS 6 BP 331 EP 343 DI 10.1016/j.npep.2004.07.006 PG 13 WC Endocrinology & Metabolism; Neurosciences SC Endocrinology & Metabolism; Neurosciences & Neurology GA 880HE UT WOS:000225778800001 PM 15567469 ER PT J AU Sweet, RA Hamilton, RL Butters, MA Mulsant, BH Pollock, BG Lewis, DA Lopez, OL DeKosky, ST Reynolds, CF AF Sweet, RA Hamilton, RL Butters, MA Mulsant, BH Pollock, BG Lewis, DA Lopez, OL DeKosky, ST Reynolds, CF TI Neuropathologic correlates of late-onset major depression SO NEUROPSYCHOPHARMACOLOGY LA English DT Article DE Alzheimer's disease; geriatric psychiatry; depression; late onset; mood disorders; neurodegenerative diseases; Lewy bodies; cerebrovascular disorders ID LATE-LIFE DEPRESSION; ALZHEIMERS-DISEASE CERAD; LAST 2 DECADES; COGNITIVE IMPAIRMENT; DOUBLE-BLIND; LEWY BODIES; INTERNATIONAL WORKSHOP; CLINICAL-DIAGNOSIS; RATING-SCALE; RISK-FACTORS AB Late life major depression (LLMD) is frequently associated with cognitive impairment, and increases the risk for subsequent dementia. Cerebrovascular disease, Alzheimer's disease ( AD), and dementia with Lewy bodies (DLB) have all been hypothesized to contribute to this increased risk, though prospective studies have yet to examine these hypotheses with autopsy confirmation of the clinical diagnoses. The aim of this study is to examine the rates of cerebrovascular, AD, and DLB pathology among the first 10 participants in an LLMD brain tissue donation program. Subjects' psychiatric diagnoses and cognitive status were prospectively determined during their participation in clinical research protocols of the Intervention Research Center for Late Life Mood Disorders. After death, final clinical diagnoses were made using all clinical information, while blind to neuropathologic diagnoses. Neuropathologic assessments were conducted blind to final clinical diagnoses. Rates of neuropathology were compared with those in a cohort of subjects with dementia, without a history of LLMD, participating in an Alzheimer Disease Research Center. Seven (70%) subjects had evidence of onset of a dementia prior to death. LLMD with dementia was significantly associated with a neuropathologic diagnosis of AD. Cerebrovascular disease and DLB pathology were also frequent in the LLMD subjects with dementia, and were found in an LLMD subject without dementia. Rates of AD, DLB, and cerebrovascular disease were similar to those in the comparison subjects. These preliminary findings suggest that AD is the predominant neuropathologic condition in LLMD subjects with dementia. Further assessment of the role of comorbid cerebrovascular disease and comorbid DLB is needed. C1 Univ Pittsburgh, Sch Med, Dept Psychiat, Pittsburgh, PA USA. Univ Pittsburgh, Sch Med, Dept Neuropathol, Pittsburgh, PA USA. Univ Pittsburgh, Sch Med, Dept Neurol, Pittsburgh, PA 15261 USA. VA Pittsburgh Hlth Care Syst, GRECC, Pittsburgh, PA USA. RP Sweet, RA (reprint author), Western Psychiat Inst & Clin, TDH, E823,3811 OHara St, Pittsburgh, PA 15213 USA. EM sweetra@upmc.edu RI Lewis, David/G-4053-2014 OI Lewis, David/0000-0002-3225-6778 FU NIA NIH HHS [P50 AG05133]; NIMH NIH HHS [MH01684, MH45156, MH52247, MH65416, MH66231] NR 49 TC 51 Z9 53 U1 1 U2 5 PU NATURE PUBLISHING GROUP PI LONDON PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND SN 0893-133X J9 NEUROPSYCHOPHARMACOL JI Neuropsychopharmacology PD DEC PY 2004 VL 29 IS 12 BP 2242 EP 2250 DI 10.1038/sj.npp.1300554 PG 9 WC Neurosciences; Pharmacology & Pharmacy; Psychiatry SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry GA 873ST UT WOS:000225302000015 PM 15354182 ER PT J AU Brody, AL Mandelkern, MA Scheibal, D Hahn, E Hsiao-Wei, L Zamora-Paja, E London, ED McCracken, JT AF Brody, AL Mandelkern, MA Scheibal, D Hahn, E Hsiao-Wei, L Zamora-Paja, E London, ED McCracken, JT TI Genetic variants in the alpha4 subunit of nachr and in COMT predict smoking-induced dopamine release in mesolimbic reward pathways SO NEUROPSYCHOPHARMACOLOGY LA English DT Meeting Abstract CT Annual Meeting of the American-College-of-Neuropsychopharmacology CY DEC 12-16, 2004 CL San Juan, PR SP Vanderbilt Univ, Sch Med, Dept Psychiaty, Amer Coll Neuropsychopharmacol C1 Univ Calif Los Angeles, Inst Neuropsychiat, Los Angeles, CA 90024 USA. Greater Los Angeles VA Healthcare Syst, Dept Nucl Med, Los Angeles, CA USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU NATURE PUBLISHING GROUP PI LONDON PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND SN 0893-133X J9 NEUROPSYCHOPHARMACOL JI Neuropsychopharmacology PD DEC PY 2004 VL 29 SU 1 BP S78 EP S79 PG 2 WC Neurosciences; Pharmacology & Pharmacy; Psychiatry SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry GA 877RO UT WOS:000225588000231 ER PT J AU Cohen, L Kornstein, S Entsuah, R Ortega-Leon, W Roy-Byrne, P Tummala, R AF Cohen, L Kornstein, S Entsuah, R Ortega-Leon, W Roy-Byrne, P Tummala, R TI Age and gender differences in antidepressant treatment: A comparative analysis of venlafaxine and selective serotonin reuptake inhibitors SO NEUROPSYCHOPHARMACOLOGY LA English DT Meeting Abstract CT Annual Meeting of the American-College-of-Neuropsychopharmacology CY DEC 12-16, 2004 CL San Juan, PR SP Vanderbilt Univ, Sch Med, Dept Psychiaty, Amer Coll Neuropsychopharmacol C1 Massachusetts Gen Hosp, Boston, MA 02114 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU NATURE PUBLISHING GROUP PI LONDON PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND SN 0893-133X J9 NEUROPSYCHOPHARMACOL JI Neuropsychopharmacology PD DEC PY 2004 VL 29 SU 1 BP S95 EP S96 PG 2 WC Neurosciences; Pharmacology & Pharmacy; Psychiatry SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry GA 877RO UT WOS:000225588000282 ER PT J AU Copland, CM Weickert, CS Kleinman, JE Davis, KL Haroutunian, V AF Copland, CM Weickert, CS Kleinman, JE Davis, KL Haroutunian, V TI Small myelin-associaed glycoprotein (S-Mag) gene expression during normal human development and in elderly schizophrenics SO NEUROPSYCHOPHARMACOLOGY LA English DT Meeting Abstract CT Annual Meeting of the American-College-of-Neuropsychopharmacology CY DEC 12-16, 2004 CL San Juan, PR SP Vanderbilt Univ, Sch Med, Dept Psychiaty, Amer Coll Neuropsychopharmacol C1 Mt Sinai Sch Med, New York, NY USA. Bronx Vet Adm Med Ctr, Bronx, NY USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU NATURE PUBLISHING GROUP PI LONDON PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND SN 0893-133X J9 NEUROPSYCHOPHARMACOL JI Neuropsychopharmacology PD DEC PY 2004 VL 29 SU 1 BP S112 EP S112 PG 1 WC Neurosciences; Pharmacology & Pharmacy; Psychiatry SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry GA 877RO UT WOS:000225588000326 ER PT J AU Dickey, CC Shenton, ME Seidman, LJ Connor, E Voglmaier, M Margaret, N Dreusicke, M McCarley, RW AF Dickey, CC Shenton, ME Seidman, LJ Connor, E Voglmaier, M Margaret, N Dreusicke, M McCarley, RW TI Simple auditory processing in schizotypal personality disorder SO NEUROPSYCHOPHARMACOLOGY LA English DT Meeting Abstract CT Annual Meeting of the American-College-of-Neuropsychopharmacology CY DEC 12-16, 2004 CL San Juan, PR SP Vanderbilt Univ, Sch Med, Dept Psychiaty, Amer Coll Neuropsychopharmacol C1 VA Boston Healthcare Syst, Brockton, MA USA. Brigham & Womens Hosp, Boston, MA 02115 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU NATURE PUBLISHING GROUP PI LONDON PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND SN 0893-133X J9 NEUROPSYCHOPHARMACOL JI Neuropsychopharmacology PD DEC PY 2004 VL 29 SU 1 BP S79 EP S79 PG 1 WC Neurosciences; Pharmacology & Pharmacy; Psychiatry SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry GA 877RO UT WOS:000225588000232 ER PT J AU Dougherty, DD Bonab, A Ottowitz, WE Livni, E Alpert, NM Rauch, SL Fischman, AJ Fava, M AF Dougherty, DD Bonab, A Ottowitz, WE Livni, E Alpert, NM Rauch, SL Fischman, AJ Fava, M TI Decreased striatal D1 binding as measured using PET and [11C]SCH 23,390 in patients with major depression with anger attacks SO NEUROPSYCHOPHARMACOLOGY LA English DT Meeting Abstract CT Annual Meeting of the American-College-of-Neuropsychopharmacology CY DEC 12-16, 2004 CL San Juan, PR SP Vanderbilt Univ, Sch Med, Dept Psychiaty, Amer Coll Neuropsychopharmacol 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 NATURE PUBLISHING GROUP PI LONDON PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND SN 0893-133X J9 NEUROPSYCHOPHARMACOL JI Neuropsychopharmacology PD DEC PY 2004 VL 29 SU 1 BP S79 EP S79 PG 1 WC Neurosciences; Pharmacology & Pharmacy; Psychiatry SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry GA 877RO UT WOS:000225588000234 ER PT J AU Fava, M Entsuah, R Tummala, R AF Fava, M Entsuah, R Tummala, R TI Comparison of the efficacy of venlafaxine, selective serotonin reuptake inhibitors, and placebo in the treatment of patients with anxious depression SO NEUROPSYCHOPHARMACOLOGY LA English DT Meeting Abstract CT Annual Meeting of the American-College-of-Neuropsychopharmacology CY DEC 12-16, 2004 CL San Juan, PR SP Vanderbilt Univ, Sch Med, Dept Psychiaty, Amer Coll Neuropsychopharmacol C1 Massachusetts Gen Hosp, Boston, MA 02114 USA. NR 0 TC 0 Z9 0 U1 2 U2 2 PU NATURE PUBLISHING GROUP PI LONDON PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND SN 0893-133X J9 NEUROPSYCHOPHARMACOL JI Neuropsychopharmacology PD DEC PY 2004 VL 29 SU 1 BP S101 EP S101 PG 1 WC Neurosciences; Pharmacology & Pharmacy; Psychiatry SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry GA 877RO UT WOS:000225588000297 ER PT J AU Gallagher, RM AF Gallagher, RM TI Pain disorders and mood disorder: Mechanisms and management SO NEUROPSYCHOPHARMACOLOGY LA English DT Meeting Abstract CT Annual Meeting of the American-College-of-Neuropsychopharmacology CY DEC 12-16, 2004 CL San Juan, PR SP Vanderbilt Univ, Sch Med, Dept Psychiaty, Amer Coll Neuropsychopharmacol C1 Philadelphia VA Med Ctr, Philadelphia, PA USA. Univ Penn, Philadelphia, PA 19104 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU NATURE PUBLISHING GROUP PI LONDON PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND SN 0893-133X J9 NEUROPSYCHOPHARMACOL JI Neuropsychopharmacology PD DEC PY 2004 VL 29 SU 1 BP S58 EP S59 PG 2 WC Neurosciences; Pharmacology & Pharmacy; Psychiatry SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry GA 877RO UT WOS:000225588000175 ER PT J AU Goldstein, JM Jerram, M Poldrack, R Harlow, B Makris, N AF Goldstein, JM Jerram, M Poldrack, R Harlow, B Makris, N TI Hormones modulate brain activity in affective arousal in normals: Implications for sex differences in psychiatric disorders SO NEUROPSYCHOPHARMACOLOGY LA English DT Meeting Abstract CT Annual Meeting of the American-College-of-Neuropsychopharmacology CY DEC 12-16, 2004 CL San Juan, PR SP Vanderbilt Univ, Sch Med, Dept Psychiaty, Amer Coll Neuropsychopharmacol C1 Brigham & Womens Hosp, Massachusetts Mental Hlth Ctr, Boston, MA 02115 USA. Massachusetts Gen Hosp, Boston, MA 02114 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU NATURE PUBLISHING GROUP PI LONDON PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND SN 0893-133X J9 NEUROPSYCHOPHARMACOL JI Neuropsychopharmacology PD DEC PY 2004 VL 29 SU 1 BP S82 EP S82 PG 1 WC Neurosciences; Pharmacology & Pharmacy; Psychiatry SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry GA 877RO UT WOS:000225588000242 ER PT J AU Green, MF Wynn, JK AF Green, MF Wynn, JK TI Visual masking in schizophrenia: Applications to neuroirnaging and electrophysiology SO NEUROPSYCHOPHARMACOLOGY LA English DT Meeting Abstract CT Annual Meeting of the American-College-of-Neuropsychopharmacology CY DEC 12-16, 2004 CL San Juan, PR SP Vanderbilt Univ, Sch Med, Dept Psychiaty, Amer Coll Neuropsychopharmacol C1 Univ Calif Los Angeles, Inst Neuropsychiat, Los Angeles, CA USA. VA Greater Los Angeles Healthcare Syst, Los Angeles, CA USA. RI Wynn, Jonathan/H-3749-2014 OI Wynn, Jonathan/0000-0002-1763-8540 NR 0 TC 0 Z9 0 U1 0 U2 1 PU NATURE PUBLISHING GROUP PI LONDON PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND SN 0893-133X J9 NEUROPSYCHOPHARMACOL JI Neuropsychopharmacology PD DEC PY 2004 VL 29 SU 1 BP S41 EP S42 PG 2 WC Neurosciences; Pharmacology & Pharmacy; Psychiatry SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry GA 877RO UT WOS:000225588000122 ER PT J AU Haroutunian, V Katsel, P Dracheva, S Copland, C Gorman, JM Davis, KL AF Haroutunian, V Katsel, P Dracheva, S Copland, C Gorman, JM Davis, KL TI Myelin-related gene expression abnormalities in 17 cortical and subcortical regions in schizophrenia SO NEUROPSYCHOPHARMACOLOGY LA English DT Meeting Abstract CT Annual Meeting of the American-College-of-Neuropsychopharmacology CY DEC 12-16, 2004 CL San Juan, PR SP Vanderbilt Univ, Sch Med, Dept Psychiaty, Amer Coll Neuropsychopharmacol C1 Mt Sinai Sch Med, New York, NY USA. Bronx Vet Adm Med Ctr, Bronx, NY USA. NR 0 TC 2 Z9 2 U1 0 U2 0 PU NATURE PUBLISHING GROUP PI LONDON PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND SN 0893-133X J9 NEUROPSYCHOPHARMACOL JI Neuropsychopharmacology PD DEC PY 2004 VL 29 SU 1 BP S32 EP S32 PG 1 WC Neurosciences; Pharmacology & Pharmacy; Psychiatry SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry GA 877RO UT WOS:000225588000098 ER PT J AU Koenigsberg, HW Siever, LJ Guo, XD New, AS Goodman, M Cheng, H Silverman, J Prohovnik, I AF Koenigsberg, HW Siever, LJ Guo, XD New, AS Goodman, M Cheng, H Silverman, J Prohovnik, I TI Emotion processing in borderline personality disorder: A functional MRI perspective SO NEUROPSYCHOPHARMACOLOGY LA English DT Meeting Abstract CT Annual Meeting of the American-College-of-Neuropsychopharmacology CY DEC 12-16, 2004 CL San Juan, PR SP Vanderbilt Univ, Sch Med, Dept Psychiaty, Amer Coll Neuropsychopharmacol C1 CUNY Mt Sinai Sch Med, New York, NY 10029 USA. Bronx Vet Affairs Med Ctr, Bronx, NY USA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU NATURE PUBLISHING GROUP PI LONDON PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND SN 0893-133X J9 NEUROPSYCHOPHARMACOL JI Neuropsychopharmacology PD DEC PY 2004 VL 29 SU 1 BP S84 EP S84 PG 1 WC Neurosciences; Pharmacology & Pharmacy; Psychiatry SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry GA 877RO UT WOS:000225588000248 ER PT J AU Kozel, FA Johnson, KA Mu, QW Grenesko, EL Laken, SJ George, MS AF Kozel, FA Johnson, KA Mu, QW Grenesko, EL Laken, SJ George, MS TI Developing functional MRI detection of deception SO NEUROPSYCHOPHARMACOLOGY LA English DT Meeting Abstract CT Annual Meeting of the American-College-of-Neuropsychopharmacology CY DEC 12-16, 2004 CL San Juan, PR SP Vanderbilt Univ, Sch Med, Dept Psychiaty, Amer Coll Neuropsychopharmacol C1 Med Univ S Carolina, Ctr Adv Imaging Res, Charleston, SC 29425 USA. Ralph H Johnson VA Med Ctr, Charleston, SC USA. RI Kozel, Frank/I-5366-2012 NR 0 TC 1 Z9 1 U1 0 U2 0 PU NATURE PUBLISHING GROUP PI LONDON PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND SN 0893-133X J9 NEUROPSYCHOPHARMACOL JI Neuropsychopharmacology PD DEC PY 2004 VL 29 SU 1 BP S84 EP S85 PG 2 WC Neurosciences; Pharmacology & Pharmacy; Psychiatry SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry GA 877RO UT WOS:000225588000249 ER PT J AU Milad, MR Orr, SP Pitman, RK Rauch, SL AF Milad, MR Orr, SP Pitman, RK Rauch, SL TI Visual contexts gate the expression of memory for fear extinction in humans: A psychophysiological study SO NEUROPSYCHOPHARMACOLOGY LA English DT Meeting Abstract CT Annual Meeting of the American-College-of-Neuropsychopharmacology CY DEC 12-16, 2004 CL San Juan, PR SP Vanderbilt Univ, Sch Med, Dept Psychiaty, Amer Coll Neuropsychopharmacol C1 Massachusetts Gen Hosp, Charlestown, MA USA. Harvard Univ, Sch Med, Charlestown, MA USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU NATURE PUBLISHING GROUP PI LONDON PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND SN 0893-133X J9 NEUROPSYCHOPHARMACOL JI Neuropsychopharmacology PD DEC PY 2004 VL 29 SU 1 BP S156 EP S157 PG 2 WC Neurosciences; Pharmacology & Pharmacy; Psychiatry SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry GA 877RO UT WOS:000225588000455 ER PT J AU Papakostas, GI Alpert, JE Nierenberg, AA Fava, M AF Papakostas, GI Alpert, JE Nierenberg, AA Fava, M TI Timing of clinical improvement and symptom resolution in the treatment of Major Depressive Disorder SO NEUROPSYCHOPHARMACOLOGY LA English DT Meeting Abstract CT Annual Meeting of the American-College-of-Neuropsychopharmacology CY DEC 12-16, 2004 CL San Juan, PR SP Vanderbilt Univ, Sch Med, Dept Psychiaty, Amer Coll Neuropsychopharmacol C1 Harvard Univ, Massachusetts Gen Hosp, Sch Med, Depress Clin & Res Program, Boston, MA USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU NATURE PUBLISHING GROUP PI LONDON PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND SN 0893-133X J9 NEUROPSYCHOPHARMACOL JI Neuropsychopharmacology PD DEC PY 2004 VL 29 SU 1 BP S161 EP S161 PG 1 WC Neurosciences; Pharmacology & Pharmacy; Psychiatry SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry GA 877RO UT WOS:000225588000469 ER PT J AU Pollack, M Whitaker, T Mangano, R Gao, B AF Pollack, M Whitaker, T Mangano, R Gao, B TI A comparison of venlafaxine XR and paroxetine in the treatment of outpatients with panic disorder SO NEUROPSYCHOPHARMACOLOGY LA English DT Meeting Abstract CT Annual Meeting of the American-College-of-Neuropsychopharmacology CY DEC 12-16, 2004 CL San Juan, PR SP Vanderbilt Univ, Sch Med, Dept Psychiaty, Amer Coll Neuropsychopharmacol C1 Massachusetts Gen Hosp, Boston, MA 02114 USA. Wyeth Pharmaceut, Collegeville, PA USA. NR 0 TC 1 Z9 1 U1 0 U2 1 PU NATURE PUBLISHING GROUP PI LONDON PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND SN 0893-133X J9 NEUROPSYCHOPHARMACOL JI Neuropsychopharmacology PD DEC PY 2004 VL 29 SU 1 BP S201 EP S202 PG 2 WC Neurosciences; Pharmacology & Pharmacy; Psychiatry SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry GA 877RO UT WOS:000225588000583 ER PT J AU Rauch, SL AF Rauch, SL TI Neuroimaging the effects of deep brain stimulation: What can we see? SO NEUROPSYCHOPHARMACOLOGY LA English DT Meeting Abstract CT Annual Meeting of the American-College-of-Neuropsychopharmacology CY DEC 12-16, 2004 CL San Juan, PR SP Vanderbilt Univ, Sch Med, Dept Psychiaty, Amer Coll Neuropsychopharmacol C1 Massachusetts Gen Hosp, Charlestown, MA USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU NATURE PUBLISHING GROUP PI LONDON PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND SN 0893-133X J9 NEUROPSYCHOPHARMACOL JI Neuropsychopharmacology PD DEC PY 2004 VL 29 SU 1 BP S31 EP S32 PG 2 WC Neurosciences; Pharmacology & Pharmacy; Psychiatry SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry GA 877RO UT WOS:000225588000096 ER PT J AU Rauch, SL AF Rauch, SL TI Cortical-basal ganglia networks in obsessive compulsive disorder: What is the role of the dorsal striatum? SO NEUROPSYCHOPHARMACOLOGY LA English DT Meeting Abstract CT Annual Meeting of the American-College-of-Neuropsychopharmacology CY DEC 12-16, 2004 CL San Juan, PR SP Vanderbilt Univ, Sch Med, Dept Psychiaty, Amer Coll Neuropsychopharmacol C1 Massachusetts Gen Hosp, Charlestown, MA USA. NR 0 TC 0 Z9 0 U1 0 U2 2 PU NATURE PUBLISHING GROUP PI LONDON PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND SN 0893-133X J9 NEUROPSYCHOPHARMACOL JI Neuropsychopharmacology PD DEC PY 2004 VL 29 SU 1 BP S16 EP S16 PG 1 WC Neurosciences; Pharmacology & Pharmacy; Psychiatry SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry GA 877RO UT WOS:000225588000048 ER PT J AU Shin, LM Wright, CI Cannistraro, PA Wedig, MM McMullin, KA Martis, B Macklin, M Lasko, N Cavanagh, SR Krangel, TS Orr, SP Pitman, RK Whalen, PJ Rauch, SL AF Shin, LM Wright, CI Cannistraro, PA Wedig, MM McMullin, KA Martis, B Macklin, M Lasko, N Cavanagh, SR Krangel, TS Orr, SP Pitman, RK Whalen, PJ Rauch, SL TI An fMRI study of amygdala and medial prefrontal cortex responses to overtly presented fearful faces in posttraumatic stress disorder SO NEUROPSYCHOPHARMACOLOGY LA English DT Meeting Abstract CT Annual Meeting of the American-College-of-Neuropsychopharmacology CY DEC 12-16, 2004 CL San Juan, PR SP Vanderbilt Univ, Sch Med, Dept Psychiaty, Amer Coll Neuropsychopharmacol C1 Tufts Univ, Medford, MA 02155 USA. Massachusetts Gen Hosp, Charlestown, MA USA. NR 0 TC 0 Z9 0 U1 3 U2 10 PU NATURE PUBLISHING GROUP PI LONDON PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND SN 0893-133X J9 NEUROPSYCHOPHARMACOL JI Neuropsychopharmacology PD DEC PY 2004 VL 29 SU 1 BP S208 EP S208 PG 1 WC Neurosciences; Pharmacology & Pharmacy; Psychiatry SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry GA 877RO UT WOS:000225588000602 ER PT J AU Simon, NM Fischmann, D Otto, MW Ostacher, MJ Demopulos, CM Nierenberg, AA Pollack, MH AF Simon, NM Fischmann, D Otto, MW Ostacher, MJ Demopulos, CM Nierenberg, AA Pollack, MH TI Exploring the association of anxiety comorbidity with suicidality in bipolar disorder SO NEUROPSYCHOPHARMACOLOGY LA English DT Meeting Abstract CT Annual Meeting of the American-College-of-Neuropsychopharmacology CY DEC 12-16, 2004 CL San Juan, PR SP Vanderbilt Univ, Sch Med, Dept Psychiaty, Amer Coll Neuropsychopharmacol C1 Massachusetts Gen Hosp, Boston, MA 02114 USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU NATURE PUBLISHING GROUP PI LONDON PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND SN 0893-133X J9 NEUROPSYCHOPHARMACOL JI Neuropsychopharmacology PD DEC PY 2004 VL 29 SU 1 BP S208 EP S209 PG 2 WC Neurosciences; Pharmacology & Pharmacy; Psychiatry SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry GA 877RO UT WOS:000225588000603 ER PT J AU Spencer, TJ Rosenbaum, JF Fischman, AJ Biederman, J Ciccone, P Dougherty, D AF Spencer, TJ Rosenbaum, JF Fischman, AJ Biederman, J Ciccone, P Dougherty, D TI A PET study examining pharmacokinetics, likability, and dopamine transporter receptor occupancy of methylphenidate formulations in adults SO NEUROPSYCHOPHARMACOLOGY LA English DT Meeting Abstract CT Annual Meeting of the American-College-of-Neuropsychopharmacology CY DEC 12-16, 2004 CL San Juan, PR SP Vanderbilt Univ, Sch Med, Dept Psychiaty, Amer Coll Neuropsychopharmacol C1 Harvard Univ, Sch Med, Boston, MA 02115 USA. Massachusetts Gen Hosp, Boston, MA 02114 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU NATURE PUBLISHING GROUP PI LONDON PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND SN 0893-133X J9 NEUROPSYCHOPHARMACOL JI Neuropsychopharmacology PD DEC PY 2004 VL 29 SU 1 BP S194 EP S194 PG 1 WC Neurosciences; Pharmacology & Pharmacy; Psychiatry SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry GA 877RO UT WOS:000225588000564 ER PT J AU Yehuda, R Yang, RK Golier, JA Bierer, LM Tischler, L Grossman, RA AF Yehuda, R Yang, RK Golier, JA Bierer, LM Tischler, L Grossman, RA TI Effect of sertraline on a peripheral glucocorticoid-mediated response in PTSD SO NEUROPSYCHOPHARMACOLOGY LA English DT Meeting Abstract CT Annual Meeting of the American-College-of-Neuropsychopharmacology CY DEC 12-16, 2004 CL San Juan, PR SP Vanderbilt Univ, Sch Med, Dept Psychiaty, Amer Coll Neuropsychopharmacol C1 Mt Sinai Sch Med, Dept Psychiat, New York, NY USA. Bronx Vet Adm Med Ctr, Mental Hlth Patient Care Ctr, Bronx, NY USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU NATURE PUBLISHING GROUP PI LONDON PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND SN 0893-133X J9 NEUROPSYCHOPHARMACOL JI Neuropsychopharmacology PD DEC PY 2004 VL 29 SU 1 BP S216 EP S216 PG 1 WC Neurosciences; Pharmacology & Pharmacy; Psychiatry SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry GA 877RO UT WOS:000225588000624 ER PT J AU Socransky, SS Haffajee, AD Smith, C Martin, L Haffajee, JA Uzel, NG Goodson, JM AF Socransky, SS Haffajee, AD Smith, C Martin, L Haffajee, JA Uzel, NG Goodson, JM TI Use of checkerboard DNA-DNA hybridization to study complex microbial ecosystems SO ORAL MICROBIOLOGY AND IMMUNOLOGY LA English DT Article DE bacteria; DNA probes; microbial ecology; microbial ecosystems; microbiology; sensitivity; specificity; subgingival plaque ID SUBGINGIVAL MICROBIOTA; MICROBIOLOGICAL PARAMETERS; PERIODONTITIS SUBJECTS; SUBTRACTION HYBRIDIZATION; ADULT PERIODONTITIS; PLAQUE; DISEASES; NORTHERN; HEALTHY; PROBES AB It has been difficult to conduct large scale studies of microbiologically complex ecosystems using conventional microbiological techniques. Molecular identification techniques in new probe-target formats, such as checkerboard DNA-DNA hybridization, permit enumeration of large numbers of species in very large numbers of samples. Digoxigenin-labeled whole genomic probes to 40 common subgingival species were tested in a checkerboard hydridization format. Chemifluorescent signals resulting from the hybridization reactions were quantified using a Fluorimager and used to evaluate sensitivity and specificity of the probes. Sensitivity of the DNA probes was adjusted to detect 10(4) cells. In all, 93.5% of potential cross-reactions to 80 cultivable species exhibited signals <5% of that detected for the homologous probe signal. Competitive hybridization and probes prepared by subtraction hybridization and polymerase chain reaction were effective in minimizing cross-reactions for closely related taxa. To demonstrate utility, the technique was used to evaluate 8887 subgingival plaque samples from 79 periodontally healthy and 272 chronic periodontitis subjects and 8126 samples from 166 subjects taken prior to and after periodontal therapy. Significant differences were detected for many taxa for mean counts, proportion of total sample, and percentage of sites colonized between samples from periodontally healthy and periodontitis subjects. Further, significant reductions were observed post therapy for many subgingival species including periodontal pathogens. DNA probes used in the checkerboard DNA-DNA format provide a useful tool for the enumeration of bacterial species in microbiologically complex systems. C1 Forsyth Inst, Dept Periodontol, Boston, MA 02115 USA. RP Socransky, SS (reprint author), Forsyth Inst, Dept Periodontol, 140 Fenway, Boston, MA 02115 USA. EM ssocransky@forsyth.org FU NIDCR NIH HHS [DE-12108, DE-10977, DE-12861, DE-13232] NR 30 TC 192 Z9 197 U1 1 U2 15 PU BLACKWELL MUNKSGAARD PI COPENHAGEN PA 35 NORRE SOGADE, PO BOX 2148, DK-1016 COPENHAGEN, DENMARK SN 0902-0055 J9 ORAL MICROBIOL IMMUN JI Oral Microbiol. Immunol. PD DEC PY 2004 VL 19 IS 6 BP 352 EP 362 DI 10.1111/j.1399-302x.2004.00168.x PG 11 WC Dentistry, Oral Surgery & Medicine; Immunology; Microbiology SC Dentistry, Oral Surgery & Medicine; Immunology; Microbiology GA 862WR UT WOS:000224522500002 PM 15491460 ER PT J AU Upadhyay, UD Holbrook, EH AF Upadhyay, UD Holbrook, EH TI Olfactory loss as a result of toxic exposure SO OTOLARYNGOLOGIC CLINICS OF NORTH AMERICA LA English DT Article ID MULTIPLE CHEMICAL-SENSITIVITY; GLUTATHIONE-S-TRANSFERASE; N-BUTYL ACETATE; HYDROGEN-SULFIDE; METHYL-BROMIDE; OCCUPATIONAL EXPOSURE; INHALATION EXPOSURE; NASAL EPITHELIUM; NERVOUS-SYSTEM; INORGANIC LEAD AB The olfactory neurons with dendrites extending to the nasal cavity are vulnerable to environmental toxins through inspired air and systemic circulation. Acute or chronic exposure to occupational and environmental agents is common and can cause transient or permanent damage to the olfactory system. Metals, gases, and solvents each have unique properties leading to loss of olfaction. Fortunately, the olfactory epithelium possesses several mechanisms for protection against potential toxins. Loss of olfaction from environmental toxins may be difficult to diagnose. Obtaining a careful detailed history is crucial, and removing the source of exposure may allow for return of function or prevention of progression. C1 Harvard Univ, Massachusetts Eye & Ear Infirm, Sch Med, Dept Otolaryngol Head & Neck Surg, Boston, MA 02114 USA. Tufts Univ, Sch Med, New England Med Ctr, Boston, MA 02111 USA. RP Holbrook, EH (reprint author), Harvard Univ, Massachusetts Eye & Ear Infirm, Sch Med, Dept Otolaryngol Head & Neck Surg, 243 Charles St, Boston, MA 02114 USA. EM Eric_Holbrook@meei.harvard.edu NR 89 TC 11 Z9 11 U1 2 U2 3 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 USA SN 0030-6665 J9 OTOLARYNG CLIN N AM JI Otolaryngol. Clin. N. Am. PD DEC PY 2004 VL 37 IS 6 BP 1185 EP + DI 10.1016/j.otc.2004.05.003 PG 24 WC Otorhinolaryngology SC Otorhinolaryngology GA 881KW UT WOS:000225867400007 PM 15563910 ER PT J AU Meltzer, EO Hamilos, DL Hadley, JA Lanza, DC Marple, BF Nicklas, RA Bachert, C Baraniuk, J Baroody, FM Benninger, MS Brook, I Chowdhury, BA Druce, HM Durham, S Ferguson, B Gwaltney, JM Kaliner, M Kennedy, DW Lund, V Naclerio, R Pawankar, R Piccirillo, JF Rohane, P Simon, R Slavin, RG Togias, A Wald, ER Zinreich, SJ AF Meltzer, EO Hamilos, DL Hadley, JA Lanza, DC Marple, BF Nicklas, RA Bachert, C Baraniuk, J Baroody, FM Benninger, MS Brook, I Chowdhury, BA Druce, HM Durham, S Ferguson, B Gwaltney, JM Kaliner, M Kennedy, DW Lund, V Naclerio, R Pawankar, R Piccirillo, JF Rohane, P Simon, R Slavin, RG Togias, A Wald, ER Zinreich, SJ TI Rhinosinusitis: Establishing definitions for clinical research and patient care SO OTOLARYNGOLOGY-HEAD AND NECK SURGERY LA English DT Review ID ALLERGIC FUNGAL SINUSITIS; CHRONIC MAXILLARY SINUSITIS; QUALITY-OF-LIFE; CHRONIC HYPERPLASTIC SINUSITIS; GASTROESOPHAGEAL-REFLUX DISEASE; MESSENGER-RNA EXPRESSION; STAPHYLOCOCCUS-AUREUS ENTEROTOXINS; INTERCELLULAR-ADHESION MOLECULE-1; INTRANASAL FLUTICASONE PROPIONATE; ACUTE BACTERIAL RHINOSINUSITIS C1 Univ Calif San Diego, Allergy & Asthma Med Grp & Res Ctr, Dept Pediat, San Diego, CA 92123 USA. Massachusetts Gen Hosp, Div Rheumatol Allergy & Immunol, Boston, MA 02114 USA. Univ Rochester, Dept Otolaryngol Head & Neck Surg, Rochester, NY USA. Sinus & Nasal Inst Florida, St Petersburg, FL USA. SW Texas State Univ, Dept Otolaryngol Head & Neck Surg, Dallas, TX USA. George Washington Univ, Dept Med, Washington, DC USA. Univ Ziekenhuis Ghent, ENT Dept, Ghent, Belgium. Univ Chicago, Dept Otolaryngol Head & Neck Surg, Chicago, IL 60637 USA. Henry Ford Hosp, Dept Otolaryngol Head & Neck Surg, Detroit, MI 48202 USA. Georgetown Univ, Dept Pediat & Med, Washington, DC USA. Walter Reed Army Med Ctr, Dept Allergy & Immunol, Washington, DC 20307 USA. Univ Med & Dent New Jersey, Dept Med, Div Allergy Immunol, Newark, NJ 07103 USA. Univ London Imperial Coll Sci Technol & Med, Natl Heart & Lung Inst, Dept Allergy & Resp Med, London, England. Univ Pittsburgh, Sch Med, Div Sino Nasal Disorders & Allergy, Dept Otolaryngol, Pittsburgh, PA USA. Univ Virginia, Sch Med, Dept Internal Med, Div Epidemiol & Virol, Charlottesville, VA 22908 USA. George Washington Univ, Sch Med, Inst Asthma & Allergy, Wheaton, MD USA. Univ Penn, Dept Otolaryngol, Philadelphia, PA 19104 USA. UCL, Dept Otolaryngol, London, England. Univ Chicago, Dept Surg, Sect Otolaryngol Head & Neck Surg, Chicago, IL 60637 USA. Nippon Med Coll, Dept Otolaryngol, Tokyo 113, Japan. Washington Univ, Dept Otolaryngol & Med, Sch Med, St Louis, MO USA. Celgene Corp, Clin Dev Inflammat, Warren, NJ USA. Scripps Clin, Div Allergy Asthma & Immunol, La Jolla, CA USA. St Louis Univ, Dept Internal Med, Sch Med, St Louis, MO 63103 USA. Johns Hopkins Univ, Sch Med, Dept Med, Baltimore, MD 21205 USA. Univ Pittsburgh, Sch Med, Dept Pediat & Otolaryngol, Pittsburgh, PA USA. Johns Hopkins Univ, Sch Med, Dept Radiol & Radiol Sci, Baltimore, MD USA. RP Meltzer, EO (reprint author), Univ Calif San Diego, Allergy & Asthma Med Grp & Res Ctr, Dept Pediat, 9610 Granite Ridge Dr,Suite B, San Diego, CA 92123 USA. EM eomeltzer@aol.com NR 352 TC 210 Z9 225 U1 3 U2 15 PU SAGE PUBLICATIONS LTD PI LONDON PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND SN 0194-5998 J9 OTOLARYNG HEAD NECK JI Otolaryngol. Head Neck Surg. PD DEC PY 2004 VL 131 IS 6 SU S BP S1 EP S62 DI 10.1016/j.otohns.2004.09.067 PG 62 WC Otorhinolaryngology; Surgery SC Otorhinolaryngology; Surgery GA 880FX UT WOS:000225775500001 PM 15577816 ER PT J AU Gallagher, RM AF Gallagher, RM TI Balancing risks and benefits in pain medicine: Wither Vioxx SO PAIN MEDICINE LA English DT Editorial Material C1 Univ Penn, Philadelphia VA Med Ctr, Philadelphia, PA 19104 USA. RP Gallagher, RM (reprint author), Univ Penn, Philadelphia VA Med Ctr, Philadelphia, PA 19104 USA. NR 0 TC 2 Z9 2 U1 0 U2 0 PU BLACKWELL PUBLISHING INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 USA SN 1526-2375 J9 PAIN MED JI Pain Med. PD DEC PY 2004 VL 5 IS 4 BP 329 EP 330 DI 10.1111/j.1526-4637.2004.04056.x PG 2 WC Medicine, General & Internal SC General & Internal Medicine GA 873FK UT WOS:000225265100001 PM 15563316 ER PT J AU Mossey, JM Gallagher, RM AF Mossey, JM Gallagher, RM TI The longitudinal occurrence and impact of comorbid chronic pain and chronic depression over two years in continuing care retirement community residents SO PAIN MEDICINE LA English DT Article DE chronic pain; chronic depression; elderly; longitudinal; subthreshold depression ID SELF-RATED HEALTH; SUBTHRESHOLD DEPRESSION; PHYSICAL-DISABILITY; OLDER-ADULTS; SYMPTOMS; POPULATION; MANAGEMENT; DIAGNOSIS; ARTHRITIS; MEDICINE AB Objective. To describe the longitudinal course of depressive symptoms and pain experienced by continuing care retirement community (CCRC) residents and to investigate the impact of comorbid chronic activity-limiting pain and chronic high depressive symptoms on physical functioning and health service use. Methods. This longitudinal study of 169 CCRC residents involved five assessments (baseline and four in-person interviews at 6-month intervals). The Geriatric Depression Scale (GDS), questions drawn from the McGill Pain Questionnaire, and self-report data on physical functioning and health care use were assessed. Individuals reporting activity-limiting pain and those with GDS scores greater than or equal to11 at three or more assessments were considered to have chronic pain or chronic depression, respectively. The analysis sample included 169 CCRC residents. Multivariate logistic regression was used to test hypotheses. Results. Pain and depressive symptoms were characterized by longitudinal stability. Of the sample, 37% met the criteria for chronic activity-limiting pain, 21% met the criteria for chronic high depressive symptoms, and 13% were comorbid. Adjusting for age and health conditions, those with chronic activity-limiting pain were five times more likely than those in the lowest pain group to persistently be in the worst two quartiles of physical functioning, as were those with even one GDS score >5. The odds of poor physical functioning were 11.2 times greater in those with comorbid chronic pain and depression. Comparable greater odds were seen in this sample for frequency of medical care visits (adjusted odds ratio [AOR]=12.4) and consistently high use of all medical services (AOR=3.5). Conclusions. Pain and depressive symptoms were both common and appeared remarkably stable over time. Depressive symptoms contributed significantly to the prediction of impairment associated with pain, and identification and treatment of such symptoms, even minor symptoms, could reduce pain-related impairment and health care costs in the elderly. C1 Drexel Univ, Sch Publ Hlth, Dept Epidemiol & Biostat, Philadelphia, PA 19102 USA. Drexel Univ, Sch Med, Dept Med, Philadelphia, PA 19102 USA. Univ Penn, Sch Med, Dept Psychiat, Philadelphia, PA 19104 USA. Univ Penn, Sch Med, Dept Anesthesiol, Philadelphia, PA 19104 USA. Philadelphia Vet Affairs Med Ctr, Pain Management Serv, Philadelphia, PA USA. RP Mossey, JM (reprint author), Drexel Univ, Sch Publ Hlth, Dept Epidemiol & Biostat, Mail Stop 660,1505 Race St,11th Floor, Philadelphia, PA 19102 USA. EM jm55@exchange1.drexel.edu FU NIA NIH HHS [AG 03934] NR 41 TC 47 Z9 49 U1 1 U2 8 PU BLACKWELL PUBLISHING INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 USA SN 1526-2375 J9 PAIN MED JI Pain Med. PD DEC PY 2004 VL 5 IS 4 BP 335 EP 348 DI 10.1111/j.1526-4637.2004.04041.x PG 14 WC Medicine, General & Internal SC General & Internal Medicine GA 873FK UT WOS:000225265100003 PM 15563319 ER PT J AU Roman, GC AF Roman, GC TI Vascular dementia - Advances in nosology, diagnosis, treatment and prevention SO PANMINERVA MEDICA LA English DT Review DE vascular dementia; stroke; vascular risk factors; cardiovascular disease; prevention; hypertension; homocysteine; lipids; cholinergic transmission ID ALZHEIMERS-DISEASE; COGNITIVE IMPAIRMENT; BLOOD-PRESSURE; RISK-FACTORS; DOUBLE-BLIND; CEREBROVASCULAR PATHOLOGY; ASSOCIATION CONFERENCE; SYSTOLIC HYPERTENSION; POSTSTROKE DEMENTIA; METABOLIC SYNDROME AB Ischemic or hemorrhagic cerebrovascular disease (CVD) produces injury of brain regions important for executive function, behavior, and memory leading to decline in cognitive functions and vascular dementia (VaD). Cardiovascular disease may cause VaD from hypoperfusion of susceptible brain areas. CVD may worsen degenerative dementias such as Alzheimer disease (AD. Currently, the global diagnostic category for cognitive impairment of vascular origin is vascular cognitive disorder (VCD). VCD ranges from vascular cognitive impairment (VCI) to VaD. The term VCI is limited to cases of cognitive impairment of vascular etiology, without dementia; VCI is equivalent to vascular mild cognitive impairment (MCI). Risk factors for VaD include age, hypertension, diabetes, smoking, cardiovascular disease (coronary heart disease, congestive heart failure, peripheral vascular disease), atrial fibrillation, left ventricular hypertrophy, hyperhomocysteinemia, orthostatic hypotension, cardiac arrhythmias, hyperfibrinogenemia, sleep apnea, infection, and high C-reactive protein. Research on biomarkers revealed increased CSF-NFL levels in VaD, whereas CSF-τ was normal. CSF-TNF-α, VEGF, and TGF-β were increased in, both AD and VaD. VaD shows low CSF acetylcholinesterase levels. This condition responds to acetylcholinesterase inhibitors, confirming the central role of cholinergic deficit in its pathogenesis. Evidence strongly suggests that control of vascular risk factors, in particular hypertension, could prevent VaD. C1 Univ Texas, Hlth Sci Ctr, Dept Med Neurol, San Antonio, TX 78229 USA. Audie L Murphy Mem Vet Adm Med Ctr, San Antonio, TX USA. RP Roman, GC (reprint author), Univ Texas, Hlth Sci Ctr, Dept Med Neurol, 7703 Floyd Curl Dr, San Antonio, TX 78229 USA. EM rornang@uthscsa.edu NR 92 TC 18 Z9 22 U1 9 U2 13 PU EDIZIONI MINERVA MEDICA PI TURIN PA CORSO BRAMANTE 83-85 INT JOURNALS DEPT., 10126 TURIN, ITALY SN 0031-0808 J9 PANMINERVA MED JI Panminerva Medica PD DEC PY 2004 VL 46 IS 4 BP 207 EP 215 PG 9 WC Medicine, General & Internal SC General & Internal Medicine GA 924UY UT WOS:000229007300001 PM 15876977 ER PT J AU Misra, M Aggarwal, A Miller, KK Almazan, C Worley, M Soyka, LA Herzog, DB Klibanski, A AF Misra, M Aggarwal, A Miller, KK Almazan, C Worley, M Soyka, LA Herzog, DB Klibanski, A TI Effects of anorexia nervosa on clinical, hematologic, biochemical, and bone density parameters in community-dwelling adolescent girls SO PEDIATRICS LA English DT Article DE adolescent health; anorexia nervosa; blood; bone mineral density; cardiovascular ID X-RAY ABSORPTIOMETRY; EATING-DISORDERS; BODY-COMPOSITION; YOUNG-WOMEN; MEDICAL COMPLICATIONS; CARDIAC ABNORMALITIES; WEIGHT RECOVERY; QT INTERVAL; PERFORMANCE; CORTISOL AB Objective. Anorexia nervosa (AN) is an eating disorder that leads to a number of medical sequelae in adult women and has a mortality rate of 5.6% per decade; known complications include effects on hematologic, biochemical, bone density, and body composition parameters. Few data regarding medical and developmental consequences of AN are available for adolescents, in particular for an outpatient community-dwelling population of girls who have this disorder. The prevalence of AN is increasing in adolescents, and it is the third most common chronic disease in adolescent girls. Therefore, it is important to determine the medical effects of this disorder in this young population. Methods. We examined clinical characteristics and performed hematologic, biochemical, hormonal, and bone density evaluations in 60 adolescent girls with AN (mean age: 15.8 +/- 1.6 years) and 58 healthy adolescent girls (mean age: 15.2 +/- 1.8 years) of comparable maturity. Nutritional and pubertal status; vital signs; a complete blood count; potassium levels; hormonal profiles; bone density at the lumbar and lateral spine; total body, hip, and femoral neck (by dual-energy x-ray absorptiometry) and body composition (by dual-energy x-ray absorptiometry) were determined. Results. All measures of nutritional status such as weight, percentage of ideal body weight, body mass index, lean body mass, fat mass, and percentage of fat mass were significantly lower in girls with AN than in control subjects. Girls with AN had significantly lower heart rates, lower systolic blood pressure, and lower body temperature compared with control subjects. Total red cell and white cell counts were lower in AN than in control subjects. Among girls with AN, 22% were anemic and 22% were leukopenic. None were hypokalemic. Mean age at menarche did not differ between the groups. However, the proportion of girls who had AN and were premenarchal was significantly higher compared with healthy control subjects who were premenarchal, despite comparable maturity as determined by bone age. Ninety-four percent of premenarchal girls with AN versus 28% of premenarchal control subjects were above the mean age at menarche for white girls, and 35% of premenarchal AN girls versus 0% of healthy adolescents were delayed >2 SD above the mean. The ratio of bone age to chronological age, a measure of delayed maturity, was significantly lower in girls with AN versus control subjects and correlated positively with duration of illness and markers of nutritional status. Serum estradiol values were lower in girls with AN than in control subjects, and luteinizing hormone values trended lower in AN. Levels of insulin- like growth factor-I were also significantly lower in girls with AN. Estradiol values correlated positively with insulin- like growth factor-I, a measure of nutritional status essential for growth (r = 0.28). All measures of bone mineral density (z scores) were lower in girls with AN than in control subjects, with lean body mass, body mass index, and age at menarche emerging as the most important predictors of bone density. Bone density z scores of < -1 at any one site were noted in 41% of girls with AN, and an additional 11% had bone density z scores of < -2. Conclusions. A high prevalence of hemodynamic, hematologic, endocrine, and bone density abnormalities are reported in this large group of community-dwelling adolescent girls with AN. Although a number of these consequences of AN are known to occur in hospitalized adolescents, the occurrence of these findings, including significant bradycardia, low blood pressure, and pubertal delay, in girls who are treated for AN on an outpatient basis is of concern and suggests the need for vigilant clinical monitoring, including that of endocrine and bone density parameters. C1 Massachusetts Gen Hosp, Neuroendocrine Unit, Boston, MA 02114 USA. Massachusetts Gen Hosp, Pediat Endocrine Unit, Boston, MA 02114 USA. Massachusetts Gen Hosp, Eating Disorders Unit, Boston, MA 02114 USA. Harvard Univ, Sch Med, Boston, MA USA. Univ Massachusetts, Sch Med, Dept Pediat, Worcester, MA USA. RP Klibanski, A (reprint author), Massachusetts Gen Hosp, Neuroendocrine Unit, Bulfinch 457,55 Fruit St, Boston, MA 02114 USA. EM aklibanski@partners.org FU NCRR NIH HHS [M01-RR-01066, K23 RR018851]; NIDDK NIH HHS [DK 062249] NR 64 TC 147 Z9 152 U1 3 U2 18 PU AMER ACAD PEDIATRICS PI ELK GROVE VILLAGE PA 141 NORTH-WEST POINT BLVD,, ELK GROVE VILLAGE, IL 60007-1098 USA SN 0031-4005 J9 PEDIATRICS JI Pediatrics PD DEC PY 2004 VL 114 IS 6 BP 1574 EP 1583 DI 10.1542/peds.2004-0540 PG 10 WC Pediatrics SC Pediatrics GA 875WN UT WOS:000225453000009 PM 15574617 ER PT J AU Elhalel, MD Wald, H Rubinger, D Gal-Moscovici, A Inoue, M Levi, M Popovtzer, MM AF Elhalel, MD Wald, H Rubinger, D Gal-Moscovici, A Inoue, M Levi, M Popovtzer, MM TI Regulation of NaPi-IIa mRNA and transporter protein in chronic renal failure: role of parathyroid hormone (PTH) and dietary phosphate (Pi) SO PFLUGERS ARCHIV-EUROPEAN JOURNAL OF PHYSIOLOGY LA English DT Article DE CRF; FEPi; PTH; NaPi-IIa; PTH/PTHrP-R; low-Pi diet; parathyroidectomy ID NA/P-I-COTRANSPORTER; DOWN-REGULATION; UREMIC RATS; ADAPTATION; HYPERPARATHYROIDISM; EXPRESSION; VESICLES; CELLS AB Chronic renal failure (CRF) is associated with a high fractional phosphate excretion (FEPi), secondary hyperparathyroidism, and resistance to parathyroid hormone (PTH). This study was undertaken to characterize the role of PTH and dietary Pi in the regulation of PTH/PTH-related peptide receptor (PTHrP-R) mRNA and NaPi-IIa mRNA and protein in CRF. The following groups of rats were studied: (1) sham-operated (control); (2) CRF: 6 weeks after 5/6 nephrectomy (NPX); (3) NPX and parathyroidectomy (NPX + PTX); (4) NPX rats fed a low-Pi diet (NPX + LP); (5) sham-operated rats fed a low-Pi diet (control + LP); (6) sham-operated after PTX (control+PTX). Expression of NaPi-IIa mRNA and PTH/PTHrP-R mRNA was determined in the renal cortex by Northern hybridization. NaPi-IIa protein abundance was determined in cortical brush border membranes by immunoblotting. In NPX rats creatinine clearance decreased to 40 +/- 4%, PTH/PTHrP-R mRNA to 52.1 +/- 2% and NaPi-IIa mRNA to 41.2 +/- 5.5% of control. The PTH/PTHrP-R and NaPi-IIa mRNA in the NPX + PTX and NPX + LP group was similar to that in NPX. NaPi-IIa protein abundance was reduced in NPX compared with control, but was increased dramatically in NPX+PTX and NPX + LP compared to NPX, paralleled by a decrease in FEPi. These findings suggest that the elevated FEPi in CRF is maintained by decreased NaPi-IIa mRNA and NaPi-IIa protein abundance. In contrast, the observed decrease in FEPi with PTX or LP diet in CRF is mediated, at least partly, by increased NaPi-IIa protein abundance with no change in NaPi-IIa mRNA, suggesting post-transcriptional regulation of the NaPi-IIa transporter. C1 Univ Arizona, Dept Med, SAVAHCS 1 111B, Tucson, AZ 85723 USA. Univ Colorado, Hlth Sci Ctr, Dept Med, Div Renal Dis & Hypertens, Denver, CO 80262 USA. Denver VAMC, Denver, CO 80262 USA. Hadassah Univ Hosp, IL-91120 Jerusalem, Israel. Univ Colorado, Hlth Sci Ctr, Dept Physiol & Biophys, Div Renal Dis & Hypertens, Denver, CO USA. RP Popovtzer, MM (reprint author), Univ Arizona, Dept Med, SAVAHCS 1 111B, 5601 S 6th Ave, Tucson, AZ 85723 USA. EM Mordecai.Popovtzer@med.va.gov OI Levi, Moshe/0000-0002-6225-946X NR 27 TC 8 Z9 10 U1 0 U2 3 PU SPRINGER PI NEW YORK PA 233 SPRING STREET, NEW YORK, NY 10013 USA SN 0031-6768 J9 PFLUG ARCH EUR J PHY JI Pflugers Arch. PD DEC PY 2004 VL 449 IS 3 BP 265 EP 270 DI 10.1007/s00424-004-1298-x PG 6 WC Physiology SC Physiology GA 882YO UT WOS:000225976500006 PM 15452708 ER PT J AU Castano, AP Demidova, TN Hamblin, MR AF Castano, Ana P. Demidova, Tatiana N. Hamblin, Michael R. TI Mechanisms in photodynamic therapy: part one-photosensitizers, photochemistry and cellular localization SO PHOTODIAGNOSIS AND PHOTODYNAMIC THERAPY LA English DT Review DE Photodynamic therapy; Photosensitizers; Photochemistry; Photophysics; Tissue optics; Subcellular localization AB The use of non-toxic dyes or photosensitizers (PS) in combination with harmless visible light that is known as photodynamic therapy (PDT) has been known for over a hundred years, but is only now becoming widely used. Originally developed as a tumor therapy, some of its most successful applications are for non-malignant disease. In a series of three reviews we will discuss the mechanisms that operate in the field of PDT. Part one discusses the recent explosion in discovery and chemical synthesis of new PS. Some guidelines on how to choose an ideal PS for a particular application are presented. The photochemistry and photophysics of PS and the two pathways known as Type I (radicals and reactive oxygen species) and Type II (singlet oxygen) photochemical processes are discussed. To carry out PDT effectively in vivo, it is necessary to ensure sufficient light reaches all the diseased tissue. This involves understanding how light travels within various tissues and the relative effects of absorption and scattering. The fact that most of the PS are also fluorescent allows various optical imaging and monitoring strategies to be combined with PDT. The most important factor governing the outcome of PDT is how the PS interacts with cells in the target tissue or tumor, and the key aspect of this interaction is the subcellular localization of the PS. Examples of PS that localize in mitochondria, lysosomes, endoplasmic reticulum, Golgi apparatus and plasma membranes are given. Finally the use of 5-aminolevulinic acid as a natural precursor of the heme biosynthetic pathway, stimulates accumulation of the PS protoporphyrin IX is described. (c) 2005 Elsevier B.V. All rights reserved. C1 [Castano, Ana P.; Demidova, Tatiana N.; Hamblin, Michael R.] Massachusetts Gen Hosp, Wellman Ctr Photomed, Boston, MA 02114 USA. [Castano, Ana P.; Hamblin, Michael R.] Harvard Univ, Sch Med, Dept Dermatol, Cambridge, MA 02138 USA. [Demidova, Tatiana N.] Tufts Univ, Dept Cellular Mol & Dev Biol, Medford, MA USA. RP Hamblin, MR (reprint author), Massachusetts Gen Hosp, Wellman Ctr Photomed, 40 Blossom St,Bartlett 3, Boston, MA 02114 USA. EM hamblin@helix.mgh.harvard.edu OI Hamblin, Michael/0000-0001-6431-4605 FU U.S. Department of Defense CDMRP Breast Cancer Research Grant; Wellman Center of Photomedicine; U.S. National Institutes of Health [R01-CA/AI838801] FX Ana P. Castano was supported by U.S. Department of Defense CDMRP Breast Cancer Research Grant. Tatiana N. Demidova was supported by a Wellman Center of Photomedicine graduate student fellowship. Michael R. Hamblin was supported by the U.S. National Institutes of Health (R01-CA/AI838801). We are grateful to Anna Yaroslavsky and Tayyaba Hasan for help and support. NR 96 TC 579 Z9 606 U1 30 U2 237 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 1572-1000 EI 1873-1597 J9 PHOTODIAGN PHOTODYN JI Photodiagnosis Photodyn. Ther. PD DEC PY 2004 VL 1 IS 4 BP 279 EP 293 DI 10.1016/S1572-1000(05)00007-4 PG 15 WC Oncology SC Oncology GA V27CG UT WOS:000208590700002 PM 25048432 ER PT J AU Shaywitz, DA Ausiello, DA AF Shaywitz, DA Ausiello, DA TI Preserving creativity in medicine SO PLOS MEDICINE LA English DT Editorial Material C1 Massachusetts Gen Hosp, Boston, MA 02114 USA. Harvard Univ, Sch Med, Cambridge, MA 02138 USA. EM dshaywitz@partners.org NR 6 TC 5 Z9 5 U1 0 U2 1 PU PUBLIC LIBRARY SCIENCE PI SAN FRANCISCO PA 185 BERRY ST, STE 1300, SAN FRANCISCO, CA 94107 USA SN 1549-1277 J9 PLOS MED JI PLos Med. PD DEC PY 2004 VL 1 IS 3 BP 176 EP 177 AR e34 DI 10.1371/journal.pmed.0010034.g001 PG 2 WC Medicine, General & Internal SC General & Internal Medicine GA 902TH UT WOS:000227378900007 PM 15630460 ER PT J AU Turner, EH AF Turner, EH TI A taxpayer-funded clinical trials registry and results database - It already exists within the US food and drug administration SO PLOS MEDICINE LA English DT Editorial Material ID PAROXETINE C1 US FDA, Rockville, MD 20857 USA. RP Turner, EH (reprint author), Portland VA Med Ctr, Mood Disorders Program, Portland, OR USA. EM turnere@ohsu.edu RI Turner, Erick/A-4848-2008 OI Turner, Erick/0000-0002-3522-3357 NR 16 TC 39 Z9 41 U1 0 U2 2 PU PUBLIC LIBRARY SCIENCE PI SAN FRANCISCO PA 185 BERRY ST, STE 1300, SAN FRANCISCO, CA 94107 USA SN 1549-1277 J9 PLOS MED JI PLos Med. PD DEC PY 2004 VL 1 IS 3 BP 180 EP 182 AR e60 DI 10.1371/journal.pmed.0010060.g001 PG 3 WC Medicine, General & Internal SC General & Internal Medicine GA 902TH UT WOS:000227378900009 PM 15562322 ER PT J AU Harisinghani, MG Weissleder, R AF Harisinghani, MG Weissleder, R TI Sensitive, noninvasive detection of lymph node metastases SO PLOS MEDICINE LA English DT Article ID SUPERPARAMAGNETIC IRON-OXIDE; BREAST-CANCER PATIENTS; CONTRAST AGENT; CARCINOMA; TOMOGRAPHY; DISSECTION; SURVIVAL; BIOPSY; TUMORS AB Background Many primary malignancies spread via lymphatic dissemination, and accurate staging therefore still relies on surgical exploration. The purpose of this study was to explore the possibility of semiautomated noninvasive nodal cancer staging using a nanoparticle-enhanced lymphotropic magnetic resonance imaging (LMRI) technique. Methods and Findings We measured magnetic tissue parameters of cancer metastases and normal unmatched lymph nodes by noninvasive LMRI using a learning dataset consisting of 97 histologically proven nodes. We then prospectively tested the accuracy of these parameters against 216 histologically validated lymph nodes from 34 patients with primary cancers, in semiautomated fashion. We found unique magnetic tissue parameters that accurately distinguished metastatic from normal nodes with an overall sensitivity of 98% and specificity of 92%. The parameters could be applied to datasets in a semiautomated fashion and be used for three-dimensional reconstruction of complete nodal anatomy for different primary cancers. Conclusion These results suggest for the first time the feasibility of semiautomated nodal cancer staging by noninvasive imaging. C1 Massachusetts Gen Hosp, Boston, MA 02114 USA. Harvard Univ, Sch Med, Boston, MA USA. RP Weissleder, R (reprint author), Massachusetts Gen Hosp, Boston, MA 02114 USA. EM weissleder@helix.mgh.harvard.edu FU NCI NIH HHS [N01-CM037008, N01CM37008, P50 CA086355, P50 CA86355] NR 30 TC 47 Z9 48 U1 1 U2 7 PU PUBLIC LIBRARY SCIENCE PI SAN FRANCISCO PA 185 BERRY ST, STE 1300, SAN FRANCISCO, CA 94107 USA SN 1549-1277 J9 PLOS MED JI PLos Med. PD DEC PY 2004 VL 1 IS 3 BP 202 EP 209 AR e66 DI 10.1371/journal.pmed.0010066 PG 8 WC Medicine, General & Internal SC General & Internal Medicine GA 902TH UT WOS:000227378900017 PM 15630471 ER PT J AU Litz, BT Williams, L Wang, J Bryant, R Engel, CC AF Litz, BT Williams, L Wang, J Bryant, R Engel, CC TI A therapist-assisted Internet self-help program for traumatic stress SO PROFESSIONAL PSYCHOLOGY-RESEARCH AND PRACTICE LA English DT Article ID POSTTRAUMATIC-STRESS; EXPOSURE THERAPY; RAPE VICTIMS; DISORDER; TELEHEALTH; INTERVENTIONS; SERVICES; FUTURE; SYSTEM AB The authors describe a therapist-assisted, Internet-based self-help intervention to treat posttraumatic stress disorder (PTSD) and discuss how it can be used as an efficient tool to treat large numbers of traumatized individuals. The intervention uses a modified form of stress inoculation training, promoted through daily homework assignments completed in vivo, using fewer therapist resources than standard face-to-face therapy. The process and structure of the treatment program (and structure of the Web site) and clinical and Internet security safeguards are described to introduce practitioners to a unique therapist-assisted self-management model of PTSD. It is hoped that the method described will lead to other novel, efficient methods of delivering interventions and treatment for PTSD in primary care and other outpatient and private practice settings. C1 Natl Ctr PTSD, Behav Sci Div, Boston Dept Vet Affairs Healthcare Syst, Boston, MA 02130 USA. Boston Univ, Dept Psychiat, Sch Med, Boston, MA 02215 USA. Boston Univ, Dept Psychol, Boston, MA 02215 USA. Univ New S Wales, Dept Psychol, Sydney, NSW, Australia. Walter Reed Army Med Ctr, Deployment Hlth Ctr, Washington, DC 20307 USA. Uniformed Serv Univ Hlth Sci, Bethesda, MD 20814 USA. RP Litz, BT (reprint author), Natl Ctr PTSD, Behav Sci Div, Boston Dept Vet Affairs Healthcare Syst, 150 S Huntington Ave, Boston, MA 02130 USA. EM brett.litz@med.va.gov OI Bryant, Richard/0000-0002-9607-819X NR 30 TC 32 Z9 33 U1 2 U2 5 PU AMER PSYCHOLOGICAL ASSOC PI WASHINGTON PA 750 FIRST ST NE, WASHINGTON, DC 20002-4242 USA SN 0735-7028 J9 PROF PSYCHOL-RES PR JI Prof. Psychol.-Res. Pract. PD DEC PY 2004 VL 35 IS 6 BP 628 EP 634 DI 10.1037/0735-7028.35.6.628 PG 7 WC Psychology, Multidisciplinary SC Psychology GA 876OV UT WOS:000225507600008 ER PT J AU Wilhelm, S AF Wilhelm, S TI Body dysmorphic disorder SO PSYCHIATRIC ANNALS LA English DT Editorial Material C1 Massachusetts Gen Hosp, Body Dysmorph Disorder Clin, Boston, MA 02114 USA. Massachusetts Gen Hosp, Obsess Compuls Disorder Clin, Boston, MA 02114 USA. Harvard Univ, Sch Med, Boston, MA USA. RP Wilhelm, S (reprint author), Massachusetts Gen Hosp, Body Dysmorph Disorder Clin, Boston, MA 02114 USA. NR 7 TC 1 Z9 1 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0048-5713 J9 PSYCHIAT ANN JI Psychiatr. Ann. PD DEC PY 2004 VL 34 IS 12 BP 902 EP 903 PG 2 WC Psychiatry SC Psychiatry GA 879MV UT WOS:000225722800002 ER PT J AU Buhlmann, U Wilhelm, S AF Buhlmann, U Wilhelm, S TI Cognitive factors in body dysmorphic SO PSYCHIATRIC ANNALS LA English DT Article ID DISORDER; ART C1 Massachusetts Gen Hosp, Obsess Compuls Disorders Clin, Boston, MA 02114 USA. RP Wilhelm, S (reprint author), Harvard Univ, Sch Med, Massachusetts Gen Hosp, OCD Clin, 149 13th St, Charlestown, MA 02102 USA. NR 24 TC 27 Z9 27 U1 0 U2 2 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0048-5713 J9 PSYCHIAT ANN JI Psychiatr. Ann. PD DEC PY 2004 VL 34 IS 12 BP 922 EP 926 PG 5 WC Psychiatry SC Psychiatry GA 879MV UT WOS:000225722800005 ER PT J AU Myrick, H Cluver, J Swavely, S Peters, H AF Myrick, H Cluver, J Swavely, S Peters, H TI Diagnosis and treatment of co-occurring affective disorders and substance use disorders SO PSYCHIATRIC CLINICS OF NORTH AMERICA LA English DT Article ID PLACEBO-CONTROLLED-TRIAL; COGNITIVE-BEHAVIORAL THERAPY; DOUBLE-BLIND; ALCOHOL-WITHDRAWAL; DEPRESSIVE-DISORDERS; FLUOXETINE TREATMENT; RELAPSE PREVENTION; DEPENDENT PATIENTS; BIPOLAR DISORDER; MENTAL-DISORDERS AB There is increasing interest in the comorbidity of affective disorders and substance use disorders. These disorders commonly co-occur, and the relationship is often complex and bidirectional. Two epidemiological surveys have emphasized the prevalence of comorbid mood and substance use disorders in community samples: the National Institute of Mental Health Epidemiologic Catchment Area (ECA) study [1] and the National Comorbidity Study (NCS) [2]. In the ECA study, an estimated 45% of individuals with alcohol use disorders and 72% of individuals with drug use disorders had at least one co-occurring psychiatric disorder. In the NCS, approximately 78% of alcohol-dependent men and 86% of alcohol-dependent women met lifetime criteria for another psychiatric disorder, including drug dependence. Interest in the co-occurrence of psychiatric and substance use disorders is clinically important as comorbidity has been found to have a negative impact on the course, treatment outcome, and prognosis of both syndromes. In this article, the relationship between substance use disorders and specific affective disorders is explored. The article begins with an overview of some of the general principles of diagnosis and treatment of co-occurring disorders; then the relationship between individual affective disorders and substance use disorders will be explored. Specifically, for major depression and bipolar disorder, the prevalence of co-occurrence with substance use, clinical characteristics, and treatment of individuals with co-occurring disorders will be reviewed. C1 Med Univ S Carolina, Ctr Drug & Alcohol Programs, Dept Psychiat & Behav Sci, Charleston, SC 29425 USA. Ralph H Johnson Vet Adm Med Ctr, Substance Abuse Treatment Ctr, Charleston, SC 29401 USA. RP Myrick, H (reprint author), Med Univ S Carolina, Ctr Drug & Alcohol Programs, Dept Psychiat & Behav Sci, 67 President St, Charleston, SC 29425 USA. EM myrickh@musc.edu FU NIAAA NIH HHS [K23 AA00314-01, 2 P50 AA10761-03] NR 46 TC 8 Z9 8 U1 5 U2 7 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 USA SN 0193-953X J9 PSYCHIAT CLIN N AM JI Psychiatr. Clin. North Amer. PD DEC PY 2004 VL 27 IS 4 BP 649 EP + DI 10.1016/j.psc.2004.06.003 PG 13 WC Psychiatry SC Psychiatry GA 879SI UT WOS:000225738800004 PM 15550285 ER PT J AU Grubaugh, AL Elhai, JD Monnier, J Frueh, BC AF Grubaugh, AL Elhai, JD Monnier, J Frueh, BC TI Service utilization among compensation-seeking veterans SO PSYCHIATRIC QUARTERLY LA English DT Article DE PTSD; combat; MMPI; service utilization ID POSTTRAUMATIC-STRESS-DISORDER; VIETNAM COMBAT VETERANS; FLOODING THERAPY; PTSD; AFFAIRS AB To examine the relationship between compensation-seeking status, symptom reporting, and health care utilization among combat veterans presenting for a Posttraumatic Stress disorder (PTSD) evaluation. Archival data for 68 veterans was drawn from electronic medical records for which compensation-seeking status was available. Consistent with previous findings, self-reports of distress and validity scale indices on the Minnesota Multiphasic Personality Inventory-2 (MMPI-2) were higher among compensation-seeking (CS) veterans than noncompensation-seeking (NCS) veterans despite a lack of difference in actual PTSD diagnoses. However, no significant differences emerged between these two groups on healthcare utilization indices. Although exploratory analyses did not yield significant group differences on various healthcare indices, there was a trend for CS veterans to use PTSD services more, suggesting the need to further explore utilization patterns among these groups. C1 Ralph H Johnson Vet Affairs Med Ctr, Charleston, SC USA. Med Univ S Carolina, Charleston, SC 29425 USA. Univ S Dakota, Disaster Mental Hlth Inst, Vermillion, SD 57069 USA. RP Frueh, BC (reprint author), VAMC, Mental Hlth Serv, 109 Bee St, Charleston, SC 29401 USA. EM fruehbe@musc.edu FU NIMH NIH HHS [MH01660, MH61983] NR 22 TC 5 Z9 5 U1 0 U2 0 PU KLUWER ACADEMIC-HUMAN SCIENCES PRESS PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013-1578 USA SN 0033-2720 J9 PSYCHIAT QUART JI Psychiatr. Q. PD WIN PY 2004 VL 75 IS 4 BP 333 EP 341 DI 10.1023/B:PSAQ.0000043509.18637.3b PG 9 WC Psychiatry SC Psychiatry GA 866KR UT WOS:000224772900003 PM 15563051 ER PT J AU Friedman, MJ Harris, WW AF Friedman, MJ Harris, WW TI Toward a national PTSD brain bank SO PSYCHIATRY-INTERPERSONAL AND BIOLOGICAL PROCESSES LA English DT Editorial Material ID POSTTRAUMATIC-STRESS-DISORDER; DISASTER VICTIMS SPEAK; EVENTS C1 VA Med Ctr, US Dept Vet Affairs, Natl Ctr PTSD, White River Jct, VT 05009 USA. Dartmouth Coll Sch Med, Dept Psychiat, Hanover, NH USA. Dartmouth Coll Sch Med, Dept Pharmacol, Hanover, NH USA. RP Friedman, MJ (reprint author), VA Med Ctr, US Dept Vet Affairs, Natl Ctr PTSD, 116D,215 N Main St, White River Jct, VT 05009 USA. EM Matthew.J.Friedman@Dartmouth.edu NR 17 TC 3 Z9 3 U1 3 U2 5 PU GUILFORD PUBLICATIONS INC PI NEW YORK PA 72 SPRING STREET, NEW YORK, NY 10012 USA SN 0033-2747 J9 PSYCHIATRY JI Psychiatry-Interpers. Biol. Process. PD WIN PY 2004 VL 67 IS 4 BP 384 EP 390 DI 10.1521/psyc.67.4.384.56564 PG 7 WC Psychiatry SC Psychiatry GA 890GJ UT WOS:000226499400005 PM 15801378 ER PT J AU Raskind, MA AF Raskind, MA TI The challenge of a PTSD brain bank SO PSYCHIATRY-INTERPERSONAL AND BIOLOGICAL PROCESSES LA English DT Editorial Material ID POSTTRAUMATIC-STRESS-DISORDER; HIPPOCAMPAL VOLUME; ALZHEIMERS-DISEASE; NOREPINEPHRINE; EFFICACY; SAFETY; MRI C1 VA Puget Sound Hlth Care Syst, Dept Psychiat & Behav Sci, Seattle, WA 98108 USA. RP Raskind, MA (reprint author), VA Puget Sound Hlth Care Syst, Dept Psychiat & Behav Sci, 116 MIRECC,1660 S Columbian Way, Seattle, WA 98108 USA. EM Murray.Raskind@med.va.gov NR 16 TC 1 Z9 1 U1 0 U2 0 PU GUILFORD PUBLICATIONS INC PI NEW YORK PA 72 SPRING STREET, NEW YORK, NY 10012 USA SN 0033-2747 J9 PSYCHIATRY JI Psychiatry-Interpers. Biol. Process. PD WIN PY 2004 VL 67 IS 4 BP 404 EP 406 DI 10.1521/psyc.67.4.404.56563 PG 3 WC Psychiatry SC Psychiatry GA 890GJ UT WOS:000226499400008 PM 15801381 ER PT J AU DeDe, G Caplan, D Kemtes, K Waters, G AF DeDe, G Caplan, D Kemtes, K Waters, G TI The relationship between age, verbal working memory, and language comprehension SO PSYCHOLOGY AND AGING LA English DT Article ID SENTENCE COMPREHENSION; OLDER ADULTS; INDIVIDUAL-DIFFERENCES; CAPACITY THEORY; SYNTACTIC AMBIGUITY; RESOURCE-ALLOCATION; ONLINE; RELIABILITY; COMPLEXITY; ABILITIES AB A structural modeling approach was used to examine the relationships between age, verbal working memory (vWM), and 3 types of language measures: online syntactic processing, sentence comprehension, and text comprehension. The best-fit model for the online-processing measure revealed a direct effect of age on online sentence processing, but no effect mediated through vWM. The best-fit models for sentence and text comprehension included an effect of age mediated through vWM and no direct effect of age. These results indicate that the relationship among age, vWM, and comprehension differs depending on the measure of language processing and support the view that individual differences in vWM do not affect individuals' online syntactic processing. C1 Boston Univ, Dept Hlth Sci, Commun Disorders Program, Boston, MA 02215 USA. Massachusetts Gen Hosp, Dept Neurol, Neuropsychol Lab, Boston, MA 02114 USA. Univ Nevada, Dept Psychol, Las Vegas, NV 89154 USA. RP Waters, G (reprint author), Boston Univ, Dept Hlth Sci, Commun Disorders Program, 635 Commonwealth Ave, Boston, MA 02215 USA. EM gwaters@bu.edu FU NIA NIH HHS [AG09661] NR 82 TC 54 Z9 57 U1 3 U2 11 PU AMER PSYCHOLOGICAL ASSOC PI WASHINGTON PA 750 FIRST ST NE, WASHINGTON, DC 20002-4242 USA SN 0882-7974 J9 PSYCHOL AGING JI Psychol. Aging PD DEC PY 2004 VL 19 IS 4 BP 601 EP 616 DI 10.1037/0882-7974.19.4.601 PG 16 WC Gerontology; Psychology, Developmental SC Geriatrics & Gerontology; Psychology GA 877DF UT WOS:000225547300005 PM 15584786 ER PT J AU Cook, JM Schnurr, PP Foa, EB AF Cook, JM Schnurr, PP Foa, EB TI Bridging the gap between posttraumatic stress disorder research and clinical practice: The example of exposure therapy SO PSYCHOTHERAPY LA English DT Article ID EMPIRICALLY SUPPORTED TREATMENTS; PSYCHOTHERAPY TREATMENT MANUALS; PSYCHOLOGISTS ATTITUDES; CHILDHOOD ABUSE; PTSD; DISSEMINATION; RECOMMENDATIONS; INTERVENTIONS; SCIENCE; TRIAL AB There are notable challenges in translating empirically supported psychosocial treatments (ESTs) into general routine clinical practice. However, there may be additional unique dissemination and implementation obstacles for ESTs for trauma-related disorders. For example, despite considerable evidence from randomized clinical trials that attests to the efficacy of exposure therapy for posttraumatic stress disorder, front-line clinicians in real-world settings rare use this treatment. Perceived and actual barriers that interfere with adoption include clinician misconceptions about what exposure entails and complex cases to which ESTs may not be readily applicable. Specific suggestions for bridging the science-into-service gap in trauma ESTs (in general) and in exposure therapy (in particular) are proposed. C1 Univ Penn, Treatment Res Ctr, Dept Psychiat, Philadelphia, PA 19104 USA. Philadephia VA Med Ctr, Dept Behav Hlth, Philadelphia, PA USA. VA Natl Ctr PTSD, Execut Div, White River Jct, VT USA. Dartmouth Coll Sch Med, Dept Psychiat, Lebanon, NH 03756 USA. RP Cook, JM (reprint author), Univ Penn, Treatment Res Ctr, Dept Psychiat, 3900 Chestnut St, Philadelphia, PA 19104 USA. EM cook_j@mail.trc.upenn.edu NR 75 TC 48 Z9 49 U1 3 U2 5 PU AMER PSYCHOLOGICAL ASSOC, DIV PSYCHOTHERAPY PI CORAL GABLES PA 1390 SOUTH DIXIE HIGHWAY, STE 2222, CORAL GABLES, FL 33146-2946 USA SN 0033-3204 J9 PSYCHOTHERAPY JI Psychotherapy PD WIN PY 2004 VL 41 IS 4 SI SI BP 374 EP 387 DI 10.1037/0033-3204.41.4.374 PG 14 WC Psychology, Clinical SC Psychology GA 906OP UT WOS:000227651800002 ER PT J AU Weingart, SN Page, D AF Weingart, SN Page, D TI Implications for practice: challenges for healthcare leaders in fostering patient safety SO QUALITY & SAFETY IN HEALTH CARE LA English DT Article ID ADVERSE DRUG EVENTS AB Although various government and regulatory organisations have identified practices that may enhance patient safety, there is little empirical or theoretical research to inform the decisions of healthcare leaders seeking to create patient safety programmes within their hospitals and clinics. In order to understand the challenges facing hospital and health system executives, we describe the experience of the Executive Session on Patient Safety. The executives identified five major problems in leading patient safety: 1) how should executives structure their organisations to deliver safe care? 2) how should executives monitor and measure their organisation's safety performance? 3) how should executives spread and sustain patient safety innovation? 4) how should executives manage the relationship with the external environment? and 5) how should executives manage their own behaviour in order to lead for safety? The organisational infrastructure needed for safer care is being developed by practitioners out in the field as a matter of necessity. Strengthening the scientific basis for organisational leadership in patient safety is a vital but neglected area of study. C1 Dana Farber Canc Inst, Ctr Patient Safety, Boston, MA 02115 USA. Fairview Hlth Serv, Minneapolis, MN USA. RP Weingart, SN (reprint author), Dana Farber Canc Inst, Ctr Patient Safety, 44 Binney St, Boston, MA 02115 USA. EM saul.weingart@dfci.harvard.edu NR 30 TC 12 Z9 12 U1 0 U2 4 PU B M J PUBLISHING GROUP PI LONDON PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND SN 1475-3898 J9 QUAL SAF HEALTH CARE JI Qual. Saf. Health Care PD DEC PY 2004 VL 13 SU 2 BP 52 EP 56 DI 10.1136/qshc.2003.009621 PG 5 WC Health Care Sciences & Services SC Health Care Sciences & Services GA 882NX UT WOS:000225946700010 ER PT J AU Cooper, JB AF Cooper, JB TI Are simulation and didactic crisis resource management (CRM) training synergistic? SO QUALITY & SAFETY IN HEALTH CARE LA English DT Editorial Material ID PERFORMANCE C1 Harvard Univ, Massachusetts Gen Hosp, Sch Med, Boston, MA 02114 USA. RP Cooper, JB (reprint author), Harvard Univ, Massachusetts Gen Hosp, Sch Med, Boston, MA 02114 USA. EM jcooper@partners.org NR 7 TC 5 Z9 5 U1 0 U2 0 PU B M J PUBLISHING GROUP PI LONDON PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND SN 1475-3898 J9 QUAL SAF HEALTH CARE JI Qual. Saf. Health Care PD DEC PY 2004 VL 13 IS 6 BP 413 EP 414 DI 10.1136/qshc.2004.011544 PG 2 WC Health Care Sciences & Services SC Health Care Sciences & Services GA 876FY UT WOS:000225483200006 PM 15576699 ER PT J AU Mahmood, U AF Mahmood, U TI Science to practice - Can MR imaging be used to track delivery of intravascularly administered stem cells? SO RADIOLOGY LA English DT Article C1 Harvard Univ, Massachusetts Gen Hosp, Sch Med, Ctr Mol Imaging Res, Charlestown, MA 02129 USA. RP Mahmood, U (reprint author), Harvard Univ, Massachusetts Gen Hosp, Sch Med, Ctr Mol Imaging Res, Bldg 149,13th St,Room 5408, Charlestown, MA 02129 USA. EM mahmood@helix.mgh.harvard.edu NR 5 TC 6 Z9 6 U1 0 U2 0 PU RADIOLOGICAL SOC NORTH AMERICA PI OAK BROOK PA 820 JORIE BLVD, OAK BROOK, IL 60523 USA SN 0033-8419 J9 RADIOLOGY JI Radiology PD DEC PY 2004 VL 233 IS 3 BP 625 EP 626 DI 10.1148/radiol.2333041190 PG 2 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA 874HV UT WOS:000225342400001 PM 15564396 ER PT J AU Thrall, JH AF Thrall, JH TI The emerging role of pay-for-performance contracting for health care services SO RADIOLOGY LA English DT Editorial Material DE perspectives; radiology and radiologists, socioeconomic issues ID INTERVENTION; PHYSICIANS; QUALITY C1 Massachusetts Gen Hosp, Dept Radiol, Boston, MA 02114 USA. RP Thrall, JH (reprint author), Massachusetts Gen Hosp, Dept Radiol, 55 Fruit St, Boston, MA 02114 USA. EM jthrall@partners.org NR 18 TC 8 Z9 8 U1 1 U2 2 PU RADIOLOGICAL SOC NORTH AMERICA PI OAK BROOK PA 820 JORIE BLVD, OAK BROOK, IL 60523 USA SN 0033-8419 J9 RADIOLOGY JI Radiology PD DEC PY 2004 VL 233 IS 3 BP 637 EP 640 DI 10.1148/radiol.2333041412 PG 4 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA 874HV UT WOS:000225342400002 PM 15564401 ER PT J AU Kalra, MK Maher, MM Toth, TL Schmidt, B Westerman, BL Morgan, HT Saini, S AF Kalra, MK Maher, MM Toth, TL Schmidt, B Westerman, BL Morgan, HT Saini, S TI Techniques and applications of automatic tube current modulation for CT SO RADIOLOGY LA English DT Review DE computed tomography (CT), image quality; computed tomography (CT), radiation exposure; computed tomography (CT), technology; radiations, exposure to patients and personnel; review ID DOSE REDUCTION; COMPUTED-TOMOGRAPHY; SPIRAL-CT; PHANTOM MEASUREMENTS; ONLINE MODULATION; IMAGE QUALITY; HELICAL CT; OPTIMIZATION; STRATEGIES; ABDOMEN AB Introduction of slip-ring technology with subsequent development of single - and multi - detector row helical computed tomographic (CT) scanners have expanded the applications of CT, leading to a substantial increase in the number of CT examinations being performed. Owing to concerns about the resultant increase in associated radiation dose, many technical innovations have been introduced. One such innovation is automatic tube current modulation. The purpose of automatic tube current modulation is to maintain constant image quality regardless of patient attenuation characteristics, thus allowing radiation dose to patients to be reduced. This review discusses the principles, clinical use, and limitations of different automatic tube current modulation techniques. C1 Emory Univ, Sch Med, Emory Univ Hosp, Dept Radiol, Atlanta, GA 30322 USA. Massachusetts Gen Hosp, Dept Radiol, Div Abdominal Imaging & Intervent, Boston, MA 02134 USA. Harvard Univ, Sch Med, Boston, MA 02134 USA. GE Med Syst, Waukesha, WI USA. Siemens Med Solut, Forchheim, Germany. Toshiba Amer Med Syst, Tustin, CA USA. Philips Med Syst, Cleveland, OH USA. RP Saini, S (reprint author), Emory Univ, Sch Med, Emory Univ Hosp, Dept Radiol, Atlanta, GA 30322 USA. EM mannudeep_k_kalra@yahoo.com NR 24 TC 344 Z9 367 U1 2 U2 22 PU RADIOLOGICAL SOC NORTH AMERICA PI OAK BROOK PA 820 JORIE BLVD, OAK BROOK, IL 60523 USA SN 0033-8419 J9 RADIOLOGY JI Radiology PD DEC PY 2004 VL 233 IS 3 BP 649 EP 657 DI 10.1148/radiol.2333031150 PG 9 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA 874HV UT WOS:000225342400005 PM 15498896 ER PT J AU Gazelle, GS McMahon, PM Beinfeld, MT Halpern, EF Weinstein, MC AF Gazelle, GS McMahon, PM Beinfeld, MT Halpern, EF Weinstein, MC TI Metastatic colorectal carcinoma: Cost-effectiveness of percutaneous radiofrequency ablation versus that of hepatic resection SO RADIOLOGY LA English DT Review DE cost-effectiveness; economics, medical; liver neoplasms; liver neoplasms, therapy; radiofrequency (RF) ablation ID PERIOPERATIVE BLOOD-TRANSFUSION; SMALL HEPATOCELLULAR-CARCINOMA; INTERSTITIAL THERMAL ABLATION; FACTORS INFLUENCING SURVIVAL; LASER-INDUCED THERMOTHERAPY; UNTREATED LIVER METASTASES; MEDICAL DECISION-MAKING; BREAST-TUMOR MODEL; QUALITY-OF-LIFE; TISSUE ABLATION AB PURPOSE: To evaluate the relative cost-effectiveness of radiofrequency (RF) ablation and hepatic resection in patients with metachronous liver metastases from colorectal carcinoma (CRC) and compare the outcomes, cost, and cost-effectiveness of a variety of treatment and follow-up strategies. MATERIALS AND METHODS: A state-transition decision model for evaluating the (societal) cost-effectiveness of RF ablation and hepatic resection in patients with CRC liver metastases was developed. The model tracks the presence, number, size, location, growth, detection, and removal of up to 15 individual metastases in each patient. Survival, quality of life, and cost are predicted on the basis of disease extent. Imaging, ablation, and resection affect outcomes through detection and elimination of individual metastases. Several patient care strategies were developed and compared on the basis of cost, effectiveness, and incremental cost-effectiveness ( expressed as dollars per quality-adjusted life-year [ QALY]). Extensive sensitivity analysis was performed to evaluate the impact of alternative scenarios and assumptions on results. RESULTS: A strategy permitting ablation of up to five metastases with computed tomographic (CT) follow-up every 4 months resulted in a gain of 0.65 QALYs relative to a no-treat strategy, at an incremental cost of $2400 per QALY. Compared with this ablation strategy, a strategy permitting resection of up to four metastases, one repeat resection, and CT follow-up every 6 months resulted in an additional gain of 0.76 QALYs at an incremental cost of $ 24 300 per QALY. Across a range of model assumptions, more aggressive treatment strategies (ie, ablation or resection of more metastases, treatment of recurrent metastases, more frequent follow-up imaging) were superior to less aggressive strategies and had incremental cost-effectiveness ratios of less than $ 35 000 per QALY. Findings were insensitive to changes in most model parameters; however, results were somewhat sensitive to changes in size thresholds for RF ablation, the number of metastases present, and surgery and treatment costs. CONCLUSION: RF ablation is a cost-effective treatment option for patients with CRC liver metastases. However, in most scenarios, hepatic resection is more effective ( in terms of QALYs gained) than RF ablation and has an incremental cost-effectiveness ratio of less than 35 000 per QALY. C1 Harvard Univ, Massachusetts Gen Hosp, Sch Med, Inst Technol Assessment, Boston, MA 02114 USA. Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Radiol, Boston, MA 02114 USA. Harvard Univ, Sch Publ Hlth, Ctr Risk Anal, Boston, MA 02115 USA. Harvard Univ, Sch Publ Hlth, Dept Hlth Policy & Management, Boston, MA 02115 USA. RP Gazelle, GS (reprint author), Harvard Univ, Massachusetts Gen Hosp, Sch Med, Inst Technol Assessment, Zero Emerson Pl,Suite 2H, Boston, MA 02114 USA. FU NCI NIH HHS [R01 CA/HS 83960] NR 123 TC 33 Z9 35 U1 1 U2 6 PU RADIOLOGICAL SOC NORTH AMERICA PI OAK BROOK PA 820 JORIE BLVD, OAK BROOK, IL 60523 USA SN 0033-8419 J9 RADIOLOGY JI Radiology PD DEC PY 2004 VL 233 IS 3 BP 729 EP 739 DI 10.1148/radiol.2333032052 PG 11 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA 874HV UT WOS:000225342400015 PM 15564408 ER PT J AU Andrew, BA Suit, H AF Andrew, BA Suit, H TI The centenary of the discovery of the Bragg peak SO RADIOTHERAPY AND ONCOLOGY LA English DT Editorial Material DE Bragg peak; charged particles; William Henry Bragg AB Bragg published curves for ionization of air by radium alpha particles in December 1904 demonstrating that ionization density increased sharply near the end of range. The accepted view was that ionization would decrease exponentially with depth. This depth dose pattern is the basis for the dose distributional advantage of charged particles relative to photons. (C) 2004 Elsevier Ireland Ltd. All rights reserved. C1 Seacoast Canc Ctr, Dover, NH 03820 USA. Massachusetts Gen Hosp, Dept Radiat Oncol, Boston, MA 02114 USA. RP Andrew, BA (reprint author), Seacoast Canc Ctr, 789 Cent Ave, Dover, NH 03820 USA. NR 8 TC 19 Z9 19 U1 0 U2 0 PU ELSEVIER SCI IRELAND LTD PI CLARE PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE, IRELAND SN 0167-8140 J9 RADIOTHER ONCOL JI Radiother. Oncol. PD DEC PY 2004 VL 73 IS 3 BP 265 EP 268 DI 10.1016/j.radonc.2004.09.008 PG 4 WC Oncology; Radiology, Nuclear Medicine & Medical Imaging SC Oncology; Radiology, Nuclear Medicine & Medical Imaging GA 885AU UT WOS:000226129000002 PM 15588869 ER PT J AU Rietzel, E Rosenthal, SJ Gierga, DP Willett, CG Chen, GTY AF Rietzel, E Rosenthal, SJ Gierga, DP Willett, CG Chen, GTY TI Moving targets: detection and tracking of internal organ motion for treatment planning and patient set-up SO RADIOTHERAPY AND ONCOLOGY LA English DT Article; Proceedings Paper CT 9th Workshop on Heavy Charged Particles in Biology and Medicine and 3rd ENLIGHT Meeting CY OCT 01-04, 2003 CL Lyon, FRANCE DE organ motion; respiratory motion; 4D Computed Tomography; motion tracking; patient set-up ID RADIATION-THERAPY; TUMOR; RADIOTHERAPY AB Background and Purpose Clinical target volumes of the thorax and abdomen are typically expanded to account for inter- and intrafractional organ motion. Usually, such expansions are based on clinical experience and planar observations of target motion during simulation. More precise, 4- dimensional motion margins for a specific patient may improve dose cove-rage of mobile targets and yet limit unnecessarily large field expansions. We are studying approaches to targeting moving tumors throughout the entire treatment process, from treatment planning to beam delivery. Material and Methods Radio-opaque markers were implanted under CT guidance in the liver at the gross tumor periphery. Organ motion during light respiration was volumetrically imaged by 4D Computed Tomography. Marker motion was also acquired by fluoroscopy and compared with 4DCT data. During treatment, daily diagnostic x-ray images were captured at end-exhale and -inhale for patient setup and target localization. Results Based on the time-resolved CT data, target volumes can be designed to account for respiratory motion during treatment. Motion of the tumor as derived from 4DCT was consistent with fluoroscopic motion analysis. Radiographs acquired in the treatment room enabled millimeter-level patient set-up and assessment of target position relative to bony anatomy. Daily positional variations between bony anatomy and implanted markers were observed. Conclusions Image guided therapy, based on 4DCT imaging, fluoroscopic imaging studies, and daily gated diagonstic energy set-up radiographs is being developed to improve beam delivery precision. Monitoring internal target motion throughout the entire treatment process will ensure adequate dose coverage of the target while sparing the maximum healthy tissue. C1 Massachusetts Gen Hosp, NE Proton Therapy Ctr, Dept Radiat Oncol, Boston, MA 02114 USA. Gesell Schwerionenforsch mbH, Biophys Abt, Darmstadt, Germany. RP Rietzel, E (reprint author), Massachusetts Gen Hosp, NE Proton Therapy Ctr, Dept Radiat Oncol, 30 Fruit St, Boston, MA 02114 USA. EM erietzel@partners.org NR 15 TC 49 Z9 49 U1 0 U2 4 PU ELSEVIER SCI IRELAND LTD PI CLARE PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE, IRELAND SN 0167-8140 J9 RADIOTHER ONCOL JI Radiother. Oncol. PD DEC PY 2004 VL 73 SU 2 BP S68 EP S72 DI 10.1016/S0167-8140(04)80018-5 PG 5 WC Oncology; Radiology, Nuclear Medicine & Medical Imaging SC Oncology; Radiology, Nuclear Medicine & Medical Imaging GA 906MY UT WOS:000227647500018 PM 15971313 ER PT J AU Robbins, LB Pender, NJ Ronis, DL Kazanis, AS Pis, MB AF Robbins, LB Pender, NJ Ronis, DL Kazanis, AS Pis, MB TI Physical activity, self-efficacy, and perceived exertion among adolescents SO RESEARCH IN NURSING & HEALTH LA English DT Article DE physical activity; exercise; self-efficacy; perceived exertion; adolescents ID EXERCISE; CHILDREN; HEALTH; YOUTH; RESPONSES; BEHAVIOR; BURDEN AB The relationship of self-efficacy, a sense of confidence in personal physical activity (PA) skills, to perceived exertion during activity was explored among 168 African American and European American boys and girls between 9 and 17 years of age. Participants walked/ran on a treadmill at a speed equivalent to 60% of their peak VO2 for 20 minutes and provided ratings of exertion every 4 minutes. Pre-activity self-efficacy Predicted Perceived exertion for boys only. Girls were lower than boys in pre-activity self-efficacy and subsequently reported greater perceived exertion. For both genders, lower perceived exertion during PA resulted in higher post-activity self-efficacy. Uncomfortable perceptions of exertion during initial efforts to increase PA are likely to discourage future activity. Interventions that can lower perceptions of exertion may enhance self-efficacy and promote a sense of competence in PA skills. (C) 2004 Wiley Periodicals, Inc. C1 Univ Michigan, Sch Nursing, Ann Arbor, MI 48109 USA. US Dept Vet Affairs, Ann Arbor, MI USA. Univ Michigan, Gerald R Ford Sch Publ Policy, Ann Arbor, MI USA. RP Robbins, LB (reprint author), Univ Michigan, Sch Nursing, 400 N Ingalls, Ann Arbor, MI 48109 USA. FU NINR NIH HHS [5 T32 NR07073-08, 1 F32 NR07509-01A1] NR 49 TC 19 Z9 19 U1 2 U2 12 PU JOHN WILEY & SONS INC PI HOBOKEN PA 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 0160-6891 J9 RES NURS HEALTH JI Res. Nurs. Health PD DEC PY 2004 VL 27 IS 6 BP 435 EP 446 DI 10.1002/nur.20042 PG 12 WC Nursing SC Nursing GA 873VU UT WOS:000225310300007 PM 15514962 ER PT J AU Kremen, WS Seidman, LJ Faraone, SV Toomey, R Tsuang, MI AF Kremen, WS Seidman, LJ Faraone, SV Toomey, R Tsuang, MI TI Heterogeneity of schizophrenia: a study of individual neuropsychological profiles SO SCHIZOPHRENIA RESEARCH LA English DT Article DE schizophrenia; neuropsychology; heterogeneity; subtypes ID COGNITIVE HETEROGENEITY; DIFFERENTIAL DEFICIT; BRAIN-DYSFUNCTION; NEGATIVE SYMPTOMS; MATCHING FALLACY; NONDEFICIT FORMS; TEMPORAL-LOBE; MEMORY; SUBTYPES; DISORDERS AB Based on a strategy developed by Seidman et al. (Seidman, L.J., Faraone, S.V, Kremen, W.S., Pepple, JR., Lyons, MI, Tsuang, M.T., 1993. Neuropsychological dysfunctions in the non-psychotic first-degree relatives of schizophrenic patients, Poster presented at the annual meeting of the Society for Research and Psychopathology. Chicago, IL) we examined neuropsychological heterogeneity in schizophrenia using clinical neuropsychological descriptions of individual cases as the starting point. We blindly rated neuropsychological profiles of 74 schizophrenia patients and 91 normal controls based primarily on prototypes from the clinical literature in neuropsychology. Patients were classified as having the following profile types: within normal limits (WNL) (23%, n= 17), frontal/abstraction (46%, n= 34), widespread/diffuse (14%, n = 10), left temporal/verbal memory (8%, n=6) and other (9%, n=7). As expected based on our classification scheme, the groups had different profile shapes (group x function interactions). They were also significantly different from one another in terms of overall severity (main effects); however, severity differences were not inherent in the definition of all groups. Longer duration of illness and greater overall cognitive impairment were observed as one went from the left temporal to the frontal to the widespread groups. Longitudinal studies are needed to determine whether the different neuropsychological profiles reflect true subgroup differences or within-person change over time. Further research-probably including neuroimaging and genetic studies-will also be needed to determine the validity and the utility of this strategy for identifying neuropsychological profile types. (C) 2004 Elsevier B.V. All rights reserved. C1 Univ Calif Davis, Sch Med, Dept Psychiat & Behav Sci, Sacramento, CA 95817 USA. Harvard Univ, Sch Med, Massachusetts Mental Hlth Ctr, Dept Psychiat, Boston, MA 02115 USA. Harvard Univ, Inst Psychiat Epidemiol & Genet, Boston, MA 02115 USA. Harvard Univ, Sch Med, Dept Psychiat, VAMC, Brockton, MA 02401 USA. Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Psychiat, Boston, MA 02114 USA. Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA. RP Kremen, WS (reprint author), Univ Calif San Diego, Dept Psychiat, 9500 Gilman Dr Mail Code 0603, La Jolla, CA 92093 USA. EM wkremen@ucsd.edu OI Faraone, Stephen/0000-0002-9217-3982 FU NIA NIH HHS [R01 AG018386]; NIMH NIH HHS [MH43518-01, MH46318] NR 93 TC 50 Z9 52 U1 0 U2 4 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0920-9964 J9 SCHIZOPHR RES JI Schizophr. Res. PD DEC 1 PY 2004 VL 71 IS 2-3 BP 307 EP 321 DI 10.1016/j.schres.2004.02.022 PG 15 WC Psychiatry SC Psychiatry GA 864VK UT WOS:000224660900010 PM 15474901 ER PT J AU Dickey, CC Salisbury, DF Nagy, AI Hirayasu, Y Lee, CU McCarley, RW Shenton, ME AF Dickey, CC Salisbury, DF Nagy, AI Hirayasu, Y Lee, CU McCarley, RW Shenton, ME TI Follow-up MRI study of prefrontal volumes in first-episode psychotic patients SO SCHIZOPHRENIA RESEARCH LA English DT Article ID SCHIZOPHRENIA; DENSITY; BRAINS C1 VA Boston Healthcare Syst, Dept Psychiat, Neurosci Lab, Clin Neurosci Div,Brockton Div, Brockton, MA 02301 USA. Harvard Univ, Sch Med, Brockton, MA 02301 USA. Brigham & Womens Hosp, Brigham Behav Neurol Grp, Boston, MA 02115 USA. McLean Hosp, Cognit Neurosci Lab, Belmont, MA 02178 USA. Yokohama City Univ, Sch Med, Yokohama, Kanagawa 232, Japan. Catholic Univ, Coll Med, Dept Psychiat, Seoul, South Korea. Brigham & Womens Hosp, MRI Div, Surg Planning Lab, Boston, MA 02115 USA. Harvard Univ, Sch Med, Dept Radiol, Boston, MA 02115 USA. RP McCarley, RW (reprint author), VA Boston Healthcare Syst, Dept Psychiat, Neurosci Lab, Clin Neurosci Div,Brockton Div, 116A,940 Belmont St, Brockton, MA 02301 USA. EM robert_mccarley@hms.harvard.edu; martha_shenton@hms.harvard.edu RI McCarley, Robert/N-5562-2014 OI McCarley, Robert/0000-0001-5705-7495 FU NIMH NIH HHS [K05 MH070047, K05 MH070047-01] NR 10 TC 22 Z9 23 U1 0 U2 1 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0920-9964 J9 SCHIZOPHR RES JI Schizophr. Res. PD DEC 1 PY 2004 VL 71 IS 2-3 BP 349 EP 351 DI 10.1016/j.schres.2004.04.010 PG 3 WC Psychiatry SC Psychiatry GA 864VK UT WOS:000224660900014 PM 15474905 ER PT J AU Buka, SL Goldstein, JM Spartos, E Tsuang, MT AF Buka, SL Goldstein, JM Spartos, E Tsuang, MT TI The retrospective measurement of prenatal and perinatal events: accuracy of maternal recall SO SCHIZOPHRENIA RESEARCH LA English DT Article DE maternal recall; pregnancy conditions; validity; measurement; interview; obstetric complications ID PREGNANCY-RELATED EVENTS; LONG-TERM RECALL; OBSTETRIC COMPLICATIONS; SCHIZOPHRENIA; VALIDITY; RELIABILITY; COHORT; BIAS; ASSOCIATION; INFECTIONS AB Adverse obstetric events have been implicated as risk factors for schizophrenia. Many studies have relied on retrospective recall of these events, given typical adult onset of schizophrenia, when most studies ascertain their samples. The goal of this study was to assess the validity of an interview for the long-term recall of prenatal and perinatal events. Ninety-six women from the Providence and Boston cohorts of the National Collaborative Perinatal Project were administered a brief structured telephone interview regarding their recall of pregnancy-related events that had occurred 22 years or more prior to interview. Women accurately reported major medical events such as cesarean section, breech delivery, and multiple birth (kappa = 1) and demographic items, such as age at birth and parity. Medical interventions and major medical conditions such as placental (kappa = -0.01) and cord (kappa = -0.10) difficulties were not accurately reported. Estimated birthweight, low birthweight, and length of gestation were recalled with reasonable accuracy. Women who completed high school generally recalled events more accurately than, those who did not. It is therefore important to attend to the sources of. information, the mode of interviewing, the specific type of event, and sociodemographic characteristics of the informant to improve the accuracy of retrospective data on obstetric events, and to increase the validity of findings relating these to the onset of schizophrenia. (C) 2004 Elsevier B.V. All rights reserved. C1 Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA. Harvard Univ, Sch Publ Hlth, Dept Soc Human Dev & Hlth, Boston, MA 02115 USA. Harvard Univ, Brigham & Womens Hosp, Sch Med, Dept Psychiat,Massachusetts Mental Hlth Ctr, Boston, MA 02115 USA. Massachusetts Gen Hosp, Boston, MA 02114 USA. Brigham & Womens Hosp, Dept Med, Div Womens Hlth, Conners Ctr Womens Hlth & Gender Biol, Boston, MA 02115 USA. Univ Calif San Diego, Dept Psychiat, San Diego, CA 92103 USA. RP Buka, SL (reprint author), Harvard Univ, Sch Publ Hlth, Dept Epidemiol, 677 Huntington Ave, Boston, MA 02115 USA. EM sbuka@hsph.harvard.edu RI Buka, Stephen/H-7335-2014 OI Buka, Stephen/0000-0002-8578-9308 FU NIMH NIH HHS [MH50647, R01 MH56956] NR 43 TC 78 Z9 78 U1 1 U2 11 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0920-9964 J9 SCHIZOPHR RES JI Schizophr. Res. PD DEC 1 PY 2004 VL 71 IS 2-3 BP 417 EP 426 DI 10.1016/j.schres.2004.04.004 PG 10 WC Psychiatry SC Psychiatry GA 864VK UT WOS:000224660900022 PM 15474913 ER PT J AU Brickman, AM Buchsbaum, MS Shihabuddin, L Byne, W Newmark, RE Brand, J Ahmed, S Mitelman, SA Hazlett, EA AF Brickman, AM Buchsbaum, MS Shihabuddin, L Byne, W Newmark, RE Brand, J Ahmed, S Mitelman, SA Hazlett, EA TI Thalamus size and outcome in schizophrenia SO SCHIZOPHRENIA RESEARCH LA English DT Article DE MRI; schizophrenia; thalamus; functional outcome ID SCHIZOTYPAL PERSONALITY-DISORDER; STRUCTURAL BRAIN ABNORMALITIES; NON-KRAEPELINIAN SCHIZOPHRENIA; SUPERIOR TEMPORAL SULCUS; METABOLIC-RATE; MEDIODORSAL NUCLEUS; PREFRONTAL CORTEX; RHESUS-MONKEYS; STRIATAL SIZE; VOLUMES AB The size of the thalamus was assessed in 106 patients with schizophrenia and 42 normal controls using high-resolution magnetic resonance imaging. The thalamus was traced at five axial levels proportionately spaced from dorsal to ventral directions. Patients with schizophrenia had significantly smaller thalamic areas at more ventral levels. Thalamic size was positively associated with frontal lobe and temporal lobe size. The effects were most marked in the patients with poorer clinical outcome (i.e., "Kraepelinian" patients). These findings are consistent with post-mortem and MRI measurement suggesting reduction in volume of the pulvinar, which occupies a large proportion of the ventral thalamus and which has prominent connections to the temporal lobe. (C) 2004 Elsevier B.V. All rights reserved. C1 CUNY Mt Sinai Sch Med, Dept Psychiat, Neurosci PET Lab, New York, NY 10029 USA. CUNY Queens Coll, Dept Psychol, Flushing, NY 11367 USA. CUNY, Grad Ctr, Flushing, NY 11367 USA. Brown Univ, Sch Med, Dept Psychiat & Human Behav, Providence, RI 02912 USA. Bronx Vet Adm Med Ctr, Dept Vet Affairs, Bronx, NY USA. RP Brickman, AM (reprint author), CUNY Mt Sinai Sch Med, Dept Psychiat, Neurosci PET Lab, Box 1505,1 Gustave L Levy Pl, New York, NY 10029 USA. EM adam.brickman@mssm.edu FU NIMH NIH HHS [MH60023, MH60384S, MH56489] NR 50 TC 34 Z9 35 U1 2 U2 2 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0920-9964 J9 SCHIZOPHR RES JI Schizophr. Res. PD DEC 1 PY 2004 VL 71 IS 2-3 BP 473 EP 484 DI 10.1016/j.schres.2004.03.011 PG 12 WC Psychiatry SC Psychiatry GA 864VK UT WOS:000224660900027 PM 15474918 ER PT J AU Rassovsky, Y Green, MF Nuechterlein, KH Breitmeyer, B Mintz, J AF Rassovsky, Y Green, MF Nuechterlein, KH Breitmeyer, B Mintz, J TI Paracontrast and metacontrast in schizophrenia: clarifying the mechanism for visual masking deficits SO SCHIZOPHRENIA RESEARCH LA English DT Article DE visual masking; backward masking; paracontrast; metacontrast; schizophrenia; neurocognition ID BACKWARD-MASKING; COLLEGE-STUDENTS; PATTERN MASKING; CHANNELS; VULNERABILITY; PERFORMANCE; DISORDERS; TRANSIENT; MANIA; LIGHT AB Schizophrenic patients consistently demonstrate performance deficits on visual masking procedures. Visual masking can occur through two distinctly different mechanisms: interruption and integration. One highly effective way to limit the masking mechanism to interruption is to use a mask that surrounds, but does not spatially overlap, the target. These procedures are called paracontrast and metacontrast (for forward and backward masking, respectively). Despite their clear advantages for interpretation, paracontrast and metacontrast have not been used previously in schizophrenia. In the present study, we examined the reliability of the paracontrast and metacontrast procedures by administering these tasks to 103 schizophrenic patients and 49 normal control subjects. In addition, we compared the results to those from a low-energy masking condition, which is an alternative way to limit masking to interruption. Patients showed deficits on both the paracontrast and metacontrast procedures. The deficits in paracontrast and metacontrast were comparable to those seen previously with low-energy masking. These results suggest that the paracontrast/metacontrast procedure and the procedure using a low-energy mask are roughly equally sensitive to deficits in early visual processing among schizophrenic patients. These results bolster previous conclusions that schizophrenic patients show deficits on visual masking tasks even when masking on those tasks occurs entirely through the interruption mechanism. (C) 2004 Elsevier B.V. All rights reserved. C1 Univ Calif Los Angeles, Dept Psychiat & Biobehav Sci, Geffen Sch Med, Los Angeles, CA 90024 USA. VA Greater Los Angeles Healthcare Syst, Los Angeles, CA USA. Univ Calif Los Angeles, Dept Psychol, Los Angeles, CA 90024 USA. Univ Houston, Dept Psychol, Houston, TX 77004 USA. RP Rassovsky, Y (reprint author), Univ Calif Los Angeles, Dept Psychiat & Biobehav Sci, Geffen Sch Med, 760 Westwood Plaza C8-747-NPI, Los Angeles, CA 90024 USA. EM yurir@ucla.edu FU NIMH NIH HHS [MH-43292, MH-37705] NR 32 TC 28 Z9 28 U1 0 U2 1 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0920-9964 J9 SCHIZOPHR RES JI Schizophr. Res. PD DEC 1 PY 2004 VL 71 IS 2-3 BP 485 EP 492 DI 10.1016/j.schres.2004.02.018 PG 8 WC Psychiatry SC Psychiatry GA 864VK UT WOS:000224660900028 PM 15474919 ER PT J AU Goss, PE AF Goss, PE TI Breaking the Barriers: Extending Endocrine Therapy Beyond Tamoxifen - Introduction SO SEMINARS IN ONCOLOGY LA English DT Editorial Material C1 Massachusetts Gen Hosp, Ctr Canc, Boston, MA 02114 USA. Harvard Univ, Sch Med, Boston, MA 02115 USA. RP Goss, PE (reprint author), Massachusetts Gen Hosp, Ctr Canc, Boston, MA 02114 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 USA SN 0093-7754 J9 SEMIN ONCOL JI Semin. Oncol. PD DEC PY 2004 VL 31 IS 6 SU 12 BP 1 EP 2 DI 10.1053/j.seminoncol.2004.09.019 PG 2 WC Oncology SC Oncology GA 884PI UT WOS:000226097600001 ER PT J AU Goss, PE AF Goss, PE TI Changing clinical practice: Extending the benefits of adjuvant endocrine therapy in breast cancer SO SEMINARS IN ONCOLOGY LA English DT Review ID AROMATASE INHIBITOR LETROZOLE; RECEPTOR-POSITIVE TUMORS; POSTMENOPAUSAL WOMEN; RANDOMIZED-TRIAL; CELL-PROLIFERATION; TAMOXIFEN THERAPY; 1ST-LINE THERAPY; PHASE-III; ANASTROZOLE; HYPERSENSITIVITY C1 Harvard Univ, Massachusetts Gen Hosp, Sch Med, Ctr Canc, Boston, MA 02114 USA. RP Goss, PE (reprint author), Harvard Univ, Massachusetts Gen Hosp, Sch Med, Ctr Canc, 55 Fruit St,Cox Bldg,Room 640, Boston, MA 02114 USA. NR 32 TC 7 Z9 7 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 0093-7754 J9 SEMIN ONCOL JI Semin. Oncol. PD DEC PY 2004 VL 31 IS 6 SU 12 BP 15 EP 22 DI 10.1053/j.seminoncol.2004.09.022 PG 8 WC Oncology SC Oncology GA 884PI UT WOS:000226097600004 PM 15719597 ER PT J AU Ng, AK Hickey, G Li, SG Neuberg, D Mauch, PM AF Ng, AK Hickey, G Li, SG Neuberg, D Mauch, PM TI A randomized phase II trial of amifostine for head and neck irradiation in lymphoma SO SEMINARS IN ONCOLOGY LA English DT Article; Proceedings Paper CT 4th International Cytoprotection Investigators Congress CY MAY, 2004 CL Philadelphia, PA ID QUALITY-OF-LIFE; MANTLE FIELD RADIOTHERAPY; LARYNGEAL-CANCER PATIENTS; SALIVARY FLOW-RATES; RADIATION-THERAPY; EUROPEAN ORGANIZATION; HODGKINS-DISEASE; ORAL FUNCTION; HEALTH; XEROSTOMIA C1 Harvard Univ, Sch Med, Brigham & Womens Hosp, Dana Farber Canc Inst, Boston, MA 02115 USA. RP Ng, AK (reprint author), Harvard Univ, Sch Med, Brigham & Womens Hosp, Dana Farber Canc Inst, 75 Francis St,ASBI-L2, Boston, MA 02115 USA. EM ang@lroc.harvard.edu NR 35 TC 0 Z9 0 U1 1 U2 2 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 USA SN 0093-7754 J9 SEMIN ONCOL JI Semin. Oncol. PD DEC PY 2004 VL 31 IS 6 SU 18 BP 20 EP 24 DI 10.1053/j.seminoncol.2004.12.007 PG 5 WC Oncology SC Oncology GA 902CR UT WOS:000227329500005 PM 15726518 ER PT J AU Anderson, KC AF Anderson, KC TI Clinical update: Novel targets in multiple myeloma SO SEMINARS IN ONCOLOGY LA English DT Article ID PROTEASOME INHIBITOR PS-341; OVERCOMES DRUG-RESISTANCE; ENDOTHELIAL GROWTH-FACTOR; THALIDOMIDE ANALOGS; SIGNALING CASCADES; MM CELLS; APOPTOSIS; INTERLEUKIN-6; MULTICENTER; ACTIVATION C1 Dana Farber Canc Inst, Boston, MA 02115 USA. RP Anderson, KC (reprint author), 44 Binney St, Boston, MA 02115 USA. NR 34 TC 11 Z9 11 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 0093-7754 J9 SEMIN ONCOL JI Semin. Oncol. PD DEC PY 2004 VL 31 IS 6 SU 16 BP 27 EP 32 DI 10.1053/j.seminoncol.2004.10.016 PG 6 WC Oncology SC Oncology GA 894QT UT WOS:000226807400006 PM 15799242 ER PT J AU Alberts, DS Muggia, FM Carmichael, J Winer, EP Jahanzeb, M Venook, AP Skubitz, KM Rivera, E Sparano, JA Dibella, NJ Stewart, SJ Kavanagh, JJ Gabizon, AA AF Alberts, DS Muggia, FM Carmichael, J Winer, EP Jahanzeb, M Venook, AP Skubitz, KM Rivera, E Sparano, JA Dibella, NJ Stewart, SJ Kavanagh, JJ Gabizon, AA TI Efficacy and safety of liposomal anthracyclines in phase I/II clinical trials SO SEMINARS IN ONCOLOGY LA English DT Review ID METASTATIC BREAST-CANCER; CELL LUNG-CANCER; GYNECOLOGIC-ONCOLOGY-GROUP; ADVANCED SOLID TUMORS; NON-HODGKINS-LYMPHOMA; SOFT-TISSUE SARCOMAS; ADVANCED HEPATOCELLULAR-CARCINOMA; ACUTE MYELOGENOUS LEUKEMIA; HAND-FOOT SYNDROME; PALMAR-PLANTAR ERYTHRODYSESTHESIA C1 Arizona Canc Ctr, Tucson, AZ USA. NYU, Inst Canc, New York, NY USA. City Hosp, Nottingham NG5 1PB, England. Dana Farber Canc Inst, Boston, MA 02115 USA. Univ Tennessee, Inst Canc, Memphis, TN USA. Univ Calif San Francisco, Ctr Canc, San Francisco, CA 94143 USA. Univ Minnesota Hosp & Clin, Minneapolis, MN 55455 USA. Univ Texas, MD Anderson Canc Ctr, Houston, TX 77030 USA. Einstein Med Sch, Bronx, NY USA. Rocky Mt Canc Ctr, Aurora, CO USA. Charing Cross Hosp, London, England. Shaare Zedek Med Ctr, Jerusalem, Israel. RP Alberts, DS (reprint author), 1515 N Campbell Ave,POB 245024, Tucson, AZ 85724 USA. EM dalberts@AZCC.Arizona.edu NR 307 TC 77 Z9 79 U1 0 U2 8 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 USA SN 0093-7754 J9 SEMIN ONCOL JI Semin. Oncol. PD DEC PY 2004 VL 31 IS 6 SU 13 BP 53 EP 90 DI 10.1053/j.seminoncol.2004.08.010 PG 38 WC Oncology SC Oncology GA 886OI UT WOS:000226237800005 PM 15717738 ER PT J AU Robert, NJ Vogel, CL Henderson, C Sparano, JA Moore, MR Silverman, P Overmoyer, BA Shapiro, CL Park, JW Colbern, GT Winer, EP Gabizon, AA AF Robert, NJ Vogel, CL Henderson, C Sparano, JA Moore, MR Silverman, P Overmoyer, BA Shapiro, CL Park, JW Colbern, GT Winer, EP Gabizon, AA TI The role of the liposomal anthracyclines and other systemic therapies in the management of advanced breast cancer SO SEMINARS IN ONCOLOGY LA English DT Review ID PHASE-II TRIAL; PROSPECTIVE RANDOMIZED-TRIAL; LOW-DOSE DOXORUBICIN; QUALITY-OF-LIFE; CONTINUOUS INTRAVENOUS-INFUSION; SOUTHWEST-ONCOLOGY-GROUP; LEUKEMIA GROUP-B; COLONY-STIMULATING FACTOR; SURGICAL ADJUVANT BREAST; SINGLE-AGENT THERAPY C1 Inova Fairfax Hosp, Ctr Canc, Falls Church, VA USA. Canc Res Network, Plantation, FL USA. Univ Calif San Francisco, Dept Med, San Francisco, CA USA. Montefiore Med Ctr, Breast Med Oncol, Weiler Div, Bronx, NY 10467 USA. Georgia Canc Specialists, Clin Res, Atlanta, GA USA. Univ Hosp Cleveland, Care Comprehens Canc Ctr, Cleveland, OH USA. Ohio State Univ, Arthur G James Canc Hosp, Columbus, OH 43210 USA. Ohio State Univ, Richard J Solove Res Inst, Columbus, OH 43210 USA. Ohio State Univ, Dept Hematol & Oncol, Columbus, OH 43210 USA. UCSF, Ctr Comprehens Canc, San Francisco, CA USA. Cell Genesys Inc, San Francisco, CA USA. Dana Farber Canc Inst, Breast Oncol Ctr, Boston, MA 02115 USA. Shaare Zedek Med Ctr, Inst Oncol, Jerusalem, Israel. Hebrew Univ Jerusalem, Fac Med, IL-91010 Jerusalem, Israel. RP Robert, NJ (reprint author), 8503 Arlington Blvd,Suite 400, Fairfax, VA 22031 USA. NR 305 TC 48 Z9 48 U1 0 U2 2 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 USA SN 0093-7754 J9 SEMIN ONCOL JI Semin. Oncol. PD DEC PY 2004 VL 31 IS 6 SU 13 BP 106 EP 146 DI 10.1053/j.seminoncol.2004.09.018 PG 41 WC Oncology SC Oncology GA 886OI UT WOS:000226237800007 PM 15717740 ER PT J AU Hussein, MA Anderson, KC AF Hussein, MA Anderson, KC TI Role of liposomal anthracyclines in the treatment of multiple myeloma SO SEMINARS IN ONCOLOGY LA English DT Review ID PLASMA-CELL MYELOMA; COOPERATIVE-ONCOLOGY-GROUP; BONE-MARROW ANGIOGENESIS; COMBINATION CHEMOTHERAPY; VAD CHEMOTHERAPY; PHASE-II; REFRACTORY PATIENTS; DOSE DEXAMETHASONE; 1ST-LINE TREATMENT; PROGNOSTIC FACTORS C1 Cleveland Clin Multiple Myeloma Res Ctr, Cleveland, OH USA. Dana Farber Canc Inst, Jerome Lipper Multiple Myeloma Ctr, Boston, MA 02115 USA. Harvard Univ, Sch Med, Boston, MA USA. RP Hussein, MA (reprint author), Cleveland Clin Fdn, 9500 Euclid Ave,R-35, Cleveland, OH 44195 USA. EM mah+sio@runbox.us NR 59 TC 23 Z9 24 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 USA SN 0093-7754 J9 SEMIN ONCOL JI Semin. Oncol. PD DEC PY 2004 VL 31 IS 6 SU 13 BP 147 EP 160 DI 10.1053/j.seminoncol.2004.08.005 PG 14 WC Oncology SC Oncology GA 886OI UT WOS:000226237800008 PM 15717741 ER PT J AU Posner, MR Haddada, RI Wirth, L Norris, CM Goguen, LA Mahadevan, A Sullivan, C Tishler, RB AF Posner, MR Haddada, RI Wirth, L Norris, CM Goguen, LA Mahadevan, A Sullivan, C Tishler, RB TI Induction chemotherapy in locally advanced squamous cell cancer of the head and neck: Evolution of the sequential treatment approach SO SEMINARS IN ONCOLOGY LA English DT Review ID PHASE-I/II TRIAL; ADVANCED LARYNGEAL-CANCER; RANDOMIZED-TRIAL; RADIATION-THERAPY; III TRIAL; CONCOMITANT CHEMORADIOTHERAPY; CONCURRENT CHEMORADIATION; NEOADJUVANT CHEMOTHERAPY; OROPHARYNGEAL CARCINOMA; ORGAN PRESERVATION C1 Dana Farber Canc Inst, Head & Neck Oncol Program, Dept Med Oncol, Boston, MA 02115 USA. Dana Farber Canc Inst, Dept Surg Oncol, Boston, MA 02115 USA. Dana Farber Canc Inst, Dept Radiat Oncol, Boston, MA 02115 USA. Beth Israel Deaconess Med Ctr, Dept Radiat Oncol, Boston, MA 02215 USA. RP Posner, MR (reprint author), Dana Farber Canc Inst, Head & Neck Oncol Program, Dept Med Oncol, SW430,44 Binney St, Boston, MA 02115 USA. EM marshall_posner@dfci.harvard.edu NR 57 TC 42 Z9 43 U1 1 U2 1 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 USA SN 0093-7754 J9 SEMIN ONCOL JI Semin. Oncol. PD DEC PY 2004 VL 31 IS 6 BP 778 EP 785 DI 10.1053/j.seminoncol.2004.09.007 PG 8 WC Oncology SC Oncology GA 882BW UT WOS:000225914500008 PM 15599855 ER PT J AU Bajwa, EK Malhotra, A Thompson, BT AF Bajwa, EK Malhotra, A Thompson, BT TI Methods of monitoring shock SO SEMINARS IN RESPIRATORY AND CRITICAL CARE MEDICINE LA English DT Review DE shock; monitoring; critical illness; intensive care unit; pulmonary artery; catheter ID CRITICALLY-ILL PATIENTS; CENTRAL VENOUS-PRESSURE; PULMONARY-ARTERY CATHETERIZATION; CAPILLARY WEDGE PRESSURE; GASTRIC INTRAMUCOSAL PH; RESPIRATORY-DISTRESS-SYNDROME; ACUTE MYOCARDIAL-INFARCTION; CARDIAC-SURGERY PATIENTS; PULSE-CONTOUR ANALYSIS; RIGHT ATRIAL PRESSURE AB Intensive monitoring is a crucial component of the management of shock. However, there is little consensus about optimal strategies for monitoring. Although the pulmonary artery catheter has been widely used, conflicting data exist about the utility of this device. A variety of other techniques have been developed in hopes of providing clinically useful information about myocardial function, intravascular volume, and indices of organ function. In addition, there is evolving evidence that targeting and monitoring certain physiological goals may be most important early in the course of shock. In this chapter, we examine many of the available monitoring techniques and the evidence supporting their use. C1 Massachusetts Gen Hosp, Pulm & Crit Care Unit, Boston, MA 02114 USA. Brigham & Womens Hosp, Boston, MA 02115 USA. RP Thompson, BT (reprint author), Massachusetts Gen Hosp, Pulm & Crit Care Unit, BUL-148,55 Fruit St, Boston, MA 02114 USA. EM tthompson1@partners.org FU NHLBI NIH HHS [R01 HL073146-02, R01 HL073146]; NIA NIH HHS [K23 AG024837-03, K23 AG024837] NR 133 TC 2 Z9 2 U1 1 U2 1 PU THIEME MEDICAL PUBL INC PI NEW YORK PA 333 SEVENTH AVE, NEW YORK, NY 10001 USA SN 1069-3424 J9 SEM RESP CRIT CARE M JI Semin. Respir. Crit. Care Med. PD DEC PY 2004 VL 25 IS 6 BP 629 EP 644 DI 10.1055/s-2004-860986 PG 16 WC Critical Care Medicine; Respiratory System SC General & Internal Medicine; Respiratory System GA 883QZ UT WOS:000226032100004 PM 16088506 ER PT J AU Bauer, KA AF Bauer, KA TI Role of thrombophilia in deciding on the duration of anticoagulation SO SEMINARS IN THROMBOSIS AND HEMOSTASIS LA English DT Article DE thrombophilia; thromboembolism; anticoagulants; INR; factor V Leiden; prothrombin G20210A mutation ID RECURRENT VENOUS THROMBOEMBOLISM; FACTOR-V-LEIDEN; ACTIVATED PROTEIN-C; DEEP-VEIN THROMBOSIS; ANTIPHOSPHOLIPID-ANTIBODY-SYNDROME; INHERITED ANTITHROMBIN DEFICIENCY; 1ST EPISODE; BLEEDING COMPLICATIONS; DECISION-ANALYSIS; PROTHROMBIN GENE AB It is now possible to identify hereditary risk factors in a substantial percentage of patients presenting with a venous thrombotic event. Discovery of the factor V Leiden and prothrombin G20210A mutations has greatly increased the percentage of patients in whom venous thrombosis can be attributed to hereditary thrombophilia. There is considerable uncertainty, however, as to how this information should be used in patient management. Although prolonged anticoagulation at an international normalized ratio (INR) of 2 to 3 is highly effective in preventing thrombotic recurrences, this benefit is partially offset by the risk of major bleeding and the inconvenience associated with oral vitamin K antagonists. Although low-intensity anticoagulation at a target INR of 1.5 to 2 has recently been shown to be effective in preventing recurrent venous thromboembolism after 3 to 6 months of treatment at an INR of 2 to 3, it has not been demonstrated to reduce the risk of major bleeding complications. A decision as to the overall benefit of extended anticoagulation therefore continues to require clinical assessment of an individual patient's risk of recurrence in the absence of treatment and the risk of bleeding at the chosen INR target range. C1 VA Boston Healthcare Syst, W Roxbury, MA 02132 USA. Harvard Univ, Beth Israel Deaconess Med Ctr, Sch Med, Boston, MA 02215 USA. RP Bauer, KA (reprint author), VA Boston Healthcare Syst, 1400 VFW Parkway, W Roxbury, MA 02132 USA. EM kbauer@bidmc.harvard.edu NR 36 TC 9 Z9 9 U1 0 U2 0 PU THIEME MEDICAL PUBL INC PI NEW YORK PA 333 SEVENTH AVE, NEW YORK, NY 10001 USA SN 0094-6176 J9 SEMIN THROMB HEMOST JI Semin. Thromb. Hemost. PD DEC PY 2004 VL 30 IS 6 BP 633 EP 637 DI 10.1055/s-2004-861505 PG 5 WC Hematology; Peripheral Vascular Disease SC Hematology; Cardiovascular System & Cardiology GA 883RA UT WOS:000226032200006 PM 15630669 ER PT J AU Chapman, VM Nimkin, K Jaramillo, D AF Chapman, VM Nimkin, K Jaramillo, D TI The pre-ossification center: normal CT and MRI findings in the trochlea SO SKELETAL RADIOLOGY LA English DT Article DE pre-ossification center; trochlea; CT; MRI AB The pre-ossification center represents the initial structural change in the development of the secondary ossification center. We report CT and MRI findings of a focus in the cartilaginous trochlea of an appropriately aged child compatible with the pre-ossification center. C1 Massachusetts Gen Hosp, Dept Radiol, Boston, MA 02114 USA. RP Chapman, VM (reprint author), Massachusetts Gen Hosp, Dept Radiol, 32 Fruit St, Boston, MA 02114 USA. EM vchapman@partners.org NR 7 TC 9 Z9 9 U1 0 U2 0 PU SPRINGER PI NEW YORK PA 233 SPRING STREET, NEW YORK, NY 10013 USA SN 0364-2348 J9 SKELETAL RADIOL JI Skeletal Radiol. PD DEC PY 2004 VL 33 IS 12 BP 725 EP 727 DI 10.1007/s00256-004-0773-y PG 3 WC Orthopedics; Radiology, Nuclear Medicine & Medical Imaging SC Orthopedics; Radiology, Nuclear Medicine & Medical Imaging GA 872WE UT WOS:000225239100006 PM 15322770 ER PT J AU LaVela, SL Smith, B Weaver, FM Miskevics, SA AF LaVela, SL Smith, B Weaver, FM Miskevics, SA TI Geographical proximity and health care utilization in veterans with SCI&D in the USA SO SOCIAL SCIENCE & MEDICINE LA English DT Article DE spinal cord injury; veterans; health care access/utilization; USA ID SPINAL-CORD-INJURY; MYOCARDIAL-INFARCTION; DISABILITIES; HOSPITALS; DISTANCE; CHOICE; READMISSION; POPULATION; MORTALITY; SERVICES AB In the USA, substantial geographic variation in health care utilization exists in the Department of Veterans Affairs (VA) health care system. Utilization of health care services is especially important for veterans with spinal cord injuries and disorders (SCI&D) who are often at high risk for secondary complications related to their SCI&D. Due to impaired mobility, access to health care for veterans with SCI&D may be even more challenging. The goal of this cross-sectional study was to describe health care utilization relative to SCI&D veteran residential geographic proximity to VA health care facilities. A negative binomial regression model was used to examine VA outpatient utilization. Veterans with SCI&D utilized outpatient services less frequently when VA facilities were farther away from their residences (p<0.000). Female (p<0.000), older (p<0.000), and non-white veterans (p<0.000), and veterans with history of respiratory (p<0.000), kidney/urinary tract (p<0.005), circulatory (p<0.000), or digestive system diseases (P<0.003) were more likely to utilize outpatient care during the study period. A Poisson model was used to examine inpatient utilization. Inpatient utilization decreased when travel distance to VA facility increased (p<0.000). Contrary to outpatient, age did not significantly affect veterans' likelihood of using inpatient health care. Marital status, gender, race, and level of injury were not related to inpatient utilization. However, history of prior illnesses including respiratory (p<0.000), kidney/urinary tract (p<0.000), circulatory (p<0.005), digestive system (p<0.015), or skin/subcutaneous tissue/breast-related illnesses (p<0.000) were associated with a greater likelihood of inpatient utilization. Geographic proximity and other factors on health care use must be considered in order to meet the health care demand patterns of veterans with SCI&D. Published by Elsevier Ltd. C1 Dept Vet Affairs, Midw Ctr Hlth Serv & Policy Res, Spinal Cord Injury Qual Enhancement Res Initiat, Edward Hines Jr Vet Affairs Hosp, Hines, IL 60141 USA. US Dept Vet Affairs, Edward Hines Jr Vet Affairs Hosp, SCI QUERI, MCHSPR,DVA, Hines, IL 60141 USA. Edward Hines Jr Vet Adm Hosp, SCI QUERI, DVA, Hines, IL 60141 USA. Northwestern Univ, Inst Hlth Serv Res & Policy Studies, Chicago, IL 60611 USA. RP LaVela, SL (reprint author), Dept Vet Affairs, Midw Ctr Hlth Serv & Policy Res, Spinal Cord Injury Qual Enhancement Res Initiat, Edward Hines Jr Vet Affairs Hosp, 5th Ave & Roosevelt Rd,151-H, Hines, IL 60141 USA. EM lavela@research.hines.med.va.gov NR 43 TC 37 Z9 37 U1 4 U2 13 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND SN 0277-9536 J9 SOC SCI MED JI Soc. Sci. Med. PD DEC PY 2004 VL 59 IS 11 BP 2387 EP 2399 DI 10.1016/j.socscimed.2004.06.033 PG 13 WC Public, Environmental & Occupational Health; Social Sciences, Biomedical SC Public, Environmental & Occupational Health; Biomedical Social Sciences GA 862WK UT WOS:000224521800016 PM 15450711 ER PT J AU Jin, M Andricioaei, L Springer, TA AF Jin, M Andricioaei, L Springer, TA TI Conversion between three conformational states of integrin I domains with a C-terminal pull spring studied with molecular dynamics SO STRUCTURE LA English DT Article ID CRYSTAL-STRUCTURE; A-DOMAIN; STRUCTURAL BASIS; DISULFIDE BOND; BINDING; PROTEINS; COMPLEX; LIGAND; FIBRONECTIN; SIMULATIONS AB We test with molecular dynamics the hypothesis that interdomain forces in integrins, simulated with a spring attached to the C-terminal alpha7-helix of an integrin I domain, can allosterically stabilize alternative I domain conformations. Depending on the force applied and timecourse, in alpha(L) and alpha(M) I domains the beta6-alpha7 loop moves successively between three ratchet positions; i.e. from closed to intermediate, and then to open. More distal, linked alterations in MIDAS loops and metal coordination closely resemble those seen when the MIDAS becomes ligated. Simulations show that the intermediate state is populated over a wider range of forces for alpha(L) than alpha(M) I domains. Simulations with mutant I domains suggest that specific ratchet residues regulate conformational equilibria. Simulations with alpha(1) and alpha(2) I domains reveal a lack of the intermediate conformation, owing to Phe to Glu substitution at the second ratchet residue. The findings have important implications for biological regulation of integrin adhesiveness. C1 Harvard Univ, Sch Med, CBR Inst Biomed Res, Dept Pathol, Boston, MA 02115 USA. Harvard Univ, Dept Chem & Biol Chem, Cambridge, MA 02138 USA. RP Springer, TA (reprint author), Harvard Univ, Sch Med, CBR Inst Biomed Res, Dept Pathol, 200 Longwood Ave, Boston, MA 02115 USA. EM springeroffice@cbr.med.harvard.edu RI Jin, Moonsoo/D-6128-2011 FU NCI NIH HHS [CA31798]; NHLBI NIH HHS [HL48675] NR 34 TC 68 Z9 69 U1 0 U2 10 PU CELL PRESS PI CAMBRIDGE PA 1100 MASSACHUSETTS AVE, CAMBRIDGE, MA 02138 USA SN 0969-2126 J9 STRUCTURE JI Structure PD DEC PY 2004 VL 12 IS 12 BP 2137 EP 2147 DI 10.1016/j.str.2004.10.005 PG 11 WC Biochemistry & Molecular Biology; Biophysics; Cell Biology SC Biochemistry & Molecular Biology; Biophysics; Cell Biology GA 880XN UT WOS:000225823600008 PM 15576028 ER PT J AU Romanus, D Iscoe, N DeAngelis, C Shear, N Einarson, TR AF Romanus, D Iscoe, N DeAngelis, C Shear, N Einarson, TR TI Cost analysis of secondary prophylaxis with oral clodronate versus pamidronate in metastatic breast cancer patients SO SUPPORTIVE CARE IN CANCER LA English DT Article DE cost analysis; clodronate; secondary prophylaxis; pamidronate; metastatic breast cancer ID PREVENTION; COMPLICATIONS; TRIAL AB Objective: We compared the direct medical costs of secondary prophylaxis with bisphosphonates (BPs) in bone metastases (BMs) of breast cancer (BCa) from a payer perspective. Patients and methods: This study adopted an incidence-based chart review of consecutive BCa patients with BMs who received prophylactic treatment with orally administered (PO) clodronate (CLODpo group), or intravenously administered (IV) pamidronate (PAM group) in 1997 at two large oncology centers in Toronto, Ontario. We evaluated the difference in costs of management of patients among the CLODpo and PAM groups using an intent-to-treat analysis from diagnosis of BMs to death, or last follow-up. The results are presented as observed mean and average lifetime (including terminal care) costs per patient. Results: The observed mean costs in the PAM and CLODpo groups were $49,472 and $50,307 (2002 Canadian dollars), respectively. The difference in costs between the CLODpo (n=34) and PAM (n=18) groups was not significant (P=0.64), and remained robust after sensitivity analyses. The corresponding average lifetime costs were $65,677 in the CLODpo group and $61,254 in the PAM group. In-patient and terminal care were the major cost drivers, comprising 45% and 25% of overall costs. Of all hospitalizations, 46% were associated with complications from BMs. Conclusions: Our analysis, which was based on a convenience sample, failed to reveal a statistically significant difference in the observed mean costs between groups of patients who initiated treatment with PO clodronate versus IV pamidronate. The cost estimates from this study can be used for future corroborative economic analyses. C1 Toronto Sunnybrook Reg Canc Ctr, Toronto, ON, Canada. Univ Toronto, Dept Med, Toronto, ON, Canada. Sunnybrook & Womens Coll, Hlth Sci Ctr, Toronto, ON, Canada. Univ Toronto, Fac Pharm, Toronto, ON, Canada. Univ Toronto, Sch Med, Dept Med, Div Clin Pharmacol, Toronto, ON, Canada. Univ Toronto, Sch Med, Dept Pharmacol, Toronto, ON, Canada. RP Romanus, D (reprint author), Dana Farber Canc Inst, 44 Binney St,454 Ste 21, Boston, MA 01810 USA. EM dorothy_romanus@dfci.harvard.edu OI De Angelis, Carlo/0000-0001-7109-4620 NR 13 TC 5 Z9 5 U1 0 U2 0 PU SPRINGER PI NEW YORK PA 233 SPRING STREET, NEW YORK, NY 10013 USA SN 0941-4355 J9 SUPPORT CARE CANCER JI Support. Care Cancer PD DEC PY 2004 VL 12 IS 12 BP 844 EP 851 DI 10.1007/s00520-004-0659-5 PG 8 WC Oncology; Health Care Sciences & Services; Rehabilitation SC Oncology; Health Care Sciences & Services; Rehabilitation GA 882WM UT WOS:000225971100005 PM 15235902 ER PT J AU Rattner, DW AF Rattner, DW TI What's in a name? The importance of "and" SO SURGICAL ENDOSCOPY AND OTHER INTERVENTIONAL TECHNIQUES LA English DT Editorial Material C1 Massachusetts Gen Hosp, Div Gen & Gastrointestinal Surg, Boston, MA 02114 USA. RP Rattner, DW (reprint author), Massachusetts Gen Hosp, Div Gen & Gastrointestinal Surg, 15 Parkman St WACC 337, Boston, MA 02114 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SPRINGER PI NEW YORK PA 233 SPRING STREET, NEW YORK, NY 10013 USA SN 0930-2794 J9 SURG ENDOSC JI Surg. Endosc. PD DEC PY 2004 VL 18 IS 12 BP 1693 EP 1693 DI 10.1007/s00464-004-8267-5 PG 1 WC Surgery SC Surgery GA 880BV UT WOS:000225764300001 PM 15809775 ER PT J AU Burns, MA He, WL Wu, CL Cheng, LL AF Burns, MA He, WL Wu, CL Cheng, LL TI Quantitative pathology in tissue MR spectroscopy based human prostate metabolomics SO TECHNOLOGY IN CANCER RESEARCH & TREATMENT LA English DT Article DE image analysis; pathology; human prostate; computer-aided; magnetic resonance; metabolomics ID EPITHELIAL-CELLS; CANCER; ANTIGEN; BENIGN; SPECTRA AB At present, the clinical utility of metabolomic profiles of human prostate tissue relies on the establishment of correlations between metabolite data and clinical measurements, particularly pathological findings. Because metabolomics is a quantitative study, its clinical value can be rigorously investigated by determining its association with other quantitative measures. The human visual assessment of prostate tissue, however, introduces both inter- and intraobserver biases that may limit the reliability of its quantitations, and therefore, the strength of its correlations with metabolomic profiles. The aim of this study was to develop a simple, feasible protocol for the computer-aided image analysis (CAIA) of prostate pathology slides in order to achieve quantitative pathology from tissue samples, following metabolomic measurement with high-resolution magic angle spinning (HRMAS) magnetic resonance spectroscopy (MRS). Thirty-eight samples from 29 prostatectomy cases were studied with HRMAS MRS. After spectroscopy analysis, samples were serial-sectioned, stained and visually assessed by pathologists. Cross-sections from these samples were then measured with the CAIA protocol. Results showed a two-fold difference between human visual assessments of the area percentages of tissue pathologies and CAIA area percentages obtained for the same features. Linear correlations were found between both metabolites indicative of normal epithelium and those indicative of prostate cancer, and the CAIA quantitative results. CAIA based quantitative pathology is more reliable than human visual assessment in establishing correlations useful for disease diagnosis between prostate pathology and metabolite concentrations. C1 Harvard Univ, Sch Med, Massachusetts Gen Hosp, Dept Pathol, Charlestown, MA 02129 USA. Harvard Univ, Sch Med, Massachusetts Gen Hosp, Dept Urol, Charlestown, MA 02129 USA. Harvard Univ, Sch Med, Massachusetts Gen Hosp, Dept Radiol, Charlestown, MA 02129 USA. RP Cheng, LL (reprint author), Harvard Univ, Sch Med, Massachusetts Gen Hosp, Dept Pathol, CNY-7,149,13th St, Charlestown, MA 02129 USA. EM cheng@nmr.mgh.harvard.edu FU NCI NIH HHS [CA095624]; NIBIB NIH HHS [EB002026] NR 21 TC 28 Z9 31 U1 1 U2 9 PU ADENINE PRESS PI SCHENECTADY PA 2066 CENTRAL AVE, SCHENECTADY, NY 12304 USA SN 1533-0346 J9 TECHNOL CANCER RES T JI Technol. Cancer Res. Treat. PD DEC PY 2004 VL 3 IS 6 BP 591 EP 598 PG 8 WC Oncology SC Oncology GA 888SD UT WOS:000226393600009 PM 15560717 ER PT J AU Frueh, BC Monnier, J Elhai, JD Grubaugh, AL Knapp, RG AF Frueh, BC Monnier, J Elhai, JD Grubaugh, AL Knapp, RG TI Telepsychiatry treatment outcome research methodology: Efficacy versus effectiveness SO TELEMEDICINE JOURNAL AND E-HEALTH LA English DT Article ID PSYCHOTHERAPY AB The use of videoconferencing technology to provide mental health services ( telepsychiatry) offers hope for addressing longstanding problems regarding work force shortages and access to care, especially in remote or rural areas. However, data on treatment outcomes ( i. e., based on randomized clinical trials) from telepsychiatry applications are virtually nonexistent, representing an important gap in the literature. An important methodological decision point in developing treatment outcome research is whether to take an efficacy or effectiveness approach. Efficacy approaches offer enhanced internal validity; however, they may have limited generalizability to real- world settings. Effectiveness approaches offer enhanced external validity. But, they are typically less controlled than efficacy studies, thereby limiting the assumptions that can be made about causality. The current state of telepsychiatry research necessitates efficacy studies, the outcomes from which can be used to inform future effectiveness studies. C1 Med Univ S Carolina, Charleston, SC 29425 USA. Univ S Dakota, Disaster Mental Hlth Inst, Vermillion, SD 57069 USA. Ralph H Johnson Vet Affairs Med Ctr, Charleston, SC USA. RP Frueh, BC (reprint author), VAMC MHS 116, 109 Bee St, Charleston, SC 29401 USA. EM fruehbc@musc.edu FU AHRQ HHS [HS11642]; NIMH NIH HHS [MH01600] NR 8 TC 15 Z9 16 U1 1 U2 1 PU MARY ANN LIEBERT INC PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 USA SN 1530-5627 J9 TELEMED J E-HEALTH JI Telemed. J. e-Health PD WIN PY 2004 VL 10 IS 4 BP 455 EP 458 DI 10.1089/tmj.2004.10.455 PG 4 WC Health Care Sciences & Services SC Health Care Sciences & Services GA 895GU UT WOS:000226849700007 PM 15689650 ER PT J AU Albers, AB Siegel, M Cheng, DM Biener, L Rigotti, NA AF Albers, AB Siegel, M Cheng, DM Biener, L Rigotti, NA TI Relation between local restaurant smoking regulations and attitudes towards the prevalence and social acceptability of smoking: a study of youths and adults who eat out predominantly at restaurants in their town SO TOBACCO CONTROL LA English DT Article ID ADOLESCENT CIGARETTE-SMOKING; TOBACCO CONTROL; NORMATIVE EXPECTATIONS; REGRESSION-MODELS; PUBLIC PLACES; UNITED-STATES; HEALTH; NORMS; PREVENTION; LAWS AB Objective: To examine the relation between strength of local restaurant smoking regulations and smoking related social norms among youths and adults. Design: We used generalised estimating equations logistic regression analysis to examine the relation between regulation strength and youths' and adults' perceptions of adult smoking prevalence and the social acceptability of smoking in their town, while controlling for baseline anti-smoking sentiment in the town. Setting: Each of the 351 Massachusetts towns were classified as having strong ( complete smoking ban), medium ( restriction of smoking to enclosed, separately ventilated areas), or weak ( all others) restaurant smoking regulations. Subjects : 1147 Massachusetts youths ages 12 - 17 years and 2116 adults who reported that they often or always eat out in their own town, drawn from a random digit dial survey. Main outcome measures: Perceived adult smoking prevalence and perceived social acceptability of smoking in restaurants, in bars, or in general. Results: Compared to youths from towns with weak regulations, youths from towns with strong regulations were more likely to perceive lower adult smoking prevalence ( odds ratio ( OR) 1.71; 95% confidence interval (CI) 1.02 to 2.84) and social unacceptability of adult smoking ( OR 2.00, 95% CI 1.29 to 3.08) in their town. Adults from towns with strong regulations were not more likely to perceive lower adult smoking prevalence, but had more than twice the odds of perceiving that smoking was unacceptable in restaurants ( OR 2.19, 95% CI 1.58 to 3.02) or bars ( OR 2.51, 95% CI 1.90 to 3.31). Conclusions: Strong local restaurant smoking regulations are associated with favourable smoking related social norms among youths and adults. C1 Boston Univ, Sch Publ Hlth, Dept Social & Behav Sci, Boston, MA 02118 USA. Boston Univ, Sch Publ Hlth, Dept Biostat, Boston, MA USA. Univ Massachusetts, Survey Res Ctr, Boston, MA 02125 USA. Massachusetts Gen Hosp, Tobacco Res & Treatment Ctr, Boston, MA 02114 USA. Massachusetts Gen Hosp, Div Gen Med, Boston, MA 02114 USA. Harvard Univ, Sch Med, Boston, MA USA. RP Siegel, M (reprint author), Boston Univ, Sch Publ Hlth, Dept Social & Behav Sci, 715 Albany St,TW2, Boston, MA 02118 USA. EM mbsiegel@bu.edu OI Biener, Lois/0000-0002-4130-8138 FU NCI NIH HHS [5 R01 CA86257-03, R01 CA086257] NR 51 TC 46 Z9 46 U1 4 U2 6 PU B M J PUBLISHING GROUP PI LONDON PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND SN 0964-4563 J9 TOB CONTROL JI Tob. Control PD DEC PY 2004 VL 13 IS 4 BP 347 EP 355 DI 10.1136/tc.2003.007336 PG 9 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA 874YJ UT WOS:000225386300014 PM 15564617 ER PT J AU Wang, J Li, W Min, J Ou, Q Chen, J Song, E AF Wang, J Li, W Min, J Ou, Q Chen, J Song, E TI Intrasplenic transplantation of allogeneic hepatocytes modified by BCL-2 gene protects rats from acute liver failure SO TRANSPLANTATION PROCEEDINGS LA English DT Article ID APOPTOTIC CELL-DEATH; SPLEEN; LIGAND AB Background. Apoptosis of donor hepatocytes may be induced by recipient cytotoxic T lymphocytes (CTLs) during acute rejection, representing a major impediment for these cell transplants. Because the mechanisms of transplanted hepatocyte loss involve Fas-mediated pathways, BCL-2 genetic modification may protect liver cells. In the present study, we further investigated whether BCL-2 transfer into transplanted liver cells rendered them resistant to Fas ligand-induced apoptosis, and protected rats from acute liver failure. Materials and Methods. Hepatocytes isolated from Sprague-Dawley rats were infected with an adenovirus vector encoding human BCL-2 gene (AdCMVBCL-2) or a control AdCMVLacZ vector. Forty-eight hours later, cells challenged with recombinant Fas ligand (rhsFasL) were assayed for apoptosis using TUNEL staining and caspase 3 activity. Other cells were transplanted into the spleens of Wistar rats with a 90% hepatectomy 12 hours later. Results. Western blot analysis and RT-PCR confirmed the expression of hBcl-2 in AdCMVhBcl-2-infected hepatocytes. Recombinant FasL produced a dose-dependent increase in TUNEL-positive percentage and caspase-3 activity in uninfected hepatocytes, but did not influence these features in AdCMVhBcl-2-infected cells. On challenge with 90% hepatectomy, the survival of Wistar rats receiving transplantation of AdCMVhBCL-2-infected hepatocytes was significantly prolonged compared with the controls. Conclusion. Adenovirus-mediated BCL-2 gene transfer protects transplanted hepatocytes from Fas-mediated cytolysis, thus holding promise for a new avenue of acute liver failure treatment. C1 Sun Yat Sen Mem Hosp, Dept Surg, Guangzhou, Peoples R China. RP Song, E (reprint author), CBR Inst Biomed Sci, WAB, Room 452, Boston, MA 02115 USA. EM songerwei@yahoo.com NR 5 TC 9 Z9 12 U1 0 U2 2 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0041-1345 J9 TRANSPLANT P JI Transplant. Proc. PD DEC PY 2004 VL 36 IS 10 BP 2924 EP 2926 DI 10.1016/j.transproceed.2004.09.069 PG 3 WC Immunology; Surgery; Transplantation SC Immunology; Surgery; Transplantation GA 894BV UT WOS:000226765800011 PM 15686661 ER PT J AU Lebeche, D Kaprielian, R del Monte, F Tomaselli, G Gwathmey, JK Schwartz, A Hajjar, RJ AF Lebeche, D Kaprielian, R del Monte, F Tomaselli, G Gwathmey, JK Schwartz, A Hajjar, RJ TI In vivo cardiac gene transfer of Kv4.3 abrogates the hypertrophic response in rats after aortic stenosis SO CIRCULATION LA English DT Article DE hypertrophy; gene therapy; ion channels; potassium; stenosis ID JUN NH2-TERMINAL KINASES; OUTWARD K+ CURRENT; HEART-FAILURE; VENTRICULAR MYOCYTES; DOWN-REGULATION; EXCITATION-CONTRACTION; MYOCARDIAL-INFARCTION; CA2+ INFLUX; CALCINEURIN; CURRENTS AB Background - Prolongation of the action potential duration (APD) and decreased transient outward K+ current (I-to) have been consistently observed in cardiac hypertrophy. The relation between electrical remodeling and cardiac hypertrophy in vivo is unknown. Methods and Results - We studied rat hearts subjected to pressure overload by surgical ascending aortic stenosis ( AS) and simultaneously infected these hearts with an adenovirus carrying either the Kv4.3 gene ( Ad. Kv4.3) or the beta-galactosidase gene (Ad.beta-gal). I-to density was reduced and APD(50) was prolonged (P < 0.05) in AS rats compared with sham rats. Kv4.2 and Kv4.3 expressions were decreased by 58% and 51%, respectively ( P < 0.05). AS rats infected with Ad.beta-gal developed cardiac hypertrophy compared with sham rats, as assessed by cellular capacitance and heart weight - body weight ratio. Associated with the development of cardiac hypertrophy, the expression of calcineurin and its downstream transcription factor nuclear factor of activated T cells ( NFAT) c1 was persistently increased by 47% and 36%, respectively ( P < 0.05) in AS myocytes infected with Ad. β-gal compared with sham myocytes. In vivo gene transfer of Kv4.3 in AS rats was shown to increase Kv4.3 expression, increase I-to density, and shorten APD(50) by 1.6-fold, 5.3-fold, and 3.6-fold, respectively ( P < 0.05). Furthermore, AS rats infected with Ad. Kv4.3 showed significant reductions in calcineurin and NFAT expression. ( P < 0.05). Conclusions - Downregulation of I-to, APD prolongation, and cardiac hypertrophy occur early after AS, and in vivo gene transfer of Kv4.3 can restore these electrical parameters and abrogate the hypertrophic response via the calcineurin pathway. C1 Harvard Univ, Sch Med, Massachusetts Gen Hosp, Cardiovasc Res Ctr, Charlestown, MA 02129 USA. Univ Cincinnati, Med Ctr, Inst Mol Pharmacol & Biophys, Cincinnati, OH 45267 USA. Johns Hopkins Univ, Sch Med, Baltimore, MD USA. Boston Univ, Sch Med, Boston, MA 02118 USA. RP Hajjar, RJ (reprint author), Harvard Univ, Sch Med, Massachusetts Gen Hosp, Cardiovasc Res Ctr, 149 13th St,CNY-4, Charlestown, MA 02129 USA. EM hajjar@cvrc.mgh.harvard.edu FU NHLBI NIH HHS [HL07382, HL 49574, HL 57623, HL 69842, HL 71763, HL076659]; PHS HHS [P01 22619] NR 33 TC 44 Z9 49 U1 1 U2 9 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0009-7322 J9 CIRCULATION JI Circulation PD NOV 30 PY 2004 VL 110 IS 22 BP 3435 EP 3443 DI 10.1161/01.CIR.0000148176.33730.3F PG 9 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 875CT UT WOS:000225398000008 PM 15557376 ER PT J AU Olenyuk, BZ Zhang, GJ Klco, JM Nickols, NG Kaelin, WG Dervan, PB AF Olenyuk, BZ Zhang, GJ Klco, JM Nickols, NG Kaelin, WG Dervan, PB TI Inhibition of vascular endothelial growth factor with a sequence-specific hypoxia response element antagonist SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE gene regulation; hypoxia-inducible factor; polyamide ID PYRROLE-IMIDAZOLE POLYAMIDES; DNA-BINDING POLYAMIDES; INDUCIBLE FACTOR-I; A BASE-PAIRS; MINOR-GROOVE; GENE-EXPRESSION; TUMOR-GROWTH; NUCLEAR-LOCALIZATION; KINASE INHIBITORS; FACTOR RECEPTOR AB Vascular endothelial growth factor (VEGF) and its receptors have been implicated as key factors in tumor angiogenesis that are up-regulated by hypoxia. We evaluated the effects of DNA-binding small molecules on hypoxia-inducible transcription of VEGF. A synthetic pyrrole-imidazole polyamide designed to bind the hypoxia response element (HRE) was found to disrupt hypoxia-inducible factor (HIF) binding to HIRE. In cultured HeLa cells, this resulted in a reduction of VEGF mRNA and secreted protein levels. The observed effects were polyamide-specific and dose-dependent. Analysis of genome-wide effects of the HIRE-specific polyamide revealed that a number of hypoxia-inducible genes were down-regulated. Pathway-based regulation of hypoxia-inducible gene expression with DNA-binding small molecules may represent a new approach for targeting angiogenesis. C1 CALTECH, Beckman Inst, Div Chem & Chem Engn, Pasadena, CA 91125 USA. Harvard Univ, Sch Med, Dana Farber Canc Inst, Dept Adult Oncol, Boston, MA 02115 USA. RP Kaelin, WG (reprint author), CALTECH, Beckman Inst, Div Chem & Chem Engn, Pasadena, CA 91125 USA. EM william_kaelin@dfci.harvard.edu; dervan@caltech.edu OI Klco, Jeffery/0000-0003-2961-6960 NR 48 TC 137 Z9 146 U1 0 U2 12 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 30 PY 2004 VL 101 IS 48 BP 16768 EP 16773 DI 10.1073/pnas.0407617101 PG 6 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA 876PC UT WOS:000225508400013 PM 15556999 ER PT J AU Goldrath, AW Luckey, CJ Park, R Benoist, C Mathis, D AF Goldrath, AW Luckey, CJ Park, R Benoist, C Mathis, D TI The molecular program induced in T cells undergoing homeostatic proliferation SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE gene-expression profiling; memory; T cell homeostasis; lymphopenia ID DRIVEN PROLIFERATION; IN-VIVO; MEMORY; NAIVE; LIGANDS; THYMUS; DIFFERENTIATION; LYMPHOCYTES; EXPRESSION; SELECTION AB Naive T cells proliferate independently of cognate antigen when introduced into lymphopenic hosts. Lymphopenia-incluced proliferation depends on low-affinity MHC/self-peptide complexes and on IL-7. To elucidate the intracellular signals mediating this proliferation, we analyzed changes in gene expression in naive CD8(+) T cells at different times after their transfer into a lymphopenic environment. The genes induced in response to lymphopenia were largely an attenuated subset of those turned up by full antigenic stimulation, including genes related to cell cycling, whereas excluding genes specifically associated with effector activity. After the initial phase of proliferation in an empty compartment, the naive T cells adopted a stable pattern of gene expression similar to that of antigen-experienced memory cells. Thus, T cells proliferating in lymphopenic hosts do not exhibit a unique gene-expression profile, instead relying on "traditional" signals for this antigenindependent proliferation; this process ultimately results in differentiation to "authentic" memory cells. C1 Harvard Univ, Sch Med, Joslin Diabet Ctr, Sect Immunol & Immunogenet, Boston, MA 02215 USA. Harvard Univ, Sch Med, Brigham & Womens Hosp, Dept Med, Boston, MA 02215 USA. RP Goldrath, AW (reprint author), Harvard Univ, Sch Med, Joslin Diabet Ctr, Sect Immunol & Immunogenet, 1 Joslin Pl, Boston, MA 02215 USA. EM cb@joslin.harvard.edu FU NHLBI NIH HHS [T32 HL007627, T32 HL07627]; NIAID NIH HHS [AI51530-01, R01 AI051530, R37 AI051530]; NIDDK NIH HHS [2P30 DK36836-17, 5 T32 DK007260-24, P30 DK036836, T32 DK007260] NR 21 TC 104 Z9 105 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 30 PY 2004 VL 101 IS 48 BP 16885 EP 16890 DI 10.1073/pnas.0407417101 PG 6 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA 876PC UT WOS:000225508400033 PM 15548615 ER PT J AU Bernhard, J Zahrieh, D Coates, AS Gelber, RD Castiglione-Gertsch, M Murray, E Forbes, JF Perey, L Collins, J Snyder, R Rudenstam, CM Crivellari, D Veronesi, A Thurlimann, B Fey, MF Price, KN Goldhirsch, A Hurny, C AF Bernhard, J Zahrieh, D Coates, AS Gelber, RD Castiglione-Gertsch, M Murray, E Forbes, JF Perey, L Collins, J Snyder, R Rudenstam, CM Crivellari, D Veronesi, A Thurlimann, B Fey, MF Price, KN Goldhirsch, A Hurny, C CA IBCSG TI Quantifying trade-offs: quality of life and quality-adjusted survival in a randomised trial of chemotherapy in postmenopausal patients with lymph node-negative breast cancer SO BRITISH JOURNAL OF CANCER LA English DT Article DE breast cancer; adjuvant therapy; quality of life; quality-adjusted survival; Q-TWiST; utility ID RECEIVING ADJUVANT THERAPY; LONG-TERM; PATIENTS PREFERENCES; CLINICAL-TRIALS; HEALTH STATES; UTILITY; IMPACT; WOMEN; EXPECTATIONS; PREVENTION AB We evaluated quality of life (QL) and quality-adjusted survival in International Breast Cancer Study Group Trial IX, a randomised trial including 1669 eligible patients receiving tamoxifen for 5 years or three prior cycles of cyclophosphamide, methotrexate and 5-fluorouracil (CMF) followed by 57 months tamoxifen. During the time with CMF toxicity (Tox), without symptoms and toxicity (TWiST), and following relapse (Rel), patients scored their QL indicators and a utility indicator for subjective health estimation between 'perfect' and 'worst' health. Scores were averaged within Tox, TWiST and Rel and transformed to utilities. Mean durations for the three transition times were weighted with utilities to obtain mean quality-adjusted TWiST (Q-TWiST). Patients receiving CMF reported significantly worse scores for most QL domains at month 3, but less hot flushes. After completing chemotherapy, there were no differences by treatment groups. Benefits evaluated by Q-TWiST favoured the additional chemotherapy. CMF provided 3 more months of Q-TWiST for patients with ER-negative tumours, but CMF provided no benefit in Q-TWiST for patients with ER-positive tumours. Q-TWiST analysis based on patient ratings is feasible in large-scale cross-cultural clinical trials. C1 IBCSG Coordinating Ctr, CH-3008 Bern, Switzerland. Inselspital Bern, Inst Med Oncol, CH-3010 Bern, Switzerland. Dana Farber Canc Inst, IBCSG Stat Ctr, Boston, MA 02115 USA. Frontier Sci & Technol Res Fdn Inc, Boston, MA USA. Canc Council Australia, Sydney, NSW, Australia. Univ Sydney, Sydney, NSW 2006, Australia. Groote Schuur Hosp, ZA-7925 Cape Town, South Africa. Univ Cape Town, ZA-7700 Rondebosch, South Africa. Australian New Zealand Breast Canc Trials Grp, Newcastle, NSW, Australia. Newcastle Mater Misericordiae Hosp, Newcastle, NSW, Australia. CHU Vaudois, Lausanne, Switzerland. Royal Melbourne Hosp, Dept Surg, Melbourne, Vic, Australia. St Vincents Hosp, Dept Oncol, Melbourne, Vic, Australia. Sahlgrens Univ Hosp, W Swedish Breast Canc Study Grp, Gothenburg, Sweden. Ctr Riferimento Oncol, I-33081 Aviano, Italy. Kantonsspital, St Gallen, Switzerland. Oncol Inst So Switzerland, Lugano, Switzerland. European Inst Oncol, Milan, Italy. Burgerspital, St Gallen, Switzerland. RP Bernhard, J (reprint author), IBCSG Coordinating Ctr, Effingerstr 40, CH-3008 Bern, Switzerland. EM juerg.bernhard@ibcsg.org FU NCI NIH HHS [CA-75362, U24 CA075362] NR 43 TC 19 Z9 20 U1 0 U2 2 PU NATURE PUBLISHING GROUP PI LONDON PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND SN 0007-0920 EI 1532-1827 J9 BRIT J CANCER JI Br. J. Cancer PD NOV 29 PY 2004 VL 91 IS 11 BP 1893 EP 1901 DI 10.1038/sj.bjc.6602230 PG 9 WC Oncology SC Oncology GA 873SQ UT WOS:000225301700007 PM 15545973 ER PT J AU Shekelle, PG AF Shekelle, PG TI Commentary: Socioeconomic inequalities in indicator scores for A diabetes: poor quality or poor measures? SO BRITISH MEDICAL JOURNAL LA English DT Editorial Material ID DISPARITIES; CARE C1 W Los Angeles Vet Affairs Med Ctr, Los Angeles, CA 90073 USA. RP Shekelle, PG (reprint author), W Los Angeles Vet Affairs Med Ctr, 11301 Wilshire Blvd, Los Angeles, CA 90073 USA. EM shekelle@rand.org NR 5 TC 2 Z9 2 U1 0 U2 0 PU B M J PUBLISHING GROUP PI LONDON PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND SN 0959-535X J9 BRIT MED J JI Br. Med. J. PD NOV 27 PY 2004 VL 329 IS 7477 BP 1269 EP 1270 DI 10.1136/bmj.38285.603692.7C PG 2 WC Medicine, General & Internal SC General & Internal Medicine GA 876FC UT WOS:000225480900017 PM 15548560 ER PT J AU Mueller, NJ Kuwaki, K Dor, FJMF Knosalla, C Gollackner, B Wilkinson, RA Sachs, DH Cooper, DKC Fishman, JA AF Mueller, NJ Kuwaki, K Dor, FJMF Knosalla, C Gollackner, B Wilkinson, RA Sachs, DH Cooper, DKC Fishman, JA TI Reduction of consumptive coagulopathy using porcine cytomegalovirus-free cardiac porcine grafts in pig-to-primate xenotransplantation SO TRANSPLANTATION LA English DT Article DE coagulopathy; heart transplantation; porcine cytomegalovirus; porcine lymphotropic herpesvirus; xenotransplantation ID TRANSPLANTATION AB Background. Xenotransplantation using pigs as the source species for organs carries a potential risk for transmission and activation of porcine herpesviruses. Activation of porcine cytomegalovirus (PCMV) in pig-to-baboon xenotransplantation is associated with xenograft injury and possibly an increased incidence of consumptive coagulopathy (CC). Methods. To further investigate the role of PCMV activation in the occurrence of CC, a strategy to exclude PCMV from the donor was developed. To exclude PCMV, piglets were early-weaned and raised separated from other swine. These piglets were used as donors in an experimental protocol of pig-to-baboon heart xenotransplantation. Results. Early weaning of piglets was successful in excluding PCMV. Use of PCMV-free cardiac porcine xenografts in baboons resulted in prolonged graft survival and prevented consumptive coagulopathy in all recipients. Conclusions. The use of PCMV-free cardiac grafts is beneficial in reducing the direct effects of PCMV activation in the graft (tissue damage) and the indirect effects of PCMV activation in the recipient (consumptive coagulopathy). C1 Harvard Univ, Massachusetts Gen Hosp, Sch Med, Div Infect Dis, Boston, MA 02114 USA. Harvard Univ, Massachusetts Gen Hosp, Transplantat Biol Res Ctr, Boston, MA 02114 USA. RP Fishman, JA (reprint author), Harvard Univ, Massachusetts Gen Hosp, Sch Med, Div Infect Dis, 55 Fruit St,GRJ 504, Boston, MA 02114 USA. EM jfishman@partners.org RI Dor, Frank/E-1032-2013; Mueller, Nicolas/B-6864-2013 OI Dor, Frank/0000-0001-7845-3075; Mueller, Nicolas/0000-0002-1059-3191 FU NIAID NIH HHS [5T32-AI07529-04, P01-AI45897] NR 11 TC 32 Z9 33 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 27 PY 2004 VL 78 IS 10 BP 1449 EP 1453 DI 10.1097/01.TP.0000141361.68446.1F PG 5 WC Immunology; Surgery; Transplantation SC Immunology; Surgery; Transplantation GA 874GY UT WOS:000225340100007 PM 15599308 ER PT J AU Yang, H Roberts, LJ Shi, MJ Zhou, LC Ballard, BR Richardson, A Guo, ZM AF Yang, H Roberts, LJ Shi, MJ Zhou, LC Ballard, BR Richardson, A Guo, ZM TI Retardation of atherosclerosis by overexpression of catalase or both Cu/Zn-superoxide dismutase and catalase in mice lacking apolipoprotein E SO CIRCULATION RESEARCH LA English DT Article DE Cu/Zn-superoxide dismutase; catalase; atherosclerosis; F-2-isoprostanes ID LOW-DENSITY-LIPOPROTEIN; APOE-DEFICIENT MICE; SMOOTH-MUSCLE CELLS; FAT-FED MICE; VITAMIN-E; OXIDATIVE STRESS; IN-VIVO; REDUCES ATHEROSCLEROSIS; ANTIOXIDANT ENZYMES; ENDOTHELIAL-CELLS AB Oxidative stress has been suggested to potentiate atherogenesis. However, studies that have investigated the effect of antioxidants on atherosclerosis showed inconsistent results, ie, atherosclerosis was either retarded or not changed by dietary antioxidants. This report directly examined the effect of overexpressing Cu/Zn-superoxide dismutase (Cu/Zn-SOD) and/or catalase on atherosclerosis and lipid peroxidation in mice lacking apolipoprotein E (ApoE(-/-)). Based on lipid staining of the en face of the aorta tree and the serial sections of the proximal aorta, ApoE(-/-) mice overexpressing catalase or both Cu/Zn-SOD and catalase had smaller and relatively early stages of atherosclerotic lesions (eg, foam cells and free lipids) when compared with ApoE(-/-) mice, who developed more advanced lesions (eg, fibrous caps and acellular areas). In addition, the retarded development of atherosclerosis was correlated with a reduced F-2-isoprostanes in the plasma and aortas in ApoE(-/-) mice overexpressing catalase or both Cu/Zn-SOD and catalase. In contrast, the levels of F-2-isoprostanes and atherosclerosis in the ApoE(-/-) mice overexpressing Cu/Zn-SOD alone were comparable to ApoE(-/-) control mice. These observations implied that endogenously produced hydrogen peroxide, but not superoxide anions, contributed to the formation of oxidized lipids and the development of atherosclerosis in ApoE(-/-) mice. C1 Meharry Med Coll, Dept Pathol Anat & Cell Biol, Nashville, TN 37208 USA. Meharry Med Coll, Dept Physiol, Nashville, TN 37208 USA. Vanderbilt Univ, Div Clin Pharmacol, Nashville, TN USA. Univ Texas, Hlth Sci Ctr, Dept Cellular Struct Biol, San Antonio, TX USA. S Texas Vet Hlth Care Syst, Audie L Murphy Div, Ctr Geriatr Res Educ & Clin, San Antonio, TX USA. RP Guo, ZM (reprint author), Meharry Med Coll, Dept Pathol Anat & Cell Biol, Nashville, TN 37208 USA. EM ZGUO@mmc.edu FU NHLBI NIH HHS [HL076623, HL071525, K01 HL076623]; NIGMS NIH HHS [GM08037, S06 GM008037] NR 38 TC 120 Z9 126 U1 0 U2 3 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0009-7330 J9 CIRC RES JI Circ.Res. PD NOV 26 PY 2004 VL 95 IS 11 BP 1075 EP 1081 DI 10.1161/01.RES.0000149564.49410.0d PG 7 WC Cardiac & Cardiovascular Systems; Hematology; Peripheral Vascular Disease SC Cardiovascular System & Cardiology; Hematology GA 874MY UT WOS:000225355700005 PM 15528470 ER PT J AU Argraves, KM Wilkerson, BA Argraves, WS Fleming, PA Obeid, LM Drake, CJ AF Argraves, KM Wilkerson, BA Argraves, WS Fleming, PA Obeid, LM Drake, CJ TI Sphingosine-1-phosphate signaling promotes critical migratory events in vasculogenesis SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID PROTEIN-COUPLED RECEPTOR; SPHINGOSINE 1-PHOSPHATE RECEPTOR; VEIN ENDOTHELIAL-CELLS; EMBRYONIC BLOOD-VESSELS; LYSOPHOSPHATIDIC ACID; MURINE ALLANTOIS; EDG-1; LIGAND; MOTILITY; ANGIOGENESIS AB Here we have investigated the role of sphingosine-1-phosphate (S1P) signaling in the process of vasculogenesis in the mouse embryo. At stages preceding the formation of blood vessels (7.5 - 8 dpc) in the embryo proper, yolk sac, and allantois, the S1P receptor S1P(2) is expressed in conjunction with S1P(1) and/or S1P(3). Additionally, sphingosine kinase-2 (SK2), an enzyme that catalyzes the formation of S1P, is expressed in these tissues throughout periods of vasculogenesis. Using the cultured mouse allantois explant model of blood vessel formation, we found that vasculogenesis was dependent on S1P signaling. We showed that S1P could replace the ability of serum to promote vasculogenesis in cultured allantois explants. Instead of small poorly reticulated clusters of rounded endothelial cells that formed under serum-free conditions, S1P promoted the formation of elongated endothelial cells that arranged into expansive branched networks of capillary-like vessels. These effects could not be reproduced by vascular endothelial growth factor or basic fibroblast growth factor administration. The ability of S1P to promote blood vessel formation was not due to effects on cell survival or on changes in numbers of endothelial cells (Flk1(+)/PECAM(+)), angioblasts (Flk1(+)/PECAM(+)), or undifferentiated mesodermal cells (Flk1(+)/PECAM(-)). The S1P effect on blood vessel formation was attributed to it promoting migratory activities of angioblasts and early endothelial cells required for the expansion of vascular networks. Together, our findings suggest that migratory events critical to the de novo formation of blood vessels are under the influence of S1P, possibly synthesized via the action of SK2, with signaling mediated by S1P receptors that include S1P(1), S1P(2), and S1P(3). C1 Med Univ S Carolina, Dept Anat & Cell Biol, Charleston, SC 29425 USA. Med Univ S Carolina, Dept Med, Charleston, SC 29425 USA. Med Univ S Carolina, Dept Biochem, Charleston, SC 29425 USA. Ralph H Johnson Vet Affairs Med Ctr, Dept Vet Affairs, Charleston, SC 29401 USA. RP Argraves, KM (reprint author), Med Univ S Carolina, Dept Anat & Cell Biol, Charleston, SC 29425 USA. EM argravek@musc.edu OI obeid, lina/0000-0002-0734-0847 FU NCI NIH HHS [CA097132]; NCRR NIH HHS [RR17677]; NHLBI NIH HHS [HL57375, HL61873, HL52813]; NIDCR NIH HHS [DE014347] NR 46 TC 42 Z9 47 U1 0 U2 3 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD NOV 26 PY 2004 VL 279 IS 48 BP 50580 EP 50590 DI 10.1074/jbc.M404432200 PG 11 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA 872SU UT WOS:000225229500122 PM 15377653 ER PT J AU Ricci, R Sumara, G Sumara, I Rozenberg, I Kurrer, M Akhmedov, A Hersberger, M Eriksson, U Eberli, FR Becher, B Boren, J Chen, M Cybulsky, MI Moore, KJ Freeman, MW Wagner, EF Matter, CM Luscher, TF AF Ricci, R Sumara, G Sumara, I Rozenberg, I Kurrer, M Akhmedov, A Hersberger, M Eriksson, U Eberli, FR Becher, B Boren, J Chen, M Cybulsky, MI Moore, KJ Freeman, MW Wagner, EF Matter, CM Luscher, TF TI Requirement of JNK2 for scavenger receptor A-mediated foam cell formation in atherogenesis SO SCIENCE LA English DT Article ID VASCULAR PROLIFERATION; DEFICIENT MICE; ATHEROSCLEROSIS; DIFFERENTIATION; EXPRESSION; LDL; INFLAMMATION; ACTIVATION; ADHESION AB In vitro studies suggest a role for c-Jun N-terminal kinases (JNKs) in proatherogenic cellular processes. We show that atherosclerosis-prone ApoE(-/-) mice simultaneously lacking JNK2 (ApoE(-/-) JNK2(-/-) mice), but not ApoE(-/-) JNK1(-/-) mice, developed less atherosclerosis than do ApoE(-/-) mice. Pharmacological inhibition of JNK activity efficiently reduced plaque formation. Macrophages lacking JNK2 displayed suppressed foam cell formation caused by defective uptake and degradation of modified lipoproteins and showed increased amounts of the modified lipoprotein-binding and -internalizing scavenger receptor A (SR-A), whose phosphorylation was markedly decreased. Macrophage-restricted deletion of JNK2 was sufficient to decrease atherogenesis. Thus, JNK2-dependent phosphorylation of SR-A promotes uptake of lipids in macrophages, thereby regulating foam cell formation, a critical step in atherogenesis. C1 Univ Zurich Hosp, Inst Physiol, CH-8057 Zurich, Switzerland. Univ Zurich Hosp, Div Cardiol, CH-8057 Zurich, Switzerland. ETH, Inst Cell Biol, CH-8093 Zurich, Switzerland. ETH, Inst Biochem, CH-8093 Zurich, Switzerland. Univ Zurich Hosp, Dept Pathol, CH-8091 Zurich, Switzerland. Univ Zurich Hosp, Inst Clin Chem, CH-8091 Zurich, Switzerland. Univ Zurich Hosp, Dept Neurol, Neuroimmunol Unit, CH-8091 Zurich, Switzerland. Univ Basel Hosp, Dept Res & Med A, CH-4031 Basel, Switzerland. Univ Gothenburg, Wallenberg Lab Cardiovasc Res, S-4345 Gothenburg, Sweden. Univ Toronto, Toronto Gen Res Inst, Toronto, ON, Canada. Univ Toronto, Dept Lab Med & Pathobiol, Toronto, ON, Canada. Harvard Univ, Sch Med, Massachusetts Gen Hosp, Lipid Metab Unit, Boston, MA 02114 USA. Inst Mol Pathol, A-1030 Vienna, Austria. RP Ricci, R (reprint author), Univ Zurich Hosp, Inst Physiol, CH-8057 Zurich, Switzerland. EM romeo.ricci@cetll.biol.ethz.ca RI Wagner, Erwin/G-9637-2012; Ricci, Romeo/K-3009-2013 OI Wagner, Erwin/0000-0001-7872-0196; Ricci, Romeo/0000-0002-9766-4369 NR 27 TC 176 Z9 187 U1 0 U2 17 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 26 PY 2004 VL 306 IS 5701 BP 1558 EP 1561 DI 10.1126/science.1101909 PG 4 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA 875ST UT WOS:000225442700060 PM 15567863 ER PT J AU Francis, NJ Kingston, RE Woodcock, CL AF Francis, NJ Kingston, RE Woodcock, CL TI Chromatin compaction by a polycomb group protein complex SO SCIENCE LA English DT Article ID STRUCTURAL BASIS; HISTONE CODE; DROSOPHILA; DNA; ACCESSIBILITY; REPRESSION; MECHANISMS; GENES; MOTIF AB Polycomb group proteins preserve body patterning through development by maintaining transcriptional silencing of homeotic genes. A long-standing hypothesis is that silencing involves creating chromatin structure that is repressive to gene transcription. We demonstrate by electron microscopy that core components of Polycomb Repressive Complex 1 induce compaction of defined nucleosomal arrays. Compaction by Polycomb proteins requires nucleosomes but not histone tails. Each Polycomb complex can compact about three nucleosomes. A region of Posterior Sex Combs that is important for gene silencing in vivo is also important for chromatin compaction, linking the two activities. This mechanism of chromatin compaction might be central to stable gene silencing by the Polycomb group. C1 Massachusetts Gen Hosp, Dept Mol Biol, Boston, MA 02114 USA. Harvard Univ, Sch Med, Dept Genet, Boston, MA 02115 USA. Univ Massachusetts, Dept Biol, Amherst, MA 01003 USA. RP Kingston, RE (reprint author), Massachusetts Gen Hosp, Dept Mol Biol, Boston, MA 02114 USA. EM kingston@molbio.mgh.harvard.edu FU NCRR NIH HHS [NIH-P41-RR01777]; NIGMS NIH HHS [GM43786] NR 26 TC 386 Z9 399 U1 4 U2 16 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 26 PY 2004 VL 306 IS 5701 BP 1574 EP 1577 DI 10.1126/science.1100576 PG 4 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA 875ST UT WOS:000225442700065 PM 15567868 ER PT J AU Stoler, JM Leach, NT Donahoe, PK Harris, NL AF Stoler, JM Leach, NT Donahoe, PK Harris, NL TI Case 36-2004: A 23-day-old infant with hypospadias and failure to thrive - Congenital abnormalities due to a chromosomal imbalance, karyotype 46,XY,rec(16)dup(16q)inv(16)(p13q22)pat, resulting from the recombination between the normal chromosome 16 and the inverted chromosome 16 in the patient's father. SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Editorial Material ID LEMLI-OPITZ SYNDROME; PERICENTRIC-INVERSION; ALCOHOL-CONSUMPTION; PREGNANCY C1 Massachusetts Gen Hosp, Dept Med Genet, Boston, MA 02114 USA. Massachusetts Gen Hosp, Dept Pediat Surg, Boston, MA 02114 USA. Brigham & Womens Hosp, Dept Pathol, 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 Surg, Boston, MA 02115 USA. RP Stoler, JM (reprint author), Massachusetts Gen Hosp, Dept Med Genet, Boston, MA 02114 USA. NR 21 TC 1 Z9 1 U1 0 U2 0 PU MASSACHUSETTS MEDICAL SOC PI WALTHAM PA WALTHAM WOODS CENTER, 860 WINTER ST,, WALTHAM, MA 02451-1413 USA SN 0028-4793 J9 NEW ENGL J MED JI N. Engl. J. Med. PD NOV 25 PY 2004 VL 351 IS 22 BP 2319 EP 2326 PG 8 WC Medicine, General & Internal SC General & Internal Medicine GA 873RH UT WOS:000225298100013 PM 15564548 ER PT J AU Wang, TJ Parise, H Levy, D Dagostino, RB Wolf, PA Vasan, RS Benjamin, EJ AF Wang, TJ Parise, H Levy, D Dagostino, RB Wolf, PA Vasan, RS Benjamin, EJ TI Obesity and the risk of new-onset atrial fibrillation SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION LA English DT Article ID LEFT-VENTRICULAR HYPERTROPHY; CORONARY-HEART-DISEASE; NATURAL-HISTORY; FRAMINGHAM; HYPERTENSION; SIZE; PREVALENCE; POPULATION; ECHOCARDIOGRAPHY; PREDICTORS AB Context Obesity is associated with atrial enlargement and ventricular diastolic dysfunction, both known predictors of atrial fibrillation (AF). However, it is unclear whether obesity is a risk factor for AF. Objective. To examine the association between body mass index (BMI) and the risk of developing AF. Design, Setting, and Participants Prospective, community-based observational cohort in Framingham, Mass. We studied 5282 participants (mean age, 57 [SD, 13] years; 2898 women [55%]) without baseline AF (electrocardiographic AF or arterial flutter). Body mass index (calculated as weight in kilograms divided by square of height in meters) was evaluated as both a continuous and a categorical variable (normal defined as <25.0; overweight, 25.0 to <30.0; and obese, greater than or equal to30.0). In addition to adjusting for clinical confounders by multivariable techniques, we also examined models including echocardiographic left atrial diameter to examine whether the influence of obesity was mediated by changes in left atrial dimensions. Main Outcome Measure Association between BMI or BMI category and risk of developing new-onset AF. Results During a mean follow-up of 13.7 years, 526 participants (234 women) developed AF. Age-adjusted incidence rates for AF increased across the 3 BMI categories in men (9.7,10.7, and 14.3 per 1000 person-years) and women (5.1, 8.6, and 9.9 per 1000 person-years). In multivariable models adjusted for cardiovascular risk factors and interim myocardial infarction or heart failure, a 4% increase in AF risk per 1-unit increase in BMI was observed in men (95% confidence interval [Cl], 1 %-7%; P=.02) and in women (95% Cl, 1%-7%; P=.009). Adjusted hazard ratios for AF associated with obesity were 1.52 (95% Cl, 1.09-2.13; P=.02) and 1.46 (95% Cl, 1.03-2.07; P=.03) for men and women, respectively, compared with individuals with normal BMI. After adjustment for echocardiographic left atrial diameter in addition to clinical risk factors, BMI was no longer associated with AF risk (adjusted hazard ratios per 1-unit increase in BMI, 1.00 [95% Cl, 0.97-1.04], P=.84 in men; 0.99 [95% Cl, 0.96-1.02], P=.56 in women). Conclusions Obesity is an important, potentially modifiable risk factor for AF. The excess risk of AF associated with obesity appears to be mediated by left atrial dilatation. These prospective data raise the possibility that interventions to promote normal weight may reduce the population. burden of AF. C1 Framingham Heart Dis Epidemiol Study, Framingham, MA 01702 USA. Harvard Univ, Sch Med, Massachusetts Gen Hosp, Div Cardiol, Boston, MA USA. Boston Univ, Dept Math, Boston, MA 02215 USA. NHLBI, Bethesda, MD 20892 USA. Boston Univ, Sch Med, Boston Med Ctr, Dept Neurol, Boston, MA 02118 USA. Boston Univ, Sch Med, Boston Med Ctr, Cardiol Sect, Boston, MA 02118 USA. Boston Univ, Sch Med, Boston Med Ctr, Prevent Med Sect, Boston, MA 02118 USA. RP Benjamin, EJ (reprint author), Framingham Heart Dis Epidemiol Study, 73 Mt Wayte Ave,Suite 2, Framingham, MA 01702 USA. EM emelia@bu.edu OI Ramachandran, Vasan/0000-0001-7357-5970; Benjamin, Emelia/0000-0003-4076-2336 FU NHLBI NIH HHS [K23-HL074077-01, K24-HL-04334, N01-HC-25195]; NINDS NIH HHS [6R01-NS-17950] NR 35 TC 502 Z9 522 U1 2 U2 14 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 24 PY 2004 VL 292 IS 20 BP 2471 EP 2477 DI 10.1001/jama.292.20.2471 PG 7 WC Medicine, General & Internal SC General & Internal Medicine GA 873TD UT WOS:000225303000021 PM 15562125 ER PT J AU Pereira, MA Swain, J Goldfine, AB Rifai, N Ludwig, DS AF Pereira, MA Swain, J Goldfine, AB Rifai, N Ludwig, DS TI Effects of a low-glycemic load diet on resting energy expenditure and heart disease risk factors during weight loss SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION LA English DT Article ID SET-POINT THEORY; METABOLIC-RATE; BODY-WEIGHT; INSULIN-RESISTANCE; YOUNG-ADULTS; LOW-CALORIE; OBESITY; NEUROENDOCRINE; PROTEIN; PLASMA AB Context Weight loss elicits physiological adaptations relating to energy intake and expenditure that antagonize ongoing weight loss. Objective To test whether dietary composition affects the physiological adaptations to weight loss, as assessed by resting energy expenditure. Design, Study, and Participants A randomized parallel-design study of 39 overweight or obese young adults aged 18 to 40 years who received an energy-restricted diet, either low-glycemic load or low-fat. Participants were studied in the General Clinical Research Centers of the Brigham and Women's Hospital and the Children's Hospital, Boston, Mass, before and after 10% weight loss. The study was conducted from January 4, 2001, to May 6, 2003. Main Outcome Measures Resting energy expenditure measured in the fasting state by indirect calorimetry, body composition by dual-energy x-ray absorptiometry, cardiovascular disease risk factors, and self-reported hunger. Results Resting energy expenditure decreased less with the low-glycemic load diet than with the low-fat diet, expressed in absolute terms (mean [SE], 96 [24] vs 176 [27] kcal/d; P=.04) or as a proportion (5.9% [1.5%] vs 10.6% [1.7%]; P=.05). Participants receiving the low-glycemic load diet reported less hunger than those receiving the low-fat diet (P=.04). Insulin resistance (P=.01), serum triglycerides (P=.01), C-reactive protein (P=.03), and blood pressure (P=.07 for both systolic and diastolic) improved more with the low-glycemic load diet. Changes in body composition (fat and lean mass) in both groups were very similar (P=.85 and P=.45, respectively). Conclusions Changes in dietary composition within prevailing norms can affect physiological adaptations that defend body weight. Reduction in glycemic load may aid in the prevention or treatment of obesity, cardiovascular disease, and diabetes mellitus. C1 Childrens Hosp, Dept Med, Boston, MA 02115 USA. Childrens Hosp, Dept Lab Med, Boston, MA 02115 USA. Brigham & Womens Hosp, Gen Clin Res Ctr, Boston, MA 02115 USA. Joslin Diabet Ctr, Boston, MA 02215 USA. RP Ludwig, DS (reprint author), Childrens Hosp, Dept Med, 300 Longwood Ave, Boston, MA 02115 USA. EM david.ludwig@childrens.harvard.edu RI Biguzzi, Felipe/E-4724-2015 FU NCRR NIH HHS [M01 RR02172, M01 RR02635]; NIDDK NIH HHS [R01 DK59240] NR 39 TC 180 Z9 188 U1 2 U2 12 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 24 PY 2004 VL 292 IS 20 BP 2482 EP 2490 DI 10.1001/jama.292.20.2482 PG 9 WC Medicine, General & Internal SC General & Internal Medicine GA 873TD UT WOS:000225303000023 PM 15562127 ER PT J AU Fox, CS Coady, S Sorlie, PD Levy, D Meigs, JB D'Agostino, RB Wilson, PWF Savage, PJ AF Fox, CS Coady, S Sorlie, PD Levy, D Meigs, JB D'Agostino, RB Wilson, PWF Savage, PJ TI Trends in cardiovascular complications of diabetes SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION LA English DT Article ID CORONARY-HEART-DISEASE; ACUTE MYOCARDIAL-INFARCTION; UNITED-STATES; DEATH CERTIFICATES; TEMPORAL TRENDS; SEX-DIFFERENCES; MEDICAL-CARE; EVENT RATES; US ADULTS; MORTALITY AB Context Despite reductions in cardiovascular disease (CVD) mortality over the past few decades, it is unclear whether adults with and without diabetes have experienced similar declines in CVD risk. Objective To determine whether adults with and without diabetes experienced similar declines in incident CVD in 1950-1995. Design, Setting, and Participants Participants aged 45-64 years from the Framingham Heart Study original and offspring cohorts who attended examinations in 1950-1966 ("earlier" time period; 4118 participants, 113 with diabetes) and 1977-1995 ("later" time period; 4063 participants, 317 with diabetes). Incidence rates of CVD among those with and without diabetes were compared between the earlier and later periods. Main Outcome Measures Myocardial infarction, coronary heart disease death, and stroke. Results Among participants with diabetes, the age- and sex-adjusted CVD incidence rate was 286.4 per 10000 person-years in the earlier period and 146.9 per 10000 in the later period, a 49.3% (95% confidence interval [Cl], 16.7%-69.4%) decline. Among participants without diabetes, the age- and sex-adjusted incidence rate was 84.6 per 10000 person-years in the earlier period and 54.3 per 10000 person-years in the later period, a 35.4% (95% Cl, 25.3%-45.4%) decline. Hazard ratios for diabetes as a predictor of incident CVD were not different in the earlier vs later periods. Conclusions We report a 50% reduction in the rate of incident CVD events among adults with diabetes, although the absolute risk of CVD is 2-fold greater than among persons without diabetes. Adults with and without diabetes have benefited similarly during the decline in CVD rates over the last several decades. More aggressive treatment of CVD risk factors and further research on diabetes-specific factors contributing to CVD, risk are needed to further reduce the high absolute risk of CVD still experienced by persons with diabetes. C1 NHLBI, Framingham Heart Study, Framingham, MA 01702 USA. NHLBI, NIH, Bethesda, MD 20892 USA. Harvard Univ, Sch Med, Brigham & Womens Hosp, Dept Endocrinol Diabet & Hypertens, Boston, MA USA. Massachusetts Gen Hosp, Dept Med, Div Gen Med, Boston, MA 02114 USA. Boston Univ, Dept Math, Boston, MA 02215 USA. Med Univ S Carolina, Dept Endocrinol Diabet & Med Genet, Charleston, SC 29425 USA. RP Fox, CS (reprint author), NHLBI, Framingham Heart Study, 73 Mt Wayte Ave,Suite 2, Framingham, MA 01702 USA. EM foxca@nhlbi.nih.gov FU NHLBI NIH HHS [N01-HC-25195] NR 45 TC 273 Z9 291 U1 0 U2 8 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 24 PY 2004 VL 292 IS 20 BP 2495 EP 2499 DI 10.1001/jama.292.20.2495 PG 5 WC Medicine, General & Internal SC General & Internal Medicine GA 873TD UT WOS:000225303000025 PM 15562129 ER PT J AU Held, KS Chen, BP Kuziel, WA Rollins, BJ Lane, TE AF Held, KS Chen, BP Kuziel, WA Rollins, BJ Lane, TE TI Differential roles of CCL2 and CCR2 in host defense to coronavirus infection SO VIROLOGY LA English DT Article DE T lymphocytes; virus; chemokines; inflammation ID CENTRAL-NERVOUS-SYSTEM; MOUSE HEPATITIS-VIRUS; MONOCYTE CHEMOATTRACTANT PROTEIN-1; CHEMOKINE RECEPTOR 2; INDUCED DEMYELINATING DISEASE; T-CELL-ACTIVATION; DENDRITIC CELLS; IFN-GAMMA; NEUROTROPIC CORONAVIRUS; VIRAL-INFECTION AB The CC chemokine ligand 2 (CCL2, monocyte chemoattractant protein-1) is important in coordinating the immune response following microbial infection by regulating T cell polarization as well as leukocyte migration and accumulation within infected tissues. The present study examines the consequences of mouse hepatitis virus (MHV) infection in mice lacking CCL2 (CCL2(-/-)) in order to determine if signaling by this chemokine is relevant in host defense. Intracerebral infection of CCL2(-/-) mice with MHV did not result in increased morbidity or mortality as compared to either wild type or CCR2(-/-) mice and CCL2(-/-) mice cleared replicating virus from the brain. In contrast, CCR2(-/-) mice displayed an impaired ability to clear virus from the brain that was accompanied by a reduction in the numbers of antigen-specific T cells as compared to both CCL2(-/-) and wild-type mice. The paucity in T cell accumulation within the central nervous system (CNS) of MHV-infected CCR2(-/-) mice was not the result of either a deficiency in antigen-presenting cell (APC) accumulation within draining cervical lymph nodes (CLN) or the generation of virus-specific T cells within this compartment. A similar reduction in macrophage infiltration into the CNS was observed in both CCL2(-/-) and CCR2(-/-) mice when compared to wild-type mice, indicating that both CCL2 and CC chemokine receptor 2 (CCR2) contribute to macrophage migration and accumulation within the CNS following MHV infection. Together, these data demonstrate that CCR2, but not CCL2, is important in host defense following viral infection of the CNS, and CCR2 ligand(s), other than CCL2, participates in generating a protective response. (C) 2004 Elsevier Inc. All rights reserved. C1 Univ Calif Irvine, Dept Mol Biol & Biochem, Irvine, CA 92697 USA. Univ Texas, Dept Mol Genet & Microbiol, Inst Cell & Mol Biol, Austin, TX 78712 USA. Harvard Univ, Sch Med, Dana Farber Canc Inst, Dept Med, Boston, MA 02115 USA. Univ Calif Irvine, Ctr Immunol, Irvine, CA 92697 USA. RP Lane, TE (reprint author), Univ Calif Irvine, Dept Mol Biol & Biochem, 3205 Bio Sci 2,McGaugh Hall, Irvine, CA 92697 USA. EM tlane@uci.edu FU NCI NIH HHS [CA53091] NR 59 TC 34 Z9 36 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 0042-6822 J9 VIROLOGY JI Virology PD NOV 24 PY 2004 VL 329 IS 2 BP 251 EP 260 DI 10.1016/j.virol.2004.09.006 PG 10 WC Virology SC Virology GA 872GH UT WOS:000225195200004 PM 15518805 ER PT J AU Bacher, CP Reichenzeller, M Athale, C Herrmann, H Eils, R AF Bacher, CP Reichenzeller, M Athale, C Herrmann, H Eils, R TI 4-D single particle tracking of synthetic and proteinaceous microspheres reveals preferential movement of nuclear particles along chromatin-poor tracks SO BMC CELL BIOLOGY LA English DT Article ID IN-VIVO; LIVING CELLS; INTERMEDIATE-FILAMENTS; BODY MOVEMENT; DIFFUSION; DYNAMICS; VIMENTIN; REGISTRATION; ORGANIZATION; COMPARTMENTS AB Background: The dynamics of nuclear organization, nuclear bodies and RNPs in particular has been the focus of many studies. To understand their function, knowledge of their spatial nuclear position and temporal translocation is essential. Typically, such studies generate a wealth of data that require novel methods in image analysis and computational tools to quantitatively track particle movement on the background of moving cells and shape changing nuclei. Results: We developed a novel 4-D image processing platform (TIKAL) for the work with laser scanning and wide field microscopes. TIKAL provides a registration software for correcting global movements and local deformations of cells as well as 2-D and 3-D tracking software. With this new tool, we studied the dynamics of two different types of nuclear particles, namely nuclear bodies made from GFP-NLS- vimentin and microinjected 0.1 mum - wide polystyrene beads, by live cell time-lapse microscopy combined with single particle tracking and mobility analysis. We now provide a tool for the automatic 3-D analysis of particle movement in parallel with the acquisition of chromatin density data. Conclusions: Kinetic analysis revealed 4 modes of movement: confined obstructed, normal diffusion and directed motion. Particle tracking on the background of stained chromatin revealed that particle movement is directly related to local reorganization of chromatin. Further a direct comparison of particle movement in the nucleoplasm and the cytoplasm exhibited an entirely different kinetic behaviour of vimentin particles in both compartments. The kinetics of nuclear particles were slightly affected by depletion of ATP and significantly disturbed by disruption of actin and microtubule networks. Moreover, the hydration state of the nucleus had a strong impact on the mobility of nuclear bodies since both normal diffusion and directed motion were entirely abolished when cells were challenged with 0.6 M sorbitol. This effect correlated with the compaction of chromatin. We conclude that alteration in chromatin density directly influences the mobility of protein assemblies within the nucleus. C1 Deutsch Krebsforschungszentrum, Div Theoret Bioinformat, D-69120 Heidelberg, Germany. Deutsch Krebsforschungszentrum, Div Cell Biol, D-69120 Heidelberg, Germany. Harvard Univ, Sch Med, Massachusetts Gen Hosp, Complex Biosyst Modeling Lab, Charlestown, MA 02129 USA. RP Eils, R (reprint author), Deutsch Krebsforschungszentrum, Div Theoret Bioinformat, Neuenheimer Feld 580, D-69120 Heidelberg, Germany. EM c.bacher@dkfz-heidelberg.de; m.reichenzeller@dkfz-heidelberg.de; cathale@partners.org; h.herrmann@dkfz-heidelberg.de; r.eils@dkfz-heidelberg.de RI Athale, Chaitanya/G-8883-2011; Eils, Roland/B-6121-2009 OI Athale, Chaitanya/0000-0002-9506-2153; Eils, Roland/0000-0002-0034-4036 NR 46 TC 40 Z9 41 U1 0 U2 8 PU BIOMED CENTRAL LTD PI LONDON PA MIDDLESEX HOUSE, 34-42 CLEVELAND ST, LONDON W1T 4LB, ENGLAND SN 1471-2121 J9 BMC CELL BIOL JI BMC Cell Biol. PD NOV 23 PY 2004 VL 5 AR 45 DI 10.1186/1471-2121-5-45 PG 14 WC Cell Biology SC Cell Biology GA 880DW UT WOS:000225770200001 PM 15560848 ER PT J AU Frangioni, JV Hajjar, RJ AF Frangioni, JV Hajjar, RJ TI In vivo tracking of stem cells for clinical trials in cardiovascular disease SO CIRCULATION LA English DT Article DE stem cells; imaging; trials; radiology ID MR CONTRAST AGENTS; BONE-MARROW; PROGENITOR CELLS; GENE-THERAPY; MYOCARDIAL-INFARCTION; HEMATOPOIETIC-CELLS; NANOPARTICLES; MIGRATION; MAGNETODENDRIMERS; BIOLUMINESCENCE AB Various stem cells hold promise for the treatment of human cardiovascular disease. Regardless of stem cell origin, future clinical trials will require that the location and number of such cells be tracked in vivo, over long periods of time. The problem of tracking small numbers of cells in the body is a difficult one, and an optimal solution does not yet exist. We review the many contrast agents and detectors that have been proposed for stem cell tracking during clinical trials, define the characteristics of an ideal imaging technology, and suggest future directions for research. C1 Beth Israel Deaconess Med Ctr, Dept Radiol, Div Hematol Oncol, Boston, MA 02215 USA. Beth Israel Deaconess Med Ctr, Mol Imaging Ctr, Boston, MA 02215 USA. Massachusetts Gen Hosp, Cardiovasc Res Ctr, Cardiol Lab Integrat Physiol & Imaging, Boston, MA 02114 USA. Harvard Univ, Sch Med, Boston, MA USA. RP Frangioni, JV (reprint author), Beth Israel Deaconess Med Ctr, Dept Radiol, Div Hematol Oncol, 330 Brookline Ave,SL-B05, Boston, MA 02215 USA. EM jfrangio@bidmc.harvard.edu FU NCI NIH HHS [R21-CA-88870, R33-CA-88256]; NHLBI NIH HHS [R01-HL-078691, R01-HL-57623, R01-HL-73756]; NIBIB NIH HHS [R33-EB-00673] NR 47 TC 164 Z9 172 U1 4 U2 11 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0009-7322 J9 CIRCULATION JI Circulation PD NOV 23 PY 2004 VL 110 IS 21 BP 3378 EP 3383 DI 10.1161/01.CIR.0000149840.46523.FC PG 6 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 873KE UT WOS:000225277900015 PM 15557385 ER PT J AU Juo, P Kaplan, JM AF Juo, P Kaplan, JM TI The anaphase-promoting the abundance of GLR-1 complex regulates glutamate receptors in the ventral nerve cord of C-elegans SO CURRENT BIOLOGY LA English DT Article ID UBIQUITIN-PROTEASOME SYSTEM; NEMATODE CAENORHABDITIS-ELEGANS; SYNAPTIC PLASTICITY; MITOSIS; ENDOCYTOSIS; EXPRESSION; METAPHASE; MEIOSIS; HOMOLOG; NEURONS AB The anaphase-promoting complex (APC) is a multisubunit E3 ubiquitin ligase that targets key cell cycle regulatory proteins for degradation. Blockade of APC activity causes mitotic arrest [1, 2]. Recent evidence suggests that the APC may have roles outside the cell cycle [3-6]. Several studies indicate that ubiquitin plays an important role in regulating synaptic strength [7-13]. We previously showed that ubiquitin is directly conjugated to GLR-1, a C. elegans non-NMDA (N-methyl-D-aspartate) class glutamate receptor (GluR), resulting in its removal from synapses [13]. By contrast, endocytosis of rodent AMPA GluRs is apparently regulated by ubiquitination of associated scaffolding proteins [12, 14]. Relatively little is known about the E3 ligases that mediate these effects. We examined the effects of perturbing APC function on postmitotic neurons in the nematode C. elegans. Temperature-sensitive mutations in APC subunits increased the abundance of GLR-1 in the ventral nerve cord. Mutations that block clathrin-mediated endocytosis blocked the effects of the APC mutations, suggesting that the APC regulates some aspect of GLR-1 recycling. Overexpression of ubiquitin decreased the density of GLR-1-containing synapses, and APC mutations blunted this effect. APC mutants had locomotion defects consistent with increased synaptic strength. This study defines a novel function for the APC in postmitotic neurons. C1 Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Mol Biol,Dept Genet, Boston, MA 02114 USA. RP Kaplan, JM (reprint author), Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Mol Biol,Dept Genet, Boston, MA 02114 USA. EM kaplan@molbio.mgh.harvard.edu FU NINDS NIH HHS [1F32NS10957, F32 NS010957, NS32196] NR 38 TC 125 Z9 136 U1 0 U2 5 PU CELL PRESS PI CAMBRIDGE PA 1100 MASSACHUSETTS AVE, CAMBRIDGE, MA 02138 USA SN 0960-9822 J9 CURR BIOL JI Curr. Biol. PD NOV 23 PY 2004 VL 14 IS 22 BP 2057 EP 2062 DI 10.1016/j.cub.2004.11.010 PG 6 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA 874LV UT WOS:000225352800028 PM 15556870 ER PT J AU Ernst, P Mabon, M Davidson, AJ Zon, LI Korsmeyer, SJ AF Ernst, P Mabon, M Davidson, AJ Zon, LI Korsmeyer, SJ TI An MII-dependent Hox program drives hematopoietic progenitor expansion SO CURRENT BIOLOGY LA English DT Article ID YOLK-SAC HEMATOPOIESIS; LINEAGE-LEUKEMIA GENE; MLL-MUTANT MICE; STEM-CELLS; DEFINITIVE HEMATOPOIESIS; EXPRESSION; APOPTOSIS; BCL-2; DIFFERENTIATION; LEUKEMOGENESIS AB Chromosomal translocations disrupting the Mixed lineage leukemia (MII gene result in leukemia, with aberrant expression of some native MII target genes (reviewed in [1]). The MII gene encodes a Trithorax-group chromatin regulator that is essential for the development of hematopoietic stem cells (HSCs) during embryogenesis [2]. Like Trithorax, MLL positively regulates clustered homeodomain or Hox genes, yet the role of Hox genes collectively in the development of the mammalian hematopoietic system has been difficult to ascertain because of redundancy among Hox paralogs. Here, we show that in the absence of MLL, early hematopoietic progenitors develop despite reduced expression of HoxA, HoxB, and HoxC genes. However, these progenitors exhibit a marked reduction in their ability to generate hematopoietic colonies, a subsequent process requiring cell division and differentiation. Reactivation of a subset of Hox genes or, remarkably, reexpression of a single Hox gene in MII-deficient progenitors rescued hematopoietic-colony frequency and growth. In contrast, expression of other MLL target genes such as Pitx2 or expression of anti-apoptotic BCL-2 failed to rescue hematopoietic-colony frequency. Furthermore, our results highlight a shared function of Hox proteins at this point in the development of the hematopoietic system. C1 Harvard Univ, Sch Med, Howard Hughes Med Inst, 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 Med, Boston, MA 02115 USA. Harvard Univ, Sch Med, Childrens Hosp, Dept Med,Div Hematol Oncol, Boston, MA USA. RP Korsmeyer, SJ (reprint author), Harvard Univ, Sch Med, Howard Hughes Med Inst, Boston, MA 02115 USA. EM stanley_korsmeyer@dfci.harvard.edu NR 35 TC 113 Z9 117 U1 1 U2 2 PU CELL PRESS PI CAMBRIDGE PA 1100 MASSACHUSETTS AVE, CAMBRIDGE, MA 02138 USA SN 0960-9822 J9 CURR BIOL JI Curr. Biol. PD NOV 23 PY 2004 VL 14 IS 22 BP 2063 EP 2069 DI 10.1016/j.cub.2004.11.012 PG 7 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA 874LV UT WOS:000225352800029 PM 15556871 ER PT J AU Traynor, BJ Zhang, H Shefner, JM Schoenfeld, D Cudkowicz, ME AF Traynor, BJ Zhang, H Shefner, JM Schoenfeld, D Cudkowicz, ME CA NEALS Consortium TI Functional outcome measures as clinical trial endpoints in ALS SO NEUROLOGY LA English DT Article ID AMYOTROPHIC-LATERAL-SCLEROSIS; PULMONARY-FUNCTION; MULTICENTER; TOPIRAMATE AB The topiramate study was a 12-month randomized placebo-controlled trial in patients with ALS. Follow-up evaluation of the placebo group (n = 97) constituted a well-described cohort of patients with ALS, in whom multiple outcome measures were assessed at 3-month intervals. During the 12-month study period, the decline of forced vital capacity (FVC%) and ALS functional rating scale (ALSFRS) was linear, whereas the decline of maximum voluntary isometric contraction-arm (MVIC-arm) and MVIC-grip Z scores was curvilinear. Rates of FVC% and ALFRS decline, but not of MVIC-arm or MVIC-grip, were independent predictors of survival. C1 Massachusetts Gen Hosp, Dept Neurol, Neurol Clin Trials Unit, Boston, MA 02114 USA. Massachusetts Gen Hosp, Dept Med, Ctr Biostat, Boston, MA 02114 USA. Upstate Med Univ, Dept Neurol, Syracuse, NY USA. Harvard MIT Hlth Sci & Technol Beth Israel Deacon, Clin Investigator Training Program, Boston, MA 02215 USA. RP Traynor, BJ (reprint author), Massachusetts Gen Hosp E, Day Lab Neuromuscular Res, Bldg 114,Room 3125,16th St, Charlestown, MA 02129 USA. EM btraynor@partners.org RI Traynor, Bryan/G-5690-2010 FU NCRR NIH HHS [M01-RR-01066] NR 10 TC 74 Z9 76 U1 0 U2 2 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0028-3878 J9 NEUROLOGY JI Neurology PD NOV 23 PY 2004 VL 63 IS 10 BP 1933 EP 1935 PG 3 WC Clinical Neurology SC Neurosciences & Neurology GA 873JE UT WOS:000225275000030 PM 15557515 ER PT J AU Cole, AJ AF Cole, AJ TI Initial individualized selection of long-term anticonvulsant drugs by neurologists - Introduction SO NEUROLOGY LA English DT Editorial Material ID AMERICAN-EPILEPSY-SOCIETY; TECHNOLOGY-ASSESSMENT SUBCOMMITTEE; QUALITY STANDARDS SUBCOMMITTEE; ACADEMY-OF-NEUROLOGY; NEW-ONSET EPILEPSY; ANTIEPILEPTIC DRUGS; REFRACTORY EPILEPSY; QSS SUBCOMMITTEES; TOLERABILITY; EFFICACY C1 Massachusetts Gen Hosp, Epilepsy Serv, Boston, MA 02114 USA. RP Cole, AJ (reprint author), Massachusetts Gen Hosp, Epilepsy Serv, VBK 830,55 Fruit St, Boston, MA 02114 USA. EM Cole.Andrew@MGH.Harvard.edu NR 4 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 23 PY 2004 VL 63 IS 10 SU 4 BP S1 EP S2 PG 2 WC Clinical Neurology SC Neurosciences & Neurology GA 874UB UT WOS:000225374200001 PM 15557545 ER PT J AU Wen, PH De Gasperi, R Sosa, MAG Elder, GA AF Wen, PH De Gasperi, R Sosa, MAG Elder, GA TI Neural progenitor cells do not differentiate prematurely in Presenilin-1 null mutant mice SO NEUROSCIENCE LETTERS LA English DT Article DE Presenilin-1; neural progenitor cells; neuronal differentiation; null mutant; telencephalon; mice ID CENTRAL-NERVOUS-SYSTEM; RAT; CORTEX; NEURONS; LOCALIZATION; CALRETININ; EXPRESSION; MIGRATION; IMMUNOREACTIVITY; CALBINDIN-D28K AB Mice with a null mutation of the presenilin-1 (PS1-/-) gene die during late intrauterine life or shortly after birth and exhibit defects in cortical development. A previous report suggested that neurons differentiate prematurely in PS1-/- brain [M. Handler, X. Yang, J. Shen, Presenilin-1 regulates neuronal differentiation during neurogenesis, Development 127 (2000) 2593-2606]. Here we reexamined the issue of whether premature neuronal differentiation occurs in PS1-/- brain using fresh cell suspensions from embryonic E11.5 and E13.5 telencephalon where individual cell phenotypes can be easily determined with cell type specific markers. Immumostaining with seven neuronal specific markers (MAP2, beta-III tubulin, GABA, reelin, GluR2/3, calbindin, and calretinin) failed to reveal any evidence of premature neuronal differentiation in PS1-/- telencephalon. We also determined the fraction of cells expressing the neural progenitor marker nestin and found no evidence for premature depletion of neural progenitor cells in PS1-/- telencephalon. Moreover, based on MAP2 staining of tissue sections from E12.5 embryos the topography of newly generated neurons also appeared to be undisturbed in the telencephalon of PS1-/- embryos. These studies thus argue that premature neuronal differentiation is unlikely to be a core pathophysiological feature underlying the aberrant cortical development that occurs in PS1-/- brain. (C) 2004 Elsevier Ireland Ltd. All rights reserved. C1 CUNY Mt Sinai Sch Med, Dept Psychiat, New York, NY 10029 USA. Bronx Vet Adm Med Ctr, Psychiat Serv 3F22, Bronx, NY 10468 USA. RP Elder, GA (reprint author), CUNY Mt Sinai Sch Med, Dept Psychiat, New York, NY 10029 USA. EM gregory.elder@mssm.edu FU NIA NIH HHS [1R01AG020139] NR 22 TC 4 Z9 4 U1 0 U2 2 PU ELSEVIER SCI IRELAND LTD PI CLARE PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE, IRELAND SN 0304-3940 J9 NEUROSCI LETT JI Neurosci. Lett. PD NOV 23 PY 2004 VL 371 IS 2-3 BP 249 EP 254 DI 10.1016/j.neulet.2004.09.038 PG 6 WC Neurosciences SC Neurosciences & Neurology GA 872JP UT WOS:000225203800034 PM 15519767 ER PT J AU Yechoor, VK Patti, ME Ueki, K Laustsen, PG Saccone, R Rauniyar, R Kahn, CR AF Yechoor, VK Patti, ME Ueki, K Laustsen, PG Saccone, R Rauniyar, R Kahn, CR TI Distinct pathways of insulin-regulated versus diabetes-regulated gene expression: An in vivo analysis in MIRKO mice SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE electron-transport chain; sirtuin ID AMYLOID BETA-PROTEIN; B SCAVENGER RECEPTOR; SKELETAL-MUSCLE; LIFE-SPAN; SACCHAROMYCES-CEREVISIAE; GLUCOSE-METABOLISM; HYPERTENSIVE-RATS; LIPID-METABOLISM/; REDOX STATE; RESISTANCE AB Diabetes mellitus is a complex metabolic disorder accompanied by alterations in cellular physiology, metabolism, and gene expression. These alterations can be primary (due to loss of direct insulin action) or secondary (due to the metabolic perturbations associated with the disease). To dissect and quantitate these two separate effects, we compared the skeletal muscle gene-expression profiles of muscle insulin receptor knockout (MIRKO) mice and their Lox controls in the basal, streptozotocin-induced diabetic, and insulin-treated diabetic states. Pure deficiency of insulin action as present in the MIRKO mouse results in regulation of 130 genes, with down-regulation of NSF (N-ethylmaleimide-sensitive fusion protein) and VAMP-2 (vesicle-associated membrane protein 2), stearoyl CoA desaturase 1, and cAMP-specific phosphodiesterase 4B, as well as up-regulation of some signaling-related genes, such as Akt2, and the fatty-acid transporter CD36. In diabetes, additional transcriptional mechanisms are activated, resulting in alterations in expression of approximate to500 genes, including a highly coordinated down-regulation of genes of the mitochondrial electron-transport chain and one of the mammalian homologues of the histone deacetylase Sir2, which has been implicated in the link between nutrition and longevity. These distinct pathways of direct and indirect regulation of gene expression provide insights into the complex mechanisms of transcriptional control in diabetes and areas of potential therapeutic targeting. C1 Harvard Univ, Sch Med, Joslin Diabet Ctr, Boston, MA 02215 USA. Harvard Univ, Sch Med, Dept Med, Boston, MA 02215 USA. RP Kahn, CR (reprint author), Harvard Univ, Sch Med, Joslin Diabet Ctr, 1 Joslin Pl, Boston, MA 02215 USA. EM c.ronald.kahn@joslin.harvard.edu FU NIDDK NIH HHS [DK33201, DK36836-15, DK45935, P30 DK036836, R01 DK033201, R01 DK045935] NR 45 TC 69 Z9 72 U1 0 U2 2 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 23 PY 2004 VL 101 IS 47 BP 16525 EP 16530 DI 10.1073/pnas.0407574101 PG 6 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA 874JT UT WOS:000225347400028 PM 15546994 ER PT J AU de Gelder, B Snyder, J Greve, D Gerard, G Hadjikhani, N AF de Gelder, B Snyder, J Greve, D Gerard, G Hadjikhani, N TI Fear fosters flight: A mechanism for fear contagion when perceiving emotion expressed by a whole body SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE emotion communication; body movement; action; social cognition; amygdala ID FACIAL EXPRESSIONS; BIOLOGICAL MOTION; NEURAL MECHANISMS; POSTERIOR CINGULATE; COORDINATE SYSTEM; CORTICAL SURFACE; PREMOTOR CORTEX; BRAIN-REGIONS; AMYGDALA; PERCEPTION AB Darwin regarded emotions as predispositions to act adaptively, thereby suggesting that characteristic body movements are associated with each emotional state. To this date, investigations of emotional cognition have predominantly concentrated on processes associated with viewing facial expressions. However, expressive body movements may be just as important for understanding the neurobiology of emotional behavior. Here, we used functional MRI to clarify how the brain recognizes happiness or fear expressed by a whole body. Our results indicate that observing fearful body expressions produces increased activity in brain areas narrowly associated with emotional processes and that this emotion-related activity occurs together with activation of areas linked with representation of action and movement. The mechanism of fear contagion hereby suggested may automatically prepare the brain for action. C1 Harvard Univ, Sch Med, Massachusetts Gen Hosp, Martinos Ctr Biomed Imaging, Charlestown, MA 02129 USA. Tilburg Univ, Cognit & Affect Neurosci Lab, NL-5000 LE Tilburg, Netherlands. RP de Gelder, B (reprint author), Harvard Univ, Sch Med, Massachusetts Gen Hosp, Martinos Ctr Biomed Imaging, 1st St Bldg 36, Charlestown, MA 02129 USA. EM degelder@nmr.mgh.harvard.edu RI Hadjikhani, Nouchine/C-2018-2008 OI Hadjikhani, Nouchine/0000-0003-4075-3106 FU NINDS NIH HHS [R01 NS044824, R01 NS44824-01] NR 55 TC 197 Z9 199 U1 3 U2 38 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 23 PY 2004 VL 101 IS 47 BP 16701 EP 16706 DI 10.1073/pnas.0407042101 PG 6 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA 874JT UT WOS:000225347400058 PM 15546983 ER PT J AU Grant, RW O'Leary, KM Weilburg, JB Singer, DE Meigs, JB AF Grant, RW O'Leary, KM Weilburg, JB Singer, DE Meigs, JB TI Impact of concurrent medication use on statin adherence and refill persistence SO ARCHIVES OF INTERNAL MEDICINE LA English DT Article ID NUTRITION EXAMINATION SURVEY; CORONARY-HEART-DISEASE; 3RD NATIONAL-HEALTH; PHARMACY RECORDS; ELDERLY PATIENTS; PRIMARY-CARE; THERAPY; COST; HYPERTENSION; POPULATION AB Background: Effective therapy for chronic illness requires daily medication adherence (DMA) for prolonged periods. Overall medical regimen complexity may represent one barrier to successful adherence. Methods: To assess the relationship between the number of concurrently prescribed medicines and adherence to 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors (statins), we analyzed a cohort of 5488 patients in a single health insurance plan who began statin therapy between July 1, 1999, and June 30, 2002. We assessed 2 parameters of statin adherence: (1) DMA ([total number of pills dispensed/total number of days between first and last prescription] x 100) and (2) refill persistence (RP) (consecutive months of refills after initial prescription). Results: The cohort was 61.6% male, with a mean +/-SD age of 52.7 +/- 9.3 vears. Patients were prescribed a mean +/-SD of 2.9 +/- 2 total medicines (range, 1-13), with a mean +/-SD statin DMA of 82.1% +/- 26.5%. By 12 months, only 68% of patients continued filling statin prescriptions. After controlling for age, income level, and treatment for hypertension or ischemic heart disease, a greater number of concurrently prescribed medicines was significantly associated with better DMA (P = .005) and longer RP (P = .03). Conclusions: In this cohort, statin DMA was generally adequate, but RP was suboptimal. Patients with more concurrently prescribed medicines had higher DMA and better RP, even after adjusting for demographic factors and cardiovascular comorbidity. Physicians should not be deterred from initiating statin therapy by a patient's medical regimen complexity but should be alert for lack of therapy persistence, particularly in younger and healthier patients. C1 Massachusetts Gen Hosp, Dept Med, Gen Med Unit, Clin Res Program, Boston, MA 02114 USA. Massachusetts Gen Hosp, Dept Psychiat, Boston, MA 02114 USA. Harvard Univ, Sch Med, Boston, MA 02115 USA. RP Grant, RW (reprint author), 50-9 Staniford St, Boston, MA 02114 USA. EM Rgrant@partners.org OI Grant, Richard/0000-0002-6164-8025 NR 34 TC 68 Z9 68 U1 0 U2 2 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 USA SN 0003-9926 J9 ARCH INTERN MED JI Arch. Intern. Med. PD NOV 22 PY 2004 VL 164 IS 21 BP 2343 EP 2348 DI 10.1001/archinte.164.21.2343 PG 6 WC Medicine, General & Internal SC General & Internal Medicine GA 874FV UT WOS:000225337200007 PM 15557413 ER PT J AU Giordano, TP Kramer, JR Souchek, J Richardson, P El-Serag, HB AF Giordano, TP Kramer, JR Souchek, J Richardson, P El-Serag, HB TI Cirrhosis and hepatocellular carcinoma in HIV-infected veterans with and without the hepatitis C virus - A cohort study, 1992-2001 SO ARCHIVES OF INTERNAL MEDICINE LA English DT Article; Proceedings Paper CT 2nd International-AIDS-Society Conference on HIV Pathogenesis and Treatment CY JUL 13-16, 2003 CL Paris, FRANCE SP Int AIDS Soc ID HUMAN-IMMUNODEFICIENCY-VIRUS; SEVERITY CLASSIFICATION-SYSTEM; MORTALITY; COINFECTION; AIDS; HOSPITALIZATIONS; MORBIDITY; THERAPIES; SURVIVAL; PATTERNS AB Background: Because they develop slowly and infrequently, the incidence and relative risk of cirrhosis at id hepatocellular carcinoma (HCC) in patients with the human immunodeficiency virus (HIV) only and in patients coinfected with the hepatitis C virus (HCV) are not known. Methods: By using national Veterans Health Administration administrative databases, we conducted a retrospective cohort study. Excluding patients with preexisting liver disease, 11678 HIV-only and 4761 coinfected patients hospitalized between October 1, 1991, and September 30, 2000, were included. Incidence rates and adjusted hazard ratios (HRs) for nonalcoholic cirrhos s and HCC after discharge were calculated through September 30, 2001. Results: The incidence rates of cirrhosis in the HIV-only, and coinfected groups were 1.47 and 15.88 per 1000 person-years, respectively. In a Cox multivariate proportion l hazards regression model, coinfected patients had an adjusted HR for cirrhosis of 9.24 compared with HIV-only patients (95% confidence interval, 6.92-12.33; P < .001). The incidence rates of HCC in the HIV-only and coinfected groups were 0.20 and 1.32 per 1000 person-years, respectively. In a Cox multivariate proportional hazards regression model, coinfected patients had an adjusted HR for HCC of 5.35 compared with HIV-only patients (95% confidence interval, 2.34-12.20; P < .00.1). Among patients identified during the highly active antiretroviral therapy era, the HR for cirrhosis was 19.06 (95% confidence interval, 10.14-35.85; P < .001), while the HR for HCC was 5.07 (95% confidence interval, 1.72-14.99; P = .003). Conclusions: To our knowledge, this study is the largest longitudinal study to examine the incidence of nonalcoholic cirrhosis and HCC in HIV-only and HCV-coinfected patients. Hepatitis C virus coinfection dramatically promotes the development of HCC (5-fold) and of cirrhosis (10- to 20-fold), and is especially associated with cirrhosis in the highly active antiretroviral therapy era. Treatment of HCV in HIV-infected patients, while often unsuccessful, should be considered. C1 Dept Vet Affairs Med Ctr, Houston Ctr Qual Care & Utilizat Studies, Hlth Serv Res & Dev Serv, Houston, TX 77030 USA. Baylor Coll Med, Dept Med, Hlth Serv Res, Infect Dis Sect, Houston, TX 77030 USA. RP Giordano, TP (reprint author), Dept Vet Affairs Med Ctr, Houston Ctr Qual Care & Utilizat Studies, Hlth Serv Res & Dev Serv, 152,2002 Holcombe Blvd, Houston, TX 77030 USA. EM tpg@bcm.tmc.edu FU NIMH NIH HHS [K23MH67505] NR 27 TC 106 Z9 116 U1 0 U2 0 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 USA SN 0003-9926 J9 ARCH INTERN MED JI Arch. Intern. Med. PD NOV 22 PY 2004 VL 164 IS 21 BP 2349 EP 2354 DI 10.1001/archinte.164.21.2349 PG 6 WC Medicine, General & Internal SC General & Internal Medicine GA 874FV UT WOS:000225337200008 PM 15557414 ER PT J AU Hermos, JA Young, MM Gagnon, DR Fiore, LD AF Hermos, JA Young, MM Gagnon, DR Fiore, LD TI Characterizations of long-term oxycodone/acetaminophen prescriptions in veteran patients SO ARCHIVES OF INTERNAL MEDICINE LA English DT Article ID CHRONIC PAIN; DRUG-ABUSE; BENZODIAZEPINES; DEPENDENCY; MANAGEMENT; MISUSE; RISKS AB Background: Long-term management of chronic pain with opioids may be stable over time or may be complicated by problematic dose increases, drug dependencies, and toxic effects. To determine clinical contexts in which stability or problems may occur, we examined the pharmacologic and clinical correlates of long-term prescriptions of oxycodone/acetaminophen, a commonly prescribed short-acting opioid formulation. Methods: We analyzed linked, archival outpatient pharmacy wand clinical databases from the New England Veterans Integrated Service Network between January 1, 1998, and June 30, 2001. Durations, doses, and dose changes of oxycodone/acetaminophen prescriptions and concurrent use of long-acting opioids, benzodiazepines, tricyclic antidepressants, and anticonvulsants were determined. Results: In aggregate, 2195 patients (31% with cancer diagnoses per the International Classification of Diseases, Ninth Revision, Clinical Modification) received oxycodone/acetaminophen for more than 9 months at a mean prescribed daily dose of 3.9 tablets per day (range, 0.5-13.0 tablets per day) with minimal changes in daily prescribed mean dose over time. Patients with cancer were more likely than other patients to receive concurrent long-acting opioids. For patients without cancer, a higher mean daily dose was associated with duration, older age, human immunodeficiency virus (HIV) and/or AIDS, and with prescribed benzodiazepines and long-acting opioids; concurrent benzodiazepine prescriptions were associated with anticonvulsant prescriptions and with psychogenic pain and alcohol abuse and/or dependence diagnoses. Conclusions: In veteran patients who received long-term oxycodone/acetaminophen prescriptions, mean daily doses were typically modest and stable, likely reflecting a selection of patients with successful, long-term management. Among patients without cancer, however, associations of higher oxycodone/acetaminophen doses with benzodiazepine prescriptions, psychogenic pain, alcohol abuse, and HIV/AIDS may portend opioid prescription management problems. C1 VA Boston Healthcare Syst, Massachusetts Vet Epidemiol Res & Informat Ctr, Pharmacoepidemiol Res Grp, Boston, MA 02130 USA. Boston Univ, Sch Publ Hlth, Boston, MA 02215 USA. RP Hermos, JA (reprint author), VA Boston Healthcare Syst, Massachusetts Vet Epidemiol Res & Informat Ctr, Pharmacoepidemiol Res Grp, 151MAV,150 Huntington Ave, Boston, MA 02130 USA. EM john.hermos@med.va.gov NR 20 TC 45 Z9 52 U1 0 U2 4 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 USA SN 0003-9926 J9 ARCH INTERN MED JI Arch. Intern. Med. PD NOV 22 PY 2004 VL 164 IS 21 BP 2361 EP 2366 DI 10.1001/archinte.164.21.2361 PG 6 WC Medicine, General & Internal SC General & Internal Medicine GA 874FV UT WOS:000225337200010 PM 15557416 ER PT J AU Sabeh, F Ota, I Holmbeck, K Birkedal-Hansen, H Soloway, P Balbin, M Lopez-Otin, C Shapiro, S Inada, M Krane, S Allen, E Chung, D Weiss, SJ AF Sabeh, F Ota, I Holmbeck, K Birkedal-Hansen, H Soloway, P Balbin, M Lopez-Otin, C Shapiro, S Inada, M Krane, S Allen, E Chung, D Weiss, SJ TI Tumor cell traffic through the extracellular matrix is controlled by the membrane-anchored collagenase MT1-MMP SO JOURNAL OF CELL BIOLOGY LA English DT Article ID I COLLAGEN; METALLOPROTEINASE ACTIVITY; PERICELLULAR PROTEOLYSIS; DEFICIENT MICE; GELATINASE-A; INVASION; CANCER; ACTIVATION; MIGRATION; EXPRESSION AB As cancer cells traverse collagen-rich extracellular matrix (ECM) barriers and intravasate, they adopt a fibroblast-like phenotype and engage undefined proteolytic cascades that mediate invasive activity. Herein, we find that fibroblasts and cancer cells express an indistinguishable pericellular collagenolytic activity that allows them to traverse the ECM. Using fibroblasts isolated from gene-targeted mice, a matrix metalloproteinase (MMP)-dependent activity is identified that drives invasion independently of plasminogen, the gelatinase A/TIMP-2 axis, gelatinase B, collogenase-3, collagenase-2, or stromelysin-1. In contrast, deleting or suppressing expression of the membrane-tethered MMP, MT1-MMP, in fibroblasts or tumor cells results in a loss of collagenolytic and invasive activity in vitro or in vivo. Thus, MT1-MMP serves as the major cell-associated proteinase necessary to confer normal or neoplastic cells with invasive activity. C1 Univ Michigan, Dept Internal Med, Div Med & Mol Genet, Ann Arbor, MI 48109 USA. Natl Inst Dent & Craniofacial Res, Bethesda, MD 20892 USA. Cornell Univ, Coll Human Ecol, Div Nutr Sci, Ithaca, NY 14853 USA. Univ Oviedo, Inst Univ Oncol, Dept Bioquim, Oviedo 33006, Spain. Harvard Univ, Sch Med, Massachusetts Gen Hosp, Boston, MA 02114 USA. RP Weiss, SJ (reprint author), Univ Michigan, Dept Internal Med, Div Med & Mol Genet, Ann Arbor, MI 48109 USA. EM sjweiss@umich.edu RI inada, masaki/D-1581-2013; Balbin, Milagros/I-4206-2015; Lopez-Otin, Carlos/C-6657-2013 OI inada, masaki/0000-0002-5066-8506; Lopez-Otin, Carlos/0000-0001-6964-1904 FU NCI NIH HHS [R01 CA071699, R01 CA088308]; NHLBI NIH HHS [P01 HL029594, P01 HL29594] NR 59 TC 375 Z9 383 U1 2 U2 20 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 22 PY 2004 VL 167 IS 4 BP 769 EP 781 DI 10.1083/jcb.200408028 PG 13 WC Cell Biology SC Cell Biology GA 875HS UT WOS:000225411600018 PM 15557125 ER PT J AU Home, P Mbanya, JC Horton, E AF Home, P Mbanya, JC Horton, E TI Standardisation of glycated haemoglobin SO BRITISH MEDICAL JOURNAL LA English DT Editorial Material ID COMPLICATIONS; HBA(1C) C1 Sch Med Sci, Newcastle Upon Tyne NE2 4HH, Tyne & Wear, England. Univ Yaounde 1, Dept Internal Med, Endocrine Unit, Yaounde 8, Cameroon. Joslin Diabet Ctr, Boston, MA 02215 USA. RP Home, P (reprint author), Sch Med Sci, Newcastle Upon Tyne NE2 4HH, Tyne & Wear, England. EM philip.home@ncl.ac.uk NR 5 TC 7 Z9 7 U1 0 U2 0 PU B M J PUBLISHING GROUP PI LONDON PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND SN 0959-535X J9 BRIT MED J JI Br. Med. J. PD NOV 20 PY 2004 VL 329 IS 7476 BP 1196 EP 1197 DI 10.1136/bmj.329.7476.1196 PG 2 WC Medicine, General & Internal SC General & Internal Medicine GA 874FG UT WOS:000225335700002 PM 15550404 ER PT J AU Cherepanov, P Devroe, E Silver, PA Engelman, A AF Cherepanov, P Devroe, E Silver, PA Engelman, A TI Identification of an evolutionarily conserved domain in human lens epithelium-derived growth factor/transcriptional co-activator p75 (LEDGF/p75) that binds HIV-1 integrase SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID IMMUNODEFICIENCY-VIRUS TYPE-1; NUCLEAR-LOCALIZATION; HUMAN-CELLS; PREINTEGRATION COMPLEXES; LTR-RETROTRANSPOSONS; HUMAN GENOME; GENE FAMILY; PWWP DOMAIN; PROTEIN; DNA AB Human lens epithelium-derived growth factor/transcriptional co-activator p75 (LEDGF/p75) protein was recently identified as a binding partner for HIV-1 integrase (IN) in human cells. In this work, we used biochemical and bioinformatic approaches to define the domain organization of LEDGF/p75. Using limited proteolysis and deletion mutagenesis we show that the protein contains a pair of evolutionarily conserved domains, assuming about 35% of its sequence. Whereas the N-terminal PWWP domain had been recognized previously, the second domain is novel. It is comprised of similar to80 amino acid residues and is both necessary and sufficient for binding to HIV-1 IN. Strikingly, the integrase binding domain (IBD) is not unique to LEDGF/p75, as a second human protein, hepatoma-derived growth factor-related protein 2 (HRP2), contains a homologous sequence. LEDGF/p75 and HRP2 IBDs avidly bound HIV-1 IN in an in vitro GST pull-down assay and each full-length protein potently stimulated HIV-1 IN activity in vitro. LEDGF/p75 and HRP2 are predicted to share a similar domain organization and have an evident evolutionary and likely functional relationship. C1 Dana Farber Canc Inst, Dept Canc Immunol & AIDS, Boston, MA 02115 USA. Dana Farber Canc Inst, Dept Canc Biol, Boston, MA 02115 USA. Harvard Univ, Sch Med, Dept Pathol, Boston, MA 02115 USA. Harvard Univ, Sch Med, Dept Syst Biol, Boston, MA 02115 USA. RP Engelman, A (reprint author), Dana Farber Canc Inst, Dept Canc Immunol & AIDS, 44 Binney St, Boston, MA 02115 USA. EM alan_engelman@dfci.harvard.edu RI Cherepanov, Peter/F-6859-2010 OI Cherepanov, Peter/0000-0002-0634-538X FU NIAID NIH HHS [AI39394] NR 59 TC 181 Z9 188 U1 0 U2 6 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 19 PY 2004 VL 279 IS 47 BP 48883 EP 48892 DI 10.1074/jbc.M406307200 PG 10 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA 870ZP UT WOS:000225098100050 PM 15371438 ER PT J AU Muller, FL Liu, YH Van Remmen, H AF Muller, FL Liu, YH Van Remmen, H TI Complex III releases superoxide to both sides of the inner mitochondrial membrane SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID CYTOCHROME BC(1) COMPLEX; HYDROGEN-PEROXIDE PRODUCTION; ELECTRON-TRANSPORT CHAIN; RESPIRATORY-CHAIN; REACTIVE OXYGEN; Q(O) SITE; HEART-MITOCHONDRIA; MUTANT MICE; UBIHYDROQUINONE OXIDATION; CHLOROPLAST THYLAKOIDS AB Mechanisms of mitochondrial superoxide formation remain poorly understood despite considerable medical interest in oxidative stress. Superoxide is produced from both Complexes I and III of the electron transport chain, and once in its anionic form it is too strongly charged to readily cross the inner mitochondrial membrane. Thus, superoxide production exhibits a distinct membrane sidedness or "topology." In the present work, using measurements of hydrogen peroxide (Amplex red) as well as superoxide ( modified Cypridina luciferin analog and aconitase), we demonstrate that Complex I-dependent superoxide is exclusively released into the matrix and that no detectable levels escape from intact mitochondria. This finding fits well with the proposed site of electron leak at Complex I, namely the iron-sulfur clusters of the (matrix-protruding) hydrophilic arm. Our data on Complex III show direct extramitochondrial release of superoxide, but measurements of hydrogen peroxide production revealed that this could only account for similar to 50% of the total electron leak even in mitochondria lacking CuZn-superoxide dismutase. We posit that the remaining similar to 50% of the electron leak must be due to superoxide released to the matrix. Measurements of ( mitochondrial matrix) aconitase inhibition, performed in the presence of exogenous superoxide dismutase and catalase, confirmed this hypothesis. Our data indicate that Complex III can release superoxide to both sides of the inner mitochondrial membrane. The locus of superoxide production in Complex III, the ubiquinol oxidation site, is situated immediately next to the intermembrane space. This explains extramitochondrial release of superoxide but raises the question of how superoxide could reach the matrix. We discuss two models explaining this result. C1 Univ Texas, Hlth Sci Ctr, Dept Cellular & Struct Biol, San Antonio, TX 78229 USA. Univ Texas, Hlth Sci Ctr, Barshop Ctr Longev Studies, San Antonio, TX 78229 USA. S Texas Vet Hlth Care Syst, Dept Cellular & Struct Biol, San Antonio, TX 78284 USA. RP Muller, FL (reprint author), Univ Texas, Hlth Sci Ctr, Dept Cellular & Struct Biol, 7703 Floyd Curl Dr,MSC 7762, San Antonio, TX 78229 USA. EM mullerf@uthscsa.edu FU NIA NIH HHS [5T3-AG021890-02, P01AG14674] NR 80 TC 485 Z9 501 U1 1 U2 22 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 19 PY 2004 VL 279 IS 47 BP 49064 EP 49073 DI 10.1074/jbc.M407715200 PG 10 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA 870ZP UT WOS:000225098100070 PM 15317809 ER PT J AU Inoue, M Digman, MA Cheng, M Breusegem, SY Halaihel, N Sorribas, V Mantulin, WW Gratton, E Barry, NP Levi, M AF Inoue, M Digman, MA Cheng, M Breusegem, SY Halaihel, N Sorribas, V Mantulin, WW Gratton, E Barry, NP Levi, M TI Partitioning of NaPi cotransporter in cholesterol-, sphingomyelin-, and glycosphingolipid-enriched membrane domains modulates NaPi protein diffusion, clustering, and activity SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID FLUORESCENCE CORRELATION SPECTROSCOPY; GPI-ANCHORED PROTEINS; GIANT UNILAMELLAR VESICLES; PHOTON-COUNTING HISTOGRAM; PROXIMAL TUBULAR CELLS; LIPID RAFTS; MODEL MEMBRANES; PHOSPHATE-TRANSPORT; BRUSH-BORDER; FLUCTUATION SPECTROSCOPY AB In dietary potassium deficiency there is a decrease in the transport activity of the type IIa sodium/phosphate cotransporter protein (NaPi) despite an increase in its apical membrane abundance. This novel posttranslational regulation of NaPi activity is mediated by the increased glycosphingolipid content of the potassium-deficient apical membrane. However, the mechanisms by which these lipids modulate NaPi activity have not been determined. We determined if in potassium deficiency NaPi is increasingly partitioned in cholesterol-, sphingomyelin-, and glycosphingolipid-enriched microdomains of the apical membrane and if the increased presence of NaPi in these microdomains modulates its activity. By using a detergent-free density gradient flotation technique, we found that 80% of the apical membrane NaPi partitions into the low density cholesterol-, sphingomyelin-, and GM1-enriched fractions characterized as "lipid raft" fractions. In potassium deficiency, a higher proportion of NaPi was localized in the lipid raft fractions. By combining fluorescence correlation spectroscopy and photon counting histogram methods for control and potassium-deficient apical membranes reconstituted into giant unilamellar vesicles, we showed a 2-fold decrease in lateral diffusion of NaPi protein and a greater than 2-fold increase in size of protein aggregates/clusters in potassium deficiency. Our results indicate that NaPi protein is localized in membrane microdomains, that in potassium deficiency a larger proportion of NaPi protein is present in these microdomains, and that NaPi lateral diffusion is slowed down and NaPi aggregation/clustering is increased in potassium deficiency, both of which could be associated with the decreased Na/P-i cotransport activity in potassium deficiency. C1 Univ Colorado, Hlth Sci Ctr, Dept Med, Div Renal Dis & Hypertens, Denver, CO 80262 USA. Univ Colorado, Hlth Sci Ctr, Dept Physiol, Div Renal Dis & Hypertens, Denver, CO 80262 USA. Univ Colorado, Hlth Sci Ctr, Dept Biophys, Div Renal Dis & Hypertens, Denver, CO 80262 USA. Denver Vet Affairs Med Ctr, Denver, CO 80262 USA. Univ Illinois, Dept Phys, Fluorescence Dynam Lab, Urbana, IL 61801 USA. Univ Zaragoza, Dept Toxicol, E-50013 Zaragoza, Spain. RP Levi, M (reprint author), Univ Colorado, Hlth Sci Ctr, Dept Med, Div Renal Dis & Hypertens, 4200 E 9th Ave, Denver, CO 80262 USA. EM Moshe.Levi@UCHSC.edu RI Halaihel , Nabil/J-2973-2016; OI Levi, Moshe/0000-0002-6225-946X; Sorribas, Victor/0000-0003-3457-323X FU NCRR NIH HHS [5 P41-RRO3155]; NIDDK NIH HHS [5R01 DK062209-02] NR 70 TC 29 Z9 29 U1 0 U2 6 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 19 PY 2004 VL 279 IS 47 BP 49160 EP 49171 DI 10.1074/jbc.M408942200 PG 12 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA 870ZP UT WOS:000225098100081 PM 15355967 ER PT J AU Wang, XZ Grammatikakis, N Siganou, A Stevenson, MA Calderwood, SK AF Wang, XZ Grammatikakis, N Siganou, A Stevenson, MA Calderwood, SK TI Interactions between extracellular signal-regulated protein kinase 1, 14-3-3 epsilon, and heat shock factor 1 during stress SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID ACTIVATED PROTEIN-KINASE; DNA-BINDING ABILITY; TRANSCRIPTIONAL ACTIVATION; FACTOR-I; GENE-TRANSCRIPTION; C-FOS; PHOSPHORYLATION; CELLS; HSF1; THERMOTOLERANCE AB Cytoprotection during the heat shock response is a complex phenomenon involving multiple inducible mechanisms. We have examined the interaction of two key molecular components in the response, heat shock transcription factor 1 (HSF1) and extracellular signal regulated protein kinase (ERK). Whereas both HSF1 and ERK are required to protect cells against apoptosis, ERK activation is paradoxically antagonistic to transactivation of hsp promoters by HSF1 and HSP accumulation during heat shock. We have found that the two pathways interact directly and that heat shock causes the physical association of ERK1 with HSF1, an interaction that promotes the kinase activity of ERK in heat-shocked cells. ERK activation results in the recruitment of the phosphoserine binding protein 14-3-3epsilon in a manner dependent on previous HSF1 phosphorylation by ERK. The effects of 14-3-3epsilon binding on HSF1 were complex, however, depending on extracellular conditions, in that HSF1-14-3-3 binding at 37degreesC led to the cytoplasmic sequestration and repression of HSF1, whereas heat shock overrode these effects and caused quantitative nuclear localization of HSF1. Although the effects of 14-3-3epsilon binding to HSF1 were overridden acutely by stress, during recovery from heat shock, 14-3-3epsilon association again led to enhanced cytoplasmic localization of HSF1, implicating a role for ERK/14-3-3epsilon in HSF1 deactivation in recovering cells. Association of HSF1 with ERK and 14-3-3epsilon during heat shock may thus modulate the amplitude of the response and lead to efficient termination of HSP expression on resumption of growth conditions. C1 Harvard Univ, Sch Med, Beth Israel Deaconess Med Ctr, Div Mol & Cellular Radiat Oncol, Boston, MA 02215 USA. Harvard Univ, Sch Med, Dana Farber Canc Inst, Boston, MA 02115 USA. Boston Univ, Sch Med, Dept Med, Boston, MA 02118 USA. RP Calderwood, SK (reprint author), Harvard Univ, Sch Med, Beth Israel Deaconess Med Ctr, Div Mol & Cellular Radiat Oncol, 21-27 Burlington Ave,Room 553B, Boston, MA 02215 USA. EM scalderw@bidmc.harvard.edu FU NCI NIH HHS [CA31303, CA47407, CA50642] NR 63 TC 41 Z9 44 U1 0 U2 3 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD NOV 19 PY 2004 VL 279 IS 47 BP 49460 EP 49469 DI 10.1074/jbc.M406059200 PG 10 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA 870ZP UT WOS:000225098100116 PM 15364926 ER PT J AU King, KR Wang, CCJ Kaazempur-Mofrad, MR Vacanti, JP Borenstein, JT AF King, KR Wang, CCJ Kaazempur-Mofrad, MR Vacanti, JP Borenstein, JT TI Biodegradable microfluidics SO ADVANCED MATERIALS LA English DT Article ID POLYMER INTERFACE; SOFT LITHOGRAPHY; SCAFFOLDS; TECHNOLOGY; DESIGN AB A biodegradable microfabrication platform for constructing 3D high-resolution devices for tissue engineering and drug delivery is presented. Biodegradable polymer films with built-in micrometer-scale features are stacked and fusion bonded to construct fully biodegradable, poly(DL-lactic-co-glycolide) (PLGA)-based, monolithic, multilayer, microfluidic networks. Integration with cells or drug compounds will enable use of these devices in therapeutic applications (scale bar: similar to 300 mum). C1 Charles Stark Draper Lab Inc, Cambridge, MA 02139 USA. MIT, Dept Mech Engn, Cambridge, MA 02139 USA. Harvard Univ, Sch Med, Dept Surg, Boston, MA 02114 USA. Massachusetts Gen Hosp, Dept Surg, Boston, MA 02114 USA. RP Borenstein, JT (reprint author), Charles Stark Draper Lab Inc, Cambridge, MA 02139 USA. EM jborenstein@draper.com NR 28 TC 117 Z9 119 U1 5 U2 48 PU WILEY-V C H VERLAG GMBH PI WEINHEIM PA PO BOX 10 11 61, D-69451 WEINHEIM, GERMANY SN 0935-9648 J9 ADV MATER JI Adv. Mater. PD NOV 18 PY 2004 VL 16 IS 22 BP 2007 EP + DI 10.1002/adma.200306522 PG 7 WC Chemistry, Multidisciplinary; Chemistry, Physical; Nanoscience & Nanotechnology; Materials Science, Multidisciplinary; Physics, Applied; Physics, Condensed Matter SC Chemistry; Science & Technology - Other Topics; Materials Science; Physics GA 884SE UT WOS:000226105600005 ER PT J AU Makris, N Gasic, GP Seidman, LJ Goldstein, JM Gastfriend, DR Elman, I Albaugh, MD Hodge, SM Ziegler, DA Sheahan, FS Caviness, VS Tsuang, MT Kennedy, DN Hyman, SE Rosen, BR Breiter, HC AF Makris, N Gasic, GP Seidman, LJ Goldstein, JM Gastfriend, DR Elman, I Albaugh, MD Hodge, SM Ziegler, DA Sheahan, FS Caviness, VS Tsuang, MT Kennedy, DN Hyman, SE Rosen, BR Breiter, HC TI Decreased absolute amygdala volume in cocaine addicts SO NEURON LA English DT Review ID LEFT-RIGHT ASYMMETRY; ADULT HUMAN BRAIN; HIPPOCAMPAL VOLUME; NUCLEUS-ACCUMBENS; SITUS-INVERSUS; WHITE-MATTER; VULNERABILITY INDICATOR; MORPHOMETRIC-ANALYSIS; 1ST-DEGREE RELATIVES; SEEKING BEHAVIOR AB The amygdala is instrumental to a set of brain processes that lead to cocaine consumption, including those that mediate reward and drug craving. This study examined the volumes of the amygdala and hippocampus in cocaine-addicted subjects and matched healthy controls and determined that the amygdala but not the hippocampus was significantly reduced in volume. The right-left amygdala asymmetry in control subjects was absent in the cocaine addicts. Topological analysis of amygdala isosurfaces (population averages) revealed that the isosurface of the cocaine-dependent group undercut the anterior and superior surfaces of the control group, implicating a difference in the corticomedial and basolateral nuclei. In cocaine addicts, amygdala volume did not correlate with any measure of cocaine use. The amygdala symmetry coefficient did correlate with baseline but not cocaine-primed craving. These findings argue for a condition that predisposes the individual to cocaine dependence by affecting the amygdala, or a primary event early in the course of cocaine use. C1 Massachusetts Gen Hosp, Dept Radiol, Motivat & Emot Neurosci Collaborat, Boston, MA 02129 USA. Massachusetts Gen Hosp, Dept Radiol, Athinoula A Martinos Ctr, Boston, MA 02129 USA. Massachusetts Gen Hosp, Dept Psychiat, Ctr Morphometr Anal Dept Neurol, Boston, MA 02129 USA. Harvard Univ, Sch Med, Boston, MA 02129 USA. Harvard Univ, Sch Med, Boston, MA 02115 USA. Massachusetts Mental Hlth Ctr, Dept Psychiat, Boston, MA 02115 USA. Brigham & Womens Hosp, Dept Psychiat, Boston, MA 02120 USA. Brigham & Womens Hosp, Div Womens Hlth, Boston, MA 02120 USA. Harvard Univ, Sch Med, Boston, MA 02120 USA. McLean Hosp, Belmont, MA 02478 USA. Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA. Univ Calif San Diego, Inst Behav Genom, Dept Psychiat, La Jolla, CA 92037 USA. Harvard Univ, Sch Med, Dept Neurobiol, Boston, MA 02115 USA. Harvard Univ, Div Addict, Cambridge, MA 02138 USA. Harvard Univ, Off Provost, Cambridge, MA 02138 USA. RP Breiter, HC (reprint author), Massachusetts Gen Hosp, Dept Radiol, Motivat & Emot Neurosci Collaborat, Boston, MA 02129 USA. EM hbreiter@partners.org RI Kennedy, David/H-3627-2012; Albaugh, Matthew/R-4349-2016 FU NIDA NIH HHS [DA00265, DA09467, DA14118]; NIMH NIH HHS [MH46318, MH00976, MH435518, MH56956, MH63951]; NINDS NIH HHS [NS34189] NR 101 TC 90 Z9 96 U1 6 U2 7 PU CELL PRESS PI CAMBRIDGE PA 1100 MASSACHUSETTS AVE, CAMBRIDGE, MA 02138 USA SN 0896-6273 J9 NEURON JI Neuron PD NOV 18 PY 2004 VL 44 IS 4 BP 729 EP 740 DI 10.1016/j.neuron.2004.10.027 PG 12 WC Neurosciences SC Neurosciences & Neurology GA 874GE UT WOS:000225338100017 PM 15541319 ER PT J AU Fazeli, A Moschella, SL Mackool, BT Harris, NL Kay, J Liu, V Axelrod, L AF Fazeli, A Moschella, SL Mackool, BT Harris, NL Kay, J Liu, V Axelrod, L TI A 68-year-old man with end-stage renal disease and thickening of the skin - Nephrogenic fibrosing dermopathy. SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Editorial Material ID EOSINOPHILIA-MYALGIA SYNDROME; DIABETES-MELLITUS; SYSTEMIC-SCLEROSIS; CLINICAL SPECTRUM; CUTANEOUS MANIFESTATIONS; DIALYSIS PATIENTS; SCLEROMYXEDEMA; CONTRACTURES; THALIDOMIDE; SCLERODERMA C1 Lahey Clin Fdn, Dept Dermatol, Burlington, MA 01805 USA. Massachusetts Gen Hosp, Dept Med, Div Rheumatol, Boston, MA 02114 USA. Massachusetts Gen Hosp, Dept Dermatol, Boston, MA 02114 USA. Massachusetts Gen Hosp, Dept Pathol, Div Dermatopathol, Boston, MA 02114 USA. Harvard Univ, Sch Med, Dept Dermatol, Cambridge, MA 02138 USA. Harvard Univ, Sch Med, Dept Med, Cambridge, MA 02138 USA. Harvard Univ, Sch Med, Dept Pathol, Cambridge, MA 02138 USA. RP Fazeli, A (reprint author), Lahey Clin Fdn, Dept Dermatol, Burlington, MA 01805 USA. NR 28 TC 31 Z9 31 U1 0 U2 0 PU MASSACHUSETTS MEDICAL SOC PI WALTHAM PA WALTHAM WOODS CENTER, 860 WINTER ST,, WALTHAM, MA 02451-1413 USA SN 0028-4793 J9 NEW ENGL J MED JI N. Engl. J. Med. PD NOV 18 PY 2004 VL 351 IS 21 BP 2219 EP 2227 PG 9 WC Medicine, General & Internal SC General & Internal Medicine GA 871UU UT WOS:000225160600014 ER PT J AU Hideshima, T Podar, K Chauhan, D Ishitsuka, K Mitsiades, C Tai, YT Hamasaki, M Raje, N Hideshima, H Schreiner, G Nguyen, AN Navas, T Munshi, NC Richardson, PG Higgins, LS Anderson, KC AF Hideshima, T Podar, K Chauhan, D Ishitsuka, K Mitsiades, C Tai, YT Hamasaki, M Raje, N Hideshima, H Schreiner, G Nguyen, AN Navas, T Munshi, NC Richardson, PG Higgins, LS Anderson, KC TI p38 MAPK inhibition enhances PS-341 (bortezomib)-induced cytotoxicity against multiple myeloma cells SO ONCOGENE LA English DT Article DE multiple myeloma; p38 MAPK inhibitor; SCIO-469; PS-341; Hsp27 ID TUMOR-NECROSIS-FACTOR; HEAT-SHOCK PROTEIN-27; MARROW STROMAL CELLS; NF-KAPPA-B; PROTEASOME INHIBITOR; DRUG-RESISTANCE; KINASE PATHWAY; THERAPEUTIC APPLICATIONS; MITOCHONDRIAL PROTEIN; MOLECULAR-MECHANISMS AB Although PS-341 (bortezomib) is a promising agent to improve multiple myeloma ( MM) patient outcome, 65% of patients with relapsed and refractory disease do not respond. We have previously shown that heat shock protein (Hsp)27 is upregulated after PS-341 treatment, that overexpression of Hsp27 confers PS-341 resistance, and that inhibition of Hsp27 overcomes PS-341 resistance. Since Hsp27 is a downstream target of p38 mitogen-activated protein kinase (MAPK)/MAPK-mitogen-activated protein kinase-2 (MAPKAPK2), we hypothesized that inhibition of p38 MAPK activity could augment PS-341 cytotoxicity by downregulating Hsp27. Although p38 MAPK inhibitor SCIO-469 (Scios Inc, CA, USA) alone did not induce significant growth inhibition, it blocked baseline and PS-341-triggered phosphorylation of p38 MAPK as well as upregulation of Hsp27, associated with enhanced cytotoxicity in MM.1S cells. Importantly, SCIO-469 enhanced phosphorylation of c-Jun NH2-terminal kinase (JNK) and augmented cleavage of caspase-8 and poly(ADP)-ribose polymerase. Moreover, SCIO-469 downregulated PS-341-induced increases in G2/M-phase cells, associated with downregulation of p21(Cip1) expression. Importantly, SCIO-469 treatment augmented cytotoxicity of PS-341 even against PS-341-resistant cell lines and patient MM cells. These studies therefore provide the framework for clinical trials of SCIO-469 to enhance sensitivity and overcome resistance to PS-341, thereby improving patient outcome in MM. C1 Dana Farber Canc Inst, Dept Med Oncol, Jerome Lipper Multiple Myeloma Ctr, Boston, MA 02115 USA. Harvard Univ, Sch Med, Boston, MA 02115 USA. Scios Inc, Fremont, CA 94555 USA. RP Anderson, KC (reprint author), Dana Farber Canc Inst, Dept Med Oncol, Jerome Lipper Multiple Myeloma Ctr, Mayer 557,44 Binney St, Boston, MA 02115 USA. EM kenneth_anderson@dfci.harvard.edu FU NCI NIH HHS [R0-1 CA 50947, IP50 CA10070-01]; PHS HHS [P0-1 78378] NR 48 TC 91 Z9 93 U1 0 U2 1 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 18 PY 2004 VL 23 IS 54 BP 8766 EP 8776 DI 10.1038/sj.onc.1208118 PG 11 WC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity GA 871VQ UT WOS:000225165100006 PM 15480425 ER PT J AU Wiederhold, T Lee, MF James, M Neujahr, R Smith, N Murthy, A Hartwig, J Gusella, JF Ramesh, V AF Wiederhold, T Lee, MF James, M Neujahr, R Smith, N Murthy, A Hartwig, J Gusella, JF Ramesh, V TI Magicin, a novel cytoskeletal protein associates with the NF2 tumor suppressor merlin and Grb2 SO ONCOGENE LA English DT Article DE NF2; merlin; tumor suppressor; Grb2; cytoskeleton ID ALDRICH-SYNDROME PROTEIN; HUMAN SCHWANNOMA CELLS; TYPE-2 GENE-PRODUCT; NEUROFIBROMATOSIS TYPE-2; TERMINAL DOMAIN; SH3 DOMAINS; F-ACTIN; N-WASP; NHE-RF; MEMBRANE AB Neurofibromatosis 2 (NF2) is a dominantly inherited disorder characterized by bilateral vestibular schwannomas and meningiomas. Merlin, the neurofibromatosis 2 tumor suppressor protein, is related to the ERM ( ezrin, radixin, moesin) proteins and, like its family members, is thought to play a role in plasma membrane-cytoskeletal interactions. We report a novel protein as a merlin-specific binding partner that we have named magicin ( merlin and Grb2 interacting cytoskeletal protein) and show that the two proteins interact in vitro and in vivo as well as colocalize beneath the plasma membrane. Magicin is a 24 kDa protein that is expressed in many cell lines and tissues. Magicin, similar to merlin, associates with the actin cytoskeleton as determined by cofractionation, immunofluorescence and electron microscopy. Analysis of the magicin sequence reveals binding motifs for the adaptor protein Grb2. Employing affinity binding, blot overlay and co-immunoprecipitation assays, we demonstrate an interaction between Grb2 and magicin. In addition, merlin is capable of forming a ternary complex with magicin and Grb2. These results support a role for merlin in receptor-mediated signaling at the cell surface, and may have implications in the regulation of cytoskeletal reorganization. C1 Massachusetts Gen Hosp, Mol Neurosci Unit, Charlestown, MA 02129 USA. Brigham & Womens Hosp, Div Expt Med, Longwood Med Res Ctr, Boston, MA 02115 USA. RP Ramesh, V (reprint author), Massachusetts Gen Hosp, Mol Neurosci Unit, Bldg 149,13th St,Rm6222, Charlestown, MA 02129 USA. EM ramesh@helix.mgh.harvard.edu FU NINDS NIH HHS [NS24279] NR 47 TC 35 Z9 38 U1 0 U2 2 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 18 PY 2004 VL 23 IS 54 BP 8815 EP 8825 DI 10.1038/sj.onc.1208110 PG 11 WC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity GA 871VQ UT WOS:000225165100011 PM 15467741 ER PT J AU Shi, JL Heegaard, CW Rasmussen, JT Gilbert, GE AF Shi, JL Heegaard, CW Rasmussen, JT Gilbert, GE TI Lactadherin binds selectively to membranes containing phosphatidyl-L-serine and increased curvature SO BIOCHIMICA ET BIOPHYSICA ACTA-BIOMEMBRANES LA English DT Article DE lactadherin; phosphatidylserine; membrane; phospholipid vesicle; blood coagulation; MFG-E8 ID LARGE UNILAMELLAR VESICLES; HUMAN-FACTOR-VIII; HUMAN-FACTOR-V; ANNEXIN-V; C2 DOMAIN; PROTHROMBINASE COMPLEX; PHOSPHOLIPID-VESICLES; BLOOD-COAGULATION; APOPTOTIC CELLS; LIGHT CHAIN AB Lactadherin, a milk protein, contains discoidin-type lectin domains with homology to the phosphatidylserine-binding domains of blood coagulation factor VIII and factor V We have found that lactadherin functions, in vitro, as a potent anticoagulant by competing with blood coagulation proteins for phospholipid binding sites [J. Shi and G.E. Gilbert, Lactadherin inhibits enzyme complexes of blood coagulation by competing for phospholipid binding sites, Blood 101 (2003) 2628-2636]. We wished to characterize the membrane-binding properties that correlate to the anticoagulant capacity. We labeled bovine lactadherin with fluorescein and evaluated binding to membranes of composition phosphatidyisefine/phosphatidylethanolamine/phosphatidylcholine, 4:20:76 supported by 2 gin diameter glass microspheres. Lactadherin bound saturably with an apparent KD of 3.3+/-0.4 nM in a Ca++-independent manner. The number of lactadherin binding sites increased proportionally to the phosphatidylserine content over a range 0-2% and less rapidly for higher phosphatidylserine content. Inclusion of phosphatidylethanolamine in phospholipid vesicles did not enhance the apparent affinity or number of lactadherin binding sites. The number of sites was at least 4-fold higher on small unilamellar vesicles than on large unilamellar vesicles, indicating that lactadherin binding is enhanced by membrane curvature. Lactadherin bound to membranes with synthetic dioleoyl phosphatidyl-L-serine but not dioleoyl phosphatidyl-D-serine indicating stereoselective recognition of phosphatidyl-L-serine. We conclude that lactadherin resembles factor VIII and V with stereoselective preference for phosphatidyl-L-serine and preference for highly curved membranes. Published by Elsevier B.V. C1 Brigham & Womens Hosp, VA Boston Healthcare Syst, Dept Med, Boston, MA 02132 USA. Harvard Univ, Sch Med, Boston, MA 02132 USA. Aarhus Univ, Dept Mol Biol, Prot Chem Lab, DK-8000 Aarhus, Denmark. RP Gilbert, GE (reprint author), VA Boston Healthcare Ctr, 1400 VFW Pkwy, Boston, MA 02132 USA. EM ggilbert@rics.bwh.harvard.edu FU NHLBI NIH HHS [R01 HL57867] NR 46 TC 102 Z9 105 U1 0 U2 10 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0005-2736 J9 BBA-BIOMEMBRANES JI Biochim. Biophys. Acta-Biomembr. PD NOV 17 PY 2004 VL 1667 IS 1 BP 82 EP 90 DI 10.1016/j.bbamem.2004.09.006 PG 9 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA 871YY UT WOS:000225173800009 PM 15533308 ER PT J AU Feezor, RJ Baker, HV Mindrinos, M Hayden, D Tannahill, CL Brownstein, BH Fay, A MacMillan, S Laramie, J Xiao, WZ Moldawer, LL Cobb, JP Laudanski, K Miller-Graziano, CL Maier, RV Schoenfeld, D Davis, RW Tompkins, RG AF Feezor, RJ Baker, HV Mindrinos, M Hayden, D Tannahill, CL Brownstein, BH Fay, A MacMillan, S Laramie, J Xiao, WZ Moldawer, LL Cobb, JP Laudanski, K Miller-Graziano, CL Maier, RV Schoenfeld, D Davis, RW Tompkins, RG CA Inflammation Host Response Injury TI Whole blood and leukocyte RNA isolation for gene expression analyses SO PHYSIOLOGICAL GENOMICS LA English DT Article DE microarray; buffy coat; PAXgene; inflammation; trauma ID CLASS DISCOVERY; MICROARRAY; STABILIZATION; PREDICTION; CARCINOMA; SURVIVAL; CANCER AB The analysis of gene expression data in clinical medicine has been plagued by the lack of a critical evaluation of accepted methodologies for the collection, processing, and labeling of RNA. In the present report, the reliability of two commonly used techniques to isolate RNA from whole blood or its leukocyte compartment was compared by examining their reproducibility, variance, and signal-to-noise ratios. Whole blood was obtained from healthy subjects and was either untreated or stimulated ex vivo with Staphylococcus enterotoxin B (SEB). Blood samples were also obtained from trauma patients but were not stimulated with SEB ex vivo. Total RNA was isolated from whole blood with the PAXgene proprietary blood collection system or from isolated leukocytes. Biotin-labeled cRNA was hybridized to Affymetrix GeneChips. The Pearson correlation coefficient for gene expression measurements in replicates from healthy subjects with both techniques was excellent, exceeding 0.985. Unsupervised analyses, including hierarchical cluster analysis, however, revealed that the RNA isolation method resulted in greater differences in gene expression than stimulation with SEB or among different trauma patients. The intraclass correlation, a measure of signal-to-noise ratio, of the difference between SEB-stimulated and unstimulated blood from healthy subjects was significantly higher in leukocyte-derived samples than in whole blood: 0.75 vs. 0.46 ( P = 0.002). At the P < 0.001 level of significance, twice as many probe sets discriminated between SEB-stimulated and unstimulated blood with leukocyte isolation than with PAXgene. The findings suggest that the method of RNA isolation from whole blood is a critical variable in the design of clinical studies using microarray analyses. C1 Harvard Univ, Massachusetts Gen Hosp, Sch Med,Dept Surg, Trauma Serv, Boston, MA 02114 USA. Univ Florida, Coll Med, Dept Surg, Gainesville, FL USA. Univ Florida, Coll Med, Dept Microbiol & Mol Genet, Gainesville, FL USA. Stanford Genome Technol Ctr, Palo Alto, CA USA. Shriners Burn Ctr, Dept Surg, Boston, MA USA. Washington Univ, Sch Med, Dept Surg, St Louis, MO 63110 USA. MIT, Dept Chem Engn, Cambridge, MA 02139 USA. Univ Rochester, Sch Med & Dent, Dept Surg, Rochester, NY USA. Univ Washington, Harborview Med Ctr, Dept Surg, Seattle, WA 98104 USA. RP Tompkins, RG (reprint author), Harvard Univ, Massachusetts Gen Hosp, Sch Med,Dept Surg, Trauma Serv, GRB 1302,55 Fruit St, Boston, MA 02114 USA. EM rtompkins@partners.org OI Laudanski, Krzysztof /0000-0002-7373-0851; xiao, wenzhong/0000-0003-4944-6380; Baker, Henry/0000-0002-8273-5320 FU NIGMS NIH HHS [T32 GM008721, U54 GM062119, U54-GM-62119-02] NR 17 TC 132 Z9 137 U1 1 U2 7 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA SN 1094-8341 J9 PHYSIOL GENOMICS JI Physiol. Genomics PD NOV 17 PY 2004 VL 19 IS 3 BP 247 EP 254 DI 10.1152/physiolgenomics.00020.2004 PG 8 WC Cell Biology; Genetics & Heredity; Physiology SC Cell Biology; Genetics & Heredity; Physiology GA 881CK UT WOS:000225840800002 PM 15548831 ER PT J AU Bjorkbacka, H Fitzgerald, KA Huet, F Li, XM Gregory, JA Lee, MA Ordija, CM Dowley, NE Golenbock, DT Freeman, MW AF Bjorkbacka, H Fitzgerald, KA Huet, F Li, XM Gregory, JA Lee, MA Ordija, CM Dowley, NE Golenbock, DT Freeman, MW TI The induction of macrophage gene expression by LPS predominantly utilizes Myd88-dindependent signaling cascades SO PHYSIOLOGICAL GENOMICS LA English DT Article DE monocytes/macrophages; lipopolysaccharide; gene regulation; signal transduction; cellular activation ID DOMAIN-CONTAINING ADAPTER; NF-KAPPA-B; MYELOID DIFFERENTIATION FACTOR-88; IFN-REGULATORY FACTOR-3; CUTTING EDGE; STAPHYLOCOCCUS-AUREUS; MYD88-DEFICIENT MICE; NEGATIVE REGULATION; INTERFERON-BETA; LIPOPOLYSACCHARIDE AB Myeloid differentiation protein-88 (MyD88) is a signal adaptor protein required for cytokine production following engagement of Toll-like receptors (TLRs) by their cognate ligands. Activation of both TLR-3 and TLR-4, however, can engage signaling events independent of MyD88 expression. The relative importance of these MyD88-dependent and - independent signaling pathways in the macrophage response to lipopolysaccharide (LPS) is unknown. Here we define these events using microarray expression profiling of LPS-stimulated macrophages taken from MyD88-null and wild-type mice. Of the 1,055 genes found to be LPS responsive, only 21.5% were dependent on MyD88 expression, with MyD88-independent genes constituting 74.7% of the genetic response. This MyD88-independent gene expression was predominantly transcriptionally regulated, as it was unaffected by cycloheximide blockade of new protein synthesis. A previously undescribed group of LPS-regulated genes (3.8%), whose induction or repression was significantly greater in the absence of MyD88, was also identified by these studies. The regulation of these genes suggested that MyD88 could serve as a molecular brake, constraining gene activity in a subset of LPS-responsive genes. The findings generated with LPS stimulation were recapitulated by exposure of macrophages to live Escherichia coli. These expression-profiling studies redefine the current dogma of TLR-4 signaling and establish that MyD88, although essential for some of the best-characterized macrophage responses to LPS, is not required for the regulation of the majority of genes engaged by macrophage exposure to endotoxin or live bacteria. C1 Massachusetts Gen Hosp, Lipid Metab Unit, Dept Mol Biol, Boston, MA 02114 USA. Univ Massachusetts, Sch Med, Div Infect Dis & Immunol, Worcester, MA USA. Harvard Univ, Dept Stat, Cambridge, MA 02138 USA. Harvard Univ, Sch Med, Boston, MA USA. RP Freeman, MW (reprint author), Massachusetts Gen Hosp, Lipid Metab Unit, Dept Mol Biol, Boston, MA 02114 USA. EM freeman@molbio.mgh.harvard.edu OI Bjorkbacka, Harry/0000-0003-3918-0857 FU NCRR NIH HHS [RR-14466]; NHLBI NIH HHS [HL-66678, HL-45098]; NIDDK NIH HHS [DK-50305]; NIGMS NIH HHS [GM-54060] NR 54 TC 184 Z9 193 U1 2 U2 4 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA SN 1094-8341 J9 PHYSIOL GENOMICS JI Physiol. Genomics PD NOV 17 PY 2004 VL 19 IS 3 BP 319 EP 330 DI 10.1152/physiolgenomics.00128.2004 PG 12 WC Cell Biology; Genetics & Heredity; Physiology SC Cell Biology; Genetics & Heredity; Physiology GA 881CK UT WOS:000225840800009 PM 15367722 ER PT J AU Fang, MC Chang, YC Hylek, EM Rosand, J Greenberg, SM Go, AS Singer, DE AF Fang, MC Chang, YC Hylek, EM Rosand, J Greenberg, SM Go, AS Singer, DE TI Advanced age, anticoagulation intensity, and risk for intracranial hemorrhage among patients taking warfarin for atrial fibrillation SO ANNALS OF INTERNAL MEDICINE LA English DT Article ID RANDOMIZED CONTROLLED-TRIALS; INTRACEREBRAL HEMORRHAGE; STROKE PREVENTION; CEREBRAL-ISCHEMIA; BLEEDING COMPLICATIONS; ANTITHROMBOTIC THERAPY; CARDIOVASCULAR HEALTH; ORAL ANTICOAGULATION; PHYSICIAN ATTITUDES; ASPIRIN AB Background: The risk for atrial fibrillation-associated stroke increases at low anticoagulation intensities. However, higher intensities increase hemorrhage risk. Optimal use of warfarin for atrial fibrillation requires precise information on the risk for intracranial hemorrhage as a function of patient age and anticoagulation intensity. Objective: To examine the relationship of age, anticoagulation intensity, and risk for intracranial hemorrhage. Design: Case-control study. Setting: Academic medical center. Patients: 170 case-patients who developed intracranial hemorrhage during warfarin therapy and 1020 matched controls who did not; both case-patients and controls were taking warfarin for atrial fibrillation. Measurements: The authors performed multivariable conditional logistic regression to determine the odds of intracranial hemorrhage with regard to age and international normalized ratio (INR), controlling for comorbid conditions and aspirin use. Results: Case-patients were older than controls (median age, 78 years vs. 75 years; P < 0.001) and had higher median INRs (2.7 vs. 2.3; P < 0.001). The risk for intracranial hemorrhage increased at 85 years of age or older (adjusted odds ratio, 2.5 [95% CI, 1.3 to 4.7]; referent age, 70 to 74 years) and at an INR range of 3.5 to 3.9 (adjusted odds ratio, 4.6 [CI, 2.3 to 9.4]; referent INR, 2.0 to 3.0). The risk for intracranial hemorrhage at INRs less than 2.0 did not differ statistically from the risk at INRs of 2.0 to 3.0 (adjusted odds ratio, 1.3 [CI, 0.8 to 2.2]). Limitations: Although duration of anticoagulation has been associated with hemorrhage in other studies, the current study could not control for this potential confounder. Conclusions: The risk for intracranial hemorrhage increases at age 85 years. International normalized ratios less than 2.0 were not associated with lower risk for intracranial hemorrhage compared with INRs between 2.0 and 3.0. Therefore, anticoagulation management should focus on maintaining INRs in the 2.0 to 3.0 range, even in elderly patients with atrial fibrillation, rather than targeting INRs less than 2.0. Similarly, INRs of 3.5 or greater should be avoided. C1 Univ Calif San Francisco, Div Gen Internal Med, Hospitalist Grp, San Francisco, CA 94143 USA. Kaiser Permanente, Oakland, CA USA. Massachusetts Gen Hosp, Boston, MA 02114 USA. RP Fang, MC (reprint author), Univ Calif San Francisco, Div Gen Internal Med, Hospitalist Grp, 533 Parnassus Ave,Box 0131, San Francisco, CA 94143 USA. EM mfang@medicine.ucsf.edu FU NIA NIH HHS [AG15478]; PHS HHS [5T32-HP-11001-14] NR 47 TC 314 Z9 331 U1 1 U2 5 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 16 PY 2004 VL 141 IS 10 BP 745 EP 752 PG 8 WC Medicine, General & Internal SC General & Internal Medicine GA 872KU UT WOS:000225206900001 PM 15545674 ER PT J AU Peabody, JW Luck, J Glassman, P Jain, S Hansen, J Spell, M Lee, M AF Peabody, JW Luck, J Glassman, P Jain, S Hansen, J Spell, M Lee, M TI Measuring the quality of physician practice by using clinical vignettes: A prospective validation study SO ANNALS OF INTERNAL MEDICINE LA English DT Article ID STANDARDIZED PATIENTS; GENERAL-PRACTITIONERS; FAMILY PHYSICIANS; CHART ABSTRACTION; NURSING RESEARCH; DECISION-MAKING; MEDICAL-RECORD; CARE; DIAGNOSIS; ILL AB Background: worldwide efforts are under way to improve the quality of clinical practice. Most quality measurements, however, are poorly validated, expensive, and difficult to compare among sites. Objective: To validate whether vignettes accurately measure the quality of clinical practice by using a comparison with standardized patients (the gold standard method), and to determine whether vignettes are a more or less accurate method than medical record abstraction. Design: Prospective, multisite study. Setting: Outpatient primary care clinics in 2 Veterans Affairs medical centers and 2 large, private medical centers. Participants: 144 of 163 eligible physicians agreed to participate, and, of these, 116 were randomly selected to see standardized patients, to complete vignettes, or both. Measurements: Scores, expressed as the percentage of explicit quality criteria correctly completed, were obtained by using 3 methods. Results: Among all physicians, the quality of clinical practice as measured by the standardized patients was 73% correct (95% CI, 72.1% to 73.4%). By using exactly the same criteria, physicians scored 68% (CI, 67.9% to 68.9%) when measured by the vignettes but only 63% (CI, 62.7% to 64.0%) when assessed by medical record abstraction. These findings were consistent across all diseases and were independent of case complexity or physician training level. Vignettes also accurately measured unnecessary care. Finally, vignettes seem to capture the range in the quality of clinical practice among physicians within a site. Limitations: Despite finding variation in the quality of clinical practice, we did not determine whether poorer quality translated into worse health status for patients. In addition, the quality scores are based on measurements from 1 patient-provider interaction. As with all other scoring criteria, vignette criteria must be regularly updated. Conclusions: Vignettes are a valid tool for measuring the quality of clinical practice. They can be used for diverse clinical settings, diseases, physician types, and situations in which case-mix variation is a concern. They are inexpensive and easy to use. Vignettes are particularly useful for comparing quality among and within sites and may be useful for longitudinal evaluations of interventions intended to change clinical practice. C1 Univ Calif San Francisco, Inst Global Hlth, San Francisco Vet Affairs Med Ctr, San Francisco, CA 94105 USA. Calif Pacific Med Ctr, San Francisco, CA USA. Univ Calif Los Angeles, Vet Affairs Greater Los Angeles Healthcare Syst, Los Angeles, CA USA. RAND Corp, Santa Monica, CA USA. Vet Affairs Ctr Study Healthcare Provider Behav, Sepulveda, CA USA. So Calif Permanente Med Grp, Los Angeles, CA 90027 USA. RP Peabody, JW (reprint author), Univ Calif San Francisco, Inst Global Hlth, San Francisco Vet Affairs Med Ctr, 74 New Montgomery,Suite 508, San Francisco, CA 94105 USA. EM peabody@psg.ucsf.edu NR 61 TC 308 Z9 308 U1 3 U2 17 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 16 PY 2004 VL 141 IS 10 BP 771 EP 780 PG 10 WC Medicine, General & Internal SC General & Internal Medicine GA 872KU UT WOS:000225206900004 PM 15545677 ER PT J AU Long, JA Chang, VW Ibrahim, SA Asch, DA AF Long, JA Chang, VW Ibrahim, SA Asch, DA TI Update on the health disparities literature SO ANNALS OF INTERNAL MEDICINE LA English DT Review ID OF-VETERANS-AFFAIRS; RENAL-TRANSPLANTATION; RACIAL-DIFFERENCES; PHYSICAL-ACTIVITY; TRENDS; RACE; MORTALITY; PATIENT; CANCER; CARE C1 Univ Penn, Sch Med, Leonard Davis Inst Hlth Econ, Vet Affairs Ctr Hlth Equ Res & Promot,Vet Affairs, Philadelphia, PA 19104 USA. Univ Pittsburgh, Sch Med, Pittsburgh, PA 15260 USA. Vet Affairs Ctr Hlth Equ Res & Promot, Pittsburgh, PA USA. RP Long, JA (reprint author), Univ Penn, Sch Med, Leonard Davis Inst Hlth Econ, Vet Affairs Ctr Hlth Equ Res & Promot,Vet Affairs, Philadelphia, PA 19104 USA. EM jalong@mail.med.upenn.edu FU NICHD NIH HHS [5-K12-HD-0435901] NR 25 TC 39 Z9 39 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 16 PY 2004 VL 141 IS 10 BP 805 EP 812 PG 8 WC Medicine, General & Internal SC General & Internal Medicine GA 872KU UT WOS:000225206900008 PM 15545681 ER PT J AU Weng, AP Ferrando, AA Lee, W Morris, JR Silverman, LB Sanchez-Irizarry, C Blacklow, SC Look, T Aster, JC AF Weng, AP Ferrando, AA Lee, W Morris, JR Silverman, LB Sanchez-Irizarry, C Blacklow, SC Look, T Aster, JC TI Gain-of-function NOTCH1 mutations occur frequently in human T cell acute lymphoblastic leukemia. SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 British Columbia Canc Agcy, Vancouver, BC V5Z 4E6, Canada. Dana Farber Canc Inst, Dept Pediat, Boston, MA 02115 USA. Brigham & Womens Hosp, Boston, MA 02115 USA. RI Weng, Andrew/I-5015-2014; Ferrando, Adolfo /Q-7026-2016 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 2004 VL 104 IS 11 MA 4 BP 5A EP 5A PN 1 PG 1 WC Hematology SC Hematology GA 871JM UT WOS:000225127500007 ER PT J AU Monti, S Savage, KJ Kutok, JL Feuerhake, F Kurtin, P Mihm, M Wu, B Pasqualucci, L Neuberg, D Aguiar, RCT Dal Cin, P Ladd, C Pinkus, GS Salles, G Harris, NL Dalla-Favera, R Habermann, TM Aster, JC Golub, TR Shipp, MA AF Monti, S Savage, KJ Kutok, JL Feuerhake, F Kurtin, P Mihm, M Wu, B Pasqualucci, L Neuberg, D Aguiar, RCT Dal Cin, P Ladd, C Pinkus, GS Salles, G Harris, NL Dalla-Favera, R Habermann, TM Aster, JC Golub, TR Shipp, MA TI Molecular profiling of diffuse large B-cell lymphoma identifies robust subtypes including one characterized by host inflammatory response. SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Broad Inst, Cambridge, MA USA. Dana Farber Canc Inst, Boston, MA USA. Brigham & Womens Hosp, Boston, MA 02115 USA. Mayo Clin, Rochester, MN USA. Massachusetts Gen Hosp, Boston, MA 02114 USA. Columbia Univ, New York, NY USA. Ctr Hosp Lyon Sud, Lyon, France. NR 0 TC 1 Z9 1 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 2004 VL 104 IS 11 MA 25 BP 11A EP 12A PN 1 PG 2 WC Hematology SC Hematology GA 871JM UT WOS:000225127500028 ER PT J AU Means, RT Dallalio, GA Fleury, TW AF Means, RT Dallalio, GA Fleury, TW TI Effects of hepcidin, ferritin, and iron deprivation on erythroid colony formation in vitro. SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Lexington VA Med Ctr, Med & Res Serv, Lexington, KY USA. Univ Kentucky, Lexington, KY USA. Ralph H Johnson VA Med Ctr, Charleston, SC USA. Med Univ S Carolina, Charleston, SC 29425 USA. RI Means, Robert/A-4454-2008 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 2004 VL 104 IS 11 MA 3704 BP 12B EP 12B PN 2 PG 1 WC Hematology SC Hematology GA 871JO UT WOS:000225127700036 ER PT J AU Wu, WS Xu, D Heinrichs, S Look, AT AF Wu, WS Xu, D Heinrichs, S Look, AT TI Slug plays an essential role in the radioprotection of hematopoietic progenitors in vivo by antagonizing p53-mediated apoptotic pathways. SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA 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 2004 VL 104 IS 11 MA 31 BP 13A EP 13A PN 1 PG 1 WC Hematology SC Hematology GA 871JM UT WOS:000225127500034 ER PT J AU Harada, H Quearry, B Korsmeyer, SJ AF Harada, H Quearry, B Korsmeyer, SJ TI Survival factor stimulates ERK-dependent phosphorylation of BIM inhibiting its association with BAX and pro-apoptotic activity. SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Virginia Commonwealth Univ, Richmond, VA 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 2004 VL 104 IS 11 MA 35 BP 14A EP 14A PN 1 PG 1 WC Hematology SC Hematology GA 871JM UT WOS:000225127500038 ER PT J AU Behler, CM Shade, SB Gregory, K Abrams, DI Volberding, PA AF Behler, CM Shade, SB Gregory, K Abrams, DI Volberding, PA TI Anemia and HIV in the antiretroviral era: Potential significance of testosterone. SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Univ Calif San Francisco, Posit Hlth Program, San Francisco, CA 94143 USA. San Francisco VA Med Ctr, San Francisco, CA 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 2004 VL 104 IS 11 MA 3722 BP 16B EP 16B PN 2 PG 1 WC Hematology SC Hematology GA 871JO UT WOS:000225127700054 ER PT J AU Means, RT Fleury, TW Dallalio, GA Brunson, CY AF Means, RT Fleury, TW Dallalio, GA Brunson, CY TI Placental growth factor concentrations in bone marrow of sickle cell patients. SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Univ Kentucky, Lexington VA Med Ctr, Med & Res Serv, Lexington, KY USA. Med Univ S Carolina, Ralph H Johnson VA Med Ctr, Div Hematol & Oncol, Charleston, SC USA. RI Means, Robert/A-4454-2008 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 2004 VL 104 IS 11 MA 3731 BP 19B EP 19B PN 2 PG 1 WC Hematology SC Hematology GA 871JO UT WOS:000225127700063 ER PT J AU Huntly, BJP Shigematzu, H Deguchi, K Lee, B Mizuno, S Duclos, N Rowan, R Amaral, S Curley, D Williams, IR Akashi, K Gilliland, G AF Huntly, BJP Shigematzu, H Deguchi, K Lee, B Mizuno, S Duclos, N Rowan, R Amaral, S Curley, D Williams, IR Akashi, K Gilliland, G TI MOZ-TIF2, but not BCR-ABL, confers properties of leukemic stem cells to committed murine hematopoietic progenitors. SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Harvard Univ, Brigham & Womens Hosp, Boston, MA 02115 USA. Harvard Univ, Dana Farber Canc Inst, Boston, MA 02115 USA. Emory Univ, Atlanta, GA 30322 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 2004 VL 104 IS 11 MA 62 BP 21A EP 22A PN 1 PG 2 WC Hematology SC Hematology GA 871JM UT WOS:000225127500065 ER PT J AU Heinrichs, S Schoch, C Neuberg, DS Look, AT AF Heinrichs, S Schoch, C Neuberg, DS Look, AT TI HOXB9 is overexpressed in blast cells from a subset of acute myeloid leukemia patients and supports proliferation of AML cell lines. SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Dana Farber Canc Inst, Dept Pediat Oncol, Boston, MA 02115 USA. LMU Grosshadern, Lab Leukemia Diagnost, Munich, Germany. Dana Farber Canc Inst, Dept Biostat Sci, 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 2004 VL 104 IS 11 MA 65 BP 22A EP 22A PN 1 PG 1 WC Hematology SC Hematology GA 871JM UT WOS:000225127500068 ER PT J AU Wu, CJ Krishnamurti, L Kutok, JL Biernacki, M Rogers, SA Antin, JH Ritz, J AF Wu, CJ Krishnamurti, L Kutok, JL Biernacki, M Rogers, SA Antin, JH Ritz, J TI Evidence for ineffective erythropoiesis in patients with severe sickle cell anemia. SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02115 USA. Brigham & Womens Hosp, Dept Med, Boston, MA 02115 USA. Brigham & Womens Hosp, Dept Pathol, Boston, MA 02115 USA. Childrens Hosp Pittsburgh, Div Hematol Oncol, Pittsburgh, PA 15213 USA. BMT, Pittsburgh, PA 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 2004 VL 104 IS 11 MA 105 BP 33A EP 34A PN 1 PG 2 WC Hematology SC Hematology GA 871JM UT WOS:000225127500108 ER PT J AU Li, LQ Greenwald, R Lafuente, EM Tzachanis, D Berezovskaya, A Freeman, GJ Sharpe, AH Boussiotis, VA AF Li, LQ Greenwald, R Lafuente, EM Tzachanis, D Berezovskaya, A Freeman, GJ Sharpe, AH Boussiotis, VA TI Rap1-GTP promotes the generation of regulatory T cells in vivo. SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Dana Farber Canc Inst, Boston, MA 02115 USA. Brigham & Womens Hosp, Boston, MA 02115 USA. Beth Israel Deaconess Med Ctr, Boston, MA 02215 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 2004 VL 104 IS 11 MA 110 BP 35A EP 35A PN 1 PG 1 WC Hematology SC Hematology GA 871JM UT WOS:000225127500113 ER PT J AU Tzachanis, D Berezovskaya, A Lafuente, EM Li, LQ Freeman, GJ Boussiotis, VA AF Tzachanis, D Berezovskaya, A Lafuente, EM Li, LQ Freeman, GJ Boussiotis, VA TI The E3 ubiquitin ligase TRIM36, a transcriptional target of Tob, is expressed in anergic T cells and mediates unresponsiveness through proteolysis of signaling proteins PLC-gamma 1 and PKC-theta. SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Beth Israel Deaconess Med Ctr, Boston, MA 02215 USA. 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 2004 VL 104 IS 11 MA 113 BP 36A EP 36A PN 1 PG 1 WC Hematology SC Hematology GA 871JM UT WOS:000225127500116 ER PT J AU Habermann, TM Weller, E Morrison, VA Cassileth, PA Cohn, J Dakhil, S Gascoyne, RD Woda, B Fisher, R Peterson, BA Horning, SJ AF Habermann, TM Weller, E Morrison, VA Cassileth, PA Cohn, J Dakhil, S Gascoyne, RD Woda, B Fisher, R Peterson, BA Horning, SJ TI Rituximab-CHOP versus CHOP with or without maintenance rituximab in patients 60 years of age or older with diffuse large B-cell lymphoma (DLBCL): An update. SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Mayo Clin, Div Hematol, Rochester, MN USA. Dana Farber Canc Inst, Boston, MA 02115 USA. Univ Minnesota, Minneapolis VA Med Ctr, Minneapolis, MN USA. Univ Miami, Miami, FL 33152 USA. Albert Einstein Canc Ctr, Philadelphia, PA USA. Wichita CCOP, Wichita, KS USA. British Columbia Canc Agcy, Vancouver, BC V5Z 4E6, Canada. Univ Massachusetts, Sch Med, Worcester, MA 01605 USA. Univ Rochester, Rochester, NY 14627 USA. Stanford Univ, Stanford, CA 94305 USA. NR 0 TC 25 Z9 26 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 2004 VL 104 IS 11 MA 127 BP 40A EP 40A PN 1 PG 1 WC Hematology SC Hematology GA 871JM UT WOS:000225127500130 ER PT J AU Cools, J Graux, C Melotte, C Quentmeier, H Ferrando, AA Levine, R Vermeesch, JR Stul, M Dutta, B Boeckx, N Bosly, A Heimann, P Uyttebroeck, A Mentens, N Somers, R MacLeod, RAF Drexler, HG Look, AT Gilliland, DG Michaux, L Vandenberghe, P Wlodarska, W Marynen, P Hagemeijer, A AF Cools, J Graux, C Melotte, C Quentmeier, H Ferrando, AA Levine, R Vermeesch, JR Stul, M Dutta, B Boeckx, N Bosly, A Heimann, P Uyttebroeck, A Mentens, N Somers, R MacLeod, RAF Drexler, HG Look, AT Gilliland, DG Michaux, L Vandenberghe, P Wlodarska, W Marynen, P Hagemeijer, A TI Fusion of NUP214 to ABL1 on amplified extrachromosomal elements in T-ALL. SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Univ Leuven, Dept Human Genet, Louvain, 02115, Belgium. Flanders Interuniv Inst Biotechnol VIB, Louvain, 02115, Belgium. Univ Leuven, Dept Hematol, Louvain, Belgium. Deutsch Sammlung Mikroorganism Zellkultur GmbH, German collect Microorganisms & Cell Cultures, B-1050 Braunschweig, Germany. Harvard Univ, Sch Med, Dana Farber Canc Inst, Boston, MA USA. Harvard Univ, Sch Med, Brigham & Womens Hosp, Div Hematol, Boston, MA 02115 USA. Clin Univ UCL Mont Godinne, Dept Hematol, Yvoir, Belgium. Free Univ Brussels, Erasme Hosp, Dept Med Genet, Brussels, Belgium. Univ Leuven, Dept Pediat Hemato Oncol, Louvain, Belgium. Howard Hughes Med Inst, 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 2004 VL 104 IS 11 MA 141 BP 43A EP 44A PN 1 PG 2 WC Hematology SC Hematology GA 871JM UT WOS:000225127500144 ER PT J AU Huang, ZW Kumar, S Choi, WT Madani, N Dong, CZ Liu, DX Wang, J An, J Sodroski, JG AF Huang, ZW Kumar, S Choi, WT Madani, N Dong, CZ Liu, DX Wang, J An, J Sodroski, JG TI A new class of chemokine analogs as useful research tools to study chemokine receptor function and promising therapeutic agents. SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Raylight Int, Chemokine Pharmaceut Inc, Drug Discovery Div, La Jolla, CA USA. Univ Illinois, Dept Biochem, Urbana, IL 61801 USA. Burnham Inst, Ctr Canc, La Jolla, CA 92037 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 2004 VL 104 IS 11 MA 3839 BP 47B EP 47B PN 2 PG 1 WC Hematology SC Hematology GA 871JO UT WOS:000225127700171 ER PT J AU Wilson, WH Dunleavy, K Pittaluga, S Grant, N Steinberg, S Raffeld, M Chabner, B Grossbard, M Jaffe, E Staudt, L Janik, J AF Wilson, WH Dunleavy, K Pittaluga, S Grant, N Steinberg, S Raffeld, M Chabner, B Grossbard, M Jaffe, E Staudt, L Janik, J TI Dose-adjusted EPOCH-rituximab is highly effective in the GCB and ABC subtypes of untreated diffuse large B-cell lymphoma. SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Natl Canc Inst, Ctr Canc Res, Bethesda, MD USA. Harvard Univ, Massachusetts Gen Hosp, Boston, MA 02115 USA. St Lukes Roosevelt Hosp, New York, NY 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 2004 VL 104 IS 11 MA 159 BP 49A EP 49A PN 1 PG 1 WC Hematology SC Hematology GA 871JM UT WOS:000225127500162 ER PT J AU Boggon, TJ Li, YQ Eck, MJ AF Boggon, TJ Li, YQ Eck, MJ TI Structural analysis of Janus kinases. SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Dana Farber Canc Inst, Boston, MA 02115 USA. Harvard Univ, 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 2004 VL 104 IS 11 MA 3863 BP 53B EP 53B PN 2 PG 1 WC Hematology SC Hematology GA 871JO UT WOS:000225127700195 ER PT J AU Rizouli, V Zahrieh, D Gorgun, G Holderried, TAW Croce, C Gribben, JG AF Rizouli, V Zahrieh, D Gorgun, G Holderried, TAW Croce, C Gribben, JG TI Gene expression profiling identifies similar CD4(+) and CD8(+) T cell defects in TCL1 transgenic mice after development of CLL to those observed in patients with CLL. SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Harvard Univ, Sch Med, Dana Farber Canc Inst, CLL Res Consortium, Boston, MA 02115 USA. Thomas Jefferson Univ, Philadelphia, PA 19107 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 2004 VL 104 IS 11 MA 180 BP 55A EP 55A PN 1 PG 1 WC Hematology SC Hematology GA 871JM UT WOS:000225127500183 ER PT J AU Alyea, EP Li, SL Kim, H Ho, VT Cutler, C Lee, SJ Gribben, J Stone, RM DeAngelo, DJ Ritz, J Antin, JH Soiffer, RJ AF Alyea, EP Li, SL Kim, H Ho, VT Cutler, C Lee, SJ Gribben, J Stone, RM DeAngelo, DJ Ritz, J Antin, JH Soiffer, RJ TI High levels of donor chimerism early after non-myeloablative transplantation predictive of overall and progression free survival but not risk of acute graft versus host disease for patients with AML or MDS. SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Dana Farber Canc Inst, Boston, MA 02115 USA. Brigham & Womens Hosp, 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 2004 VL 104 IS 11 MA 185 BP 57A EP 57A PN 1 PG 1 WC Hematology SC Hematology GA 871JM UT WOS:000225127500188 ER PT J AU Liu, TX Becker, M Hsu, K Jelinek, J Deng, M Bloomfield, C Issa, JP Clarke, MF Look, AT AF Liu, TX Becker, M Hsu, K Jelinek, J Deng, M Bloomfield, C Issa, JP Clarke, MF Look, AT TI Epigenetic suppression of the CTNNA1 gene, encoding the alpha-catenin protein, which is located in the 5q31 critical deleted region in malignant myeloid disorders with del(5q). SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Dana Farber Canc Inst, Boston, MA 02115 USA. Univ Michigan, Ann Arbor, MI 48109 USA. MD Anderson Canc Ctr, Sect Acute Leukemias, Houston, TX USA. RI Jelinek, Jaroslav/A-8476-2008; Jelinek, Jaroslav/D-2282-2012 OI Jelinek, Jaroslav/0000-0002-2533-0220 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 2004 VL 104 IS 11 MA 203 BP 62A EP 62A PN 1 PG 1 WC Hematology SC Hematology GA 871JM UT WOS:000225127500206 ER PT J AU Rajkumar, SV Blood, E Vesole, DH Shepard, R Greipp, PR AF Rajkumar, SV Blood, E Vesole, DH Shepard, R Greipp, PR TI Thalidomide plus dexamethasone versus dexamethasone alone in newly diagnosed multiple myeloma (E1AOO): Results of a phase III trial coordinated by the eastern cooperative oncology group. SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Mayo Clin, Div Hematol, Rochester, MN USA. Dana Farber Canc Inst, Dept Biostat, Boston, MA 02115 USA. Med Coll Wisconsin, Div Hematol Oncol, Milwaukee, WI 53226 USA. Univ Virginia, Div Hematol Oncol, Charlottesville, VA USA. NR 0 TC 19 Z9 19 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 2004 VL 104 IS 11 MA 205 BP 63A EP 63A PN 1 PG 1 WC Hematology SC Hematology GA 871JM UT WOS:000225127500208 ER PT J AU Han, ZC Li, ZJ Wang, ZZ Zheng, YZ Xu, B Yang, RC Scadden, DT AF Han, ZC Li, ZJ Wang, ZZ Zheng, YZ Xu, B Yang, RC Scadden, DT TI Unique expression of platelet endothelial cell adhesion molecule-1 (PECAM-1/CD31) on embryonic stem cells. SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 PUMC, Tianjin, Peoples R China. CAMS, State Key Lab Expt Hematol, Inst Hematol, Tianjin, Peoples R China. CAMS, Blood Dis Hosp, Tianjin, Peoples R China. Harvard Univ, Sch Med, Massachusetts Gen Hosp, Ctr Regenerat 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 2004 VL 104 IS 11 MA 3914 BP 65B EP 65B PN 2 PG 1 WC Hematology SC Hematology GA 871JO UT WOS:000225127700246 ER PT J AU Iwasaki, H Arinobu, Y Mizuno, S Shigematsu, H Takatsu, K Tenen, DG Akashi, K AF Iwasaki, H Arinobu, Y Mizuno, S Shigematsu, H Takatsu, K Tenen, DG Akashi, K TI The ordered expression of transcription factors directs hierarchical lineage specification of eosinophils, basophils and mast cells. SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Dana Farber Canc Inst, Dept Canc Immunol & AIDS, Boston, MA 02115 USA. Harvard Univ, Sch Med, Boston, MA USA. Univ Tokyo, Inst Med Sci, Div Immunol, Dept Microbiol & Immunol, Tokyo, Japan. Harvard Univ, Sch Med, Harvard Inst Med, 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 2004 VL 104 IS 11 MA 224 BP 68A EP 68A PN 1 PG 1 WC Hematology SC Hematology GA 871JM UT WOS:000225127500227 ER PT J AU Wang, Y Yates, F Dikovskaia, E Ernst, P Davidson, AJ Zon, LI Daley, GQ AF Wang, Y Yates, F Dikovskaia, E Ernst, P Davidson, AJ Zon, LI Daley, GQ TI Derivation of hematopoietic stem cells from embryonic stem cells. SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Harvard Univ, Sch Med, Childrens Hosp, Boston, MA USA. Harvard Univ, Sch Med, Dept Biol Chem & Mol Pharmacol, Boston, MA USA. Dana Farber Canc Inst, Howard Hughes Med Inst, Boston, MA 02115 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 2004 VL 104 IS 11 MA 223 BP 68A EP 68A PN 1 PG 1 WC Hematology SC Hematology GA 871JM UT WOS:000225127500226 ER PT J AU Growney, JD Shigematsu, H Li, Z Lee, BH Adelsperger, J Rowan, R Curley, DP Akashi, K Williams, IR Speck, NA Gilliland, DG AF Growney, JD Shigematsu, H Li, Z Lee, BH Adelsperger, J Rowan, R Curley, DP Akashi, K Williams, IR Speck, NA Gilliland, DG TI Loss of Runx1 perturbs adult hematopoiesis and is associated with a myeloproliferative phenotype. SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Brigham & Womens Hosp, Div Hematol, Boston, MA 02115 USA. Dana Farber Canc Inst, Boston, MA 02115 USA. Dartmouth Coll Sch Med, Dept Biochem, Hanover, NH USA. Brigham & Womens Hosp, Dept Pathol, Boston, MA 02115 USA. Emory Univ, Atlanta, GA 30322 USA. Harvard Univ, Sch Med, Howard Hughes Med 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 2004 VL 104 IS 11 MA 227 BP 69A EP 69A PN 1 PG 1 WC Hematology SC Hematology GA 871JM UT WOS:000225127500230 ER PT J AU Lee, SJ Sullivan, AM Back, AL Block, SD Goldman, R Tulsky, JA Alexander, SC Kirkpatrick, T Stewart, SK Weeks, JC AF Lee, SJ Sullivan, AM Back, AL Block, SD Goldman, R Tulsky, JA Alexander, SC Kirkpatrick, T Stewart, SK Weeks, JC TI Patient-physician communication about hematologic malignancies. SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Dana Farber Canc Inst, Boston, MA 02115 USA. Univ Washington, Seattle, WA 98195 USA. Brown Univ, Providence, RI 02912 USA. VA & Duke Univ, Durham, NC USA. Blood & Marrow Transplant Informat Network, Highland Pk, IL 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 2004 VL 104 IS 11 MA 230 BP 69A EP 70A PN 1 PG 2 WC Hematology SC Hematology GA 871JM UT WOS:000225127500233 ER PT J AU Feuerhake, F Kutok, JL Monti, S Cattoretti, G Kurtin, P Pinkus, GS de Leval, L Harris, NL Savage, KJ Habermann, TM Dalla-Favera, R Golub, TR Aster, JC Shipp, MA AF Feuerhake, F Kutok, JL Monti, S Cattoretti, G Kurtin, P Pinkus, GS de Leval, L Harris, NL Savage, KJ Habermann, TM Dalla-Favera, R Golub, TR Aster, JC Shipp, MA TI NF kappa B activation in primary mediastinal large B-cell lymphoma: Nuclear localization of c-REL and coordinate Upregulation of NF kappa B target genes. SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Dana Farber Canc Inst, Boston, MA 02115 USA. Brigham & Womens Hosp, Boston, MA 02115 USA. Broad Inst, Cambridge, MA USA. Columbia Univ, Inst Canc Genet, New York, NY USA. Mayo Clin, Rochester, MN USA. Massachusetts Gen Hosp, Boston, MA 02114 USA. RI Cattoretti, Giorgio/H-2340-2011 NR 0 TC 0 Z9 0 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 2004 VL 104 IS 11 MA 243 BP 73A EP 73A PN 1 PG 1 WC Hematology SC Hematology GA 871JM UT WOS:000225127500246 ER PT J AU Giles, F Schiffer, C Kantarjian, H Fischer, T Paquette, R Pelov, DM Resta, DJ Cohen, PS Wang, YF Stone, R AF Giles, F Schiffer, C Kantarjian, H Fischer, T Paquette, R Pelov, DM Resta, DJ Cohen, PS Wang, YF Stone, R TI Phase 1 study of PKC412, an oral FLT3 kinase inhibitor, in sequential and concomitant combinations with daunorubicin and cytarabine (DA) induction and high-dose cytarabine (HDAra-C) consolidation in newly diagnosed patients with AML SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 MD Anderson Canc Ctr, Houston, TX USA. Barbara Ann Karmanos Canc Inst, Div Hematol & Oncol, Detroit, MI USA. Univ Mainz, Dept Med 3, D-6500 Mainz, Germany. Univ Calif Los Angeles, Dept Med, Los Angeles, CA 90024 USA. Dana Farber Canc Ctr, Boston, MA USA. Novartis Oncol, E Hanover, NJ 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 2004 VL 104 IS 11 MA 262 BP 78A EP 78A PN 1 PG 1 WC Hematology SC Hematology GA 871JM UT WOS:000225127500264 ER PT J AU Wadleigh, M Kirkpatrick, T Gonzales, A Levine, R Gilliland, DG Lee, SJ AF Wadleigh, M Kirkpatrick, T Gonzales, A Levine, R Gilliland, DG Lee, SJ TI Creating a national cohort of myeloproliferative disorders using the Internet: A feasibility study SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 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 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 2004 VL 104 IS 11 MA 270 BP 80A EP 81A PN 1 PG 2 WC Hematology SC Hematology GA 871JM UT WOS:000225127500272 ER PT J AU Mitsiades, CS Rouleau, C Menon, K Teicher, B Iacobelli, M Anderson, KC Richardson, PG AF Mitsiades, CS Rouleau, C Menon, K Teicher, B Iacobelli, M Anderson, KC Richardson, PG TI Defibrotide (DF) targets tumor-microenvironmental interactions and sensitizes multiple myeloma and solid tumor cells to cytotoxic chemotherapeutics SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Dana Farber Canc Inst, Jerome Lipper Multiple Myeloma Ctr, Dept Med Oncol, Boston, MA 02115 USA. Harvard Univ, Sch Med, Dept Med, Boston, MA USA. Gentium SpA, Como, Italy. 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 2004 VL 104 IS 11 MA 286 BP 85A EP 85A PN 1 PG 1 WC Hematology SC Hematology GA 871JM UT WOS:000225127500288 ER PT J AU Shringarpure, R Bhole, D Burger, R Catley, L Podar, K Tai, YT Hideshima, T Mitsiades, C Munshi, NC Chauhan, D Anderson, KC AF Shringarpure, R Bhole, D Burger, R Catley, L Podar, K Tai, YT Hideshima, T Mitsiades, C Munshi, NC Chauhan, D Anderson, KC TI Increased TCF-4 expression correlates with reduced caspase-3 induction and confers resistance to Bortezomib SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Harvard Univ, Sch Med, Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02115 USA. Harvard Univ, Sch Med, Dept Med, Boston, MA USA. Harvard Univ, Sch Med, Brigham & Womens Hosp, Dept Anesthesia,CET & RI, 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 2004 VL 104 IS 11 MA 285 BP 85A EP 85A PN 1 PG 1 WC Hematology SC Hematology GA 871JM UT WOS:000225127500287 ER PT J AU Miklos, DB Miller, KH Kim, HT Lee, SJ Alyea, EP Cutler, C Antin, JH Soiffer, RJ Ritz, J AF Miklos, DB Miller, KH Kim, HT Lee, SJ Alyea, EP Cutler, C Antin, JH Soiffer, RJ Ritz, J TI Allogeneic B cell response to H-Y minor histocompatibility antigens after donor lymphocyte infusion correlates with disease response SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Stanford Univ, Sch Med, Stanford, CA 94305 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 2004 VL 104 IS 11 MA 296 BP 88A EP 88A PN 1 PG 1 WC Hematology SC Hematology GA 871JM UT WOS:000225127500298 ER PT J AU Alyea, EP Kim, H Cutler, C Ho, VT Gribben, J DeAngelo, DJ Lee, SJ Windawi, S Stone, R Ritz, J Antin, JH Robert, RJ AF Alyea, EP Kim, H Cutler, C Ho, VT Gribben, J DeAngelo, DJ Lee, SJ Windawi, S Stone, R Ritz, J Antin, JH Robert, RJ TI Similar outcome of non-myeloablative and myeloablative allogeneic hematopoietic cell transplantation for patients greater than fifty years of age. SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Dana Farber Canc Inst, Boston, MA 02115 USA. Brigham & Womens Hosp, 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 2004 VL 104 IS 11 MA 300 BP 89A EP 89A PN 1 PG 1 WC Hematology SC Hematology GA 871JM UT WOS:000225127500302 ER PT J AU Li, LQ Godfrey, WR Porter, SB Ge, Y June, CH Blazar, BR Boussiotis, VA AF Li, LQ Godfrey, WR Porter, SB Ge, Y June, CH Blazar, BR Boussiotis, VA TI CD4(+)CD25(+) regulatory T cells from cord blood have functional and molecular properties of T cell anergy. SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Dana Farber Canc Inst, Boston, MA USA. Univ Minnesota, Minneapolis, MN USA. Univ Penn, Ctr Canc, Philadelphia, PA 19104 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 2004 VL 104 IS 11 MA 316 BP 94A EP 94A PN 1 PG 1 WC Hematology SC Hematology GA 871JM UT WOS:000225127500318 ER PT J AU Zhou, JB Li, AH Goldwasser, MA Wang, HJ Dalton, V Lyons, C McBride, KD Sallan, SE Silverman, LB Gribben, JG AF Zhou, JB Li, AH Goldwasser, MA Wang, HJ Dalton, V Lyons, C McBride, KD Sallan, SE Silverman, LB Gribben, JG TI Quantitative analysis of minimal residual disease at the completion of induction therapy predicts relapse in children with B-lineage acute lymphoblastic leukemia in DFCI ALL consortium protocol 95-01. SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Dana Farber Canc Inst, Boston, MA 02115 USA. Childrens Hosp, 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 2004 VL 104 IS 11 MA 323 BP 96A EP 96A PN 1 PG 1 WC Hematology SC Hematology GA 871JM UT WOS:000225127500325 ER PT J AU Bergmeier, W Crittenden, JR Piffath, CL Wagner, DD Housman, DE Graybiel, AM AF Bergmeier, W Crittenden, JR Piffath, CL Wagner, DD Housman, DE Graybiel, AM TI CalDAG-GEFI is a key signal integrator in platelet activation and thrombus formation SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Harvard Univ, Sch Med, CBR Inst Biomed Res, Boston, MA 02115 USA. Harvard Univ, Sch Med, Dept Pathol, Boston, MA 02115 USA. MIT, Dept Brain & Cognit Sci, Cambridge, MA USA. MIT, McGovern Inst Brain Res, Cambridge, MA USA. MIT, Ctr Canc Res, Cambridge, MA 02139 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 2004 VL 104 IS 11 MA 326 BP 97A EP 97A PN 1 PG 1 WC Hematology SC Hematology GA 871JM UT WOS:000225127500328 ER PT J AU Springer, TA Takagi, J Coller, BS Wang, JH Xiao, T AF Springer, TA Takagi, J Coller, BS Wang, JH Xiao, T TI Crystal structure of the integrin alpha IIB beta 3 headpiece at 2.7-3.1 angstrom: Structure, mechanisms of activation and ligand binding, inhibition by eptifibatide, tirofiban, and mAb 10E5, and structure of the HPA-1 alloantigen epitope. SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Harvard Univ, Sch Med, CBR Inst Biomed Res, Boston, MA 02115 USA. Rockefeller Univ, Lab Blood & Vasc Biol, New York, NY 10021 USA. Dana Farber Canc Inst, Boston, MA 02115 USA. RI Xiao, Tsan/A-8590-2010; Xiao, Tsan/I-7616-2013 OI Xiao, Tsan/0000-0001-9688-475X 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 2004 VL 104 IS 11 MA 327 BP 97A EP 97A PN 1 PG 1 WC Hematology SC Hematology GA 871JM UT WOS:000225127500329 ER PT J AU Richardson, PG Chanan-Khan, A Schlossman, RL Munshi, NC Wen, P Briemberg, H Kuter, D Oaklander, AL Lonial, S Hassoun, H Doss, D Colson, K McKenney, M Hande, K Koryzna, A Stoklas, B Lunde, L Gorelik, S McAlister, C Freeman, A Warren, D Collins, D Esseltine, D Amato, A Anderson, KC AF Richardson, PG Chanan-Khan, A Schlossman, RL Munshi, NC Wen, P Briemberg, H Kuter, D Oaklander, AL Lonial, S Hassoun, H Doss, D Colson, K McKenney, M Hande, K Koryzna, A Stoklas, B Lunde, L Gorelik, S McAlister, C Freeman, A Warren, D Collins, D Esseltine, D Amato, A Anderson, KC TI Phase II trial of single agent bortezomib (VELCADE (R)) in patients with previously untreated multiple myeloma (MM) SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Dana Farber Canc Inst, Jerome Lipper Multiple Myeloma Ctr, Boston, MA 02115 USA. Brigham & Womens Hosp, Boston, MA 02115 USA. Roswell Pk Canc Inst, Buffalo, NY 14263 USA. Massachusetts Gen Hosp, Boston, MA 02114 USA. Emory Univ, Atlanta, GA 30322 USA. Mem Sloan Kettering Canc Ctr, New York, NY 10021 USA. Millennium Pharmaceut Inc, Cambridge, MA USA. NR 0 TC 21 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 2004 VL 104 IS 11 MA 336 BP 100A EP 100A PN 1 PG 1 WC Hematology SC Hematology GA 871JM UT WOS:000225127500338 ER PT J AU Rosenbauer, F Steidl, U Owens, B Clayton, L Wagner, K Kutok, JL Le Beau, MM Tenen, DG AF Rosenbauer, F Steidl, U Owens, B Clayton, L Wagner, K Kutok, JL Le Beau, MM Tenen, DG TI Deletion of a key PU.1 gene regulatory element induces T-Cell lymphoma SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Harvard Univ, Inst Med, Dana Farber Canc Inst, Boston, MA 02115 USA. Brigham & Womens Hosp, Boston, MA 02115 USA. Univ Chicago, Chicago, IL 60637 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 2004 VL 104 IS 11 MA 344 BP 102A EP 102A PN 1 PG 1 WC Hematology SC Hematology GA 871JM UT WOS:000225127500346 ER PT J AU Richardson, PG Soiffer, RJ Antin, JH Voss, SD Jin, Z Kurtzberg, J Martin, PL Hockenbery, D Murray, KF Vogelsang, GB Chen, A Krishnan, A Kernan, NA Avigan, D Spitzer, TR Iannone, R Giralt, S Warren, D Momtaz, P Bradwin, G Iacobelli, M McDonald, GB Guinan, EC AF Richardson, PG Soiffer, RJ Antin, JH Voss, SD Jin, Z Kurtzberg, J Martin, PL Hockenbery, D Murray, KF Vogelsang, GB Chen, A Krishnan, A Kernan, NA Avigan, D Spitzer, TR Iannone, R Giralt, S Warren, D Momtaz, P Bradwin, G Iacobelli, M McDonald, GB Guinan, EC TI Defibrotide (DF) for the treatment of severe veno-occlusive disease (VOD) and multi-system organ failure (MOF) post SCT: Final results of a phase II, multicenter, randomized study and preliminary analyses of surrogate markers and ultrasound findings SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Dana Farber Canc Inst, BIDMC, Mass Gen Childrens Hosp, Boston, MA 02115 USA. Columbia Univ, New York, NY USA. Duke Univ, Ctr Med, Durham, NC 27706 USA. Johns Hopkins Oncol Ctr, Baltimore, MD USA. Fred Hutchinson Canc Res Ctr, Seattle, WA 98104 USA. City Hope Canc Ctr, Duarte, CA USA. Mem Sloan Kettering Canc Ctr, Bronx, NY USA. Univ Texas, MD Anderson Canc Ctr, Houston, TX 77030 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 2004 VL 104 IS 11 MA 350 BP 103A EP 104A PN 1 PG 2 WC Hematology SC Hematology GA 871JM UT WOS:000225127500352 ER PT J AU Cutler, C Li, SL Kim, HT Laglenne, P Ford, C Ho, V Lee, SJ Alyea, E Soiffer, R Antin, JH Sonis, S AF Cutler, C Li, SL Kim, HT Laglenne, P Ford, C Ho, V Lee, SJ Alyea, E Soiffer, R Antin, JH Sonis, S TI Oral mucositis incidence and severity after methotrexate and non-methotrexate containing GVHD prophylaxis regimens SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Dana Farber Canc Inst, Boston, MA 02115 USA. Brigham & Womens Hosp, Boston, MA 02115 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 2004 VL 104 IS 11 MA 351 BP 104A EP 104A PN 1 PG 1 WC Hematology SC Hematology GA 871JM UT WOS:000225127500353 ER PT J AU Yanik, GA Levine, JE Ferrara, JLM Uberti, JP Ho, VT Antin, JH Cooke, KR AF Yanik, GA Levine, JE Ferrara, JLM Uberti, JP Ho, VT Antin, JH Cooke, KR TI Survival following etanercept therapy for the treatment of Idiopathic Pneumonia Syndrome post allogeneic stem cell transplantation SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Univ Michigan, Blood & Marrow Transplantat Program, Ann Arbor, MI 48109 USA. Dana Farber Canc Inst, Dept Adult Oncol, 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 2004 VL 104 IS 11 MA 354 BP 104A EP 105A PN 1 PG 2 WC Hematology SC Hematology GA 871JM UT WOS:000225127500356 ER PT J AU Richardson, P Sonneveld, P Schuster, M Irwin, D Stadtmauer, E Facon, T Harousseau, J Ben-Yehuda, D Lonial, S Goldschmidt, H Reece, D Miguel, JS Blade, J Boccadoro, M Cavenagh, J Dalton, W Boral, A Schenkein, D Anderson, K AF Richardson, P Sonneveld, P Schuster, M Irwin, D Stadtmauer, E Facon, T Harousseau, J Ben-Yehuda, D Lonial, S Goldschmidt, H Reece, D Miguel, JS Blade, J Boccadoro, M Cavenagh, J Dalton, W Boral, A Schenkein, D Anderson, K TI Bortezomib demonstrates superior efficacy to high-dose dexamethasone in relapsed multiple myeloma: Final report of the APEX study SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Dana Farber Canc Inst, Boston, MA 02115 USA. Univ Rotterdam Hosp, Rotterdam, Netherlands. NY Presbyterian Hosp, New York, NY USA. Univ Penn, Ctr Canc, Philadelphia, PA 19104 USA. Hadassah Univ Hosp, IL-91120 Jerusalem, Israel. Emory Univ, Atlanta, GA 30322 USA. Univ Heidelberg, Heidelberg, Germany. Princess Margaret Hosp, Toronto, ON M4X 1K9, Canada. Hosp Univ Salamanca, Salamanca, Spain. Univ Barcelona, Barcelona, Spain. Univ Turin, Turin, Italy. St Bartholomews Hosp, London, England. H Lee Moffitt Canc Ctr & Res Inst, Tampa, FL USA. RI FACON, THIERRY/M-9736-2014 OI FACON, THIERRY/0000-0001-7705-8460 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 2004 VL 104 IS 11 MA 366.5 BP 108A EP 108A PN 1 PG 1 WC Hematology SC Hematology GA 871JM UT WOS:000225127500369 ER PT J AU Shigematsu, H Iwasaki, H Mizuno, S Sternberg, DW Huntly, BJP Gilliland, DG Akashi, K AF Shigematsu, H Iwasaki, H Mizuno, S Sternberg, DW Huntly, BJP Gilliland, DG Akashi, K TI TEL/PDGF beta R trosine kinase fusion specifically activates myeloid differentiation programs, and converts lymphoid progenitors into the myeloid lineage. SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Harvard Univ, Sch Med, Dana Farber Canc Inst, Dept Canc Immunol & AIDS, Boston, MA 02115 USA. Mt Sinai Sch Med, Dept Hematol Oncol, New York, NY 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 2004 VL 104 IS 11 MA 387 BP 114A EP 114A PN 1 PG 1 WC Hematology SC Hematology GA 871JM UT WOS:000225127500390 ER PT J AU Gu, TL Tam, WF Chen, J Lee, BH Wang, AZ Cooper, MR Monti, S Golub, T Gilliland, GD AF Gu, TL Tam, WF Chen, J Lee, BH Wang, AZ Cooper, MR Monti, S Golub, T Gilliland, GD TI Oncogenic tyrosine kinases regulate proliferative and survival signals through activation of Id1. SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Brigham & Womens Hosp, Div Hematol, Boston, MA 02115 USA. Harvard Univ, Sch Med, Howard Hughes Med Inst, Boston, MA 02115 USA. Harvard Univ, Sch Med, Boston, MA USA. Millennium Pharmaceut Inc, Cambridge, MA USA. Harvard Univ, Ctr Genome Res, Cambridge, MA USA. Broad Inst MIT, Cambridge, 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 2004 VL 104 IS 11 MA 417 BP 122A EP 122A PN 1 PG 1 WC Hematology SC Hematology GA 871JM UT WOS:000225127500420 ER PT J AU Palomero, T Odom, DT O'Neil, J Ferrando, AA Winter, SS Larson, RS Young, RA Look, AT AF Palomero, T Odom, DT O'Neil, J Ferrando, AA Winter, SS Larson, RS Young, RA Look, AT TI Genome-wide transcriptional regulatory networks downstream of TAL1/SCL in T-cell acute lymphoblastic leukemia. SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Dana Farber Canc Inst, Boston, MA 02115 USA. Whitehead Inst Biomed Res, Cambridge, MA 02142 USA. Univ New Mexico, Hlth Sci Ctr, Albuquerque, NM USA. Univ New Mexico, Sch Med, Dept Pathol, Albuquerque, NM 87131 USA. RI Young, Richard/F-6495-2012 OI Young, Richard/0000-0001-8855-8647 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 2004 VL 104 IS 11 MA 416 BP 122A EP 122A PN 1 PG 1 WC Hematology SC Hematology GA 871JM UT WOS:000225127500419 ER PT J AU DeAngelo, DJ Alyea, EP Borrello, IM Levitsky, HI Stock, W Sher, D Damon, LE Linker, CA Donnelly, A Hege, KM AF DeAngelo, DJ Alyea, EP Borrello, IM Levitsky, HI Stock, W Sher, D Damon, LE Linker, CA Donnelly, A Hege, KM TI Posttransplant immunotherapy with a GM-CSF-based tumor vaccine (GVAX (R)) following autologous stem cell transplant (ASCT) for acute myeloid leukemia (AML) SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Dana Farber Canc Inst, Partners Canc Ctr, Boston, MA 02115 USA. Johns Hopkins Univ, Baltimore, MD 21218 USA. Univ Chicago, Chicago, IL 60637 USA. Univ Calif San Francisco, San Francisco, CA 94143 USA. Cell Genesys, 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 2004 VL 104 IS 11 MA 441 BP 129A EP 129A PN 1 PG 1 WC Hematology SC Hematology GA 871JM UT WOS:000225127500444 ER PT J AU Vianello, F Papeta, N Kircher, MF Toner, M Weissleder, R Irimia, D Poznansky, MC AF Vianello, F Papeta, N Kircher, MF Toner, M Weissleder, R Irimia, D Poznansky, MC TI Murine melanomas expressing high levels of SDF-1 repel and escape control by tumor specific T-cells SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Massachusetts Gen Hosp, AIDS Res & Canc Ctr, Charlestown, MA USA. Massachusetts Gen Hosp, Ctr Mol Imaging Res, Charlestown, MA USA. Massachusetts Gen Hosp, Ctr Engn Med, Charlestown, MA USA. RI Vianello, Fabrizio/M-5211-2016 OI Vianello, Fabrizio/0000-0002-7174-4651 NR 0 TC 0 Z9 0 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 2004 VL 104 IS 11 MA 445 BP 130A EP 130A PN 1 PG 1 WC Hematology SC Hematology GA 871JM UT WOS:000225127500448 ER PT J AU Heidel, F Breitenbuecher, F Kindler, T Solem, FK Carius, B Thiede, HM Cohen, PS Roesel, J Estey, EH Feldman, E Ehninger, G Schiller, GJ Klimek, V Nimer, S DeAngelo, D Giles, F Stone, RM Huber, C Fischer, T AF Heidel, F Breitenbuecher, F Kindler, T Solem, FK Carius, B Thiede, HM Cohen, PS Roesel, J Estey, EH Feldman, E Ehninger, G Schiller, GJ Klimek, V Nimer, S DeAngelo, D Giles, F Stone, RM Huber, C Fischer, T TI Mechanisms of resistance to the FLT3-tyrosine kinase inhibitor PKC412 in patients with AML SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Univ Mainz, D-6500 Mainz, Germany. Univ Carl Gustav Carus, Dresden, Germany. Novartis Oncol, Florham Pk, NJ USA. Novartis Pharma, Basel, Switzerland. Univ Texas, MD Anderson Canc Ctr, Houston, TX 77030 USA. Cornell Univ, Ctr Canc, New York, NY 14853 USA. Univ Calif Los Angeles, Med Ctr, Los Angeles, CA 90024 USA. MSKCC, New York, NY USA. Dana Farber Canc Ctr, Boston, MA USA. NR 0 TC 6 Z9 6 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 2004 VL 104 IS 11 MA 454 BP 133A EP 133A PN 1 PG 1 WC Hematology SC Hematology GA 871JM UT WOS:000225127500457 ER PT J AU Li, Z Godinho, F Garriga-Canut, M Yu, CN Orkin, SH AF Li, Z Godinho, F Garriga-Canut, M Yu, CN Orkin, SH TI Developmental stage-selective effect of somatically mutated GATA-1 in Down syndrome AML M7 - A potential basis for transient myeloproliferative disorder SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA 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 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 2004 VL 104 IS 11 MA 463 BP 135A EP 135A PN 1 PG 1 WC Hematology SC Hematology GA 871JM UT WOS:000225127500466 ER PT J AU Berkofsky-Fessler, WD McConnell, MJ Neuberg, DS Licht, JD AF Berkofsky-Fessler, WD McConnell, MJ Neuberg, DS Licht, JD TI Identification of genes affected during myeloid differentiation induced by valproic acid and retinoic acid: The choice of array pre-processing and normalization algorithm has a critical effect on results SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 CUNY Mt Sinai Sch Med, Div Hematol Oncol, Dept Med, New York, NY 10029 USA. Dana Farber Canc Inst, Dept Biostat Sci, 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 2004 VL 104 IS 11 MA 4207 BP 138B EP 138B PN 2 PG 1 WC Hematology SC Hematology GA 871JO UT WOS:000225127700536 ER PT J AU Byrd, JC Gribben, JG Peterson, B Grever, MR Lozanski, G Lucas, DM Larson, RA Caligiuri, MA Heerema, NA AF Byrd, JC Gribben, JG Peterson, B Grever, MR Lozanski, G Lucas, DM Larson, RA Caligiuri, MA Heerema, NA TI Select high risk genetic features predict earlier progression following chemoimmunotherapy with fludarabine and rituximab in chronic lymphocytic leukemia (CLL): Preliminary justification for risk-adapted therapy. SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Ohio State Univ, Columbus, OH 43210 USA. Dana Farber Canc Inst, Boston, MA 02115 USA. Duke Univ, Med Ctr, Durham, NC 27706 USA. Univ Chicago, Chicago, IL 60637 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 2004 VL 104 IS 11 MA 476 BP 139A EP 139A PN 1 PG 1 WC Hematology SC Hematology GA 871JM UT WOS:000225127500479 ER PT J AU Luo, HY Mang, D Patrinos, GP Wu, CJY Eung, SH Pourfarzad, F Whitacre, J Rosenfield, CG Daoust, PR Braun, A Grosveld, FG Steinberg, MH Chui, DHK AF Luo, HY Mang, D Patrinos, GP Wu, CJY Eung, SH Pourfarzad, F Whitacre, J Rosenfield, CG Daoust, PR Braun, A Grosveld, FG Steinberg, MH Chui, DHK TI A mutation in a GATA-1 binding site 5 ' to the (G)gamma-globin gene (nt-567, T > G) may be associated with increased levels of fetal hemoglobin. SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Boston Univ, Sch Med, Boston, MA 02215 USA. Dana Farber Canc Inst, Boston, MA 02115 USA. Tufts Univ, New England Med Ctr, Boston, MA 02111 USA. Erasmus Univ, Rotterdam, Netherlands. Sequenom Inc, San Diego, CA 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 2004 VL 104 IS 11 MA 500 BP 145A EP 146A PN 1 PG 2 WC Hematology SC Hematology GA 871JM UT WOS:000225127500503 ER PT J AU Kuter, D Bussel, JB Aledort, LM George, J Lyons, RM Conklin, GT Lichtin, AE Nieva, J Kelly, R Chen, CF Nichol, JL AF Kuter, D Bussel, JB Aledort, LM George, J Lyons, RM Conklin, GT Lichtin, AE Nieva, J Kelly, R Chen, CF Nichol, JL TI A phase 2 placebo controlled study evaluating the platelet response and safety of weekly dosing with a novel thrombopoietic protein (AMG531) in thrombocytopenic adult patients (pts) with immune thrombocytopenic purpura (ITP). SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Massachusetts Gen Hosp, Boston, MA 02114 USA. Cornell Univ, Weill Med Coll, New York, NY USA. Univ Oklahoma, Hlth Sci Ctr, Oklahoma City, OK USA. Hematol Oncol Assoc So Texas, San Antonio, TX USA. Cleveland Clin Fdn, Cleveland, OH 44195 USA. Scripps Clin, La Jolla, CA USA. Amgen Inc, Dev, Thousand Oaks, CA 91320 USA. Mt Sinai Hosp, New York, NY 10029 USA. Diagnost Clin Houston, Houston, TX 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 2004 VL 104 IS 11 MA 511 BP 148A EP 149A PN 1 PG 2 WC Hematology SC Hematology GA 871JM UT WOS:000225127500514 ER PT J AU Lafuente, EM Carman, CV Krause, M Springer, TA Gertler, FB Boussiotis, VA AF Lafuente, EM Carman, CV Krause, M Springer, TA Gertler, FB Boussiotis, VA TI RIAM, a new Rap1 effector, functions downstream of Rap1 and regulates rapl localization at the plasma membrane and Rap1-induced adhesion. SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Dana Farber Canc Inst, Boston, MA 02115 USA. Harvard Univ, Sch Med, Ctr Blood Res, Boston, MA 02115 USA. MIT, Dept Biol, Boston, MA 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 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 2004 VL 104 IS 11 MA 510 BP 148A EP 148A PN 1 PG 1 WC Hematology SC Hematology GA 871JM UT WOS:000225127500513 ER PT J AU Batista, A Barata, JT Costa, LF Sallan, SE Carlesso, N Nadler, LM Cardoso, AA AF Batista, A Barata, JT Costa, LF Sallan, SE Carlesso, N Nadler, LM Cardoso, AA TI MTOR as therapeutic target for T-cell leukemia: Synergism with conventional cytotoxic drugs and signaling inhibitors. SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Dana Farber Canc Inst, Boston, MA 02115 USA. Inst Mol Med, Lisbon, Portugal. Massachusetts Gen Hosp, Ctr Regenerat Med, 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 2004 VL 104 IS 11 MA 521 BP 151A EP 151A PN 1 PG 1 WC Hematology SC Hematology GA 871JM UT WOS:000225127500524 ER PT J AU Stam, RW den Boer, ML Passier, M Sallan, SE Armstrong, SA Pieters, P AF Stam, RW den Boer, ML Passier, M Sallan, SE Armstrong, SA Pieters, P TI MLL rearranged infant acute lymphoblastic leukemia is characterized by silencing of the putative tumor suppressor gene FHIT. SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Sophia Childrens Univ Hosp, Erasmus Med Ctr, Rotterdam, Netherlands. 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 2004 VL 104 IS 11 MA 525 BP 152A EP 152A PN 1 PG 1 WC Hematology SC Hematology GA 871JM UT WOS:000225127500528 ER PT J AU Nestoridi, E Kushak, R Ingelfinger, JR Grabowski, EF AF Nestoridi, E Kushak, R Ingelfinger, JR Grabowski, EF TI Active site-inactivated recombinant factor VIIa blocks Shiga toxin-induced upregulation of tissue factor activity on human glomerular endothelial cells and human proximal tubular epithelial cells. SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Harvard Univ, Sch Med, Massachusetts Gen Hosp, Dept Pediat,Cardiovasc Thrombosis Lab, Boston, MA 02115 USA. Harvard Univ, Sch Med, Massachusetts Gen Hosp, Dept Pediat,Pediat Nephrol Lab, 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 2004 VL 104 IS 11 MA 532 BP 154A EP 155A PN 1 PG 2 WC Hematology SC Hematology GA 871JM UT WOS:000225127500535 ER PT J AU O'Neil, J Ferrando, AA Palomero, T Look, AT AF O'Neil, J Ferrando, AA Palomero, T Look, AT TI Identification of TAL1/SCL target genes through siRNA and microarray expression analysis. SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA 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 2004 VL 104 IS 11 MA 4294 BP 158B EP 158B PN 2 PG 1 WC Hematology SC Hematology GA 871JO UT WOS:000225127700624 ER PT J AU Griffin, JD Fabbro, D Fendrieh, G Huntly, B Jacob, S Kung, A Mestan, J Weisberg, E Gilliland, DG Manley, PW AF Griffin, JD Fabbro, D Fendrieh, G Huntly, B Jacob, S Kung, A Mestan, J Weisberg, E Gilliland, DG Manley, PW TI AMD107: Efficacy as a selective inhibitor of the tyrosine kinase activity of BCR-ABL in murine leukemia models. SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02115 USA. Novartis Inst Biomed Res, Basel, Switzerland. Brigham & Womens Hosp, 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 2004 VL 104 IS 11 MA 551 BP 160A EP 160A PN 1 PG 1 WC Hematology SC Hematology GA 871JM UT WOS:000225127500554 ER PT J AU Chiaretti, S Guarini, A De Propris, MS Intoppa, S Vitale, A Ariola, C Ritz, J Foa, R AF Chiaretti, S Guarini, A De Propris, MS Intoppa, S Vitale, A Ariola, C Ritz, J Foa, R TI ZAP-70 expression in acute lymphoblastic leukemia: Association with the E2A/PBX1 rearrangement and with the pre-B stage of differentiation. SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Univ Roma La Sapienza, Div Hematol, Rome, Italy. Dana Farber Canc Inst, Dept Med Oncol, 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 2004 VL 104 IS 11 MA 4305 BP 161B EP 161B PN 2 PG 1 WC Hematology SC Hematology GA 871JO UT WOS:000225127700635 ER PT J AU Sattler, M Balbendreier, E Chu, SC Gramlich, JL Podar, K Griffin, JD AF Sattler, M Balbendreier, E Chu, SC Gramlich, JL Podar, K Griffin, JD TI Pim kinases mediate viability signals downstream of the tyrosine kinase Oncogenes BCR-ABL and FLT3-ITD. SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 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 2004 VL 104 IS 11 MA 557 BP 161A EP 161A PN 1 PG 1 WC Hematology SC Hematology GA 871JM UT WOS:000225127500560 ER PT J AU Mitsiades, CS Mitsiades, N Fanourakis, G Goudopoulou, A McMullan, CJ Voutsinas, G Munshi, NC Anderson, KC AF Mitsiades, CS Mitsiades, N Fanourakis, G Goudopoulou, A McMullan, CJ Voutsinas, G Munshi, NC Anderson, KC TI Evaluation of the Ras/B-Raf/SHP-2 axis in B cell malignancies. SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Harvard Univ, Sch Med, Dana Farber Canc Inst, Dept Med,Dept Med Oncol, Boston, MA 02115 USA. Univ Athens, Dept Pathol, Athens, Greece. NCSR Demokritos, Inst Biol, GR-15310 Athens, Greece. 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 2004 VL 104 IS 11 MA 4344 BP 170B EP 170B PN 2 PG 1 WC Hematology SC Hematology GA 871JO UT WOS:000225127700674 ER PT J AU Chakraverty, R Buchli, J Zhao, GL Sykes, M AF Chakraverty, R Buchli, J Zhao, GL Sykes, M TI Proliferation, expansion, effector differentiation and survival of GVH-reactive T cells following delayed DLI to mixed chimeras. SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Massachusetts Gen Hosp, Transplantat Biol Res Ctr, 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 2004 VL 104 IS 11 MA 594 BP 171A EP 172A PN 1 PG 2 WC Hematology SC Hematology GA 871JM UT WOS:000225127500597 ER PT J AU Haining, WN Neuberg, D Keczkemethy, H Evans, J Rivoli, S Guenaga, J Douek, D Sallan, S Guinan, E Nadler, L AF Haining, WN Neuberg, D Keczkemethy, H Evans, J Rivoli, S Guenaga, J Douek, D Sallan, S Guinan, E Nadler, L TI Protective, antigen-specific immunity in children treated for ALL is due to selective preservation of T-cell memory SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Dana Farber Canc Inst, Boston, MA 02115 USA. NIAID, NIH, Vaccine Res Ctr, 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 2004 VL 104 IS 11 MA 600 BP 173A EP 173A PN 1 PG 1 WC Hematology SC Hematology GA 871JM UT WOS:000225127500603 ER PT J AU Huang, ZW Liu, DX Madani, N Kumar, S Choi, WT Cao, R Li, Y Gao, YG Dong, CZ Wang, J An, J Sodroski, JG AF Huang, ZW Liu, DX Madani, N Kumar, S Choi, WT Cao, R Li, Y Gao, YG Dong, CZ Wang, J An, J Sodroski, JG TI A novel synthetic chemokine containing D-amino acids that binds to the CXCR4 receptor and inhibits HIV-1 infection SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Chemokine Pharmaceut Inc, Raylight Int, Drug Discovery Div, La Jolla, CA USA. Univ Illinois, Dept Biochem, Urbana, IL 61801 USA. Burnham Inst, Ctr Canc, La Jolla, CA 92037 USA. Harvard Univ, Sch Med, Dana Farber Canc Inst, Dept Canc Immunol & AIDS, 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 2004 VL 104 IS 11 MA 603 BP 174A EP 174A PN 1 PG 1 WC Hematology SC Hematology GA 871JM UT WOS:000225127500606 ER PT J AU Stine, K Becton, D Dahl, GV Ravindranath, Y Raimondi, SC Behm, FG Chang, M Weinstein, H AF Stine, K Becton, D Dahl, GV Ravindranath, Y Raimondi, SC Behm, FG Chang, M Weinstein, H TI Genetic randomization to allogeneic bone marrow transplant in first remission pediatric acute myeloid leukemia patients, pediatric oncology group 9421 (Now childrens oncology group) SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Univ Arkansas Med Sci, Little Rock, AR 72205 USA. Childrens Hosp Michigan, Detroit, MI 48201 USA. St Jude Childrens Res Hosp, Memphis, TN 38105 USA. Ctr Data, Childrens Oncol Grp, Gainesville, FL USA. Massachusetts Gen Hosp, Boston, MA 02114 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 2004 VL 104 IS 11 MA 616 BP 178A EP 178A PN 1 PG 1 WC Hematology SC Hematology GA 871JM UT WOS:000225127500619 ER PT J AU Le Gouill, S Podar, K Amiot, M Hideshima, T Chauhan, D Ishitsuka, K Kumar, S Raje, N Richardson, P Harousseau, JL Anderson, K AF Le Gouill, S Podar, K Amiot, M Hideshima, T Chauhan, D Ishitsuka, K Kumar, S Raje, N Richardson, P Harousseau, JL Anderson, K TI VEGF upregulates Mcl-1 expression and protects multiple myeloma cells against starvation induced-apoptosis. SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Dana Farber Canc Inst, Jerome Lipper Multiple Myeloma Ctr, Dept Med Oncol, Boston, MA 02115 USA. CHU Nantes, Hotel Dieu, Serv Hematol Clin, F-44035 Nantes 01, France. INSERM, U0161, Inst Biol, Nantes, France. 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 2004 VL 104 IS 11 MA 631 BP 182A EP 182A PN 1 PG 1 WC Hematology SC Hematology GA 871JM UT WOS:000225127500634 ER PT J AU Nimmanapalli, R Gerbino, E Dalton, WS Alsina, M AF Nimmanapalli, R Gerbino, E Dalton, WS Alsina, M TI Telomerase inhibition, telomere shortening and apoptotic cell death in multiple myeloma cells following exposure to a novel and potent telomerase inhibitor (GRN163L), targeting RNA component of telomerase. SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 VA Boston Healthcare Syst, Dept Med, W Roxbury, MA USA. Dana Farber Canc Inst, Dept Med Oncol, Jerome Lipper Multiple Myeloma Ctr, Boston, MA 02115 USA. Harvard Univ, Sch Med, Boston, MA 02115 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 2004 VL 104 IS 11 MA 638 BP 184A EP 184A PN 1 PG 1 WC Hematology SC Hematology GA 871JM UT WOS:000225127500641 ER PT J AU Burger, R Legouill, S Tai, YT Shringarpure, R Podar, K Catley, L Tassone, P Neri, P Hideshima, T Chauhan, D Fridman, JS Anderson, KC AF Burger, R Legouill, S Tai, YT Shringarpure, R Podar, K Catley, L Tassone, P Neri, P Hideshima, T Chauhan, D Fridman, JS Anderson, KC TI Inhibition of human plasmacytoma cell growth by a novel JAK kinase inhibitor. SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02115 USA. Incyte Corp, Wilmington, DE 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 2004 VL 104 IS 11 MA 644 BP 186A EP 186A PN 1 PG 1 WC Hematology SC Hematology GA 871JM UT WOS:000225127500647 ER PT J AU Frost, P Hoang, B Gera, J Sharma, A Shi, YJ Yan, HJ Lichtenstein, A AF Frost, P Hoang, B Gera, J Sharma, A Shi, YJ Yan, HJ Lichtenstein, A TI AKT activity regulates sensitivity of multiple myeloma cells to mTor inhibitors. SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 W Los Angeles Vet Affairs Med Ctr, Dept Hematol Oncol, Los Angeles, CA 90073 USA. Washington Univ, Dept Arts & Sci, St Louis, MO 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 2004 VL 104 IS 11 MA 646 BP 186A EP 186A PN 1 PG 1 WC Hematology SC Hematology GA 871JM UT WOS:000225127500649 ER PT J AU Shimaoka, M Salas, A Yang, W Weitz-Schmidt, G Springer, TA AF Shimaoka, M Salas, A Yang, W Weitz-Schmidt, G Springer, TA TI A small-molecule antagonist to integrin LFA-1 reveals a crucial inter-domain communication as a novel therapeutic target. SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Harvard Univ, Sch Med, CBR Inst Biomed Res, Boston, MA 02115 USA. Novartis Pharma AG, Basel, Switzerland. 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 2004 VL 104 IS 11 MA 650 BP 187A EP 188A PN 1 PG 2 WC Hematology SC Hematology GA 871JM UT WOS:000225127500653 ER PT J AU Sipkins, DA Wei, XB Wu, JW Means, TK Luster, AD Lin, CP Scadden, DT AF Sipkins, DA Wei, XB Wu, JW Means, TK Luster, AD Lin, CP Scadden, DT TI Specialized bone marrow endothelium defines microdomains for tumor and stem cell engraftment. SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Massachusetts Gen Hosp, Wellman Ctr Photomed, 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 2004 VL 104 IS 11 MA 663 BP 191A EP 191A PN 1 PG 1 WC Hematology SC Hematology GA 871JM UT WOS:000225127500666 ER PT J AU Stier, S Ko, Y Forkert, R Lutz, C Neuhaus, T Gruenewald, E Dombkowski, D Rittling, SR Scadden, DT AF Stier, S Ko, Y Forkert, R Lutz, C Neuhaus, T Gruenewald, E Dombkowski, D Rittling, SR Scadden, DT TI Matrix glycoprotein osteopontin is a stem cell niche constituent that constrains the hematopoietic stem cell pool size. SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Univ Bonn, Med Poliklin, D-5300 Bonn, Germany. Harvard Univ, Sch Med, Massachusetts Gen Hosp, Ctr regenerat Med & Technol, Boston, MA 02115 USA. Rutgers State Univ, Dept Cell Biol & Neurosci, Piscataway, NJ 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 2004 VL 104 IS 11 BP 191A EP 191A PN 1 PG 1 WC Hematology SC Hematology GA 871JM UT WOS:000225127500667 ER PT J AU Down, JD Parmar, K Clyne, J Mauch, PM Sackstein, R AF Down, JD Parmar, K Clyne, J Mauch, PM Sackstein, R TI Defining the bone marrow stem cell niche according to a Hoechst dye diffusion gradient and hypoxia. SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Harvard Inst Med, Dept Dermatol, Boston, MA USA. Brigham & Womens Hosp, Dept Radiat Oncol, Boston, MA 02115 USA. Dana Farber Canc Inst, Boston, MA 02115 USA. NR 0 TC 1 Z9 1 U1 2 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 2004 VL 104 IS 11 MA 666 BP 192A EP 192A PN 1 PG 1 WC Hematology SC Hematology GA 871JM UT WOS:000225127500669 ER PT J AU Ebihara, Y Masuya, M Owens, R Yang, S Visconti, RP Fleming, PA Minamiguchi, H Drake, CJ Ogawa, M AF Ebihara, Y Masuya, M Owens, R Yang, S Visconti, RP Fleming, PA Minamiguchi, H Drake, CJ Ogawa, M TI Hematopoietic origin of fibroblasts and their precursors. SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Ralph H Johnson VA Med Ctr, Res Serv, Charleston, SC USA. Med Univ S Carolina, Charleston, SC 29425 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 2004 VL 104 IS 11 MA 672 BP 193A EP 193A PN 1 PG 1 WC Hematology SC Hematology GA 871JM UT WOS:000225127500675 ER PT J AU LaRue, AC Masuya, M Fleming, PA Visconti, RP Ogawa, M Drake, CJ AF LaRue, AC Masuya, M Fleming, PA Visconti, RP Ogawa, M Drake, CJ TI The hematopoietic origin of tumor fibroblasts and pericytes. SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Ralph H Johnson VA Med Ctr, Res Serv, Charleston, SC USA. Med Univ S Carolina, Dept Med, Charleston, SC 29425 USA. Med Univ S Carolina, Dept Anat & Cell Biol, Charleston, SC 29425 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 2004 VL 104 IS 11 MA 673 BP 193A EP 194A PN 1 PG 2 WC Hematology SC Hematology GA 871JM UT WOS:000225127500676 ER PT J AU Silverman, LB Levy, DE Dalton, VK Lipshultz, SE Gelber, RD Sallan, SE AF Silverman, LB Levy, DE Dalton, VK Lipshultz, SE Gelber, RD Sallan, SE TI Outcome of Dana-Farber Cancer Institute (DFCI) consortium protocol 95-01 for children with newly diagnosed acute lymphoblastic leukemia (ALL). SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Childrens Hosp, Dana Farber Canc Inst, Dept Pediat Oncol, Boston, MA 02115 USA. Dana Farber Canc Inst, Dept Biostat Sci, Boston, MA 02115 USA. Univ Miami, Sch Med, Dept Pediat, Miami, FL 33152 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 2004 VL 104 IS 11 MA 679 BP 195A EP 195A PN 1 PG 1 WC Hematology SC Hematology GA 871JM UT WOS:000225127500682 ER PT J AU Attar, EC Learner, E Amerin, PC AF Attar, EC Learner, E Amerin, PC TI In vitro studies of bortezomib with daunorubicin and cytarabine: Sequence of administration affects leukemia cell chemosensitivity SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Massachusetts Gen Hosp, Ctr Canc, Hematol Oncol Unit, 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 2004 VL 104 IS 11 MA 4464 BP 198B EP 198B PN 2 PG 1 WC Hematology SC Hematology GA 871JO UT WOS:000225127700794 ER PT J AU Gazda, HT Sanoudou, D Kho, AT Zaucha, JM Sieff, CA Beggs, AH AF Gazda, HT Sanoudou, D Kho, AT Zaucha, JM Sieff, CA Beggs, AH TI Gene expression changes in bone marrow cells from diamond-Blackfan anemia patients. SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Dana Farber Canc Inst, Boston, MA 02115 USA. Childrens Hosp, Genom Program, Boston, MA 02115 USA. Childrens Hosp, Div Genet, Boston, MA 02115 USA. Harvard Univ, Sch Med, Boston, MA USA. Childrens Hosp, Informat Program, Boston, MA 02115 USA. Univ Gdansk, Sch Med, Dept Hematol Oncol, PL-80952 Gdansk, Poland. Childrens Hosp, Dept Hematol, 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 2004 VL 104 IS 11 MA 720 BP 206A EP 207A PN 1 PG 2 WC Hematology SC Hematology GA 871JM UT WOS:000225127500723 ER PT J AU Ebert, BL Lee, M Pretz, J Golub, TR Sieff, C AF Ebert, BL Lee, M Pretz, J Golub, TR Sieff, C TI An RNA interference model of RPS19 deficiency in Diamond Blackfan Anemia recapitulates defective erythropoiesis and rescue by dexamethasone: Identification of dexamethasone responsive genes by microarray. SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Dana Farber Canc Inst, Dept Adult Oncol, Boston, MA USA. Dana Farber Canc Inst, Dept Pediat Oncol, Boston, MA USA. Harvard Univ, Broad Inst, Cambridge, MD USA. MIT, Cambridge, 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 2004 VL 104 IS 11 MA 721 BP 207A EP 207A PN 1 PG 1 WC Hematology SC Hematology GA 871JM UT WOS:000225127500724 ER PT J AU Shimamura, A Leary, R Stotsky, M Moreau, LA D'Andrea, AD AF Shimamura, A Leary, R Stotsky, M Moreau, LA D'Andrea, AD TI Monoubiquitinated FANCD2 is both necessary and sufficient for mitomycin C resistance in the absence of a functional Fanconi anemia core complex. SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Dana Farber Canc Inst, Boston, MA 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 2004 VL 104 IS 11 MA 722 BP 207A EP 207A PN 1 PG 1 WC Hematology SC Hematology GA 871JM UT WOS:000225127500725 ER PT J AU Alyea, EP Li, SL Kim, H Cutler, C Ho, V Lee, SJ Gribben, J Ritz, J Fisher, DC Soiffer, RJ Antin, JH AF Alyea, EP Li, SL Kim, H Cutler, C Ho, V Lee, SJ Gribben, J Ritz, J Fisher, DC Soiffer, RJ Antin, JH TI Sirolimus, tacrolimus and reduced-dose methotrexate as graft versus host disease (GVHD) prophylaxis after non-myeloablative stem cell transplantation: Low incidence of acute GVHD compared with tacrolimus/methotrexate or cyclosporine/prednisone. SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Brigham & Womens Hosp, Boston, MA 02115 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 2004 VL 104 IS 11 MA 730 BP 209A EP 209A PN 1 PG 1 WC Hematology SC Hematology GA 871JM UT WOS:000225127500733 ER PT J AU Avigan, D Vasir, B Wu, ZI Uhl, L Desliva, T Rosenblatt, J Levine, JD Joyce, R Miller, K Munshi, N Richardson, P Proper, J Gillombardo, N Forino, P Villaroel, M Anderson, K Kufe, D AF Avigan, D Vasir, B Wu, ZI Uhl, L Desliva, T Rosenblatt, J Levine, JD Joyce, R Miller, K Munshi, N Richardson, P Proper, J Gillombardo, N Forino, P Villaroel, M Anderson, K Kufe, D TI Dendritic cell myeloma fusions stimulate anti-tumor immunity: Results from pre-clinical studies and a clinical trial. SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA 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 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 2004 VL 104 IS 11 MA 751 BP 215A EP 215A PN 1 PG 1 WC Hematology SC Hematology GA 871JM UT WOS:000225127500753 ER PT J AU Treon, SP Branagan, A Wasi, P Emmanouilides, CA Frankel, SR Lister, A Morel, P Matous, J Enschede, SH Kimby, E AF Treon, SP Branagan, A Wasi, P Emmanouilides, CA Frankel, SR Lister, A Morel, P Matous, J Enschede, SH Kimby, E TI Combination therapy with rituximab and fludarabine in Waldenstrom's Macroglobulinemia. SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Dana Farber Canc Inst, Bing Program Waldenstroms Macrolgobulinemia, Boston, MA 02115 USA. Harvard Univ, Sch Med, Boston, MA USA. McMaster Univ, Med Ctr, Hamilton, ON, Canada. Univ Calif Los Angeles, Ctr Med, Los Angeles, CA 90024 USA. Greenbaum Canc Ctr, Baltimore, MD USA. St Bartholomews Hosp & Canc Res, London, England. Ctr Hosp Schaffner, Lens, France. Mt Canc Ctr, Denver, CO USA. Rush Presbyterian Med Ctr, Chicago, IL USA. Karolinska Inst, Stockholm, Sweden. NR 0 TC 4 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 2004 VL 104 IS 11 MA 753 BP 215A EP 215A PN 1 PG 1 WC Hematology SC Hematology GA 871JM UT WOS:000225127500755 ER PT J AU Darabi, K Tester, W Daskal, L Cohn, J AF Darabi, K Tester, W Daskal, L Cohn, J TI Syncytial variant of nodular sclerosing Hodgkin's disease. SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Massachusetts Gen Hosp, Blood Transfus Serv, Boston, MA 02114 USA. Albert Einstein Med Ctr, Einstein Canc Ctr, Philadelphia, PA 19141 USA. Albert Einstein Med Ctr, Dept Pathol, Philadelphia, PA 19141 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 2004 VL 104 IS 11 MA 4533 BP 217B EP 217B PN 2 PG 1 WC Hematology SC Hematology GA 871JO UT WOS:000225127700863 ER PT J AU Bradner, J Kim, YS Koehler, A Kawasumi, M Li, XD Schreiber, SL Nghiem, P AF Bradner, J Kim, YS Koehler, A Kawasumi, M Li, XD Schreiber, SL Nghiem, P TI Identification and characterization of novel small-molecule inhibitors of the replication checkpoint. SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Harvard Univ, Dept Chem & Biol Chem, Cambridge, MA 02138 USA. Massachusetts Gen Hosp, Cutaneous Biol Res Ctr, Boston, MA 02114 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 2004 VL 104 IS 11 MA 763 BP 218A EP 218A PN 1 PG 1 WC Hematology SC Hematology GA 871JM UT WOS:000225127500765 ER PT J AU Chauhan, D Li, GL Hideshima, T Podar, K Tassone, P Neri, PE Mitsiades, C Mitsiades, N Raje, N Kumar, S Schlossman, R Sharma, S Munshi, N Zawel, L Anderson, KC AF Chauhan, D Li, GL Hideshima, T Podar, K Tassone, P Neri, PE Mitsiades, C Mitsiades, N Raje, N Kumar, S Schlossman, R Sharma, S Munshi, N Zawel, L Anderson, KC TI Targeting mitochondrial factor Smac/DIABLO as therapy for multiple myeloma (MM) SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Dana Farber Canc Inst, Boston, MA 02115 USA. Novartis, Biomed Res Inst, Cambridge, 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 2004 VL 104 IS 11 MA 764 BP 219A EP 219A PN 1 PG 1 WC Hematology SC Hematology GA 871JM UT WOS:000225127500766 ER PT J AU McMullan, CJ Poulaki, V Shringarpure, R Libermann, TA Hideshima, T Chauhan, D Schlossman, RL Richardson, PG Munshi, NC Echeverria, CG Hoffmann, F Anderson, KC Mitsiades, CS AF McMullan, CJ Poulaki, V Shringarpure, R Libermann, TA Hideshima, T Chauhan, D Schlossman, RL Richardson, PG Munshi, NC Echeverria, CG Hoffmann, F Anderson, KC Mitsiades, CS TI NVP-AEW541: A selective small molecule IGF-1R tyrosine kinase inhibitor is active against multiple myeloma and other hematologic neoplasias and solid tumors SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Harvard Univ, Sch Med, Dept Med, Beth Israel Deaconess Med Ctr, Boston, MA USA. Harvard Univ, Sch Med, Dana Farber Canc Inst, Jerome Lipper Multiple Myeloma Ctr,Dept Med Oncol, Boston, MA USA. Harvard Univ, Inst Med, Genom Ctr, Boston, MA 02115 USA. Novartis Pharmaceut AG, Novartis Inst Biomed Res, Basel, Switzerland. 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 2004 VL 104 IS 11 MA 766 BP 219A EP 219A PN 1 PG 1 WC Hematology SC Hematology GA 871JM UT WOS:000225127500768 ER PT J AU Arinobu, Y Iwasaki, H Gurish, MR Mizuno, S Shigematsu, H Akashi, K AF Arinobu, Y Iwasaki, H Gurish, MR Mizuno, S Shigematsu, H Akashi, K TI Identification of progenitors committed to basophil and/or mast cell lineage SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Harvard Univ, Sch Med, Dept Canc Immunol & AIDS, Dana Farber Canc Inst, Boston, MA USA. Brigham & Womens Hosp, Dept Med, Div Rheumatol Immunmol & Allergy, 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 2004 VL 104 IS 11 MA 779 BP 223A EP 223A PN 1 PG 1 WC Hematology SC Hematology GA 871JM UT WOS:000225127500781 ER PT J AU Carrasco, R Tonon, G Brennan, C Protopopov, A Sinha, R Feng, B Leo, C Zhang, YY Zhang, J Zhan, FH Protopopova, M Mitsiades, C Munshi, N Chin, L Bergsagel, P Kuehl, M Shaughnessy, J Anderson, K DePinho, R AF Carrasco, R Tonon, G Brennan, C Protopopov, A Sinha, R Feng, B Leo, C Zhang, YY Zhang, J Zhan, FH Protopopova, M Mitsiades, C Munshi, N Chin, L Bergsagel, P Kuehl, M Shaughnessy, J Anderson, K DePinho, R TI Comprehensive genome-wide profile of regional gains and losses in multiple myeloma using array-CGH: The 1q21 amplification and potential role of the BCL-9 gene in multiple myeloma pathogenesis SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Dana Farber Canc Inst, Dept Med Oncol, Boston, MA USA. NCI, Genet Dept, Bethesda, MD USA. Univ Arkansas, Lambert Lab Myeloma Genet, Little Rock, AR USA. Cornell Univ, Dept Med, New York, NY 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 2004 VL 104 IS 11 MA 785 BP 225A EP 225A PN 1 PG 1 WC Hematology SC Hematology GA 871JM UT WOS:000225127500787 ER PT J AU Berkofsky-Fessler, WD Licht, JD McConnell, MJ Neuberg, DS Bowler, TS Fruchtman, SM AF Berkofsky-Fessler, WD Licht, JD McConnell, MJ Neuberg, DS Bowler, TS Fruchtman, SM TI The transcriptional program of polycythemia vera revelas altered expression of multiple putative tumor suppressor genes SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Mt Sinai Sch Med, Dept Med, Div Hematol Oncol, New York, NY 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 2004 VL 104 IS 11 MA 796 BP 227A EP 227A PN 1 PG 1 WC Hematology SC Hematology GA 871JM UT WOS:000225127500798 ER PT J AU Klement, G Kikuchi, L Kieran, M Almog, N Yip, TT Folkman, J AF Klement, G Kikuchi, L Kieran, M Almog, N Yip, TT Folkman, J TI Early tumor detection using platelet uptake of angiogenesis regulators. SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Childrens Hosp, Vasc Biol Program, Boston, MA 02115 USA. Childrens Hosp, Dept Surg, Boston, MA 02115 USA. Harvard Univ, Sch Med, Boston, MA 02115 USA. Dana Farber Canc Inst, Boston, MA USA. Harvard Univ, Sch Med, Boston, MA USA. Ciphergen Biosyst Inc, Fremont, CA USA. NR 0 TC 10 Z9 10 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 2004 VL 104 IS 11 MA 839 BP 239A EP 240A PN 1 PG 2 WC Hematology SC Hematology GA 871JM UT WOS:000225127500841 ER PT J AU Bergmeier, W Piffath, CL Cheng, GY Dole, VS Zhang, YH von Andrian, UH Wagner, DD AF Bergmeier, W Piffath, CL Cheng, GY Dole, VS Zhang, YH von Andrian, UH Wagner, DD TI Tumor necrosis factor-alpha converting enzyme (ADAM17) mediates GPIb alpha shedding from platelets in vitro and in vivo SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Harvard Univ, Sch Med, CBR Inst Biomed Res, Boston, MA USA. Harvard Univ, Sch Med, Dept Pathol, Boston, MA USA. Wyeth 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 2004 VL 104 IS 11 MA 841 BP 240A EP 240A PN 1 PG 1 WC Hematology SC Hematology GA 871JM UT WOS:000225127500843 ER PT J AU Bartlett, NL Gribben, JC Boccia, RV Milder, MS Aboulafia, DM Castro, J Flinn, I Hayes-Lattin, B Kaplan, L Lin, T Lucas, JB Maloney, DG McLaughlin, P McSweeney, PA Mohrbacher, A Redfern, C Steis, R Stephenson, JJ Strair, R Berenson, RJ Frohlich, MW AF Bartlett, NL Gribben, JC Boccia, RV Milder, MS Aboulafia, DM Castro, J Flinn, I Hayes-Lattin, B Kaplan, L Lin, T Lucas, JB Maloney, DG McLaughlin, P McSweeney, PA Mohrbacher, A Redfern, C Steis, R Stephenson, JJ Strair, R Berenson, RJ Frohlich, MW TI A phase II study of Xcellerated T cells (TM) in patients with relapsed or refractory indolent non-Hodgkin's lymphoma (NHL). SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Washington Univ, Sch Med, St Louis, MO USA. Dana Farber Canc Inst, Boston, MA 02115 USA. Ctr Canc & Blood Disorders, Bethesda, MD USA. Swedish Canc Ctr, Seattle, WA USA. Virginia Mason Canc Inst, Seattle, WA USA. Univ Calif San Diego, San Diego, CA 92103 USA. Johns Hopkins Oncol Ctr, Baltimore, MD USA. Oregon Hlth Sci Univ, Portland, OR 97201 USA. Univ Calif San Francisco, San Francisco, CA 94143 USA. Ohio State Univ, Columbus, OH 43210 USA. Calif Canc Care, Greenbrae, CA USA. Rocky Mt Canc Ctr, Denver, CO USA. Univ So Calif, Los Angeles, CA USA. Sharp Healthcare, San Diego, CA USA. Atlanta Canc Care, Roswell, GA USA. Canc Ctr Carolinas, Greenville, SC USA. Fred Hutchinson Canc Res Ctr, Seattle, WA 98104 USA. MD Anderson Canc Ctr, Houston, TX USA. Canc Inst New Jersey, New Brunswick, NJ USA. Xcyte Therapies Inc, Seattle, WA 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 2004 VL 104 IS 11 MA 4640 BP 244B EP 244B PN 2 PG 1 WC Hematology SC Hematology GA 871JO UT WOS:000225127700970 ER PT J AU Raponi, M Lowenberg, B Lancet, JE Harousseau, JL Stone, R Rackoff, W Thibault, A Zhang, Y Atkins, D Wang, YX AF Raponi, M Lowenberg, B Lancet, JE Harousseau, JL Stone, R Rackoff, W Thibault, A Zhang, Y Atkins, D Wang, YX TI Identification of molecular predictors of response to ZARNESTRA (TM) (tipifarnib, R115777) in relapsed and refractory acute myeloid leukemia. SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Veridex LLC, Mol Diagnost, San Diego, CA USA. Johnson & Johnson Pharmaceut Res & Dev LLC, Drug Dev, Raritan, NJ USA. Univ Rochester, James P Wilmot Canc Ctr, Rochester, NY USA. Hop Hotel Dieu, Serv Hematol, Nantes, France. Dana Farber Canc Inst, Adult Leukemia Program, Boston, MA 02115 USA. Erasmus Univ, Dept Hematol, Rotterdam, Netherlands. NR 0 TC 6 Z9 7 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 2004 VL 104 IS 11 MA 861 BP 246A EP 246A PN 1 PG 1 WC Hematology SC Hematology GA 871JM UT WOS:000225127500863 ER PT J AU Stone, RM Moser, B Schulman, P Barrier, RC Kolitz, JE Allen, SL Stock, W Galinsky, IA Khoury, H Larson, RA AF Stone, RM Moser, B Schulman, P Barrier, RC Kolitz, JE Allen, SL Stock, W Galinsky, IA Khoury, H Larson, RA TI A dose escalation and phase II study of gemtuzumab ozogamicin (GO) with high-dose cytarabine (HiDAC) for patients (Pts) with refractory or relapsed acute myeloid leukemia (AML): CALGB 19902. SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Dana Farber Canc Inst, Boston, MA 02115 USA. Duke Univ, Ctr Stat, Durham, NC USA. Mem Sloan Kettering Canc Ctr, New York, NY 10021 USA. N Shore Univ Hosp, Manhasset, NY USA. Washington Univ, Sch Med, St Louis, MO USA. Univ Chicago Hosp, Chicago, IL 60637 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 2004 VL 104 IS 11 MA 873 BP 249A EP 249A PN 1 PG 1 WC Hematology SC Hematology GA 871JM UT WOS:000225127500875 ER PT J AU Damon, L Niedzwiecki, D Johnson, J Cheson, B Hurd, D Barlett, N Kelly, M Linker, C Canellos, G AF Damon, L Niedzwiecki, D Johnson, J Cheson, B Hurd, D Barlett, N Kelly, M Linker, C Canellos, G TI Intense immunochemotherapy (IC) and autologous stem, cell transplant (ASCT) for untreated patients (pts) with mantle cell lymphoma (MCL): CALGB 59909. A preliminary report. SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Univ Calif San Francisco, Dept Hematol, San Francisco, CA 94143 USA. CALGB, Ctr Stat, Durham, NC USA. Georgetown Univ, Vincent T Lombardi Canc Res Ctr, Washington, DC USA. Wake Forest Univ, Winston Salem, NC 27109 USA. Washington Univ, Sch Med, St Louis, MO USA. Univ Chicago, Chicago, IL 60637 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 2004 VL 104 IS 11 MA 895 BP 255A EP 256A PN 1 PG 2 WC Hematology SC Hematology GA 871JM UT WOS:000225127500897 ER PT J AU Berman, JN Heinrichs, S Ortiz, TM Kornblau, SM Neuberg, DS Estey, EH Look, AT AF Berman, JN Heinrichs, S Ortiz, TM Kornblau, SM Neuberg, DS Estey, EH Look, AT TI CD34+cell selection is required to accurately measure HOXA9 levels by quantitative RT-PCR in patients with myelodysplastic syndrome. SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Dana Farber Canc Inst, Dept Pediat Oncol, Boston, MA 02115 USA. Dana Farber Canc Inst, Dept Biostat Sci, Boston, MA 02115 USA. Childrens Hosp, Dept Pediat Hematol Oncol, Boston, MA 02115 USA. Univ Texas, MD Anderson Canc Ctr, Dept Leukemia, Houston, TX 77030 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 2004 VL 104 IS 11 MA 4733 BP 266B EP 267B PN 2 PG 2 WC Hematology SC Hematology GA 871JO UT WOS:000225127701059 ER PT J AU Dey, BR Cox, B Chien, AJ Caron, M McAfee, SL Colby, C Spitzer, TR AF Dey, BR Cox, B Chien, AJ Caron, M McAfee, SL Colby, C Spitzer, TR TI Influence of first-line regimens on the outcomes of high-dose chemotherapy with autologous hematopoietic stem-cell transplantation for patients with newly diagnosed multiple myeloma. SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 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 2004 VL 104 IS 11 MA 931 BP 267A EP 267A PN 1 PG 1 WC Hematology SC Hematology GA 871JM UT WOS:000225127500933 ER PT J AU Lucas, DM Dewald, GW Neuberg, DS Byrd, JC Lozanski, G Harbison, J Cunningham, KD Flinn, IW Appelbaum, FR Larson, RA Tallman, MS Grever, MR AF Lucas, DM Dewald, GW Neuberg, DS Byrd, JC Lozanski, G Harbison, J Cunningham, KD Flinn, IW Appelbaum, FR Larson, RA Tallman, MS Grever, MR TI Clinical, laboratory, and treatment outcome characteristics of chronic lymphocytic leukemia (CLL) patients with p53 mutations or del(17p) enrolled on a prospective phase III clinical trial: Short progression free survival, irrespective of fludarabine-based treatment used. SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Ohio State Univ, Columbus, OH 43210 USA. Mayo Clin, Rochester, MN USA. Dana Farber Canc Inst, Boston, MA 02115 USA. Ohio State Univ, Columbus, OH 43210 USA. Johns Hopkins, Baltimore, MD USA. Northwestern Univ, Chicago, IL 60611 USA. Fred Hutchinson Canc Res Ctr, Seattle, WA 98104 USA. Univ Chicago, Chicago, IL 60637 USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 2021 L ST NW, SUITE 900, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2004 VL 104 IS 11 MA 949 BP 272A EP 272A PN 1 PG 1 WC Hematology SC Hematology GA 871JM UT WOS:000225127500951 ER PT J AU Holderried, TAW Gorgun, G Gribben, JG AF Holderried, TAW Gorgun, G Gribben, JG TI Cell contact with CLL cells induces defects in T cell differentiation and effector pathways: Impact of silencing specific cytokine production. SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Harvard Univ, Sch Med, Dana Farber Canc Inst, Boston, MA 02115 USA. CLL Res Consortium, 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 2004 VL 104 IS 11 MA 955 BP 273A EP 274A PN 1 PG 2 WC Hematology SC Hematology GA 871JM UT WOS:000225127500957 ER PT J AU Kitada, S Reed, JC David, MLI Neuberg, DS Gribben, JG Dewald, GW Flinn, IW Appelbaum, FR Larson, RA Tallman, MS Byrd, JC Grever, MR AF Kitada, S Reed, JC David, MLI Neuberg, DS Gribben, JG Dewald, GW Flinn, IW Appelbaum, FR Larson, RA Tallman, MS Byrd, JC Grever, MR TI Critical molecular studies to strategically plan therapy in chronic lymphocytic leukemia (CLL): Correlating cellular proteins with defined prognostic patient subsets and their response to treatment. SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Burnham Inst, La Jolla, CA 92037 USA. Ohio State Univ, Columbus, OH 43210 USA. Dana Farber Canc Inst, Boston, MA 02115 USA. Mayo Clin, Rochester, MN USA. Johns Hopkins, Baltimore, MD USA. Northwestern Univ, Chicago, IL 60611 USA. Fred Hutchinson Canc Res Ctr, Seattle, WA 98104 USA. Univ Chicago, Chicago, IL 60637 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 2004 VL 104 IS 11 MA 956 BP 274A EP 274A PN 1 PG 1 WC Hematology SC Hematology GA 871JM UT WOS:000225127500958 ER PT J AU Mauerer, K Zahrieh, D Ansen, S Li, AH Xia, ZN Gribben, JG AF Mauerer, K Zahrieh, D Ansen, S Li, AH Xia, ZN Gribben, JG TI Somatic hypermutation does not increase the binding affinity of Ig derived peptides to MHC class I or II - Implications for Ig peptide vaccination strategies. SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Harvard Univ, Sch Med, CLL Res Consortium, 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 2004 VL 104 IS 11 MA 960 BP 275A EP 275A PN 1 PG 1 WC Hematology SC Hematology GA 871JM UT WOS:000225127500962 ER PT J AU Battle, TE Arbiser, J Frank, DA AF Battle, TE Arbiser, J Frank, DA TI The natural product honokiol induces caspase-dependent apoptosis in chronic lymphocytic leukmemia (CLL) cells. SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02115 USA. Emory Univ, Sch Med, Dept Dermatol, Atlanta, GA 30322 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 2004 VL 104 IS 11 MA 4777 BP 277B EP 277B PN 2 PG 1 WC Hematology SC Hematology GA 871JO UT WOS:000225127701103 ER PT J AU Battle, TE Frank, DA AF Battle, TE Frank, DA TI Molecular events underlying the induced differentiation of CLL cells are recapitulated in CESS B cells. SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 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 2004 VL 104 IS 11 MA 4778 BP 277B EP 277B PN 2 PG 1 WC Hematology SC Hematology GA 871JO UT WOS:000225127701104 ER PT J AU Mauerer, K Zahrieh, D Gorgun, G Li, AH Zhou, JB Rassenti, L Gribben, JG AF Mauerer, K Zahrieh, D Gorgun, G Li, AH Zhou, JB Rassenti, L Gribben, JG TI Distinct VDJ-H gene usage between mutated and unmutated patients in B-CLL: Implications for pathogenesis and correlation with clinical outcome. SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Harvard Univ, Sch Med, Dana Farber Canc Inst, Boston, MA USA. Univ Calif San Diego, CLL Res Consortium, La Jolla, CA 92093 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 2004 VL 104 IS 11 MA 970 BP 278A EP 278A PN 1 PG 1 WC Hematology SC Hematology GA 871JM UT WOS:000225127500972 ER PT J AU Maia, S Rao, SP Sallan, SE Nadler, LM Cardoso, AA AF Maia, S Rao, SP Sallan, SE Nadler, LM Cardoso, AA TI Aberrant expression of BAFF system molecules on B-cell precursor leukemia modulates tumor cell survival: Novel targets for therapeutic intervention. SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Dana Farber Canc Inst, Boston, MA 02115 USA. Biogen IDEC, Mol & Cell Biol, Cambridge, MA USA. Dana Farber Canc Inst, Boston, MA 02115 USA. RI Maia, Sara/B-2513-2013 OI Maia, Sara/0000-0001-8638-0566 NR 0 TC 0 Z9 0 U1 2 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 2004 VL 104 IS 11 MA 989 BP 283A EP 283A PN 1 PG 1 WC Hematology SC Hematology GA 871JM UT WOS:000225127500991 ER PT J AU Faderl, S Rai, KR Gribben, J Flinn, I Byrd, JC McConkey, D Schenkein, D Esseltine, D Browning, ML Keating, MJ AF Faderl, S Rai, KR Gribben, J Flinn, I Byrd, JC McConkey, D Schenkein, D Esseltine, D Browning, ML Keating, MJ TI Phase 2 study of three doses of single agent bortezomib in patients with fludarabine-refractory B-cell CLL. SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Univ Texas, MD Anderson Canc Ctr, Dept Leukemia, Houston, TX 77030 USA. Long Isl Jewish Med Ctr, New York, NY USA. Dana Farber Canc Inst, Boston, MA 02115 USA. Ohio State Univ, Columbus, OH 43210 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 2004 VL 104 IS 11 MA 4841 BP 293B EP 293B PN 2 PG 1 WC Hematology SC Hematology GA 871JO UT WOS:000225127701167 ER PT J AU Raje, N Kumar, S Hideshima, T Ishitsuka, K Roccaro, A Yasui, H Hamasaki, M Shiraisi, N Munshi, NC Elford, H Anderson, KC AF Raje, N Kumar, S Hideshima, T Ishitsuka, K Roccaro, A Yasui, H Hamasaki, M Shiraisi, N Munshi, NC Elford, H Anderson, KC TI Induction of apoptosis by didox via down-regulation of Bcl-2 family proteins in multiple myeloma (MM). SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Harvard Univ, Sch Med, Boston, MA 02115 USA. Dana Farber Canc Inst, Boston, MA 02115 USA. Mol Hlth Inc, Richmond, VA 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 2004 VL 104 IS 11 MA 4842 BP 293B EP 293B PN 2 PG 1 WC Hematology SC Hematology GA 871JO UT WOS:000225127701168 ER PT J AU Hunter, ZR Branagan, AR Santos, DD Tournilhac, O Hatjiharissi, E Xu, L Manning, RJ Treon, SP AF Hunter, ZR Branagan, AR Santos, DD Tournilhac, O Hatjiharissi, E Xu, L Manning, RJ Treon, SP TI High levels of soluble immunoregulatory receptors in patients with Waldenstrom's macroglobulinemia. SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Dana Farber Canc Inst, Bing Program Waldenstroms Macroglobulinemia, Boston, MA 02115 USA. Harvard Univ, Sch Med, Boston, MA 02115 USA. RI Hunter, Zachary/H-3018-2013 OI Hunter, Zachary/0000-0002-1689-1691 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 2004 VL 104 IS 11 MA 4881 BP 303B EP 303B PN 2 PG 1 WC Hematology SC Hematology GA 871JO UT WOS:000225127701207 ER PT J AU Santos, DD Hatjiarissi, E Tournilhac, O Xu, L Branagan, A Hunter, Z Catsells, M Anderson, KC Treon, SP AF Santos, DD Hatjiarissi, E Tournilhac, O Xu, L Branagan, A Hunter, Z Catsells, M Anderson, KC Treon, SP TI CD52 is expressed on human mast cells and is a therapeutic target for the anti-CD52 monoclonal antibody Campath-1H in Waldenstrom's macroglobulinemia and mast cell disorders. SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Dana Farber Canc Inst, Bing Program Waldenstroms Macroglobulinemia, Boston, MA USA. Brigham & Womens Hosp, Boston, MA 02115 USA. Harvard Univ, Sch Med, Boston, MA 02115 USA. RI Hunter, Zachary/H-3018-2013 OI Hunter, Zachary/0000-0002-1689-1691 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 2004 VL 104 IS 11 MA 4885 BP 304B EP 304B PN 2 PG 1 WC Hematology SC Hematology GA 871JO UT WOS:000225127701211 ER PT J AU Tournilhac, O Le Gouill, S Santos, DD Podar, K Xu, L Hatjiharissi, E Tai, YT Hunter, Z Branagan, A Anderson, KC Treon, SP AF Tournilhac, O Le Gouill, S Santos, DD Podar, K Xu, L Hatjiharissi, E Tai, YT Hunter, Z Branagan, A Anderson, KC Treon, SP TI Vascular endothelial growth factor (VEGF) is a growth and survival factor in Waldenstrom's macroglobulinemia. SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Dana Farber Canc Inst, Bing Program Waldenstroms Macrolgobulinemia, Boston, MA USA. Dana Farber Canc Inst, Jerome Lipper Multiple Myeloma Ctr, Boston, MA USA. Harvard Univ, Sch Med, Boston, MA 02115 USA. RI Hunter, Zachary/H-3018-2013 OI Hunter, Zachary/0000-0002-1689-1691 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 2004 VL 104 IS 11 MA 4892 BP 305B EP 305B PN 2 PG 1 WC Hematology SC Hematology GA 871JO UT WOS:000225127701218 ER PT J AU Treon, S Branagan, A Hunter, Z Santos, DD Tournilhac, O Hatjiharissi, E Xu, L Manning, R AF Treon, S Branagan, A Hunter, Z Santos, DD Tournilhac, O Hatjiharissi, E Xu, L Manning, R TI IgA and IgG hypogammaglobulinemia persists in most patients with Waldenstrom's macroglobulinemia despite therapeutic responses, including complete remissions. SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Dana Farber Canc Inst, Bing Program Waldenstroms Macroglobulinemia, Boston, MA USA. Harvard Univ, Sch Med, Boston, MA 02115 USA. RI Hunter, Zachary/H-3018-2013 OI Hunter, Zachary/0000-0002-1689-1691 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 2004 VL 104 IS 11 MA 4896 BP 306B EP 306B PN 2 PG 1 WC Hematology SC Hematology GA 871JO UT WOS:000225127701222 ER PT J AU Li, AH Zhou, JB Wang, HJ Goldwasser, MA Lyons, C Sallan, SE Silverman, LB Gribben, JG AF Li, AH Zhou, JB Wang, HJ Goldwasser, MA Lyons, C Sallan, SE Silverman, LB Gribben, JG TI Molecular analysis of T-cell receptor gene rearrangements in children with T-cell acute lymphoblast leukemia on DFCI ALL consortium protocol 95-01 SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Umea Univ, Umea, Sweden. Harvard Univ, Sch Med, Dana Farber Canc Inst, Childrens Hosp, 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 2004 VL 104 IS 11 MA 1084 BP 308A EP 308A PN 1 PG 1 WC Hematology SC Hematology GA 871JM UT WOS:000225127501086 ER PT J AU Roccaro, AM Hideshima, T Raje, N Kumar, S Ishitsuka, K Yasui, H Shiraishi, N Hamasaki, M Richardson, PG Anderson, KC AF Roccaro, AM Hideshima, T Raje, N Kumar, S Ishitsuka, K Yasui, H Shiraishi, N Hamasaki, M Richardson, PG Anderson, KC TI Bortezomib targets multiple myeloma endothelial cells. SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA 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 2004 VL 104 IS 11 MA 4903 BP 308B EP 308B PN 2 PG 1 WC Hematology SC Hematology GA 871JO UT WOS:000225127701229 ER PT J AU Palombella, VJ Normant, E Ali, J Barrett, J Foley, M Gao, Y Ge, JN Georges, AT Grayzel, D Grenier, L Hudak, J Pak, R Patterson, J Pien, C Pink, M Porter, J Sang, JB Spear, K Sydor, J Wright, J Mitsiades, CS Anderson, KC Adams, J Tong, J AF Palombella, VJ Normant, E Ali, J Barrett, J Foley, M Gao, Y Ge, JN Georges, AT Grayzel, D Grenier, L Hudak, J Pak, R Patterson, J Pien, C Pink, M Porter, J Sang, JB Spear, K Sydor, J Wright, J Mitsiades, CS Anderson, KC Adams, J Tong, J TI Anti-tumor activity of IPI-504, a novel Hsp90 inhibitor in multiple myeloma. SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Infin Pharmaceut Inc, Dept Res & Dev, Cambridge, MA USA. Harvard Univ, Sch Med, Dana Farber Canc Inst, Dept Med Oncol,Jerome Lipper Multiple Myeloma Ctr, Boston, MA 02115 USA. NR 0 TC 2 Z9 2 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 2004 VL 104 IS 11 MA 4922 BP 312B EP 313B PN 2 PG 2 WC Hematology SC Hematology GA 871JO UT WOS:000225127701248 ER PT J AU Hunter, ZR Branagan, AR Treon, SP AF Hunter, ZR Branagan, AR Treon, SP TI Campath-1H in WaIdenstrom's macroglobulinemia. SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Dana Farber Canc Inst, Bing Program Waldenstroms Macroglobulinemia, Boston, MA USA. Harvard Univ, Sch Med, Boston, MA 02115 USA. RI Hunter, Zachary/H-3018-2013 OI Hunter, Zachary/0000-0002-1689-1691 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 2004 VL 104 IS 11 BP 313B EP 313B PN 2 PG 1 WC Hematology SC Hematology GA 871JO UT WOS:000225127701250 ER PT J AU Treon, SR Tournilhac, O Branagan, A Hunter, Z Xu, LA Hatjiharissi, E Santos, DD AF Treon, SR Tournilhac, O Branagan, A Hunter, Z Xu, LA Hatjiharissi, E Santos, DD TI Clinical responses to sildenafil in Waldenstrom's macroglobulinemia. SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Dana Farber Canc Inst, Bing Program Waldenstroms Macroglobulinemia, Boston, MA USA. Harvard Univ, Sch Med, Boston, MA 02115 USA. RI Hunter, Zachary/H-3018-2013 OI Hunter, Zachary/0000-0002-1689-1691 NR 0 TC 0 Z9 0 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 2004 VL 104 IS 11 MA 4926 BP 313B EP 313B PN 2 PG 1 WC Hematology SC Hematology GA 871JO UT WOS:000225127701252 ER PT J AU Hunter, Z Branagan, A Treon, S AF Hunter, Z Branagan, A Treon, S TI CHOP plus rituximab (CHOP-R) in Waldenstrom's macroglobulinemia (WM). SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Dana Farber Canc Inst, Bing Program Waldenstroms Macroglobulinemia, Boston, MA USA. Harvard Univ, Sch Med, Boston, MA 02115 USA. RI Hunter, Zachary/H-3018-2013 OI Hunter, Zachary/0000-0002-1689-1691 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 2004 VL 104 IS 11 MA 4930 BP 314B EP 314B PN 2 PG 1 WC Hematology SC Hematology GA 871JO UT WOS:000225127701256 ER PT J AU Tournilhac, O Santos, DD Xu, LA Hatjiharissi, E Tai, YT Catley, L Hunter, Z Branagan, A Burger, R Shringarpure, R Boyce, J Anderson, KC Treon, SP AF Tournilhac, O Santos, DD Xu, LA Hatjiharissi, E Tai, YT Catley, L Hunter, Z Branagan, A Burger, R Shringarpure, R Boyce, J Anderson, KC Treon, SP TI Lymphoplasmacytic cells and mast cells are targets for imatinib Mesylate (Gleevee, glivec) in Waldenstrom's macroglobulinemia. SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Dana Farber Canc Inst, Bing Program Waldenstroms Macroglobulinemia, Boston, MA USA. Brigham & Womens Hosp, Boston, MA 02115 USA. Harvard Univ, Sch Med, Boston, MA 02115 USA. RI Hunter, Zachary/H-3018-2013; Catley, Laurence/E-5313-2013 OI Hunter, Zachary/0000-0002-1689-1691; 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 2004 VL 104 IS 11 MA 4929 BP 314B EP 314B PN 2 PG 1 WC Hematology SC Hematology GA 871JO UT WOS:000225127701255 ER PT J AU Steidl, U Rosenbauer, F Gu, XS Owens, B Klippel, S Wagner, K Aivado, M Libermann, TA Tenen, DG AF Steidl, U Rosenbauer, F Gu, XS Owens, B Klippel, S Wagner, K Aivado, M Libermann, TA Tenen, DG TI Knockdown of the transcription factor PU.1 causes characteristic transcriptional changes in hematopoietic stem cells prior to leukemic transformation SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Harvard Inst Med, Div Hematol Oncol, Boston, MA USA. Beth Israel Deaconess Med Ctr, BIDMC Genom Ctr, Boston, MA 02215 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 2004 VL 104 IS 11 MA 1112 BP 316A EP 316A PN 1 PG 1 WC Hematology SC Hematology GA 871JM UT WOS:000225127501114 ER PT J AU Bourquin, JP Langebrake, C Subramanian, A Li, XC Reinhardt, D Bernard, O Zwaan, CM Hasle, H Schrappe, M Golub, TR Orkin, SH AF Bourquin, JP Langebrake, C Subramanian, A Li, XC Reinhardt, D Bernard, O Zwaan, CM Hasle, H Schrappe, M Golub, TR Orkin, SH TI A molecular signature of the transcription factor GATA1 in acute megakaryoblastic leukemia of childhood SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Dana Farber Canc Inst, Boston, MA 02115 USA. Childrens Hosp, Boston, MA 02115 USA. MIT, Whitehead Inst, CGR, Cambridge, MA 02139 USA. RI Schrappe, Martin/A-8109-2010; Reinhardt, Dirk/D-3939-2011 OI Reinhardt, Dirk/0000-0003-4313-9056 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 2004 VL 104 IS 11 MA 1117 BP 317A EP 317A PN 1 PG 1 WC Hematology SC Hematology GA 871JM UT WOS:000225127501119 ER PT J AU Chiaretti, S Li, XC Gentleman, R Li, C Vitale, A Mancini, M Mecucci, C Foa, R Ritz, J AF Chiaretti, S Li, XC Gentleman, R Li, C Vitale, A Mancini, M Mecucci, C Foa, R Ritz, J TI Identification of a LOH region on chromosome 9p associated with a specific gene expression signature in adult B-lineage ALL through integration of high density microarray expression and SNP analyses SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Univ Roma La Sapienza, Div Hematol, Rome, Italy. Dana Farber Canc Inst, Dept Biostat Sci, Boston, MA 02115 USA. Univ Perugia, Monteluce Policlin, Haematol & Bone Marrow Transplantat Unit, I-06100 Perugia, Italy. Dana Farber Canc Inst, Dept Med Oncol, 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 2004 VL 104 IS 11 MA 1119 BP 317A EP 317A PN 1 PG 1 WC Hematology SC Hematology GA 871JM UT WOS:000225127501121 ER PT J AU Zhou, DC Kim, H Tallman, MS Gallagher, RE AF Zhou, DC Kim, H Tallman, MS Gallagher, RE TI Relapse of acute promyelocytic leukemia (APL) is associated with increased methylation of the retinoic acid receptor-beta2 (RAR beta 2) gene promoter SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Albert Einstein Canc Ctr, Bronx, NY USA. Dana Farber Canc Inst, Boston, MA 02115 USA. Northwestern Univ, Feinberg Sch Med, Chicago, IL 60611 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 2004 VL 104 IS 11 MA 1124 BP 318A EP 319A PN 1 PG 2 WC Hematology SC Hematology GA 871JM UT WOS:000225127501126 ER PT J AU Vallat, LD Kemper, CA Park, Y Rassenti, LZ Fisher, JW Gribben, JG AF Vallat, LD Kemper, CA Park, Y Rassenti, LZ Fisher, JW Gribben, JG TI Reprogramming the transcriptional response of chronic lymphocytic leukemia (CLL) cells: Influencing the temporal gene regulatory network SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Harvard Univ, Sch Med, Dana Farber Canc Inst, Boston, MA 02115 USA. MIT, Cambridge, MA 02139 USA. Harvard Univ, Sch Publ Hlth, Boston, MA 02115 USA. Univ Calif San Diego, CLL Res Consortium, La Jolla, CA 92093 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 2004 VL 104 IS 11 MA 1128 BP 319A EP 320A PN 1 PG 2 WC Hematology SC Hematology GA 871JM UT WOS:000225127501130 ER PT J AU Zorn, E Floyd, B Tweel, A Miklos, DB Bellucci, R Canning, C Soiffer, RJ Antin, J Ritz, J AF Zorn, E Floyd, B Tweel, A Miklos, DB Bellucci, R Canning, C Soiffer, RJ Antin, J Ritz, J TI The Y-specific gene PRY is expressed in normal blood cells as well as leukemia cells and can elicit a specific antibody response in male recipients of hematopoietic stem cells from female donors. SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA 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 2004 VL 104 IS 11 MA 4976 BP 325B EP 325B PN 2 PG 1 WC Hematology SC Hematology GA 871JO UT WOS:000225127701302 ER PT J AU Cutler, C Li, SL Kim, HT Alyea, E Ho, V Lee, SJ Fisher, DC Schlossman, R Miklos, D Sonis, S Soiffer, R Antin, JH AF Cutler, C Li, SL Kim, HT Alyea, E Ho, V Lee, SJ Fisher, DC Schlossman, R Miklos, D Sonis, S Soiffer, R Antin, JH TI Sirolimus and tacrolimus as graft-vs.-host disease prophylaxis in allogeneic stem cell transplantation: The Dana-Farber cancer institute experience. SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA 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 2004 VL 104 IS 11 MA 1227 BP 346A EP 347A PN 1 PG 2 WC Hematology SC Hematology GA 871JM UT WOS:000225127501229 ER PT J AU Brandao, JG Barata, JT Nunes, R Nadler, LM Cardoso, AA AF Brandao, JG Barata, JT Nunes, R Nadler, LM Cardoso, AA TI Crosstalk between breast cancer cells and bone marrow endothelium require the engagement of PI3K/Akt signaling. SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Dana Farber Canc Inst, Dept Med Oncol, Boston, MA USA. Inst Mol Med, 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 2004 VL 104 IS 11 MA 1299 BP 366A EP 366A PN 1 PG 1 WC Hematology SC Hematology GA 871JM UT WOS:000225127501302 ER PT J AU Westervelt, P Holmes, W Emmons, R Becker, P Lowry, P Traynor, A Ballen, K AF Westervelt, P Holmes, W Emmons, R Becker, P Lowry, P Traynor, A Ballen, K TI Favorable outcomes with acceptable toxicity using a reduced intensity conditioning regimen for patients otherwise ineligible for related donor allogeneic stem cell transplantation. SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Univ Washington, Sch Med, Seattle, WA 98195 USA. Univ Massachusetts, Sch Med, Worcester, MA 01605 USA. Temple Univ, Sch Med, Philadelphia, PA 19122 USA. 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 2004 VL 104 IS 11 MA 5137 BP 368B EP 368B PN 2 PG 1 WC Hematology SC Hematology GA 871JO UT WOS:000225127701463 ER PT J AU Ng, AK Hua, L Wu, BY Neuberg, D Silver, B Mauch, PM AF Ng, AK Hua, L Wu, BY Neuberg, D Silver, B Mauch, PM TI A prospective study on pulmonary function in patients receiving Hodgkin's disease therapy. SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 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 2004 VL 104 IS 11 MA 1319 BP 371A EP 371A PN 1 PG 1 WC Hematology SC Hematology GA 871JM UT WOS:000225127501322 ER PT J AU Hirano, N Butler, MO Xia, ZN Nadler, LM AF Hirano, N Butler, MO Xia, ZN Nadler, LM TI Highly efficient presentation of endogenously processed class I peptides by artificial APC for the generation of effective anti-tumor responses. SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02115 USA. Harvard Univ, 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 2004 VL 104 IS 11 MA 1355 BP 381A EP 381A PN 1 PG 1 WC Hematology SC Hematology GA 871JM UT WOS:000225127501358 ER PT J AU Kriangkum, J Taylor, BJ Strachan, ER Treon, SP Mant, MJ Reiman, T Belch, AR Pilarski, LM AF Kriangkum, J Taylor, BJ Strachan, ER Treon, SP Mant, MJ Reiman, T Belch, AR Pilarski, LM TI Mutator genes UDG and AID appear to be normal in class-switch deficient and clonally homogeneous Waidenstrom's macroglobulinemias having either germline or hypermutated clonotypic IgH VDJ. SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA 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 2004 VL 104 IS 11 MA 1359 BP 382A EP 382A PN 1 PG 1 WC Hematology SC Hematology GA 871JM UT WOS:000225127501362 ER PT J AU Adamia, S Treon, SP Mant, MJ Larratt, LM Reiman, T Belch, AR Pilarski, LM AF Adamia, S Treon, SP Mant, MJ Larratt, LM Reiman, T Belch, AR Pilarski, LM TI Polymorphisms in the hyaluronan synthase 1 gene may be predisposing factors for Waidenstrom's macroglobulinemia. SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Univ Alberta, Edmonton, AB T6G 2M7, Canada. Cross Canc Inst, Edmonton, AB T6G 1Z2, Canada. Dana Farber Canc Inst, Dept Adult 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 2004 VL 104 IS 11 MA 1363 BP 383A EP 383A PN 1 PG 1 WC Hematology SC Hematology GA 871JM UT WOS:000225127501366 ER PT J AU Shenkier, T Blay, JY O'Neill, BP Poortmans, P Janke, K Abrey, LE Neuwelt, E Tsang, R Batchelor, T Harris, N Ferreri, AJ Ponzoni, M O'Brien, P Rubenstein, J Connors, JM AF Shenkier, T Blay, JY O'Neill, BP Poortmans, P Janke, K Abrey, LE Neuwelt, E Tsang, R Batchelor, T Harris, N Ferreri, AJ Ponzoni, M O'Brien, P Rubenstein, J Connors, JM TI Primary central nervous system lymphoma of T cell origin: A descriptive analysis of 45 cases from the International PCNSL Collaborative Group. SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 British Columbia Canc Agcy, Vancouver, BC V5Z 4E6, Canada. Hop Edouard Herriot, Unite Cytokines & Canc, Ctr Leon Berard, Lyon, France. Mayo Clin, Ctr Canc, Neurooncol Program, Rochester, MN USA. Dr Bernard Verbeeten Inst, Tilburg, Netherlands. Charite, Berlin, Germany. Mem Sloan Kettering Canc Ctr, Dept Neurol, New York, NY 10021 USA. Oregon Hlth & Sci Univ, Dept Neurol & Neurosurg, Portland, OR 97201 USA. Princess Margaret Hosp, Dept Radiat Oncol, Toronto, ON M4X 1K9, Canada. Harvard Univ, Sch Med, Massachusetts Gen Hosp, Dept Neurol, Boston, MA 02115 USA. Harvard Univ, Sch Med, Massachusetts Gen Hosp, Dept Pathol, Boston, MA 02115 USA. Ist Sci San Raffaele, Dept Radiochemotherapy, I-20132 Milan, Italy. Ist Sci San Raffaele, Dept Pathol, I-20132 Milan, Italy. Newcastle Mater Hosp, Dept Radiat Oncol, Newcastle, NSW, Australia. Univ Calif San Francisco, San Francisco, CA 94143 USA. RI Ferreri, Andres Jose Maria/A-6662-2013; Poortmans, P.M.P./L-4581-2015; Blay, Jean-Yves/N-3966-2016 OI Ferreri, Andres Jose Maria/0000-0001-9606-6124; Blay, Jean-Yves/0000-0001-7190-120X NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 2021 L ST NW, SUITE 900, WASHINGTON, DC 20036 USA SN 0006-4971 EI 1528-0020 J9 BLOOD JI Blood PD NOV 16 PY 2004 VL 104 IS 11 MA 1372 BP 385A EP 385A PN 1 PG 1 WC Hematology SC Hematology GA 871JM UT WOS:000225127501375 ER PT J AU Friedberg, JW Kho, ME Lepisto, EM Rodriguez, MA TerVeer, A LaCasce, AS Nademanee, AP Millenson, M Czuczman, M Niland, J Zelenetz, AD Weeks, JC AF Friedberg, JW Kho, ME Lepisto, EM Rodriguez, MA TerVeer, A LaCasce, AS Nademanee, AP Millenson, M Czuczman, M Niland, J Zelenetz, AD Weeks, JC TI Newly diagnosed follicular (FL), mantle cell (MCL), and diffuse large B cell (DLCL) non-Hodgkin's lymphoma (NHL) in 5 United States comprehensive cancer centers: An analysis from the national comprehensive cancer network (NCCN) NHL outcomes project. SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Wilmot Canc Ctr, Lymphoma Program, Rochester, NY USA. Dana Farber Canc Inst, Boston, MA 02115 USA. Natl Comprehens Canc Network, Jenkintown, PA USA. City Hope Natl Med Ctr, Duarte, CA 91010 USA. Fox Chase Canc Ctr, Philadelphia, PA 19111 USA. Univ Texas, MD Anderson Canc Ctr, Houston, TX 77030 USA. Mem Sloan Kettering Canc Ctr, New York, NY 10021 USA. Roswell Pk Canc Inst, Buffalo, NY 14263 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 2004 VL 104 IS 11 MA 1391 BP 391A EP 391A PN 1 PG 1 WC Hematology SC Hematology GA 871JM UT WOS:000225127501394 ER PT J AU Freedman, AS Gribben, JG Neuberg, D Li, S Kim, H Mauch, P Nadler, LM AF Freedman, AS Gribben, JG Neuberg, D Li, S Kim, H Mauch, P Nadler, LM TI Autologous bone marrow transplantation for follicular lymphoma in first remission: Long term follow up of two sequential trials with standard dose and high dose CHOP induction SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA 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 2004 VL 104 IS 11 MA 5243 BP 396B EP 396B PN 2 PG 1 WC Hematology SC Hematology GA 871JO UT WOS:000225127701569 ER PT J AU Shammas, MA Koley, H Shah, S Batchu, RB Tassone, P Anderson, KC Munshi, NC AF Shammas, MA Koley, H Shah, S Batchu, RB Tassone, P Anderson, KC Munshi, NC TI Dysregulated apurinic/apyrimidinic endonucleases (Ape1 and Ape2) lead to genetic instability in multiple myeloma. SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 VA Boston Healthcare Syst, Med Serv, W Roxbury, MA USA. Dana Farber Canc Inst, Jerome Lipper Multiple Myeloma Ctr, Dept Med Oncol, Boston, MA 02115 USA. Harvard Univ, 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 2004 VL 104 IS 11 MA 1418 BP 397A EP 398A PN 1 PG 2 WC Hematology SC Hematology GA 871JM UT WOS:000225127501421 ER PT J AU van Ness, B Blood, E Greipp, P Kay, N Rajkumar, V Kyle, R Oken, M Fonseca, R Zhao, FY AF van Ness, B Blood, E Greipp, P Kay, N Rajkumar, V Kyle, R Oken, M Fonseca, R Zhao, FY TI Associations of DNA repair gene polymorphisms in XRCC1 and ERCC2 with clinical outcome in ECOG trial E9486. SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Univ Minnesota, Dept Genet Cell Biol & Dev, Minneapolis, MN USA. Dana Farber Canc Inst, Dept Biostat Sci, Boston, MA 02115 USA. Mayo Clin, Div Hematol, Rochester, MN USA. N Mem Hosp, Dept Med, Robbinsdale, MN USA. Mayo Clin, Div Hematol, Scottsdale, AZ 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 2004 VL 104 IS 11 MA 1475 BP 412A EP 413A PN 1 PG 2 WC Hematology SC Hematology GA 871JM UT WOS:000225127501478 ER PT J AU Branagan, AR Hunter, Z Santos, D Moran, J Treon, SP AF Branagan, AR Hunter, Z Santos, D Moran, J Treon, SP TI Thalidomide and rituximab in Waldenstrorm's macroglobulinemia. SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Harvard Univ, Sch Med, Dana Farber Canc Inst, Bing Program Waldenstroms Macroglobulinemia, Boston, MA 02115 USA. RI Hunter, Zachary/H-3018-2013 OI Hunter, Zachary/0000-0002-1689-1691 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 2004 VL 104 IS 11 MA 1484 BP 415A EP 415A PN 1 PG 1 WC Hematology SC Hematology GA 871JM UT WOS:000225127501486 ER PT J AU Ishitsuka, K Hideshima, T Hamasaki, M Noopur, R Shaji, K Hideshima, H Shiraishi, N Richardson, P Munshi, NC Chauhan, D Arbiser, J Anderson, KC AF Ishitsuka, K Hideshima, T Hamasaki, M Noopur, R Shaji, K Hideshima, H Shiraishi, N Richardson, P Munshi, NC Chauhan, D Arbiser, J Anderson, KC TI Honokiol overcomes conventional drug resistance in human multiple myeloma. SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Dana Farber Canc Inst, Dept Med Oncol, Jerome Lipper Multiple Myeloma Ctr, Boston, MA 02115 USA. Harvard Univ, Sch Med, Boston, MA USA. Emory Univ, Sch Med, Dept Dermatol, Atlanta, GA 30322 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 2004 VL 104 IS 11 MA 1488 BP 416A EP 416A PN 1 PG 1 WC Hematology SC Hematology GA 871JM UT WOS:000225127501490 ER PT J AU Raje, N Kumar, S Hideshima, T Ishitsuka, K Chauhan, D Mitsiades, C Podar, K Le Gouill, S Richardson, P Munshi, NC Stirling, DI Antin, JH Anderson, KC AF Raje, N Kumar, S Hideshima, T Ishitsuka, K Chauhan, D Mitsiades, C Podar, K Le Gouill, S Richardson, P Munshi, NC Stirling, DI Antin, JH Anderson, KC TI Combination of the mTOR inhibitor rapamycin and Revlimid (TM) (CC-5013) has synergistic activity in multiple myeloma (MM) SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Dana Farber Canc Inst, Boston, MA 02115 USA. Mayo Clin, Div Hematol, Rochester, MN USA. Celgene Corp, NA, Warren, NJ USA. RI Kumar, Shaji/A-9853-2008 OI Kumar, Shaji/0000-0001-5392-9284 NR 0 TC 4 Z9 4 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 2004 VL 104 IS 11 MA 1492 BP 417A EP 417A PN 1 PG 1 WC Hematology SC Hematology GA 871JM UT WOS:000225127501494 ER PT J AU Mitsiades, N McMullan, C Poulaki, V Negri, J Raje, N Kumar, S Sikoutri, D Hideshima, T Chauhan, D Richardson, PG Schlossman, RL Kung, AL Lane, H Munshi, NC Anderson, KC Mitsiades, CS AF Mitsiades, N McMullan, C Poulaki, V Negri, J Raje, N Kumar, S Sikoutri, D Hideshima, T Chauhan, D Richardson, PG Schlossman, RL Kung, AL Lane, H Munshi, NC Anderson, KC Mitsiades, CS TI The mTOR inhibitor RAD001 (everolimus) is active against multiple myeloma cells in vitro and in vivo SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Beth Israel Deaconess Med Ctr, Dept Med, Boston, MA 02215 USA. Harvard Univ, Sch Med, Jerome Lipper Multiple Myeloma Ctr, Dept Med Oncol,Dana Farber Canc Inst, Boston, MA USA. Harvard Univ, Sch Med, Dept Pediat Oncol, Dana Farber Canc Inst, Boston, MA USA. Novartis Pharma AG, Basel, Switzerland. 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 2004 VL 104 IS 11 MA 1496 BP 418A EP 418A PN 1 PG 1 WC Hematology SC Hematology GA 871JM UT WOS:000225127501498 ER PT J AU Tai, YT Catley, L Li, XF Hamasaki, M Podar, K Hideshima, T Chauhan, D Schlossman, R Richardson, P Streon, SP Munshi, NC Anderson, KC AF Tai, YT Catley, L Li, XF Hamasaki, M Podar, K Hideshima, T Chauhan, D Schlossman, R Richardson, P Streon, SP Munshi, NC Anderson, KC TI Enhanced cytotoxicity of monoclonal antibody SGN-40 and immunomodulatory drug IMiD3 against human multiple myeloma SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Dana Farber Canc Inst, Jerome Lipper Multiple Myeloma Ctr, Dept Med Oncol, 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 2004 VL 104 IS 11 MA 1498 BP 418A EP 419A PN 1 PG 2 WC Hematology SC Hematology GA 871JM UT WOS:000225127501500 ER PT J AU Richardson, P Schlossman, RL Mitsiades, CS Munshi, NC Colson, K Doss, D McKenney, M Hande, K Gorelik, S Lunde, L Stepanek, A Freeman, A Dinand, K Hayes, S Michelle, R Doucet, K Warren, D Mitsiades, N Richon, VM Chiao, J Anderson, KC AF Richardson, P Schlossman, RL Mitsiades, CS Munshi, NC Colson, K Doss, D McKenney, M Hande, K Gorelik, S Lunde, L Stepanek, A Freeman, A Dinand, K Hayes, S Michelle, R Doucet, K Warren, D Mitsiades, N Richon, VM Chiao, J Anderson, KC TI Phase I clinical trial of oral administration of the histone deacetylase (HDAC) inhibitor suberoylanilide hydroxamic acid (SAHA) in patients with relapsed/refractory multiple myeloma SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Harvard Univ, Sch Med, Jerome Lipper Multiple Myeloma Ctr, Dep Med Omcol,Dana Farber Canc Inst, Boston, MA 02115 USA. Atom Pharma, Merck & Co Inc, Tarrytown, NY USA. 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 2004 VL 104 IS 11 MA 1503 BP 420A EP 420A PN 1 PG 1 WC Hematology SC Hematology GA 871JM UT WOS:000225127501505 ER PT J AU Okuda, K Sonoda, Y Griffin, JD AF Okuda, K Sonoda, Y Griffin, JD TI A new model to evaluate signaling of Raf in hematopoietic cells SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Kyoto Prefectural Univ Med, Kyoto, 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 2004 VL 104 IS 11 MA 1533 BP 429A EP 429A PN 1 PG 1 WC Hematology SC Hematology GA 871JM UT WOS:000225127501535 ER PT J AU Wu, CJ Gladwin, MT Krishnamurti, L Biernacki, M Rogers, SA Wang, XD Antin, JH Ritz, J AF Wu, CJ Gladwin, MT Krishnamurti, L Biernacki, M Rogers, SA Wang, XD Antin, JH Ritz, J TI Mixed chimerism following nonmyeloablative stem cell transplantation for sickle cell disease prevents intravascular hemolysis and restores endothelial function. SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02115 USA. Brigham & Womens Hosp, Dept Med, Boston, MA 02115 USA. Childrens Hosp Pittsburgh, Div Hematol Oncol, Pittsburgh, PA 15213 USA. Childrens Hosp Pittsburgh, BMT, Pittsburgh, PA 15213 USA. NHLBI, Vasc Therapeut Sect, Cardiovasc Branch, NIH, Bethesda, MD 20892 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 2004 VL 104 IS 11 MA 1679 BP 467A EP 467A PN 1 PG 1 WC Hematology SC Hematology GA 871JM UT WOS:000225127501681 ER PT J AU Miyake, N Brun, ACM Magnusson, M Scadden, DT Karlsson, S AF Miyake, N Brun, ACM Magnusson, M Scadden, DT Karlsson, S TI Hematopoietic stem cell expansion by HOXB4 is greatly enhanced in p21 deficient stem cells. SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Univ Lund Hosp, S-22185 Lund, Sweden. Harvard Univ, Massachusetts Gen Hosp, Sch Med, Ctr Regenerat Med & Technol, 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 2004 VL 104 IS 11 MA 1688 BP 469A EP 470A PN 1 PG 2 WC Hematology SC Hematology GA 871JM UT WOS:000225127501690 ER PT J AU Gilbert, GE Kaufman, RJ Price, P Mao, H Pipe, SW AF Gilbert, GE Kaufman, RJ Price, P Mao, H Pipe, SW TI His2315/Gln2316 of the factor VIIIC2 domain interact with phospholipid membranes and influence activity of the factor Xase complex SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Boston VA Healthcare Syst, Boston, MA USA. Brigham & Womens Hosp, Boston, MA 02115 USA. Harvard Univ, Sch Med, Boston, MA 02115 USA. Univ Michigan, Ann Arbor, MI 48109 USA. Howard Hughes Med Inst, Ann Arbor, MI USA. Univ Michigan, Ann Arbor, MI 48109 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 2004 VL 104 IS 11 MA 1727 BP 479A EP 479A PN 1 PG 1 WC Hematology SC Hematology GA 871JM UT WOS:000225127501729 ER PT J AU Gilbert, GE Bhimavarapu, A Price, P Jacquemin, M AF Gilbert, GE Bhimavarapu, A Price, P Jacquemin, M TI Antibody to C1 domain of factor VIII alters interaction of factor Xase complex with factor X SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Boston VA Healthcare Syst, Boston, MA USA. Brigham & Womens Hosp, Boston, MA 02115 USA. Harvard Univ, Sch Med, Boston, MA 02115 USA. Katholieke Univ Leuven, Louvain, Belgium. 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 2004 VL 104 IS 11 MA 1738 BP 482A EP 482A PN 1 PG 1 WC Hematology SC Hematology GA 871JM UT WOS:000225127501740 ER PT J AU Bradner, J Hallisey, RK Kuter, DJ AF Bradner, J Hallisey, RK Kuter, DJ TI Fondaparinux in the treatment of heparin-induced thrombocytopenia SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Massachusetts Gen Hosp, Dept Hematol Oncol, Boston, MA 02114 USA. Massachusetts Gen Hosp, Dept Pharm, Boston, MA 02114 USA. NR 0 TC 8 Z9 8 U1 1 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 2004 VL 104 IS 11 MA 1775 BP 492A EP 492A PN 1 PG 1 WC Hematology SC Hematology GA 871JM UT WOS:000225127501777 ER PT J AU De Angelo, DJ Stone, RM Heaney, ML Nimer, SD Paquette, R Bruner-Klisovic, R Caligiuri, MA Cooper, MR Le-Cerf, JM Iyer, G AF De Angelo, DJ Stone, RM Heaney, ML Nimer, SD Paquette, R Bruner-Klisovic, R Caligiuri, MA Cooper, MR Le-Cerf, JM Iyer, G TI Phase II evaluation of the tyrosine kinase inhibitor MLN518 in patients with acute myeloid leukemia (AML) bearing a FLT3 internal tandem duplication (ITD) mutation. SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Dana Farber Canc Inst, Dept Med, Boston, MA 02115 USA. Mem Sloan Kettering Canc Ctr, Div Hematol Oncol, New York, NY 10021 USA. Univ Calif Los Angeles, Dept Med, Los Angeles, CA 90024 USA. Ohio State Univ, Ctr Comprehens Canc, Columbus, OH 43210 USA. Millennium Pharmaceut, Cambridge, MA USA. Oregon Hlth Sci Univ, Dept Med, Portland, OR 97201 USA. NR 0 TC 12 Z9 12 U1 1 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 2004 VL 104 IS 11 MA 1792 BP 496A EP 497A PN 1 PG 2 WC Hematology SC Hematology GA 871JM UT WOS:000225127501793 ER PT J AU Attar, EC DeAngelo, DJ Ballen, KK Learner, E Trehu, EG Schenkein, DP Levine, JD Stone, RM Amrein, PC AF Attar, EC DeAngelo, DJ Ballen, KK Learner, E Trehu, EG Schenkein, DP Levine, JD Stone, RM Amrein, PC TI Phase I dose escalating trial of bortezomib (Veleade (R)) in combination with idarubicin and cytarabine in patients with acute myeloid leukemia. SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Massachusetts Gen Hosp, Hematol Oncol Unit, Ctr Canc, Boston, MA 02114 USA. Dana Farber Canc Inst, Adult Leukemia Program, Boston, MA 02115 USA. Beth Israel Deaconess Med Ctr, Div Hematol Oncol, Boston, MA 02215 USA. Millenium Pharmaceut Inc, Cambridge, MA 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 2004 VL 104 IS 11 MA 1799 BP 498A EP 499A PN 1 PG 2 WC Hematology SC Hematology GA 871JM UT WOS:000225127501800 ER PT J AU Henry, NL Li, SL Kim, HT Magee, C Alyea, E Ho, V Lee, SJ Soiffer, R Antin, JH Cutler, C AF Henry, NL Li, SL Kim, HT Magee, C Alyea, E Ho, V Lee, SJ Soiffer, R Antin, JH Cutler, C TI Sirolimus and thrombotic microangiopathy after allogeneic stem cell transplantation. SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Dana Farber Canc Inst, Boston, MA 02115 USA. Brigham & Womens Hosp, Boston, MA 02115 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 2004 VL 104 IS 11 MA 1834 BP 508A EP 508A PN 1 PG 1 WC Hematology SC Hematology GA 871JM UT WOS:000225127501835 ER PT J AU Spitzer, TR Cox, B Sepe, P McAfee, SL Dey, BR Ballan, K Scadden, D AF Spitzer, TR Cox, B Sepe, P McAfee, SL Dey, BR Ballan, K Scadden, D TI Dose adjusted IV busulfan/cyclophosphamide (BU/CY) and autologous (AU) stem cell transplantation (SCT) for recurrent lymphoma. SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Massachusetts Gen Hosp, Bone Marrow Transplant Program, Boston, MA 02114 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 2004 VL 104 IS 11 MA 1884 BP 522A EP 522A PN 1 PG 1 WC Hematology SC Hematology GA 871JM UT WOS:000225127501885 ER PT J AU Zhou, JB Xia, ZN Li, AH Gribben, JG AF Zhou, JB Xia, ZN Li, AH Gribben, JG TI Mapping low molecular weight plasma proteome of chronic lymphoblastic leukemia patients using MALDI-TOF mass spectrometry. SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Harvard Univ, Sch Med, CLL Res Consortium, 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 2004 VL 104 IS 11 MA 1910 BP 528A EP 528A PN 1 PG 1 WC Hematology SC Hematology GA 871JM UT WOS:000225127501911 ER PT J AU Mestan, J Ellen, W Sandra, CJ Doriano, F Pascal, F Gabriele, F Gerard, G Dominique, K Markus, G James, GD Paul, MW AF Mestan, J Ellen, W Sandra, CJ Doriano, F Pascal, F Gabriele, F Gerard, G Dominique, K Markus, G James, GD Paul, MW TI AMN107: In vitro profile of a new inhibitor of the tyrosine kinase activity of Bcr-Abl. SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Novartis Inst Biomed Res, Basel, Switzerland. Dana Farber Canc Inst, Boston, MA 02115 USA. NR 0 TC 3 Z9 3 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 2004 VL 104 IS 11 MA 1978 BP 546A EP 546A PN 1 PG 1 WC Hematology SC Hematology GA 871JM UT WOS:000225127501979 ER PT J AU Juszczynski, P Kutok, JL Aguiar, RCT Mitra, J Shipp, MA AF Juszczynski, P Kutok, JL Aguiar, RCT Mitra, J Shipp, MA TI B-Aggressive lymphoma gene (BAL) is a risk-related, gamma-IFN-inducible gene that is expressed in primary diffuse large B-cell lymphomas with a brisk host inflammatory response. SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA 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 2004 VL 104 IS 11 MA 2035 BP 561A EP 561A PN 1 PG 1 WC Hematology SC Hematology GA 871JM UT WOS:000225127502036 ER PT J AU Chandra, J Tracy, J Gorre, M Talpaz, M Griffin, J Verstovsek, S Beran, M Sawyers, C Sausville, E Kaufmann, S AF Chandra, J Tracy, J Gorre, M Talpaz, M Griffin, J Verstovsek, S Beran, M Sawyers, C Sausville, E Kaufmann, S TI Effects of adaphostin, a novel tyrphostin inhibitor, in diverse models of imatinib mesylate resistance. SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 MD Anderson Canc Ctr, Dept Pediat Res, Houston, TX USA. MD Anderson Canc Ctr, Dept Leukemia, Houston, TX USA. Univ Calif Los Angeles, Div Hematol Oncol, Los Angeles, CA USA. Dana Farber Canc Inst, Dept Adult Oncol, Boston, MA 02115 USA. NCI, Dev Therapeut Program, Div Canc Treatment & Diag, Bethesda, MD 20892 USA. Mayo Clin, Div Oncol Res & Hematol, Rochester, MN USA. RI Sawyers, Charles/G-5327-2016 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 2004 VL 104 IS 11 MA 2097 BP 577A EP 577A PN 1 PG 1 WC Hematology SC Hematology GA 871JM UT WOS:000225127502098 ER PT J AU Bellucci, R Gallagher, M Nguyen, HN Alyea, EP Zorn, E Anderson, KC Munshi, NC Ritz, J AF Bellucci, R Gallagher, M Nguyen, HN Alyea, EP Zorn, E Anderson, KC Munshi, NC Ritz, J TI PDC-E2, a common auto antigen in primary biliary cirrhosis (PBC) is also a target of an antibody response in patients who achieve complete remission after donor lymphocyte infusion. SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA 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 2004 VL 104 IS 11 MA 2121 BP 583A EP 583A PN 1 PG 1 WC Hematology SC Hematology GA 871JM UT WOS:000225127502122 ER PT J AU Saito, TI Rubio, MT Sykes, M AF Saito, TI Rubio, MT Sykes, M TI Clinical relevance of recipient leukocyte infusion (RLI) therapy. SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA 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 2004 VL 104 IS 11 MA 2120 BP 583A EP 583A PN 1 PG 1 WC Hematology SC Hematology GA 871JM UT WOS:000225127502121 ER PT J AU Hochberg, EP Miklos, D Zorn, E Levin, J Reynolds, C Canning, C Soiffer, RJ Ritz, J AF Hochberg, EP Miklos, D Zorn, E Levin, J Reynolds, C Canning, C Soiffer, RJ Ritz, J TI Genetic disparity between stem cell transplant patients and their donors assessed by high density single nucleotide polymorphism (SNP) microarray typing is seen in specific genomic regions. SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Massachusetts Gen Hosp, Boston, MA 02114 USA. Dana Farber Canc Inst, Div Hematol Malignancies, 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 2004 VL 104 IS 11 MA 2127 BP 585A EP 585A PN 1 PG 1 WC Hematology SC Hematology GA 871JM UT WOS:000225127502128 ER PT J AU Zorn, E Lista, D Kim, H Bellucci, R Canning, C Soiffer, RJ Ritz, J AF Zorn, E Lista, D Kim, H Bellucci, R Canning, C Soiffer, RJ Ritz, J TI Low-dose administration of recombinant IL-2 following T cell depleted bone marrow transplantaion induces expansion of CD4+CD25+FOXP3+regulatory T cells in vivo. SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA 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 2004 VL 104 IS 11 MA 2136 BP 588A EP 588A PN 1 PG 1 WC Hematology SC Hematology GA 871JM UT WOS:000225127502137 ER PT J AU Colvin, GA Abedi, M Rathore, R Lum, LG Ballen, KK Dey, B Elfenbein, GJ Quesenberry, PJ AF Colvin, GA Abedi, M Rathore, R Lum, LG Ballen, KK Dey, B Elfenbein, GJ Quesenberry, PJ TI Mini-haploidentical transplantation for refractory acute myeloid leukemia. SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Roger Williams Med Ctr, Dept Res, Providence, RI USA. Massachusetts Gen Hosp, Div Hematol Oncol, Boston, MA 02114 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 2004 VL 104 IS 11 MA 2150 BP 591A EP 591A PN 1 PG 1 WC Hematology SC Hematology GA 871JM UT WOS:000225127502151 ER PT J AU Toro, JJ Morales, M Loberiza, FR Freytes, CO AF Toro, JJ Morales, M Loberiza, FR Freytes, CO TI Patterns of use of vascular access devices (VAD) in patients undergoing hematopoietic stem cell transplantation (HSCT): Results of an international survey. SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 S Texas Vet Hlth Care Syst, San Antonio, TX USA. Univ Hosp Nuestra Senora de Candelaria, Med Oncol Serv, Santa Cruz de Tenerife, Canary Islands, Spain. Med Coll Wisconsin, Hlth Policy Inst, Milwaukee, WI 53226 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 2004 VL 104 IS 11 MA 2195 BP 603A EP 603A PN 1 PG 1 WC Hematology SC Hematology GA 871JM UT WOS:000225127502196 ER PT J AU Haining, WN Evans, J Seth, N Callaway, G Wucherpfennig, K Nadler, L Guinan, E AF Haining, WN Evans, J Seth, N Callaway, G Wucherpfennig, K Nadler, L Guinan, E TI Rapid T cell response to vaccination can occur without antibody response in children post HSCT. SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Dana Farber Canc Inst, Boston, MA 02115 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 2004 VL 104 IS 11 MA 2235 BP 614A EP 614A PN 1 PG 1 WC Hematology SC Hematology GA 871JM UT WOS:000225127502236 ER PT J AU Cutler, C Miklos, D Lee, SJ Woo, SB Treister, N Bienfang, D Klickstein, L Levin, J Miller, KH Reynolds, C Pasek, M Ho, V Ritz, J Antin, JH Soiffer, R Alyea, E AF Cutler, C Miklos, D Lee, SJ Woo, SB Treister, N Bienfang, D Klickstein, L Levin, J Miller, KH Reynolds, C Pasek, M Ho, V Ritz, J Antin, JH Soiffer, R Alyea, E TI Rituximab therapy for steroid-refractory chronic GVHD: Safety and efficacy analysis. SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Dana Farber Canc Inst, Boston, MA 02115 USA. Brigham & Womens Hosp, Boston, MA 02115 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 2004 VL 104 IS 11 MA 2251 BP 619A EP 620A PN 1 PG 2 WC Hematology SC Hematology GA 871JM UT WOS:000225127502252 ER PT J AU Scott, BL Maris, M Sandmaier, B Storer, B Chauncey, T Maloney, DG Sorror, M Storb, R Deeg, HJ AF Scott, BL Maris, M Sandmaier, B Storer, B Chauncey, T Maloney, DG Sorror, M Storb, R Deeg, HJ TI Myeloablative versus nonmyeloablative hemopoietic cell transplantation (HCT) for patients with myelodysplasia (MDS) or AML with multilineage dysplasia following MDS (tAML). SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Fred Hutchinson Canc Res Ctr, Div Clin Res, Seattle, WA 98104 USA. Univ Washington, Seattle, WA 98195 USA. VA Puget Sound, Seattle, WA 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 2004 VL 104 IS 11 MA 2320 BP 638A EP 638A PN 1 PG 1 WC Hematology SC Hematology GA 871JM UT WOS:000225127502321 ER PT J AU Tournilhac, O Santos, DD Xu, L Kutok, J Tai, YT Le Gouill, S Hatjiharissi, E Catley, L Hunter, Z Branagan, A Anderson, KC Treon, SP AF Tournilhac, O Santos, DD Xu, L Kutok, J Tai, YT Le Gouill, S Hatjiharissi, E Catley, L Hunter, Z Branagan, A Anderson, KC Treon, SP TI Constitutive expression of CD40L on bone marrow mast cells supports the growth of lymphoplasmacytic cells in patients with Waldenstrom's macroglobulinemia. SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Dana Farber Canc Inst, Bing Program Waldenstroms Macroglobulinemia, Boston, MA 02115 USA. Dana Farber Canc Inst, Jerome Lipper Multiple Myeloma Ctr, Boston, MA 02115 USA. Brigham & Womens Hosp, Boston, MA 02115 USA. Harvard Univ, Sch Med, Boston, MA USA. RI Hunter, Zachary/H-3018-2013; Catley, Laurence/E-5313-2013 OI Hunter, Zachary/0000-0002-1689-1691; 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 2004 VL 104 IS 11 MA 2350 BP 646A EP 646A PN 1 PG 1 WC Hematology SC Hematology GA 871JM UT WOS:000225127502351 ER PT J AU Hideshima, T Tassone, P Chauhan, D Ishitsuka, K Mitsiades, C Raje, N Kumar, S Hamasaki, M Hideshima, H Munshi, NC Richardson, PG Schenkein, D Anderson, KC AF Hideshima, T Tassone, P Chauhan, D Ishitsuka, K Mitsiades, C Raje, N Kumar, S Hamasaki, M Hideshima, H Munshi, NC Richardson, PG Schenkein, D Anderson, KC TI Targeting IKK inhibits multiple myeloma (MM) cell growth in the bone marrow microenvironment. SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Dana Farber Canc Inst, Jerome Lipper Multiple Myeloma Ctr, Boston, MA 02115 USA. Mayo Clin, Dept Internal Med, Rochester, MN USA. Millennium Pharmaceut, Cambridge, 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 2004 VL 104 IS 11 MA 2351 BP 647A EP 647A PN 1 PG 1 WC Hematology SC Hematology GA 871JM UT WOS:000225127502352 ER PT J AU Kumar, S Raje, N Hideshima, T Podar, K Ishitsuka, K Rocarro, A Chauhan, D Munshi, NC Anderson, KC AF Kumar, S Raje, N Hideshima, T Podar, K Ishitsuka, K Rocarro, A Chauhan, D Munshi, NC Anderson, KC TI Endothelial cells induce multiple myeloma cell proliferation protect against conventional and novel therapies. SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Dana Farber Canc Inst, Boston, MA 02115 USA. Harvard Univ, Sch Med, Boston, MA USA. Mayo Clin, Div Hematol, Rochester, MN USA. Mayo Clin, Div Internal Med, Rochester, MN 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 2004 VL 104 IS 11 MA 2354 BP 647A EP 647A PN 1 PG 1 WC Hematology SC Hematology GA 871JM UT WOS:000225127502355 ER PT J AU Hayashi, T Hideshima, T Podar, K Richardson, P Munoz, O Hamasaki, M Ishitsuka, K Yasui, H Murphy, A McEnroe, G Chakravarty, S Dugar, S Higgins, LS Chauhan, D Anderson, KC AF Hayashi, T Hideshima, T Podar, K Richardson, P Munoz, O Hamasaki, M Ishitsuka, K Yasui, H Murphy, A McEnroe, G Chakravarty, S Dugar, S Higgins, LS Chauhan, D Anderson, KC TI TGF-beta receptor I kinase inhibitor downregulates cytokine secretion and multiple myeloma cell growth in the bone marrow microenvironment. SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02115 USA. Harvard Univ, Sch Med, Dept Med, Boston, MA USA. Sapporo Med Univ, Dept Internal Med 1, Sapporo, Hokkaido, Japan. SCIOS Inc, Sunnyvale, 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 2004 VL 104 IS 11 MA 2355 BP 648A EP 648A PN 1 PG 1 WC Hematology SC Hematology GA 871JM UT WOS:000225127502356 ER PT J AU Aivado, M Spentzos, D Germing, U Alterovitz, G Meng, XY Grall, F Giagounidis, AAN Klement, G Steidl, U Otu, HH Iking-Konert, C Czibere, A Prall, WC Shayne, M Ramoni, MF Gattermann, N Mitsiades, CS Haas, R Fung, ET Libermann, TA AF Aivado, M Spentzos, D Germing, U Alterovitz, G Meng, XY Grall, F Giagounidis, AAN Klement, G Steidl, U Otu, HH Iking-Konert, C Czibere, A Prall, WC Shayne, M Ramoni, MF Gattermann, N Mitsiades, CS Haas, R Fung, ET Libermann, TA TI Serum protein profiling with mass spectrometry for the diagnosis of myelodysplastic syndromes. SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Harvard Univ, Dana Farber Canc Inst, Ctr Canc, Boston, MA 02115 USA. Univ Duesseldorf, Dusseldorf, Germany. Ciphergen, Fremont, 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 2004 VL 104 IS 11 MA 2362 BP 649A EP 649A PN 1 PG 1 WC Hematology SC Hematology GA 871JM UT WOS:000225127502362 ER PT J AU Hamasaki, M Hideshima, T Tassone, P Neli, P Ishitsuka, K Akiyama, M Hayashi, T Yasui, H Shiraishi, N Chauhan, D Mitsiades, C Podar, K Gupta, D Picker, DH Jacob, GS Richardson, PG Munshi, NC Anderson, KC AF Hamasaki, M Hideshima, T Tassone, P Neli, P Ishitsuka, K Akiyama, M Hayashi, T Yasui, H Shiraishi, N Chauhan, D Mitsiades, C Podar, K Gupta, D Picker, DH Jacob, GS Richardson, PG Munshi, NC Anderson, KC TI Atiprimod (N-N-diethl-8,8-dipropyl-2-azaspiro[4.5] decane-2-propanamine) inhibits myeloma in vivo SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02115 USA. Callisto Pharmaceut Inc, New York, NY 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 2004 VL 104 IS 11 MA 2401 BP 660A EP 660A PN 1 PG 1 WC Hematology SC Hematology GA 871JM UT WOS:000225127502401 ER PT J AU Kumar, S Blood, E Oken, MM Greipp, PR AF Kumar, S Blood, E Oken, MM Greipp, PR TI Prognostic value of syndecan-1 in multiple myeloma and its relationship with other prognostic factors SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Dana Farber Canc Inst, Eastern Cooperat Oncol Grp, Ctr Stat, Boston, MA 02115 USA. Mayo Clin, Div Hematol, Rochester, MN USA. N Mem Med Ctr, Hubert H Humphrey Canc Ctr, Robbinsdale, MN USA. RI Kumar, Shaji/A-9853-2008 OI Kumar, Shaji/0000-0001-5392-9284 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 2004 VL 104 IS 11 MA 2402 BP 660A EP 660A PN 1 PG 1 WC Hematology SC Hematology GA 871JM UT WOS:000225127502402 ER PT J AU Mitsiades, CS Mitsiades, N Rooney, M Hideshima, T Chauhan, D Munshi, NC Johnson, R Hannah, A Richardson, PG Anderson, KC AF Mitsiades, CS Mitsiades, N Rooney, M Hideshima, T Chauhan, D Munshi, NC Johnson, R Hannah, A Richardson, PG Anderson, KC TI Anti-tumor activity of KOS-953, a cremophor-based formulation of the hsp90 inhibitor 17-AAG SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA 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. Kosan Biosci Inc, Hayward, CA 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 2004 VL 104 IS 11 MA 2404 BP 660A EP 661A PN 1 PG 2 WC Hematology SC Hematology GA 871JM UT WOS:000225127502404 ER PT J AU Mitsiades, CS Mitsiades, N Rooney, M Negri, J Geer, CC Pink, M Pien, C Hideshima, T Chauhan, D Munshi, NC Richardson, PG Barrett, J Tong, JK Grayzel, D Palombella V Adams, J Anderson, KC AF Mitsiades, CS Mitsiades, N Rooney, M Negri, J Geer, CC Pink, M Pien, C Hideshima, T Chauhan, D Munshi, NC Richardson, PG Barrett, J Tong, JK Grayzel, D Palombella, V Adams, J Anderson, KC TI IPI-504: A novel hsp90 inhibitor with in vitro and in vivo antitumor activity SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA 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, Dept Med, Beth Israel Deaconess Med Ctr, Boston, MA 02115 USA. Infin Pharmaceut, Cambridge, 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 2004 VL 104 IS 11 MA 2403 BP 660A EP 660A PN 1 PG 1 WC Hematology SC Hematology GA 871JM UT WOS:000225127502403 ER PT J AU Chauhan, D Li, GL Podar, K Hideshima, T Shrigarpure, R Catley, L Mitsiades, C Munshi, N Sclossman, R Bahjat, R Neuteboom, S Richardson, P Palladino, M Anderson, KC AF Chauhan, D Li, GL Podar, K Hideshima, T Shrigarpure, R Catley, L Mitsiades, C Munshi, N Sclossman, R Bahjat, R Neuteboom, S Richardson, P Palladino, M Anderson, KC TI A novel orally available proteasome inhibitor NPI-0052 induces killing in multiple myeloma (MM) cells resistant to conventional and bortezomib therapies SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Nereus Pharmaceut, San Diego, CA USA. Dana Farber Canc Inst, Boston, MA 02115 USA. RI Catley, Laurence/E-5313-2013 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 2004 VL 104 IS 11 MA 2405 BP 661A EP 661A PN 1 PG 1 WC Hematology SC Hematology GA 871JM UT WOS:000225127502405 ER PT J AU Kumar, S Raje, N Hideshima, T Ishitsuka, K Roccaro, A Shiraishi, N Hamasaki, M Yasui, H Munshi, NC Figg, WD Anderson, KC AF Kumar, S Raje, N Hideshima, T Ishitsuka, K Roccaro, A Shiraishi, N Hamasaki, M Yasui, H Munshi, NC Figg, WD Anderson, KC TI Anti-myeloma activity of two novel N-substituted and tetraflourinated thalidomide analogues SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Dana Farber Canc Inst, Boston, MA 02115 USA. Harvard Univ, Sch Med, Boston, MA USA. Mayo Clin & Mayo Fdn, Rochester, MN 55905 USA. NCI, Mol Pharmacol Sect, Canc Therapeut Branch, NIH, Bethesda, MD 20892 USA. RI Kumar, Shaji/A-9853-2008; Figg Sr, William/M-2411-2016 OI Kumar, Shaji/0000-0001-5392-9284; 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 2004 VL 104 IS 11 MA 2406 BP 661A EP 661A PN 1 PG 1 WC Hematology SC Hematology GA 871JM UT WOS:000225127502406 ER PT J AU Hideshima, T Chauhan, D Ishitsuka, K Raje, N Kumar, S Podar, K Mitsiades, C Hideshima, H Bonham, L Munshi, NC Richardson, PG Singer, JW Anderson, KC AF Hideshima, T Chauhan, D Ishitsuka, K Raje, N Kumar, S Podar, K Mitsiades, C Hideshima, H Bonham, L Munshi, NC Richardson, PG Singer, JW Anderson, KC TI Molecular characterization of PS-341 (bortezomib) resistance: Implications for overcoming resistance using lysophosphatidic acid acyltransferase (LPAAT)-beta inhibitors SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Dana Farber Canc Inst, Jerome Lipper Multiple Myeloma Ctr, Boston, MA 02115 USA. Mayo Clin, Dept Internal Med, Rochester, MN USA. Cell Therapeut Inc, Seattle, WA USA. RI Kumar, Shaji/A-9853-2008 OI Kumar, Shaji/0000-0001-5392-9284 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 2004 VL 104 IS 11 MA 2411 BP 663A EP 663A PN 1 PG 1 WC Hematology SC Hematology GA 871JM UT WOS:000225127502411 ER PT J AU Hussein, MA Niesvizky, R Munshi, N Berenson, JC Anderson, KC Ryan, K Baumgartner, K Miller, DM McDonald, M AF Hussein, MA Niesvizky, R Munshi, N Berenson, JC Anderson, KC Ryan, K Baumgartner, K Miller, DM McDonald, M TI A phase I, multi-dose, dose escalation study of SGN-40 (anti-huCD40 mAb) in patients with refractory or recurrent multiple myeloma SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Cleveland Clin Multiple Myeloma Res Progam, Taussig Canc Ctr, Cleveland, OH USA. Cornell Univ, Weill Med Coll, New York, NY USA. Dana Farber Canc Inst, Boston, MA 02115 USA. Inst Myeloma & Bone Canc Res, Los Angeles, CA USA. Seattle Genet Inc, Bothell, WA 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 2004 VL 104 IS 11 MA 2413 BP 663A EP 663A PN 1 PG 1 WC Hematology SC Hematology GA 871JM UT WOS:000225127502413 ER PT J AU Tai, YT Li, XF Tong, X Catley, L Santos, D Tournilhac, O Schlossman, R Richardson, P Munshi, NC Luqman, M Anderson, KC AF Tai, YT Li, XF Tong, X Catley, L Santos, D Tournilhac, O Schlossman, R Richardson, P Munshi, NC Luqman, M Anderson, KC TI A fully human antagonist anti-CD40 antibody triggers significant antitumor activity against human multiple myeloma SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Dana Farber Canc Inst, Dept Med Oncol, 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 2004 VL 104 IS 11 MA 2414 BP 663A EP 664A PN 1 PG 2 WC Hematology SC Hematology GA 871JM UT WOS:000225127502414 ER PT J AU Schittenhelm, M Shiraga, S Lee, FY Heinrich, MC AF Schittenhelm, M Shiraga, S Lee, FY Heinrich, MC TI BMS-354825 potently inhibits the kinase activity of KIT activation loop mutations associated with systemic mastocytosis and induces apoptosis of mastocytosis cell lines SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Univ Tubingen, Dept Hematol Oncol Rheumatol & Immunol, Tubingen, Germany. Portland VA Med Ctr, Portland, OR USA. OHSU, Div Hematol Med Oncol, Inst Canc, Portland, OR USA. Bristol Myers Squibb Co, Oncol Drug Discovery, Princeton, NJ USA. NR 0 TC 5 Z9 5 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 2004 VL 104 IS 11 MA 2424 BP 666A EP 666A PN 1 PG 1 WC Hematology SC Hematology GA 871JM UT WOS:000225127502424 ER PT J AU Le Gouill, S Podar, K Hideshima, T Zorn, E Simoncini, M Harousseau, JL Anderson, KC AF Le Gouill, S Podar, K Hideshima, T Zorn, E Simoncini, M Harousseau, JL Anderson, KC TI Lack of Mcl-1 confers resistance to bortezomid in multiple myeloma. SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Dana Farber Canc Inst, Jerome Lipper Multiple Myeloma Ctr, Dept Med Oncol, Boston, MA 02115 USA. CHU Nantes, Hotel Dieu, Serv Hematol Clin, F-44035 Nantes 01, France. 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 2004 VL 104 IS 11 MA 2445 BP 671A EP 672A PN 1 PG 2 WC Hematology SC Hematology GA 871JM UT WOS:000225127502445 ER PT J AU Chen, J Lee, BH Williams, IR Kutok, JL Duclos, N Cohen, S Adelsperger, J Okabe, R Coburn, A Moore, S Huntly, BJP Mitsiades, CS Anderson, KC Griffin, JD Fabbro, D Gilliland, DG AF Chen, J Lee, BH Williams, IR Kutok, JL Duclos, N Cohen, S Adelsperger, J Okabe, R Coburn, A Moore, S Huntly, BJP Mitsiades, CS Anderson, KC Griffin, JD Fabbro, D Gilliland, DG TI PKC412 effectively inhibits constitutively activated FGFR3 mutants in murine leukemia models and t(4;14) myeloma cell lines. SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Harvard Univ, Sch Med, Howard Hughes Med Inst, Boston, MA 02115 USA. Brigham & Womens Hosp, Boston, MA 02115 USA. Emory Univ, Atlanta, GA 30322 USA. Novartis Pharma AG, Basel, Switzerland. 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 2004 VL 104 IS 11 MA 2448 BP 672A EP 672A PN 1 PG 1 WC Hematology SC Hematology GA 871JM UT WOS:000225127502448 ER PT J AU Podar, K Simoncini, M Le Gouill, S Tai, YT Kumar, S Tassone, P Catley, LP Pandite, LN Kumar, R Hideshima, T Chauhan, D Anderson, KC AF Podar, K Simoncini, M Le Gouill, S Tai, YT Kumar, S Tassone, P Catley, LP Pandite, LN Kumar, R Hideshima, T Chauhan, D Anderson, KC TI Effects of the indazolylpyrimidine GW786034 on angiogenesis and MM cell growth: Therapeutic implications. SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Dana Farber Canc Inst, Jerome Lipper Multiple Myeloma Ctr, Boston, MA 02115 USA. GlaxoSmithKline Inc, Res Triangle Pk, NC USA. 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 2004 VL 104 IS 11 MA 2452 BP 673A EP 673A PN 1 PG 1 WC Hematology SC Hematology GA 871JM UT WOS:000225127502452 ER PT J AU Podar, K Shringarpure, R Tai, YT Simoncini, M Sattler, M Ishitsuka, K Richardson, PG Hideshima, T Chauhan, D Kenneth, AC AF Podar, K Shringarpure, R Tai, YT Simoncini, M Sattler, M Ishitsuka, K Richardson, PG Hideshima, T Chauhan, D Kenneth, AC TI Caveolin-1 is required for VEGF-triggered multiple myeloma cell migration and is targeted by bortezomib (Velcade (R)). SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA 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 2004 VL 104 IS 11 MA 2453 BP 673A EP 674A PN 1 PG 2 WC Hematology SC Hematology GA 871JM UT WOS:000225127502453 ER PT J AU Chauhan, D Li, GL Podar, K Hideshima, T Ishitsuka, K Catley, L Sattler, M Tai, YT Burger, R Richardson, P Chang, Y Schindler, J Carver, B Anderson, KC AF Chauhan, D Li, GL Podar, K Hideshima, T Ishitsuka, K Catley, L Sattler, M Tai, YT Burger, R Richardson, P Chang, Y Schindler, J Carver, B Anderson, KC TI Mitochondria and caspase-independent cell-death triggered by GCS-100, a novel carbohydrate-based therapeutic in multiple myeloma (MM) cells. SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Dana Farber Canc Inst, Boston, MA 02115 USA. GlycoGenesys Inc, Boston, MA USA. 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 2004 VL 104 IS 11 MA 2456 BP 674A EP 674A PN 1 PG 1 WC Hematology SC Hematology GA 871JM UT WOS:000225127502456 ER PT J AU Tassone, P Neri, P Carrasco, DR Burger, R Catley, L Venuta, S Anderson, KC Munshi, NC AF Tassone, P Neri, P Carrasco, DR Burger, R Catley, L Venuta, S Anderson, KC Munshi, NC TI A clinically relevant SCID-hu in vivo model of human multiple myeloma. SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Dana Farber Canc Inst, Jerome Lipper Multiple Myeloma Ctr, Boston, MA 02115 USA. Harvard Univ, Sch Med, Boston, MA 02115 USA. VA Boston Healthcare Syst, Boston, MA USA. Univ Magne Graecia, Catanzaro, Italy. 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 2004 VL 104 IS 11 MA 2455 BP 674A EP 674A PN 1 PG 1 WC Hematology SC Hematology GA 871JM UT WOS:000225127502455 ER PT J AU Shammas, MA Koley, H Batchu, RB Neri, P Tassone, P Prabhala, R Anderson, KC Munshi, NC AF Shammas, MA Koley, H Batchu, RB Neri, P Tassone, P Prabhala, R Anderson, KC Munshi, NC TI Specific killing of multiple myeloma cancer cells by epigallocatechin-3-gallate extracted from green tea. SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 VA Boston Healthcare Syst, Med Serv, W Roxbury, MA USA. Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02115 USA. Harvard Univ, Sch 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 2004 VL 104 IS 11 MA 2461 BP 675A EP 676A PN 1 PG 2 WC Hematology SC Hematology GA 871JM UT WOS:000225127502461 ER PT J AU Ishitsuka, K Hideshima, T Hamasaki, M Noopur, R Shaji, K Yasui, H Roccaro, AM Chauhan, D Podar, K Tai, YZ Jain, J Anderson, KC AF Ishitsuka, K Hideshima, T Hamasaki, M Noopur, R Shaji, K Yasui, H Roccaro, AM Chauhan, D Podar, K Tai, YZ Jain, J Anderson, KC TI A novel inosine monophosphate dehydrogenase inhibitor VX-944 overcomes conventional drug-resistance in multiple mueloma cells in the bone marrow microenvironment. SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Harvard Univ, Sch Med, Boston, MA 02115 USA. Dana Farber Canc Inst, Dept Med Oncol, Jerome Lipper Multiple Myeloma Ctr, Boston, MA 02115 USA. Vertex Pharmaceut Inc, 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 2004 VL 104 IS 11 MA 2468 BP 677A EP 677A PN 1 PG 1 WC Hematology SC Hematology GA 871JM UT WOS:000225127502468 ER PT J AU Prabhala, R Neri, P Tassone, P Shammas, MA Bae, J Cumming, VM Allam, CK Daley, JF Desarneud, F Chauhan, D Blanchard, E Anderson, K Munshi, NC AF Prabhala, R Neri, P Tassone, P Shammas, MA Bae, J Cumming, VM Allam, CK Daley, JF Desarneud, F Chauhan, D Blanchard, E Anderson, K Munshi, NC TI Dysregulated CD4(+)CD25(+) T-regulatory cells and TLRs in myeloma. SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 VA Boston Healthcare Syst, Med Serv, W Roxbury, MA USA. Harvard Univ, Sch Med, 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 2004 VL 104 IS 11 MA 2466 BP 677A EP 677A PN 1 PG 1 WC Hematology SC Hematology GA 871JM UT WOS:000225127502466 ER PT J AU Prabhala, R Cheema, P Shammas, MA Song, WH Blanchard, E Chauhan, D Neri, P Tassone, P Stirling, D Anderson, K Munshi, NC AF Prabhala, R Cheema, P Shammas, MA Song, WH Blanchard, E Chauhan, D Neri, P Tassone, P Stirling, D Anderson, K Munshi, NC TI Effect of thalidomide and revlimid on the gene expression that reveals molecular circuitries involved in T cell co-activation. SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 VA Boston Healthcare Syst, Med Serv, W Roxbury, MA USA. Harvard Univ, Sch Med, Dept Med Oncol, Dana Farber Canc Inst, Boston, MA 02115 USA. Celgene Corp, Warren, NJ 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 2004 VL 104 IS 11 MA 2472 BP 678A EP 678A PN 1 PG 1 WC Hematology SC Hematology GA 871JM UT WOS:000225127502472 ER PT J AU Czuczman, MS Porcu, P Johnson, J Niedzwiecki, D Canellos, GP Cheson, BD AF Czuczman, MS Porcu, P Johnson, J Niedzwiecki, D Canellos, GP Cheson, BD TI CALGB 59901: Results of a phase II study of 506U78 in CTCL and PTCL. SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Roswell Pk Canc Inst, Lymphoma Myeloma Sect, Buffalo, NY 14263 USA. OSU Canc Ctr, Columbus, OH USA. CALGB Stat Ctr, Durham, NC USA. Dana Farber Canc Ctr, Boston, MA USA. Vincent T Lombardi Canc Res Ctr, Washington, DC USA. NR 0 TC 2 Z9 2 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 2004 VL 104 IS 11 MA 2486 BP 682A EP 682A PN 1 PG 1 WC Hematology SC Hematology GA 871JM UT WOS:000225127502486 ER PT J AU Smith, SM Johnson, JL Niedzwiecki, D Eder, JP Canellos, GP Cheson, BD Bartlett, NL AF Smith, SM Johnson, JL Niedzwiecki, D Eder, JP Canellos, GP Cheson, BD Bartlett, NL TI Sequential topoisomerase I (topo I) and topoisomerase II (topo II) inhibitors in relapsed/refractory aggressive NHL: Results of CALGB 59906, a phase II study of doxorubicin and topotecan. SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Univ Chicago, Dept Med, Chicago, IL 60637 USA. Duke Univ, Canc & Leukemia Grp B, Ctr Stat, Durham, NC USA. Dana Farber Canc Inst, Boston, MA 02115 USA. Georgetown Univ, Vincent T Lombardi Canc Res Ctr, Washington, DC 20007 USA. Washington Univ, St Louis, MO 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 2004 VL 104 IS 11 MA 2500 BP 685A EP 686A PN 1 PG 2 WC Hematology SC Hematology GA 871JM UT WOS:000225127502500 ER PT J AU Chen, J DeAngelo, DJ Kutok, JL Williams, IR Lee, BH Wadleigh, M Duclos, N Cohen, S Adelsperger, J Okabe, R Coburn, A Galinsky, I Huntly, BJP Cohen, P Meyer, T Fabbro, D Banerji, L Griffin, JD Xiao, S Fletcher, JA Stone, RM Gilliland, DG AF Chen, J DeAngelo, DJ Kutok, JL Williams, IR Lee, BH Wadleigh, M Duclos, N Cohen, S Adelsperger, J Okabe, R Coburn, A Galinsky, I Huntly, BJP Cohen, P Meyer, T Fabbro, D Banerji, L Griffin, JD Xiao, S Fletcher, JA Stone, RM Gilliland, DG TI PKC412 inhibits the ZNF198-FGFR1 fusion tyrosine kinase and is efficacious in treatment of t(8;13)(p11;q12) associated stem cell myeloproliferative disease. SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Harvard Univ, Sch Med, Howard Hughes Med Inst, Boston, MA 02115 USA. Dana Farber Canc Inst, Boston, MA 02115 USA. Brigham & Womens Hosp, Boston, MA 02115 USA. Emory Univ, Atlanta, GA 30322 USA. Novartis Pharma AG, Basel, Switzerland. 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 2004 VL 104 IS 11 MA 2549 BP 698A EP 698A PN 1 PG 1 WC Hematology SC Hematology GA 871JM UT WOS:000225127502549 ER PT J AU Matuskova, J Cambien, B Piffath, C Wagner, DD AF Matuskova, J Cambien, B Piffath, C Wagner, DD TI Reduced plasma fibronectin leads to delayed thrombus growth in the injured arterioles in vivo. SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 CBR Inst Biomed Res, Ctr Blood Res, 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 2004 VL 104 IS 11 MA 2619 BP 716A EP 717A PN 1 PG 2 WC Hematology SC Hematology GA 871JM UT WOS:000225127502620 ER PT J AU Forero-Torres, A Bernstein, S Gopal, A Foss, F Leonard, J Rosenblatt, J Bartlett, N Younes, A Fisher, D Cheson, B Carabasi, M Bociek, G Hart, B McDonald, M AF Forero-Torres, A Bernstein, S Gopal, A Foss, F Leonard, J Rosenblatt, J Bartlett, N Younes, A Fisher, D Cheson, B Carabasi, M Bociek, G Hart, B McDonald, M TI SGN-30 (anti-CD30 monoclonal antibody) is active and well tolerated in patients with refractory or recurrent systemic anaplastic large cell lymphoma. SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Univ Alabama, Ctr Comprehens Canc, Birmingham, AL 35294 USA. Univ Rochester, Med Ctr, Rochester, NY 14627 USA. Univ Washington, Seattle Canc Care Alliance, Seattle, WA 98195 USA. Tufts New England Med Ctr, Boston, MA USA. Cornell Univ, Weill Med Coll, New York, NY USA. Univ Miami, Sylvester Comprehens Canc Ctr, Miami, FL 33152 USA. Washington Univ, Siteman Canc Ctr, St Louis, MO 63130 USA. Univ Texas, MD Anderson Canc Ctr, Houston, TX 77030 USA. Dana Farber Canc Inst, Boston, MA 02115 USA. Georgetown Univ, Washington, DC 20057 USA. Univ So Calif, Norris Canc Ctr, Los Angeles, CA 90089 USA. Nebraska Med Ctr, Omaha, NE USA. Seattle Genet, Bothell, WA 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 2004 VL 104 IS 11 MA 2637 BP 721A EP 722A PN 1 PG 2 WC Hematology SC Hematology GA 871JM UT WOS:000225127502638 ER PT J AU Leonard, JP Rosenblatt, JD Bartlett, NL Gopal, A Younes, A Fisher, D Foss, F Forero, A Bernstein, S Cheson, B Carabasi, MH Bociek, RG Hart, B McDonald, M AF Leonard, JP Rosenblatt, JD Bartlett, NL Gopal, A Younes, A Fisher, D Foss, F Forero, A Bernstein, S Cheson, B Carabasi, MH Bociek, RG Hart, B McDonald, M TI Phase II study of SGN-30 (anti-CD30 monoclonal antibody) in patients with refractory or recurrent Hodgkin's disease. SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Cornell Univ, Weil Med Coll, Ctr Lymphoma & Myeloma, New York, NY USA. Univ Miami, Sylvester Comprehens Canc Ctr, Miami, FL 33152 USA. Washington Univ, Siteman Canc Ctr, St Louis, MO 63130 USA. Univ Washington, Seattle Canc Care Alliance, Seattle, WA 98195 USA. Univ Texas, MD Anderson Canc Ctr, Houston, TX 77030 USA. Dana Farber Canc Inst, Boston, MA 02115 USA. Tufts New England Med Ctr, Boston, MA USA. Univ Alabama, Birmingham, AL USA. Univ Rochester, Med Ctr, Rochester, NY 14627 USA. Georgetown Univ, Med Ctr, Washington, DC 20057 USA. Univ So Calif, Norris Cotton Canc Ctr, Los Angeles, CA 90089 USA. Univ Nebraska, Ctr Med, Omaha, NE 68182 USA. Seattle Genet Inc, Bothell, WA 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 2004 VL 104 IS 11 MA 2635 BP 721A EP 721A PN 1 PG 1 WC Hematology SC Hematology GA 871JM UT WOS:000225127502636 ER PT J AU Vianello, F Kraft, P Hart, W Mok, YT Poznansky, MC AF Vianello, F Kraft, P Hart, W Mok, YT Poznansky, MC TI CXCR4-dependent repulsion of mature single-positive CD4 cells mediates emigration from thymus SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Massachusetts Gen Hosp, AIDS Res & Canc Ctr, Charlestown, MA USA. RI Vianello, Fabrizio/M-5211-2016 OI Vianello, Fabrizio/0000-0002-7174-4651 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 2004 VL 104 IS 11 MA 2649 BP 724A EP 725A PN 1 PG 2 WC Hematology SC Hematology GA 871JM UT WOS:000225127502650 ER PT J AU Hirano, N Butler, MO Nadler, LM AF Hirano, N Butler, MO Nadler, LM TI 4-1BB (CD137) or CD40 signaling fails to improve the expansion of antigen specific T cells demonstrated with engagement of TCR, CD28 and CD83 ligand SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02115 USA. Harvard Univ, Sch Med, Boston, MA 02115 USA. NR 0 TC 1 Z9 1 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 2004 VL 104 IS 11 MA 2665 BP 728A EP 728A PN 1 PG 1 WC Hematology SC Hematology GA 871JM UT WOS:000225127502665 ER PT J AU Gekas, C Dieterien-Lievre, F Orkin, SH AF Gekas, C Dieterien-Lievre, F Orkin, SH TI Placenta is a niche for hematopoietic stem cells SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Dana Farber Canc Inst, Boston, MA 02115 USA. Coll France, CNRS, Lab Embryol Cellulaire & Mol, Nogent Sur Marne, 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 2004 VL 104 IS 11 MA 2671 BP 730A EP 730A PN 1 PG 1 WC Hematology SC Hematology GA 871JM UT WOS:000225127502671 ER PT J AU Wagers, AJ Prohaska, SS Passegue, E Price, J Weissman, IL AF Wagers, AJ Prohaska, SS Passegue, E Price, J Weissman, IL TI Phenotype, function, and regulation of migrating hematopoietic stem cells SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Joslin Diabet Ctr, Sect Dev & Stem Cell Biol, Boston, MA 02215 USA. Stanford Univ, Sch Med, Dept Pathol, Stanford, CA 94305 USA. Stanford Univ, Sch Med, Dept Dev Biol, Stanford, CA 94305 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 2004 VL 104 IS 11 MA 2680 BP 732A EP 732A PN 1 PG 1 WC Hematology SC Hematology GA 871JM UT WOS:000225127502680 ER PT J AU Vallat, LD Park, Y Rassenti, L Gribben, JG AF Vallat, LD Park, Y Rassenti, L Gribben, JG TI Temporal gene expression after BCR-crosslinking based upon Zap70 related genomic features. SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Harvard Univ, Sch Med, Dana Farber Canc Inst, Boston, MA 02115 USA. Harvard Univ, Sch Publ Hlth, Boston, MA 02115 USA. Univ Calif San Diego, CLL Res Consortium, La Jolla, CA 92093 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 2004 VL 104 IS 11 MA 2795 BP 765A EP 765A PN 1 PG 1 WC Hematology SC Hematology GA 871JM UT WOS:000225127502796 ER PT J AU Motiwala, T Ghoshal, K Majumder, S Kutay, H Neuberg, DS Kitada, S Reed, JC Dewald, GW Flinn, IW Appelbaum, FR Larson, RA Tallman, MA Liu, T Plass, C Lucas, DM Byrd, JC Jacob, ST Grever, MR AF Motiwala, T Ghoshal, K Majumder, S Kutay, H Neuberg, DS Kitada, S Reed, JC Dewald, GW Flinn, IW Appelbaum, FR Larson, RA Tallman, MA Liu, T Plass, C Lucas, DM Byrd, JC Jacob, ST Grever, MR TI Methylation of the tumor suppressor gene PTPRO (receptor-type protein tyrosine phosphatase) is associated with expression of important apoptosis-related proteins in chronic lymphocytic leukemia (CLL) SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Ohio State Univ, Columbus, OH 43210 USA. Dana Farber Canc Inst, Boston, MA 02115 USA. Burnham Inst, La Jolla, CA 92037 USA. Mayo Clin, Rochester, MN USA. Northwestern Univ, Chicago, IL 60611 USA. Fred Hutchinson Canc Res Ctr, Seattle, WA 98104 USA. Univ Chicago, Chicago, IL 60637 USA. RI Plass, Christoph/H-7192-2014; Motiwala, Tasneem/D-4687-2016 OI Motiwala, Tasneem/0000-0002-5863-7704 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 2004 VL 104 IS 11 MA 2804 BP 767A EP 767A PN 1 PG 1 WC Hematology SC Hematology GA 871JM UT WOS:000225127502805 ER PT J AU Rassenti, LZ Neuberg, DS Keating, MJ Gribben, JG Flinn, IW Rai, KR Byrd, JC Kay, NE Kipps, TJ AF Rassenti, LZ Neuberg, DS Keating, MJ Gribben, JG Flinn, IW Rai, KR Byrd, JC Kay, NE Kipps, TJ TI CD38 compared with ZAP-70 or immmunoglobulin mutation status as predictor of disease progression in chronic lymphocytic leukemia. SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Univ Calif San Diego, La Jolla, CA 92093 USA. Dana Farber Canc Inst, Boston, MA 02115 USA. Univ Texas, MD Anderson Canc Ctr, Leukemia Dept, Houston, TX 77030 USA. Long Isl Jewish Med Ctr, New Hyde Pk, NY 11042 USA. Ohio State Univ, Columbus, OH 43210 USA. Mayo Clin, Div Hematol, Rochester, MN USA. Univ Calif San Diego, CLL Res Consortium, La Jolla, CA 92093 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 2004 VL 104 IS 11 MA 2805 BP 767A EP 768A PN 1 PG 2 WC Hematology SC Hematology GA 871JM UT WOS:000225127502806 ER PT J AU Eom, HS Chakraverty, R Sachs, J Zhao, GL Sykes, M AF Eom, HS Chakraverty, R Sachs, J Zhao, GL Sykes, M TI Requirement for CD4 help for optimal GVL effects of alloreactive T cells given to established mixed chimeras but not freshly irradiated mice. SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Harvard Univ, Sch Med, Massachusetts Gen Hosp, Transplantat Biol Res Ctr, 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 2004 VL 104 IS 11 MA 3044 BP 831A EP 832A PN 1 PG 2 WC Hematology SC Hematology GA 871JM UT WOS:000225127503045 ER PT J AU Chakraverty, R Buchli, J Zhao, GL Hsu, R Sykes, M AF Chakraverty, R Buchli, J Zhao, GL Hsu, R Sykes, M TI Host environment dictates the outcome following transfer of graft-versus-host reactive effector/memory T cells. SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Massachusetts Gen Hosp, Transplantat Biol Res Ctr, 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 2004 VL 104 IS 11 MA 3046 BP 832A EP 832A PN 1 PG 1 WC Hematology SC Hematology GA 871JM UT WOS:000225127503047 ER PT J AU Chakraverty, R Buchli, J Zhao, GL Hsu, R Croft, M Sykes, M AF Chakraverty, R Buchli, J Zhao, GL Hsu, R Croft, M Sykes, M TI Sequential blockade and engagement of co-stimulatory pathways: A potential strategy for amplifying graft-versus-leukemia responses without GVHD. SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Massachusetts Gen Hosp, Transplantat Biol Res Ctr, Boston, MA 02114 USA. La Jolla Inst Allergy & Immunol, Div Mol Immnunol, San Diego, 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 2004 VL 104 IS 11 MA 3075 BP 840A EP 840A PN 1 PG 1 WC Hematology SC Hematology GA 871JM UT WOS:000225127503076 ER PT J AU Abel, GA Hays, JT Decker, P Croghan, G Kuter, DJ Rigotti, NA AF Abel, GA Hays, JT Decker, P Croghan, G Kuter, DJ Rigotti, NA TI Effects of biochemically-confirmed smoking cessation on periperhal leukocyte count SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Harvard Univ, Sch Med, Massachusetts Gen Hosp, Dept Med, Boston, MA 02115 USA. Mayo Clin & Mayo Fdn, Mayo Med Sch, Rochester, MN 55905 USA. Harvard Univ, Sch Med, Massachusetts Gen Hosp, Tobacco Res & Treatment Ctr, Boston, MA 02115 USA. Mayo Clin & Mayo Fdn, Nicotine Dependence Ctr, Rochester, MN 55905 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 2004 VL 104 IS 11 MA 3148 BP 861A EP 861A PN 1 PG 1 WC Hematology SC Hematology GA 871JM UT WOS:000225127503150 ER PT J AU Berman, JN Berry, W Wang, M Neuberg, DS Guinan, EC AF Berman, JN Berry, W Wang, M Neuberg, DS Guinan, EC TI Herpes zoster (HZ) infection in the post-hematopoietic stem cell transplant pediatric population may be preceded by transaminitis SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Dana Farber Canc Inst, Dept Pediat Oncol, Boston, MA USA. Dana Farber Canc Inst, Dept Biostat Sci, Boston, MA 02115 USA. Childrens Hosp, Dept Pediat Hematol Oncol, 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 2004 VL 104 IS 11 MA 3167 BP 866A EP 866A PN 1 PG 1 WC Hematology SC Hematology GA 871JM UT WOS:000225127503169 ER PT J AU Butler, MO Hirano, N Lee, JS Beecham, EJ Chung, M Ripley, R Murray, AP Mulligan, RC Nadler, LM AF Butler, MO Hirano, N Lee, JS Beecham, EJ Chung, M Ripley, R Murray, AP Mulligan, RC Nadler, LM TI Off the shelf, GMP grade artificial APC efficiently generates large numbers of antigen specific CTLs sufficient for the treatment of cancer and infectious disease SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Dana Farber Canc Inst, Boston, MA 02115 USA. Childrens Hosp, Boston, MA USA. Harvard Univ, 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 2004 VL 104 IS 11 MA 3172 BP 867A EP 867A PN 1 PG 1 WC Hematology SC Hematology GA 871JM UT WOS:000225127503174 ER PT J AU Cutler, C Li, SL Kim, HT Alyea, E Miklos, D Soiffer, R Antin, JH AF Cutler, C Li, SL Kim, HT Alyea, E Miklos, D Soiffer, R Antin, JH TI Prevention of acute GVHD with sirolimus does not abrogate the risk of chronic GVHD. SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA 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 2004 VL 104 IS 11 MA 3317 BP 906A EP 906A PN 1 PG 1 WC Hematology SC Hematology GA 871JM UT WOS:000225127503319 ER PT J AU Andorsky, DJ Lee, SJ AF Andorsky, DJ Lee, SJ TI Baseline physical and mental functioning are strong predictors of post-stem cell transplant function and quality of life. SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 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 2004 VL 104 IS 11 MA 3322 BP 907A EP 908A PN 1 PG 2 WC Hematology SC Hematology GA 871JM UT WOS:000225127503324 ER PT J AU Thornley, I Eapen, M Sung, L Lee, SJ Davies, SM Joffe, S AF Thornley, I Eapen, M Sung, L Lee, SJ Davies, SM Joffe, S TI Family cord blood banking: Experience and views of pediatric hematopoietic stem cell transplant physicians. SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Dana Farber Canc Inst, Boston, MA 02115 USA. Med Coll Wisconsin, IBMTR, Milwaukee, WI 53226 USA. Hosp Sick Children, Toronto, ON M5G 1X8, Canada. Childrens Hosp, Med Ctr, Cincinnati, OH 45229 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 2004 VL 104 IS 11 MA 3323 BP 908A EP 908A PN 1 PG 1 WC Hematology SC Hematology GA 871JM UT WOS:000225127503325 ER PT J AU Neelapu, SS Munshi, NC Jagannath, S Watson, TM Pennington, R Barlogie, B Kwak, LW AF Neelapu, SS Munshi, NC Jagannath, S Watson, TM Pennington, R Barlogie, B Kwak, LW TI Tumor antigen immunization of sibling stem cell transplant donors in multiple myeloma. SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Univ Texas, MD Anderson Canc Ctr, Houston, TX 77030 USA. Harvard Univ, Sch Med, Dana Farber Canc Inst, Boston, MA 02115 USA. St Vincents Catholic Med Ctr, New York, NY USA. NCI, Expt & Transplantat Immunol Branch, Canc Res Ctr, NIH, Bethesda, MD 20892 USA. NCI, Frederick Canc Res & Dev Ctr, SAIC, Frederick, MD USA. Univ Arkansas Med Sci, Myeloma Inst Res & Therapy, Little Rock, AR 72205 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 2004 VL 104 IS 11 MA 3340 BP 913A EP 913A PN 1 PG 1 WC Hematology SC Hematology GA 871JM UT WOS:000225127503342 ER PT J AU Desarnaud, FJ Shammas, M Neri, P Koley, H Prabhala, R Cheng, L Ryung, SK Chauhan, D Tassone, P Bae, J Anderson, KC Munshi, NC AF Desarnaud, FJ Shammas, M Neri, P Koley, H Prabhala, R Cheng, L Ryung, SK Chauhan, D Tassone, P Bae, J Anderson, KC Munshi, NC TI The polycomb group transcriptional repressor Bmi-1 is constitutively expressed in multiple myeloma (MM) cells and modulates proliferation through a mechanism independent of the INK4a/ARF locus. SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 VA Boston Hlth Care Syst, Dept Med, W Roxbury, MA USA. Dana Farber Canc Inst, Boston, MA 02115 USA. Harvard Univ, 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 2004 VL 104 IS 11 MA 3346 BP 914A EP 914A PN 1 PG 1 WC Hematology SC Hematology GA 871JM UT WOS:000225127503348 ER PT J AU Gullo, CA Hwang, W Au, M Greenfield, EA Anderson, KC Teoh, G AF Gullo, CA Hwang, W Au, M Greenfield, EA Anderson, KC Teoh, G TI CD40 ligand stimulation of multiple myeloma cells results in upregulation of surface expressed heat shock proteins and increased antigenicity. SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Singapore Gen Hosp, Dept Clin Res, Singapore 0316, Singapore. SingHlth, Multiple Myeloma Res Lab, Singapore, Singapore. Singapore Gen Hosp, Dept Haematol, Singapore 0316, Singapore. Singapore Gen Hosp, Div Res, Singapore 0316, Singapore. Millennium Pharmaceut Inc, Holding Facil, Cambridge, MA USA. Dana Farber Canc Inst, Jerome Lipper Multiple Myeloma Ctr, 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 2004 VL 104 IS 11 MA 3351 BP 915A EP 915A PN 1 PG 1 WC Hematology SC Hematology GA 871JM UT WOS:000225127503353 ER PT J AU Hideshima, T Podar, K Chauhan, D Ishitsuka, K Mitsiades, C Tai, YT Hamasaki, M Raje, N Hideshima, H Schreiner, G Nguyen, A Navas, T Munshi, NC Richardson, PG Higgins, LS Anderson, KC AF Hideshima, T Podar, K Chauhan, D Ishitsuka, K Mitsiades, C Tai, YT Hamasaki, M Raje, N Hideshima, H Schreiner, G Nguyen, A Navas, T Munshi, NC Richardson, PG Higgins, LS Anderson, KC TI p38 MAPK inhibition enhances PS-341 (bortezomib)-induced cytotoxicity against multiple myeloma cells. SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Dana Farber Canc Inst, Jerome Lipper Multiple Myeloma, Boston, MA 02115 USA. Scios Inc, Fremont, 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 2004 VL 104 IS 11 MA 3348 BP 915A EP 915A PN 1 PG 1 WC Hematology SC Hematology GA 871JM UT WOS:000225127503350 ER PT J AU Podar, K Simoncini, M Tai, YT Sattler, M Ishitsuka, K Le Gouill, S Hamasaki, M Burger, R Raje, N Hideshima, TC Chauhan, D Anderson, K AF Podar, K Simoncini, M Tai, YT Sattler, M Ishitsuka, K Le Gouill, S Hamasaki, M Burger, R Raje, N Hideshima, TC Chauhan, D Anderson, K TI The tyrosine kinase inhibitor adaphostin (NSC 680410), but not imatinib mesylate, inhibits survival and Src tyrosine kinase family-triggered signaling pathways of MM cells. SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA 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 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 2004 VL 104 IS 11 MA 3352 BP 916A EP 916A PN 1 PG 1 WC Hematology SC Hematology GA 871JM UT WOS:000225127503354 ER PT J AU Guenther, A Gordon, S Bakker, F Burger, R Green, JR Rogers, M Gramatzki, M AF Guenther, A Gordon, S Bakker, F Burger, R Green, JR Rogers, M Gramatzki, M TI Zoledronic acid inhibits protein prenylation in plasmacytoma tumors in vivo and enhances survival in the INA-6 SCID mouse model. SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Univ Kiel, Dept Med 2, Div Stem Cell & Immunotherapy, D-24098 Kiel, Germany. Univ Aberdeen, Inst Med Sci, Bone Res Grp, Aberdeen AB9 1FX, Scotland. Dana Farber Canc Inst, Boston, MA 02115 USA. Novartis Pharma, Basel, Switzerland. RI Gramatzki, Martin/A-9533-2010 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 2004 VL 104 IS 11 MA 3360 BP 917A EP 917A PN 1 PG 1 WC Hematology SC Hematology GA 871JM UT WOS:000225127503362 ER PT J AU Raje, N Kumar, S Hideshima, T Ishitsuka, K Roccaro, A Yasui, H Hamasaki, M Shiraishi, N Chauhan, D Munshi, NC Green, SR Anderson, KC AF Raje, N Kumar, S Hideshima, T Ishitsuka, K Roccaro, A Yasui, H Hamasaki, M Shiraishi, N Chauhan, D Munshi, NC Green, SR Anderson, KC TI In vitro activity of a novel small molecule cyclin dependent kinase inhibitor, CYC202 (seliciclib or R-roscovitine), in multiple myeloma (MM). SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Dana Farber Canc Inst, Boston, MA 02115 USA. Harvard Univ, Sch Med, Boston, MA USA. Cyclacel Ltd, Dundee DD, Scotland. 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 2004 VL 104 IS 11 MA 3359 BP 917A EP 917A PN 1 PG 1 WC Hematology SC Hematology GA 871JM UT WOS:000225127503361 ER PT J AU Santos, DD Tournilhac, O Xu, L Evdoxia, H Hunter, Z Branagan, A Manning, R Anderson, KC Grewal, I Treon, SP AF Santos, DD Tournilhac, O Xu, L Evdoxia, H Hunter, Z Branagan, A Manning, R Anderson, KC Grewal, I Treon, SP TI B-lymphocyte stimulator protein (BLYS) is expressed by bone marrow mast and lymphoplasmacytic cells in Waldenstrom's macroglobulinemia, and provides signaling for growth, survival and IgM secretion. SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Dana Farber Canc Inst, Bing ProgramWaldenstroms Macroglobulinemia, Boston, MA 02115 USA. Dana Farber Canc Inst, Jerome Lipper Multiple Myeloma Ctr, Boston, MA 02115 USA. Harvard Univ, Sch Med, Boston, MA USA. Genentech Inc, Dept Immunobiol, San Francisco, CA 94080 USA. RI Hunter, Zachary/H-3018-2013 OI Hunter, Zachary/0000-0002-1689-1691 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 2004 VL 104 IS 11 MA 3358 BP 917A EP 917A PN 1 PG 1 WC Hematology SC Hematology GA 871JM UT WOS:000225127503360 ER PT J AU Mitsiades, N McMullan, CJ Poulabi, V Negri, J Geer, DC Haridas, V Munshi, NC Gutterman, J Anderson, KC Mitsiades, CS AF Mitsiades, N McMullan, CJ Poulabi, V Negri, J Geer, DC Haridas, V Munshi, NC Gutterman, J Anderson, KC Mitsiades, CS TI Avicins: A novel class of anti-myeloma agents. SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA 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. Beth Israel Deaconess Med Ctr, Dept Med, Boston, MA 02215 USA. Univ Texas, MD Anderson Canc Ctr, Houston, TX 77030 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 2004 VL 104 IS 11 MA 3405 BP 929A EP 929A PN 1 PG 1 WC Hematology SC Hematology GA 871JM UT WOS:000225127503407 ER PT J AU Shammas, MA Koley, H Li, C Anderson, KC Reis, RJS Munshi, NC AF Shammas, MA Koley, H Li, C Anderson, KC Reis, RJS Munshi, NC TI Molecular mechanisms underlying the development of drug resistance in multiple myeloma. SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 VA Boston Healthcare Syst, Dept Med, Boston, MA USA. Dana Farber Canc Inst, Jerome Lipper Multiple Myeloma Ctr, Dept Med Oncol, Boston, MA 02115 USA. Harvard Univ, Sch Med, Boston, MA USA. Univ Arkansas Med Sci, Dept Geriatr, Little Rock, AR 72205 USA. 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 2004 VL 104 IS 11 MA 3409 BP 930A EP 930A PN 1 PG 1 WC Hematology SC Hematology GA 871JM UT WOS:000225127503411 ER PT J AU Catley, L Tai, YT Shringarpure, R Burger, R Son, M Podar, K Chauhan, D Hideshima, T Denis, L Richardson, PG Munshi, NC Anderson, KC AF Catley, L Tai, YT Shringarpure, R Burger, R Son, M Podar, K Chauhan, D Hideshima, T Denis, L Richardson, PG Munshi, NC Anderson, KC TI JNK activation and Fas up-regulation precede proteasomal degradation of topoisomerase I in SN38-mediated cytotoxicity against multiple myeloma. SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Dana Farber Canc Inst, Boston, MA 02115 USA. Pfizer, New London, CT USA. RI Catley, Laurence/E-5313-2013 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 2004 VL 104 IS 11 MA 3413 BP 931A EP 931A PN 1 PG 1 WC Hematology SC Hematology GA 871JM UT WOS:000225127503415 ER PT J AU Hirano, N Butler, MO Xia, ZN Kojima, S Nadler, LM AF Hirano, N Butler, MO Xia, ZN Kojima, S Nadler, LM TI gamma-globin, a tumor-associated antigen for juvenile myelomonocytic leukemia (JMML): A cell-based approach to identify tumor antigenic epitopes that are naturally processed and presented. SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02115 USA. Harvard Univ, Sch Med, 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 2004 VL 104 IS 11 MA 3418 BP 932A EP 932A PN 1 PG 1 WC Hematology SC Hematology GA 871JM UT WOS:000225127503420 ER PT J AU Yasui, H Hideshima, T Roccaro, AM Shiraishi, N Hamasaki, M Ishitsuka, K Kumar, S Raje, N Li, GL Tai, YT Podar, K Chauhan, D Anderson, KC AF Yasui, H Hideshima, T Roccaro, AM Shiraishi, N Hamasaki, M Ishitsuka, K Kumar, S Raje, N Li, GL Tai, YT Podar, K Chauhan, D Anderson, KC TI Anti-tumor activity of a novel immunosuppressant FTY720 in multiple myeloma. SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Dana Farber Canc Inst, Jerome Lipper Multiple Myeloma Ctr, Boston, MA 02115 USA. Harvard Univ, 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 2004 VL 104 IS 11 MA 3456 BP 941A EP 942A PN 1 PG 2 WC Hematology SC Hematology GA 871JM UT WOS:000225127503458 ER PT J AU Hamasaki, M Hideshima, T Ishitsuka, K Yasui, H Shiraishi, N Kumar, S Raje, N Roccaro, AM Tai, YT Shiringarpure, R Leoni, L Kanekal, S Elliott, G Munshi, NC Anderson, KC AF Hamasaki, M Hideshima, T Ishitsuka, K Yasui, H Shiraishi, N Kumar, S Raje, N Roccaro, AM Tai, YT Shiringarpure, R Leoni, L Kanekal, S Elliott, G Munshi, NC Anderson, KC TI SDX-101 is cytotoxic and overcomes drug resistance in multiple myeloma. SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02115 USA. Salmedix Inc, San Diego, CA 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 2004 VL 104 IS 11 MA 3466 BP 944A EP 944A PN 1 PG 1 WC Hematology SC Hematology GA 871JM UT WOS:000225127503468 ER PT J AU Grever, MR Lucas, DM Dewald, GW Neuberg, DS Flinn, IW Appelbaum, FR Larson, RA Tallman, MS Gribben, JG Byrd, JC AF Grever, MR Lucas, DM Dewald, GW Neuberg, DS Flinn, IW Appelbaum, FR Larson, RA Tallman, MS Gribben, JG Byrd, JC TI Outcome of treatment with fludarabine versus fludarabine and cyclophosphamide in chronic lymphocytic leukemia (CLL) is adversely impacted by high risk genetic features: Results from ECOG 2997. SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Ohio State Univ, Columbus, OH 43210 USA. Mayo Clin, Rochester, MN USA. Dana Farber Canc Inst, Boston, MA 02115 USA. Johns Hopkins, Baltimore, MD USA. Northwestern Univ, Chicago, IL 60611 USA. Fred Hutchinson Canc Res Ctr, Seattle, WA 98104 USA. Univ Chicago, Chicago, IL 60637 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 2004 VL 104 IS 11 MA 3487 BP 950A EP 951A PN 1 PG 2 WC Hematology SC Hematology GA 871JM UT WOS:000225127503489 ER PT J AU Shi, JL Rasmussen, JT Heegaard, CW Gilbert, GE AF Shi, JL Rasmussen, JT Heegaard, CW Gilbert, GE TI Reversible exposure of phosphatidylserine on thrombin-stimulated platelets detected by binding of lactadherin. SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Boston VA Healthcare Syst, Boston, MA USA. Brigham & Womens Hosp, Boston, MA 02115 USA. Harvard Univ, Sch Med, Boston, MA USA. Univ Aarhus, Aarhus, Denmark. 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 2004 VL 104 IS 11 MA 3537 BP 963A EP 963A PN 1 PG 1 WC Hematology SC Hematology GA 871JM UT WOS:000225127503538 ER PT J AU Zhou, GP Surks, HK Schnell, JR Chou, JJ Mendelsohn, ME Rigby, AC AF Zhou, GP Surks, HK Schnell, JR Chou, JJ Mendelsohn, ME Rigby, AC TI The three-dimensional structure of the cGMP-dependent protein kinase I-alpha leucine zipper domain and its interaction with the myosin binding subunit. SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Harvard Univ, Sch Med, BIDMC, Div Hemostasis & Thrombosis, Boston, MA USA. Tufts Univ New England Med Ctr, Mol Cardiol Res Inst, Boston, MA 02111 USA. Tufts Univ, Boston, MA 02111 USA. RI Chou, James/N-9840-2013 NR 0 TC 9 Z9 9 U1 2 U2 5 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 2004 VL 104 IS 11 MA 3539 BP 963A EP 963A PN 1 PG 1 WC Hematology SC Hematology GA 871JM UT WOS:000225127503540 ER PT J AU Banerji, L Scheijen, B Griffffin, JD AF Banerji, L Scheijen, B Griffffin, JD TI Identification of common target genes of the BCR/ABL and FLT3-ITD tyrosine kinases by microarray analysis SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA 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 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 2004 VL 104 IS 11 MA 3551 BP 966A EP 966A PN 1 PG 1 WC Hematology SC Hematology GA 871JM UT WOS:000225127503552 ER PT J AU Tassone, P Neri, P Kutok, J Tournilhac, O Santos, DD Hatjiharissi, E Venuta, S Anderson, KC Treon, S Munshi, NC AF Tassone, P Neri, P Kutok, J Tournilhac, O Santos, DD Hatjiharissi, E Venuta, S Anderson, KC Treon, S Munshi, NC TI A novel murine model for human Waldenstrom's macroglobulinemia. SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Dana Farber Canc Inst, Boston, MA 02115 USA. Harvard Univ, Sch Med, VA Boston Healthcare Syst, Boston, MA 02115 USA. Brigham & Womens Hosp, Boston, MA 02115 USA. Univ Magna Graecia, Catanzaro, Italy. 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 2004 VL 104 IS 11 MA 3646 BP 991A EP 991A PN 1 PG 1 WC Hematology SC Hematology GA 871JM UT WOS:000225127503647 ER PT J AU Blanchard, EM Lawler, E Brophy, M Fiore, L Munshi, NC AF Blanchard, EM Lawler, E Brophy, M Fiore, L Munshi, NC TI Chronic inflammation may predispose to the development of plasma cell dyscrasias. SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Boston Univ, Ctr Med, Boston, MA 02215 USA. VA Boston, VA Cooperat Studies Program, Mass Vet Epidemiol Res & Informat Ctr, Jamaica Plain, 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 2004 VL 104 IS 11 MA 3650 BP 993A EP 993A PN 1 PG 1 WC Hematology SC Hematology GA 871JM UT WOS:000225127503651 ER PT J AU Bergmeier, W Piffath, CL Ruggeri, ZM Ware, JL Wagner, DD AF Bergmeier, W Piffath, CL Ruggeri, ZM Ware, JL Wagner, DD TI GPIb alpha is essential for platelet adhesion during thrombus formation: Studies with mutant mice deficient in the extracellular domain of GPIb alpha. SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Harvard Univ, Sch Med, CBR Inst Biomed Res, Boston, MA 02115 USA. Harvard Univ, Sch Med, Dept Pathol, Boston, MA 02115 USA. Scripps Res Inst, Dept Mol & Expt Med, Roon Res Ctr Arteriosclerosis & Thrombosis, La Jolla, CA USA. Scripps Res Inst, Dept Vasc Biol, Roon Res Ctr Arteriosclerosis & Thrombosis, La Jolla, CA USA. Univ Arkansas Med Sci, Dept Physiol & Biophys, Little Rock, AR 72205 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 2004 VL 104 IS 11 MA 3659 BP 995A EP 995A PN 1 PG 1 WC Hematology SC Hematology GA 871JM UT WOS:000225127503660 ER PT J AU Marchese, P Kanaji, T Wagner, DD Ware, J Ruggeri, ZM AF Marchese, P Kanaji, T Wagner, DD Ware, J Ruggeri, ZM TI Elevated threshold shear rate for the dependence of glycoprotein Ib alpha-mediated platelet thrombus formation onto immobilized von Willebrand factor in mouse blood. SO BLOOD LA English DT Meeting Abstract CT 46th Annual Meeting of the American-Society-of-Hematology CY DEC 04-07, 2004 CL San Diego, CA SP Amer Soc Hematol C1 Scripps Res Inst, Dept Mol & Expt Med, La Jolla, CA USA. Harvard Univ, Sch Med, CBR Inst Biomed Res, Boston, MA 02115 USA. Harvard Univ, Sch Med, Dept Pathol, Boston, MA 02115 USA. Univ Arkansas Med Sci, Dept Physiol & Biophys, Little Rock, AR 72205 USA. NR 0 TC 1 Z9 1 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 2004 VL 104 IS 11 MA 3662 BP 996A EP 996A PN 1 PG 1 WC Hematology SC Hematology GA 871JM UT WOS:000225127503663 ER PT J AU Kampschulte, A Ferguson, MS Kerwin, WS Polissar, NL Chu, B Saam, T Hatsukami, TS Yuan, C AF Kampschulte, A Ferguson, MS Kerwin, WS Polissar, NL Chu, B Saam, T Hatsukami, TS Yuan, C TI Differentiation of intraplaque versus juxtaluminal hemorrhage/thrombus in advanced human carotid atherosclerotic lesions by in vivo magnetic resonance imaging SO CIRCULATION LA English DT Article DE magnetic resonance imaging; atherosclerosis; carotid arteries; plaque; hemorrhage ID HIGH-RESOLUTION MRI; CEREBRAL-ISCHEMIA; PLAQUE HEMORRHAGE; ARTERY STENOSIS; CLASSIFICATION; RUPTURE; ACCURACY; DISEASE; DEATH AB Background - Intraplaque hemorrhage and juxtaluminal hemorrhage/thrombus may differ in cause and clinical implications. This study tested the hypothesis that MRI can distinguish between intraplaque hemorrhage and juxtaluminal hemorrhage/thrombus and investigated the association between hemorrhage and underlying lesion types. Methods and Results - Twenty-six patients scheduled for carotid endarterectomy were imaged with a 1.5-T GE scanner by a multicontrast-weighted MRI technique. Hemorrhages were identified with previously established MRI criteria, and differentiations were made between intraplaque and juxtaluminal hemorrhage/ thrombus. Corresponding histology was used to confirm the magnetic resonance findings. Tissues underlying areas of hemorrhage/ thrombus were histologically categorized according to modified American Heart Association criteria. Of 190 matched sections, 140 contained areas of hemorrhage by histology, of which MRI correctly detected 134. The sensitivity and specificity for MRI to correctly identify cross sections that contained hemorrhage were 96% and 82%, respectively. Furthermore, MRI was able to distinguish juxtaluminal hemorrhage/ thrombus from intraplaque hemorrhage with an accuracy of 96%. The distribution of lesion types underlying hemorrhages differed significantly (P = 0.004). Intraplaque hemorrhage had an underlying lipid-rich type IV/V lesion in 55% of histological sections, whereas juxtaluminal hemorrhage/ thrombus had an underlying calcified lesion type VII in 70% of sections. Conclusions - In vivo high-resolution MRI can detect and differentiate intraplaque hemorrhage from juxtaluminal hemorrhage/ thrombus with good accuracy. The association of hemorrhage and lesion types suggests potential differences in origin. Noninvasive MRI therefore provides a possible tool for prospectively studying differences in origin of plaque hemorrhage and the association of plaque progression and instability. C1 Univ Washington, Dept Radiol, Seattle, WA 98195 USA. Univ Washington, Dept Surg, Seattle, WA 98195 USA. VA Puget Sound Hlth Care Syst, Seattle, WA USA. Mt Whisper Light Stat Consulting, Seattle, WA USA. Univ Heidelberg, Dept Radiol, Heidelberg, Germany. RP Yuan, C (reprint author), Univ Washington, Dept Radiol, 1959 NE Pacific Ave,Box 357115, Seattle, WA 98195 USA. EM cyuan@u.washington.edu FU NHLBI NIH HHS [HL56874] NR 33 TC 98 Z9 105 U1 0 U2 5 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0009-7322 J9 CIRCULATION JI Circulation PD NOV 16 PY 2004 VL 110 IS 20 BP 3239 EP 3244 DI 10.1161/01.CIR.0000147287.23741.9A PG 6 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 871DQ UT WOS:000225109900014 PM 15533871 ER PT J AU Gregory, SA Desai, AS Fifer, MA AF Gregory, SA Desai, AS Fifer, MA TI Isolated right ventricular infarction resulting from occlusion of a nondominant right coronary artery SO CIRCULATION LA English DT Editorial Material C1 Massachusetts Gen Hosp, Div Cardiol, Dept Med, Boston, MA 02114 USA. Harvard Univ, Sch Med, Boston, MA USA. Brigham & Womens Hosp, Dept Med, Div Cardiovasc, Boston, MA 02115 USA. RP Gregory, SA (reprint author), Massachusetts Gen Hosp, Div Cardiol, Dept Med, Yawkey Ctr,Suite 5800,55 Fruit St, Boston, MA 02114 USA. EM sagregory@partners.org NR 0 TC 6 Z9 7 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 16 PY 2004 VL 110 IS 20 BP E500 EP E501 DI 10.1161/01.CIR.0000147608.81302.D3 PG 2 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 871DQ UT WOS:000225109900021 PM 15545523 ER PT J AU Sabatine, MS Morrow, DA de Lemos, JA Omland, T Desai, MY Tanasijevic, M Hall, C McCabe, CH Braunwald, E AF Sabatine, MS Morrow, DA de Lemos, JA Omland, T Desai, MY Tanasijevic, M Hall, C McCabe, CH Braunwald, E TI Acute changes in circulating natriuretic peptide levels in relation to myocardial ischemia SO JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY LA English DT Article ID PLASMA-LEVELS; HEART-FAILURE; BRAIN; ATRIAL; ELEVATION; EXERCISE; DISEASE; IDENTIFICATION; INFARCTION; SECRETION AB OBJECTIVES The aim of this study was to determine the effect of transient myocardial ischemia on circulating natriuretic peptide levels. BACKGROUND Natriuretic peptides are released by the heart in response to wall stress. We hypothesized that transient myocardial ischemia would cause acute changes in circulating natriuretic peptide levels. METHODS B-type natriuretic peptide (BNP), N-terminal fragment of BNP pro-hormone (NT-pro-BNP), and N-terminal fragment of atrial natriuretic peptide pro-hormone (NT-pro-ANP) levels were measured in 112 patients before, immediately after, and 4 h after exercise testing with nuclear perfusion imaging. RESULTS Baseline levels of BNP were associated with the subsequent severity of provoked ischemia, with median levels of 43, 62, and 101 pg/ml in patients with none, mild- to-moderate, and severe inducible ischemia, respectively (p = 0.03). Immediately after exercise, the median increase in BNP was 14.2 pg/ml in patients with mild-to-moderate ischemia (p = 0.0005) and 23.7 pg/ml in those with severe ischemia (p = 0.017). In contrast, BNP levels only rose by 2.3 pg/ml in those who did not develop ischemia (p = 0.31). A similar relationship was seen between baseline NT-pro-BNP levels and inducible ischemia, but the changes in response to ischemia were less pronounced. NT-pro-ANP levels rose with exercise in both ischemic and non-Ischemic patients. When added to traditional clinical predictors of ischemia, a post-stress test BNP greater than or equal to80 pg/ml remained a strong and independent predictor of inducible myocardial ischemia (odds ratio 3.0, p = 0.025). CONCLUSIONS Transient myocardial ischemia was associated with an immediate rise in circulating BNP levels, and the magnitude of rise was proportional to the severity of ischemia. These findings demonstrate an important link between the severity of an acute ischemic insult and the circulating levels of BNP. (C) 2004 by the American College of Cardiology Foundation. C1 Brigham & Womens Hosp, Div Cardiovasc, TIMI Study Grp, Boston, MA 02115 USA. Univ Texas, SW Med Ctr, Dallas, TX USA. Aker Hosp, Dept Med, N-0514 Oslo, Norway. Johns Hopkins Univ, Div Cardiol, Baltimore, MD USA. Brigham & Womens Hosp, Dept Pathol, Div Clin Labs, Boston, MA 02115 USA. Univ Oslo, Rikshosp, Inst Clin Biochem, N-0027 Oslo, Norway. RP Sabatine, MS (reprint author), Brigham & Womens Hosp, Div Cardiovasc, TIMI Study Grp, 75 Francis St, Boston, MA 02115 USA. EM msabatine@partners.org FU NHLBI NIH HHS [F32 HL68455-01] NR 18 TC 213 Z9 229 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 16 PY 2004 VL 44 IS 10 BP 1988 EP 1995 DI 10.1016/j.jacc.2004.07.057 PG 8 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA 871ZI UT WOS:000225174900008 PM 15542281 ER PT J AU Song, HD Sun, XJ Deng, M Zhang, GW Zhou, Y Wu, XY Sheng, Y Chen, Y Ruan, Z Jiang, CL Fan, HY Zon, LI Kanki, JP Liu, TX Look, AT Chen, Z AF Song, HD Sun, XJ Deng, M Zhang, GW Zhou, Y Wu, XY Sheng, Y Chen, Y Ruan, Z Jiang, CL Fan, HY Zon, LI Kanki, JP Liu, TX Look, AT Chen, Z TI Hematopoietic gene expression profile in zebrafish kidney marrow SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article ID ACUTE MYELOID-LEUKEMIA; ACUTE MYELOMONOCYTIC LEUKEMIA; STEM/PROGENITOR CELLS; CLONING; MLL; FUSION; IDENTIFICATION; TRANSLOCATION; MYELOPOIESIS; EVOLUTIONARY AB The zebrafish kidney marrow is considered to be the organ of definitive hematopoiesis, analogous to the mammalian bone marrow. We have sequenced 26,143 ESTs and isolated 304 cDNAs with putative full-length ORF from a zebrafish kidney marrow cDNA library. The ESTs formed 7,742 assemblies, representing both previously identified zebrafish ESTs (56%) and recently discovered zebrafish ESTs (44%). About 30% of these EST assemblies have orthologues in humans, including 1,282 disease-associated genes in the Online Mendelian inheritance in Man (OMIM) database. Comparison of the effective and regulatory molecules related to erythroid functions across species suggests a good conservation from zebrafish to human. Interestingly, both embryonic and adult zebrafish globin genes showed higher homology to the human embryonic globin genes than to the human fetal/adult ones, consistent with evo-devo correlation hypothesis. In addition, conservation of a whole set of transcription factors involved in globin gene switch suggests the regulatory network for such remodeling mechanism existed before the divergence of the teleost and the ancestor of mammals. We also carried out whole-mount mRNA in situ hybridization assays for 493 cDNAs and identified 80 genes (16%) with tissue-specific expression during the first five days of zebrafish development. Twenty-six of these genes were specifically expressed in hematopoietic or vascular tissues, including three previously unidentified zebrafish genes: coro1a, nephrosin, and dab2. Our results indicate that conserved genetic programs regulate vertebrate hematopoiesis and vasculogenesis, and support the role of the zebrafish as an important animal model for studying both normal development and the molecular pathogenesis of human blood diseases. C1 Dana Farber Canc Inst, Dept Pediat Oncol, Medford, MA 02155 USA. Shanghai Med Univ 2, Ruijin Hosp, Shanghai Inst Hematol, State Key Lab Med Genomics, Shanghai 200025, Peoples R China. Shanghai Med Univ 2, Hlth Sci Ctr, Shanghai 200025, Peoples R China. Chinese Acad Sci, Shanghai Inst Biol Sci, Shanghai 200025, Peoples R China. Harvard Univ, Sch Med, Boston, MA 02115 USA. Childrens Hosp, Howard Hughes Med Inst, Boston, MA 02115 USA. Childrens Hosp, Div Hematol & Oncol, Boston, MA 02115 USA. RP Look, AT (reprint author), Dana Farber Canc Inst, Dept Pediat Oncol, Medford, MA 02155 USA. EM thomas_look@dfci.harvard.edu; zchen@stn.sh.cn RI Sun, Xiao-Jian/D-1560-2011; Song, Huai-Dong/G-8961-2011 OI Sun, Xiao-Jian/0000-0001-8826-4614; FU NIDDK NIH HHS [U01 DK063328] NR 30 TC 88 Z9 192 U1 2 U2 16 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 16 PY 2004 VL 101 IS 46 BP 16240 EP 16245 DI 10.1073/pnas.0407241101 PG 6 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA 872RO UT WOS:000225226200029 PM 15520368 ER PT J AU Chen, JH Magavi, SSP Macklis, JD AF Chen, JH Magavi, SSP Macklis, JD TI Neurogenesis of corticospinal motor neurons extending spinal projections in adult mice SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article ID MICROTUBULE-ASSOCIATED PROTEIN; CENTRAL-NERVOUS-SYSTEM; CELL-DEATH; HIPPOCAMPAL NEUROGENESIS; EMBRYONIC NEURONS; PYRAMIDAL NEURONS; PURKINJE NEURONS; MAMMALIAN BRAIN; OLFACTORY-BULB; DENTATE GYRUS AB The adult mammalian CNS shows a very limited capacity to regenerate after injury. However, endogenous precursors, or stem cells, provide a potential source of new neurons in the adult brain. Here, we induce the birth of new corticospinal motor neurons (CSMN), the CNS neurons that die in motor neuron degenerative diseases, including amyotrophic lateral sclerosis, and that cause loss of motor function in spinal cord injury. We induced synchronous apoptotic degeneration of CSMN and examined the fates of newborn cells arising from endogenous precursors, using markers for DNA replication, neuroblast migration, and progressive neuronal differentiation, combined with retrograde labeling from the spinal cord. We observed neuroblasts entering the neocortex and progressively differentiating into mature pyramidal neurons in cortical layer V. We found 20-30 new neurons per mm(3) in experimental mice vs. 0 in controls. A subset of these newborn neurons projected axons into the spinal cord and survived >56 weeks. These results demonstrate that endogenous precursors can differentiate into even highly complex long-projection CSMN in the adult mammalian brain and send new projections to spinal cord targets, suggesting that molecular manipulation of endgenous neural precursors in situ may offer future therapeutic possibilities for motor neuron degenerative disease and spinal cord injury. C1 Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Neurosurg, Boston, MA 02114 USA. Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Neurol, Boston, MA 02114 USA. Harvard Univ, Massachusetts Gen Hosp, Sch Med, Program Neurosci,Ctr Nervous Syst Repair, Boston, MA 02114 USA. RP Macklis, JD (reprint author), Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Neurosurg, Boston, MA 02114 USA. EM jeffrey_macklis@hms.harvard.edu NR 43 TC 161 Z9 170 U1 0 U2 2 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 16 PY 2004 VL 101 IS 46 BP 16357 EP 16362 DI 10.1073/pnas.0406795101 PG 6 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA 872RO UT WOS:000225226200049 PM 15534207 ER PT J AU Moselewski, F Ropers, D Pohle, K Hoffmann, M Ferencik, M Chan, RC Cury, RC Abbara, S Jang, IK Brady, TJ Daniel, WG Achenbach, S AF Moselewski, F Ropers, D Pohle, K Hoffmann, M Ferencik, M Chan, RC Cury, RC Abbara, S Jang, IK Brady, TJ Daniel, WG Achenbach, S TI Comparison of measurement of cross-sectional coronary atherosclerotic plaque and vessel areas by 16-slice multidetector computed tomography versus intravascular ultrasound SO AMERICAN JOURNAL OF CARDIOLOGY LA English DT Article ID ACUTE MYOCARDIAL-INFARCTION; MULTISLICE SPIRAL CT; IMAGE QUALITY; ANGIOGRAPHY; ARTERY; ACCURACY AB In 26 patients, 16-slice multicletector computed tomography (MDCT) with 0.75-mm collimation and intravascular ultrasound (IVUS) of 1 coronary artery were performed. At 100 sites within the coronary arteries, the measurement of cross-sectional luminal area and, if detectable, the cross-sectional area of atherosclerotic plaque was performed independently with IVUS and MDCT. The mean luminal area (r = 0.92), measured at 100 sites, and plaque area (r = 0.55), measured at 65 sites, were significantly correlated (p < 0.001) between MDCT and IVUS. The mean luminal area and mean plaque area were slightly but significantly overestimated with MDCT. MDCT permits the noninvasive measurement of coronary cross-sectional luminal and plaque areas with moderate accuracy. (C) 2004 by Excerpta Medica, Inc. C1 Massachusetts Gen Hosp, Dept Radiol, Boston, MA 02114 USA. Univ Erlangen Nurnberg, Dept Internal Med 2 Cardiol, Erlangen, Germany. Massachusetts Gen Hosp, Div Cardiol, Boston, MA 02114 USA. RP Moselewski, F (reprint author), Univ Erlangen Nurnberg, Dept Internal Med 2, Ullmenweg 18, D-91054 Erlangen, Germany. EM stephan.achenbach@med2.med.uni-erlangen.de NR 16 TC 113 Z9 117 U1 0 U2 3 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 15 PY 2004 VL 94 IS 10 BP 1294 EP 1297 DI 10.1016/j.amjcard.2004.07.117 PG 4 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA 872LC UT WOS:000225207700016 PM 15541250 ER PT J AU Bent, S Padula, A Neuhaus, J AF Bent, S Padula, A Neuhaus, J TI Safety and efficacy of citrus aurantium for weight loss SO AMERICAN JOURNAL OF CARDIOLOGY LA English DT Article ID EPHEDRA; ADULTS AB To examine the safety and efficacy of citrus aurantium, an herb now commonly used as a substitute for ephedra in dietary supplements marketed to promote weight loss, we conducted a systematic review. An extensive search of MEDLINE, EMBASE, BIOSIS, and the Cochrane Collaboration Database identified only 1 eligible randomized placebo controlled trial, which followed 20 patients for 6 weeks, demonstrated no statistically significant benefit for weight loss, and provided limited information about the safety of the herb. (C) 2004 by Excerpta Medica, Inc. C1 San Francisco VA Med Ctr, Dept Med, San Francisco, CA 94121 USA. Univ Calif San Francisco, Osher Ctr Integrat Med, San Francisco, CA 94143 USA. Univ Calif San Francisco, Dept Epidemiol & Biostat, San Francisco, CA 94143 USA. RP Bent, S (reprint author), San Francisco VA Med Ctr, Dept Med, 111-A1,4150 Clement St, San Francisco, CA 94121 USA. EM bent@itsa.ucsf.edu FU NCCIH NIH HHS [1 K08 ATO1338-01] NR 14 TC 55 Z9 60 U1 0 U2 6 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 15 PY 2004 VL 94 IS 10 BP 1359 EP 1361 DI 10.1016/j.amjcard.2004.07.137 PG 3 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA 872LC UT WOS:000225207700036 PM 15541270 ER PT J AU Brown, AM Gordon, D Lee, H Caudy, M Hardy, J Haroutunian, V Blass, JP AF Brown, AM Gordon, D Lee, H Caudy, M Hardy, J Haroutunian, V Blass, JP TI Association of the dihydrolipoamide dehydrogenase gene with Alzheimer's disease in an Ashkenazi Jewish population SO AMERICAN JOURNAL OF MEDICAL GENETICS PART B-NEUROPSYCHIATRIC GENETICS LA English DT Article ID OBSESSIVE-COMPULSIVE DISORDER; HARDY-WEINBERG PROPORTIONS; APOLIPOPROTEIN-E; MITOCHONDRIAL DISEASES; FREQUENCY ESTIMATION; COMPLEX ACTIVITY; ALPHA-SUBUNIT; TYPE-4 ALLELE; ONSET; MUTATIONS AB Abundant biochemical evidence links deficient activity of mitochondrial a-ketoglutarate dehydrogenase with neuropathologically confirmed Alzheimer's disease (AD). Reduced a-ketoglutarate dehydrogenase activity has also been associated with anti-mortem measures of clinical disability. One of the genes encoding this complex, namely, DLD, lies within a chromosome 7 region that is in linkage disequilibrium. with AD. We therefore examined the hypothesis that variation in DLD is associated with AD risk. Denaturing HPLC was used to search for sequence variations in the coding and flanking regions of all exons of DLD, but no abundant variants that alter protein sequence were found. However, four common SNPs were identified and genotyped in a case-control series of 297 Caucasians from New York City, including 229 residents of a Jewish nursing home. Logistic regression analysis was performed for the four-locus DLD genotype, sex, and ApoE4 status to determine the association of these independent variables with AD. Significant associations with AD were observed for ApoE4 (P<10(-6)) and sex combined with DLD genotype (P=0.013). The association with the DLD genotypes appears only in the male population in both the Caucasian series (P=0.0009, n=83) and the Ashkenazi Jewish subseries (P=0.017, n=49). The DLD genotype appears to operate independently of APOE in conferring AD risk. (C) 2004 Wiley-Liss, Inc. C1 Dementia Res Serv, Burke Med Res Inst, White Plains, NY 10605 USA. Cornell Univ, Weill Med Coll, Dept Biochem, New York, NY USA. Cornell Univ, Weill Med Coll, Dept Neurol & Neurosci, New York, NY USA. Cornell Univ, Weill Med Coll, Dept Med, New York, NY USA. Rockefeller Univ, Lab Stat Genet, New York, NY 10021 USA. NINDS, Neurogenet Lab, Bethesda, MD 20892 USA. Mt Sinai Sch Med, Dept Psychiat, New York, NY USA. Bronx Vet Adm Med Ctr, Bronx, NY USA. RP Brown, AM (reprint author), Dementia Res Serv, Burke Med Res Inst, 785 Mamaroneck Ave, White Plains, NY 10605 USA. EM ambrown@med.cornell.edu RI Hardy, John/C-2451-2009 FU NHGRI NIH HHS [K01-HG00055]; NIA NIH HHS [P01-AG02219, P01-AG14930]; NIMH NIH HHS [MH44292] NR 48 TC 11 Z9 11 U1 0 U2 1 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 0148-7299 J9 AM J MED GENET B JI Am. J. Med. Genet. B PD NOV 15 PY 2004 VL 131B IS 1 BP 60 EP 66 DI 10.1002/ajmg.b.30008 PG 7 WC Genetics & Heredity; Psychiatry SC Genetics & Heredity; Psychiatry GA 866RP UT WOS:000224790900011 PM 15389771 ER PT J AU Tsai, KY Tsao, H AF Tsai, KY Tsao, H TI The genetics of skin cancer SO AMERICAN JOURNAL OF MEDICAL GENETICS PART C-SEMINARS IN MEDICAL GENETICS LA English DT Review DE basal cell carcinoma; squamous cell carcinoma; melanoma; cutaneous lymphoma ID BASAL-CELL CARCINOMAS; DUPRE-CHRISTOL SYNDROME; PRIMITIVE NEUROECTODERMAL TUMORS; MELANOCORTIN-1 RECEPTOR MC1R; PAPILLOMAVIRUS TYPE-16 E6; HUMAN-MALIGNANT MELANOMA; CENTRAL-NERVOUS-SYSTEM; COARSE SPARSE HAIR; SUN-EXPOSED SKIN; N-RAS MUTATIONS AB Recent advances in molecular genetics have led to a better understanding of the biological underpinnings of skin cancer formation. As with most cancers, the RB, p53, and RAS pathways appear to play prominent roles in the pathogenesis of several skin cancer types. Although various components of these pathways may be differentially altered in squamous cell carcinoma (SCC), basal cell carcinoma (BCC), and cutaneous melanoma, the final biochemical expression of these defects may be the same. With the unraveling of these genetic mechanisms, a more targeted approach to diagnosis and treatment maybe possible in the near future. (C) 2004 Wiley-Liss, Inc. C1 Massachusetts Gen Hosp, Wellman Ctr Photomed, Dept Dermatol, Boston, MA 02114 USA. Harvard Univ, Sch Med, Dept Dermatol, Cambridge, MA 02138 USA. Massachusetts Gen Hosp, Melanoma Genet Program, Boston, MA 02114 USA. Massachusetts Gen Hosp, Pigmented Les Clin, Boston, MA 02114 USA. RP Tsao, H (reprint author), Massachusetts Gen Hosp, Wellman Ctr Photomed, Dept Dermatol, Bartlett Hall,622,48 Blossom St, Boston, MA 02114 USA. EM htsao@partners.org NR 154 TC 43 Z9 43 U1 1 U2 6 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 0148-7299 J9 AM J MED GENET C JI Am. J. Med. Genet. C PD NOV 15 PY 2004 VL 131C IS 1 BP 82 EP 92 DI 10.1002/ajmg.c.30037 PG 11 WC Genetics & Heredity SC Genetics & Heredity GA 868YL UT WOS:000224949000010 PM 15468170 ER PT J AU McNaughton-Collins, M Fowler, FJ Caubet, JF Bates, DW Lee, JM Hauser, A Barry, MJ AF McNaughton-Collins, M Fowler, FJ Caubet, JF Bates, DW Lee, JM Hauser, A Barry, MJ TI Psychological effects of a suspicious prostate cancer screening test followed by a benign biopsy result SO AMERICAN JOURNAL OF MEDICINE LA English DT Article ID FALSE-POSITIVE MAMMOGRAM; QUALITY-OF-LIFE; BREAST-CANCER; LOCAL-ANESTHESIA; ANTIGEN; PATIENT; HEALTH; TRIAL; MEN AB PURPOSE: To evaluate the psychological implications of an apparently false-positive screening result for prostate cancer. METHODS: The sample comprised 167 men with a benign biopsy result in response to a Suspicious screening test result (biopsy group) and 233 men with a normal prostate-specific antigen (PSA) test result (control group). The men responded to a questionnaire within about 6 weeks of their biopsy or PSA results. They were asked about demographic characteristics, medical history, psychological effects, biopsy experience, and prostate cancer knowledge. RESULTS: The survey response rate was 85% (400/471). The mean (+/- SD) age of respondents was 60 +/- 9 years (range, 40 to 88 years); 88% (n = 350) were white. Forty-nine percent (81/167) of men in the biopsy group reported having thought about prostate cancer either "a lot" or "some of the time", compared with 18% (42/230) in the control group (P < 0.001). In addition, 40% (67/167) in the biopsy group reported having worried "a lot" or "some of the time" that they may develop prostate cancer, compared with 8% (18/231) in the control group (P < 0.001). CONCLUSION: Men who underwent prostate biopsy more often reported having thought and worried about prostate cancer, despite having received a benign result. This underrecognized human cost of screening should be considered in the debate about the benefits and harms of prostate cancer screening. (C) 2004 by Elsevier Inc. C1 Massachusetts Gen Hosp, Gen Med Div, Boston, MA 02114 USA. Univ Massachusetts, Ctr Survey Res, Boston, MA 02125 USA. Brigham & Womens Hosp, Gen Med Div, Boston, MA 02115 USA. Boston Med Ctr, Gen Med Div, Boston, MA USA. RP McNaughton-Collins, M (reprint author), Massachusetts Gen Hosp, Gen Med Div, 50 Staniford St,9th Floor, Boston, MA 02114 USA. EM mmcnaughtoncollins@partners.org NR 29 TC 56 Z9 57 U1 0 U2 3 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 15 PY 2004 VL 117 IS 10 BP 719 EP 725 DI 10.1016/j.amjmed.2004.06.036 PG 7 WC Medicine, General & Internal SC General & Internal Medicine GA 872UA UT WOS:000225232900001 PM 15541320 ER PT J AU Mortensen, EM Restrepo, M Anzueto, A Pugh, J AF Mortensen, EM Restrepo, M Anzueto, A Pugh, J TI Effects of guideline-concordant antimicrobial therapy on mortality among patients with community-acquired pneumonia SO AMERICAN JOURNAL OF MEDICINE LA English DT Article ID ELDERLY-PATIENTS; MANAGEMENT; DIAGNOSIS; SEVERITY; OUTCOMES; QUALITY; ADULTS; CARE AB PURPOSE: National practice guidelines have recommended specific initial empiric antimicrobial regimens for patients with community-acquired pneumonia. Our aim was to determine the association between the use of guideline-concordant antimicrobial therapy and 30-day mortality in patients with pneumonia. METHODS: We conducted a retrospective cohort study at two tertiary teaching hospitals. Eligible patients were admitted with a diagnosis of community-acquired pneumonia, had a chest radiograph consistent with pneumonia, and had a discharge diagnosis of pneumonia. All eligible patients were identified and a random sample was abstracted. We determined whether the use of guideline-concordant antibiotics was associated with 30-day mortality in an analysis that adjusted for potential confounders using propensity scores. RESULTS: Information was obtained on 420 patients with pneumonia. The mean (+/- SD) age was 63 +/- 16 years, 355 were men, and 82 patients were initially admitted to the intensive care unit. At 30 days after presentation, 41 patients (9.8%) had died: 21 of 97 (21.7%) in the non-guideline-concordant group and 20 of 323 (6.2%) in the guideline-concordant group. Antibiotics were concordant with national guidelines in 323 patients. In the regression analysis, after adjustment for the propensity score, failure to comply with antimicrobial therapy guidelines was associated with increased 30-day mortality (odds ratio = 5.7; 95% confidence interval: 2.0 to 16.0). CONCLUSION: Receipt of antimicrobial regimens concordant with national published guidelines may reduce 30-day mortality among patients hospitalized with pneumonia. (C) 2004 by Elsevier Inc. C1 UTHSCSA, ALMD, Vet Evidence Based Res Disseminat & Implementat C, Div Gen Internal Med, San Antonio, TX 78284 USA. S Texas Vet Hlth Care Syst, Div Pulm Crit Care Med, San Antonio, TX USA. RP Mortensen, EM (reprint author), UTHSCSA, ALMD, Vet Evidence Based Res Disseminat & Implementat C, Div Gen Internal Med, 7400 Merton Minter Blvd, San Antonio, TX 78284 USA. EM mortensen@verdict.uthscsa.edu OI Pugh, Jacqueline/0000-0003-4933-141X; Mortensen, Eric/0000-0002-3880-5563 NR 17 TC 86 Z9 89 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 15 PY 2004 VL 117 IS 10 BP 726 EP 731 DI 10.1016/j.amjmed.2004.06.028 PG 6 WC Medicine, General & Internal SC General & Internal Medicine GA 872UA UT WOS:000225232900002 PM 15541321 ER PT J AU Arterburn, DE McDonell, MB Hedrick, SC Diehr, P Fihn, SD AF Arterburn, DE McDonell, MB Hedrick, SC Diehr, P Fihn, SD TI Association of body weight with condition-specific quality of life in male veterans SO AMERICAN JOURNAL OF MEDICINE LA English DT Article ID PRIMARY-CARE PATIENTS; HEALTH-STATUS; OBESITY; QUESTIONNAIRE; OVERWEIGHT; DISEASE; POPULATION; DEPRESSION; GUIDELINES; ADULTS AB PURPOSE: We hypothesized that obese adults with coronary heart disease, obstructive lung disease, or depression would report greater impairments in health-related quality of life owing to their angina, dyspnea, or depressive symptoms as compared with persons with normal body weight. METHODS: We analyzed cross-sectional data from the Ambulatory Care Quality Improvement Project, a multicenter Study of veterans enrolled in general internal medicine clinics. Health-related quality of life was assessed using the Medical Outcomes Study Short Form-36, the Seattle Angina Questionnaire, the Seattle Obstructive Lung Disease Questionnaire, and the Hopkins Symptom Checklist for Depression. RESULTS: Compared with patients of normal weight (body mass index: 18.5 to 24.9 kg/m(2)), underweight patients (body mass index <18.5 kg/m(2)) reported health-related quality-of-life scores that were at least 5% lower (worse) in all 15 quality-of-life domains examined. Patients with class III obesity (body 2 mass index greater than or equal to40 kg/m(2)) reported quality-of-life scores that were at least 5% lower than those of normal weight patients in eight domains. Scores of overweight patients (body mass index: 25 to 29.9 kg/m(2)) were higher (better) than those of normal weight patients in I I domains. CONCLUSION: Body mass index was strongly associated with generic- and condition-specific health-related quality of life. Our results suggest that, when considering health-related quality-of-life outcomes among veterans, the optimal body mass index may be above the "normal" range. Further research should test the validity of the 1998 National Institutes of Health body mass index categories as predictors of health outcomes among veterans. (C) 2004 by Elsevier Inc. C1 Cincinnati Vet Affairs Med Ctr, Hlth Serv Res & Dev, Cincinnati, OH 45220 USA. Univ Cincinnati, Ctr Med, Dept Internal Med, Div Gen Internal Med,Sect Outcomes Res, Cincinnati, OH USA. Univ Cincinnati, Inst Hlth Policy & Hlth Serv Res, Cincinnati, OH USA. Vet Affairs Puget Sound Hlth Care Syst, NW Hlth Serv Res, Seattle, WA USA. Vet Affairs Puget Sound Hlth Care Syst, Dev Ctr Excellence, Seattle, WA USA. Univ Washington, Dept Hlth Serv, Seattle, WA USA. Univ Washington, Dept Biostat, Seattle, WA USA. Univ Washington, Dept Med, Seattle, WA USA. RP Arterburn, DE (reprint author), Cincinnati Vet Affairs Med Ctr, Hlth Serv Res & Dev, 3200 Vine St 151, Cincinnati, OH 45220 USA. EM David.Arterburn@uc.edu NR 30 TC 24 Z9 25 U1 1 U2 2 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 15 PY 2004 VL 117 IS 10 BP 738 EP 746 DI 10.1016/j.amjmed.2004.06.031 PG 9 WC Medicine, General & Internal SC General & Internal Medicine GA 872UA UT WOS:000225232900004 PM 15541323 ER PT J AU Steinman, MA Fischer, MA Shlipak, MG Bosworth, HB Oddone, EZ Hoffman, BB Goldstein, MK AF Steinman, MA Fischer, MA Shlipak, MG Bosworth, HB Oddone, EZ Hoffman, BB Goldstein, MK TI Clinician awareness of adherence to hypertension guidelines SO AMERICAN JOURNAL OF MEDICINE LA English DT Article ID PRIMARY-CARE PHYSICIANS; BLOOD-PRESSURE; SELF-ASSESSMENTS; PERFORMANCE; MEDICINE; MANAGEMENT; INFORMATION; ATTITUDES; ACCURACY; FEEDBACK AB PURPOSE: Little is known about how well clinicians are aware of their own adherence to clinical guidelines, an important indicator of quality. We compared clinicians' beliefs about their adherence to hypertension guidelines with data on their actual performance. METHODS: We surveyed 139 primary care clinicians at three Veterans Affairs medical centers, asking them to assess their own adherence to hypertension guidelines. We then extracted data from the centers' clinical databases on guideline-concordant medication use and blood pressure control for patients cared for by these providers during a 6-month period. Data were collected for patients with hypertension and diabetes, hypertension and coronary disease, or hypertension with neither of these comorbid conditions. RESULTS: Eighty-six clinicians (62%) completed the survey. Each clinician saw a median of 94 patients with hypertension (mean age, 65 years). Patients were treated with an average of 1.6 antihypertensive medications. Overall, clinicians overestimated the proportion of their patients who were prescribed guideline-concordant medications (75% perceived vs. 67% actual, P <0.001) and who had blood pressure levels <140/90 mm Hg on their last visit (68% perceived vs. 43% actual, P <0.001). Among individual clinicians, there were no significant correlations between perceived and actual guideline adherence (r = 0.18 for medications, r = 0.14 for blood pressure control; P greater than or equal to0.10 for both). Clinicians with relatively low actual guideline performance were most likely to overestimate their adherence to medication recommendations and blood pressure targets. CONCLUSION: Clinicians appear to overestimate their adherence to hypertension guidelines, particularly with regards to the proportion of their patients with controlled blood pressure. This limited awareness may represent a barrier to successful implementation of guidelines, and could be addressed through the use of provider profiles and point-of-service feedback to clinicians. (C) 2004 by Elsevier Inc. C1 San Francisco VA Med Ctr, Div Geriatr, San Francisco, CA 94121 USA. San Francisco VA Med Ctr, Div Gen Internal Med, San Francisco, CA 94121 USA. Univ Calif San Francisco, San Francisco, CA 94143 USA. Univ Massachusetts, Ctr Med, Dept Med, Worcester, MA USA. Durham VA Med Ctr, Ctr Hlth Serv Res Primary Care, Durham, NC USA. Duke Univ, Div Gen Internal Med, Dept Med, Durham, NC 27706 USA. Harvard Univ, Sch Med, Boston, MA USA. VA Boston, Dept Med, Boston, MA USA. Stanford Univ, Dept Med, Ctr Primary Care & Outcomes Res, Palo Alto, CA 94304 USA. VA Palo Alto Hlth Care Syst, Geriatr Res Educ & Clin Ctr, Palo Alto, CA USA. RP Steinman, MA (reprint author), San Francisco VA Med Ctr, Div Geriatr, 4150 Clement St,Box 181-G, San Francisco, CA 94121 USA. EM mstein@itsa.ucsf.edu NR 30 TC 57 Z9 57 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 15 PY 2004 VL 117 IS 10 BP 747 EP 754 DI 10.1016/j.amjmed.2004.03.035 PG 8 WC Medicine, General & Internal SC General & Internal Medicine GA 872UA UT WOS:000225232900005 PM 15541324 ER PT J AU Delaunoit, T Goldberg, RM Sargent, DJ Morton, RF Fuchs, CS Findlay, BP Thomas, SP Salim, M Schaefer, PL Stella, PJ Green, E Mailliard, JA AF Delaunoit, T Goldberg, RM Sargent, DJ Morton, RF Fuchs, CS Findlay, BP Thomas, SP Salim, M Schaefer, PL Stella, PJ Green, E Mailliard, JA TI Mortality associated with daily bolus 5-fluorouracil/leucovorin administered in combination with either irinotecan or oxaliplatin - Results from Intergroup Trial N09741 SO CANCER LA English DT Article DE 5-fluorouracil; leucovorin; irinotecan; oxaliplatin; colorectal carcinoma; gastrointestinal toxicity; treatment related mortality ID METASTATIC COLORECTAL-CANCER; MULTICENTER RANDOMIZED-TRIAL; 1ST-LINE TREATMENT; PHASE-II; FLUOROURACIL; LEUCOVORIN; INFUSION AB BACKGROUND. Intergroup Trial N9741 evaluated 5-fluorouracil (5-FU)/leucovorin (LV) administered in conjunction with either irinotecan or oxaliplatin in the first-line treatment of advanced colorectal carcinoma (CRC). The current report describes two treatment arms that were withdrawn from the protocol due to unexpected treatment-related toxicities and a high mortality rate. The complications observed in these arms highlight the importance of aggressive and immediate supportive care in the management of digestive toxicity. METHODS. In Trial N9741, patients were randomly assigned to receive one of the following six regimens: 1) irinotecan plus bolus 5-FU/LV (Arm A); 2) sequential irinotecan plus bolus 5-FU/LV (Arm B); 3) bolus 5-FU/LV only (Mayo Clinic regimen; Arm D); 4) oxaliplatin plus bolus 5-FU/LV (Arm E); 5) oxaliplatin plus infusional 5-FU/LV (Arm F); or 6) oxaliplatin plus irinotecan (Arm G). In the current study, the authors investigated treatment-related toxicity in patients who received either of the two combination regimens containing daily bolus 5-FU (i.e., patients in Arm B or Arm E). RESULTS. Sixty-one and 47 patients were enrolled in Arm B and Arm E, respectively. Diarrhea and neutropenia were the most common toxicities in both groups. Five patients in Arm B (8.2%) and 4 patients in Arm E (8.5%) died within 60 days of study entry. All fatal toxicities occurred within 15 days of treatment administration, and all deaths were associated with the simultaneous occurrence of multiple symptoms, which were dominated by Grade 3 diarrhea. CONCLUSIONS. Combination regimens containing daily bolus 5-FU/LV and oxaliplatin or irinotecan can be associated with severe gastrointestinal toxicity and high mortality rates. Therefore, the authors recommend the use of more tolerable infusional 5-FU-based regimens in the treatment of metastatic CRC. Cancer 2004; 101:2170-6. (C) 2004 American Cancer Society. C1 Mayo Clin, Canc Ctr Stat Unit, Rochester, MN 55905 USA. Mayo Clin, Dept Oncol, Rochester, MI USA. Univ N Carolina, Dept Med, Chapel Hill, NC USA. Iowa Oncol Res Assoc, Community Clin Oncol Program, Des Moines, IA USA. Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02115 USA. Natl Canc Inst Canada, St Catharines, ON, Canada. Oncol Hematol Associates, Peoria, IL USA. Allen Blair Canc Ctr, Regina, SK, Canada. Toledo Community Clin Oncol Program, Toledo, OH USA. St Joseph Mercy Hlth Syst, Alex Canc Care Ctr, Ann Arbor, MI USA. Missouri Valley Canc Consortium, Community Clin Oncol Program, Omaha, NE USA. RP Sargent, DJ (reprint author), Mayo Clin, Canc Ctr Stat Unit, Kahler 1A,200 1st St SW, Rochester, MN 55905 USA. EM sargent.daniel@mayo.edu RI Goldberg , Richard/M-1311-2013 NR 21 TC 52 Z9 54 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 2004 VL 101 IS 10 BP 2170 EP 2176 DI 10.1002/cncr.20594 PG 7 WC Oncology SC Oncology GA 870TN UT WOS:000225081300005 PM 15470715 ER PT J AU Ahles, TA Herndon, JE Small, EJ Vogelzang, NJ Kornblith, AB Ratain, MJ Stadler, W Palchak, D Marshall, ME Wilding, G Petrylak, D Holland, JC AF Ahles, TA Herndon, JE Small, EJ Vogelzang, NJ Kornblith, AB Ratain, MJ Stadler, W Palchak, D Marshall, ME Wilding, G Petrylak, D Holland, JC TI Quality of life impact of three different doses of suramin in patients with metastatic hormone-refractory prostate carcinoma - Results of Intergroup 0159/Cancer and Leukemia Group B 9480 SO CANCER LA English DT Article DE prostate carcinoma; quality of life; suramin; hormone-refractory adenocarcinoma ID CANCER; MEN; THERAPY; PAIN AB BACKGROUND. Research has suggested that men with hormone-refractory prostate carcinoma have a lower quality of life (QOL) compared with men who have hormone-sensitive prostate carcinoma and that quality of life (QOL) steadily declines over the last year of life for men with prostate carcinoma. The primary purpose of the current study was to evaluate whether there was evidence of palliative effects associated with suramin at any of the three doses administered in the original clinical trial. METHODS. Patients with histologically confirmed advanced hormone-refractory adenocarcinoma of the prostate were randomized to receive suramin at a low dose (n = 129; median age, 69 years), an intermediate dose (n = 129; median age, 71 years), or a high dose (n = 127; median age, 70 years) as part of the Intergroup 0159/Cancer and Leukemia Group B 9480 trial. Patients completed a battery of assessment tools, including the Functional Assessment of Cancer Therapy (FACT)-Prostate, the Center for Epidemiological Studies-Depression Scale (CES-D), the Brief Pain Inventory, and an opioid medication log, at baseline, on Day 1 of the sixth week of active therapy, during the second week after treatment termination, and 3 months after administration of the final suramin dose. RESULTS. Patients who received low-dose suramin reported improvement in QOL (FACT-General: P < 0.01; FACT-Treatment Outcome Index: P < 0.01) and decreased levels of depression (CES-D: P < 0.0006) during treatment compared with patients in the intermediate- and high-dose arms. After treatment, all groups experienced equal decreases in FACT and CES-D scores. CONCLUSIONS. The pattern of results suggests that the lowest dose of suramin administered had a palliative effect in terms of improvement in QOL and decreased levels of depression and that this effect was lost once suramin was discontinued. Cancer 2004;101:2202-8. (C) 2004 American Cancer Society. C1 Dartmouth Hitchcock Med Ctr, Norris Cotton Canc Ctr, Dept Psychiat, Lebanon, NH 03756 USA. Ctr Stat, Canc & Leukemia Grp B, Durham, NC USA. Univ Calif San Francisco, Dept Med, Ctr Comprehens Canc, San Francisco, CA USA. Univ Chicago, Dept Med, Chicago, IL 60637 USA. Dana Farber Canc Inst, Dept Adult Oncol, Boston, MA 02115 USA. Univ Calif San Diego, Dept Med, Ctr Canc, San Diego, CA 92103 USA. SE Canc Control Consortium Inc, Community Clin Oncol Program, Goldsboro, NC USA. Univ Wisconsin, Ctr Comprehens Canc, Dept Med, Madison, WI USA. Columbia Presbyterian Med Ctr, Dept Med, New York, NY 10032 USA. Mem Sloan Kettering Canc Ctr, Dept Psychiat & Behav Sci, New York, NY 10032 USA. RP Ahles, TA (reprint author), Dartmouth Hitchcock Med Ctr, Norris Cotton Canc Ctr, Dept Psychiat, 1 Med Ctr Dr, Lebanon, NH 03756 USA. EM Tim.A.Ahles@Dartmouth.edu FU NCI NIH HHS [CA12046, CA31983, CA77406, CA365091, CA11028, CA47577, CA77298, CA47559, CA33601, CA12449, CA45389, CA47545, CA47555, CA03927, CA11789, CA02599, CA21060, CA71323, CA35421, CA07968, CA08025, CA45374, CA26806, CA77658, CA41287, CA45808, CA60138, CA16450, CA04326, CA04457, CA74811, CA31946, CA45418, CA32291] NR 15 TC 23 Z9 25 U1 0 U2 1 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 2004 VL 101 IS 10 BP 2202 EP 2208 DI 10.1002/cncr.20655 PG 7 WC Oncology SC Oncology GA 870TN UT WOS:000225081300009 PM 15484217 ER PT J AU Argiris, A Li, Y Forastiere, A AF Argiris, A Li, Y Forastiere, A TI Prognostic factors and long-term survivorship in patients with recurrent or metastatic carcinoma of the head and neck - An analysis of two Eastern Cooperative Oncology Group randomized trials SO CANCER LA English DT Article DE prognostic factors; squamous cell carcinoma; head and neck carcinoma; chemotherapy; metastatic; recurrent ID SQUAMOUS-CELL CARCINOMA; CISPLATIN-BASED CHEMOTHERAPY; FULL-DOSE REIRRADIATION; PHASE-III; CANCER; 5-FLUOROURACIL; METHOTREXATE; FLUOROURACIL; HYDROXYUREA; PACLITAXEL AB BACKGROUND. The current study was conducted to identify prognostic factors and report the characteristics of long-term survivors in patients with recurrent or metastatic carcinoma of the head and neck who were treated with cisplatin-based combination chemotherapy in two randomized, Phase III trials conducted by the Eastern Oncology Cooperative Group (ECOG) (E1393 and E1395). METHODS. The authors analyzed prognostic factors for response and survival by combining data from the E1393 trial, which compared cisplatin plus paclitaxel at two dose levels, with data from the E1395 trial, which compared cisplatin plus paclitaxel with cisplatin plus 5-fluorouracil (5-FU), using logistic regression and Cox regression models. RESULTS. A total of 399 eligible patients were included. The median follow-up was 4.7 years. The 1-year overall survival (OS) rate for all patients was 32%, the median OS was 7.8 months, and the objective response rate was 32%. On multivariate analysis, the following were found to be independent unfavorable predictors of objective response: weight loss of > 5%, an ECOG performance status of I (vs. 0), residual disease at the primary tumor site, a primary tumor site other than the oropharynx, prior radiation therapy (RT) (P = 0.056), and well/moderate tumor cell differentiation (P = 0.067). Independent unfavorable prognostic factors for OS were weight loss, an ECOG performance status of I (vs. 0), well/moderate tumor cell differentiation, a primary tumor in the oral cavity or hypopharynx, and prior RT. The following were found to be independent unfavorable prognostic facotrs for time to disease progression: well/ moderate tumor cell differentiation, a oral cavity or hypopharyngeal primary tumor, and prior RT. Patients with greater than or equal to 2 adverse prognostic factors were reported to have a median OS of I year, whereas patients with 3-5 adverse prognostic factors were found to have a median OS of 0.5 years (P < 0.0001). Forty-nine patients (12%) survived for greater than or equal to 2 years and 6 patients were alive at 5 years. Two-year survivors were more likely to have achieved an objective response to chemotherapy, have poor tumor cell differentiation, be white, have an ECOG performance status of 0, and have received no prior RT. CONCLUSIONS. Clinical parameters and tumor cell differentiation appear to be strong pretreatment predictors of outcome in patients with carcinoma of the head and neck and should be considered in the design of future randomized trials. A small percentage of patients with recurrent head and neck carcinoma can achieve long-term survival. Cancer 2004;101:2222-9. (C) 2004 American Cancer Society. C1 Northwestern Univ, Feinberg Sch Med, Div Hematol Oncol, Dept Med, Chicago, IL 60611 USA. Northwestern Univ, Robert H Lurie Comprehens Canc Ctr, Chicago, IL 60611 USA. Dana Farber Canc Inst, Dept Biostat & Computat Biol, Boston, MA 02115 USA. Johns Hopkins Univ, Sch Med, Dept Oncol, Baltimore, MD 21205 USA. RP Argiris, A (reprint author), Northwestern Univ, Feinberg Sch Med, Div Hematol Oncol, Dept Med, 676 N St Clair,Suite 850, Chicago, IL 60611 USA. EM a-argiris@northwestern.edu NR 16 TC 76 Z9 76 U1 0 U2 2 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 2004 VL 101 IS 10 BP 2222 EP 2229 DI 10.1002/cncr.20640 PG 8 WC Oncology SC Oncology GA 870TN UT WOS:000225081300012 PM 15452834 ER PT J AU Hayashi, T Hideshima, T Nguyen, AN Munoz, O Podar, K Hamasaki, M Ishitsuka, K Yasui, H Richardson, P Chakravarty, S Murphy, A Chauhan, D Higgins, LS Anderson, KC AF Hayashi, T Hideshima, T Nguyen, AN Munoz, O Podar, K Hamasaki, M Ishitsuka, K Yasui, H Richardson, P Chakravarty, S Murphy, A Chauhan, D Higgins, LS Anderson, KC TI Transforming growth factor beta receptor I kinase inhibitor down-regulates cytokine secretion and multiple myeloma cell growth in the bone marrow microenvironment SO CLINICAL CANCER RESEARCH LA English DT Article ID RESISTANCE CAM-DR; INTERLEUKIN-6; APOPTOSIS; THALIDOMIDE; ADHESION; GROWTH-FACTOR-BETA-1; HEMATOPOIESIS; ANGIOGENESIS; EXPRESSION; INDUCTION AB Purpose: Transforming growth factors (TGFs) have pleiotropic biological effects on tumor cells and their environment. In multiple myeloma (MM), we have reported that bone marrow stromal cells (BMSCs) from MM patients produce more TGF-beta1 than BMSCs from healthy donors, which in turn induces interleukin (IL)-6 secretion. We show here that the TGF-beta receptor I kinase inhibitor SD-208 significantly decreases secretion of both IL-6 and vascular endothelial growth factor (VEGF) from BMSCs, as well as tumor cell growth triggered by MM cell adhesion to BMSCs. Experimental Design: Cytokine production and MM cell proliferation triggered by TGF-beta1 or adhesion to BMSCs were examined in the presence or absence of SD-208. Effects of SD-208 on TGF-beta1-induced signaling pathways triggering IL-6 and VEGF transcription in BMSCs were also delineated. Results: SD-208 significantly inhibits not only transcription but also secretion of both IL-6 and VEGF from BMSCs triggered by either TGF-beta1 or adhesion of MM cells to BMSCs. Moreover, SD-208 decreased tumor cell growth triggered by MM cell adhesion to BMSCs. SD-208 works, at least in part, by blocking TGF-beta1-triggered nuclear accumulation of Smad2/3 and hypoxia-inducible factor la, as well as related production of IL-6 and VEGF, respectively. Conclusions: These studies indicate that SD-208 inhibits production of cytokines mediating MM cell growth, survival, drug resistance, and migration in the BM milieu, thereby providing the preclinical rationale for clinical evaluation of SD-208 to improve patient outcome in MM. C1 Harvard Univ, Sch Med, Dana Farber Canc Inst, Dept Med Oncol,Dept Med,Jerome Lipper Multiple My, Boston, MA 02115 USA. SCIOS Inc, Sunnyvale, CA USA. RP Anderson, KC (reprint author), Harvard Univ, Sch Med, Dana Farber Canc Inst, Dept Med Oncol,Dept Med,Jerome Lipper Multiple My, 44 Binney St, Boston, MA 02115 USA. EM kenneth_anderson@dfci.harvard.edu FU PHS HHS [P0-1 78378] NR 32 TC 60 Z9 71 U1 0 U2 0 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA SN 1078-0432 J9 CLIN CANCER RES JI Clin. Cancer Res. PD NOV 15 PY 2004 VL 10 IS 22 BP 7540 EP 7546 DI 10.1158/1078-0432.CCR-04-0632 PG 7 WC Oncology SC Oncology GA 874LH UT WOS:000225351400012 PM 15569984 ER PT J AU Hu, KK Veenstra, DL Lipsky, BA Saint, S AF Hu, KK Veenstra, DL Lipsky, BA Saint, S TI Use of maximal sterile barriers during central venous catheter insertion: Clinical and economic outcomes SO CLINICAL INFECTIOUS DISEASES LA English DT Article ID BLOOD-STREAM INFECTION; CRITICALLY-ILL PATIENTS; POVIDONE-IODINE; SITE CARE; PREVENTION; MORTALITY; RISK; SEPSIS; CONSEQUENCES; METAANALYSIS AB Background. We performed a cost-effectiveness analysis to determine the effect of maximal sterile barriers (MSBs) on reducing central venous catheter (CVC)-related infections. Use of MSBs when placing CVCs may reduce the risk of infections but is more cumbersome, time-consuming, and expensive than other techniques. Methods. We developed a decision analytic model in which a patient could have a CVC placed with either an MSB or a less stringent technique. We calculated total direct medical costs and the incidences of catheterrelated bloodstream infections, catheter colonization, and death. Results. Use of MSBs lowered costs (from $621 to $369 per catheter insertion) and decreased the incidences of catheter-related bloodstream infections (from 5.3% to 2.8%), catheter colonization with local infection (from 5.5% to 2.9%) and death (from 0.8% to 0.4%). MSBs improved patient safety throughout all sensitivity analyses. Conclusions. Use of MSBs during CVC insertion likely lowers medical costs and decreases the incidences of catheter colonization, catheter-related bloodstream infections, and death. Cost savings were found over a wide range of clinical and economic assumptions, suggesting that MSBs should be routinely used when CVCs are inserted. C1 Univ Washington, VA Puget Sound Hlth Care Syst, Seattle, WA 98108 USA. Univ Washington, NW Hlth Serv Res & Dev Program, Seattle, WA 98108 USA. Univ Washington, Pharmaceut Outcomes Res & Policy Program, Seattle, WA 98108 USA. Univ Washington, Dept Med, Seattle, WA 98108 USA. Univ Michigan, Dept Internal Med, Ann Arbor, MI 48109 USA. Univ Michigan, Patient Safety Enhancement Program, Ann Arbor, MI 48109 USA. Ann Arbor Vet Affairs Med Ctr, Hlth Serv Res & Dev Ctr Excellence, Ann Arbor, MI USA. RP Hu, KK (reprint author), Univ Washington, VA Puget Sound Hlth Care Syst, 1660 S Columbian Way,HSR&D 152, Seattle, WA 98108 USA. EM kenthu@u.washington.edu OI Lipsky, Benjamin A./0000-0001-9886-5114 FU AHRQ HHS [P20-HS11540] NR 29 TC 32 Z9 35 U1 0 U2 0 PU OXFORD UNIV PRESS INC PI CARY PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA SN 1058-4838 J9 CLIN INFECT DIS JI Clin. Infect. Dis. PD NOV 15 PY 2004 VL 39 IS 10 BP 1441 EP 1445 DI 10.1086/425309 PG 5 WC Immunology; Infectious Diseases; Microbiology SC Immunology; Infectious Diseases; Microbiology GA 904JH UT WOS:000227492000007 PM 15546079 ER PT J AU Bray, NJ Jehu, L Moskvina, V Buxbaum, JD Dracheva, S Haroutunian, V Williams, J Buckland, PR Owen, MJ O'Donovan, MC AF Bray, NJ Jehu, L Moskvina, V Buxbaum, JD Dracheva, S Haroutunian, V Williams, J Buckland, PR Owen, MJ O'Donovan, MC TI Allelic expression of APOE in human brain: effects of epsilon status and promoter haplotypes SO HUMAN MOLECULAR GENETICS LA English DT Article ID SPORADIC ALZHEIMERS-DISEASE; APOLIPOPROTEIN-E; CEREBROSPINAL-FLUID; REGULATORY REGION; MESSENGER-RNA; TYPE-4 ALLELE; GENE; POLYMORPHISM; RISK; PLASMA AB The epsilon4 haplotype of APOE is the only undisputed genetic risk factor for late-onset Alzheimer's disease (LOAD). It has been proposed that at least two other polymorphisms in the promoter of the APOE gene (-219G>T and -491A>T) might also contribute to disease susceptibility, and modulate the impact of structural changes in the ApoE protein, by altering its expression. In order to assess the extent of cis-acting influences on APOE expression in human brain, highly quantitative measures of allele discrimination were applied to cortical RNA from individuals heterozygous for the epsilon alleles. A small, but significant, increase in the expression of epsilon4 allele was observed relative to that of the epsilon3 and epsilon2 alleles (P<0.0001). Similar differences were observed in brain tissue from confirmed LOAD subjects, and between cortical regions BA10 (frontopolar) and BA20 (inferior temporal). Stratification of epsilon4/epsilon3 allelic expression ratios according to heterozygosity for the -219G>T promoter polymorphism revealed significantly lower relative expression of haplotypes containing the -219T allele (P=0.02). Our data indicate that, in human brain, most of the cis-acting variance in APOE expression is accounted for by the epsilon4 haplotype, but there are additional, small, cis-acting influences associated with promoter genotype. C1 Univ Wales Coll Cardiff, Dept Psychol Med, Sch Med, Cardiff CF14 4XN, S Glam, Wales. Univ Wales Coll Cardiff, Biostat Bioinformat Unit, Sch Med, Cardiff CF14 4XN, S Glam, Wales. CUNY, Mt Sinai Med Ctr, Dept Psychiat, New York, NY 10021 USA. Bronx Vet Affairs Med Ctr, MIRECC, Bronx, NY 10468 USA. RP O'Donovan, MC (reprint author), Univ Wales Coll Cardiff, Dept Psychol Med, Sch Med, Heath Pk, Cardiff CF14 4XN, S Glam, Wales. EM odonovanmc@cardiff.ac.uk RI turton, miranda/F-4682-2011; OI O'Donovan, Michael/0000-0001-7073-2379; Buxbaum, Joseph/0000-0001-8898-8313; Escott-Price, Valentina/0000-0003-1784-5483 NR 27 TC 31 Z9 32 U1 0 U2 2 PU OXFORD UNIV PRESS PI OXFORD PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND SN 0964-6906 J9 HUM MOL GENET JI Hum. Mol. Genet. PD NOV 15 PY 2004 VL 13 IS 22 BP 2885 EP 2892 DI 10.1093/hmg/ddh299 PG 8 WC Biochemistry & Molecular Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Genetics & Heredity GA 873BG UT WOS:000225253100015 PM 15385439 ER PT J AU Armanios, M Xu, RH Forastiere, AA Haller, DG Kugler, JW Benson, AB AF Armanios, M Xu, RH Forastiere, AA Haller, DG Kugler, JW Benson, AB TI Adjuvant chemotherapy for resected adenocarcinoma of the esophagus, gastro-esophageal junction, and cardia: Phase II trial (E8296) of the Eastern Cooperative Oncology Group SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Article; Proceedings Paper CT 39th Annual Meeting of the American-Society-of-Clinical-Oncology CY MAY 31-JUN 03, 2003 CL CHICAGO, IL SP Amer Soc Clin Oncol ID POSITRON-EMISSION-TOMOGRAPHY; SQUAMOUS-CELL CARCINOMA; PREOPERATIVE CHEMORADIATION; CANCER; SURGERY; THERAPY; CHEMORADIOTHERAPY; PACLITAXEL; CISPLATIN; TAXOL AB Purpose To evaluate the effect of postoperative paclitaxel and cisplatin on 2-year survival in patients with completely resected adenocarcinoma of the distal esophagus, gastro-esophageal (GE) junction, and cardia. Patients and Methods We conducted a multicenter phase II trial. Patients had pathologically staged T2 node-positive to T3-4, any node status adenocarcinoma of the distal esophagus, GE junction, or gastric cardia with negative margins (R0). Treatment consisted of four cycles of paclitaxel 175 mg/m(2) intravenously (IV) over 3 hours followed by cisplatin 75 mg/m(2) IV every 21 days. A positive outcome was considered to be an improvement in 2-year survival rate by greater than or equal to20% compared to historic controls. Results Fifty-nine patients were recruited from 20 centers. Of 55 eligible patients, 49 (89%) had lymph node involvement. Forty-six patients (84%) completed all four cycles. Of the total 59 patients, 31 (56%) developed grade 3 or 4 toxicity with leukopenia/neutropenia, nausea/vomiting, and metabolic toxicities were most common. The median follow-up for surviving patients was 4 years. At 2 years, 33 patients were alive and 22 were dead, with a survival rate of 60% (95% CI, 46% to 73%; one-sided P = .0008 compared with the historic controls). Conclusion Our data suggest that adjuvant paclitaxel and cisplatin may improve survival in R0 resected patients with locally advanced adenocarcinoma of the distal esophagus, GE junction, and cardia. These results warrant further testing in randomized trials. (C) 2004 by American Society of Clinical Oncology. C1 Johns Hopkins Univ, Baltimore, MD 21205 USA. Dana Farber Canc Inst, Boston, MA 02115 USA. Univ Penn, Philadelphia, PA 19104 USA. Illinois Oncol Res Assoc, Peoria, IL USA. Northwestern Univ, Chicago, IL 60611 USA. RP Armanios, M (reprint author), Johns Hopkins Univ, 1650 Orleans St,CRB 186, Baltimore, MD 21205 USA. EM marmani1@jhmi.edu FU NCI NIH HHS [CA15488, CA13650, CA16116, CA17145, CA21115, CA23318, CA66636] NR 24 TC 32 Z9 37 U1 0 U2 0 PU AMER SOC CLINICAL ONCOLOGY PI ALEXANDRIA PA 330 JOHN CARLYLE ST, STE 300, ALEXANDRIA, VA 22314 USA SN 0732-183X J9 J CLIN ONCOL JI J. Clin. Oncol. PD NOV 15 PY 2004 VL 22 IS 22 BP 4495 EP 4499 DI 10.1200/JCO.2004.06.533 PG 5 WC Oncology SC Oncology GA 871ZP UT WOS:000225175600010 PM 15542799 ER PT J AU Hudson, MM Krasin, M Link, MP Donaldson, SS Billups, C Merchant, TE Kun, L Billet, AL Kaste, S Tarbell, NJ Howard, S Friedmann, AM Hurwitz, CA Young, JA Marcus, KC Rai, S Cowan, T Weinstein, HJ AF Hudson, MM Krasin, M Link, MP Donaldson, SS Billups, C Merchant, TE Kun, L Billet, AL Kaste, S Tarbell, NJ Howard, S Friedmann, AM Hurwitz, CA Young, JA Marcus, KC Rai, S Cowan, T Weinstein, HJ TI Risk-adapted, combined-modality therapy with VAMP/COP and response-based, involved-field radiation for unfavorable pediatric Hodgkin's disease SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Article ID LOW-DOSE RADIATION; 2ND MALIGNANT NEOPLASMS; LONG-TERM SURVIVORS; CANCER-STUDY-GROUP; FRENCH SOCIETY; ONCOLOGY-GROUP; BREAST-CANCER; CHILDHOOD; CHILDREN; CHEMOTHERAPY AB Purpose To evaluate the efficacy of vinblastine, doxorubicin, methotrexate, and prednisone (VAMP) and cyclophosphamide, vincristine, and procarbazine (COP) chemotherapy and response-based, involved-field radiation, a combined-modality regimen that limits doses of alkylating agents, anthracyclines, and radiation, in children with advanced and unfavorable Hodgkin's disease. Patients and Methods From 1993 to 2000, 159 children and adolescents with unfavorable Hodgkin's disease received three alternating cycles (total of six cycles) of VAMP/COP chemotherapy followed by response-based, involved-field radiation therapy: 15 Gy was administered to patients achieving a complete response, and 25.5 Gy was administered to those achieving a partial response after the first two cycles of chemotherapy and to all sites of bulky lymphadenopathy. Unfavorable disease was defined as clinical stage I and II with bulky peripheral nodal disease greater than 6 cm, initial bulky mediastinal mass 33% or more of the intrathoracic diameter, and/or "B" symptoms and all stage III and IV. Results Study enrollment was closed after an interim analysis estimated a 5-year event-free survival (EFS) rate below a predefined level. Disease presentation was localized (stage I/II) in 77 patients (48.4%) and advanced (stage III/IV) in 82 patients (51.6%). At a median follow-up of 5.8 years (range, 1.3 to 10.0 years), 38 patients had events, including relapse/progression (n = 35), second malignancy (n = 2), and accidental death (n = 1); nine relapses (25.7%) occurred greater than 4 years from diagnosis. Five-year survival and EFS estimates are 92.7% +/- 2.5% and 75.6% +/- 4.1%, respectively. Conclusion Risk-adapted combined-modality therapy with VAMP/COP and response-based, involved-field radiation therapy results in an unsatisfactory outcome for pediatric patients with unfavorable presentations of Hodgkin's disease. (C) 2004 by American Society of Clinical Oncology. C1 St Jude Childrens Res Hosp, Dept Hematol Oncol, Memphis, TN 38105 USA. St Jude Childrens Res Hosp, Dept Radiol Sci, Memphis, TN USA. St Jude Childrens Res Hosp, Dept Biostat, Memphis, TN USA. Univ Tennessee, Coll Med, Memphis, TN USA. Stanford Univ, Med Ctr, Stanford, CA 94305 USA. Massachusetts Gen Hosp, Boston, MA 02114 USA. Dana Farber Canc Inst, Boston, MA 02115 USA. Barbara Bush Childrens Hosp, Portland, ME USA. Maine Med Ctr, Portland, ME 04102 USA. RP Hudson, MM (reprint author), St Jude Childrens Res Hosp, Dept Hematol Oncol, 332 N Lauderdale St, Memphis, TN 38105 USA. EM melissa.hudson@stjude.org RI Howard, Scott/K-3401-2013 OI Howard, Scott/0000-0003-2244-1686 FU NCI NIH HHS [CA 21765] NR 40 TC 48 Z9 50 U1 0 U2 1 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 2004 VL 22 IS 22 BP 4541 EP 4550 DI 10.1200/JCO.2004.02.139 PG 10 WC Oncology SC Oncology GA 871ZP UT WOS:000225175600016 PM 15542805 ER PT J AU van Santen, HM Benoist, C Mathis, D AF van Santen, HM Benoist, C Mathis, D TI Number of T reg cells that differentiate does not increase upon encounter of agonist ligand on thymic epithelial cells SO JOURNAL OF EXPERIMENTAL MEDICINE LA English DT Article DE Foxp3; thymocytes; clonal deletion; inducible expression; transgenic ID IMMUNOLOGICAL SELF-TOLERANCE; TRANSGENIC MICE; REGULATORY CELLS; GENE-EXPRESSION; IN-VITRO; SYSTEMIC AUTOIMMUNITY; IMMUNE DYSREGULATION; NEGATIVE SELECTION; INVARIANT CHAIN; RECEPTOR AB It has been reported that the differentiation of CD4(+)CD25(+) regulatory T cells (T reg cells) can be induced by agonist peptide/major histocompatibility complex ligands in the thymus. Exploiting a transgenic mouse line wherein expression of a particular T cell epitope can be controlled temporally and quantitatively, we found that diversion of differentiating thymocytes into the FoxP3 T reg cell pathway by this agonist ligand was essentially nonexistent. However, CD4(+)CD25(+) thymocytes were much less sensitive than their CD4(+)CD25(-) companions, by two to three orders of magnitude, to agonist-induced clonal deletion, such that their proportion increased, giving the false impression of induced differentiation. To account for these and prior observations, one can propose that differentiation along the CD4(+)CD25(+) pathway is induced by cues other than recognition of self-agonist cues, which are poorly read by thymocytes, whose T cell receptors are conducive to selection toward the conventional CD4(+)CD25(-) lineage. Thus, selective survival, rather than induced differentiation, may explain the apparent enrichment observed here and in previous studies. C1 Harvard Univ, Sect Immunol & Immunogenet, Brigham & Womens Hosp, Joslin Diabet Ctr,Sch Med, Boston, MA 02215 USA. Harvard Univ, Brigham & Womens Hosp, Dept Med, Sch Med, Boston, MA 02215 USA. RP Mathis, D (reprint author), Harvard Univ, Sect Immunol & Immunogenet, Brigham & Womens Hosp, Joslin Diabet Ctr,Sch Med, 1 Joslin Pl, Boston, MA 02215 USA. EM cbdm@joslin.harvard.edu RI van Santen, Hisse Martien/E-8103-2013 FU NIAID NIH HHS [1 R01 AI51530-01, R01 AI051530]; NIDDK NIH HHS [2 P30 DK36836-17, P30 DK036836] NR 54 TC 182 Z9 186 U1 0 U2 5 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 15 PY 2004 VL 200 IS 10 BP 1221 EP 1230 DI 10.1084/jem.20041022 PG 10 WC Immunology; Medicine, Research & Experimental SC Immunology; Research & Experimental Medicine GA 875EY UT WOS:000225404300001 PM 15534371 ER PT J AU Roers, A Siewe, L Strittmatter, E Deckert, M Schluter, D Stenzel, W Gruber, AD Krieg, T Rajewsky, K Muller, W AF Roers, A Siewe, L Strittmatter, E Deckert, M Schluter, D Stenzel, W Gruber, AD Krieg, T Rajewsky, K Muller, W TI T cell-specific inactivation of the interleukin 10 gene in mice results in enhanced T cell responses but normal innate responses to lipopolysaccharide or skin irritation SO JOURNAL OF EXPERIMENTAL MEDICINE LA English DT Article DE cytokines; gene targeting; inflammation; inflammatory bowel disease; allergic contact dermatitis ID KERATINOCYTE-DERIVED IL-10; DENDRITIC CELLS; TOXOPLASMA-GONDII; IMMUNE-RESPONSE; INTESTINAL INFLAMMATION; CYTOKINE REQUIREMENTS; RESPIRATORY-TRACT; HELPER-CELL; IN-VITRO; COLITIS AB Interleukin (IL)-10 is a regulator of inflammatory responses and is secreted by a variety of different cell types including T cells. T regulatory cells have been shown to suppress immune responses by IL-10-dependent, but also IL-10-independent, mechanisms. Herein, we address the role of T cell-derived IL-10 in mice with an inactivation of the IL-10 gene restricted to T cells generated by Cre/loxP-mediated targeting of the IL-10 gene. Splenocytes from this T cell-specific mutant secrete increased amounts of proinflammatory cytokines after activation in vitro compared with show enhanced contact hypersensitivity reactions, and succumb to severe immunopathology upon infection with Toxoplasma gondii. Despite intact IL-10 genes in other cell types, the dysregulation of T cell responses observed in the T cell-specific IL-10 mutant closely resembles the phenotype in complete IL-10 deficiency. However, in contrast to complete IL-10 deficiency, sensitivity to endotoxic shock and irritant responses of the skin are not enhanced in the T cell-specific IL-10 mutant. Our data highlight the importance of T cell-derived IL-10 in the regulation of T cell responses and demonstrate that endotoxic shock and the irritant response of the skin are controlled by IL-10 from other cell types. C1 Univ Cologne, Dept Dermatol, D-50931 Cologne, Germany. Univ Cologne, Dept Neuropathol, D-50931 Cologne, Germany. Otto Von Guericke Univ, Inst Med Mikrobiol, D-39120 Magdeburg, Germany. Univ Hosp Mannheim, Dept Med Microbiol & Hyg, D-68167 Mannheim, Germany. Sch Vet Med, Dept Pathol, D-30559 Hannover, Germany. Harvard Univ, Sch Med, Ctr Blood Res, Boston, MA 02115 USA. German Res Ctr Biotechnol, Dept Expt Immunol, D-38124 Braunschweig, Germany. RP Roers, A (reprint author), Univ Cologne, Dept Dermatol, Josef Stelzmann Str 9, D-50931 Cologne, Germany. EM axel.roers@uni-koeln.de RI Muller, Werner/B-9044-2008; Deckert, Martina/P-2842-2016 OI Muller, Werner/0000-0002-1297-9725; NR 44 TC 160 Z9 165 U1 0 U2 6 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 15 PY 2004 VL 200 IS 10 BP 1289 EP 1297 DI 10.1084/jem.20041789 PG 9 WC Immunology; Medicine, Research & Experimental SC Immunology; Research & Experimental Medicine GA 875EY UT WOS:000225404300007 PM 15534372 ER PT J AU Zhang, XK Gallant, S Molano, I Moussa, OM Ruiz, P Spyropoulos, DD Watson, DK Gilkeson, G AF Zhang, XK Gallant, S Molano, I Moussa, OM Ruiz, P Spyropoulos, DD Watson, DK Gilkeson, G TI Decreased expression of the Ets family transcription factor Fli-1 markedly prolongs survival and significantly reduces renal disease in MRL/lpr mice SO JOURNAL OF IMMUNOLOGY LA English DT Article ID SYSTEMIC-LUPUS-ERYTHEMATOSUS; AUTOIMMUNE-DISEASE; MRL-FAS(LPR) MICE; MURINE LUPUS; GENE; GAMMA; ACTIVATION; MEMBER; ELF-1; CHAIN AB Increased Fli-1 mRNA is present in PBLs from systemic lupus erythematosus patients, and transgenic overexpression of Fli-1 in normal mice leads to a lupus-like disease. We report in this study that MRL/lpr mice, an animal model of systemic lupus erythematosus, have increased splenic expression of Fli-1 protein compared with BALB/c mice. Using mice with targeted gene disruption, we examined the effect of reduced Fli-1 expression on disease development in MRL/lpr mice. Complete knockout of Fli-1 is lethal in utero. Fli-1 protein expression in heterozygous MRL/lpr (Fli-l(+/-)) mice was reduced by 50% compared with wild-type MRL/lpr (Fli-1(+/+)) mice. Fli-1(+/-) MRL/lpr mice had significantly decreased serum levels of total IgG and anti-dsDNA Abs as disease progressed. Fli-1(+/-) MRL/lpr mice had significantly increased splenic CD8(+) and naive T cells compared with Fli-1(+/+) MRL/lpr mice. Both in vivo and in vitro production of MCP-1 were significantly decreased in Fli-1+/- MRL/lpr mice. The Fli-1(+/-) mice had markedly decreased proteinuria and significantly lower pathologic renal scores. At 48 wk of age, survival was significantly increased in the Fli-1(+/-) MRL/lpr mice, as 100% of Fli-1+/- MRL/lpr mice were alive, in contrast to only 27% of Fli-1(+/+) mice. These findings indicate that Fli-1 expression is important in lupus-like disease development, and that modulation of Fli-1 expression profoundly decreases renal disease and improves survival in MRL/lpr mice. C1 Med Univ S Carolina, Dept Med, Div Rheumatol & Immunol, Med Res Serv,Ralph H Johnson Vet Affairs Med Ctr, Charleston, SC 29425 USA. Med Univ S Carolina, Dept Pathol & Lab Med, Charleston, SC 29425 USA. Univ Miami, Sch Med, Miami, FL 33136 USA. RP Zhang, XK (reprint author), Med Univ S Carolina, Dept Med, Div Rheumatol & Immunol, Med Res Serv,Ralph H Johnson Vet Affairs Med Ctr, 96 Jonathon Lucas St,POB 250623, Charleston, SC 29425 USA. EM zhangjo@musc.edu FU NCI NIH HHS [P01 CA 78582]; NIAMS NIH HHS [AR 47451, K01 AR051385] NR 36 TC 40 Z9 42 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 2004 VL 173 IS 10 BP 6481 EP 6489 PG 9 WC Immunology SC Immunology GA 869QL UT WOS:000224999000070 PM 15528390 ER PT J AU Erkinjuntti, T Roman, G Gauthier, S AF Erkinjuntti, T Roman, G Gauthier, S TI Treatment of vascular dementia - evidence from clinical trials with cholinesterase inhibitors SO JOURNAL OF THE NEUROLOGICAL SCIENCES LA English DT Article; Proceedings Paper CT 1st Congress of the International-Society-for-Vascular-Behavioural-and-Cognitive-Disorders (VAS-COG 2003) CY AUG 28-31, 2003 CL Goteborg, SWEDEN SP Int Soc Vasc Behav Cognit Disorders DE vascular dementia; Alzheimer's disease; cholinesterase inhibitors ID ALZHEIMERS-DISEASE; CEREBROVASCULAR-DISEASE; COGNITIVE DECLINE; EFFICACY; RIVASTIGMINE; GALANTAMINE; DONEPEZIL; TOLERABILITY AB Cerebrovascular disease (CVD), as well as secondary ischemic brain injury from cardiovascular disease, are common causes of dementia and cognitive decline in the elderly. In addition, CVD frequently contributes to cognitive loss in patients with Alzheimer's disease (AD). Progress in understanding the pathogenetic mechanism involved in vascular cognitive impairment (VCI) and vascular dementia (VaD) has resulted in promising treatments of these conditions. Cholinergic deficits in VaD are due to ischemia of basal forebrain nuclei and of cholinergic pathways and can be treated with the use of the cholinesterase inhibitor agents used in AD. Controlled clinical trials with donepezil, galantamine and rivastigmine in VaD, as well as in patients with AD plus CVD, have demonstrated improvements in cognition, behavior and activities of daily living. (C) 2004 Elsevier B.V. All rights reserved. C1 Univ Helsinki, Cent Hosp, Helsinki, Finland. Univ Texas, Hlth Sci Ctr, San Antonio, TX 78229 USA. A Murphy Vet Adm Hosp, San Antonio, TX 78229 USA. McGill Ctr Studies Aging, MCSA, Alzheimers Dis Res Unit, Montreal, PQ, Canada. RP Erkinjuntti, T (reprint author), Univ Helsinki, Cent Hosp, Helsinki, Finland. EM Timo.Erkinjuntti@HUS.fi NR 21 TC 38 Z9 48 U1 1 U2 2 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0022-510X J9 J NEUROL SCI JI J. Neurol. Sci. PD NOV 15 PY 2004 VL 226 IS 1-2 BP 63 EP 66 DI 10.1016/j.jns.2004.09.018 PG 4 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA 873XI UT WOS:000225314400014 PM 15537522 ER PT J AU Roman, GC Sachdev, P Royall, DR Bullock, RA Orgogozo, JM Lopez-Pousa, S Arizaga, R Wallin, A AF Roman, GC Sachdev, P Royall, DR Bullock, RA Orgogozo, JM Lopez-Pousa, S Arizaga, R Wallin, A TI Vascular cognitive disorder: a new diagnostic category updating vascular cognitive impairment and vascular dementia SO JOURNAL OF THE NEUROLOGICAL SCIENCES LA English DT Article; Proceedings Paper CT 1st Congress of the International-Society-for-Vascular-Behavioural-and-Cognitive-Disorders (VAS-COG 2003) CY AUG 28-31, 2003 CL Goteborg, SWEDEN SP Int Soc Vasc Behav Cognit Disorders DE aging; cerebrovascular disease; cognition; dementia; vascular cognitive disorder; vascular cognitive impairment; vascular dementia ID EXECUTIVE CONTROL FUNCTION; ALZHEIMERS-DISEASE; SILENT EPIDEMIC; DONEPEZIL; TOLERABILITY; DYSFUNCTION; EFFICACY; RETIREES; CRITERIA AB Vascular cognitive impairment (VCI) was proposed as an umbrella term to include subjects affected with any degree of cognitive impairment resulting from cerebrovascular disease (CVD), ranging from mild cognitive impairment (MCI) to vascular dementia. VCI may or may not exclude the host of "focal" circumscribed impairments of specialized functions such as language (aphasia), intentional gesture (apraxia), or categorical recognition (agnosia), among others, that may result from a stroke. Therefore, there are no universally accepted diagnostic criteria for VCI. We conclude that this concept could be more useful if it were to be limited to cases of vascular MCI without dementia, by analogy with the concept of amnestic MCI, currently considered the earliest clinically diagnosable stage of Alzheimer disease (AD). In agreement with our view, the Canadian Study on Health and Aging successfully implemented a restricted definition of VCI, excluding cases of dementia (i.e., vascular cognitive impairment no dementia, VCI-ND). The Canadian definition and diagnostic criteria could be utilized for future studies of VCI. This definition excludes isolated impairments of specialized cognitive functions. Vascular dementia (VaD): The main problem of this diagnostic category stems from the currently accepted definition of dementia that requires memory loss as the sine qua non for the diagnosis. This may result in over-sampling of patients with AD worsened by stroke (AD+CVD). This problem was minimized in controlled clinical trials of VaD by excluding patients with a prior diagnosis of AD, those with pre-existing memory loss before the index stroke, and those with amnestic MCI. We propose a definition of dementia in VaD based on presence of abnormal executive control function, severe enough to interfere with social or occupational functioning. Vascular cognitive disorder (VCD): This term, proposed by Sachdev [P. Sachdev, Vascular cognitive disorder. Int J Geriat Psychiatry 14 (1999) 402-403.] would become the global diagnostic category for cognitive impairment of vascular origin, ranging from VCI to VaD. It would include specific disease entities such as post-stroke VCI, post-stroke VaD, CADASIL, Binswanger disease, and AD plus CVD. This category explicitly excludes isolated cognitive dysfunctions such as those mentioned above. (C) 2004 Elsevier B.V. All rights reserved. C1 Univ Texas, Hlth Sci Ctr, Dept Med Neurol, San Antonio, TX 78229 USA. Audie L Murphy Mem Vet Adm Med Ctr, San Antonio, TX 78229 USA. Univ New S Wales, Sch Psychiat, Sydney, NSW, Australia. Prince Wales Hosp, Inst Neuropsychiat, Sydney, NSW, Australia. Univ Texas, Hlth Sci Ctr, Dept Psychiat, San Antonio, TX 78229 USA. Univ Texas, Hlth Sci Ctr, Dept Med, San Antonio, TX 78229 USA. Univ Texas, Hlth Sci Ctr, Dept Pharmacol, San Antonio, TX 78229 USA. Victoria Hosp, Kingshill Res Ctr, Swindon, Wilts, England. CHU Pellegrin, Bordeaux, France. Hosp Santa Catarina, Memory & Dementia Unit, Girona, Spain. Natl Inst Social Serv Retirees, Memory Disorders Res Ctr, Buenos Aires, DF, Argentina. Natl Inst Social Serv Retirees, Neuroepidemiol Branch, Buenos Aires, DF, Argentina. Sahlgrens Univ Hosp, Inst Clin Neurosci, Molndal, Sweden. RP Roman, GC (reprint author), Univ Texas, Hlth Sci Ctr, Dept Med Neurol, 7703 Floyd Curl Dr,Mail Code 7883, San Antonio, TX 78229 USA. EM romang@uthscsa.edu; p.sachdev@unsw.edu.au; uvamid@ias.scs.es; anders.wallin@neuro.gu.se OI Sachdev, Perminder/0000-0002-9595-3220 NR 48 TC 133 Z9 146 U1 2 U2 15 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0022-510X J9 J NEUROL SCI JI J. Neurol. Sci. PD NOV 15 PY 2004 VL 226 IS 1-2 BP 81 EP 87 DI 10.1016/j.jns.2004.09.016 PG 7 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA 873XI UT WOS:000225314400018 PM 15537526 ER PT J AU Yun, SH Tearney, GJ de Boer, JF Bouma, BE AF Yun, SH Tearney, GJ de Boer, JF Bouma, BE TI Pulsed-source and swept-source spectral-domain optical coherence tomography with reduced motion artifacts SO OPTICS EXPRESS LA English DT Article ID HIGH-SPEED; ULTRAHIGH-RESOLUTION; SUPERCONTINUUM; WAVELENGTH; LASER AB Significant motion artifacts may arise in conventional spectral-domain optical coherence tomography due to sample or probe motion during the exposure time of a CCD array. We show, for the first time to our knowledge, that the motion artifacts can be greatly reduced by short illumination of individual CCD pixels and that this can be accomplished by use of two distinct classes of light sources: broadband pulsed sources and cw wavelength-swept sources. We experimentally demonstrate the benefit of these techniques in terms of the reduction of signal fading due to an axially moving sample and fiber-optic catheter at a high rotational speed. (C) 2004 Optical Society of America. C1 Harvard Univ, Sch Med, Boston, MA 02114 USA. Massachusetts Gen Hosp, Wellman Ctr Photomed, Boston, MA 02114 USA. RP Yun, SH (reprint author), Harvard Univ, Sch Med, 50 Blossom St,BAR-718, Boston, MA 02114 USA. EM syun@hms.harvard.edu RI de Boer, Johannes/B-7590-2012 OI de Boer, Johannes/0000-0003-1253-4950 FU NCI NIH HHS [R01 CA103769, R01 CA103769-03, R33 CA110130, R33 CA110130-02]; NCRR NIH HHS [R01 RR019768, R01 RR019768-02]; NHLBI NIH HHS [R01 HL070039, R01 HL070039-02] NR 22 TC 31 Z9 31 U1 0 U2 9 PU OPTICAL SOC AMER PI WASHINGTON PA 2010 MASSACHUSETTS AVE NW, WASHINGTON, DC 20036 USA SN 1094-4087 J9 OPT EXPRESS JI Opt. Express PD NOV 15 PY 2004 VL 12 IS 23 BP 5614 EP 5624 DI 10.1364/OPEX.12.005614 PG 11 WC Optics SC Optics GA 872SH UT WOS:000225228200004 PM 19488195 ER PT J AU Jiang, HY Zhou, XH AF Jiang, HY Zhou, XH TI Bootstrap confidence intervals for medical costs with censored observations SO STATISTICS IN MEDICINE LA English DT Article DE skewed distribution; censored data; cost data; bootstrap method AB Medical costs data with administratively censored observations often arise in cost-effectiveness studies of treatments for life-threatening diseases. Mean of medical costs incurred from the start of a treatment until death or a certain time point after the implementation of treatment is frequently of interest. In many situations, due to the skewed nature of the cost distribution and non-uniform rate of cost accumulation over time, the currently available normal approximation confidence interval has poor coverage accuracy. In this paper, we propose a bootstrap confidence interval for the mean of medical costs with censored observations. In simulation studies, we show that the proposed bootstrap confidence interval had much better coverage accuracy than the normal approximation one when medical costs had a skewed distribution. When there is light censoring on medical costs (less than or equal to,25 per cent), we found that the bootstrap confidence interval based on the simple weighted estimator is preferred due to its simplicity and good coverage accuracy. For heavily censored cost data (censoring rate greater than or equal to30 per cent) with larger sample sizes (n greater than or equal to 200), the bootstrap confidence intervals based on the partitioned estimator has superior performance in terms of both efficiency and coverage accuracy. We also illustrate the use of our methods in a real example. Copyright (C) 2004 John Wiley Sons, Ltd. C1 Univ Washington, Dept Biostat, Seattle, WA 98195 USA. Harvard Univ, Sch Publ Hlth, Dept Biostat, Boston, MA 02115 USA. VA Puget Sound Hlth Care Syst, NW HSR&D Ctr Excellence, Biostat Unit, Seattle, WA USA. RP Zhou, XH (reprint author), Univ Washington, Dept Biostat, Seattle, WA 98195 USA. EM azhou@u.washington.edu FU AHRQ HHS [R01HS013105]; NIAID NIH HHS [R01AI24643] NR 12 TC 15 Z9 16 U1 0 U2 3 PU JOHN WILEY & SONS LTD PI CHICHESTER PA THE ATRIUM, SOUTHERN GATE, CHICHESTER PO19 8SQ, W SUSSEX, ENGLAND SN 0277-6715 J9 STAT MED JI Stat. Med. PD NOV 15 PY 2004 VL 23 IS 21 BP 3365 EP 3376 DI 10.1002/sim.1556 PG 12 WC Mathematical & Computational Biology; Public, Environmental & Occupational Health; Medical Informatics; Medicine, Research & Experimental; Statistics & Probability SC Mathematical & Computational Biology; Public, Environmental & Occupational Health; Medical Informatics; Research & Experimental Medicine; Mathematics GA 867UO UT WOS:000224868200009 PM 15490430 ER PT J AU Sherwood, RI Christensen, JL Conboy, IM Conboy, MJ Rando, TA Weissman, IL Wagers, AJ AF Sherwood, RI Christensen, JL Conboy, IM Conboy, MJ Rando, TA Weissman, IL Wagers, AJ TI Isolation of adult mouse myogenic progenitors: Functional heterogeneity of cells within and engrafting skeletal muscle SO CELL LA English DT Article ID HEMATOPOIETIC STEM-CELLS; BONE-MARROW; SATELLITE CELLS; REGENERATION; EXPRESSION; MICE; TRANSPLANTATION; IDENTIFICATION; SPECIFICATION; POPULATION AB Skeletal muscle regeneration in adults is thought to occur through the action of myogenic satellite cells located in close association with mature musclefibers; however, these precursor cells have not been prospectively isolated, and recent studies have suggested that additional muscle progenitors, including cells of bone marrow or hematopoietic origin, may exist. To clarify the origin(s) of adult myogenic cells, we used phenotypic, morphological, and functional criteria to identify and prospectively isolate a subset of myofiber-associated cells capable at the single cell level of generating myogenic colonies at high frequency. Importantly, although muscle-engrafted cells from marrow and/or circulation localized to the same anatomic compartment as myogenic satellite cells and expressed some though not all satellite cell markers, they displayed no intrinsic myogenicity. Together, these studies describe the clonal isolation of functional adult myogenic progenitors and demonstrate that these cells do not arise from hematopoietic or other bone marrow or circulating precursors. C1 Stanford Univ, Sch Med, Dept Pathol, Stanford, CA 94305 USA. Stanford Univ, Sch Med, Dept Dev Biol, Stanford, CA 94305 USA. Stanford Univ, Sch Med, Dept Neurol & Neurol Sci, Stanford, CA 94305 USA. Vet Affairs Palo alto Hlth Care Syst, GRECC, Palo Alto, CA 94304 USA. Vet Affairs Palo alto Hlth Care Syst, Serv Neurol, Palo Alto, CA 94304 USA. RP Wagers, AJ (reprint author), Joslin Diabet Ctr, Sect Dev & Stem Cell Biol, Boston, MA 02215 USA. EM amy.wagers@joslin.harvard.edu FU NCI NIH HHS [CA86065]; NIA NIH HHS [AG05902]; NINDS NIH HHS [R01-NS36409] NR 35 TC 299 Z9 308 U1 2 U2 17 PU CELL PRESS PI CAMBRIDGE PA 1100 MASSACHUSETTS AVE, CAMBRIDGE, MA 02138 USA SN 0092-8674 J9 CELL JI Cell PD NOV 12 PY 2004 VL 119 IS 4 BP 543 EP 554 DI 10.1016/j.cell.2004.10.021 PG 12 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA 872CI UT WOS:000225183200012 PM 15537543 ER PT J AU Fitzgerald, ML Okuhira, K Short, GF Manning, JJ Bell, SA Freeman, MW AF Fitzgerald, ML Okuhira, K Short, GF Manning, JJ Bell, SA Freeman, MW TI ATP-binding cassette transporter A1 contains a novel C-terminal VFVNFA motif that is required for its cholesterol efflux and ApoA-I binding activities SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID APOLIPOPROTEIN-A-I; TANGIER-DISEASE; ABCA1 TRANSPORTER; GUANYLATE KINASES; PDZ DOMAINS; PROTEIN; MECHANISM; MUTATIONS; COMPLEX; EVOLUTION AB The stimulation of cellular cholesterol and phospholipid efflux by apolipoprotein A-I is mediated by the activity of the ATP-binding cassette transporter A1 (ABCA1). Individuals with Tangier disease harbor loss-of-function mutations in this transporter that have proven useful in illuminating its activity. Here, we analyze a mutation that deletes the last 46 residues of the 2261 amino acid transporter (Delta46) and eliminates its lipid efflux. As the final four amino acids of the C terminus represent a putative PDZ-binding motif, we initially characterized deletion mutants lacking only these residues. Although a moderate decline in lipid efflux was detected, this decline was not as profound as that seen in the Delta46 mutant. Subsequent systematic analysis of the ABCA1 C terminus revealed a novel, highly conserved motif (VFVNFA) that was required for lipid efflux. Alteration of this motif, which is present in some but not all members of the ABCA family, did not prevent trafficking of the transporter to the plasma membrane but did eliminate its binding of apoA-I. Chimeric transporters, generated by substituting the C termini of either ABCA4 or ABCA7 for the endogenous terminus, demonstrated that ABCA1 could stimulate cholesterol efflux without its PDZ-binding motif but not without the VFVNFA motif. When a peptide containing the VFVNFA sequence was introduced into ABCA1-expressing cells, ABCA1-mediated lipid efflux was also markedly inhibited. These results indicate that the C-terminal VFVNFA motif of ABCA1 is essential for its lipid efflux activity. The data also suggest that this motif participates in novel protein-protein interactions that may be shared among members of the ABCA family. C1 Massachusetts Gen Hosp, Lipid Metab Unit, Boston, MA 02114 USA. Harvard Univ, Sch Med, Boston, MA 02114 USA. RP Fitzgerald, ML (reprint author), Massachusetts Gen Hosp, Lipid Metab Unit, Boston, MA 02114 USA. EM mfitzger@molbio.mgh.harvard.edu; freeman@molbio.mg.harvard.edu FU NHLBI NIH HHS [HL45098, HL68988, HL72358] NR 42 TC 46 Z9 48 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 12 PY 2004 VL 279 IS 46 BP 48477 EP 48485 DI 10.1074/jbc.M409848200 PG 9 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA 869BJ UT WOS:000224957000125 PM 15347662 ER PT J AU Calsyn, DA Saxon, AJ Bush, KR Howell, DN Baer, JS Sloan, KL Malte, CA Kivlahan, DR AF Calsyn, DA Saxon, AJ Bush, KR Howell, DN Baer, JS Sloan, KL Malte, CA Kivlahan, DR TI The addiction severity index medical and psychiatric composite scores measure similar domains as the SF-36 in substance-dependent veterans: concurrent and discriminant validity SO DRUG AND ALCOHOL DEPENDENCE LA English DT Article DE functional status; quality of life; substance dependence; assessment; medical illness; co-morbidity ID QUALITY-OF-LIFE; FUNCTIONAL IMPAIRMENT; MENTAL-DISORDERS; ABUSE TREATMENT; HEALTH-STATUS; ALCOHOL; COMORBIDITY; SERVICES; DRUG; PREDICTORS AB Background: Recently attention has focused on the assessment of functional health status in substance-dependent individuals. The addiction severity index (ASI) is a widely used assessment instrument that includes scales to reflect current medical and psychiatric status. This study examines the concurrent validity of these ASI composite scores in relation to the short form 36-item health survey (SF-36), a well-established measure of health-related quality of life/functional health status. Methods: Veterans (n = 674) were assessed at admission to substance dependence treatment. Correlations were performed between ASI composite scores and SF-36 scales and the physical and mental summary components (PSC and MSC, respectively). Areas under receiver operating characteristic (ROC) curves determined the descriminative ability of the ASI composites to ascertain impairment. Results: The ASI medical composite score demonstrated robust correlations with the four SF-36 scales that relate to physical health and with the PCS. The ASI psychiatric composite score had robust correlations with the four SF-36 scales related to mental health and with the mental component summary (MCS). ROC curves indicated that the ASI medical (AUC = 0.83) and psychiatric composites (AUC = 0.90) accurately detected subjects with impairment. Conclusions: ASI medical and psychiatric composite scores provide effective initial screening for patients with impaired functional status as measured by the corresponding SF-36 component summary scores. (C) 2004 Elsevier Ireland Ltd. All rights reserved. C1 Ctr Excellence Substance Abuse Treatment & Educ, VA Puget Sound Hlth Care Syst, Seattle, WA 98108 USA. Univ Washington, Sch Med, Dept Psychiat & Behav Sci, Seattle, WA 98195 USA. Pacific Grad Sch Psychol, Palo Alto, CA 94303 USA. Univ Washington, Dept Psychol, Seattle, WA 98195 USA. RP Calsyn, DA (reprint author), Ctr Excellence Substance Abuse Treatment & Educ, VA Puget Sound Hlth Care Syst, 1660 S Columbian Way, Seattle, WA 98108 USA. EM donald.calsyn@med.va.gov NR 25 TC 35 Z9 36 U1 2 U2 5 PU ELSEVIER SCI IRELAND LTD PI CLARE PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE, IRELAND SN 0376-8716 J9 DRUG ALCOHOL DEPEN JI Drug Alcohol Depend. PD NOV 11 PY 2004 VL 76 IS 2 BP 165 EP 171 DI 10.1016/j.drugalcdep.2004.04.018 PG 7 WC Substance Abuse; Psychiatry SC Substance Abuse; Psychiatry GA 870KV UT WOS:000225056900006 PM 15488340 ER PT J AU Braunwald, E Pfeffer, MA Domanski, M Fowler, S Rice, M Rosenberg, Y Dunlap, M Flaker, G Geller, N Gersh, B Goldberg, A Hsia, J Limacher, M Maggioni, A Mills, P Rouleau, J Warnica, J Wasserman, A Domanski, M Rosenberg, Y Geller, N Mills, P Fowler, S Cleary, P Close, N Davey, T Green, J Hsia, J Jablonski, K Mason, D Pakalapati, S Rice, M Verter, J Wasserman, A Weir, J Yalamanchili, V Maggioni, A Fabbri, G Gorini, M Lorimer, A Lucci, D Sarti, L Hsia, J Clemenza, F Cuddy, T Goldberg, A Huynh, T Maggioni, A Starling, M Title, L Zabalgoitia, M Fye, C Gagne, W Steffes, M Bucksa, J Rynders, G Frye, R Cooper, E Davis, C Grimes, C Nanda, N Pellegrino, E Stokes, L Dunlap, M Ortiz, J Fleegle, R Armstrong, A Jafri, S Goldberg, A Frank, D Piotrowski, K Kotlewski, A Mahrer, P Browning, R Sharma, A Nediratta, S Ely, G Allen, V Goodfield, P Tredinnick, K Hundley, R Mabry, V Sparrow, T Cunningham, P Owens, S Nelson, D Lewis, S Kelley, D Starling, M Majors, C Flaker, G Belew, K Rodeheffer, R Anderson, P Dodin, E Vold, D Wertheimer, J McKinney, V Ouyang, P Wingo, J Erenrich, N Grumbach, C Serfas, D Oskins, D Denny, D VanVactor, B Chaitman, B Aubuchon, S Brachfeld, C McKinster, B Logemann, T Joyce, D Smith, E Pacheco, R Limacher, M Bryant, B Wolinsky, D Westlake-Hicks, L Lopez, M Schenks, R Graham, S Jackson, J Durr, S De Raad, R Solomon, S Mercier, R Lader, E Meyer, M Wickemeyer, W Young, N Omar, B Clark, L Reddy, P Norwood, T Perry, J Romero, T Eastburn, T Hicks, K Jain, A Limon, L Vetrovec, G Damico, K Liang, CS Perkins, E Katz, R Arevalo, J Thadani, U Thresher, M Weiss, R Brennan, B Ackell, P Noble, M Kahl, F Soots, S Marzo, K Hodnett, P Seaworth, J Farris, S Jiang, L Duquette, M Ziperman, D Greene-Nashold, J Timmis, G Clark, C Colfer, H Ronquist, M Wagner, S Olliges, M Mohiuddin, S Rasmussen, L Sheikh, K Hengerer-Yates, T Palmeri, S Casazza, L Leimbach, W Ritter, D Zabalgoitia, M Paredes, A Golden, J McCaskill, B Duvernoy, W Cunningham, D Goldman, S Ohm, J McBride, J Foster, B Rosenson, R Dahle, K Schmidt, P Ness, C Patton, J Davison, C Riba, A Draus, C Herzog, E Tormey, D Keller, A Obeid, M Hendrix, G Schulz, M Larry, J Homan, J Kutscher, A Calhoon, W Medici, S Amidi, M Bell, M Khadra, S Bax, J Wool, K Parker, J Smith, M Feick, P Schulman, P Folger, J Shanes, J Guard, K Solomon, S English, M Ellis, J Kelly, D Menapace, F Kleman, M Fitzpatrick, P Sass, A Gillespie, J Cohen, L Kowey, P Heaney, S Kussmaul, W Mark, L Bugni, W Sweeney, S Kereiakes, D Ibanez, K Slater, W Guerra, B Brown, E Valeria, A Fifer, M Benard, P Feicht, C Crist, K Capone, R Omorogbe, T Desai, V Pierre-Louis, J Jutzy, K Bishop, V Dadkhah, S Fisch, A Costantino, T Basilious, M Smitherman, T Rosenfelder, D Canaday, D Baxter, J DeWood, M Chapman, D Olson, W Lamas, G Hussein, S Stein, R Varvatsas, J Smith, E Davison, C Kazmierski, J O'Mara, K Smith, J Cromer, C DiCola, J Dolan, S Martin, W Manns, H Kipperman, R Zhang, Y Grossman, D Morrison, B Chiaramida, A Gaven, R DeQuattro, V Song, Z Bergin, P Masengil, J Ely, D Reynolds, F Dennish, G Horton, N Bates, E Luciano, A Moloo, J Kaminski, M Geltman, E Flanagan, J Hayden, CT Felicetta, J Beckner, L Kaushik, V Mueco, A Lee, R Metcalf, A Fowles, R Summers, K Heerema, M Jacobson, M Diggs, P Roeske, M Rosenstein, R Dawley, D Dorst, D Warnica, J Smith, B Walker, L Scarcelli, D Tam, J Cuddy, T Courcelles, P Miller, N Gosselin, G Ducharme, A Marquis, J Lamy, M Title, L Johnstone, D Francis, M Cossett, J Dion, D St-Hilaire, R Morissette, A Poulin, F Arnold, M Krupa, M Boulianne, M Campeau, J Ouimet, F Roberge, B Huynh, T Finkenbine, S St Jacques, B Boudreault, C Borts, D Bonafede, N Burtcher, J Edwards, C Baigrie, R Gee, F Judge, J Reilly, K Bernstein, V MacDonald, K Mooney, S Rouleau, J Vienneau, R Mayer, JP Mitges, S Nawaz, S Dhaliwal, R Talbot, P Talbot, M Sussex, B Newman, S Baird, M Fraser, M Guimond, C Leboeuf, J Moe, G Day, D Rajakumar, G Kroeger, B Khouri, M Zello, N Lee, H Barban, K Kostuk, W Powell, AM Smilovitch, M Toyota, V Phaneuf, D Duclos, R Goulet, G Primeau, L Machel, T Morash, J Gossard, D Boutin, L Vizel, S Fox, B Stanton, E Lawrence, M Sullivan, H Paterson, R Hoag, G Ilott, K Dufton, J Sweeney, R Garcia-Palmieri, M Banchs, H Gonzalez, M Perez, M Colon, P Vazquez, N Schweiger, C Frisinghelli, A Galati, A Palma, P Di Pasquale, P Clemenza, F Filorizzo, G Petacchi, R Cogo, R Ferrari, M Battaglia, A Mancino, F D'Alessandro, B Truncellito, L Maina, M Romanzi, S Chieffo, C Cardillo, A De Lorenzi, E Bergarno, A Boccalatte, A Gaeta, G Neri, G Masaro, G Perticone, F Maio, R De Biase, M Carrone, M Scrutinio, D La Gioia, R Leonzio, L Tullio, D Santarone, M Tagliagambe, L Zonzin, P Capanna, M Di Giovanni, N Fiore, I Gavazzi, A Mazzoleni, D Pinelli, G Ribani, M Mangiameli, S Rubino, V Viecca, M Sala, R Porcu, M Salis, S Amici, R Patteri, G Bortolini, F Turelli, A Maresta, A Dalla Valle, G Braschi, G Abrignani, M Terrosu, P Castellaccio, M Boccanelli, A Morosetti, P Tartarini, G Levantesi, D Grieco, A Cazzaniga, A Poggio, G Giani, S Ferrari, G Belluschi, R Del Citerna, F Balli, E Maiolino, P Pedon, L Mininni, N Monda, V AF Braunwald, E Pfeffer, MA Domanski, M Fowler, S Rice, M Rosenberg, Y Dunlap, M Flaker, G Geller, N Gersh, B Goldberg, A Hsia, J Limacher, M Maggioni, A Mills, P Rouleau, J Warnica, J Wasserman, A Domanski, M Rosenberg, Y Geller, N Mills, P Fowler, S Cleary, P Close, N Davey, T Green, J Hsia, J Jablonski, K Mason, D Pakalapati, S Rice, M Verter, J Wasserman, A Weir, J Yalamanchili, V Maggioni, A Fabbri, G Gorini, M Lorimer, A Lucci, D Sarti, L Hsia, J Clemenza, F Cuddy, T Goldberg, A Huynh, T Maggioni, A Starling, M Title, L Zabalgoitia, M Fye, C Gagne, W Steffes, M Bucksa, J Rynders, G Frye, R Cooper, E Davis, C Grimes, C Nanda, N Pellegrino, E Stokes, L Dunlap, M Ortiz, J Fleegle, R Armstrong, A Jafri, S Goldberg, A Frank, D Piotrowski, K Kotlewski, A Mahrer, P Browning, R Sharma, A Nediratta, S Ely, G Allen, V Goodfield, P Tredinnick, K Hundley, R Mabry, V Sparrow, T Cunningham, P Owens, S Nelson, D Lewis, S Kelley, D Starling, M Majors, C Flaker, G Belew, K Rodeheffer, R Anderson, P Dodin, E Vold, D Wertheimer, J McKinney, V Ouyang, P Wingo, J Erenrich, N Grumbach, C Serfas, D Oskins, D Denny, D VanVactor, B Chaitman, B Aubuchon, S Brachfeld, C McKinster, B Logemann, T Joyce, D Smith, E Pacheco, R Limacher, M Bryant, B Wolinsky, D Westlake-Hicks, L Lopez, M Schenks, R Graham, S Jackson, J Durr, S De Raad, R Solomon, S Mercier, R Lader, E Meyer, M Wickemeyer, W Young, N Omar, B Clark, L Reddy, P Norwood, T Perry, J Romero, T Eastburn, T Hicks, K Jain, A Limon, L Vetrovec, G Damico, K Liang, CS Perkins, E Katz, R Arevalo, J Thadani, U Thresher, M Weiss, R Brennan, B Ackell, P Noble, M Kahl, F Soots, S Marzo, K Hodnett, P Seaworth, J Farris, S Jiang, L Duquette, M Ziperman, D Greene-Nashold, J Timmis, G Clark, C Colfer, H Ronquist, M Wagner, S Olliges, M Mohiuddin, S Rasmussen, L Sheikh, K Hengerer-Yates, T Palmeri, S Casazza, L Leimbach, W Ritter, D Zabalgoitia, M Paredes, A Golden, J McCaskill, B Duvernoy, W Cunningham, D Goldman, S Ohm, J McBride, J Foster, B Rosenson, R Dahle, K Schmidt, P Ness, C Patton, J Davison, C Riba, A Draus, C Herzog, E Tormey, D Keller, A Obeid, M Hendrix, G Schulz, M Larry, J Homan, J Kutscher, A Calhoon, W Medici, S Amidi, M Bell, M Khadra, S Bax, J Wool, K Parker, J Smith, M Feick, P Schulman, P Folger, J Shanes, J Guard, K Solomon, S English, M Ellis, J Kelly, D Menapace, F Kleman, M Fitzpatrick, P Sass, A Gillespie, J Cohen, L Kowey, P Heaney, S Kussmaul, W Mark, L Bugni, W Sweeney, S Kereiakes, D Ibanez, K Slater, W Guerra, B Brown, E Valeria, A Fifer, M Benard, P Feicht, C Crist, K Capone, R Omorogbe, T Desai, V Pierre-Louis, J Jutzy, K Bishop, V Dadkhah, S Fisch, A Costantino, T Basilious, M Smitherman, T Rosenfelder, D Canaday, D Baxter, J DeWood, M Chapman, D Olson, W Lamas, G Hussein, S Stein, R Varvatsas, J Smith, E Davison, C Kazmierski, J O'Mara, K Smith, J Cromer, C DiCola, J Dolan, S Martin, W Manns, H Kipperman, R Zhang, Y Grossman, D Morrison, B Chiaramida, A Gaven, R DeQuattro, V Song, Z Bergin, P Masengil, J Ely, D Reynolds, F Dennish, G Horton, N Bates, E Luciano, A Moloo, J Kaminski, M Geltman, E Flanagan, J Hayden, CT Felicetta, J Beckner, L Kaushik, V Mueco, A Lee, R Metcalf, A Fowles, R Summers, K Heerema, M Jacobson, M Diggs, P Roeske, M Rosenstein, R Dawley, D Dorst, D Warnica, J Smith, B Walker, L Scarcelli, D Tam, J Cuddy, T Courcelles, P Miller, N Gosselin, G Ducharme, A Marquis, J Lamy, M Title, L Johnstone, D Francis, M Cossett, J Dion, D St-Hilaire, R Morissette, A Poulin, F Arnold, M Krupa, M Boulianne, M Campeau, J Ouimet, F Roberge, B Huynh, T Finkenbine, S St Jacques, B Boudreault, C Borts, D Bonafede, N Burtcher, J Edwards, C Baigrie, R Gee, F Judge, J Reilly, K Bernstein, V MacDonald, K Mooney, S Rouleau, J Vienneau, R Mayer, JP Mitges, S Nawaz, S Dhaliwal, R Talbot, P Talbot, M Sussex, B Newman, S Baird, M Fraser, M Guimond, C Leboeuf, J Moe, G Day, D Rajakumar, G Kroeger, B Khouri, M Zello, N Lee, H Barban, K Kostuk, W Powell, AM Smilovitch, M Toyota, V Phaneuf, D Duclos, R Goulet, G Primeau, L Machel, T Morash, J Gossard, D Boutin, L Vizel, S Fox, B Stanton, E Lawrence, M Sullivan, H Paterson, R Hoag, G Ilott, K Dufton, J Sweeney, R Garcia-Palmieri, M Banchs, H Gonzalez, M Perez, M Colon, P Vazquez, N Schweiger, C Frisinghelli, A Galati, A Palma, P Di Pasquale, P Clemenza, F Filorizzo, G Petacchi, R Cogo, R Ferrari, M Battaglia, A Mancino, F D'Alessandro, B Truncellito, L Maina, M Romanzi, S Chieffo, C Cardillo, A De Lorenzi, E Bergarno, A Boccalatte, A Gaeta, G Neri, G Masaro, G Perticone, F Maio, R De Biase, M Carrone, M Scrutinio, D La Gioia, R Leonzio, L Tullio, D Santarone, M Tagliagambe, L Zonzin, P Capanna, M Di Giovanni, N Fiore, I Gavazzi, A Mazzoleni, D Pinelli, G Ribani, M Mangiameli, S Rubino, V Viecca, M Sala, R Porcu, M Salis, S Amici, R Patteri, G Bortolini, F Turelli, A Maresta, A Dalla Valle, G Braschi, G Abrignani, M Terrosu, P Castellaccio, M Boccanelli, A Morosetti, P Tartarini, G Levantesi, D Grieco, A Cazzaniga, A Poggio, G Giani, S Ferrari, G Belluschi, R Del Citerna, F Balli, E Maiolino, P Pedon, L Mininni, N Monda, V CA PEACE Trial Investigators TI Angiotensin-converting-enzyme inhibition in stable coronary artery disease SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Article ID LEFT-VENTRICULAR DYSFUNCTION; CONGESTIVE-HEART-FAILURE; MYOCARDIAL-INFARCTION; EJECTION FRACTIONS; CARDIOVASCULAR EVENTS; ENLARGEMENT TRIAL; AMERICAN-COLLEGE; CLINICAL-TRIALS; TASK-FORCE; ENALAPRIL AB Background: Angiotensin-converting-enzyme (ACE) inhibitors are effective in reducing the risk of heart failure, myocardial infarction, and death from cardiovascular causes in patients with left ventricular systolic dysfunction or heart failure. ACE inhibitors have also been shown to reduce atherosclerotic complications in patients who have vascular disease without heart failure. Methods: In the Prevention of Events with Angiotensin Converting Enzyme Inhibition (PEACE) Trial, we tested the hypothesis that patients with stable coronary artery disease and normal or slightly reduced left ventricular function derive therapeutic benefit from the addition of ACE inhibitors to modern conventional therapy. The trial was a double-blind, placebo-controlled study in which 8290 patients were randomly assigned to receive either trandolapril at a target dose of 4 mg per day (4158 patients) or matching placebo (4132 patients). Results: The mean (+/-SD) age of the patients was 64+/-8 years, the mean blood pressure 133+/-17/78+/-10 mm Hg, and the mean left ventricular ejection fraction 58+/-9 percent. The patients received intensive treatment, with 72 percent having previously undergone coronary revascularization and 70 percent receiving lipid-lowering drugs. The incidence of the primary end point -- death from cardiovascular causes, myocardial infarction, or coronary revascularization -- was 21.9 percent in the trandolapril group, as compared with 22.5 percent in the placebo group (hazard ratio in the trandolapril group, 0.96; 95 percent confidence interval, 0.88 to 1.06; P=0.43) over a median follow-up period of 4.8 years. Conclusions: In patients with stable coronary heart disease and preserved left ventricular function who are receiving ``current standard'' therapy and in whom the rate of cardiovascular events is lower than in previous trials of ACE inhibitors in patients with vascular disease, there is no evidence that the addition of an ACE inhibitor provides further benefit in terms of death from cardiovascular causes, myocardial infarction, or coronary revascularization. C1 Brigham & Womens Hosp, TIMI Study Grp, Boston, MA 02115 USA. Harvard Univ, Sch Med, Boston, MA USA. NHLBI, Bethesda, MD 20892 USA. George Washington Univ, Rockville, MD USA. Mayo Clin Fdn, Rochester, MN USA. George Washington Univ, Washington, DC USA. Univ Montreal, Montreal, PQ, Canada. RP Braunwald, E (reprint author), Brigham & Womens Hosp, TIMI Study Grp, 350 Longwood Ave, Boston, MA 02115 USA. FU NHLBI NIH HHS [N01 HC065149-12, N01 HC065149] NR 30 TC 641 Z9 677 U1 2 U2 19 PU MASSACHUSETTS MEDICAL SOC PI WALTHAM PA WALTHAM WOODS CENTER, 860 WINTER ST,, WALTHAM, MA 02451-1413 USA SN 0028-4793 J9 NEW ENGL J MED JI N. Engl. J. Med. PD NOV 11 PY 2004 VL 351 IS 20 BP 2058 EP 2068 PG 11 WC Medicine, General & Internal SC General & Internal Medicine GA 869TM UT WOS:000225007200007 PM 15531767 ER PT J AU Dahl, DM Mueller, PR Young, RH Kaufman, DS Harisinghani, M Young, RH McDougal, WS AF Dahl, DM Mueller, PR Young, RH Kaufman, DS Harisinghani, M Young, RH McDougal, WS TI A man with right flank pain and Hematuria - Papillary transitional-cell carcinoma of the renal pelvis, low grade SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Editorial Material ID LAPAROSCOPIC NEPHROURETERECTOMY; MICROSCOPIC HEMATURIA; HELICAL CT; FOLLOW-UP; MANAGEMENT; UROGRAPHY C1 Massachusetts Gen Hosp, Dept Urol, Boston, MA 02114 USA. Massachusetts Gen Hosp, Dept Radiol, Boston, MA 02114 USA. Massachusetts Gen Hosp, Dept Pathol, Boston, MA 02114 USA. Harvard Univ, Sch Med, Dept Surg, Cambridge, MA 02138 USA. Harvard Univ, Sch Med, Dept Radiol, Cambridge, MA 02138 USA. Harvard Univ, Sch Med, Dept Pathol, Cambridge, MA 02138 USA. RP Dahl, DM (reprint author), Massachusetts Gen Hosp, Dept Urol, Boston, MA 02114 USA. NR 17 TC 0 Z9 0 U1 0 U2 1 PU MASSACHUSETTS MEDICAL SOC PI WALTHAM PA WALTHAM WOODS CENTER, 860 WINTER ST,, WALTHAM, MA 02451-1413 USA SN 0028-4793 J9 NEW ENGL J MED JI N. Engl. J. Med. PD NOV 11 PY 2004 VL 351 IS 20 BP 2102 EP 2110 PG 9 WC Medicine, General & Internal SC General & Internal Medicine GA 869TM UT WOS:000225007200013 PM 15537909 ER PT J AU Mutter, GL Zahrieh, D Liu, CM Neuberg, D Finkelstein, D Baker, HE Warrington, JA AF Mutter, GL Zahrieh, D Liu, CM Neuberg, D Finkelstein, D Baker, HE Warrington, JA TI Comparison of frozen and RNALater solid tissue storage methods for use in RNA expression microarrays SO BMC GENOMICS LA English DT Article ID HIGH-QUALITY RNA; MESSENGER-RNA; SAMPLES; YIELD; TUMOR; PCR AB Background: Primary human tissues are an invaluable widely used tool for discovery of gene expression patterns which characterize disease states. Tissue processing methods remain unstandardized, leading to unanswered concerns of how to best store collected tissues and maintain reproducibility between laboratories. We subdivided uterine myometrial tissue specimens and stored split aliquots using the most common tissue processing methods (fresh, frozen, RNALater) before comparing quantitative RNA expression profiles on the Affymetrix U133 human expression array. Split samples and inclusion of duplicates within each processing group allowed us to undertake a formal genome-wide analysis comparing the magnitude of result variation contributed by sample source (different patients), processing protocol (fresh vs. frozen vs. 24 or 72 hours RNALater), and random background (duplicates). The dataset was randomly permuted to define a baseline pattern of ANOVA test statistic values against which the observed results could be interpreted. Results: 14,639 of 22,283 genes were expressed in at least one sample. Patient subjects provided the greatest sources of variation in the mixed model ANOVA, with replicates and processing method the least. The magnitude of variation conferred by processing method (24 hours RNALater vs 72 hours RNALater vs. fresh vs frozen) was similar to the variability seen within replicates. Subset analysis of the test statistic according to gene functional class showed that the frequency of "outlier" ANOVA results within each functional class is overall no greater than expected by chance. Conclusions: Ambient storage of tissues for 24 or 72 hours in RNALater did not contribute any systematic shift in quantitative RNA expression results relative to the alternatives of fresh or frozen tissue. This nontoxic preservative enables decentralized tissue collection for expression array analysis without a requirement for specialized equipment. C1 Brigham & Womens Hosp, Dept Pathol, Boston, MA 02115 USA. Dana Farber Canc Inst, Dept Biostat Sci, Boston, MA 02115 USA. Affymetrix Inc, Santa Clara, CA USA. RP Mutter, GL (reprint author), Brigham & Womens Hosp, Dept Pathol, 75 Francis St, Boston, MA 02115 USA. EM gmutter@rics.bwh.harvard.edu; zahrieh@jimmy.harvard.edu; Chunmei_Liu@affymetrix.com; neuberg@jimmy.harvard.edu; David.Finkelstein@STJUDE.ORG; crumbsbaker@yahoo.com; janet_warrington@affymetrix.com RI Mutter, George/C-5819-2009 NR 18 TC 100 Z9 107 U1 3 U2 17 PU BIOMED CENTRAL LTD PI LONDON PA MIDDLESEX HOUSE, 34-42 CLEVELAND ST, LONDON W1T 4LB, ENGLAND SN 1471-2164 J9 BMC GENOMICS JI BMC Genomics PD NOV 10 PY 2004 VL 5 AR 88 DI 10.1186/1471-2164-5-88 PG 7 WC Biotechnology & Applied Microbiology; Genetics & Heredity SC Biotechnology & Applied Microbiology; Genetics & Heredity GA 878BF UT WOS:000225620800001 PM 15537428 ER PT J AU Rojo, E Martin, R Carter, C Zouhar, J Pan, SQ Plotnikova, J Jin, HL Paneque, M Sanchez-Serrano, JJ Baker, B Ausubel, FM Raikhel, NV AF Rojo, E Martin, R Carter, C Zouhar, J Pan, SQ Plotnikova, J Jin, HL Paneque, M Sanchez-Serrano, JJ Baker, B Ausubel, FM Raikhel, NV TI VPE gamma exhibits a caspase-like activity that contributes to defense against pathogens SO CURRENT BIOLOGY LA English DT Article ID PROGRAMMED CELL-DEATH; VACUOLAR PROCESSING ENZYME; ARABIDOPSIS-THALIANA; HYPERSENSITIVE RESPONSE; ASPARAGINYL ENDOPEPTIDASE; CYSTEINE ENDOPEPTIDASE; STORAGE PROTEINS; PLANTS; DEGRADATION; PROTEASE AB Background: Caspases are a family of aspartate-specific cysteine proteases that play an essential role in initiating and executing programmed cell death (PCD) in metazoans. Caspase-like activities have been shown to be required for the initiation of PCD in plants, but the genes encoding those activities have not been identified. VPEgamma, a cysteine protease, is induced during senescence, a form of PCD in plants, and is localized in precursor protease vesicles and vacuoles, compartments associated with PCD processes in plants. Results: We show that VPEgamma binds in vivo to a general caspase inhibitor and to caspase-1-specific inhibitors, which block the activity of VPEgamma. A cysteine protease inhibitor, cystatin, accumulates to 20-fold higher levels in vpegamma mutants. Homologs of cystatin are known to suppress hypersensitive cell death in plant and animal systems. We also report that infection with an avirulent strain of Pseudomonas syringae results in an increase of caspase-1 activity, and this increase is partially suppressed in vpegamma mutants. Plants overexpressing VPEgamma exhibit a greater amount of ion leakage during infection with P. syringae, suggesting that VPEgamma may regulate cell death progression during plant-pathogen interaction. VPEgamma expression is induced after infection with P. syringae, Botrytis cinerea, and turnip mosaic virus, and knockout of VPEgamma results in increased susceptibility to these pathogens. Conclusions: We conclude that VPEgamma is a caspase-like enzyme that has been recruited in plants to regulate vacuole-mediated cell dismantling during cell death, a process that has significant influence in the outcome of a diverse set of plant-pathogen interactions. C1 Univ Calif Riverside, Ctr Plant Cell Biol, Riverside, CA 92521 USA. Univ Calif Riverside, Dept Bot & Plant Sci, Riverside, CA 92521 USA. CSIC, Ctr Nacl Biotecnol, Dept Genet Mol Plantas, E-28049 Madrid, Spain. Harvard Univ, Sch Med, Dept Genet, Boston, MA 02114 USA. Massachusetts Gen Hosp, Dept Mol Biol, Boston, MA 02114 USA. USDA, Albany, CA 94710 USA. Univ Calif Berkeley, Ctr Plant Gene Express, Albany, CA 94710 USA. RP Rojo, E (reprint author), Univ Calif Riverside, Ctr Plant Cell Biol, 2109 Batchelor Hall, Riverside, CA 92521 USA. EM erojo@cnb.uam.es; natasha.raikhel@ucr.edu RI Paneque, Manuel/A-6930-2015; Sanchez Serrano, Jose/H-6955-2015; Baker, Barbara/L-7198-2016; OI Paneque, Manuel/0000-0002-8731-0233; Sanchez Serrano, Jose/0000-0002-4489-4785; Baker, Barbara/0000-0002-1276-971X; Rojo, Enrique/0000-0001-9886-2917 FU NIGMS NIH HHS [GM069087, GM48707] NR 35 TC 157 Z9 173 U1 0 U2 19 PU CELL PRESS PI CAMBRIDGE PA 1100 MASSACHUSETTS AVE, CAMBRIDGE, MA 02138 USA SN 0960-9822 J9 CURR BIOL JI Curr. Biol. PD NOV 9 PY 2004 VL 14 IS 21 BP 1897 EP 1906 DI 10.1016/j.cub.2004.09.056 PG 10 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA 870QY UT WOS:000225074100018 PM 15530390 ER PT J AU Smith, EE Gurol, ME Eng, JA Engel, CR Nguyen, TN Rosand, J Greenberg, SM AF Smith, EE Gurol, ME Eng, JA Engel, CR Nguyen, TN Rosand, J Greenberg, SM TI White matter lesions, cognition, and recurrent hemorrhage in lobar intracerebral hemorrhage SO NEUROLOGY LA English DT Article ID CEREBRAL AMYLOID ANGIOPATHY; APOLIPOPROTEIN-E EPSILON-2; ISCHEMIC-STROKE; ROTTERDAM-SCAN; ELDERLY-PEOPLE; RISK-FACTORS; AGING BRAIN; MR-IMAGES; DEMENTIA; LEUKOARAIOSIS AB Background: Accumulating evidence suggests that white matter lesions are associated with vascular cognitive impairment. The authors investigated the relationships between white matter lesions, cognitive impairment, and risk of recurrent hemorrhage in a prospectively identified cohort of patients with lobar intracerebral hemorrhage (ICH). Methods: The authors collected clinical and genetic information on 182 consecutive patients age greater than or equal to 55 who had CT scan at admission for lobar ICH. White matter disease was graded on CT in all subjects and on MRI in a subset of 82 patients. All scans were interpreted blinded to clinical information. Survivors were followed for recurrent ICH by telephone interview. Results: White matter damage was common (present on CT in 77%) and severe (advanced CT grade in 32%). White matter damage was correlated with the total number of hemorrhages on gradient-echo MRI and with risk of recurrent ICH. Subjects with cognitive impairment prior to their index ICH were more likely to have severe white matter damage on CT (OR 3.6, 95% CI 1.6 to 8.1, p = 0.003) and more likely to have advanced periventricular hyperintensities on MRI. The relationships between white matter damage and cognitive impairment were similar in the subset of 88 subjects meeting criteria for probable or definite cerebral amyloid angiopathy and remained independent after adjustment for age, cortical atrophy, and APOE genotype. Conclusions: White matter damage in lobar ICH is common and is associated with cognitive impairment. These data support the possibility that an underlying vasculopathy in lobar ICH patients, possibly cerebral amyloid angiopathy, can cause clinically important vascular dysfunction. C1 Massachusetts Gen Hosp, Dept Neurol, Boston, MA 02114 USA. Harvard Univ, Sch Med, Boston, MA USA. RP Smith, EE (reprint author), Massachusetts Gen Hosp, Dept Neurol, VBK 725,55 Fruit St, Boston, MA 02114 USA. EM eesmith@partners.org RI Gurol, Edip/J-2279-2014; OI Gurol, Edip/0000-0002-2169-4457; Smith, Eric/0000-0003-3956-1668 NR 56 TC 123 Z9 125 U1 2 U2 6 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0028-3878 J9 NEUROLOGY JI Neurology PD NOV 9 PY 2004 VL 63 IS 9 BP 1606 EP 1612 PG 7 WC Clinical Neurology SC Neurosciences & Neurology GA 869MJ UT WOS:000224987700013 PM 15534243 ER PT J AU Li, G Higdon, R Kukull, WA Peskind, E Moore, KV Tsuang, D van Belle, G McCormick, W Bowen, JD Teri, L Schellenberg, GD Larson, EB AF Li, G Higdon, R Kukull, WA Peskind, E Moore, KV Tsuang, D van Belle, G McCormick, W Bowen, JD Teri, L Schellenberg, GD Larson, EB TI Statin therapy and risk of dementia in the elderly - A community-based prospective cohort study SO NEUROLOGY LA English DT Article ID COA REDUCTASE INHIBITORS; CORONARY-HEART-DISEASE; ALZHEIMERS-DISEASE; CONTROLLED TRIAL; APOLIPOPROTEIN-E; CHOLESTEROL; SIMVASTATIN; STROKE; INDIVIDUALS; MONOTHERAPY AB Objective: To assess the association between statin therapy and risk of Alzheimer disease ( AD) in a prospective cohort study with documented statin exposure and incident dementia. Methods: This is a prospective, cohort study of statin use and incident dementia and probable AD. A cohort of 2,356 cognitively intact persons, aged 65 and older, were randomly selected from a health maintenance organization (HMO), and were assessed biennially for dementia. Statin use was identified using the HMO pharmacy database. A proportional hazards model with statin use as a time-dependent covariate was used to assess the statin-dementia/AD association. Results: Among 312 participants with incident dementia, 168 had probable AD. The unadjusted hazard ratios (HRs) with statin use were 1.33 (95% CI 0.95 to 1.85) for all-cause dementia and 0.90 (CI 0.54 to 1.51) for probable AD. Adjusted corresponding HRs were 1.19 (CI 0.82 to 1.75) and 0.82 (CI 0.46 to 1.46). A subgroup analysis of participants with at least one APOE-epsilon4 allele who entered the study before age 80 produced an adjusted HR of 0.33 (CI 0.10 to 1.04). Conclusion: Employing time-dependent proportional hazards modeling, the authors found no significant association between statin use and incident dementia or probable AD. In contrast, when the data were analyzed, inappropriately, as a case-control study, the authors found an OR of 0.55 for probable AD, falsely indicating a protective effect of statins. Study design and analytic methods may explain the discrepancy between the current null findings and earlier findings. C1 VA Puget Sound Hlth Care Syst, Mental Illness Res & Educ Clin Ctr, Seattle, WA 98108 USA. Univ Washington, Dept Psychiat & Behav Sci, Seattle, WA 98195 USA. Univ Washington, Dept Epidemiol, Seattle, WA 98195 USA. Univ Washington, Dept Environm Hlth & Biostat, Seattle, WA 98195 USA. Univ Washington, Dept Neurol, Seattle, WA 98195 USA. Univ Washington, Dept Psychosocial & Commun Hlth, Seattle, WA 98195 USA. Univ Washington, Dept Geriatr & Gerontol, Seattle, WA 98195 USA. VA Puget Sound Hlth Care Syst, Ctr Geriatr Res Educ & Clin, Seattle, WA 98108 USA. Grp Hlth Cooperat Puget Sound, Ctr Hlth Studies, Seattle, WA 98101 USA. RP Li, G (reprint author), VA Puget Sound Hlth Care Syst, Mental Illness Res & Educ Clin Ctr, 1660 S Columbian Way,Mailstop S-116 MIRECC, Seattle, WA 98108 USA. EM gli@u.washington.edu RI Tsuang, Debby/L-7234-2016; OI Tsuang, Debby/0000-0002-4716-1894; Kukull, Walter/0000-0001-8761-9014 FU NIA NIH HHS [AG05136, AG06781, AG16976, AG20020] NR 30 TC 167 Z9 181 U1 1 U2 5 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0028-3878 J9 NEUROLOGY JI Neurology PD NOV 9 PY 2004 VL 63 IS 9 BP 1624 EP 1628 PG 5 WC Clinical Neurology SC Neurosciences & Neurology GA 869MJ UT WOS:000224987700016 PM 15534246 ER PT J AU Shefner, JM Cudkowicz, ME Schoenfeld, D Conrad, T Taft, J Chilton, M Urbinelli, L Qureshi, M Zhang, H Pestronk, A Caress, J Donofrio, P Sorenson, E Bradley, W Lomen-Hoerth, C Pioro, E Rezania, K Ross, M Pascuzzi, R Heiman-Patterson, T Tandan, R Mitsumoto, H Rothstein, J Smith-Palmer, T MacDonald, D Burke, D AF Shefner, JM Cudkowicz, ME Schoenfeld, D Conrad, T Taft, J Chilton, M Urbinelli, L Qureshi, M Zhang, H Pestronk, A Caress, J Donofrio, P Sorenson, E Bradley, W Lomen-Hoerth, C Pioro, E Rezania, K Ross, M Pascuzzi, R Heiman-Patterson, T Tandan, R Mitsumoto, H Rothstein, J Smith-Palmer, T MacDonald, D Burke, D CA NEALS Consortium TI A clinical trial of creatine in ALS SO NEUROLOGY LA English DT Article ID AMYOTROPHIC-LATERAL-SCLEROSIS; UNIT NUMBER ESTIMATION; MOTOR-NEURON DISEASE; TRANSGENIC MICE; SOD1 MUTATION; GLUTAMATE; NEUROFILAMENTS; MODEL; DEGENERATION; DYSFUNCTION AB Background: Mitochondrial dysfunction occurs early in the course of ALS, and the mitochondria may be an important site for therapeutic intervention. Creatine stabilizes the mitochondrial transition pore, and is important in mitochondrial ATP production. In a transgenic mouse model of ALS, administration of creatine prolongs survival and preserves motor function and motor neurons. Methods: The authors conducted a randomized double-blind, placebo controlled trial on 104 patients with ALS from 14 sites to evaluate the efficacy of creatine supplementation in ALS. The primary outcome measure was maximum voluntary isometric contraction of eight upper extremity muscles, with secondary outcomes including grip strength, ALS Functional Rating Scale-Revised, and motor unit number estimates. Patients were treated for 6 months, and evaluated monthly. Results: Creatine was tolerated well, but no benefit of creatine could be demonstrated in any outcome measure. CI analysis showed that the study, although powered to detect a 50% or greater change in rate of decline of muscle strength, actually made an effect size of greater than 23% unlikely. It was also demonstrated that motor unit number estimation was performed with acceptable reproducibility and tolerability, and may be a useful outcome measure in future clinical trials. Conclusion: Any beneficial effect of creatine at 5 g per day in ALS must be small. Other agents should be considered in future studies of therapeutic agents to address mitochondrial dysfunction in ALS. In addition, motor unit number estimation may be a useful outcome measure for future clinical trials in ALS. C1 SUNY Upstate Med Univ, Dept Neurol, Syracuse, NY 13104 USA. Massachusetts Gen Hosp, Dept Neurol, Boston, MA 02114 USA. Massachusetts Gen Hosp, Ctr Biostat, Boston, MA 02114 USA. Washington Univ, Dept Neurol, St Louis, MO USA. Wake Forest Univ, Dept Neurol, Winston Salem, NC 27109 USA. Mayo Clin & Mayo Fdn, Dept Neurol, Rochester, MN 55905 USA. Univ Miami, Dept Neurol, Coral Gables, FL 33124 USA. Univ Calif San Francisco, Dept Neurol, San Francisco, CA 94143 USA. Cleveland Clin, Dept Neurol, Cleveland, OH 44106 USA. Univ Chicago, Dept Neurol, Chicago, IL 60637 USA. Univ Kentucky, Dept Neurol, Lexington, KY 40506 USA. Indiana Univ, Dept Neurol, Bloomington, IN 47405 USA. MCP Hahnemann, Dept Neurol, Philadelphia, PA USA. Univ Vermont, Dept Neurol, Burlington, VT 05405 USA. Columbia Univ, Dept Neurol, New York, NY 10027 USA. Johns Hopkins Univ, Dept Neurol, Baltimore, MD 21218 USA. St Francis Xavier Univ, Dept Chem, Antigonish, NS B2G 1C0, Canada. RP Shefner, JM (reprint author), SUNY Upstate Med Univ, Dept Neurol, 750 E Adams St, Syracuse, NY 13104 USA. EM shefnerj@upstate.edu RI rothstein, jeffrey/C-9470-2013; OI Caress, James/0000-0002-5814-6083 NR 39 TC 173 Z9 180 U1 0 U2 8 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0028-3878 J9 NEUROLOGY JI Neurology PD NOV 9 PY 2004 VL 63 IS 9 BP 1656 EP 1661 PG 6 WC Clinical Neurology SC Neurosciences & Neurology GA 869MJ UT WOS:000224987700021 PM 15534251 ER PT J AU Yaffe, K Clemons, TE McBee, WL Lindblad, AS AF Yaffe, K Clemons, TE McBee, WL Lindblad, AS CA Age-Related Eye Dis Study Res Grp TI Impact of antioxidants, zinc, and copper on cognition in the elderly - A randomized, controlled trial SO NEUROLOGY LA English DT Article ID ALZHEIMER-DISEASE; DIETARY-INTAKE; VITAMIN-E; RISK; SUPPLEMENTS; ASSOCIATION AB Participants in the Age-Related Eye Disease Study were randomly assigned to receive daily antioxidants (vitamin C, 500 mg; vitamin E, 400 IU; beta carotene, 15 mg), zinc and copper ( zinc, 80 mg; cupric oxide, 2 mg), antioxidants plus zinc and copper, or placebo. A cognitive battery was administered to 2,166 elderly persons after a median of 6.9 years of treatment. Treatment groups did not differ on any of the six cognitive tests (p > 0.05 for all). These results do not support a beneficial or harmful effect of antioxidants or zinc and copper on cognition in older adults. C1 EMMES Corp, AREDS Coordinating Ctr, Rockville, MD 20850 USA. Univ Calif San Francisco, Dept Psychiat, San Francisco, CA 94143 USA. Univ Calif San Francisco, Dept Neurol, San Francisco, CA 94143 USA. Univ Calif San Francisco, Dept Epidemiol, San Francisco, CA 94143 USA. San Francisco VA Med Ctr, San Francisco, CA USA. RP Yaffe, K (reprint author), EMMES Corp, AREDS Coordinating Ctr, 401 N Washington St,Suite 700, Rockville, MD 20850 USA. EM aredspub@emmes.com FU NEI NIH HHS [Z01 EY000394-03] NR 10 TC 77 Z9 79 U1 1 U2 8 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0028-3878 J9 NEUROLOGY JI Neurology PD NOV 9 PY 2004 VL 63 IS 9 BP 1705 EP 1707 PG 3 WC Clinical Neurology SC Neurosciences & Neurology GA 869MJ UT WOS:000224987700031 PM 15534261 ER PT J AU Gutschalk, A Harting, I Cantz, M Springer, C Rohrschneider, K Meinck, HM AF Gutschalk, A Harting, I Cantz, M Springer, C Rohrschneider, K Meinck, HM TI Adult alpha-mannosidosis - Clinical progression in the absence of demyelination SO NEUROLOGY LA English DT Article ID NERVOUS-SYSTEM AB alpha-Mannosidosis is an inherited lysosomal storage disease. The authors report three siblings ( ages 38 to 47 years) with the rare adult variant. All three had late-onset ataxia and retinal degeneration, adding to hearing loss, cognitive impairment, and dysotosis multiplex. One sibling also had psychosis. MRI revealed cerebellar atrophy and predominantly parieto-occipital white matter changes. MR spectroscopy showed no evidence for demyelination. It appears that the disabling course of adult alpha-mannosidosis is caused by lysosomal accumulation rather than demyelination. C1 Univ Heidelberg, Dept Neurol, D-6900 Heidelberg, Germany. Univ Heidelberg, Dept Neuroradiol, D-6900 Heidelberg, Germany. Univ Heidelberg, Dept Pathol, D-6900 Heidelberg, Germany. Univ Heidelberg, Dept Ophthalmol, D-6900 Heidelberg, Germany. RP Gutschalk, A (reprint author), Massachusetts Eye & Ear Infirm, Eaton Peabody Lab, 243 Charles St, Boston, MA 02114 USA. EM Alexander_Gutschalk@meei.harvard.edu NR 10 TC 21 Z9 21 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 9 PY 2004 VL 63 IS 9 BP 1744 EP 1746 PG 3 WC Clinical Neurology SC Neurosciences & Neurology GA 869MJ UT WOS:000224987700044 PM 15534274 ER PT J AU Lee, DU Rao, A AF Lee, DU Rao, A TI Molecular analysis of a locus control region in the T helper 2 cytokine gene cluster: A target for STAT6 but not GATA3 SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article ID T-CELL DIFFERENTIATION; IL-4 GENE; COORDINATE REGULATOR; HISTONE ACETYLATION; CHROMATIN-STRUCTURE; TH2 DEVELOPMENT; EXPRESSION; TRANSCRIPTION; SEQUENCE; MICE AB The linked IL-4 and IL-13 cytokine genes, which are activated and silenced in T helper (Th) 2 and Th1 cells, respectively, are flanked by the equivalently expressed RAD50 and KIF3A genes. A scan of DNase I hypersensitivity and DNA methylation across approximate to100 kb of the KIF3A/IL-4/IL-13/RAD50 cluster revealed differences in chromatin structure between Th1 and Th2 cells at the 3' end of the RAD50 gene, a region previously shown to contain a locus control region (LCR) regulating Th2-specific expression of IL-4 and IL-13. Naive CD4T cells did not exhibit any DNase I hypersensitivity in this region, but stimulation under either Th1 or Th2 conditions caused rapid development of three hypersensitive sites. An additional hypersensitive site developed rapidly only under Th2 conditions, through a mechanism dependent on signal transducers and activators of transcription 6 (STAT6) but not GATA3. Our data point to a physical separation in the actions of STAT6 and its downstream effector GATA3 during Th2 differentiation: STAT6 directly remodels the RAD50 LCR, whereas GATA3 acts only in the vicinity of the IL-4 gene. We suggest that the RAD50 LCR has a complex and dual role in Th1 and Th2 differentiation, communicating early T cell antigen receptor and cytokine signals to the IL-4/IL-13 locus in both differentiating cell types. C1 Harvard Univ, Sch Med, Boston, MA 02115 USA. CBR Inst Biomed Res, Boston, MA 02115 USA. Harvard Univ, Sch Med, Div Med Sci, Grad Program Immunol, Boston, MA 02115 USA. RP Rao, A (reprint author), Harvard Univ, Sch Med, Alpert Bldg,Room 152,200 Longwood Ave, Boston, MA 02115 USA. EM arao@cbr.med.harvard.edu FU NHLBI NIH HHS [P01 HL067664, P01 HL 67664]; NIAID NIH HHS [R01 AI044432, R012 AI 44432] NR 48 TC 65 Z9 68 U1 0 U2 0 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 9 PY 2004 VL 101 IS 45 BP 16010 EP 16015 DI 10.1073/pnas.0407031101 PG 6 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA 872GX UT WOS:000225196800036 PM 15507491 ER PT J AU Poon, EG Gandhi, TK Seduist, TD Murff, HJ Karson, AVS Bates, DW AF Poon, EG Gandhi, TK Seduist, TD Murff, HJ Karson, AVS Bates, DW TI "I wish I had seen this test result earlier!" SO ARCHIVES OF INTERNAL MEDICINE LA English DT Article ID ABNORMAL PAP-SMEARS; FOLLOW-UP; WOMEN; NOTIFICATION; SYSTEMS; TRIAL; CARE AB Background: Failure to review and follow up on outpatient test results in a timely manner represents a patient safety and malpractice concern. Therefore, we sought to identify problems in current test result management systems and possible ways to improve these systems. Methods: We surveyed 262 physicians working in 15 internal medicine practices affiliated with 2 large urban teaching hospitals (response rate, 64%). We asked physicians about systems they used and the amount of time they spent managing test results. We asked them to report delays in reviewing test results and their overall satisfaction with their management of test results. We also asked physicians to rate features they would find useful in a new test result management system. Results: Overall, 83% of respondents reported at least 1 delay in reviewing test results during the previous 2 months. Despite reporting that they spent on average 74 minutes per clinical day managing test results, only 41% of physicians reported being satisfied with how they managed test results. Satisfaction was associated with fewer self-reported delays in reviewing test results. Physicians who actively tracked their test orders to completion were also more likely to be satisfied. The most highly desired features of a test result management system were tools to help physicians generate result letters to patients, prioritize their workflow, and track test orders to completion. Conclusions: Delays in test result review are common, and many physicians are not satisfied with how they manage test results. Tools to improve test result management in office practices need to improve workflow efficiency and track test orders to completion. C1 Brigham & Womens Hosp, Div Gen Med & Primary Care, Boston, MA 02120 USA. Vanderbilt Univ, Med Ctr, Nashville, TN USA. Massachusetts Gen Hosp, Boston, MA 02114 USA. RP Poon, EG (reprint author), Brigham & Womens Hosp, Div Gen Med & Primary Care, 3-F 1620 Tremont St, Boston, MA 02120 USA. EM epoon@partners.org FU AHRQ HHS [R01 1U18 HS11046-03] NR 24 TC 146 Z9 146 U1 1 U2 3 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 USA SN 0003-9926 J9 ARCH INTERN MED JI Arch. Intern. Med. PD NOV 8 PY 2004 VL 164 IS 20 BP 2223 EP 2228 DI 10.1001/archinte.164.20.2223 PG 6 WC Medicine, General & Internal SC General & Internal Medicine GA 869EG UT WOS:000224965600006 PM 15534158 ER PT J AU Prochazka, AV Kick, S Steinbrunn, C Miyoshi, T Fryer, GE AF Prochazka, AV Kick, S Steinbrunn, C Miyoshi, T Fryer, GE TI A randomized trial of nortriptyline combined with transdermal nicotine for smoking cessation SO ARCHIVES OF INTERNAL MEDICINE LA English DT Article ID SUSTAINED-RELEASE BUPROPION; DOUBLE-BLIND; WITHDRAWAL; PLACEBO; CLONIDINE; SMOKERS; HEAVY AB Background: Smoking cessation rates with current therapy are suboptimal. Tricyclic antidepressants improve cessation rates. We hypothesized that addition of nortriptyline hydrochloride to transdermal nicotine would enhance cessation rates. Methods: We conducted a randomized, double-blind, placebo-controlled trial at a Department of Veterans Affairs medical center. Subjects were aged 18 to 65 years, smoked 10 or more cigarettes per day, and did not have current major depression. Nortriptyline hydrochloride or matched placebo was started at 25 mg 14 days before quit day. titrated to 75 mg/d as tolerated, and continued for 12 weeks after quit day. Transdermal nicotine (21 mg/d) was started on quit day and continued for 8 weeks. The behavioral intervention consisted of 12 brief, individual visits. Withdrawal symptoms were measured by means of a daily diary, and smoking cessation was defined as self-reported abstinence, expired carbon monoxide level of 9 ppm or less, and a 6-month urine cotinine level less than 50 ng/mL (284 nmol/L). Results: A total of 158 patients were randomized (79 to nortriptyline and 79 to placebo). There was no significant reduction in withdrawal symptoms. The cessation rates at 6 months were 23% (18/79) and 10% (8/79), respectively (absolute difference, 13%; 95% confidence interval, 1.3%-24.5%; P=.052). Nortriptyline caused frequent side effects, including dry mouth (38%) and sedation (20%). Conclusions: Nortriptyline combined with transdermal nicotine resulted in an increased cessation rate with little effect on withdrawal symptoms. This combination may represent an option for smokers in whom standard therapy has failed. C1 Univ Colorado, Hlth Sci Ctr, Div Gen Internal Med, Denver, CO 80262 USA. Univ Colorado, Hlth Sci Ctr, Dept Family Med, Denver, CO USA. Denver Vet Affairs Med Ctr, Ambulat Care, Denver, CO USA. Amer Acad Family Phys, Robert Graham Ctr Policy Studies Family Practice, Washington, DC USA. RP Prochazka, AV (reprint author), Ambulat Care 11B, 1055 Clermont, Denver, CO 80220 USA. EM Allan.Prochazka@med.va.gov NR 26 TC 35 Z9 39 U1 0 U2 0 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 USA SN 0003-9926 J9 ARCH INTERN MED JI Arch. Intern. Med. PD NOV 8 PY 2004 VL 164 IS 20 BP 2229 EP 2233 DI 10.1001/archinte.164.20.2229 PG 5 WC Medicine, General & Internal SC General & Internal Medicine GA 869EG UT WOS:000224965600007 PM 15534159 ER PT J AU Buckland, PR Hoogendoom, B Guy, CA Coleman, SL Smith, SK Buxbaum, JD Haroutunian, V O'Donovan, MC AF Buckland, PR Hoogendoom, B Guy, CA Coleman, SL Smith, SK Buxbaum, JD Haroutunian, V O'Donovan, MC TI A high proportion of polymorphisms in the promoters of brain expressed genes influences transcriptional activity SO BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR BASIS OF DISEASE LA English DT Article DE Tf; NPY; PCSK1; NEFL; LM04; HSPA1B ID FUNCTIONAL-ANALYSIS; NEUROPEPTIDE-Y; SCHIZOPHRENIA; SUSCEPTIBILITY; ASSOCIATION; IDENTIFICATION; NEUREGULIN-1; DATABASE; ELEMENT; DISEASE AB There is increasing interest in the possibility that polymorphisms affecting gene expression are responsible for a significant proportion of heritable human phenotypic variation, including human disease. We have sought to determine if polymorphisms in the promoters of brain expressed genes are commonly functional. We screened for polymorphism 56 genes previously reported to be differentially expressed in the brains of schizophrenics [Y Hakak, JR. Walker, C. Li, W.H. Wong, K.L. Davis, J.D. Buxbaum, V Haroutunian, A.A. Fienberg, Genome-wide expression analysis reveals dysregulation of myelination-related genes in chronic schizophrenia. Proc. Natl. Acad. Sci. 98 (2001) 4746-4751.]. We found 60 variants distributed across 31 of the genes. A total of 77 haplotypes representing 28 different putative promoters were analyzed in a reporter gene assay in two. cell lines. Of a total of 54 sequence variants represented in the haplotypes, 12 (or around 22%) were functional according to a highly conservative definition. These were found in the promoters of eight genes: NPY, PCSK1, NEFL, KIAA0513, LMO4, HSPA1B, TF and MDH1. We therefore estimate that around 20-25% of promoter polymorphisms in brain expressed genes are functional, and this is likely to be an underestimate. Our data therefore provide for the first time empirical evidence that promoter element polymorphisms, at least in brain expressed genes, should be afforded a high priority for molecular genetic studies. (C) 2004 Elsevier B.V. All rights reserved. C1 Univ Wales Coll Med, Dept Med Psychol, Cardiff CF14 4XN, S Glam, Wales. Mt Sinai Sch Med, Dept Psychiat, New York, NY 10021 USA. Bronx Vet Affairs Med Ctr, MIRECC, Bronx, NY 10468 USA. RP Buckland, PR (reprint author), Univ Wales Coll Med, Dept Med Psychol, Heath Pk, Cardiff CF14 4XN, S Glam, Wales. EM buckland@cardiff.ac.uk OI O'Donovan, Michael/0000-0001-7073-2379; Hoogendoorn, Bastiaan/0000-0001-9753-169X; Buxbaum, Joseph/0000-0001-8898-8313 FU Medical Research Council [G9810900]; NIMH NIH HHS [P50 MH66932] NR 35 TC 50 Z9 53 U1 0 U2 2 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0925-4439 J9 BBA-MOL BASIS DIS JI Biochim. Biophys. Acta-Mol. Basis Dis. PD NOV 5 PY 2004 VL 1690 IS 3 BP 238 EP 249 DI 10.1016/j.bbadis.2004.06.023 PG 12 WC Biochemistry & Molecular Biology; Biophysics; Cell Biology SC Biochemistry & Molecular Biology; Biophysics; Cell Biology GA 870LG UT WOS:000225058000007 PM 15511631 ER PT J AU Browner, NC Dey, NB Boch, KD Lincoln, TM AF Browner, NC Dey, NB Boch, KD Lincoln, TM TI Regulation of cGMP-dependent protein kinase expression by soluble guanylyl cyclase in vascular smooth muscle cells SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID REDUCES NEOINTIMA FORMATION; NITRIC-OXIDE RECEPTOR; CYCLIC-GMP; ACTIVITY REQUIRES; ENZYME SUBUNITS; DOWN-REGULATION; GENE-TRANSFER; RATS; NO; DESENSITIZATION AB Vascular smooth muscle cells (VSMC) undergo many phenotypic changes when placed in culture. Several studies have shown that the levels of expression of soluble guanylyl cyclase (sGC) or cGMP-dependent protein kinase (PKG) are altered in cultured VSMC. In this study the mechanisms involved in the coordinated expression of sGC and PKG were examined. Pro-inflammatory cytokines that increase the expression of type II NO synthase (inducible NO synthase, or iNOS) decreased PKG expression in freshly isolated, non-passaged bovine aortic SMC. However, in several passaged VSMC lines (i.e. bovine aortic SMC, human aortic SMC, and A7r5 cells), PKG protein expression was not suppressed by cytokines or NO. sGC was highly expressed in non-passaged bovine aortic SMC but not in passaged cell lines. Restoration of expression of sGC to passaged bovine SMC using adenovirus encoding the alpha(1) and beta(1) subunits of sGC restored the capacity of the cells to increase cGMP in response to NO. Furthermore, treatment of these sGC-transduced cells with NO donors for 48 h resulted in decreased PKG protein expression. In contrast, passaged rat aortic SMC expressed high levels of NO-responsive sGC but demonstrated reduced expression of PKG. Adenovirus-mediated expression of the PKG catalytically active domain in rat aortic SMC caused a reduction in the expression of sGC in these cells. These results suggest that there is a mechanism for the coordinated expression of sGC and PKG in VSMC and that prolonged activation of sGC down-regulates PKG expression. Likewise, the loss of PKG expression appears to increase sGC expression. These effects may be an adaptive mechanism allowing growth and survival of VSMC in vitro. C1 Univ S Alabama, Dept Physiol, Mobile, AL 36688 USA. Univ Alabama, Dept Pharmacol & Toxicol, Birmingham, AL 35294 USA. Univ Hartford, Sch Med, Massachusetts Gen Hosp, Dept Med,Cardiovasc Div, Charlestown, MA 02129 USA. Univ Hartford, Sch Med, Massachusetts Gen Hosp, Cardiovasc Res Ctr, Charlestown, MA 02129 USA. RP Lincoln, TM (reprint author), Univ S Alabama, Dept Physiol, Med Sci Bldg,Rm 3024, Mobile, AL 36688 USA. EM tlincoln@usouthal.edu FU NHLBI NIH HHS [HL66164, HL53426, R01 HL053426, R01 HL066164] NR 38 TC 35 Z9 37 U1 0 U2 2 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 5 PY 2004 VL 279 IS 45 BP 46631 EP 46636 DI 10.1074/jbc.M408518200 PG 6 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA 867HE UT WOS:000224832400037 PM 15337747 ER PT J AU Im, SH Hueber, A Monticelli, S Kang, KH Rao, A AF Im, SH Hueber, A Monticelli, S Kang, KH Rao, A TI Chromatin-level regulation of the IL10 gene in T cells SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID HISTONE ACETYLATION; INTERFERON-GAMMA; IN-VIVO; INTERLEUKIN-10; TRANSCRIPTION; DIFFERENTIATION; ACTIVATION; ENHANCER; RECEPTOR; EXPRESSION AB The immunoregulatory cytokine interleukin 10 (IL-10) modulates the function of diverse immune and non-immune cells. Here, we examine the chromatin structural changes associated with IL10 gene transcription by naive and differentiated murine T cells. Naive T cells lack DNase I hypersensitive (HS) sites in the vicinity of the IL10 gene, whereas differentiated T cells display a strong 3' constitutive HS site as well as several inducible sites. The majority of HS sites map to regions that are strongly conserved in sequence between mouse and human genomes. In committed Th1 cells, the mechanism of IL10 gene silencing is associated with the development of repressive histone modifications near the IL10 promoter and also near intronic hypersensitive regions of the IL10 gene. Our results constitute the first report of chromatin structural differences within the IL10 gene in differentiated Th1 and Th2 cells and emphasize the surprising diversity of mechanisms used to regulate cytokine gene expression at the chromatin level. C1 Gwangju Inst Sci & Technol, Dept Life Sci, Kwangju 500712, South Korea. Harvard Univ, Sch Med, Ctr Blood Res, Boston, MA 02115 USA. Harvard Univ, Sch Med, Dept Pathol, Boston, MA 02115 USA. RP Im, SH (reprint author), Gwangju Inst Sci & Technol, Dept Life Sci, 1 Oryong Dong, Kwangju 500712, South Korea. EM imsh@gist.ac.kr RI Im, Sin-Hyeog/E-6811-2013 OI Im, Sin-Hyeog/0000-0002-3173-1856 FU NCI NIH HHS [R01-CA42471]; NIAID NIH HHS [R01-AI48213] NR 24 TC 76 Z9 79 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 5 PY 2004 VL 279 IS 45 BP 46818 EP 46825 DI 10.1074/jbc.M401722200 PG 8 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA 867HE UT WOS:000224832400062 PM 15319439 ER PT J AU Saoncella, S Calautti, E Neveu, W Goetinck, PF AF Saoncella, S Calautti, E Neveu, W Goetinck, PF TI Syndecan-4 regulates ATF-2 transcriptional activity in a Rac1-dependent manner SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID FOCAL ADHESION KINASE; ACTIVATED PROTEIN-KINASES; ACTIN STRESS FIBERS; SIGNALING PATHWAYS; GENE-EXPRESSION; RHO-GTPASES; RAC; TRANSDUCTION; INTEGRINS; BINDING AB Syndecan-4 is a transmembrane heparan sulfate proteoglycan that co-operates with integrins during cell-matrix interactions for the assembly of focal adhesions and actin stress fibers and in the phosphorylation of focal adhesion kinase (FAK) on Tyr(397). These cellular events are regulated by the small GTPase Rho, and in the absence of syndecan-4 ligation, cellular levels of GTP-bound Rho are decreased implicating syndecan-4 in the regulation of the small GTPases. In the present study we report that, compared with wild type cells, fibronectin-adherent syndecan-4-null fibroblasts showed enhanced lamellipodia and increased Rac1 activity that could be down-regulated by re-expression of syndecan-4 in the mutant cells. Consistent with the role for Rac1 in activating p38 and JNK signaling, syndecan-4-null cells display higher levels of active p38 MAPK and JNK that were abolished by the expression of a dominant-negative RacN17 mutant. Since p38 and JNK regulate gene expression by phosphorylating and activating transcription factors, we compared both the phosphorylation state and the transcriptional activity of the ATF-2 transcription factor, as a direct p38 and JNK target in syndecan-4-null and wild type cells. In the absence of syndecan-4, both ATF-2 phosphorylation and transcriptional activity were significantly more elevated compared with wild type cells, and both activities were decreased either by the re-expression of syndecan-4 or by the expression of RacN17. Our results reveal a novel function for syndecan-4 in modulating nuclear transcriptional activity and indicate an underlying mechanism that acts at the level of Rac1-p38/JNK signaling. C1 Harvard Univ, Sch Med, Massachusetts Gen Hosp, Cutaneous Biol Res Ctr, Charlestown, MA 02129 USA. RP Goetinck, PF (reprint author), MGH E, Cutaneous Biol Res Ctr, Bldg 149,13th St, Charlestown, MA 02129 USA. EM paul.goetinck@cbrc2.mgh.harvard.edu OI CALAUTTI, Vincenzo/0000-0002-4439-9709 FU NICHD NIH HHS [HD-37490] NR 36 TC 26 Z9 26 U1 0 U2 0 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD NOV 5 PY 2004 VL 279 IS 45 BP 47172 EP 47176 DI 10.1074/jbc.C400299200 PG 5 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA 867HE UT WOS:000224832400104 PM 15371457 ER PT J AU Shen, BZ Goodman, HM AF Shen, BZ Goodman, HM TI Uridine addition after microRNA-directed cleavage SO SCIENCE LA English DT Article ID MESSENGER-RNA; ARABIDOPSIS; TARGETS; MIRNA C1 Harvard Univ, Sch Med, Dept Genet, Boston, MA 02114 USA. Massachusetts Gen Hosp, Dept Mol Biol, Boston, MA 02114 USA. RP Goodman, HM (reprint author), Harvard Univ, Sch Med, Dept Genet, 50 Blossom St, Boston, MA 02114 USA. EM goodman@motbio.mgh.harvard.edu NR 6 TC 136 Z9 143 U1 1 U2 9 PU AMER ASSOC ADVANCEMENT SCIENCE PI WASHINGTON PA 1200 NEW YORK AVE, NW, WASHINGTON, DC 20005 USA SN 0036-8075 J9 SCIENCE JI Science PD NOV 5 PY 2004 VL 306 IS 5698 BP 997 EP 997 DI 10.1126/science.1103521 PG 1 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA 869RG UT WOS:000225001100032 PM 15528436 ER PT J AU Xiao, T Takagi, J Coller, BS Wang, JH Springer, TA AF Xiao, T Takagi, J Coller, BS Wang, JH Springer, TA TI Structural basis for allostery in integrins and binding to fibrinogen-mimetic therapeutics SO NATURE LA English DT Article ID GLYCOPROTEIN-IIB-IIIA; INSIDE-OUT ACTIVATION; LIGAND-BINDING; CRYSTAL-STRUCTURE; A-DOMAIN; EXTRACELLULAR SEGMENT; SIGNAL-TRANSDUCTION; BETA(3) SUBUNIT; HYBRID DOMAIN; GPIIB-IIIA AB Integrins are important adhesion receptors in all Metazoa that transmit conformational change bidirectionally across the membrane. Integrin alpha and beta subunits form a head and two long legs in the ectodomain and span the membrane. Here, we define with crystal structures the atomic basis for allosteric regulation of the conformation and affinity for ligand of the integrin ectodomain, and how fibrinogen- mimetic therapeutics bind to platelet integrin alpha(IIb)beta(3). Allostery in the beta(3)I domain alters three metal binding sites, associated loops and alpha1- and alpha7-helices. Piston-like displacement of the alpha7-helix causes a 62degrees reorientation between the beta(3)I and hybrid domains. Transmission through the rigidly connected plexin/semaphorin/integrin ( PSI) domain in the upper beta(3) leg causes a 70 Angstrom separation between the knees of the alpha and beta legs. Allostery in the head thus disrupts interaction between the legs in a previously described low-affinity bent integrin conformation, and leg extension positions the high-affinity head far above the cell surface. C1 Harvard Univ, Sch Med, CBR Inst Biomed Res, Boston, MA 02115 USA. Harvard Univ, Sch Med, Dept Pathol, Boston, MA 02115 USA. Rockefeller Univ, Lab Blood & Vasc Biol, New York, NY 10021 USA. Harvard Univ, Sch Med, Dana Farber Canc Inst, Boston, MA 02115 USA. Harvard Univ, Sch Med, Dept Pediat, Boston, MA 02115 USA. Harvard Univ, Sch Med, Dept Biol Chem & Mol Pharmacol, Boston, MA 02115 USA. RP Springer, TA (reprint author), Harvard Univ, Sch Med, CBR Inst Biomed Res, 200 Longwood Ave, Boston, MA 02115 USA. EM springer@cbr.med.harvard.edu RI Xiao, Tsan/A-8590-2010; Xiao, Tsan/I-7616-2013 OI Xiao, Tsan/0000-0001-9688-475X FU NHLBI NIH HHS [P01 HL048675] NR 50 TC 489 Z9 503 U1 3 U2 42 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 4 PY 2004 VL 432 IS 7013 BP 59 EP 67 DI 10.1038/nature02976 PG 9 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA 867PQ UT WOS:000224854900038 PM 15378069 ER PT J AU Bhatt, DL Roe, MT Peterson, ED Li, Y Chen, AY Harrington, RA Greenbaum, AB Berger, PB Cannon, CP Cohen, DJ Gibson, CM Saucedo, JF Kleiman, NS Hochman, JS Boden, WE Brindis, RG Peacock, WF Smith, SC Pollack, CV Gibler, WB Ohman, EM AF Bhatt, DL Roe, MT Peterson, ED Li, Y Chen, AY Harrington, RA Greenbaum, AB Berger, PB Cannon, CP Cohen, DJ Gibson, CM Saucedo, JF Kleiman, NS Hochman, JS Boden, WE Brindis, RG Peacock, WF Smith, SC Pollack, CV Gibler, WB Ohman, EM CA CRUSADE Investigators TI Utilization of early invasive management strategies for high-risk patients with non-ST-segment elevation acute coronary syndromes - Results from the CRUSADE quality improvement initiative SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION LA English DT Article ID PLATELET GLYCOPROTEIN IIB/IIIA; ACUTE MYOCARDIAL-INFARCTION; UNSTABLE ANGINA; ARTERY-DISEASE; ACC/AHA GUIDELINES; HEART-ASSOCIATION; ELDERLY-PATIENTS; TRIAL; CARE; ANGIOGRAPHY AB Context The American College of Cardiology/American Heart Association (ACC/ AHA) guidelines for the management of non-ST-segment elevation acute coronary syndromes (NSTE ACS) recommend early invasive management for high-risk patients, given the benefits with this approach demonstrated in randomized clinical trials. Objectives To determine the use and predictors of early invasive management strategies (cardiac catheterization <48 hours following presentation) in high-risk patients with NSTE ACS and to examine the association of early invasive management with mortality. Design, Setting, and Patients The CRUSADE (Can Rapid Risk Stratification of Unstable Angina Patients Suppress Adverse Outcomes With Early Implementation of the ACC/AHA Guidelines) Quality Improvement Initiative evaluated care patterns and outcomes for 17926 high-risk NSTE ACS patients (positive cardiac markers and/or ischemic electrocardiographic changes) based on ACC/AHA guidelines recommendations at 248 US hospitals with catheterization and revascularization facilities between March 2000 and September 2002. Main Outcome Measures Use of early invasive management within 48 hours of presentation, predictors of early invasive management, and in-hospital mortality. Results Of the 17926 patients analyzed, 8037 (44.8%) underwent early cardiac catheterization less than 48 hours following presentation. Predictors of early invasive management included cardiology care, younger age, lack of prior or current congestive heart failure, lack of renal insufficiency, ischemic electrocardiographic changes, positive cardiac markers, white race, and male sex. Patients treated with early invasive management were more likely to be treated with medications and interventions recommended by the ACC/AHA guidelines and had a lower risk of in-hospital mortality after adjusting for differences in clinical characteristics and after comparing propensity-matched pairs (2.5% vs 3.7%, P<.001). Conclusions An early invasive management strategy is not utilized in the majority of high-risk patients with NSTE ACS. This strategy appears to be reserved for patients without significant comorbidities and those cared for by cardiologists and is associated with a lower risk of in-hospital mortality. C1 Cleveland Clin Fdn, Dept Cardiovasc Med, Cleveland, OH 44195 USA. Duke Clin Res Inst, Durham, NC USA. Henry Ford Heart & Vasc Inst, Detroit, MI USA. Brigham & Womens Hosp, Boston, MA 02115 USA. Beth Israel Deaconess Med Ctr, Boston, MA 02215 USA. Harvard Univ, Sch Med, TIMI Study Grp, Boston, MA USA. Univ Oklahoma, Hlth Sci Ctr, Oklahoma City, OK USA. Baylor Coll Med, Houston, TX 77030 USA. NYU, Sch Med, New York, NY USA. Univ Connecticut, Hartford, CT 06112 USA. Kaiser Permanente Hlth Syst, San Francisco, CA USA. Univ N Carolina, Chapel Hill, NC USA. Penn Hosp, Philadelphia, PA 19107 USA. Univ Cincinnati, Cincinnati, OH USA. RP Bhatt, DL (reprint author), Cleveland Clin Fdn, Dept Cardiovasc Med, Desk F25,9500 Euclid Ave, Cleveland, OH 44195 USA. EM bhattd@ccf.org NR 36 TC 355 Z9 368 U1 2 U2 11 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 3 PY 2004 VL 292 IS 17 BP 2096 EP 2104 DI 10.1001/jama.292.17.2096 PG 9 WC Medicine, General & Internal SC General & Internal Medicine GA 868OC UT WOS:000224921900022 PM 15523070 ER PT J AU Roberts, TG Goulart, BH Squitieri, L Stallings, SC Halpern, EF Chabner, BA Gazelle, GS Finkelstein, SN Clark, JW AF Roberts, TG Goulart, BH Squitieri, L Stallings, SC Halpern, EF Chabner, BA Gazelle, GS Finkelstein, SN Clark, JW TI Trends in the risks and benefits to patients with cancer participating in phase 1 clinical trials SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION LA English DT Article; Proceedings Paper CT 38th Annual Meeting of the American-Society-of-Clinical-Oncology CY MAY 18-21, 2002 CL ORLANDO, FL SP Amer Soc Clin Oncol ID INFORMED-CONSENT; I TRIALS; ONCOLOGY; ETHICS; IMPACT; PERCEPTIONS; PHYSICIANS; THERAPY; QUALITY; AGENTS AB Context In the past, cancer patients entering phase 1 studies confronted the prospects of high risk and unlikely benefit. Over the last decade, cancer drugs under development have become more targeted, and the clinical research environment has become more scrutinized. The impact of these changes on the risks and benefits to patients who participate in phase 1 cancer trials is unknown. Objective To determine trends in the rates of treatment-related (toxic) death, objective response, and serious toxicity and to identify factors associated with these outcomes. Data Sources We searched abstracts and journal articles reporting the results of phase 1 cancer treatment trials originally submitted to annual meetings of the American Society of Clinical Oncology (ASCO) from 1991 through 2002. Study Selection We focused on published single-agent trials that enrolled patients with advanced solid tumors and excluded studies testing agents already approved by the US Food and Drug Administration at the time of the ASCO presentation. Data Extraction Multiple observers independently extracted information on trial design, location, sponsorship, types of tumors treated, drug class, route of administration, and clinical outcomes. Data Synthesis The overall toxic death rate for 213 studies (involving 6474 cancer patients) published in peer-reviewed journals was 0.54%, while the overall objective response rate was 3.8%. Toxic death rates decreased over the study period, from 1.1% over the first 4 years of the study (1991-1994) to 0.06% over the most recent 4-year period (1999-2002) (P<.01). Response rates also decreased but by proportionally much less. After adjusting for characteristics of the experimental trials and the investigational agents, the odds of a patient dying from an experimental treatment while participating in a trial submitted during the most recent 4-year period were less than one tenth those of a patient participating in a trial submitted during the first 4-year period (odds ratio, 0.09; 95% confidence interval, 0.01-0.67; P=.009). In comparison, the adjusted odds of a patient experiencing an objective response over the same time periods decreased by approximately half (odds ratio, 0.46; 95% confidence interval, 0.32-0.66; P<.001). Conclusions The level of risk experienced by cancer patients who participate in phase 1 treatment trials appears to have improved over the 12-year period from 1991 through 2002. Because toxic death rates have decreased more quickly than have objective response rates, the ratio of risk to benefit may have also improved. These changes relate in part to the targeted and less-toxic nature of newer cancer drugs and are coincident with the increased attention that has been paid to the safety of clinical research over the time period we analyzed. C1 Harvard Univ, Massachusetts Gen Hosp, Sch Med, Div Hematol Oncol, Boston, MA 02114 USA. MIT, Program Pharmaceut Ind, Cambridge, MA 02139 USA. Massachusetts Gen Hosp, Inst Technol Assessment, Boston, MA 02114 USA. Harvard Univ, Sch Med, Dana Farber Harvard Canc Ctr, Cambridge, MA 02138 USA. RP Roberts, TG (reprint author), Harvard Univ, Massachusetts Gen Hosp, Sch Med, Div Hematol Oncol, Cox 640,100 Blossom St, Boston, MA 02114 USA. EM troberts@partners.org FU NCI NIH HHS [R25 CA092203, R25T CA 92203] NR 42 TC 157 Z9 158 U1 0 U2 7 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 3 PY 2004 VL 292 IS 17 BP 2130 EP 2140 DI 10.1001/jama.292.17.2130 PG 11 WC Medicine, General & Internal SC General & Internal Medicine GA 868OC UT WOS:000224921900026 PM 15523074 ER PT J AU Hurwitz, CA Duncan, J Wolfe, J AF Hurwitz, CA Duncan, J Wolfe, J TI Caring for the child with cancer at the close of life - "There are people who make it, and I'm hoping I'm one of them" SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION LA English DT Article ID PEDIATRIC PALLIATIVE CARE; MALIGNANT-DISEASE; TERMINAL CANCER; ILL PATIENTS; SYMPTOMS; END; PAIN; METHYLPHENIDATE; HYDRATION; DYSPNEA AB Approximately 25% of children with cancer die of their disease. Early in the course of a patient's illness, it is often impossible to determine whether the disease will be cured with cancer-directed treatment. When potentially curative therapy is no longer an option, the patient, family, and oncology team face enormous medical, psychological, and spiritual challenges. Optimal palliative care requires willingness on the part of the physician and caregiver team to engage the patient and family in discussions of their hopes and fears and to provide solace and support for emotional and physical pain. Using the comments of a child in the terminal phase of acute leukemia, his mother, and his physician, we describe opportunities and important lessons often revealed only when families and their caregivers face the end of a child's life. A broad-minded assessment of the patient's and family's physical, emotional, and spiritual needs and clarification of realistic goals and hopes not only improves the clinical care that the patient receives but also contributes to the sense of satisfaction and meaning that the physician can gain from the experience of caring for children at the end of life. C1 Dana Farber Canc Inst, Dept Pediat Oncol, Pediat Adv Care Team, Boston, MA 02115 USA. Childrens Hosp, Div Hematol Oncol, Boston, MA 02115 USA. Harvard Univ, Sch Med, Dept Pediat, Boston, MA 02115 USA. Maine Med Ctr, Maine Childrens Canc Program, Portland, ME USA. Maine Med Ctr, Barbara Bush Childrens Hosp, Portland, ME USA. RP Wolfe, J (reprint author), Dana Farber Canc Inst, Dept Pediat Oncol, Pediat Adv Care Team, 44 Binney St, Boston, MA 02115 USA. EM joanne_wolfe@dfci.harvard.edu NR 72 TC 51 Z9 52 U1 2 U2 5 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 3 PY 2004 VL 292 IS 17 BP 2141 EP 2149 DI 10.1001/jama.292.17.2141 PG 9 WC Medicine, General & Internal SC General & Internal Medicine GA 868OC UT WOS:000224921900027 PM 15523075 ER PT J AU Linseman, DA Butts, BD Precht, TA Phelps, RA Le, SS Laessig, TA Bouchard, RJ Florez-McClure, ML Heidenreich, KA AF Linseman, DA Butts, BD Precht, TA Phelps, RA Le, SS Laessig, TA Bouchard, RJ Florez-McClure, ML Heidenreich, KA TI Glycogen synthase kinase-3 beta phosphorylates bax and promotes its mitochondrial localization during neuronal apoptosis SO JOURNAL OF NEUROSCIENCE LA English DT Article DE glycogen synthase kinase; cerebellar granule neuron; apoptosis; mitochondria; Bax; phosphorylation ID CEREBELLAR GRANULE NEURONS; PROGRAMMED CELL-DEATH; GROWTH-FACTOR-I; BCL-2 FAMILY; KINASE; SURVIVAL; PATHWAY; GSK3-BETA; DISEASE; TRANSLOCATION AB Glycogen synthase kinase-3beta(GSK-3beta)is a critical activator of neuronal apoptosis induced by a diverse array of neurotoxic insults. However, the downstream substrates of GSK-3beta that ultimately induce neuronal death are unknown. Here, we show that GSK-3beta phosphorylates and regulates the activity of Bax, a pro-apoptotic Bcl-2 family member that stimulates the intrinsic ( mitochondrial) death pathway by eliciting cytochrome c release from mitochondria. In cerebellar granule neurons undergoing apoptosis, inhibition of GSK-3beta suppressed both the mitochondrial translocation of an expressed green fluorescent protein (GFP)-Bax(alpha) fusion protein and the conformational activation of endogenous Bax. GSK-3beta directly phosphorylated Bax(alpha) on Ser163, a residue found within a species-conserved, putative GSK-3beta phosphorylation motif. Coexpression of GFP-Bax(alpha) with a constitutively active mutant of GSK-3beta, GSK-3beta(Ser9Ala), enhanced the in vivo phosphorylation of wild-type Bax(alpha), but not a Ser163Ala mutant of Bax(alpha), in transfected human embryonic kidney 293 (HEK293) cells. Moreover, cotransfection with constitutively active GSK-3beta promoted the localization of Bax(alpha) to mitochondria and induced apoptosis in both transfected HEK293 cells and cerebellar granule neurons. In contrast, neither a Ser163Ala point mutant of Bax(alpha) nor a naturally occurring splice variant that lacks 13 amino acids encompassing Ser163 (Bax(sigma)) were driven to mitochondria in HEK293 cells coexpressing constitutively active GSK-3beta. In a similar manner, either mutation or deletion of the identified GSK-3beta phosphorylation motif prevented the localization of Bax to mitochondria in cerebellar granule neurons undergoing apoptosis. Our results indicate that GSK-3beta exerts some of its pro-apoptotic effects in neurons by regulating the mitochondrial localization of Bax, a key component of the intrinsic apoptotic cascade. C1 Univ Colorado, Hlth Sci Ctr Fitzsimons, Dept Pharmacol, Aurora, CO 80045 USA. Denver Vet Affairs Med Ctr, Denver, CO 80262 USA. RP Heidenreich, KA (reprint author), Univ Colorado, Hlth Sci Ctr Fitzsimons, Dept Pharmacol, POB 6511,Mail Stop 8303, Aurora, CO 80045 USA. EM Kim.Heidenreich@UCHSC.edu FU NIDDK NIH HHS [P30-DK57516]; NINDS NIH HHS [NS38619] NR 39 TC 239 Z9 252 U1 0 U2 4 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 3 PY 2004 VL 24 IS 44 BP 9993 EP 10002 DI 10.1523/JNEUROSCI.2057-04.2004 PG 10 WC Neurosciences SC Neurosciences & Neurology GA 867VC UT WOS:000224869600030 PM 15525785 ER PT J AU Maeder, M Klein, M Fehr, T Rickli, H AF Maeder, M Klein, M Fehr, T Rickli, H TI Contrast nephropathy: Review focusing on prevention SO JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY LA English DT Review ID ACUTE-RENAL-FAILURE; RANDOMIZED CONTROLLED-TRIAL; RADIOCONTRAST-INDUCED NEPHROPATHY; AGENT-ASSOCIATED NEPHROTOXICITY; HIGH-RISK PATIENTS; CYSTATIN-C LEVELS; CORONARY-ANGIOGRAPHY; N-ACETYLCYSTEINE; SERUM CREATININE; CARDIAC-CATHETERIZATION AB Contrast nephropathy (CN) accounts for significant morbidity and mortality. Patients with pre-existing renal insufficiency, especially those with diabetic nephropathy, are at particular risk. Medullary hypoxia due to decreased renal blood flow and direct cytotoxicity contribute to the pathogenesis. Contrast nephropathy is usually defined as an increase in serum creatinine concentration >0.5 mg/dl or 25% above the baseline level within 48 h. Intravenous hydration (saline 0.45%, if tolerated 0.9% at a rate of 1 ml/kg/h) 12 h before and after contrast exposure and the use of low or iso-osmolality contrast agents are advisable. The benefit of low-dose dopamine as well as the selective dopamine-1 receptor agonist fenoldopam is unproven. Studies on the effectiveness of the adenosine antagonist theophylline have led to conflicting results. Because theophylline has a narrow therapeutic range and may be associated with adverse effects, it is not a prophylactic agent of first choice. The administration of N-acetylcysteine (NAC) has been evaluated in several trials with inconsistent results. Newer data suggest a benefit of high-dose NAC (1,200 mg twice daily) for patients receiving high doses (>140 ml) of contrast agent, or those with advanced renal insufficiency (creatinine >2.5 mg/dl). Whereas prophylactic hemodialysis does not prevent CN, a recent study demonstrated a marked benefit of prophylactic hemofiltration. (C) 2004 by the American College of Cardiology Foundation. C1 Kantonsspital, Div Cardiol, Dept Internal Med, CH-9007 St Gallen, Switzerland. Kantonsspital, Div Gen Internal Med, Dept Internal Med, CH-9007 St Gallen, Switzerland. Massachusetts Gen Hosp, Transplantat Biol Res Ctr, Boston, MA 02114 USA. RP Maeder, M (reprint author), Kantonsspital, Div Cardiol, Dept Internal Med, Rorschacherstr 95, CH-9007 St Gallen, Switzerland. EM micha.maeder@kssg.ch NR 66 TC 128 Z9 138 U1 1 U2 5 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 2 PY 2004 VL 44 IS 9 BP 1763 EP 1771 DI 10.1016/j.jacc.2004.06.075 PG 9 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA 866OF UT WOS:000224782100001 PM 15519005 ER PT J AU Wong, SL Zhang, LV Tong, AHY Li, ZJ Goldberg, DS King, OD Lesage, G Vidal, M Andrews, B Bussey, H Boone, C Roth, FP AF Wong, SL Zhang, LV Tong, AHY Li, ZJ Goldberg, DS King, OD Lesage, G Vidal, M Andrews, B Bussey, H Boone, C Roth, FP TI Combining biological networks to predict genetic interactions SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article ID PROTEIN-PROTEIN INTERACTIONS; SACCHAROMYCES-CEREVISIAE; DROSOPHILA-MELANOGASTER; SYNTHETIC LETHALITY; DUPLICATE GENES; YEAST; EXPRESSION; EVOLUTION; COMPLEXES; MAP AB Genetic interactions define overlapping functions and compensatory pathways. In particular, synthetic sick or lethal (SSL) genetic interactions are important for understanding how an organism tolerates random mutation, i.e., genetic robustness. Comprehensive identification of SSL relationships remains far from complete in any organism, because mapping these networks is highly labor intensive. The ability to predict SSL interactions, however, could efficiently guide further SSL discovery. Toward this end, we predicted pairs of SSL genes in Saccharomyces cerevisiae by using probabilistic decision trees to integrate multiple types of data, including localization, mRNA expression, physical interaction, protein function, and characteristics of network topology. Experimental evidence demonstrated the reliability of this strategy, which, when extended to human SSL interactions, may prove valuable in discovering drug targets for cancer therapy and in identifying genes responsible for multigenic diseases. C1 Harvard Univ, Sch Med, Dept Biol Chem & Mol Pharmacol, Boston, MA 02115 USA. Univ Toronto, Banting & Best Dept Med Res, Toronto, ON M5G 1L6, Canada. Univ Toronto, Dept Med Genet & Microbiol, Toronto, ON M5G 1L6, Canada. McGill Univ, Dept Biol, Montreal, PQ H3A 1B1, Canada. Harvard Univ, Sch Med, Dana Farber Canc Inst, Boston, MA 02115 USA. Harvard Univ, Sch Med, Dept Genet, Boston, MA 02115 USA. RP Roth, FP (reprint author), Harvard Univ, Sch Med, Dept Biol Chem & Mol Pharmacol, 250 Longwood Ave, Boston, MA 02115 USA. EM fritz_roth@hms.harvard.edu RI Roth, Frederick/H-6308-2011; OI Roth, Frederick/0000-0002-6628-649X NR 45 TC 143 Z9 149 U1 2 U2 4 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 2 PY 2004 VL 101 IS 44 BP 15682 EP 15687 DI 10.1073/pnas.0406614101 PG 6 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA 868OG UT WOS:000224922300026 PM 15496468 ER PT J AU Herrlich, A Leitch, V King, LS AF Herrlich, A Leitch, V King, LS TI Role of proneuregulin 1 cleavage and human epidermal growth factor receptor activation in hypertonic aquaporin induction SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE cell volume; epithelium; osmotic stress; proteolytic cleavage; extracellular signal-regulated kinase ID AIRWAY SURFACE FLUID; GENE-EXPRESSION; MAP KINASE; SIGNAL-TRANSDUCTION; HYPEROSMOTIC SHOCK; EPITHELIAL-CELLS; STRESS; PROTEIN; LIGAND; NEUREGULIN AB Mammalian cells. are confronted with changes in extracellular osmolality at various sites, including the aqueous layer above the lung epithelium. Hypertonic shock induces the activation of mitogen-activated protein kinases and the expression of a defined set of genes, including aquaporins. We investigated upstream components of the response to hypertonicity in lung epithelial cells and found that before extracellular signal-regulated kinase activation and aquaporin synthesis, the membrane-bound prohormone neuregulin 1-beta is cleaved and binds to human epidermal growth factor receptor 3 (HER3). The signaling is prevented by matrix metalloproteinase inhibition, inhibition of neuregulin 1-beta binding to HER3, and inhibition of HER tyrosine kinase activity. Inhibition of HER activation interferes with the hypertonic induction of two different aquaporins in three distinct cell lines of mouse and human origin. We propose that ligand-dependent HER activation constitutes a generalized signaling principle in the mammalian hypertonic stress response relevant to aquaporin expression. C1 Massachusetts Gen Hosp, Renal Unit, Boston, MA 02114 USA. MIT, Whitehead Inst Biomed Res, Cambridge, MA 02142 USA. Johns Hopkins Univ, Sch Med, Div Pulm & Crit Care Med, Baltimore, MD 21224 USA. Johns Hopkins Univ, Sch Med, Dept Med, Baltimore, MD 21224 USA. Johns Hopkins Univ, Sch Med, Dept Biol Chem, Baltimore, MD 21224 USA. RP King, LS (reprint author), Johns Hopkins Asthma & Allergy Ctr, 4B-64,5501 Hopkins Bayview Circle, Baltimore, MD 21224 USA. EM lsking@jhmi.edu FU NHLBI NIH HHS [HL 70217, R01 HL070217] NR 59 TC 14 Z9 14 U1 0 U2 0 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 2 PY 2004 VL 101 IS 44 BP 15799 EP 15804 DI 10.1073/pnas.04068543101 PG 6 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA 868OG UT WOS:000224922300046 PM 15498868 ER PT J AU Vozenilek, J Huff, JS Reznek, M Gordon, JA AF Vozenilek, J Huff, JS Reznek, M Gordon, JA TI See one, do one, teach one: Advanced technology in medical education SO ACADEMIC EMERGENCY MEDICINE LA English DT Article; Proceedings Paper CT 2004 AEM Consensus Conference CY MAY 15, 2004 CL Orlando, FL SP AEM DE medical education; Web-based education; virtual reality; patient simulation ID HIGH-FIDELITY SIMULATION; EMERGENCY-MEDICINE; VIRTUAL-REALITY; ENVIRONMENT; COMPETENCE; INFORMATION; REVOLUTION; MANAGEMENT; RESIDENTS; KNOWLEDGE AB The concept of "learning by doing" has become less acceptable, particularly when invasive procedures and high-risk care are required. Restrictions on medical educators have prompted them to seek alternative methods to teach medical knowledge and gain procedural experience. Fortunately, the last decade has seen an explosion of the number of tools available to enhance medical education: web-based education, virtual reality, and high fidelity patient simulation. This paper presents some of the consensus statements in regard to these tools agreed upon by members of the Educational Technology Section of the 2004 AEM Consensus Conference for Informatics and Technology in Emergency Department Health Care, held in Orlando, Florida. Findings: Web-based teaching: 1) Every ED should have access to medical educational materials via the Internet, computer-based training, and other effective education methods for point-of-service information, continuing medical education, and training. 2) Real-time automated tools should be integrated into Emergency Department Information Systems [EDIS] for contemporaneous education. Virtual reality [VR]: 1) Emergency physicians and emergency medicine societies should become more involved in VR development and assessment. 2) Nationally accepted protocols for the proper assessment of VR applications should be adopted and large multi-center groups should be formed to perform these studies. High-fidelity simulation: Emergency medicine residency programs should consider the use of high-fidelity patient simulators to enhance the teaching and evaluation of core competencies among trainees. Conclusions: Across specialties, patient simulation, virtual reality and the Web will soon enable medical students and residents to... see one, simulate many, do one competently, and teach everyone. C1 Simulat Technol Acad & Res, Evanston Northwestern Hlth Care Ctr, Div Emergency Med, Evanston, IL 60201 USA. Univ Virginia, Hlth Sci Ctr, Dept Emergency Med, Charlottesville, VA USA. Wayne State Univ, Detroit Receiving Hosp, Dept Emergency Med, Detroit, MI USA. Massachusetts Gen Hosp, Dept Emergency Med, Boston, MA USA. Harvard Univ, Sch Med, GS Beckwith Gilbert & Katharine S Gilbert Med Edu, Boston, MA USA. RP Vozenilek, J (reprint author), Simulat Technol Acad & Res, Evanston Northwestern Hlth Care Ctr, Div Emergency Med, 2650 Ridge Ave, Evanston, IL 60201 USA. EM vozonline@ameritech.net OI Vozenilek, John/0000-0001-7955-4089 NR 44 TC 99 Z9 107 U1 5 U2 18 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 2004 VL 11 IS 11 BP 1149 EP 1154 DI 10.1197/j.aem.2004.08.003 PG 6 WC Emergency Medicine SC Emergency Medicine GA 870WG UT WOS:000225088900008 PM 15528578 ER PT J AU Schwamm, LH Rosenthal, ES Hirshberg, A Schaefer, PW Little, EA Kvedar, JC Petkovska, I Koroshetz, WJ Levine, SR AF Schwamm, LH Rosenthal, ES Hirshberg, A Schaefer, PW Little, EA Kvedar, JC Petkovska, I Koroshetz, WJ Levine, SR TI Virtual TeleStroke support for the emergency department evaluation of acute stroke SO ACADEMIC EMERGENCY MEDICINE LA English DT Article DE stroke consultation; TeleStroke; tPA; videoconference; telemedicine ID ACUTE ISCHEMIC-STROKE; TISSUE-PLASMINOGEN ACTIVATOR; TELEMEDICINE; RELIABILITY; TELENEUROLOGY; SCALE C1 Massachusetts Gen Hosp, Dept Neurol, Boston, MA 02114 USA. Massachusetts Gen Hosp, Dept Radiol, Boston, MA 02114 USA. Massachusetts Gen Hosp, Dept Telemed, Boston, MA 02114 USA. Marthas Vineyard Hosp, Dept Emergency Med, Oak Bluffs, MA USA. Mt Sinai Sch Med, Dept Neurol, New York, NY 10029 USA. RP Schwamm, LH (reprint author), Massachusetts Gen Hosp, Dept Neurol, VBK 915, Boston, MA 02114 USA. EM lschwamm@partners.org OI Schwamm, Lee/0000-0003-0592-9145 NR 11 TC 101 Z9 101 U1 0 U2 4 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 2004 VL 11 IS 11 BP 1193 EP 1197 DI 10.1197/j.aem.2004.08.014 PG 5 WC Emergency Medicine SC Emergency Medicine GA 870WG UT WOS:000225088900014 PM 15528584 ER PT J AU Hoh, BL Curry, WT Carter, BS Ogilvy, CS AF Hoh, BL Curry, WT Carter, BS Ogilvy, CS TI Computed tomographic demonstrated infarcts after surgical and endovascular treatment of aneurysmal subarachnoid hemorrhage SO ACTA NEUROCHIRURGICA LA English DT Article DE aneurysm; computed tomography; endovascular; subarachnoid hemorrhage; stroke; surgery ID DETACHABLE COIL EMBOLIZATION; CEREBRAL VASOSPASM; INTRACRANIAL ANEURYSMS; MANAGEMENT; RISK AB Background. Cerebral infarction is a sequela of vasospasm. Other etiologies for infarction after subarachnoid hemorrhage (SAH), however, have not been well-studied. To determine the incidence and etiologies for infarction after SAH, we reviewed the head CT scans of all SAH patients at our center from 1993-2000. Methods. From 1993-2000, 679 consecutive patients were admitted with SAH, of which 619 patients underwent surgical or endovascular treatment. Two reviewers examined the head CT scans of all 619 patients for new infarct. Clinical outcome was collected from a prospective database. Findings. 505 patients were treated with surgical clipping; 114 with endovascular coiling. There were CT findings of new infarct in 189 patients (30%): 140 in the surgical group (28%) and 49 in the endovascular group (43%). The etiologies for infarct in the surgical group were vasospasm 79 (15%), perforator occlusion 40 (8%), large vessel occlusion 14 (3%), elevated intracranial pressure 4 (1%), thromboembolism 2 (0.4%), and systemic hypotension 1 (0.2%). Infarcts in the endovascular group were due to vasospasm 20 (18%), thromboembolism 12 (11%), large vessel occlusion/dissection 9 (8%), elevated intracranial pressure 4 (4%), perforator occlusion 3 (3%), and systemic hypotension 1 (1%). Hunt Hess Grade (P<0.001), Fisher Score (P<0.0001), and MGH Grade (P<0.001) were significantly associated with CT-demonstrated infarct. There was no significant difference in incidence of CT-infarcts when the period 1993-1996 was compared to 1997-2000. Conclusions. Despite advances in the treatment of SAH, there is still a significant incidence of associated radiographic infarcts. Hunt Hess Grade, Fisher Score, and MGH Grade were significantly associated with CT-demonstrated infarct. C1 Harvard Univ, Massachusetts Gen Hosp, Sch Med, Brain Aneurysm AVM Ctr,Neurosurg Serv, Boston, MA 02114 USA. RP Hoh, BL (reprint author), Harvard Univ, Massachusetts Gen Hosp, Sch Med, Brain Aneurysm AVM Ctr,Neurosurg Serv, VBK-710,55 Fruit St, Boston, MA 02114 USA. NR 18 TC 30 Z9 31 U1 0 U2 0 PU SPRINGER WIEN PI VIENNA PA SACHSENPLATZ 4-6, PO BOX 89, A-1201 VIENNA, AUSTRIA SN 0001-6268 J9 ACTA NEUROCHIR JI Acta Neurochir. PD NOV PY 2004 VL 146 IS 11 BP 1177 EP 1183 DI 10.1007/s00701-004-0349-6 PG 7 WC Clinical Neurology; Surgery SC Neurosciences & Neurology; Surgery GA 864ES UT WOS:000224617300002 PM 15349755 ER PT J AU Berg, MB Mimiaga, MJ Safren, SA AF Berg, MB Mimiaga, MJ Safren, SA TI Mental health concerns of HIV-infected gay and bisexual men seeking mental health services: An observational study SO AIDS PATIENT CARE AND STDS LA English DT Article ID PROTEASE INHIBITORS; ALCOHOL-USE; PREDICTORS; ADHERENCE; PREVALENCE; WOMEN; RISK; AIDS; MEDICATION; DEPRESSION AB Addressing mental health concerns of HIV-positive individuals is an important component of providing quality HIV care. Mental health intake information from patients with HIV can be an important source of data to complement existing research on HIV and mental health because the intake information contains concerns that are both from the perspective of the patients and are significant enough to bring them into treatment. The current study describes the mental health intake information of HIV-positive men who have sex with men (MSM) at an urban community health clinic over a 1-year period. This information included presenting problems, current symptoms from a symptom checklist, ratings of impairments in functioning, and client histories (e. g., substance abuse, emotional, physical, and sexual abuse, previous treatment). It also included clinicians' Diagnostic and Statistical Manual of Mental Disorders, 4th edition (DSM-IV) diagnoses of the participants, and recommended treatments. Depression was the most prevalent presenting problem (58.1% of clients), followed by anxiety (38.2%). Consistently, depression (96.3%) and low energy (78.2%) were the most frequently endorsed symptoms on a symptom checklist, followed by anxiety (69.2%). HIV-specific problems also played a large role both directly, as a presenting problem, and indirectly as they related to such concerns as relationship issues. Axis I diagnoses included adjustment disorders (50.0%), major depressive disorder (21.4%), and dysthymia (a less severe but more chronic depression) (8.9%). This review highlights the mental health issues that HIV-positive MSM feel are significant enough to require treatment. Because mental health is a key component of overall quality of life, HIV providers who work with MSM can use these data to increase awareness of the types of mental concerns that are most distressing to this population. C1 Harvard Univ, Sch Med, Massachusetts Gen Hosp, Psychiat Dept,ACC 812, Boston, MA 02114 USA. Wheaton Coll, Norton, MA 02766 USA. Fenway Community Hlth, Boston, MA USA. Harvard Univ, Sch Publ Hlth, Boston, MA 02115 USA. RP Safren, SA (reprint author), Harvard Univ, Sch Med, Massachusetts Gen Hosp, Psychiat Dept,ACC 812, 15 Parkman St, Boston, MA 02114 USA. EM ssafren@partners.org FU NIMH NIH HHS [MH 66660] NR 32 TC 26 Z9 27 U1 1 U2 3 PU MARY ANN LIEBERT INC PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 USA SN 1087-2914 J9 AIDS PATIENT CARE ST JI Aids Patient Care STDS PD NOV PY 2004 VL 18 IS 11 BP 635 EP 643 DI 10.1089/apc.2004.18.635 PG 9 WC Public, Environmental & Occupational Health; Infectious Diseases SC Public, Environmental & Occupational Health; Infectious Diseases GA 875CE UT WOS:000225396500003 PM 15633261 ER EF