FN Thomson Reuters Web of Science™ VR 1.0 PT J AU Brown, AF Gregg, EW Stevens, MR Karter, A Weinberger, M Safford, MM Gary, TL Caputo, DA Waitzfelder, B Kim, C Beckles, GL AF Brown, AF Gregg, EW Stevens, MR Karter, A Weinberger, M Safford, MM Gary, TL Caputo, DA Waitzfelder, B Kim, C Beckles, GL TI Race, ethnicity, socioeconomic position, and quality of care for adults with diabetes enrolled in managed care: the Translating Research Into Action for Diabetes (TRIAD) study SO DIABETES CARE LA English DT Article ID RACIAL-DIFFERENCES; GLYCEMIC CONTROL; RACIAL/ETHNIC DIFFERENCES; AFRICAN-AMERICANS; US ADULTS; POPULATION; DISPARITIES; MORTALITY; RETINOPATHY; HEALTH AB OBJECTIVE - To examine racial/ethnic and socioeconomic variation in diabetes care in managed-care settings. RESEARCH DESIGN AND METHODS - We studied 7,456 adults enrolled in health plans participating in the Translating Research Into Action for Diabetes study, a six-center cohort study of diabetes in managed care. Cross-sectional analyses using hierarchical regression models assessed processes of care (HbA(1C) [A1C], lipid, and proteinuria assessment; foot and dilated eye examinations; use or advice to use aspirin-, and influenza vaccination) and intermediate health outcomes (A1C, LDL, and blood pressure control). RESULTS - Most quality indicators and intermediate outcomes were comparable across race/ethnicity and socioeconomic position (SEP). Latinos and Asians/Pacific Islanders had similar or better processes and intermediate outcomes than whites with the exception of slightly higher A1C levels. Compared with whites, African Americans had lower rates of A1C and LDL measurement and influenza vaccination, higher rates of foot and dilated eye examinations, and the poorest blood pressure and lipid control. The main SEP difference was lower rates of dilated eye examinations among poorer and less educated individuals. In almost all instances, racial/ethnic minorities or low SEP participants with poor glycemic, blood pressure, and lipid control received similar or more appropriate intensification of therapy relative to whites or those with higher SEP. CONCLUSIONS - In these managed-care settings, minority race/ethnicity was not consistently associated With worse processes or outcomes, and not all differences favored whites. The only notable SEP disparity was in rates of dilated eye examinations. Social disparities in health may be reduced in managed-care settings. C1 Univ Calif Los Angeles, David Geffen Sch Med, Dept Med, Div Gen Internal Med & Hlth Serv Res, Los Angeles, CA 90095 USA. Ctr Dis Control & Prevent, Atlanta, GA USA. Kaiser Permanente, Div Res, Oakland, CA USA. Univ N Carolina, Dept Hlth Policy & Adm, Chapel Hill, NC USA. Durham VAMC, Ctr Hlth Serv Res Primary Care, Durham, NC USA. Birmingham VA Med Ctr, Deep S Ctr Effectiveness, Birmingham, AL USA. Univ Alabama, Dept Prevent Med, Birmingham, AL USA. Johns Hopkins Univ, Bloomberg Sch Publ Hlth, Dept Epidemiol, Baltimore, MD USA. Univ Med & Dent New Jersey, New Brunswick, NJ USA. Pacific Hlth Res Inst, Honolulu, HI USA. Univ Michigan, Dept Med, Ann Arbor, MI 48109 USA. Univ Michigan, Dept Obstet Gynecol, Ann Arbor, MI 48109 USA. RP Brown, AF (reprint author), Univ Calif Los Angeles, David Geffen Sch Med, Dept Med, Div Gen Internal Med & Hlth Serv Res, Los Angeles, CA 90095 USA. EM abrown@mednet.ucla.edu FU NIA NIH HHS [AG 02004] NR 44 TC 114 Z9 114 U1 0 U2 2 PU AMER DIABETES ASSOC PI ALEXANDRIA PA 1701 N BEAUREGARD ST, ALEXANDRIA, VA 22311-1717 USA SN 0149-5992 J9 DIABETES CARE JI Diabetes Care PD DEC PY 2005 VL 28 IS 12 BP 2864 EP 2870 DI 10.2337/diacare.28.12.2864 PG 7 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA 988HJ UT WOS:000233583500008 PM 16306546 ER PT J AU Nagle, JA Wilbur, DC Pitman, MB AF Nagle, JA Wilbur, DC Pitman, MB TI Cytomorphology of gastric and duodenal epithelium and reactivity to B72.3: A baseline for comparison to pancreatic lesions aspirated by EUS-FNAB SO DIAGNOSTIC CYTOPATHOLOGY LA English DT Article DE gastrointestinal contamination; endoscopic ultrasound-guided fine-needle aspiration biopsy; pancreas; B72.3 ID FINE-NEEDLE-ASPIRATION; MUCINOUS TUMORS; CYTOLOGY AB Endoscopic ultrasound-guided fine-needle aspiration biopsy (EUS-FNAB) has become a widely used method of pre-operatively evaluating pancreatic masses. This technique introduces gastrointestinal contamination into the specimen, which poses a diagnostic pitfall. The cytomorphologic features of these contaminants have not been fully characterized. The current study was designed to systematically document the cytomorphology of gastric and duodenal epithelium on fixed and air-dried smears, as well as ThinPrep((R)) (TP) preparations, and to assess the reactivity of the epithelial cells to the tumor marker B72.3 so as to establish a baseline for future comparative studies with EUS-FNAB of the pancreas. Air-dried and fixed smears and TP specimens were obtained using a cytobrush from gastric (GM) and duodenal (DM) mucosa from 14 Whipple specimens. Cytologic features of cell architecture, cellular features and smear background were analysed. Immunocytochemical staining with B72.3 was performed in 10114 cases. Mucin was present in all preparations except one case from the duodenum. It was consistently present as isolated thick to thin clumps but never as diffuse 'colloid-type' mucin; it was most prominent on air-dried smears, and most abundant from the GM. Epithelial cells were admixed with mucin, but degenerated cells and inflammation were not present within the mucin. Mucin on TP appeared as fragmented wisps of pale blue staining material. Background inflammation and debris were not significant findings. The epithelial cells were arranged in large and small monolayered sheets. Smaller groups were more common from GM on smears and more abundant on TP than smears. Luminal edges (DM > GM) were a prominent feature, with a brush border noted in DM. The nuclei of GM and DM were round, evenly spaced and without atypia, and dense, non-vacuolated cytoplasm was the rule, with the exception of goblet cells and occasional gastric foveolar cells noted in one case. In both GM and DM, B72.3 stained goblet cells with a strong, coarsely granular pattern and stained epithelial cells focally in a finely granular, punctate, perinuclear distribution; mucin also stained strongly in all cases. These baseline characteristics provide a template for assessing mucin and epithelial GM and DM contamination on pancreatic EUS-FNAB specimens. C1 Harvard Univ, Dept Pathol, Sch Med, Massachusetts Gen Hosp, Boston, MA 02114 USA. RP Pitman, MB (reprint author), Harvard Univ, Dept Pathol, Sch Med, Massachusetts Gen Hosp, 55 Fruit St, Boston, MA 02114 USA. EM mpitman@partners.org NR 7 TC 20 Z9 21 U1 0 U2 0 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 8755-1039 J9 DIAGN CYTOPATHOL JI Diagn. Cytopathol. PD DEC PY 2005 VL 33 IS 6 BP 381 EP 386 DI 10.1002/dc.20343 PG 6 WC Medical Laboratory Technology; Pathology SC Medical Laboratory Technology; Pathology GA 990WB UT WOS:000233772800004 PM 16299750 ER PT J AU Enzinger, PC Kulke, MH Clark, JW Ryan, DP Kim, H Earle, CC Vincitore, MM Michelini, AL Mayer, RJ Fuchs, CS AF Enzinger, PC Kulke, MH Clark, JW Ryan, DP Kim, H Earle, CC Vincitore, MM Michelini, AL Mayer, RJ Fuchs, CS TI A phase II trial of irinotecan in patients with previously untreated advanced esophageal and gastric adenocarcinoma SO DIGESTIVE DISEASES AND SCIENCES LA English DT Article DE esophageal adenocarcinoma; gastric adenocarcinoma; irinotecan; chemotherapy; phase II trial ID GASTROESOPHAGEAL JUNCTION CARCINOMA; CONTACT-SENSITIVE PLATES; DNA TOPOISOMERASE-I; ANTITUMOR-ACTIVITY; 20(S)-CAMPTOTHECIN DERIVATIVES; CHEMICAL MODIFICATION; COLORECTAL-CARCINOMA; CANCER STATISTICS; PLUS CISPLATIN; CPT-11 AB Chemotherapy options for esophagogastric adenocarcinoma remain limited. Irinotecan has demonstrated broad activity in a variety of epithelial malignancies. Forty-six patients with previously untreated, measurable, unresectable, or metastatic esophagooastric adenocarcinoma were enrolled. Patients received irinotecan (125 mg/m(2) intravenously over 90 min weekly) for 4 consecutive weeks followed by a 2-week rest. Forty-three patients received at least one treatment and were evaluable for response and toxicity. One complete and five partial responses were observed, for an overall response rate of 14% (95% CI, 4-24%). Median survival for all 43 patients was 6.4 months (95% Cl, 4.6-8.2 months). Grade 3 to 4 toxicity included 10 patients (23%) with neutropenia, 13 patients (30%) with late diarrhea, 6 patients (14%) with vomiting, and 6 patients (14%) with fatigue. We conclude that although single-agent irinotecan is an active agent for esophagogastric adenocarcinoma, the schedule utilized in this trial is associated with moderate toxicity. When used as a single-agent, a triweekly schedule may be preferable for this patient population. C1 Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02115 USA. Dana Farber Canc Inst, Dept Biostat, Boston, MA 02115 USA. Massachusetts Gen Hosp, Div Hematol Oncol, Boston, MA 02114 USA. Brigham & Womens Hosp, Channing Lab, Boston, MA 02115 USA. RP Enzinger, PC (reprint author), Dana Farber Canc Inst, Dept Med Oncol, 44 Binney St, Boston, MA 02115 USA. EM Peter_Enzinger@dfci.harvard.edu NR 34 TC 26 Z9 28 U1 0 U2 0 PU SPRINGER PI DORDRECHT PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS SN 0163-2116 J9 DIGEST DIS SCI JI Dig. Dis. Sci. PD DEC PY 2005 VL 50 IS 12 BP 2218 EP 2223 DI 10.1007/s10620-005-3038-2 PG 6 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA 999HK UT WOS:000234380200006 PM 16416165 ER PT J AU McGory, ML Maggard, MA Kang, HJ O'Connell, JB Ko, CY AF McGory, ML Maggard, MA Kang, HJ O'Connell, JB Ko, CY TI Malignancies of the appendix: Beyond case series reports SO DISEASES OF THE COLON & RECTUM LA English DT Article; Proceedings Paper CT Annual Meeting of the American-Society-of-Colon-and-Rectal-Surgeons CY APR 30-MAY 05, 2005 CL Philadelphia, PA SP Amer Soc Colon & Rectal Surg DE appendiceal carcinoma; carcinoid; noncarcinoid; outcomes; surveillance; epidemiology and end results (SEER) ID CARCINOID-TUMORS; RIGHT HEMICOLECTOMY; PERITONEAL DISSEMINATION; MANAGEMENT; SURGERY; ADENOCARCINOMA; THERAPY AB PURPOSE: A comprehensive analysis was performed for five histologic types of appendiceal tumors to compare incidence, clinicopathologic features, survival, and appropriateness of surgery. METHODS: All patients diagnosed with mucinous adenocarcinoma (n = 951), adenocarcinoma (n 646), carcinoid (n = 435), goblet (n = 369), and signet-ring cell (n = 113) in the Surveillance, Epidemiology, and End Results database (1973-2001) were analyzed. Evaluation of incidence, stage, and five-year relative survival were determined for each histology. The appropriateness of the operative procedure (i.e., appendectomy vs. colectomy) was examined by tumor type and size. RESULTS: Tumor incidence, patient demographics, survival outcomes, and appropriateness of surgery varied significantly among the different appendiceal tumor histologies. The most common appendiceal tumors were mucinous. With regard to patient demographics, carcinoids presented at an earlier mean age of 41 years and 71 percent were female (P < 0.001 for both). Overall five-year survival was highest for carcinoid (83 percent) and lowest for signet ring (18 percent). Although current guidelines specify that a right hemicolectomy (rather than an appendectomy) be performed for all noncarcinoid tumors and carcinoid tumors >2 cm, we found that 30 percent of noncarcinoids underwent appendectomv. Similarly, 28 percent of carcinoids >2 cm underwent appendectomy, which is a lesser resection than is indicated. CONCLUSIONS: This study provides a population-based analysis of epidemiology, tumor characteristics, survival, and quality of care for appendiceal carcinomas. This characterization provides a novel description of the presentation and outcomes for malignancies of the appendix and highlights that it substantial number of patients with appendiceal tumors may not be receiving appropriate surgical resection. C1 Univ Calif Los Angeles, David Geffen Sch Med, Dept Surg, Hlth Sci Ctr, Los Angeles, CA 90095 USA. Daehang Hosp, Dept Surg, Seoul, South Korea. VA Greater Los Angeles Healthcare Syst, Dept Surg, Los Angeles, CA USA. RP McGory, ML (reprint author), Univ Calif Los Angeles, David Geffen Sch Med, Dept Surg, Hlth Sci Ctr, 10833 Conte Ave,72-215,Box 956904, Los Angeles, CA 90095 USA. EM mmcgory@mednet.ucla.edu NR 24 TC 80 Z9 89 U1 0 U2 3 PU SPRINGER PI NEW YORK PA 233 SPRING STREET, NEW YORK, NY 10013 USA SN 0012-3706 J9 DIS COLON RECTUM JI Dis. Colon Rectum PD DEC PY 2005 VL 48 IS 12 BP 2264 EP 2271 DI 10.1007/s10-005-0196-4 PG 8 WC Gastroenterology & Hepatology; Surgery SC Gastroenterology & Hepatology; Surgery GA 990VW UT WOS:000233772300013 PM 16258711 ER PT J AU Gilbert, RJ Napadow, VJ AF Gilbert, RJ Napadow, VJ TI Three-dimensional muscular architecture of the human tongue determined in vivo with diffusion tensor magnetic resonance imaging SO DYSPHAGIA LA English DT Article DE lingual anatomy; myoarchitecture; magnetic resonance imaging; deglutition; deglutition disorders ID FIBER ARCHITECTURE; RESTRICTED DIFFUSION; WEIGHTED MRI; MUSCLE; TISSUE; WATER; FLOW; NMR; DEFORMATION; DEGLUTITION AB The myoarchitecture of the tongue is believed to consist of a complex network of interwoven fibers, which function together to produce a near limitless array of functional deformations. These deformations contribute mechanically to speech production and to oral cavity food handling during swallowing. We have previously imaged the 3D myoarchitecture of the mammalian tongue in excised tissue with diffusion tensor MRI, a technique which derives the 3D orientation of intramural fibers as a function of the extent. to which a direction-specific MR signal attenuates under diffusion-encoding magnetic gradients. The resulting 3D diffusion tensor defines the relative orientations of the myofiber populations within a region of tissue. In this study, we have extended the use of this method to assess lingual myoarchitecture in normal human subjects in vivo. Subjects Were imaged using a diffusion-sensitive stimulated-echo pulse sequence with single-shot echoplanar spatial encoding in the midsagittal plane. Differences in lingual fiber orientation were manifested by graduated changes in fiber direction throughout the tissue, without clear anatomical demarcations between regions of the tissue. The anterior tissue was:composed generally of orthogonally oriented fibers surrounded by an axially oriented ring of tissue, whereas the posterior portion of the tissue was composed mostly of fibers projecting in the superior and posterior directions. The bulk of the tissue displayed a highly homogeneous, vertically oriented set of fibers, including the anteroinferior region of the tissue and extending nearly to the superior surface. Further analysis of the tissue in terms of diffusion anisotropy demonstrated that the tissue could be represented by varying degrees of anisotropy, with a tendency toward high anisotropy in the dorsal and anteroventral periphery and low anisotropy in the central region of the tissue. These findings demonstrate that the muscular anatomy of the tongue can be displayed as a continuous array of structural units, or tensors, representing fibers of varying orientations throughout the tissue. C1 MIT, Dept Mech Engn, Cambridge, MA 02139 USA. Massachusetts Gen Hosp, Dept Radiol, Athinoula A Martinos Imaging Ctr, Boston, MA 02114 USA. RP Gilbert, RJ (reprint author), MIT, Dept Mech Engn, 77 Massachusetts Ave, Cambridge, MA 02139 USA. EM rgilbert@mit.edug NR 28 TC 25 Z9 26 U1 0 U2 7 PU SPRINGER PI NEW YORK PA 233 SPRING STREET, NEW YORK, NY 10013 USA SN 0179-051X J9 DYSPHAGIA JI Dysphagia PD WIN PY 2005 VL 20 IS 1 BP 1 EP 7 DI 10.1007/s000455-003-0505-9 PG 7 WC Otorhinolaryngology SC Otorhinolaryngology GA 908JX UT WOS:000227784400001 PM 15886960 ER PT J AU Saito, S Sidis, Y Mukherjee, A Xia, Y Schneyer, A AF Saito, S Sidis, Y Mukherjee, A Xia, Y Schneyer, A TI Differential biosynthesis and intracellular transport of follistatin isoforms and follistatin-like-3 SO ENDOCRINOLOGY LA English DT Article ID HORMONE-RELATED PROTEIN; ACTIVIN-BINDING PROTEIN; NUCLEAR; LOCALIZATION; TRAFFICKING; GENE; PROTEOGLYCANS; RECEPTORS; PATHWAYS; CELLS AB Follistatin (FST) and FST-like-3 (FSTL3) are structurally related proteins that bind and neutralize activin and closely related members of the TGF beta superfamily. Three FST isoforms (FST288, FST303, and FST315) are produced from the Fst gene that are primarily secreted proteins. FSTL3 is secreted, but is also observed within the nucleus of most cells. We used pulse-chase S-35 labeling to examine the biosynthetic and intracellular transport patterns that lead to differential secretion and intracellular retention of these proteins. Among the FST isoforms, FST315 was secreted fastest and FST288 was secreted more slowly, with some remaining intracellular. In contrast, FSTL3 was secreted the slowest, with newly synthesized proteins being both secreted and trafficked to the nucleus. This nuclear FSTL3 wasN-glycosylated, although not to the same degree as secreted FSTL3. Both FST and FSTL3 have two Mets in their signal sequence. Mutation of the first Met in FST288 eliminated protein translation, whereas FSTL3 could be translated from either Met. However, although FSTL3 translated from the second Met, which had no signal sequence, was confined to the nucleus, it was not glycosylated. Interestingly, this FSTL3 retained activin-antagonizing activity. Thus, although bioactive, nuclear FSTL3 can be translated from the second Met when the first Met is mutated, the glycosylated nuclear FSTL3 produced endogenously indicates that a different mechanism must be used under natural conditions that apparently includes N-glycosylation. Moreover, the differential biosynthetic and intracellular transport patterns for FST288 and FSTL3 suggest that these two activin-binding proteins may have distinct intracellular roles. C1 Harvard Univ, Sch Med, Massachusetts Gen Hosp, Reprod Endocrine Unit, Boston, MA 02114 USA. RP Schneyer, A (reprint author), Harvard Univ, Sch Med, Massachusetts Gen Hosp, Reprod Endocrine Unit, 55 Fruit St,BHX-5, Boston, MA 02114 USA. EM schneyer.alan@mgh.harvard.edu FU NICHD NIH HHS [R01-HD-39777]; NIDDK NIH HHS [R01-DK-55838] NR 27 TC 23 Z9 26 U1 0 U2 1 PU ENDOCRINE SOC PI CHEVY CHASE PA 8401 CONNECTICUT AVE, SUITE 900, CHEVY CHASE, MD 20815-5817 USA SN 0013-7227 J9 ENDOCRINOLOGY JI Endocrinology PD DEC PY 2005 VL 146 IS 12 BP 5052 EP 5062 DI 10.1210/en.2005-0833 PG 11 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA 984JY UT WOS:000233301000004 PM 16150905 ER PT J AU van Dijk, G de Vries, K Nyakas, C Buwalda, B Adage, T Kuipers, F Kas, MJH Adan, RAH Wilkinson, CW Thiele, TE Scheurink, AJW AF van Dijk, G de Vries, K Nyakas, C Buwalda, B Adage, T Kuipers, F Kas, MJH Adan, RAH Wilkinson, CW Thiele, TE Scheurink, AJW TI Reduced anorexigenic efficacy of leptin, but not of the melanocortin receptor agonist melanotan-II, predicts diet-induced obesity in rats SO ENDOCRINOLOGY LA English DT Article ID CORTICOTROPIN-RELEASING HORMONE; MELANOCYTE-STIMULATING HORMONE; HYPOTHALAMIC PARAVENTRICULAR NUCLEUS; FOOD-INTAKE; INSULIN SENSITIVITY; CENTRAL INFUSION; WEIGHT-LOSS; RESPONSES; NEURONS; EXPRESSION AB Leptin gains access to the central nervous system where it influences activity of neuronal networks involved in ingestive behavior, neuroendocrine activity, and metabolism. In particular, the brain melanocortin (MC) system is important in leptin signaling and maintenance of energy balance. Although leptin or MC receptor insensitivity has been proposed to be associated with obesity, the present study compared central leptin and MC receptor stimulation on some of the above-mentioned parameters and investigated whether these treatments predict proneness to diet-induced obesity (DIO) in out-bred Wistar rats. Third-cerebroventricular administration of equianorexigenic doses of leptin and of the MC agonist melanotan-II caused comparable increases in plasma ACTH and corticosterone levels and c-Fos-labeling in approximately 70% of paraventricular hypothalamic (PVN) neuronal cell bodies containing CRH. This reinforces involvement of paraventricular CRH neurons in the short-term neuroendocrine and ingestive effects of leptin and melanocortins. In the DIO prediction study, anorexigenic efficacy of melanotan-II was not correlated with any parameter linked to DIO but was highly correlated with MC in situ binding (with labeled [Nle(4),D-Phe(7)] alpha-MSH) as well as CRH immunoreactivity in the PVN of DIO rats. This suggests intricate relationships among MC signaling, the CRH system, and ingestive behavior unrelated to DIO. In the same animals, leptin's anorexigenic efficacy was not correlated with PVN MC in situ binding or CRH immunoreactivity but correlated inversely to post-DIO plasma leptin, liver weight, and abdominal adiposity, the latter being correlated to insulin resistance. Thus, differences in leptin but not MC signaling might underlie DIO, visceral obesity, and insulin resistance. C1 Ctr Biol, Dept Anim Physiol, NL-9751 NN Haren, Netherlands. Univ Groningen, Med Ctr, Dept Pediat, Ctr Liver Pediat Digest & Metab Dis, NL-9747 AG Groningen, Netherlands. Semmelweis Univ, Hungarian Acad Sci, Brain Physiol Res Grp, H-1085 Budapest, Hungary. Univ Utrecht, Med Ctr, Dept Pharmacol & Anat, Rudolf Magnus Inst Neurosci, Utrecht, Netherlands. Univ Washington, Dept Psychiat & Behav Sci, Seattle, WA 98108 USA. Ctr Geriatr Res Educ & Clin, Vet Affairs Puget Sound Hlth Care Syst, Seattle, WA 98108 USA. Univ N Carolina, Dept Psychol, Chapel Hill, NC 27514 USA. RP van Dijk, G (reprint author), Kerklaan 30, NL-9751 NN Haren, Netherlands. EM gertjan.van.dijk@rug.nl RI Buwalda, Bauke/L-1427-2013; OI van Dijk, Gertjan/0000-0002-6565-4019 FU NIAAA NIH HHS [R01 AA013573, R01 AA015148, AA013573, AA015148] NR 66 TC 6 Z9 6 U1 0 U2 1 PU ENDOCRINE SOC PI CHEVY CHASE PA 8401 CONNECTICUT AVE, SUITE 900, CHEVY CHASE, MD 20815-5817 USA SN 0013-7227 J9 ENDOCRINOLOGY JI Endocrinology PD DEC PY 2005 VL 146 IS 12 BP 5247 EP 5256 DI 10.1210/en.2005-0472 PG 10 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA 984JY UT WOS:000233301000025 PM 16166222 ER PT J AU Rodriguez, L Tu, CL Cheng, ZQ Chen, TH Bikle, D Shoback, D Chang, WH AF Rodriguez, L Tu, CL Cheng, ZQ Chen, TH Bikle, D Shoback, D Chang, WH TI Expression and functional assessment of an alternatively spliced extracellular Ca2+-sensing receptor in growth plate chondrocytes SO ENDOCRINOLOGY LA English DT Article ID CALCIUM-SENSING RECEPTOR; BOVINE PARATHYROID CELLS; VITAMIN-D-RECEPTOR; FAMILIAL HYPOCALCIURIC HYPERCALCEMIA; NEONATAL SEVERE HYPERPARATHYROIDISM; MINERAL ION HOMEOSTASIS; N-LINKED GLYCOSYLATION; HUMAN CA2+ RECEPTOR; SKELETAL PHENOTYPE; SURFACE EXPRESSION AB The extracellular Ca-2 - sensing receptor (CaR) plays an essential role in mineral homeostasis. Studies to generate CaR-knockout (CaR-/-) mice indicate that insertion of a neomycin cassette into exon 5 of the mouse CaR gene blocks the expression of full-length CaRs. This strategy, however, allows for the expression of alternatively spliced CaRs missing exon 5 [(Exon5(-))CaRs]. These experiments addressed whether growth plate chondrocytes (GPCs) from CaR-/- mice express (Exon5(-)) CaRs and whether these receptors activate signaling. RT- PCR and immunocytochemistry confirmed the expression of (Exon5(-)) CaR in growth plates from CaR-/- mice. In Chinese hamster ovary or human embryonic kidney-293 cells, recombinant human (Exon5(-)) CaRs failed to activate phospholipase C likely due to their inability to reach the cell surface as assessed by intact-cell ELISA and immunocytochemistry. Human (Exon5(-)) CaRs, however, trafficked normally to the cell surface when overexpressed in wild-type or CaR-/- GPCs. Immunocytochemistry of growth plate sections and cultured GPCs from CaR-/- mice showed easily detectable cell-membrane expression of endogenous CaRs (presumably (Exon5(-)) CaRs), suggesting that trafficking of this receptor form to the membrane can occur in GPCs. In GPCs from CaR-/- mice, high extracellular [Ca2+] ([Ca2+](e)) increased inositol phosphate production with a potency comparable with that of wild-type GPCs. Raising [Ca2+](e) also promoted the differentiation of CaR-/- GPCs as indicated by changes in proteoglycan accumulation, mineral deposition, and matrix gene expression. Taken together, our data support the idea that expression of (Exon5(-)) CaRs may compensate for the loss of full-length CaRs and be responsible for sensing changes in [Ca2+](e) in GPCs in CaR-/- mice. C1 Univ Calif San Francisco, Endocrine Res Unit, San Francisco Vet Affairs Med Ctr, Dept Vet Affairs Med Ctr,Dept Med, San Francisco, CA 94121 USA. RP Chang, WH (reprint author), Univ Calif San Francisco, Endocrine Res Unit, San Francisco Vet Affairs Med Ctr, Dept Vet Affairs Med Ctr,Dept Med, 111N,4150 Clement St, San Francisco, CA 94121 USA. EM bambam@itsa.ucsf.edu FU NIA NIH HHS [AG-21353]; NIAMS NIH HHS [AR-050662] NR 53 TC 51 Z9 53 U1 0 U2 0 PU ENDOCRINE SOC PI WASHINGTON PA 2055 L ST NW, SUITE 600, WASHINGTON, DC 20036 USA SN 0013-7227 EI 1945-7170 J9 ENDOCRINOLOGY JI Endocrinology PD DEC PY 2005 VL 146 IS 12 BP 5294 EP 5303 DI 10.1210/en.2005-0256 PG 10 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA 984JY UT WOS:000233301000030 PM 16166224 ER PT J AU Ao, Y Toy, N Song, MK Go, VLW Yang, H AF Ao, Y Toy, N Song, MK Go, VLW Yang, H TI Altered glucose and insulin responses to brain medullary thyrotropin-releasing hormone (TRH)-induced autonomic activation in type 2 diabetic Goto-Kakizaki rats SO ENDOCRINOLOGY LA English DT Article ID DORSAL VAGAL COMPLEX; ISLET BLOOD-FLOW; RAPHE PALLIDUS NEURONS; GASTRIC-ACID-SECRETION; NERVOUS-SYSTEM; GK-RAT; PHYSIOPHARMACOLOGICAL INVESTIGATIONS; STIMULATED HYPERGLYCEMIA; URETHANE ANESTHESIA; INTRACISTERNAL TRH AB Insulin secretion is impaired in type 2 diabetes (T2D). The insulin and glucose responses to central autonomic activation induced by excitation of brain medullary TRH receptors were studied in T2D Goto-Kakizaki (GK) rats. Blood glucose levels in normally fed, pentobarbital-anesthetized GK and nondiabetic Wistar rats were 193 and 119 mg/100 ml in males and 214 and 131 mg/100 ml in females. Intracisternal injection (ic) of the stable TRH analog RX 77368 (10 ng) induced significantly higher insulin response in both genders of overnight-fasted GK rats compared with Wistar rats and slightly increased blood glucose in female Wistar rats but significantly decreased it from 193 to 145 mg/100 ml in female GK rats. RX 77368 (50 ng) ic induced markedly greater glucose and relatively weaker insulin responses in male GK rats than Wistar rats. Bilateral vagotomy blocked ic RX 77368-induced insulin secretion, whereas adrenalectomy abolished its hyperglycemic effect. In adrenalectomized male GK but not Wistar rats, ic RX 77368 (50 ng) dramatically increased serum insulin levels by 6.5-fold and decreased blood glucose levels from 154 to 98 mg/100 ml; these changes were prevented by vagotomy. GK rats had higher basal pancreatic insulin II mRNA levels but a lower response to ic RX 77368 (50 ng) compared with Wistar rats. These results indicate that central-vagal activation-induced insulin secretion is susceptible in T2D GK rats. However, the dominant sympathetic-adrenal response to medullary TRH plays a suppressing role on vagal-mediated insulin secretion. This unbalanced vago-sympathetic activation by medullary TRH may contribute to the impaired insulin secretion in T2D. C1 Univ Calif Los Angeles, Digest Dis Res Ctr, Ctr Ulcer Res & Educ, Dept Med,Div Digest Dis & Brain Res Inst, Los Angeles, CA 90073 USA. Vet Affairs Greater Los Angeles Healthcare Syst, Dept Vet Affairs, Los Angeles, CA 90073 USA. RP Yang, H (reprint author), Univ Calif Los Angeles, Digest Dis Res Ctr, Ctr Ulcer Res & Educ, Dept Med,Div Digest Dis & Brain Res Inst, Vet Affairs Greater Los Angeles Healthcare Syst B, Los Angeles, CA 90073 USA. EM hoyang@ucla.edu FU NIDDK NIH HHS [DK-41301] NR 57 TC 8 Z9 8 U1 0 U2 1 PU ENDOCRINE SOC PI CHEVY CHASE PA 8401 CONNECTICUT AVE, SUITE 900, CHEVY CHASE, MD 20815-5817 USA SN 0013-7227 J9 ENDOCRINOLOGY JI Endocrinology PD DEC PY 2005 VL 146 IS 12 BP 5425 EP 5432 DI 10.1210/en.2005-0553 PG 8 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA 984JY UT WOS:000233301000045 PM 16179412 ER PT J AU Handforth, A DeLorey, TM Homanics, GE Olsen, RW AF Handforth, A DeLorey, TM Homanics, GE Olsen, RW TI Pharmacologic evidence for abnormal thalamocortical functioning in GABA(A) receptor beta 3 subunit-deficient mice, a model of Angelman syndrome SO EPILEPSIA LA English DT Article DE Angelman; GABA receptor; ethosuximide; thalamus; electroencephalogram; seizures ID RECIPROCAL INHIBITORY CONNECTIONS; GENERALIZED ABSENCE SEIZURES; IN-VITRO; SYNCHRONIZED OSCILLATIONS; GAMMA-HYDROXYBUTYRATE; INDUCED CONVULSIONS; BETA(3) SUBUNIT; EPILEPSY; NUCLEUS; THALAMUS AB Purpose:gamma-Aminobutyric acid receptor (GABA(A)r) subunit beta 3-deficient mice model Angelman syndrome by displaying impaired learning, abnormal EEG with interictal spikes and slowing, myoclonus, and convulsions. The beta 3-subunit deficiency causes a failure of intrathalamic reticular nucleus inhibition, leading to abnormally synchronized thalamocortical oscillations. We postulated that this pathophysiology underlies the abnormal cortical EEG and triggers interictal spikes and seizures, but extrathalamic regions also contribute to interictal spikes and seizures, so that the EEG slowing should reveal an absence-like response profile, whereas spikes and seizures have dual responsiveness to absence and partial-seizure drugs. Methods: Recording electrodes were implanted over the parietal cortices of wild-type, heterozygotes, and homozygous null mice. In each experiment, EEG was recorded for 45 min, either drug or vehicle administered, and EEG recorded for another 3 h. Each EEG was scored for slow-wave activity, interictal spikes, and seizures by a reader blinded to treatments. Results: Interictal spiking and percentage of time in EEG slowing in heterozygotes were increased by the proabsence drug baclofen (GABA(B)-receptor agonist), whereas CGP 35348 (GABA(B)-receptor antagonist) had the opposite effect. The antiabsence drug ethosuximide markedly suppressed EEG slowing and interictal spiking in heterozygote and null mice. Broad-spectrum clonazepam and valproate were more effective on interictal spiking than on EEG slowing, and fosphenytoin suppressed only interictal spiking. Conclusions: The results suggest that this model of Angelman syndrome, although not expressing typical absence seizures, is characterized by hypersynchronous thalamocortical oscillations that possess absence-like pharmacologic responsiveness and promote EEG slowing, interictal spikes, and convulsive seizures. C1 VA Greater Los Angeles Healthcare Syst, Dept Neurol W127, Los Angeles, CA 90073 USA. Univ Calif Los Angeles, Dept Mol & Med Pharmacol, Los Angeles, CA USA. Univ Pittsburgh, Dept Anesthesiol, Pittsburgh, PA USA. Univ Pittsburgh, Dept Pharmacol, Pittsburgh, PA 15261 USA. Mol Res Inst, Mountain View, CA USA. RP Handforth, A (reprint author), VA Greater Los Angeles Healthcare Syst, Dept Neurol W127, 11301 Wilshire Blvd, Los Angeles, CA 90073 USA. EM charles.handforth@med.va.gov FU NIAAA NIH HHS [AA10422]; NIGMS NIH HHS [GM52035]; NINDS NIH HHS [NS28772, NS35985] NR 49 TC 12 Z9 12 U1 0 U2 2 PU BLACKWELL PUBLISHING PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DQ, OXON, ENGLAND SN 0013-9580 J9 EPILEPSIA JI Epilepsia PD DEC PY 2005 VL 46 IS 12 BP 1860 EP 1870 DI 10.1111/j.1528-1167.2005.00287.x PG 11 WC Clinical Neurology SC Neurosciences & Neurology GA 988CI UT WOS:000233568600001 PM 16393151 ER PT J AU Fujikawa, DG AF Fujikawa, DG TI Prolonged seizures and cellular injury: Understanding the connection SO EPILEPSY & BEHAVIOR LA English DT Article; Proceedings Paper CT 58th Annual Meeting of the American-Epilepsy-Society CY DEC 03-07, 2004 CL New Orleans, LA SP Amer Epilepsy Soc DE seizures; status epilepticus; cellular injury; neuroprotection; excitotoxicity ID APOPTOSIS-INDUCING FACTOR; INDUCED NEURONAL DEATH; EPILEPTIC BRAIN-DAMAGE; SUSTAINED ELECTRICAL-STIMULATION; INTERNUCLEOSOMAL DNA CLEAVAGE; NMDA RECEPTOR ANTAGONIST; CASPASE-ACTIVATED DNASE; KAINIC ACID; RAT-BRAIN; CEREBRAL-ISCHEMIA AB Status epilepticus (SE)-induced neuronal death is morphologically necrotic and is initiated by excessive glutamate release, which activates postsynaptic N-methyl-D-aspartate (NMDA) receptors and triggers receptor-mediated calcium influx (excitotoxicity). This results in activation of intracellular proteases and neuronal nitric oxide synthase, with generation of free radicals, and damage to cellular membranes, structural proteins, and essential enzymes. Programmed cell death mechanisms, such as p53 activation, activation of cell deathpromoting Bcl-2 family members, and endonuclease-induced DNA laddering, occur in SE-induced neuronal death. Caspase-independent excitotoxic mechanisms, such as NMDA-induced calpain I activation, with activation and translocation of the cell death-promoting Bcl-2 family member Bid from cytoplasm to mitochondria, and subsequent translocation of apoptosis-inducing factor and endonuclease G to nuclei (which cause large-scale and internucleosomal DNA cleavage, respectively), may be triggered by SE. Poly(ADP-ribose) polymerase-1 (PARP-1) activation and cysteinyl cathepsin and DNase II release from lysosomes may occur following SE as well, but these events await future investigation. In the future, rational combinations of central nervous system-penetrable neuroprotective agents, based on our knowledge of excitotoxic mechanisms, may be useful in refractory human SE. Published by Elsevier Inc. C1 VA Greater Los Angeles Healthcare Syst, Expt Neurol Lab, Sepulveda, CA USA. Univ Calif Los Angeles, Dept Neurol, David Geffen Sch Med, Los Angeles, CA 90024 USA. Univ Calif Los Angeles, Brain Res Inst, Los Angeles, CA 90024 USA. RP Fujikawa, DG (reprint author), VA Greater Los Angeles Healthcare Syst, Expt Neurol Lab, Sepulveda, CA USA. EM dfujikaw@ucla.edu NR 70 TC 110 Z9 112 U1 0 U2 4 PU ACADEMIC PRESS INC ELSEVIER SCIENCE PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA SN 1525-5050 J9 EPILEPSY BEHAV JI Epilepsy Behav. PD DEC PY 2005 VL 7 SU 3 BP S3 EP S11 DI 10.1016/j.yebeh.2005.08.003 PG 9 WC Behavioral Sciences; Clinical Neurology; Psychiatry SC Behavioral Sciences; Neurosciences & Neurology; Psychiatry GA 995XK UT WOS:000234138000002 PM 16278099 ER PT J AU Illes, Z Stern, JNH Keskin, DB Reddy, J Brosnan, CF Waldner, H Santambrogio, L Kuchroo, VK Strominger, JL AF Illes, Z Stern, JNH Keskin, DB Reddy, J Brosnan, CF Waldner, H Santambrogio, L Kuchroo, VK Strominger, JL TI Copolymer effects on microglia and T cells in the central nervous system of humanized mice SO EUROPEAN JOURNAL OF IMMUNOLOGY LA English DT Article DE T lymphocyte; antigen; MHC class II; multimer; suppression/anergy ID MYELIN BASIC-PROTEIN; TRANSCRIPTION FACTOR GATA-3; AMINO-ACID COPOLYMERS; MULTIPLE-SCLEROSIS; PROTEOLIPID PROTEIN; GLATIRAMER ACETATE; ENCEPHALOMYELITIS; EXPRESSION; APOPTOSIS; PEPTIDE AB The random amino acid copolymers FYAK and VWAK ameliorate EAE in a humanized mouse model expressing both a human transgenic myelin basic protein (MBP)85-99-specific T cell receptor and HLA-DR2. Here we show that microglia isolated from the central nervous system (CNS) of humanized mice with EAE induced by MBP85-99 and treated with these copolymers had reduced expression of HLA-DR, and thus reduced capacity to present MBP85-99 and activate transgenic T cells. In vitro microglia upregulated empty HLA-DR2 upon activation with GM-CSF with or without LPS or IFN-gamma, but not with IL-4 or IL-10. Correspondingly, gene chip arrays showed that the CNS of untreated and YFAK-treated mice differentially expressed pro- and anti-inflammatory molecules during MBP85-99-induced EAE. Interestingly, microglia expressed the full-length y gamma beta and alpha beta subunits of the tetrameric adaptor protein complexes AP-1 and AP-2 respectively, but after treatment with GM-CSF these complexes were cleaved, as had been found in immature dendritic cells derived from bone marrow. Strikingly, in vivo the perivascular lymphocyte infiltration seen in untreated mice immunized with MBP85-99 was composed of equal numbers of hV beta 2(+) MPB85-99-specific transgenic and hV beta 2(-) endogenous T cells, while the much smaller infiltration seen after treatment with YFAK was composed predominantly of hV beta 2(-) endogenous T cells. C1 Harvard Univ, Dept Mol & Cellular Biol, Cambridge, MA 02138 USA. Harvard Univ, Brigham & Womens Hosp, Sch Med, Harvard Inst Med,Ctr Neurol Dis, Boston, MA 02115 USA. Albert Einstein Coll Med, Dept Pathol, Bronx, NY 10467 USA. Dana Farber Canc Inst, Dept Canc Immunol & AIDS, Boston, MA 02115 USA. RP Strominger, JL (reprint author), Harvard Univ, Dept Mol & Cellular Biol, 7 Divin Ave, Cambridge, MA 02138 USA. EM jlstrom@fas.harvard.edu RI Reddy, Jay/K-7200-2014; OI Reddy, Jay/0000-0003-4082-9254; Stern, Joel N.H./0000-0002-1259-2256 FU NIAID NIH HHS [R01AI49524]; NINDS NIH HHS [R01NS38037, R01NS30843] NR 31 TC 13 Z9 13 U1 0 U2 2 PU WILEY-BLACKWELL PI HOBOKEN PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA SN 0014-2980 EI 1521-4141 J9 EUR J IMMUNOL JI Eur. J. Immunol. PD DEC PY 2005 VL 35 IS 12 BP 3683 EP 3693 DI 10.1002/eji.200526121 PG 11 WC Immunology SC Immunology GA 996VN UT WOS:000234203400031 PM 16259003 ER PT J AU Clement, JP Kassarjian, A Palmer, WE AF Clement, JP Kassarjian, A Palmer, WE TI Synovial inflammatory processes in the hand SO EUROPEAN JOURNAL OF RADIOLOGY LA English DT Article DE MR imaging; synovial inflammation; finger ID EARLY RHEUMATOID-ARTHRITIS; JUVENILE IDIOPATHIC ARTHRITIS; FOREIGN-BODY REACTION; FINGER JOINTS; PSORIATIC-ARTHRITIS; MRI FEATURES; FOLLOW-UP; SILICONE; WRIST; METACARPOPHALANGEAL AB The numerous synovial articulations and tendon sheaths of the hand afford it a central role in the diagnosis and management of inflammatory arthropathies. Inflammation may be idiopathic, infectious, post-traumatic, or secondary to deposition diseases. In most cases, synovial inflammation represents the primal event in the onset of destructive arthropathies. We review the imaging features of acute and chronic synovitis in the hand. Magnetic resonance imaging is very sensitive to the earliest changes of synovitis and provides a modality for early detection of disease. Additionally, once a diagnosis is established, magnetic resonance imaging has an emerging role in rapid assessment of response to therapy. Positron emission tomography and ultrasound also show promise in the evaluation and treatment of inflammatory arthropathies. Although highly sensitive to the presence of inflammation these more advanced imaging techniques often lack specificity. Therefore, the radiographic evaluation of the pattern of bone destruction remains critical to distinguishing among the different synovial inflammatory processes. (C) 2005 Elsevier Ireland Ltd. All rights reserved. C1 Massachusetts Gen Hosp, Boston, MA 02114 USA. RP Palmer, WE (reprint author), Massachusetts Gen Hosp, Boston, MA 02114 USA. EM palmer.william@mgh.harvard.edu NR 40 TC 5 Z9 5 U1 0 U2 2 PU ELSEVIER IRELAND LTD PI CLARE PA ELSEVIER HOUSE, BROOKVALE PLAZA, EAST PARK SHANNON, CO, CLARE, 00000, IRELAND SN 0720-048X J9 EUR J RADIOL JI Eur. J. Radiol. PD DEC PY 2005 VL 56 IS 3 BP 307 EP 318 DI 10.1016/j.ejrad.2005.03.012 PG 12 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA 994ZF UT WOS:000234069000005 PM 16298676 ER PT J AU Restrepo, MI Anzueto, A AF Restrepo, MI Anzueto, A TI Guidelines for the diagnoses and treatment of adult lower respiratory tract infections: a true ''European cooperative effort'' SO EUROPEAN RESPIRATORY JOURNAL LA English DT Editorial Material ID COMMUNITY-ACQUIRED PNEUMONIA; OBSTRUCTIVE PULMONARY-DISEASE; LENGTH-OF-STAY; ANTIMICROBIAL THERAPY; ANTIBIOTIC-THERAPY; CONTROLLED-TRIAL; MANAGEMENT; MORTALITY; PATHWAY; CARE C1 Univ Texas, Hlth Sci Ctr, Div Pulm & Crit Care Med, S Texas Vet Hlth Care Syst Audie L Murphy Div San, San Antonio, TX 78284 USA. S Texas Vet hlth Care Syst, Audie L Murphy VA Hosp, VERDICT, San Antonio, TX USA. RP Anzueto, A (reprint author), Univ Texas, Hlth Sci Ctr, Div Pulm & Crit Care Med, S Texas Vet Hlth Care Syst Audie L Murphy Div San, 7400 Merton Minter Blvd, San Antonio, TX 78284 USA. EM anzueto@uthscsa.edu RI Restrepo, Marcos/H-4442-2014 NR 28 TC 4 Z9 5 U1 0 U2 1 PU EUROPEAN RESPIRATORY SOC JOURNALS LTD PI SHEFFIELD PA 146 WEST ST, STE 2.4, HUTTONS BLDG, SHEFFIELD S1 4ES, ENGLAND SN 0903-1936 J9 EUR RESPIR J JI Eur. Resp. J. PD DEC PY 2005 VL 26 IS 6 BP 979 EP 981 DI 10.1183/09031936.05.00102105 PG 3 WC Respiratory System SC Respiratory System GA 996VK UT WOS:000234203100001 PM 16319322 ER PT J AU Chiappelli, F Prolo, P Cajulis, OS AF Chiappelli, F Prolo, P Cajulis, OS TI Evidence-based research in complementary and alternative medicine I: History SO EVIDENCE-BASED COMPLEMENTARY AND ALTERNATIVE MEDICINE LA English DT Article DE evidence-based research; complementary and alternative medicine; mind-body interactions AB Contemporary Western medicine has witnessed a fragmentation of our conceptualization of the medical endeavor into 'traditional medicine' and 'non-traditional medicine'. The former is meant to refer to the Western medical tradition, the latter encompasses both 'complementary' and 'alternative' medical practices. Complementary medicine complements conventional medical treatments, and alternative modes of medical interventions are meant to replace traditional Western medicine. Evidence-based research must be directed at establishing the best available evidence in complementary and alternative medicine. This paper is the first of a set of four 'lectures' that reviews the process of evidence-based research, and discusses its implications and applications for the early decades of the 21st century. The purpose of this paper is to introduce the series by examining some of the historical and philosophical foundations of this research endeavor. C1 Univ Calif Los Angeles, Sch Dent, Div Oral Biol & Med, Los Angeles, CA 90095 USA. W Los Angeles Vet Affairs Med Ctr, Los Angeles, CA 90073 USA. Psychoneuroimmunol Grp Inc, Los Angeles, CA 90073 USA. Dent Grp Sherman Oaks, Los Angeles, CA USA. RP Chiappelli, F (reprint author), Univ Calif Los Angeles, Sch Dent, Div Oral Biol & Med, CHS 63-090, Los Angeles, CA 90095 USA. EM chiappelli@dent.ucla.edu NR 15 TC 26 Z9 29 U1 0 U2 3 PU OXFORD UNIV PRESS PI OXFORD PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND SN 1741-427X J9 EVID-BASED COMPL ALT JI Evid.-based Complement Altern. Med. PD DEC PY 2005 VL 2 IS 4 BP 453 EP 458 DI 10.1093/ecam/neh106 PG 6 WC Integrative & Complementary Medicine SC Integrative & Complementary Medicine GA 988XT UT WOS:000233638200004 PM 16322801 ER PT J AU Kradin, R Matsubara, O Mark, EJ AF Kradin, R Matsubara, O Mark, EJ TI Endothelial nitric oxide synthase expression in pulmonary capillary hemangiomatosis SO EXPERIMENTAL AND MOLECULAR PATHOLOGY LA English DT Article DE pulmonary capillary hemangiomatosis; angiogenesis; nitric oxide; nitric oxide synthase; pulmonary hypertension ID HYPERTENSION; LUNGS; VASOCONSTRICTION; ANGIOGENESIS; AUTOPSY AB Pulmonary capillary hemangiomatosis (PCH) is an unusual disorder characterized by the proliferation of capillaries in the alveolar septa and pulmonary interstitium. Originally conceived as a primary idiopathic disorder of the pulmonary microcirculation, recent studies have demonstrated that PCH may be associated with other pathologies. Nitric oxide (NO) is a gaseous free radical with protean biological effects that is released during the intracellular conversion of arginine to citrulline. Nitric oxide synthases (NOS) mediate the production of NO and the release of NO in the microvasculature is specifically catalyzed by endothelial NOS (NOS-III). As NOS contributes to angiogenesis and is reduced in the hypertensive pulmonary microcirculation, we examined the expression of NOS-III protein in situ in the lungs of patients with PCH. Reduced microvascular expression of NOS-III protein by endothelial cells was observed in 4/6 (67%) cases of PCH, and all of these showed concomitant pulmonary vascular hypertensive remodeling. In 2/6 (33%) cases of PCH with no morphologic evidence of pulmonary hypertensive arteriopathy, endothelial expression of NOS-III protein was judged to be either minimally reduced or normal. These findings suggest that NOS-III is specifically reduced in PCH when pulmonary arterial hypertensive remodeling is concomitantly present. (C) 2005 Elsevier Inc. All rights reserved. C1 Massachusetts Gen Hosp, Dept Pathol, Boston, MA 02114 USA. Massachusetts Gen Hosp, Dept Med, Boston, MA 02114 USA. Natl Def Med Coll, Dept Pathol, Saitama, Japan. RP Kradin, R (reprint author), Massachusetts Gen Hosp, Dept Pathol, Warren 2, Boston, MA 02114 USA. EM Rkradin@partners.org NR 20 TC 10 Z9 10 U1 0 U2 0 PU ACADEMIC PRESS INC ELSEVIER SCIENCE PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA SN 0014-4800 J9 EXP MOL PATHOL JI Exp. Mol. Pathol. PD DEC PY 2005 VL 79 IS 3 BP 194 EP 197 DI 10.1016/j.yexmp.2005.08.010 PG 4 WC Pathology SC Pathology GA 985IG UT WOS:000233370200002 PM 16246326 ER PT J AU Ballen, KK Colvin, G Dey, BR Porter, D Westervelt, P Spitzer, TR Quesenberry, PJ AF Ballen, KK Colvin, G Dey, BR Porter, D Westervelt, P Spitzer, TR Quesenberry, PJ TI Cellular immune therapy for refractory cancers: novel therapeutic strategies SO EXPERIMENTAL HEMATOLOGY LA English DT Review ID BONE-MARROW-TRANSPLANTATION; VERSUS-HOST-DISEASE; DONOR LEUKOCYTE INFUSIONS; UMBILICAL-CORD BLOOD; STEM-CELL; HEMATOLOGIC MALIGNANCIES; MYELOGENOUS LEUKEMIA; ANTITUMOR RESPONSE; MYELOID-LEUKEMIA; MIXED CHIMERISM AB Objective. Allogeneic stem cell transplantation is curative for certain cancers, but the high doses of chemotherapy and radiotherapy may lead to toxicity. This review summarizes the field of cellular immune therapy using very-low-dose conditioning for refractory cancers. Methods. In our initial study, we treated 25 patients with refractory cancers with 100 cGy total body irradiation followed by allogeneic, nonmobilized peripheral blood cells. Eighteen patients received sibling and seven patients received unrelated cord blood stem cells. Results. None of the 13 patients with solid tumors achieved donor chimerism or had a sustained response. Twelve patients with hematologic malignancies were treated, 1 received a cord blood transplant and 11 received sibling donor cells. Nine of these 11 patients achieved donor chimerism, ranging from 5% to 100%. Four patients had sustained complete remission of their cancers. The patients who received cord blood transplants did not respond. Development of chimerism correlated with total previous myelotoxic chemotherapy (p < 0.001). We review additional studies in this area, including data in the haploidentical and unrelated donor setting. The data presented comprises studies performed at the four institutions represented by the authors, and a review of other pertinent studies in this area. Conclusions. Cellular immune therapy is an emerging application of transplantation therapy, which may be appropriate for refractory cancers. New studies in solid tumors, and with alternative donors, will expand the application of this new and promising treatment. (c) 2005 International Society for Experimental Hematology. Published by Elsevier Inc. C1 Massachusetts Gen Hosp, Div Hematol Oncol, Boston, MA 02114 USA. Roger Williams Med Ctr, Ctr Canc, Providence, RI USA. Hosp Univ Penn, Div Hematol Oncol, Philadelphia, PA 19104 USA. Univ Massachusetts, Mem Hlth Care, Worcester, MA 01605 USA. RP Ballen, KK (reprint author), Massachusetts Gen Hosp, Div Hematol Oncol, Cox 640,100 Blossom St, Boston, MA 02114 USA. EM kballen@partners.org FU NCI NIH HHS [L30 CA104092-01, L30 CA104092-02] NR 54 TC 10 Z9 16 U1 1 U2 2 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0301-472X J9 EXP HEMATOL JI Exp. Hematol. PD DEC PY 2005 VL 33 IS 12 BP 1427 EP 1435 DI 10.1016/j.exphem.2005.06.032 PG 9 WC Hematology; Medicine, Research & Experimental SC Hematology; Research & Experimental Medicine GA 999MK UT WOS:000234393400001 PM 16338484 ER PT J AU Eom, HS Rubio, MT Means, TK Luster, AD Sykes, M AF Eom, HS Rubio, MT Means, TK Luster, AD Sykes, M TI T-cell P/E-selectin ligand alpha(1,3)fucosylation is not required for graft-vs-host disease induction SO EXPERIMENTAL HEMATOLOGY LA English DT Article ID BONE-MARROW-TRANSPLANTATION; SERUM CYTOKINE LEVELS; INTERFERON-GAMMA; P-SELECTIN; LEUKOCYTE TRAFFICKING; ADHESION MOLECULE-1; DENDRITIC CELLS; ACUTE GVHD; FUCT-VII; MICE AB Objective. Recognition of E- and P-selectins on vascular endothelium by their leukocyte glycoprotein counterreceptor P-selectin glycoprotein ligand-1 (PSGL-1) initiates and sustains leukocyte rolling, culminating in extravasation of lymphocytes from blood into organs. PSGL-1 is rendered functional by terminal glycosylation steps, which occur mainly in activated Th1 but not Th2 cells. alpha(1,3)Fucosyltransferases IV and VII control this glycosylation pathway. Mice lacking these transferases (Fuc-TIV-/-/Fuc-TVII-/-) lack functional E- and P-selectin ligands. We hypothesized that Fuc-TIV-/-/Fuc-TVII-/- donor T cells might have reduced capacity to roll on vessels of inflamed target tissues and mediate graft-vs-host disease (GVHD). Materials and Methods. We compared the ability of Fuc-TIV-/-/Fuc-TVII-/- and wild-type (WT) C57BL/6 (136) spleen cells (SPCs) to produce GVHD in lethally irradiated major histocompatibility complex (MHC) haplotype-mismatched B6D2F1 recipients. Clinical GVHD, GVHD pathology in target organs, memory phenotype conversion, proliferation of donor T cells, and tissue and serum cytokine expression were examined. Results. Surprisingly, clinical GVHD was not reduced in lethally irradiated mice receiving full haplotype MHC mismatched or matched Fuc-TIV-/-/Fuc-TVII-/- SPCs compared to those receiving WT SPCs. GVHD pathology in target organs, memory phenotype conversion, and proliferation of donor T cells were similar in both groups. However, reduced interferon-gamma was detected in liver and lung, and serum levels of tumor necrosis factor-alpha were higher in mice receiving Fuc-TIV-/-/Fuc-TVII-/- SPCs compared with WT SPCs. Conclusions. These results suggest that donor T cells, including Th1, are capable of trafficking to GVHD target tissues independently of P- and E- selectin ligand in conditioned hosts. (c) 2005 International Society for Experimental Hematology. Published by Elsevier Inc. C1 Harvard Univ, Massachusetts Gen Hosp, Sch Med, Transplantat Biol Res Ctr,Bone Marrow Transplanta, Boston, MA 02129 USA. Harvard Univ, Massachusetts Gen Hosp, Sch Med, Ctr Immunol & Inflammatory Dis,Div Rheumatol Alle, Boston, MA 02115 USA. RP Sykes, M (reprint author), Harvard Univ, Massachusetts Gen Hosp, Sch Med, Transplantat Biol Res Ctr,Bone Marrow Transplanta, MGH E Bldg 149-5102,13th St, Boston, MA 02129 USA. EM Megan.Sykes@tbrc.mgh.harvard.edu FU NCI NIH HHS [R01 CA79989] NR 46 TC 2 Z9 2 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0301-472X J9 EXP HEMATOL JI Exp. Hematol. PD DEC PY 2005 VL 33 IS 12 BP 1564 EP 1573 DI 10.1016/j.exphem.2005.08.003 PG 10 WC Hematology; Medicine, Research & Experimental SC Hematology; Research & Experimental Medicine GA 999MK UT WOS:000234393400016 PM 16338500 ER PT J AU Cornia, PB Anawalt, BD AF Cornia, PB Anawalt, BD TI Male hormonal contraceptives: a potentially patentable and profitable product SO EXPERT OPINION ON THERAPEUTIC PATENTS LA English DT Review DE androgen; gonadotropin-releasing hormone analogue; gonadotropins; male contraception; progestogen; spermatogenesis; testosterone ID EFFECTIVELY SUPPRESSES SPERMATOGENESIS; TESTOSTERONE-DEPENDENT RESTORATION; DEPOT-MEDROXYPROGESTERONE ACETATE; NORMAL MEN; CYPROTERONE-ACETATE; CLINICAL-TRIAL; 5-ALPHA-REDUCTASE INHIBITOR; ETONOGESTREL IMPLANTS; NORETHISTERONE ENANTHATE; INJECTABLE TESTOSTERONE AB Although women have traditionally shouldered the responsibility of contraception, up to one-third of couples worldwide employ a male form of contraception (e.g., vasectomy or condoms). Vasectomy should be considered irreversible and long-term use of condoms is associated with a relatively high failure rate (pregnancy). Because many women are unable to use hormonal contraception and men want more contraceptive options, there is a need for a safe, effective, reversible and well-tolerated male hormonal contraceptive agent. Two large multicentre, multinational trials sponsored by the World Health Organization in the 1990s showed that high-dosage exogenous testosterone provided contraceptive efficacy similar to currently available female oral contraceptives. However, the supraphysiological dosages of testosterone used resulted in androgen-related adverse effects such as weight gain and suppression of high-density lipoprotein cholesterol levels. Subsequent efforts have been directed at combining testosterone with other agents, such as progestogens or gonaclotropin-releasing hormone analogues, to decrease the dosage of testosterone (and thus androgen-related side effects) whilst achieving uniform azoospermia. In this article, the latest developments in male hormonal contraception supporting the feasibility of such an agent will be reviewed and suggestions for future directions of research and development will be offered. C1 Univ Washington, VA Puget Sound Healthcare Syst, Seattle, WA 98108 USA. Univ Washington, Dept Med, Seattle, WA 98108 USA. RP Cornia, PB (reprint author), Univ Washington, VA Puget Sound Healthcare Syst, 1660 S Columbian Way,S-111-GIMC, Seattle, WA 98108 USA. EM paul.cornia@med.va.gov NR 73 TC 1 Z9 1 U1 0 U2 5 PU ASHLEY PUBLICATIONS LTD PI LONDON PA TELEPHONE HOUSE, 69-77 PAUL STREET, LONDON EC2A 4LQ, ENGLAND SN 1354-3776 J9 EXPERT OPIN THER PAT JI Expert Opin. Ther. Patents PD DEC PY 2005 VL 15 IS 12 BP 1727 EP 1737 DI 10.1517/13543776.15.12.1727 PG 11 WC Chemistry, Medicinal; Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA 000NJ UT WOS:000234468600005 ER PT J AU Taha, TA Kitatani, K El-Alwani, M Bielawski, J Hannun, YA Obeid, LM AF Taha, TA Kitatani, K El-Alwani, M Bielawski, J Hannun, YA Obeid, LM TI Loss of sphingosine kinase-1 activates the intrinsic pathway of programmed cell death: modulation of sphingolipid levels and the induction of apoptosis SO FASEB JOURNAL LA English DT Article DE ceramide; Bax; mitochondria ID NECROSIS-FACTOR-ALPHA; PROSTATE-CANCER CELLS; SPHINGOSINE-1-PHOSPHATE PHOSPHOHYDROLASE; SIGNAL-TRANSDUCTION; INHIBITS APOPTOSIS; ENDOTHELIAL-CELLS; MOLECULAR-CLONING; CYTOCHROME-C; CA2+ SIGNALS; TNF-ALPHA AB Activation of sphingosine kinase-1 (SK1) by overexpression or agonist stimulation promotes cell proliferation, survival, and anti-apoptosis. Studies on the function of endogenous SK1 are lacking. Endogenous SK1 has been shown to be down-regulated under stress, and knockdown of the enzyme reduces the percentage of viable MCF-7 breast cancer cells (Taha, T. A. et al. 2004. J. Biol. Chem. 279, 20546- 20554). In this study, we examined the mechanisms by which SK1 loss affects the growth of cells. Knockdown of the enzyme by small interfering RNA caused cell cycle arrest and induced apoptosis. Cell death involved effector caspase activation, cytochrome c release and Bax oligomerization in the mitochondrial membrane, thus placing SK1 knockdown upstream of the mitochondrial pathway of apoptosis. SK1 knockdown also induced significant increases in ceramide levels in whole cells and in mitochondria enriched fractions of cells. Inhibition of de novo sphingolipid biosynthesis with myriocin significantly attenuated Bax oligomerization and downstream caspase activation after SK1 loss. These studies for the first time implicate endogenous SK1 as an important survival enzyme in MCF-7 cells and link the biological consequences of knocking down the enzyme to its biochemical role as a regulator of sphingolipid metabolism. C1 Med Univ S Carolina, Dept Med, Charleston, SC 29425 USA. Ralph H Johnson Vet Adm Hosp, Div Gen Internal Med, Charleston, SC 29401 USA. RP Obeid, LM (reprint author), Med Univ S Carolina, Dept Med, 114 Doughty St,POB 250779, Charleston, SC 29425 USA. EM obeidl@musc.edu OI Kitatani, Kazuyuki/0000-0002-8516-6135; obeid, lina/0000-0002-0734-0847 NR 75 TC 4 Z9 4 U1 0 U2 1 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD DEC PY 2005 VL 19 IS 14 BP 482 EP + DI 10.1096/fj.05-4412fje PG 24 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 999QR UT WOS:000234405500015 ER PT J AU Blackwood, CB Yuen, TJ Sangeorzan, BJ Ledoux, WR AF Blackwood, CB Yuen, TJ Sangeorzan, BJ Ledoux, WR TI The midtarsal joint locking mechanism SO FOOT & ANKLE INTERNATIONAL LA English DT Article DE biomechanics; foot; gait AB Background. The midtarsal joint, consisting of the talonavicular and the calcaneocuboid joints, is presumed to be responsible for the foot being both flexible and rigid during different parts of the stance phase of gait. However, this mechanism has never been well quantified. This study explores the midtarsal joint locking mechanism by comparing the effect of hindfoot inversion and eversion on midfoot and forefoot mobility. Methods: Motion of the tibia, talus, calcaneus, navicular, cuboid and the first, second, and fifth metatarsals were measured in nine cadaver feet using Polhemus Fastrak (R) electromagnetic sensors (EST GmbH & Co. KG, Kaiserslautern, Germany). The talus was fixed to the tibia, and then the forefoot was maximally dorsiflexed, plantarflexed, inverted, and everted, with the hindfoot in maximal eversion and inversion, for a total of eight test positions. The range of motion of the individual bones between maximal forefoot dorsiflexion and plantarflexion and between maximal forefoot inversion and eversion was calculated for the hindfoot in maximal eversion and inversion. Results: For the range of motion from maximal dorsiflexion to maximal plantarflexion there was significantly increased movement of the first, second, and fifth metatarsals in the sagittal plane (p-value = 0.003, 0.007, and 0.002, respectively) when the calcaneus was maximally everted compared to when the calcaneus was maximally inverted. No significant differences were detected for the range of motion from forefoot inversion to eversion for the two hindfoot positions. Conclusions: This study demonstrated that motion in the forefoot is influenced by hindfoot position through the midtarsal joint. Specifically, the sagittal plane range of motion of the metatarsals is increased when the hindfoot is in valgus. C1 VA Puget Sound, Healthcare Syst, Dept Vet Affairs, RRD Ctr Excellence Limb Loss Prevent & Prosthet E, Seattle, WA 98108 USA. Univ Washington, Dept Mech Engn, Seattle, WA 98195 USA. RP Ledoux, WR (reprint author), VA Puget Sound, Healthcare Syst, Dept Vet Affairs, RRD Ctr Excellence Limb Loss Prevent & Prosthet E, MS 151,1660 S Columbian Way, Seattle, WA 98108 USA. EM wrledoux@u.washington.edu RI Ledoux, William/K-6815-2015 OI Ledoux, William/0000-0003-4982-7714 NR 10 TC 36 Z9 37 U1 0 U2 10 PU AMER ORTHOPAEDIC FOOT & ANKLE SOC, INC PI SEATTLE PA 2517 EASTLAKE AVE EAST, STE 200, SEATTLE, WA 98102 USA SN 1071-1007 J9 FOOT ANKLE INT JI Foot Ankle Int. PD DEC PY 2005 VL 26 IS 12 BP 1074 EP 1080 PG 7 WC Orthopedics SC Orthopedics GA 993AH UT WOS:000233924600013 PM 16390642 ER PT J AU Esrailian, E Gralnek, IM AF Esrailian, E Gralnek, IM TI Nonvariceal upper gastrointestinal bleeding: Epidemiology and diagnosis SO GASTROENTEROLOGY CLINICS OF NORTH AMERICA LA English DT Review ID UPPER-GI HEMORRHAGE; PEPTIC-ULCER HEMORRHAGE; CHRONIC-RENAL-FAILURE; PORTAL HYPERTENSIVE GASTROPATHY; ENDOSCOPIC HEMOCLIP PLACEMENT; RANDOMIZED CONTROLLED-TRIAL; ANTRAL VASCULAR ECTASIA; MALLORY-WEISS-SYNDROME; VON-WILLEBRAND-FACTOR; DIEULAFOYS LESION AB Nonvariceal upper gastrointestinal bleeding remains an important cause of patient morbidity, mortality, and use of considerable health care resources. An early and accurate diagnosis is critical for guiding appropriate management and facilitating patient care. Ibis article reviews the most recent epidemiologic data on acute nonvariceal upper gastrointestinal bleeding and outlines important aspects of making the diagnosis. C1 Univ Calif Los Angeles, David Geffen Sch Med, VA Greater Los Angeles Healthcare Syst, UCLA VA Ctr Outcomes Res & Educ, Los Angeles, CA 90073 USA. RP Gralnek, IM (reprint author), Univ Calif Los Angeles, David Geffen Sch Med, VA Greater Los Angeles Healthcare Syst, UCLA VA Ctr Outcomes Res & Educ, 11301 Wilshire Blvd,CURE Bldg 115,Room 215, Los Angeles, CA 90073 USA. EM i_gralnek@rambam.health.gov.il NR 123 TC 36 Z9 37 U1 0 U2 1 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 USA SN 0889-8553 J9 GASTROENTEROL CLIN N JI Gastroenterol. Clin. North Am. PD DEC PY 2005 VL 34 IS 4 BP 589 EP + DI 10.1016/j.gtc.2005.08.006 PG 18 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA 994ZP UT WOS:000234070000003 PM 16303572 ER PT J AU Lorenzen, JA Bonacci, BB Palmer, RE Wells, C Zhang, J Haber, DA Goldstein, AM Mayer, AN AF Lorenzen, JA Bonacci, BB Palmer, RE Wells, C Zhang, J Haber, DA Goldstein, AM Mayer, AN TI Rbm19 is a nucleolar protein expressed in crypt/progenitor cells of the intestinal epithelium SO GENE EXPRESSION PATTERNS LA English DT Article DE intestine; Rbm19; development; nucleolus; progenitor; stem cell; differentiation; morphogenesis; organogenesis; Caco-2 cells; intestinal crypt; RNA-binding proteins; nucleophosmin; nucleolin; C23; B23; preribosomal RNA processing; ribosome biogenesis; colorectal adenocarcinoma; colon cancer; mitosis ID RIBOSOMAL-RNA; DIGESTIVE ORGANS; BINDING PROTEIN; STEM-CELL; C-MYC; MORPHOGENESIS; ZEBRAFISH; COMPONENTS; RBD-1 AB Intestinal development and homeostasis rely on the coordination of proliferation and differentiation of the epithelium. To better understand this process, we are studying Rbm 19, a gene expressed in the gut epithelium that is essential for intestinal morphogenesis and differentiation in the zebrafish (Development 130, 3917). Here we analyzed the expression of Rbm19 in several biological contexts that feature proliferation/differentiation cell fate decisions. In the undifferentiated embryonic gut tube, Rbm19 is expressed throughout the epithelium, but then becomes localized to the crypts of Lieberkuhn of the adult intestine. Consistent with its expression in adult crypt/progenitor cells, expression is widespread in human colorectal carcinomas and dividing Caco-2 cells. Its expression in Caco-2 cells recapitulates the in vivo pattern, declining when the cells undergo confluence-induced arrest and differentiation. Rbm19 protein localizes to the nucleolus during interphase and to the perichromosomal sheath during mitosis, in accordance with the pattern described for other nucleolar proteins implicated in ribosome biogenesis. Interestingly, the loss of nucleolar rbm19, nucleolin/C23, and nucleophosmin/B23 in confluent Caco-2 cells did not signify loss of nucleoli as detected by electron microscopy. Taken together, these data point to the nucleolus as a possible locus for regulating the proliferation/differentiation cell fate decision in the intestinal epithelium. (c) 2005 Elsevier B.V. All rights reserved. C1 Med Coll Wisconsin, Dept Pediat, Gastroenterol Sect, Milwaukee, WI 53226 USA. Massachusetts Gen Hosp, Ctr Canc, Boston, MA 02129 USA. Harvard Univ, Sch Med, Boston, MA 02129 USA. Med Coll Wisconsin, Dept Cell Biol Neurobiol & Anat, Milwaukee, WI 53226 USA. Childrens Res Inst, Milwaukee, WI 53226 USA. Massachusetts Gen Hosp, Dept Pediat Surg, Boston, MA 02129 USA. RP Mayer, AN (reprint author), Med Coll Wisconsin, Dept Pediat, Gastroenterol Sect, 8703 Watertown Plank Rd, Milwaukee, WI 53226 USA. EM alanmayer@mac.com FU NIDDK NIH HHS [R03DK067176-01] NR 26 TC 10 Z9 12 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 1567-133X J9 GENE EXPR PATTERNS JI Gene Expr. Patterns PD DEC PY 2005 VL 6 IS 1 BP 45 EP 56 DI 10.1016/j.modgep.2005.05.001 PG 12 WC Developmental Biology; Genetics & Heredity SC Developmental Biology; Genetics & Heredity GA 994RB UT WOS:000234047800006 PM 16027046 ER PT J AU Koochekpour, S Zhang, YJ Beroukhim, R Hsieh, CL Hofer, MD Zhau, HE Hiraiwa, M Pattan, DY Ware, JL Luftig, RB Sandhoff, K Sawyers, CL Pienta, KJ Rubin, MA Vessella, RL Sellers, WR Sartor, O AF Koochekpour, S Zhang, YJ Beroukhim, R Hsieh, CL Hofer, MD Zhau, HE Hiraiwa, M Pattan, DY Ware, JL Luftig, RB Sandhoff, K Sawyers, CL Pienta, KJ Rubin, MA Vessella, RL Sellers, WR Sartor, O TI Amplification and overexpression of prosaposin in prostate cancer SO GENES CHROMOSOMES & CANCER LA English DT Article ID COMPARATIVE GENOMIC HYBRIDIZATION; XENOGRAFT MODEL; TARGETED DISRUPTION; GENETIC ALTERATIONS; SIGNALING PATHWAYS; STIMULATES GROWTH; EPITHELIAL-CELLS; BONE METASTASIS; UROKINASE GENE; SCHWANN-CELLS AB We identified prosaposin (PSAP) as a secreted protein expressed in androgen-independent (AI) prostate cancer cells by cloning/ sequencing, after probing a PC-3 cDNA library expressed in the lambda TriplEx phagemid expression vector with a polyclonal rabbit antibody generated against pooled human seminal plasma. PSAP is a neurotrophic molecule; its deficiency or inactivation has proved to be lethal in man and mice, and in mice, it leads to abnormal development and atrophy of the prostate gland, despite normal testosterone levels. We used Southern hybridization, quantitative real-time polymerase chain reaction, and/or single nucleotide polymorphism (SNP) array analysis, and we now report the genomic amplification of PSAP in the metastatic AI prostate cancer cell lines, PC-3, DU-145, MDA-PCa 2b, M-12, and NCI-H660. In addition, by using SNP arrays and a set of 25 punch biopsy samples of human prostate cancer xenografts (LAPC3, LuCaP 23.1, 35, 49, 58, 73, 77, 81, 86.2, 92.1, 93, 96, 105, and 115), lymph nodes, and visceral-organ metastases, we detected amplification of the PSAP locus (10q22.1) in LuCaP 58 and 96 xenografts and two lymph node metastases. In addition, AI metastatic prostate cancer cell lines C4-2B and IA8-ARCaP over-expressed PSAP mRNA without evidence of genomic amplification. Taken together with prior data that demonstrated the growth-, migration-, and invasion-promoting activities, the activation of multiple signal transduction pathways, and the antiapoptotic effect of PSAP (or one of its active domains, saposin C) in prostate cancer cells, our current observation of PSAP amplification or overexpression in prostate cancer suggests, for the first time, a role for this molecule in the process of carcinogenesis or cancer progression in the prostate. (c) 2005 Wiley-Liss, Inc. C1 Louisiana State Univ, Hlth Sci Ctr, Stanley S Scott Canc Ctr, Dept Microbiol Immunol & Parasitol, New Orleans, LA 70112 USA. Harvard Univ, Sch Med, Boston, MA USA. Dana Farber Canc Inst, Boston, MA 02115 USA. Emory Univ, Sch Med, Winship Canc Inst, Dept Urol,Mol Urol & Therapeut Program, Atlanta, GA USA. Brigham & Womens Hosp, Dept Pathol, Boston, MA 02115 USA. Univ Calif San Diego, Ctr Genet Mol, Dept Neurosci, La Jolla, CA USA. Virginia Commonwealth Univ, Med Coll Virginia, Dept Pathol, Richmond, VA 23298 USA. Univ Bonn, Kekule Inst Organ Chem & Biochem, Bonn, Germany. Univ Calif Los Angeles, David Geffen Sch Med, Howard Hughes Med Inst, Los Angeles, CA USA. Univ Calif Los Angeles, David Geffen Sch Med, Dept Med, Los Angeles, CA USA. Univ Calif Los Angeles, David Geffen Sch Med, Dept Urol, Los Angeles, CA USA. Univ Calif Los Angeles, David Geffen Sch Med, Dept Mol & Med Pharmacol, Los Angeles, CA USA. Univ Calif Los Angeles, David Geffen Sch Med, Jonsson Comprehens Canc Ctr, Los Angeles, CA USA. Univ Michigan, Ctr Comprehens Canc, Urol Ctr, Div Hematol & Oncol,Dept Urol, Ann Arbor, MI USA. Univ Washington, Dept Urol, Seattle, WA 98195 USA. Louisiana State Univ, Hlth Sci Ctr, Dept Med, New Orleans, LA USA. RP Koochekpour, S (reprint author), Louisiana State Univ, Hlth Sci Ctr, Stanley S Scott Canc Ctr, Dept Microbiol Immunol & Parasitol, 533 Bolivar St,CSRB 4-17, New Orleans, LA 70112 USA. EM skooch@lsuhsc.edu RI Sawyers, Charles/G-5327-2016; Pienta, Kenneth/E-7679-2015; OI Pienta, Kenneth/0000-0002-4138-2186; Rubin, Mark/0000-0002-8321-9950 FU NCI NIH HHS [P01 CA85859, 5T32CA09172-30, T32 CA009172] NR 64 TC 27 Z9 34 U1 1 U2 2 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 1045-2257 J9 GENE CHROMOSOME CANC JI Gene Chromosomes Cancer PD DEC PY 2005 VL 44 IS 4 BP 351 EP 364 DI 10.1002/gcc.20249 PG 14 WC Oncology; Genetics & Heredity SC Oncology; Genetics & Heredity GA 972BN UT WOS:000232428900002 PM 16080200 ER PT J AU Delalle, I Pfleger, CM Buff, E Lueras, P Hariharan, IK AF Delalle, I Pfleger, CM Buff, E Lueras, P Hariharan, IK TI Mutations in the drosophila orthologs of the F-actin capping protein alpha- and beta-subunits cause actin accumulation and subsequent retinal degeneration SO GENETICS LA English DT Article ID HUMAN NEURODEGENERATIVE DISEASE; PARKINSONS-DISEASE; CELL-PROLIFERATION; BEHAVIORAL-CHANGES; GENOME PROJECT; BARBED END; GENE; POLYMERIZATION; EXPRESSION; VERTEBRATES AB The progression of several human neurodegenerative diseases is characterized by the appearance of intracellular inclusions or cytoskeletal abnormalities. An important question is whether these abnormalities actually contribute to the degenerative process or whether they are merely manifestations of cells that are already destined for degeneration. We have conducted a large screen in Drosophila for mutations that alter the growth or differentiation of cells during eye development. We have used mitotic recombination to generate patches of homozygous Mutant cells. In our entire screen, mutations in only two different loci, burned (bnd) and scorched (scrd), resulted in eyes in which the mutant patches appeared black and the mutant tissue appeared to have undergone degeneration. In larval imaginal discs, growth and cell fate specification occur normally in mutant cells, but there is an accumulation of F-actin. Mutant cells degenerate much later during the pupal phase of development. burned mutations are allelic to mutations in the previously described cpb locus that encodes the P-subunit of the F-actin capping protein, while scorched mutations disrupt the gene encoding its a-subunit (cpa). The alpha/beta-heterodimer caps the barbed ends of an actin filament and restricts its growth. In its absence, cells progressively accumulate actin filaments and eventually die. A possible role for their human orthologs in neurodegenerative disease merits further investigation. C1 Massachusetts Gen Hosp, Ctr Canc, Charlestown, MA 02139 USA. Boston Univ, Sch Med, Dept Pathol, Boston, MA 02118 USA. Univ Calif Berkeley, Dept Mol & Cell Biol, Berkeley, CA 94720 USA. RP Hariharan, IK (reprint author), Massachusetts Gen Hosp, Ctr Canc, Charlestown, MA 02139 USA. EM ikh@berkeley.edu FU NCI NIH HHS [P01 CA095281, CA 95281]; NEI NIH HHS [K08 EY013639, K08 EY 13639 A]; NIGMS NIH HHS [R01 GM061672, GM 61672] NR 59 TC 27 Z9 28 U1 0 U2 2 PU GENETICS PI BALTIMORE PA 428 EAST PRESTON ST, BALTIMORE, MD 21202 USA SN 0016-6731 J9 GENETICS JI Genetics PD DEC PY 2005 VL 171 IS 4 BP 1757 EP 1765 DI 10.1534/genetics.105.049213 PG 9 WC Genetics & Heredity SC Genetics & Heredity GA 999RB UT WOS:000234407100028 PM 16143599 ER PT J AU Rowan, AJ AF Rowan, AJ TI Epilepsy in older adults - Common morbidities influence development, treatment strategies, and expected outcomes SO GERIATRICS LA English DT Article DE antiepileptic drugs (AEDs); epilepsy; seizures; elderly; geriatrics ID TONIC CLONIC SEIZURES; CARBAMAZEPINE AB Given that that the average person has one chronic illness for each decade over age 50, one would expect that patients who develop seizures in late life would have associated medical and/or neurologic conditions. Cerebrovascular disease, hypertension, heart disease, diabetes mellitus, renal disease, and dementia all relate to epilepsy. Comorbidities not only contribute to the causation and consequences of seizures, they also interfere with effective treatment and optimal functioning. Because seizures in older individuals can lead to serious consequences, safe and effective treatment is essential. Yet, antiepileptic drugs (AEDs) may cause adverse effects that may be worse in older patients when compared to younger patients. Multiple medications lead to a high probability that medically significant drug interactions may occur and must be monitored for in geriatric patients. C1 Mt Sinai Sch Med, Dept Neurol, New York, NY 10029 USA. Bronx Vet Adm Med Ctr, Bronx, NY USA. Harvard Univ, Sch Med, Boston, MA 02115 USA. Harvard Univ, Osher Inst, Boston, MA 02115 USA. St Josephs Hosp, HealthE Neurovasc Inst, St Paul, MN USA. Mt Sinai Sch Med, Brookdale Dept Geriatr & Adult Dev, New York, NY 10029 USA. RP Rowan, AJ (reprint author), Mt Sinai Sch Med, Dept Neurol, New York, NY 10029 USA. NR 13 TC 18 Z9 18 U1 0 U2 3 PU ADVANSTAR COMMUNICATIONS PI DULUTH PA 131 W FIRST ST, DULUTH, MN 55802 USA SN 0016-867X J9 GERIATRICS JI Geriatrics PD DEC PY 2005 VL 60 IS 12 BP 30 EP + PG 4 WC Geriatrics & Gerontology SC Geriatrics & Gerontology GA 995CA UT WOS:000234076300016 PM 16343034 ER PT J AU Bates-Jensen, BM Simmons, SF Schnelle, JF Alessi, C AF Bates-Jensen, BM Simmons, SF Schnelle, JF Alessi, C TI Evaluating the accuracy of minimum data set bed-mobility ratings against independent performance assessments: Systematic error and directions for improvement SO GERONTOLOGIST LA English DT Article DE activities of daily living assessment; bed mobility; minimum data set accuracy; physical performance assessments ID NURSING-HOME RESIDENTS; URINARY-INCONTINENCE; REFLECT DIFFERENCES; QUALITY INDICATORS; FUNCTIONAL STATUS; CARE; HEALTH; STABILITY; STAFF AB Purpose: The Minimum Data Set (MDS) Activities of Daily Living (ADL) bed-mobility item, which rates the staff-assistance level necessary for bed movement, is used to target scheduled repositioning interventions and to identify physical function changes in nursing home residents; however, accuracy of the item is uncertain. The purpose of this study was to evaluate the accuracy of the MDS ADL bed-mobility item as completed by nursing home nurses with independent performance assessments conducted by research staff. Design and Methods: A convenience sample of 197 long-stay residents from 26 California nursing homes participating in a larger project was used in this cross-sectional study to compare independent research-staff performance assessments (using graduated assistance protocols of residents' ability to move in bed) and nursing home nurse MDS bed-mobility ratings. Participants also wore movement monitors to verify performance assessments. Results: Poor agreement existed between the nursing home nurse MDS bed-mobility ratings and the research-staff performance assessments across all assistance levels (kappa range, kappa = 0.007, p = .918 to kappa = 0.484, p < .001), with better agreement seen in totally dependent participants and with fewer elapsed days between MDS ratings and performance assessments. The odds of nursing home nurse errors (underestimating or overestimating dependency) on the MDS bed-mobility item were 2.1 times higher for participants judged independent by research staff compared with participants judged as requiring physical assistance by research staff (95% confidence interval, 1.14-4.03) when adjusted for number of days between nurse MDS ratings and research-staff performance assessments. Implications: Nursing home nurses overestimated resident dependency in bed mobility. The systematic inaccuracies in MDS bed-mobility ratings have implications for their use as a basis for targeting residents for repositioning programs and determining changes in residents' physical function. Performance assessments utilizing graduated assistance protocols are recommended as a method of improving the accuracy of MDS bed-mobility ratings. C1 Univ Calif Los Angeles, Borun Ctr Gerontol Res, Jewish Home Aging, Reseda, CA 91335 USA. Univ Calif Los Angeles, Sch Med, Borun Ctr Gerontol Res, Los Angeles, CA 90024 USA. Vet Adm Greater Los Angeles Healthcare Syst, Sepulveda, CA USA. Ctr Geriatr Res Educ & Clin, Sepulveda, CA USA. RP Bates-Jensen, BM (reprint author), Univ Calif Los Angeles, Borun Ctr Gerontol Res, Jewish Home Aging, 7150 Tampa Ave, Reseda, CA 91335 USA. EM batesjen@ucla.edu NR 27 TC 10 Z9 10 U1 2 U2 4 PU GERONTOLOGICAL SOCIETY AMER PI WASHINGTON PA 1275 K STREET NW SUITE 350, WASHINGTON, DC 20005-4006 USA SN 0016-9013 J9 GERONTOLOGIST JI Gerontologist PD DEC PY 2005 VL 45 IS 6 BP 731 EP 738 PG 8 WC Gerontology SC Geriatrics & Gerontology GA 989UN UT WOS:000233699500002 PM 16326654 ER PT J AU Canada, AL Parker, PA Basen-Engquist, K de Moor, JS Ramondetta, LM AF Canada, AL Parker, PA Basen-Engquist, K de Moor, JS Ramondetta, LM TI Active coping mediates the association between religion/spirituality and functional well-being in ovarian cancer SO GYNECOLOGIC ONCOLOGY LA English DT Editorial Material C1 Univ Texas, MD Anderson Canc Ctr, Dept Behav Sci, Houston, TX 77030 USA. Dana Farber Canc Inst, Boston, MA 02115 USA. Harvard Univ, Sch Publ Hlth, Boston, MA 02115 USA. Univ Texas, MD Anderson Canc Ctr, Dept Gynecol Oncol, Houston, TX 77030 USA. RP Canada, AL (reprint author), Univ Texas, MD Anderson Canc Ctr, Dept Behav Sci, 1515 Holcombe Blvd,Unit 1330, Houston, TX 77030 USA. EM alcanada@mdanderson.org NR 1 TC 7 Z9 7 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 0090-8258 J9 GYNECOL ONCOL JI Gynecol. Oncol. PD DEC PY 2005 VL 99 IS 3 SU 1 BP S125 EP S125 DI 10.1016/j.ygyno.2005.07.057 PG 1 WC Oncology; Obstetrics & Gynecology SC Oncology; Obstetrics & Gynecology GA 000ZV UT WOS:000234502500027 PM 16450431 ER PT J AU Chang, SK Pavlova, I Marin, NM Follen, M Richards-Kortum, R AF Chang, SK Pavlova, I Marin, NM Follen, M Richards-Kortum, R TI Fluorescence spectroscopy as a diagnostic tool for detecting cervical pre-cancer SO GYNECOLOGIC ONCOLOGY LA English DT Editorial Material ID AUTOFLUORESCENCE SPECTROSCOPY; RESOLVED FLUORESCENCE; IN-VIVO; NEOPLASIA; TISSUE; MODEL C1 Massachusetts Gen Hosp, Wellman Ctr Photomed, Boston, MA 02114 USA. Univ Texas, Dept Biomed Engn, Austin, TX 78712 USA. Univ Texas, MD Anderson Canc Ctr, Dept Gynecol Oncol, Houston, TX 77030 USA. Rice Univ, Dept Bioengn, Houston, TX 77251 USA. RP Chang, SK (reprint author), Massachusetts Gen Hosp, Wellman Ctr Photomed, Boston, MA 02114 USA. EM skchang@partners.org RI Pavlova, Ina/I-5332-2012; Richards-Kortum, Rebecca/P-4074-2014 OI Richards-Kortum, Rebecca/0000-0003-2347-9467 NR 11 TC 7 Z9 7 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 0090-8258 J9 GYNECOL ONCOL JI Gynecol. Oncol. PD DEC PY 2005 VL 99 IS 3 SU 1 BP S61 EP S63 DI 10.1016/j.ygyno.2005.07.045 PG 3 WC Oncology; Obstetrics & Gynecology SC Oncology; Obstetrics & Gynecology GA 000ZV UT WOS:000234502500014 PM 16419187 ER PT J AU Goodman, A AF Goodman, A TI Religious and cultural interpretation of illness in the Boston Haitian community and its impact on healthcare SO GYNECOLOGIC ONCOLOGY LA English DT Editorial Material C1 Harvard Univ, Sch Med, Massachusetts Gen Hosp, Gillette Ctr Womens Canc, Boston, MA 02114 USA. RP Goodman, A (reprint author), Harvard Univ, Sch Med, Massachusetts Gen Hosp, Gillette Ctr Womens Canc, Yawkey 9,Fruit St, Boston, MA 02114 USA. EM agoodman@partners.org NR 0 TC 2 Z9 2 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 0090-8258 J9 GYNECOL ONCOL JI Gynecol. Oncol. PD DEC PY 2005 VL 99 IS 3 SU 1 BP S199 EP S200 DI 10.1016/j.ygyno.2005.07.082 PG 2 WC Oncology; Obstetrics & Gynecology SC Oncology; Obstetrics & Gynecology GA 000ZV UT WOS:000234502500052 PM 16419207 ER PT J AU Dowd, BE Coulam, RF Feldman, R Pizer, SD AF Dowd, BE Coulam, RF Feldman, R Pizer, SD TI Fee-for-service Medicare in a competitive market environment SO HEALTH CARE FINANCING REVIEW LA English DT Article ID REGIONAL-VARIATIONS; MANAGED CARE; REFORM AB Since its inception, the Medicare Program has allowed for the participation of private health plans, but the relationship of private plans to the government-sponsored fee-for-service (FFS) plan has been the subject of debate. Increased payments to private plans, the introduction of regional preferred provider organizations (PPOs), and a mandated demonstration of price competition that includes FFS Medicare reflect an ongoing attempt to define the role of Private Plans. The purpose of this article is to explore the roles of private plans and FFS Medicare and to attempt to identify the advantages and disadvantages of each. C1 Univ Minnesota, Sch Publ Hlth, Div Hlth Serv Res & Policy, Minneapolis, MN 55455 USA. VA Boston Hlth Care Syst, Jamaica Plain, MA USA. RP Dowd, BE (reprint author), Univ Minnesota, Sch Publ Hlth, Div Hlth Serv Res & Policy, Box 729 MMC, Minneapolis, MN 55455 USA. EM dowdx001@umn.edu NR 24 TC 4 Z9 4 U1 0 U2 1 PU CENTERS FOR MEDICARE & MEDICAID SERVICES PI BALTIMORE PA 7500 SECURITY BOULEVARD, BALTIMORE, MD 21244-1850 USA SN 0195-8631 J9 HEALTH CARE FINANC R JI Health Care Finan. Rev. PD WIN PY 2005 VL 27 IS 2 BP 113 EP 126 PG 14 WC Health Care Sciences & Services; Health Policy & Services SC Health Care Sciences & Services GA 018RE UT WOS:000235781700011 PM 17290642 ER PT J AU Moffett, ML Morgan, RO Ashton, CM AF Moffett, ML Morgan, RO Ashton, CM TI Strategic opportunities in the oversight of the US hospital accreditation system SO HEALTH POLICY LA English DT Article DE hospital regulation; accreditation; JCAHO; double moral hazard ID ACUTE MYOCARDIAL-INFARCTION; QUALITY; CARE AB Hospital accreditation and state certification are the means that the Centers for Medicare & Medicaid Services (CMS) employs to meet quality of care requirements for medical care reimbursement. Hospitals can choose to use either a national accrediting agency or a state certification inspection in order to receive Medicare payments. Approximately, 80% of hospitals choose the Joint Commission on Accreditation of Healthcare Organizations (JCAHO). The purpose of this paper is to analyze and discuss improvements on the structure of the accreditation process in a Principal-Agent-Supervisor framework with a special emphasis on the oversight by the principal (CMS) of the supervisor (JCAHO). Published by Elsevier Ireland Ltd C1 Baylor Coll Med, Houston Ctr Qual Care & Utilizat Studies, Michael E DeBakey Vet Affairs Med Ctr 152, Houston, TX 77030 USA. RP Moffett, ML (reprint author), Baylor Coll Med, Houston Ctr Qual Care & Utilizat Studies, Michael E DeBakey Vet Affairs Med Ctr 152, 2002 Holcombe Blvd, Houston, TX 77030 USA. EM mauricem@bcm.tmc.edu; rmorgan@bcm.tmc.edu; cashton@bcm.tmc.edu RI Morgan, Robert/A-8577-2009; Moffett, Maurice/I-6664-2013 OI Moffett, Maurice/0000-0002-4536-9843 NR 19 TC 3 Z9 3 U1 1 U2 2 PU ELSEVIER IRELAND LTD PI CLARE PA ELSEVIER HOUSE, BROOKVALE PLAZA, EAST PARK SHANNON, CO, CLARE, 00000, IRELAND SN 0168-8510 J9 HEALTH POLICY JI Health Policy PD DEC PY 2005 VL 75 IS 1 BP 109 EP 115 DI 10.1016/j.healthpol.2005.03.005 PG 7 WC Health Care Sciences & Services; Health Policy & Services SC Health Care Sciences & Services GA 991WY UT WOS:000233846500010 PM 16298233 ER PT J AU Songer, JE Rosowski, JJ AF Songer, JE Rosowski, JJ TI The effect of superior canal dehiscence on cochlear potential in response to air-conducted stimuli in chinchilla SO HEARING RESEARCH LA English DT Article DE superior canal dehiscence; third-window hypothesis; auditory mechanisms ID HEARING-LOSS; MECHANISMS; EARPHONES; VERTIGO; MODEL AB A superior semicircular canal dehiscence (SCD) is a break or hole in the bony wall of the superior semicircular canal. Patients with SCD syndrome present with a variety of symptoms: some with vestibular symptoms, others with auditory symptoms (including low-frequency conductive hearing loss) and yet others with both. We are interested in whether or not mechanically altering the superior canal by introducing a dehiscence is sufficient to cause the low-frequency conductive hearing loss associated with SCD syndrome. We evaluated the effect of a surgically introduced dehiscence on auditory responses to air-conducted (AC) stimuli in 11 chinchilla ears. Cochlear potential (CP) was recorded at the round-window before and after a dehiscence was introduced. In each ear, a decrease in CP in response to low frequency (<2 kHz) sound stimuli was observed after the introduction of the dehiscence. The dehiscence was then patched with cyanoacrylate glue leading to a reversal of the dehiscence-induced changes in CP. The reversible decrease in auditory sensitivity observed in chinchilla is consistent with the elevated AC thresholds observed in patients with SCD. According to the 'third-window' hypothesis the SCD shunts sound-induced stapes velocity away from the cochlea, resulting in decreased auditory sensitivity to AC sounds. The data collected in this study are consistent with predictions of this hypothesis. (c) 2005 Elsevier B.V. All rights reserved. C1 Massachusetts Eye & Ear Infirm, Eaton Peabody Lab Auditory Physiol, Boston, MA 02114 USA. Harvard Univ, MIT, Cambridge, MA 02138 USA. Harvard Univ, Sch Med, Dept Otol & Laryngol, Boston, MA 02115 USA. RP Songer, JE (reprint author), Massachusetts Eye & Ear Infirm, Eaton Peabody Lab Auditory Physiol, 243 Charles St, Boston, MA 02114 USA. EM jocelyns@mit.edu; John_Rosowski@meei.harvard.edu FU NIDCD NIH HHS [R01 DC000194] NR 22 TC 37 Z9 41 U1 0 U2 4 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD DEC PY 2005 VL 210 IS 1-2 BP 53 EP 62 DI 10.1016/j.heares.2005.07.003 PG 10 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 991EQ UT WOS:000233795500006 PM 16150562 ER PT J AU Cury, RC Abbara, S Schmidt, S Malchano, ZJ Neuzil, P Weichet, J Ferencik, M Hoffmann, U Ruskin, JN Brady, TJ Reddy, VY AF Cury, RC Abbara, S Schmidt, S Malchano, ZJ Neuzil, P Weichet, J Ferencik, M Hoffmann, U Ruskin, JN Brady, TJ Reddy, VY TI Relationship of the esophagus and aorta to the left atrium and pulmonary veins: Implications for catheter ablation of atrial fibrillation SO HEART RHYTHM LA English DT Article DE catheter ablation; multidetector computed tomography; complications; atrial fibrillation; esophagus ID RADIOFREQUENCY ABLATION; TRANSCATHETER; COMPLICATION; FISTULA; LESIONS AB Background A potential complication during ablation of atrial fibrillation (AF) is damage to adjacent structures such as the esophagus and aorta. Fatal atrio-esophageal fistulas have developed after surgery- or catheter-based AF ablation procedures. Objectives The purpose of this study was to analyze multidetector computed tomography (MDCT) angiographic images to determine the anatomic relationship of the aorta and esophagus to the left atrium (LA). Methods Sixty-five subjects underwent CT imaging using a 16-slice MDCT scanner: 24 with paroxysmal AF, 21 with chronic AF, and 20 "control" subjects without a history of AF. Measurements assessed included LA diameters, width of the esophagus and aorta in contact with the posterior LA wall, and distance from the esophagus to the four pulmonary veins (PVs), spine, and LA endocardium. Results Mean LA diameters were significantly larger in patients with AF vs the control group (P=.003 for anteroposterior diameter; P=.009 for transverse diameter). The anterior aspect of the esophagus was directly apposed to the LA in all cases (contact width 18.9 +/- 4.4 mm). The position of the esophagus varied in the posterior mediastinum but on average was closer to the ostia of the left PVs (P=.0001). The descending aorta was in contact with the LA and/or left PVs in 50 of 65 subjects. The esophagus was closer to the spine in the chronic AF vs control group (P=.007), likely due to increased LA dimension. Conclusion In addition to its ability to assess PV anatomy, preprocedural MDCT imaging can investigate the variable relationship of adjacent structures, such as the esophagus and aorta to the LA and PVs. C1 Harvard Univ, Sch Med, Massachusetts Gen Hosp, Cardiac Arrhythmia Serv, Boston, MA 02114 USA. Harvard Univ, Sch Med, Massachusetts Gen Hosp, Cardiac CT Unit, Boston, MA 02114 USA. Na Homolce Hosp, Cardiac Arrhythmia Serv, Prague, Czech Republic. RP Reddy, VY (reprint author), Harvard Univ, Sch Med, Massachusetts Gen Hosp, Cardiac Arrhythmia Serv, 55 Fruit St,Gray Bigelow 109, Boston, MA 02114 USA. EM vreddy@partners.org FU NHLBI NIH HHS [K23 HL68064-02] NR 15 TC 48 Z9 50 U1 0 U2 4 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 1547-5271 J9 HEART RHYTHM JI Heart Rhythm PD DEC PY 2005 VL 2 IS 12 BP 1317 EP 1323 DI 10.1016/j.hrthm.2005.09.012 PG 7 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA 997JJ UT WOS:000234241200007 PM 16360083 ER PT J AU Armato, SG Oxnard, GR AF Armato, SG Oxnard, GR TI The radiologic measurement of mesothelioma SO HEMATOLOGY-ONCOLOGY CLINICS OF NORTH AMERICA LA English DT Article ID MALIGNANT PLEURAL MESOTHELIOMA; LEUKEMIA GROUP-B; PHASE-II TRIAL; SOLID TUMORS; INTRAOBSERVER VARIABILITY; RESPONSE EVALUATION; RECIST CRITERIA; LUNG LESIONS; CT SCANS; ONCOLOGY AB The radiologic evaluation of disease, which now includes the quantification of disease, has become an essential part of clinical medicine. The unique circumferential and often scalloped morphology of mesothelioma, however, distinguishes it from other thoracic neoplasms. The challenges of measuring mesothelioma are many. In this article, the authors explore the demands, the current standard of clinical practice, and the opportunities associated with the radiologic measurement of mesothelioma. C1 Univ Chicago, Dept Radiol, Chicago, IL 60637 USA. Massachusetts Gen Hosp, Dept Med, Boston, MA 02114 USA. RP Armato, SG (reprint author), Univ Chicago, Dept Radiol, 5841 S Maryland Ave,MC 2026, Chicago, IL 60637 USA. EM s-armato@uchicago.edu NR 39 TC 1 Z9 1 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 USA SN 0889-8588 J9 HEMATOL ONCOL CLIN N JI Hematol. Oncol. Clin. North Am. PD DEC PY 2005 VL 19 IS 6 BP 1053 EP + DI 10.1016/j.hoc.2005.09.002 PG 15 WC Oncology; Hematology SC Oncology; Hematology GA 998PZ UT WOS:000234332600005 PM 16325123 ER PT J AU Isomoto, H Kobayashi, S Werneburg, NW Bronk, SF Guicciardi, ME Frank, DA Gores, GJ AF Isomoto, H Kobayashi, S Werneburg, NW Bronk, SF Guicciardi, ME Frank, DA Gores, GJ TI Interleukin 6 upregulates myeloid cell leukemia-1 expression through a STAT3 pathway in cholanglocarcinoma cells SO HEPATOLOGY LA English DT Article ID ACTIVATED PROTEIN-KINASE; CHOLANGIOCARCINOMA CELLS; SIGNALING PATHWAY; GROWTH-FACTOR; MCL-1; LINE; APOPTOSIS; ESTABLISHMENT; PROLIFERATION; INHIBITION AB Interleukin 6 (IL-6) contributes to the pathogenesis of cholangiocarcinoma by upregulating myeloid cell leukemia- 1 (Mcl-1), a key antiapoptotic Bd-2 family member protein. IL-6 can after gene transcription via Janus kinases UAK) and signal transducer and activator of transcription (STAT) signal cascade. We examined this cascade in IL-6 regulation of Mcl-1 transcription in human cholangiocarcinoma cell lines. STAT3 was constitutively activated (i.e., tyrosine-phosphorylated) in cholangiocarcinoma cells but not in nonmalignant cholangiocytes. Treatment with anti-IL-6 antisera or the JAK inhibitor AG490 or transfection with dominant negative STAT3 diminished Mcl-1 messenger RNA and protein levels. Likewise, these attempts to interrupt the STAT3 cascade also reduced Mcl-1 promoter activity. Site-directed mutagenesis of a putative STAT3 consensus binding sequence decreased Mcl-1 promoter activity. Chromatin immunoprecipitation analysis demonstrated a direct binding of STAT3 to the putative STAT3 binding sequences in the Mcl-1 promoter. Downregulation of Mcl-1 by AG490 sensitized the cells to apoptosis mediated by tumor necrosis factor-related apoptosis-inducing ligand. In conclusion, we have directly demonstrated a STAT3 regulatory element in the Mcl-1 promoter. Downregulation of Mcl-1 transcription by inhibiting this cascade is a potential strategy for the treatment of this cancer. Supplementary material for this article can be found on the HEPATOLOGY website (http://interscience.wiley.com/jpages/0270-9139/uppmat/index.html). C1 Mayo Clin & Mayo Fdn, Rochester, MN 55905 USA. Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02115 USA. RP Gores, GJ (reprint author), Mayo Clin & Mayo Fdn, 200 1st St SW, Rochester, MN 55905 USA. EM gores.gregory@mayo.edu FU NIDDK NIH HHS [DK-59427] NR 34 TC 122 Z9 134 U1 0 U2 1 PU JOHN WILEY & SONS INC PI HOBOKEN PA 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 0270-9139 J9 HEPATOLOGY JI Hepatology PD DEC PY 2005 VL 42 IS 6 BP 1329 EP 1338 DI 10.1002/hep.20966 PG 10 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA 989TS UT WOS:000233697400015 PM 16317687 ER PT J AU Schiano, TD Gutierrez, JA Walewski, JL Fiel, MI Cheng, B Bodenheimer, H Thung, SN Chung, RT Schwartz, ME Bodian, C Branch, AD AF Schiano, TD Gutierrez, JA Walewski, JL Fiel, MI Cheng, B Bodenheimer, H Thung, SN Chung, RT Schwartz, ME Bodian, C Branch, AD TI Accelerated hepatitis C virus kinetics but similar survival rates in recipients of liver grafts from living versus deceased donors SO HEPATOLOGY LA English DT Article ID RIGHT LOBE ADULT; TRANSPLANT RECIPIENTS; CORE ANTIGEN; HISTOLOGIC RECURRENCE; PATIENT SURVIVAL; HCV RNA; ALLOGRAFT; INFECTION; DAMAGE AB This study tested the hypothesis that hepatitis C virus (HCV) RNA and core antigen levels rise more rapidly after liver transplantation (LT) in recipients of grafts from living donors (LD) versus deceased donors (DD). Eleven consecutive LD and 15 DD recipients were followed prospectively. Before LT, median HCV RNA levels were similar: 5.42 (LDLT) and 5.07 (DDLT) log(10) IU/mL (P = NS). During the first 7 hours after LT a trend toward a greater HCV RNA decrease in LDLT patients was seen, although they received fewer blood replacement products during surgery. HCV RNA levels rose more rapidly in LDLT patients between days 1 and 3 (P = .0059) and were higher in this group on days 2, 3, 4, and 5. Core antigen levels were significantly higher in LDLT patients on days 3 and 5, although they were similar before LT (P = NS). Alanine aminotransferase (ALT) values were higher among LDLT patients from 8 to 14 days and from 4 to 24 months. Two-year graft and patient survival were 73% for LDLT patients and 80% for DDLT patients (P = NS). In conclusion, viral load rose more rapidly in LD recipients and reached higher levels shortly after surgery. Greater ALT elevations were evident in the LDLT group, but survival rates were similar. The trend toward a greater initial viral load decrease in patients with LD grafts and the significantly sharper increase suggest that the liver plays a predominant role in both HCV clearance and replication. C1 Mt Sinai Sch Med, Div Liver Dis, Dept Med, New York, NY 10029 USA. Mt Sinai Hosp, Recanati Miller Transplantat Inst, New York, NY 10029 USA. Mt Sinai Sch Med, Dept Pathol, New York, NY 10029 USA. Mt Sinai Sch Med, Dept Surg, New York, NY 10029 USA. Mt Sinai Sch Med, Dept Anesthesiol, New York, NY 10029 USA. Beth Israel Med Ctr, Div Digest Dis, New York, NY 10003 USA. Massachusetts Gen Hosp, Gastrointestinal Unit, Boston, MA 02114 USA. RP Branch, AD (reprint author), Mt Sinai Sch Med, Div Liver Dis, Dept Med, 1425 Madison Ave, New York, NY 10029 USA. EM andrea.brancb@mssm.edu FU NIDA NIH HHS [DA 016156]; NIDDK NIH HHS [DK 066939, DK 052071] NR 37 TC 30 Z9 31 U1 0 U2 0 PU JOHN WILEY & SONS INC PI HOBOKEN PA 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 0270-9139 J9 HEPATOLOGY JI Hepatology PD DEC PY 2005 VL 42 IS 6 BP 1420 EP 1428 DI 10.1002/hep.20947 PG 9 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA 989TS UT WOS:000233697400026 PM 16317672 ER PT J AU Brown, AB Mahmood, U Cortes, ML Tang, Y Dai, G Stemmer-Rachamimov, A Prabhakar, S Leishear, K Onda, H Kwiatkowski, D Weissleder, R Breakefield, X AF Brown, AB Mahmood, U Cortes, ML Tang, Y Dai, G Stemmer-Rachamimov, A Prabhakar, S Leishear, K Onda, H Kwiatkowski, D Weissleder, R Breakefield, X TI Magnetic resonance imaging and characterization of spontaneous lesions in a transgenic mouse model of tuberous sclerosis as a model for endothelial cell-based transgene delivery SO HUMAN GENE THERAPY LA English DT Article ID TUBEROUS-SCLEROSIS-COMPLEX-2 TSC2; EMBRYONIC LETHALITY; DIRECT TARGET; GENE; RHEB; COMPLEX; GROWTH; MICE; MTOR; LINE AB Tuberous sclerosis (TSC) is an autosomal dominant genetic disorder characterized by abnormalities in cellular migration, proliferation, and differentiation in many tissues. Benign hamartomas develop in multiple organs, believed to be caused by somatic mutation in addition to germ line mutation to cause loss of both alleles of either the TSC1 or TSC2 tumor suppressor gene, with resultant dysregulated growth due to loss of hamartin or tuberin function, respectively. This study focuses on detecting spontaneous lesions in a knockout mouse model of TSC2 by magnetic resonance imaging (MRI) and exploring the efficiency of introducing gene products into lesions, using transduced endothelial cells as gene vehicles. MRI was shown to be effective in detecting spontaneous lesions in multiple tissues as a means of assessing the prevalence of tumors. Tsc2(-/+) heterozygous mice were screened at 12-24 months of age. MRI detected 100% of the renal lesions (cystadenomas, renal cell carcinomas) and 75% of the hepatic lesions (hemangiosarcomas), later identified by histology. Cell-mediated gene delivery was evaluated by immunohistochemical analysis of renal, hepatic, and lung lesions after intravenous delivery of MS1 mouse endothelial cells, transduced to express an enhanced form of green fluorescent protein (EGFP). Preliminary immunohistochemical analysis, using a polyclonal antibody to EGFP and a horseradish peroxidase-diaminobenzidine detection system, revealed these cells throughout liver, kidney, and lung sections from injected animals, organs that are frequently affected in TSC2 patients, as well as within the lesions themselves. C1 Massachusetts Gen Hosp, Brain Tumor Ctr, Boston, MA 02114 USA. Harvard Univ, Sch Med, Boston, MA 02114 USA. Massachusetts Gen Hosp, Dept Neurol, Mol Neurogenet Unit, Boston, MA 02114 USA. Massachusetts Gen Hosp, Ctr Mol Imagen Res, Boston, MA 02114 USA. Harvard Univ, Sch Med, Boston, MA 02115 USA. Brigham & Womens Hosp, Dept Med, Boston, MA 02115 USA. Massachusetts Gen Hosp, Dept Radiol, Martinos Ctr, Boston, MA 02114 USA. Massachusetts Gen Hosp, Dept Pathol, Boston, MA 02114 USA. RP Brown, AB (reprint author), Massachusetts Gen Hosp, Brain Tumor Ctr, Cox 315,100 Blossom St, Boston, MA 02114 USA. EM abrown2@caregroup.harvard.edu FU NCI NIH HHS [R24 CA92782, P50 CA86355, CA69246]; NINDS NIH HHS [NS24279] NR 28 TC 2 Z9 2 U1 0 U2 3 PU MARY ANN LIEBERT, INC PI NEW ROCHELLE PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA SN 1043-0342 EI 1557-7422 J9 HUM GENE THER JI Hum. Gene Ther. PD DEC PY 2005 VL 16 IS 12 BP 1367 EP 1376 DI 10.1089/hum.2005.16.1367 PG 10 WC Biotechnology & Applied Microbiology; Genetics & Heredity; Medicine, Research & Experimental SC Biotechnology & Applied Microbiology; Genetics & Heredity; Research & Experimental Medicine GA 997NP UT WOS:000234253000002 PM 16390268 ER PT J AU Thadhani, RI Johnson, RJ Karumanchi, SA AF Thadhani, RI Johnson, RJ Karumanchi, SA TI Hypertension during pregnancy - A disorder begging for pathophysiological support SO HYPERTENSION LA English DT Editorial Material ID PLACENTAL GROWTH-FACTOR; SERUM URIC-ACID; ENDOTHELIAL DYSFUNCTION; TYROSINE KINASE-1; PREECLAMPSIA; RISK; ANGIOGENESIS; URATE C1 Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Med, Boston, MA 02114 USA. Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Obstet & Gynecol, Boston, MA 02114 USA. Harvard Univ, Sch Med, Beth Israel Deaconess Med Ctr, Dept Med, Boston, MA 02114 USA. Harvard Univ, Sch Med, Beth Israel Deaconess Med Ctr, Dept Obstet & Gynecol, Boston, MA 02114 USA. Univ Florida, Div Nephrol Hypertens & Transplantat, Gainesville, FL USA. RP Thadhani, RI (reprint author), Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Med, Bullfinch 127,55 Fruit St, Boston, MA 02114 USA. EM thadhani.r@mgh.harvard.edu FU NHLBI NIH HHS [HL079594, HL068607]; NICHD NIH HHS [HD39223]; NIDDK NIH HHS [DK067397] NR 26 TC 17 Z9 17 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3261 USA SN 0194-911X J9 HYPERTENSION JI Hypertension PD DEC PY 2005 VL 46 IS 6 BP 1250 EP 1251 DI 10.1161/01.HYP.0000188701.24418.64 PG 2 WC Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 987ZX UT WOS:000233557700004 PM 16246974 ER PT J AU Chang, HC Tan, KM Ouyang, J Parisini, E Liu, JH Le, Y Wang, XS Reinherz, EL Wang, JH AF Chang, HC Tan, KM Ouyang, J Parisini, E Liu, JH Le, Y Wang, XS Reinherz, EL Wang, JH TI Structural and mutational analyses of a CD8 alpha beta heterodimer and comparison with the CD8 alpha alpha homodimer SO IMMUNITY LA English DT Article ID CLASS-I MOLECULE; T-CELL-RECEPTOR; CD8 BETA-CHAIN; IMMUNOGLOBULIN SUPERFAMILY DOMAINS; CRYSTAL-STRUCTURE; CORECEPTOR FUNCTION; DIFFERENTIAL EXPRESSION; ECTODOMAIN FRAGMENT; POSITIVE SELECTION; VARIABLE DOMAINS AB The crystal structure of a recombinant mouse single chain CD8 alpha beta ectodomains at 2.4 A resolution reveals paired immunoglobulin variable region-like domains with a striking resemblance to CD8 alpha alpha in size, shape, and surface electrostatic potential of complementarity determining regions (CDR), despite < 20% sequence identity between the CD8 alpha and CD8 beta subunits. Unlike the CD8 alpha subunit(s) in the heterodimer or homodimer, the CDR1 loop of CD8 beta tilts away from its corresponding CDR2 and CDR3 loops. Consistent with this observation, independent mutational studies reveal that alanine substitutions of residues in the CDR1 loop of CD8 beta have no effect on CD8 alpha beta coreceptor function, whereas mutations in CD8 beta CDR2 and CDR3 loops abolish CD8 alpha beta coreceptor activity. The implications of these findings and additional CD8 alpha beta mutational studies for CD8 alpha beta- versus CD8 alpha-MHCI binding are discussed. C1 Harvard Univ, Sch Med, Dana Farber Canc Inst, Lab Immunobiol,Dept Med Oncol,Dept Med, Boston, MA 02115 USA. Harvard Univ, Sch Med, Dept Pediat, Dept Biol Chem & Mol Pharmacol, Boston, MA 02115 USA. RP Chang, HC (reprint author), Harvard Univ, Sch Med, Dana Farber Canc Inst, Lab Immunobiol,Dept Med Oncol,Dept Med, 44 Binney St, Boston, MA 02115 USA. EM hsiu-ching_chang@dfci.harvard.edu FU NHLBI NIH HHS [HL48675]; NIAID NIH HHS [AI19807, AI45789] NR 63 TC 27 Z9 29 U1 1 U2 5 PU CELL PRESS PI CAMBRIDGE PA 1100 MASSACHUSETTS AVE, CAMBRIDGE, MA 02138 USA SN 1074-7613 J9 IMMUNITY JI Immunity PD DEC PY 2005 VL 23 IS 6 BP 661 EP 671 DI 10.1016/j.immuni.2005.11.002 PG 11 WC Immunology SC Immunology GA 998KH UT WOS:000234316900012 PM 16356863 ER PT J AU Ehrlich, LA Roodman, GD AF Ehrlich, LA Roodman, GD TI The role of immune cells and inflammatory cytokines in Paget's disease and multiple myeloma SO IMMUNOLOGICAL REVIEWS LA English DT Review ID NECROSIS-FACTOR-ALPHA; MARROW STROMAL CELLS; KAPPA-B LIGAND; COLONY-STIMULATING FACTOR; HUMAN BONE-MARROW; PLASMA-CELLS; OSTEOCLAST DIFFERENTIATION; MULTINUCLEATED CELLS; RECEPTOR ACTIVATOR; DENDRITIC CELLS AB The osteoclast (OCL) is the primary cell involved in the pathogenesis of Paget's disease (PD) and the destructive bone process in multiple myeloma (MM). Both of these diseases are characterized by increased numbers of OCLs actively resorbing bone, but they differ in that bone formation is greatly increased in PD and is suppressed in MM. The marrow microenvironment plays a critical role in both disease processes, through the increased expression of inflammatory cytokines that enhance osteoclastogenesis and, in the case of MM, also suppress osteoblast (OBL) activity. In addition, the OCLs in PD are intrinsically abnormal, are markedly increased in number and size, and are hyper-responsive to inflammatory cytokines and 1,25-(OH)(2)D-3. This article discusses the role of immune cells and inflammatory cytokines and chemokines in the increased OCL activity in PD and MM bone disease, as well as the potential role of interleukin-3 in the suppression of OBL activity in MM. C1 VA Pittsburth Healthcare Syst, Pittsburgh, PA 15240 USA. Univ Pittsburgh, Dept Med Hematol Oncol, Pittsburgh, PA USA. RP Roodman, GD (reprint author), VA Pittsburth Healthcare Syst, R&D,151 U,Room 2E-113,Univ Dr C, Pittsburgh, PA 15240 USA. EM roodmangd@upmc.edu NR 111 TC 45 Z9 45 U1 0 U2 3 PU BLACKWELL PUBLISHING PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DQ, OXON, ENGLAND SN 0105-2896 J9 IMMUNOL REV JI Immunol. Rev. PD DEC PY 2005 VL 208 BP 252 EP 266 DI 10.1111/j.0105-2896.2005.00323.x PG 15 WC Immunology SC Immunology GA 986JN UT WOS:000233446000018 PM 16313353 ER PT J AU Mora, JR Iwata, M Eksteen, B Song, SY Senman, B Adams, DH von Andrian, UH AF Mora, JR Iwata, M Eksteen, B Song, SY Senman, B Adams, DH von Andrian, UH TI Dynamic control of lymphocyte homing by dendritic cells and retinoids SO IMMUNOLOGY LA English DT Meeting Abstract C1 Harvard Univ, Sch Med, CBRI, Boston, MA 02115 USA. Tokushima Bunri Univ, Lab Biodef Res, Tokushima 7708514, Japan. Univ Birmingham, Queen Elizabeth Hosp, Birmingham B15 2TT, W Midlands, England. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL PUBLISHING PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DQ, OXON, ENGLAND SN 0019-2805 J9 IMMUNOLOGY JI Immunology PD DEC PY 2005 VL 116 SU 1 BP 27 EP 27 PG 1 WC Immunology SC Immunology GA 987QC UT WOS:000233531400116 ER PT J AU Reinecker, HC AF Reinecker, HC TI Pathways for antigen acquisition and presentation in the intestine SO IMMUNOLOGY LA English DT Meeting Abstract C1 Massachusetts Gen Hosp, Boston, MA 02114 USA. NR 0 TC 0 Z9 0 U1 1 U2 1 PU BLACKWELL PUBLISHING PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DQ, OXON, ENGLAND SN 0019-2805 J9 IMMUNOLOGY JI Immunology PD DEC PY 2005 VL 116 SU 1 BP 27 EP 27 PG 1 WC Immunology SC Immunology GA 987QC UT WOS:000233531400118 ER PT J AU Takahashi, K Shi, L Gowda, LD Ezekowitz, RAB AF Takahashi, K Shi, L Gowda, LD Ezekowitz, RAB TI Relative roles of complement factor 3 and mannose-binding lectin in host defense against infection SO INFECTION AND IMMUNITY LA English DT Article ID STAPHYLOCOCCUS-AUREUS; SERINE-PROTEASE; ACTIVATES COMPLEMENT; IMMUNE-RESPONSE; INNATE IMMUNITY; DEFICIENT MICE; COMPONENT C3; RECEPTOR; SERUM; PATHWAY AB Staphylococcus aureus is a major cause of severe nosocomial and community-acquired infections. Phagocytes and humoral molecules, including complement, have been proposed to cooperate in host defense against gram-positive bacteria. Circumstantial evidence indicates a role for complement, but this has not been formally defined. Complement activation is initiated by the classical, alternative, or lectin pathway, with the latter requiring mannose-binding lectin (MBL, also known as mannose-binding protein). MBL is an oligomeric serum protein that recognizes carbohydrates decorating a broad range of infectious agents, including S. aureus. We previously reported that MBL null mice were highly susceptible to S. aureus infection, confirming that MBL plays a key role in first-line host defense. In this study, we evaluated the relative roles of C3 and MBL against S. aureus infection by generating MBL X C3 null mice to compare with C3 single null mice. C3 deficiency alone significantly reduced survival to 19% from 97% of wild-type mice (P < 0.0001). Surprisingly, an additional MBL deficiency reduced the survival further to 7% (P < 0.0001). However, the MBL deficiency alone had a smaller though significant effect on survival, which was 77% (P = 0.018 versus wild-type mice). These results confirm an essential function for complement in host resistance against S. aureus infection but also identify an MBL-dependent mechanism that is C3 independent. C1 Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Pediat,Lab Dev Immunol, Boston, MA 02114 USA. RP Takahashi, K (reprint author), Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Pediat,Lab Dev Immunol, 55 Fruit St,GRJ 1402, Boston, MA 02114 USA. EM ktakahashi1@partners.org FU NIAID NIH HHS [R01 AI042788, R01AI42788] NR 49 TC 23 Z9 23 U1 0 U2 1 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA SN 0019-9567 J9 INFECT IMMUN JI Infect. Immun. PD DEC PY 2005 VL 73 IS 12 BP 8188 EP 8193 DI 10.1128/IAI.73.12.8188-8193.2005 PG 6 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA 986WK UT WOS:000233480200047 PM 16299314 ER PT J AU Tang, RJ Breger, J Idnurm, A Gerik, KJ Lodge, JK Heitman, J Calderwood, SB Mylonakis, E AF Tang, RJ Breger, J Idnurm, A Gerik, KJ Lodge, JK Heitman, J Calderwood, SB Mylonakis, E TI Cryptococcus neoformans gene involved in mammalian pathogenesis identified by a Caenorhabditis elegans progeny-based approach SO INFECTION AND IMMUNITY LA English DT Article ID MAP KINASE PATHWAYS; SACCHAROMYCES-CEREVISIAE; EXCHANGE FACTOR; CELL INTEGRITY; VIRULENCE; PROTEIN; MODEL; HOMOLOG; HOST; PKC1 AB Caenorhabditis elegans can serve as a substitute host for the study of microbial pathogenesis. We found that mutations in genes of the fungal pathogen Cryptococcus neoformians involved in mammalian virulence allow C. elegans to produce greater numbers of progeny than when exposed to wild-type fungus. We used this property to screen a library of C. neoformans mutants for strains that permit larger C. elegans brood sizes. In this screen, we identified a gene homologous to Saccharomyces cerevisiae ROM2. C. neoformans rom2 mutation resulted in a defect in mating and growth defects at elevated temperature or in the presence of cell wall or hyperosmolar stresses. An effect of the C. neoformans rom2 mutation in virulence was confirmed in a murine inhalation infection model. We propose that a screen for progeny-permissive mutants of microorganisms can serve as a high-throughput method for identifying novel loci related to mammalian pathogenesis. C1 Massachusetts Gen Hosp, Div Infect Dis, Boston, MA 02114 USA. Duke Univ, Med Ctr, Dept Mol Genet & Microbiol, Durham, NC 27710 USA. Duke Univ, Med Ctr, Div Infect Dis, Durham, NC 27710 USA. Duke Univ, Med Ctr, Dept Med, Durham, NC 27710 USA. Duke Univ, Med Ctr, Howard Hughes Med Inst, Durham, NC 27710 USA. St Louis Univ, Sch Med, Edward A Doisy Dept Biochem & Mol Biol, St Louis, MO 63104 USA. St Louis Univ, Sch Med, Dept Mol Microbiol & Immunol, St Louis, MO 63104 USA. Harvard Univ, Sch Med, Dept Microbiol & Mol Genet, Boston, MA 02114 USA. RP Mylonakis, E (reprint author), Massachusetts Gen Hosp, Div Infect Dis, Gray Jackson 504,55 Fruit St, Boston, MA 02114 USA. EM emylonakis@partners.org RI Idnurm, Alexander/K-8558-2013 OI Idnurm, Alexander/0000-0001-5995-7040 FU NIAID NIH HHS [K08 AI63084-01, K08 AI063084] NR 41 TC 38 Z9 41 U1 1 U2 5 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA SN 0019-9567 J9 INFECT IMMUN JI Infect. Immun. PD DEC PY 2005 VL 73 IS 12 BP 8219 EP 8225 DI 10.1128/IAI.73.12.8219-8225.2005 PG 7 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA 986WK UT WOS:000233480200051 PM 16299318 ER PT J AU Zeng, XY Moore, TA Newstead, MW Deng, JC Kunkel, SL Luster, AD Standiford, TJ AF Zeng, XY Moore, TA Newstead, MW Deng, JC Kunkel, SL Luster, AD Standiford, TJ TI Interferon-inducible protein 10, but not monokine induced by gamma interferon, promotes protective type 1 immunity in murine Klebsiella pneumoniae pneumonia SO INFECTION AND IMMUNITY LA English DT Article ID MONONUCLEAR-CELL ACCUMULATION; INDUCIBLE PROTEIN-10; T-CELLS; LEGIONELLA-PNEUMOPHILA; TRANSGENIC EXPRESSION; ALVEOLAR MACROPHAGES; BACTERIAL CLEARANCE; PULMONARY DEFENSES; DENDRITIC CELLS; CXC CHEMOKINES AB CXC chemokines that lack the ELR motif, including interferon-inducible protein 10 [IP-10 (CXCL10)] and monokine induced by gamma interferon (IFN-gamma) [MIG (CXCL9)], have been shown to mediate the generation of type I immune responses. In this study, we found that intrapulmonary administration of the gram-negative bacterium Klebsiella pneumoniae resulted in the local and systemic expression of IP-10, followed sequentially by MIG expression. MIG mRNA expression in the lungs of Klebsiella-infected mice required the endogenous production of IFN-gamma, whereas IP-10 was expressed in both an IFN-gamma-dependent and an IFN-gamma-independent fashion. Antibody-mediated neutralization of IP-10 resulted in reduced bacterial clearance and decreased survival, whereas bacterial clearance was unaltered in mice treated with anti-MIG antibody. Impaired bacterial clearance in anti-IP-10 antibody-treated mice was associated with significant reductions in the number and/or activational status of NK and NK-T cells, CD4(+) T cells, and gamma delta T cells, as well as a reduction in the expression of IFN-gamma. Conversely, the transient transgenic expression of murine IP-10 using adenovirus-mediated gene transfer resulted in improved bacterial clearance when IP-10 adenovirus was given concomitant with intrapulmonary bacterial challenge. These results indicate that IP-10 is an important component of innate immunity against extracellular bacterial pathogens of the lung and may represent a candidate molecule for immunotherapy in the setting of severe respiratory tract infection. C1 Univ Michigan, Med Ctr, Div Pulm & Crit Care Med, Dept Pathol, Ann Arbor, MI 48109 USA. Univ Michigan, Med Ctr, Div Pulm & Crit Care Med, Dept Med, Ann Arbor, MI 48109 USA. Massachusetts Gen Hosp, Dept Med, Div Rheumatol Allergy & Immunol, Boston, MA 02114 USA. RP Standiford, TJ (reprint author), Univ Michigan, Med Ctr, Div Pulm & Crit Care Med, Dept Pathol, 6301 MSRB 3,1150 W Med Ctr Dr, Ann Arbor, MI 48109 USA. EM tstandif@umich.edu FU NHLBI NIH HHS [HL57243, P05 HL60289, R01 HL057243] NR 41 TC 36 Z9 36 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA SN 0019-9567 J9 INFECT IMMUN JI Infect. Immun. PD DEC PY 2005 VL 73 IS 12 BP 8226 EP 8236 DI 10.1128/IAI.73.12.8226-8236.2005 PG 11 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA 986WK UT WOS:000233480200052 PM 16299319 ER PT J AU Shibolet, O Alper, R Ilan, Y Weidenfeld, J AF Shibolet, O Alper, R Ilan, Y Weidenfeld, J TI Regulatory role of the pituitary-adrenal axis in experimental colitis: Effect of adrenalectomy on the clinical course and the T(H)1/T(H)2 immune profile SO INFLAMMATORY BOWEL DISEASES LA English DT Article DE hypothalamus-pituitary-adrenal axis; adrenalectomy; trinitrobenzene sulfonic acid colitis ID INFLAMMATORY-BOWEL-DISEASE; EXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITIS; NEUROENDOCRINE REGULATION; NERVOUS-SYSTEM; HPA-AXIS; GLUCOCORTICOIDS; ACTIVATION; CELLS; RATS; RECEPTORS AB Background: The hypothalalkic-pituitary-adrenal (HPA) axis plays an important role in modulating immune reactions in inflammatory bowel disease. Our aim was to assess the role of the HPA axis in the pathogenesis of immunomediated colitis in mice. Methods: Trinitrobenzene sulfonic acid (TNBS) colitis was induced in Balb/c mice. Sham operation (sham+TNBS) or bilateral adrenalectomy (Adex+TNBS) was performed 3 days later. Control groups underwent adrenalectomy Without colitis induction (Adex) or were untreated [naive mice (Naive)]. Mice were monitored for Survival, Weight loss, and macroscopic and microscopic scores of colitis. FACS analysis of CD4(+), CD8(+), natural killer T lymphocytes, and serum levels of adrenocorticotropic hormone (ACTI-1), corticosterone (CS), interferon-gamma (IFN-gamma), interleukin-10 (IL-10), and IL-1 beta were Measured. Production of prostaglandin E(2) (PGE(2)) and binding capacity to glucocorticoid receptor (GR) in Colonic mucosa were also assessed. Results: By day 7 following induction of colitis there was it marked increase in ACTH and CS levels in the colitis as compared with the control group (86 +/- 6.5 pg/mL and 16 +/- 1.9 pg/mL, and 23.3 +/- 2 pg/mL and 2.8 +/- 0.8 pg/mL, respectively). There was a decrease in ACTH and CS levels by day 28 in the colitis group, but file levels were still significantly higher than the levels in controls. Adrenalectomy markedly exacerbated colitis. The macroscopic and microscopic scores increased from 2.79 +/- 0.03 and 2.0 +/- 0.1 in the sham+TNBS group to 3.3 +/- 0.3 and 3.2 +/- 0.3 in the Adex+TNBS group. Survival and weight loss correlated with these differences. A significant increase in IL-10, IFN-gamma, and PGE2 was noted in the Adex+TNBS group compared with the shanl+TNBS group. Splenic CD4(+) lymphocytes decreased in the sham+TNBS and Adex+TNBS groups as compared with control groups (Adex and naive). The CD8(+)/CD4(+) ratio was significantly higher in the Adex+TNBS compared with the sham+TNBS group. Colitis also Caused a significant decrease in the specific binding capacity of labeled dexamethasone to Colonic mucosa. Conclusions: TNBS induced colitis activated the HPA axis and reduced file sensitivity of the inflamed mucosa to circulating glucocorticoids. Adrenalectomy markedly exacerbated TNBS-induced colitis. The effect was associated with changes in the peripheral CDS(+)/CD4(+) ratio and with it T(H)l cytokine shift. Our results suggest that adrenocortical hormones play all important role in the regulation of the immune system in experimental colitis. C1 Hebrew Univ Jerusalem, Hadassah Med Ctr, Liver Unit, Div Med, Jerusalem, Israel. Hebrew Univ Jerusalem, Hadassah Med Ctr, Dept Neurol, Agnes Ginges Ctr Human Neurogenet, Jerusalem, Israel. RP Shibolet, O (reprint author), Massachusetts Gen Hosp, Gastroenterol Unit GRJ715, 55 Fruit St, Boston, MA 02114 USA. EM oshibolet@partners.org NR 27 TC 10 Z9 11 U1 0 U2 2 PU WILEY-BLACKWELL PI MALDEN PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA SN 1078-0998 J9 INFLAMM BOWEL DIS JI Inflamm. Bowel Dis. PD DEC PY 2005 VL 11 IS 12 BP 1053 EP 1059 DI 10.1097/01.MIB.0000191610.97842.51 PG 7 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA 990PA UT WOS:000233754500004 PM 16306767 ER PT J AU Rubio, MT Means, TK Chakraverty, R Shaffer, J Fudaba, Y Chittenden, M Luster, AD Sykes, M AF Rubio, MT Means, TK Chakraverty, R Shaffer, J Fudaba, Y Chittenden, M Luster, AD Sykes, M TI Maturation of human monocyte-derived dendritic cells (MoDCs) in the presence of prostaglandin E-2 optimizes CD4 and CD8 T cell-mediated responses to protein antigens: role of PGE(2) in chemokine and cytokine expression by MoDCs SO INTERNATIONAL IMMUNOLOGY LA English DT Article DE dendritic cells; human; prostaglandin E-2; T helper 1; T helper 2 ID NECROSIS-FACTOR-ALPHA; IN-VITRO; DIFFERENTIAL DEACTIVATION; PHYSIOLOGICAL STIMULI; RECEPTOR EXPRESSION; FINAL MATURATION; P40 HOMODIMER; HELPER-CELLS; IFN-GAMMA; INTERLEUKIN-12 AB Prostaglandin E-2 (PGE(2)) acts in synergy with other inflammatory stimuli such as tumor necrosis factor (TNF) to induce the maturation of migratory-type monocyte-derived dendritic cells (MoDCs). However, PGE(2) has been reported to inhibit IL-12p70 production by MoDCs and to promote the generation of Th2 T cell responses. We demonstrate here that the addition of PGE(2) to TNF for the maturation of MoDCs enhanced CD4 and CD8 T cell proliferative responses to neoantigen and recall antigen, and enhanced Th1-type responses. The increased stimulatory capacity of MoDCs matured with PGE(2) was associated with a fully mature, migratory-type MoDC phenotype and more rapid down-regulation of the expression of inflammatory chemokines, with up-regulated expression of the constitutive chemokines TARC and MDC. In addition, although MoDCs matured with TNF and PGE(2) selectively produced the inhibitory IL-12p40 subunit at steady state, they were able to produce the bioactive IL-12p70 heterodimer after stimulation with CD40 ligand and/or IFN-gamma. Despite increased IL-6 mRNA expression, MoDCs matured with PGE(2) did not overcome the suppressive effects of CD4(+)CD25(+) T cells in allogeneic mixed lymphocyte reactions. In conclusion, MoDCs matured in the presence of PGE(2) display characteristics of more efficient antigen-presenting cells that might be optimal for use in cancer vaccine-based clinical trials. C1 Massachusetts Gen Hosp, Bone Marrow Transplantat Sect, Transplantat Biol Res Ctr, Boston, MA 02129 USA. Harvard Univ, Sch Med, Boston, MA 02129 USA. Massachusetts Gen Hosp, Ctr Immunol & Inflammatory Dis, Boston, MA 02129 USA. Massachusetts Gen Hosp, Div Rheumatol Allergy & Immunol, Boston, MA 02129 USA. RP Sykes, M (reprint author), Massachusetts Gen Hosp, Bone Marrow Transplantat Sect, Transplantat Biol Res Ctr, Bldg 149-5102,13th St, Boston, MA 02129 USA. EM megan.sykes@tbrc.mgh.harvard.edu FU NCI NIH HHS [R01-CA69212, R01-CA79986]; NHLBI NIH HHS [R01-HL63474]; NIDDK NIH HHS [P01-DK50305] NR 60 TC 27 Z9 28 U1 0 U2 1 PU OXFORD UNIV PRESS PI OXFORD PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND SN 0953-8178 J9 INT IMMUNOL JI Int. Immunol. PD DEC PY 2005 VL 17 IS 12 BP 1561 EP 1572 DI 10.1093/intimm/dxh335 PG 12 WC Immunology SC Immunology GA 989JP UT WOS:000233669100005 PM 16303787 ER PT J AU Earle, CC Neville, BA Landrum, MB Souza, JM Weeks, JC Block, SD Grunfeld, E Ayanian, JZ AF Earle, CC Neville, BA Landrum, MB Souza, JM Weeks, JC Block, SD Grunfeld, E Ayanian, JZ TI Evaluating claims-based indicators of the intensity of end-of-life cancer care SO INTERNATIONAL JOURNAL FOR QUALITY IN HEALTH CARE LA English DT Article DE administrative data; benchmarking; cancer; claims data; indicators development; performance measures; quality of care; terminally ill patients ID COMORBIDITY INDEX; QUALITY AB Objective. To evaluate measures that could use existing administrative data to assess the intensity of end-of-life cancer care. Methods. Benchmarking standards and statistical variation were evaluated using Medicare claims of 48,906 patients who died from cancer from 1991 through 1996 in 11 regions of the United States. We assessed accuracy by comparing administrative data to 150 medical records in one hospital and affiliated cancer treatment center. Results. Systems not providing overly aggressive care near the end of life would be ones in which less than 10% of patients receive chemotherapy in the last 14 days of life, less than 2% start a new chemotherapy regimen in the last 30 days of life, less than 4% have multiple hospitalizations or emergency room visits or are admitted to the intensive care unit (ICU) in the last month of life, and less than 17% die in an acute care institution. At least 55% of patients would receive hospice services before death from cancer, and less than 8% of those would be admitted to hospice within only 3 days of death. All measures were found to have accuracy ranging from 85 to 97% and 2- to 5-fold adjusted variability between the 5th and 95th percentiles of performance. Conclusions. The usefulness of these measures will depend on whether the concept of intensity of care near death can be further validated as an acceptable and important quality issue among patients, their families, health care providers, and other stakeholders in oncology. C1 Dana Farber Canc Inst, Ctr Outcomes & Policy Res, Dept Med Oncol, Div Populat Sci, Boston, MA 02115 USA. Harvard Univ, Sch Med, Dept Hlth Care Policy, Boston, MA 02115 USA. Brigham & Womens Hosp, Dept Psychiat, Div Psychosocial Oncol & Palliat Care, Boston, MA 02115 USA. Dalhousie Univ, Halifax, NS B3H 3J5, Canada. Canc Care Nova Scotia, Halifax, NS, Canada. Brigham & Womens Hosp, Dept Med, Div Gen Med, Boston, MA 02115 USA. RP Earle, CC (reprint author), Dana Farber Canc Inst, Ctr Outcomes & Policy Res, Dept Med Oncol, Div Populat Sci, 44 Binney St,454-STE 21-24, Boston, MA 02115 USA. EM craig_earle@dfci.harvard.edu FU NCI NIH HHS [CA 91753-02] NR 21 TC 109 Z9 111 U1 1 U2 4 PU OXFORD UNIV PRESS PI OXFORD PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND SN 1353-4505 J9 INT J QUAL HEALTH C JI Int. J. Qual. Health Care PD DEC PY 2005 VL 17 IS 6 BP 505 EP 509 DI 10.1093/intqhc/mzi061 PG 5 WC Health Care Sciences & Services; Health Policy & Services SC Health Care Sciences & Services GA 985YN UT WOS:000233414900007 PM 15985505 ER PT J AU Calderwood, SK Theriault, JR Gong, JL AF Calderwood, SK Theriault, JR Gong, JL TI How is the immune response affected by hyperthermia and heat shock proteins? SO INTERNATIONAL JOURNAL OF HYPERTHERMIA LA English DT Article; Proceedings Paper CT Workshop on Thermal Medicine, Heat Shock Proteins and Cancer CY MAR 31, 2005 CL NIH, Natcher Ctr, Bethesda, MD HO NIH, Natcher Ctr DE heat shock protein; peptide complex; extracellular hyperthermia; tumor immune response ID ANTIGEN-PRESENTING CELLS; TOLERANCE; RECEPTOR; BINDING AB There is growing body of evidence linking the cellular response to heat stress with the response of the immune system to cancer. The anti-tumor immune response can be markedly enhanced by treatment with hyperthermia particularly in the fever range. In addition, the heat shock proteins (hsp) which are produced in abundant quantities in cells exposed to heat are potent immune modulators and can lead to stimulation of both the innate and adaptive immune responses to tumors. Immunostimulation by hyperthermia involves both direct effects of heat on the behavior of immune cells as well as indirect effects mediated through hsp release. In addition, the hsp can be deployed as components of antitumor vaccines in protocols that do not include hyperthermia. Understanding these process may permit the effective deployment of hyperthermia and hsp based vaccines in tumor treatment. C1 Harvard Univ, Sch Med, BIDMC, Boston, MA 02215 USA. BUMC, Ctr Mol Stress Response, Boston, MA USA. RP Calderwood, SK (reprint author), Harvard Univ, Sch Med, BIDMC, Boston, MA 02215 USA. EM scalderw@bidmc.harvard.edu FU NCI NIH HHS [CA31303, CA47407, CA50642] NR 11 TC 48 Z9 52 U1 2 U2 4 PU TAYLOR & FRANCIS LTD PI ABINGDON PA 4 PARK SQUARE, MILTON PARK, ABINGDON OX14 4RN, OXON, ENGLAND SN 0265-6736 J9 INT J HYPERTHER JI Int. J. Hyperthermia PD DEC PY 2005 VL 21 IS 8 BP 713 EP 716 DI 10.1080/02656730500340794 PG 4 WC Oncology; Radiology, Nuclear Medicine & Medical Imaging SC Oncology; Radiology, Nuclear Medicine & Medical Imaging GA 992TJ UT WOS:000233906600007 PM 16338853 ER PT J AU Papakostas, GI Petersen, T Lebowitz, BD Mischoulon, D Ryan, JL Nierenberg, AA Bottiglieri, T Alpert, JE Rosenbaum, JF Fava, M AF Papakostas, GI Petersen, T Lebowitz, BD Mischoulon, D Ryan, JL Nierenberg, AA Bottiglieri, T Alpert, JE Rosenbaum, JF Fava, M TI The relationship between serum folate, vitamin B12, and homocysteine levels in major depressive disorder and the timing of improvement with fluoxetine SO INTERNATIONAL JOURNAL OF NEUROPSYCHOPHARMACOLOGY LA English DT Article DE fluoxetine; folate; homocysteine; onset; response; vitamin B12 ID ADENOSYL-L-METHIONINE; FOLIC-ACID; ANTIDEPRESSANT; ONSET; DEFICIENCY; PLASMA AB The objective of the present study was to examine the relationship between serum folate, vitamin B12, and homocysteine levels and the timing of clinical improvement to fluoxetine in major depressive disorder (MDD) patients. A total of 110 outpatients with MDD who responded to an 8-wk trial of fluoxetine had serum folate, B12, and homocysteine measurements at baseline (prior to fluoxetine initiation). Onset of clinical improvement was defined as a 30% decrease in Hamilton Depression Scale scores that led to a 50% decrease by week S. Patients with low folate levels (<= 2.5 ng/ml) were more likely to experience a later onset of clinical improvement than eufolatemic patients (p=0.0028). B12 and homocysteine level status did not predict time to clinical improvement (p > 0.05). In conclusion, low serum folate levels were found to be associated with a delayed onset of clinical improvement during treatment with fluoxetine in MDD by, on average, 1.5 wk. C1 Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Psychiat,Depress Clin & Res Program, Boston, MA 02114 USA. NIMH, Adult & Geriatr Treatment & Prevent Intervent Res, Bethesda, MD 20892 USA. Baylor Univ, Sch Med, Inst Metab Dis, Waco, TX 76798 USA. RP Papakostas, GI (reprint author), Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Psychiat,Depress Clin & Res Program, 15 Parkman St,WACC 812, Boston, MA 02114 USA. EM gpapakostas@partners.org RI Papakostas, George/I-6905-2013; OI Papakostas, George/0000-0002-2465-5103; Alpert, Jonathan/0000-0002-4332-908X FU NIMH NIH HHS [K23-MH069629-1, R01-MH-48-483-05] NR 26 TC 44 Z9 47 U1 0 U2 6 PU CAMBRIDGE UNIV PRESS PI NEW YORK PA 40 WEST 20TH ST, NEW YORK, NY 10011-4211 USA SN 1461-1457 J9 INT J NEUROPSYCHOPH JI Int. J. Neuropsychopharmacol. PD DEC PY 2005 VL 8 IS 4 BP 523 EP 528 DI 10.1017/S1461145705005195 PG 6 WC Clinical Neurology; Neurosciences; Pharmacology & Pharmacy; Psychiatry SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry GA 986VB UT WOS:000233476700005 PM 15877935 ER PT J AU Zimmermann, CE Troulis, MJ Kaban, LB AF Zimmermann, CE Troulis, MJ Kaban, LB TI Pediatric facial fractures: recent advances in prevention, diagnosis and management SO INTERNATIONAL JOURNAL OF ORAL AND MAXILLOFACIAL SURGERY LA English DT Review ID MOTOR-VEHICLE COLLISIONS; RIGID PLATE FIXATION; CHILD RESTRAINT LAW; MANDIBULAR FRACTURES; MAXILLOFACIAL TRAUMA; CONDYLAR FRACTURES; BONE-FRACTURES; CRANIOFACIAL SURGERY; MIDFACIAL FRACTURES; INJURIES AB During the last 25 years, there have been considerable advances in the prevention, diagnosis and management of craniomaxillofacial injuries in children. When compared to adults, the pattern of fractures and frequency of associated injuries are similar but the overall incidence is much lower. Diagnosis is more difficult than in adults and fractures are easily overlooked. Clinical diagnosis is best confirmed by computed tomographic (CT) scans. Treatment is usually performed without delay and can be limited to observation or closed reduction in non-displaced or minimally displaced fractures. Operative management should involve minimal manipulation and may be modified by the stage of skeletal and dental development. Open reduction and rigid internal fixation is indicated for severely displaced fractures. Primary bone grafting is preferred over secondary reconstruction and alloplastic materials should be avoided when possible. Children require long-term follow-up to monitor potential growth abnormalities. This article is a review of the epidemiology, diagnosis and management of facial fractures in children. C1 Massachusetts Gen Hosp, Dept Oral & Maxillofacial Surg, Boston, MA 02114 USA. RP Kaban, LB (reprint author), Massachusetts Gen Hosp, Dept Oral & Maxillofacial Surg, 55 Fruit St, Boston, MA 02114 USA. EM LKaban@partners.org NR 138 TC 26 Z9 28 U1 1 U2 3 PU CHURCHILL LIVINGSTONE PI EDINBURGH PA JOURNAL PRODUCTION DEPT, ROBERT STEVENSON HOUSE, 1-3 BAXTERS PLACE, LEITH WALK, EDINBURGH EH1 3AF, MIDLOTHIAN, SCOTLAND SN 0901-5027 J9 INT J ORAL MAX SURG JI Int. J. Oral Maxillofac. Surg. PD DEC PY 2005 VL 34 IS 8 BP 823 EP 833 DI 10.1016/j.ijom.2005.06.015 PG 11 WC Dentistry, Oral Surgery & Medicine; Surgery SC Dentistry, Oral Surgery & Medicine; Surgery GA 985OM UT WOS:000233387500001 PM 16154722 ER PT J AU Galer, C Holbrook, E Treves, J Leopold, D AF Galer, C Holbrook, E Treves, J Leopold, D TI Grisel's syndrome: A case report and review of the literature SO INTERNATIONAL JOURNAL OF PEDIATRIC OTORHINOLARYNGOLOGY LA English DT Article DE atlantoaxial subluxation; Grisel's syndrome; potential sequelae ID SUBLUXATION; TORTICOLLIS AB Grisel's syndrome is non-traumatic atlantoaxial subluxation (AAS) secondary to an inflammatory process in the upper neck. It is a rare condition that occurs almost exclusively in children and has been associated with upper cervical infections and otolaryngologic procedures. A case of AAS secondary to an upper cervical infection is presented. Potential sequelae can be severe; early diagnosis and treatment of Grisel's syndrome can prevent tragic outcome. (c) 2005 Elsevier Ireland Ltd. All rights reserved. C1 Univ Nebraska, Med Ctr, Dept Otolaryngol, Nebraska Med Ctr 981225, Omaha, NE 68198 USA. Massachusetts Eye & Ear Infirm, Dept Otolaryngol, Nebraska Med Ctr 981225, Omaha, NE 68198 USA. Univ Nebraska, Med Ctr, Neurosurg Sect, Nebraska Med Ctr 981225, Omaha, NE 68198 USA. RP Galer, C (reprint author), Univ Nebraska, Med Ctr, Dept Otolaryngol, Nebraska Med Ctr 981225, 600 S 42nd St, Omaha, NE 68198 USA. EM cgaler@unmc.edu NR 13 TC 9 Z9 9 U1 0 U2 0 PU ELSEVIER IRELAND LTD PI CLARE PA ELSEVIER HOUSE, BROOKVALE PLAZA, EAST PARK SHANNON, CO, CLARE, 00000, IRELAND SN 0165-5876 J9 INT J PEDIATR OTORHI JI Int. J. Pediatr. Otorhinolaryngol. PD DEC PY 2005 VL 69 IS 12 BP 1689 EP 1692 DI 10.1016/j.ijporl.2005.03.046 PG 4 WC Otorhinolaryngology; Pediatrics SC Otorhinolaryngology; Pediatrics GA 991AS UT WOS:000233785100012 PM 15978678 ER PT J AU Chen, AB Killoran, J Kim, H Mamon, H AF Chen, AB Killoran, J Kim, H Mamon, H TI Treatment planning for resected abdominal tumors: Differences in organ position between diagnostic and radiation-planning computed tomography scans SO INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS LA English DT Article DE radiation therapy; organ position; radiation planning ID RESPIRATION-INDUCED MOTION; RADIOTHERAPY; THERAPY; KIDNEYS AB Purpose: To evaluate whether organ location, determined from preoperative diagnostic computed tomography scans (CTs), accurately reflects organ location when patients are positioned for radiation therapy. Methods and Materials: We identified patients with upper abdominal malignancies treated with surgery and/or radiation therapy. Comparisons of organ position relative to fixed bony landmarks were made among preoperative diagnostic CTs, postoperative diagnostic CTs, and radiation-planning CTs. We studied 18 patients who had CTs differing only in scanning technique, 11 patients who had CTs differing only in operative state, and 7 patients with CTs differing in both scanning technique and operative state. Results: For patients with diagnostic CTs and radiation-planning CTs that were either both preoperative or both postoperative, mean organ position, measured relative to a fixed bony landmark, ranged from 1.9 to 3.2 cm superior on radiation-planning CTs compared with diagnostic CTs (p < 0.0001). Mean organ position ranged from 0.9 to 1.7 cm posterior on radiation-planning CTs compared with diagnostic CTs (p <= 0.008). Shifts in the right-left direction were small and variable. For patients with pre- and postoperative diagnostic CTs, organ shifts were variable and not significant. Organ shifts for patients with preoperative diagnostic CTs and postoperative radiation-planning CTs were similar to shifts observed for the first group. Conclusions: Relative to bony landmarks, there are superior and posterior shifts in organ position for radiation-planning CTs compared with diagnostic CTs. These shifts should be considered during treatment planning for resected abdominal tumors. (c) 2005 Elsevier Inc. C1 Brigham & Womens Hosp, Dept Radiat Oncol, Dana Farber Canc Inst, Boston, MA 02115 USA. Dana Farber Canc Inst, Dept Biostat Sci, Boston, MA 02115 USA. RP Mamon, H (reprint author), Brigham & Womens Hosp, Dept Radiat Oncol, Dana Farber Canc Inst, 75 Francis St,ASB1-L2, Boston, MA 02115 USA. EM hmamon@lroc.harvard.edu OI Chen, Aileen/0000-0002-5385-3360 NR 9 TC 2 Z9 2 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0360-3016 J9 INT J RADIAT ONCOL JI Int. J. Radiat. Oncol. Biol. Phys. PD DEC 1 PY 2005 VL 63 IS 5 BP 1613 EP 1620 DI 10.1016/j.ijrobp.2005.05.031 PG 8 WC Oncology; Radiology, Nuclear Medicine & Medical Imaging SC Oncology; Radiology, Nuclear Medicine & Medical Imaging GA 986VH UT WOS:000233477300046 PM 16115738 ER PT J AU Siebert, U Sroczynski, G AF Siebert, U Sroczynski, G CA German Hepatitis C Model Grp HTA Expert Panel Hepatitis C TI Effectiveness and cost-effectiveness of initial combination therapy with interferon/peginterferon plus ribavirin in patients with chronic hepatitis C in Germany: A health technology assessment commissioned by the German Federal Ministry of Health and Social Security SO INTERNATIONAL JOURNAL OF TECHNOLOGY ASSESSMENT IN HEALTH CARE LA English DT Article DE chronic hepatitis C; antiviral therapy; health technology assessment; decision analysis ID LONG-TERM EFFICACY; NAIVE PATIENTS; FOLLOW-UP; NON-A; NON-B; POSTTRANSFUSION HEPATITIS; VIRUS-INFECTION; RANDOMIZED-TRIAL; INTERFERON-ALFA; DISEASE AB Objectives: The purpose of this health technology assessment (HTA), commissioned by the German Federal Ministry of Health and Social Security, was to systematically review the evidence for the effectiveness and cost-effectiveness of antiviral treatment (AVT) with interferon (INF) or peginterferon (PegIFN) in combination with ribavirin (RBV) in treatment-naive patients with chronic hepatitis C (CHC) and to apply these data in the context of the German health-care system. Methods: We performed a systematic literature search on effectiveness and cost-effectiveness of AVT and summarized results using meta-analysis and evidence tables. We applied the German Hepatitis C Model (GEHMO), a decision-analytic Markov model, to determine long-term clinical effectiveness, costs, and incremental cost-effectiveness ratios (ICER) of the examined treatment strategies. Model parameters were derived from German databases, published international randomized clinical trials (RCT), and a Cochrane Review. Results: Overall, nine RCTs, two HTA reports, one Cochrane review, two meta-analyses, and seven economic evaluations met the inclusion criteria. These studies indicate that PegIFN + RBV achieved the highest sustained virological response rates (SVR) (54-61 percent), followed by IFN + RBV (38-54 percent) and IFN monotherapy (11-21 percent). Based on our meta-analysis, PegIFN + RBV reduced cases without SVR by 17 percent compared with INF + RBV. International cost-effectiveness studies indicate that INF + RBV is cost-effective when compared with INF monotherapy. For PegIFN + RBV, our decision analysis yielded an ICER of Euro 9,800 per quality-adjusted life-year gained. Conclusions: This HTA suggests that initial combination therapy prolongs life, improves quality of life, and is cost-effective in patients with CHC. Peginterferon plus ribavirin is the most effective and efficient treatment among the examined options. However, because not all chronic hepatitis C patients will develop progressive liver disease, a thorough assessment of the eligibility and appropriateness of treatment with combination therapy must be performed in each individual patient. C1 Harvard Univ, Massachusetts Gen Hosp, Sch Med, Inst Technol Assessment, Boston, MA 02114 USA. Univ Munich, Inst Med Informat Biometry & Epidemiol, Bavarian Publ Hlth Res & Coordinat Ctr, Program Hlth Technol Assessment & Decis Sci, D-81377 Munich, Germany. RP Siebert, U (reprint author), Harvard Univ, Massachusetts Gen Hosp, Sch Med, Inst Technol Assessment, 101 Merrimac St,10th Floor, Boston, MA 02114 USA. EM usiebert@hsph.harvard.edu; gaby@mgh-ita.org NR 60 TC 24 Z9 25 U1 0 U2 0 PU CAMBRIDGE UNIV PRESS PI NEW YORK PA 40 WEST 20TH ST, NEW YORK, NY 10011-4211 USA SN 0266-4623 J9 INT J TECHNOL ASSESS JI Int. J. Technol. Assess. Health Care PD WIN PY 2005 VL 21 IS 1 BP 55 EP 65 PG 11 WC Health Care Sciences & Services; Public, Environmental & Occupational Health; Medical Informatics SC Health Care Sciences & Services; Public, Environmental & Occupational Health; Medical Informatics GA 898JT UT WOS:000227073800007 PM 15736515 ER PT J AU Censor, Y Elfving, T Kopf, N Bortfeld, T AF Censor, Y Elfving, T Kopf, N Bortfeld, T TI The multiple-sets split feasibility problem and its applications for inverse problems SO INVERSE PROBLEMS LA English DT Article ID SPARSE SYSTEMS; PROJECTIONS; RECONSTRUCTION; CONSTRAINTS; ALGORITHMS AB The multiple-sets split feasibility problem requires finding a point closest to a family of closed convex sets in one space such that its image under a linear transformation will be closest to another family of closed convex sets in the image space. It can be a model for many inverse problems where constraints are imposed on the solutions in the domain of a linear operator as well as in the operator's range. It generalizes the convex feasibility problem as well as the two-sets split feasibility problem. We propose a projection algorithm that minimizes a proximity function that measures the distance of a point from all sets. The formulation, as well as the algorithm, generalize earlier work on the split feasibility problem. We offer also a generalization to proximity functions with Bregman distances. Application of the method to the inverse problem of intensity-modulated radiation therapy treatment planning is studied in a separate companion paper and is here only described briefly. C1 Univ Haifa, Dept Math, IL-31905 Haifa, Israel. Linkoping Univ, Dept Math, SE-58183 Linkoping, Sweden. Massachusetts Gen Hosp, Dept Radiat Oncol, Boston, MA 02114 USA. Harvard Univ, Sch Med, Boston, MA 02114 USA. RP Censor, Y (reprint author), Univ Haifa, Dept Math, Mt Carmel, IL-31905 Haifa, Israel. EM yair@math.haifa.ac.it; toelf@mai.liu.se; nirit_kopf@hotmail.com; tbortfeld@hms.harvard.edu RI Censor, Yair/H-5740-2011 NR 37 TC 191 Z9 198 U1 0 U2 1 PU IOP PUBLISHING LTD PI BRISTOL PA DIRAC HOUSE, TEMPLE BACK, BRISTOL BS1 6BE, ENGLAND SN 0266-5611 J9 INVERSE PROBL JI Inverse Probl. PD DEC PY 2005 VL 21 IS 6 BP 2071 EP 2084 DI 10.1088/0266-5611/21/6/017 PG 14 WC Mathematics, Applied; Physics, Mathematical SC Mathematics; Physics GA 996UP UT WOS:000234200900029 ER PT J AU Chen, L Cursiefen, C Barabino, S Zhang, Q Dana, MR AF Chen, L Cursiefen, C Barabino, S Zhang, Q Dana, MR TI Novel expression and characterization of lymphatic vessel endothelial hyaluronate receptor 1 (LYVE-1) by conjunctival cells SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Article ID INFLAMMATORY NEOVASCULARIZATION; LYMPHATIC ENDOTHELIUM; LYMPHANGIOGENESIS; HYALURONAN; REJECTION; HEMANGIOGENESIS; RECEPTOR; SYSTEM AB PURPOSE. Lymphatic vessel endothelial hyaluronic acid receptor (LYVE-1) is a newly discovered lymphatic-specific marker. To date, there is no report of its expression on conjunctival cells. The purpose of this study was to investigate the expression of LYVE-1 in normal conjunctiva, to phenotype LYVE-1(+) cells, and to study changes in their expression levels during corneal inflammation. METHODS. Flatmounted conjunctivae or cross sections of eyeballs were harvested from BALB/c mice (6-8 weeks of age) for immunofluorescent confocal microscopic studies. RESULTS. The data demonstrate, for the first time, that in addition to its expression on lymphatic vessels, LYVE-1 was expressed on CD45(+), CD11b(+), and CD31(-) conjunctival cells, indicating a bone-marrow-derived monocytic lineage. Surprisingly, the number of cells that expressed LYVE-1 decreased during corneal inflammation, in conjunction with ingrowth of lymphatics into the cornea. CONCLUSIONS. A new population of monocytic cells has been found to express LYVE-1 in normal conjunctiva. These cells that normally express LYVE-1 may act as a reservoir for lymphangiogenesis and cell recruitment when the immune system is challenged. C1 Harvard Univ, Massachusetts Eye & Ear Infirm, Sch Med, Dept Ophthalmol,Schepens Eye Res Inst,Lab Immunol, Boston, MA 02114 USA. RP Dana, MR (reprint author), Harvard Univ, Massachusetts Eye & Ear Infirm, Sch Med, Dept Ophthalmol,Schepens Eye Res Inst,Lab Immunol, Boston, MA 02114 USA. EM dana@vision.eri.harvard.edu FU NEI NIH HHS [EY-12963, R01 EY012963, EY-014786, F32 EY014786] NR 22 TC 37 Z9 38 U1 0 U2 0 PU ASSOC RESEARCH VISION OPHTHALMOLOGY INC PI ROCKVILLE PA 12300 TWINBROOK PARKWAY, ROCKVILLE, MD 20852-1606 USA SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD DEC PY 2005 VL 46 IS 12 BP 4536 EP 4540 DI 10.1167/iovs.05-0975 PG 5 WC Ophthalmology SC Ophthalmology GA 988FV UT WOS:000233578600027 PM 16303945 ER PT J AU Campbell, EG Koski, G Zinner, DE Blumenthal, D AF Campbell, EG Koski, G Zinner, DE Blumenthal, D TI Managing the triple helix in the life sciences SO ISSUES IN SCIENCE AND TECHNOLOGY LA English DT Article C1 Harvard Univ, Inst Hlth Policy, Sch Med, Cambridge, MA 02138 USA. Massachusetts Gen Hosp, Boston, MA 02114 USA. Harvard Univ, Sch Business, Cambridge, MA 02138 USA. RP Campbell, EG (reprint author), Harvard Univ, Inst Hlth Policy, Sch Med, Cambridge, MA 02138 USA. EM ecampbell@partners.org NR 0 TC 0 Z9 0 U1 0 U2 1 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA SN 0748-5492 J9 ISSUES SCI TECHNOL JI Issues Sci. Technol. PD WIN PY 2005 VL 21 IS 2 BP 48 EP 54 PG 7 WC Engineering, Multidisciplinary; Engineering, Industrial; Multidisciplinary Sciences; Social Issues SC Engineering; Science & Technology - Other Topics; Social Issues GA 887IB UT WOS:000226298100034 ER PT J AU Martin, BK Wu, AW Gelman, R Mitsuyasu, RT AF Martin, BK Wu, AW Gelman, R Mitsuyasu, RT CA Adult AIDS Clinical Trials Grp TI Quality of life in a clinical trial of highly active antiretroviral therapy alone or with intravenous or subcutaneous interleukin-2 administration SO JAIDS-JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES LA English DT Article DE HIV; AIDS; interleukin-2; highly active antiretroviral therapy; clinical trial; health-related quality of life ID HUMAN-IMMUNODEFICIENCY-VIRUS; RANDOMIZED CONTROLLED-TRIAL; CD4(+) CELL COUNTS; PHASE-II TRIAL; HIV-1 INFECTION; HIV/AIDS; TYPE-1; IMPACT AB Objective: To assess the impact of subcutaneous and intravenous interleukin-2 (IL-2) on health-related quality of life (HRQOL) in adults with HIV-1 receiving highly active antiretroviral therapy (HAART). Design: Randomized clinical trial. Setting: Twenty-two institutions from the Adult AIDS Clinical Trials Group. Patients: One hundred forty-eight HIV-infected adults randomized, with baseline HRQOL data. Methods: HAART (indinavir plus 2 nucleoside analogues) for 12 weeks, followed by 72 weeks of continued HAART alone, HAART plus subcutaneous IL-2, or HAART plus intravenous IL-2. Outcome Measures: Scores for 8 dimensions of HRQOL, an unweighted summary score, and a visual analogue health rating score. Results: The IL-2 subcutaneous group had the best mean change in 6 of 8 dimension subscales and in the summary scale at 28 weeks (16 weeks after baseline). At 52 weeks, the IL-2 subcutaneous group had the best mean change in all the subscales and the summary scale. The differences were statistically significant for 3 subscales and the summary scale. Midcycle changes were statistically significantly worse for the subcutaneous IL-2 group for 4 subscales and the summary scale. Conclusions: We found evidence of a short-term but not long-term adverse impact of IL-2 on HRQOL and some evidence of long-term benefit for the subcutaneous group. C1 Johns Hopkins Bloomberg Sch Publ Hlth, John Hopkins Ctr Clin Trials, Baltimore, MD 21205 USA. Johns Hopkins Sch Med, Baltimore, MD USA. Dana Farber Canc Inst, Boston, MA 02115 USA. Harvard Univ, Sch Publ Hlth, Boston, MA 02115 USA. Univ Calif Los Angeles, Sch Med, Los Angeles, CA USA. RP Martin, BK (reprint author), Johns Hopkins Bloomberg Sch Publ Hlth, John Hopkins Ctr Clin Trials, 615 N Wolfe St,Suite W5010, Baltimore, MD 21205 USA. EM bmartin@jhsph.edu FU NCRR NIH HHS [RR-00046, RR-00052, RR-05096, RR-00865, RR-00047]; NIAID NIH HHS [AI-27658, AI-27663, AI-34853, AI-38844, AI-36219, AI-25903, AI-32782, AI-39156, AI-27665, AI-50410, AI-32770, AI-46370, AI-27673, AI-32775, AI-25924, AI-25859, AI-27659, AI-27666, AI-27660, U01 AI-38858, AI-46386, AI-27767, AI-27668, AI-25868, AI-25879, AI-27661] NR 21 TC 5 Z9 5 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3261 USA SN 1525-4135 J9 JAIDS-J ACQ IMM DEF JI JAIDS PD DEC 1 PY 2005 VL 40 IS 4 BP 428 EP 433 DI 10.1097/01.qai.0000182848.45722.b7 PG 6 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA 986UE UT WOS:000233474400007 PM 16280697 ER PT J AU Rasgon, NL Reynolds, MF Elman, S Saad, M Frye, MA Bauer, M Altshuler, LL AF Rasgon, NL Reynolds, MF Elman, S Saad, M Frye, MA Bauer, M Altshuler, LL TI Longitudinal evaluation of reproductive function in women treated for bipolar disorder SO JOURNAL OF AFFECTIVE DISORDERS LA English DT Article DE bipolar disorder; women; menstrual abnormalities; testosterone; insulin resistance; valproate ID POLYCYSTIC-OVARY-SYNDROME; ENDOCRINE DISORDERS; INSULIN RESISTANCE; VALPROATE; EPILEPSY; DEPRESSION; OBESITY; RISK; ABNORMALITIES AB Background: We assessed reproductive endocrine and metabolic markers in women treated for bipolar disorder over a 2-year time period, controlling for valproate use. Methods: Twenty-five women ages 18-45 with bipolar disorder underwent longitudinal evaluations. Subjects completed a reproductive health questionnaire and endocrinological exam at baseline. Total and free testosterone, progesterone, LH, FSH, fasting insulin and glucose, and other hormones were measured across the menstrual cycle at baseline and at 2-year follow-up. Results: Ten subjects were currently receiving valproate as a mood stabilizing agent; of the remaining subjects, six received lithium and five received atypical antipsychotics. Of all subjects, 41.7% reported current oligomenorrhea, while 40% reported oligomenorrhea before starting medication. Rates of oligomenorrhea and clinical hyperandrogenism did not differ by medication use. Eighty percent of women had a high homeostatic model assessment of insulin resistance (HOMA-IR) at baseline; all other measures were normal. Over time, all subjects exhibited a significant decrease in luteal phase progesterone and increase in free testosterone concentrations. Valproate use was associated with an increase over time in total testosterone. Baseline values and changes in BMI were similar across groups. Limitations: Limitations include small sample size and the absence of a control group. Conclusion: We confirm our previous observations of high rates of menstrual abnormalities, hyperandrogenemia and insulin resistance in women with bipolar disorder. These results tentatively support the role of valproate in hyperandrogenemia; however, rates of oligomenorrhea and clinical hyperandrogenism did not differ between medication groups. (c) 2005 Elsevier B.V. All rights reserved. C1 Stanford Univ, Sch Med, Dept Psychiat & Behav Sci, Stanford, CA 94305 USA. Univ Calif Los Angeles, Dept Psychiat & Biobehav Sci, Los Angeles, CA 90024 USA. VA Greater Los Angeles Healthcare Syst, W Los Angeles Healthcare Ctr, Dept Psychiat, Los Angeles, CA USA. Charite Univ Med Berlin, Dept Psychiat & Psychotherapy, Berlin, Germany. Univ Calif Los Angeles, Neuropsychiat Inst & Hosp, Dept Psychiat & Biobehav Sci, Los Angeles, CA USA. RP Rasgon, NL (reprint author), Stanford Univ, Sch Med, Dept Psychiat & Behav Sci, 401 Quarry Rd, Stanford, CA 94305 USA. EM nrasgon@stanford.edu NR 27 TC 28 Z9 29 U1 0 U2 6 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0165-0327 J9 J AFFECT DISORDERS JI J. Affect. Disord. PD DEC PY 2005 VL 89 IS 1-3 BP 217 EP 225 DI 10.1016/j.jad.2005.08.002 PG 9 WC Clinical Neurology; Psychiatry SC Neurosciences & Neurology; Psychiatry GA 998YJ UT WOS:000234355500025 PM 16171873 ER PT J AU Hamilos, DL Lanza, DC Kennedy, DW AF Hamilos, DL Lanza, DC Kennedy, DW TI Rhinosinusitis and the revised "Sinusitis practice parameters" SO JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY LA English DT Editorial Material DE rhinosinusitis; sinusitis; practice parameters C1 Massachusetts Gen Hosp, Div Rheumatol Allergy & Immunol, Boston, MA 02114 USA. Sinus & Nasal Inst, St Petersburg, FL USA. Univ Penn, Hlth Syst, Philadelphia, PA 19104 USA. RP Hamilos, DL (reprint author), Massachusetts Gen Hosp, Div Rheumatol Allergy & Immunol, Bulfinch 422,55 Fruit St, Boston, MA 02114 USA. EM dhamilos@partners.org NR 10 TC 3 Z9 4 U1 0 U2 0 PU MOSBY, INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 USA SN 0091-6749 J9 J ALLERGY CLIN IMMUN JI J. Allergy Clin. Immunol. PD DEC PY 2005 VL 116 IS 6 BP 1267 EP 1268 DI 10.1016/j.jaci.2005.09.011 PG 2 WC Allergy; Immunology SC Allergy; Immunology GA 017IJ UT WOS:000235687000015 PM 16337456 ER PT J AU Brau, N AF Brau, N TI Chronic hepatitis C in patients with HIV/AIDS: a new challenge in antiviral therapy SO JOURNAL OF ANTIMICROBIAL CHEMOTHERAPY LA English DT Article DE pegylated interferon; ribavirin; highly active antiretroviral therapy; drug interactions ID INTERFERON-ALPHA-2B PLUS RIBAVIRIN; RANDOMIZED CONTROLLED-TRIAL; HIV-INFECTED PATIENTS; VIRUS-INFECTION; MITOCHONDRIAL TOXICITY; HIV/HCV-COINFECTION; CIRRHOSIS; ALPHA AB HIV-infected patients are living longer since the introduction of highly active antiretroviral therapy. However, coinfection with the hepatitis C virus (HCV) leads to increased morbidity from liver disease and higher overall mortality. The prevalence of chronic hepatitis C among patients with HIV/AIDS ranges from 7% (sexual transmission of HIV) to > 90% (injection drug use). Uncontrolled HIV infection seems to accelerate the progression of HCV-induced liver fibrosis. Forty-eight weeks of combination therapy with pegylated interferon alpha (2a or 2b) plus ribavirin achieves a sustained viral response in coinfected individuals in up to 38% with HCV genotype 1 and up to 73% with genotypes 2 or 3. The safety profile of this treatment is similar to therapy in HCV-monoinfected patients with influenza-like symptoms, cytopenia and neuropsychiatric symptoms dominating. However, HIV/HCV-coinfected patients who also take zidovudine develop more profound anaemia than those on other HIV nucleoside analogue therapy. Didanosine and stavudine are associated with rare but serious mitochondrial toxicity, such as pancreatitis or lactic acidosis. It does not appear that the addition of ribavirin increases that risk. There is currently no evidence that in HIV/HCV coinfection one pegylated interferon product is superior to the other. Contrary to common perception, it is also unproven that HIV/HCV-coinfected patients respond less well to therapy with peginterferon alpha plus ribavirin than HCV-monoinfected patients. Given the safety and efficacy of combination therapy with peginterferon plus ribavirin and the deleterious effects of chronic hepatitis C, all HIV/HCV-coinfected patients should be evaluated for therapy. C1 Bronx Vet Affairs Med Ctr, Mt Sinai Sch Med, Infect Dis Sect, Dept Med,Div Infect Dis, Bronx, NY 10468 USA. Mt Sinai Sch Med, Div Liver Dis, Bronx, NY 10468 USA. Vet Affairs Med Ctr, Bronx, NY USA. RP Brau, N (reprint author), Bronx Vet Affairs Med Ctr, Mt Sinai Sch Med, Infect Dis Sect, Dept Med,Div Infect Dis, 130 W Kingsbridge Rd, Bronx, NY 10468 USA. EM norbert.brau@med.va.gov NR 24 TC 8 Z9 8 U1 0 U2 0 PU OXFORD UNIV PRESS PI OXFORD PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND SN 0305-7453 J9 J ANTIMICROB CHEMOTH JI J. Antimicrob. Chemother. PD DEC PY 2005 VL 56 IS 6 BP 991 EP 995 DI 10.1093/jac/dki392 PG 5 WC Infectious Diseases; Microbiology; Pharmacology & Pharmacy SC Infectious Diseases; Microbiology; Pharmacology & Pharmacy GA 993XE UT WOS:000233989900001 PM 16308419 ER PT J AU Tgavalekos, NT Tawhai, M Harris, RS Mush, G Vidal-Melo, M Venegas, JG Lutchen, KR AF Tgavalekos, NT Tawhai, M Harris, RS Mush, G Vidal-Melo, M Venegas, JG Lutchen, KR TI Identifying airways responsible for heterogeneous ventilation and mechanical dysfunction in asthma: an image functional modeling approach SO JOURNAL OF APPLIED PHYSIOLOGY LA English DT Article DE morphometric lung model; constriction; closure ID BRONCHIAL TREE; LUNG; RESISTANCE AB We present an image functional modeling approach, which synthesizes imaging and mechanical data with anatomically explicit computational models. This approach is utilized to identify the relative importance of small and large airways in the simultaneous deterioration of mechanical function and ventilation in asthma. Positron emission tomographic ( PET) images provide the spatial distribution and relative extent of ventilation defects in asthmatic subjects postbronchoconstriction. We also measured lung resistance and elastance from 0.15 to 8 Hz. The first step in image functional modeling involves mapping ventilation three- dimensional images to the computational model and identifying the largest sized airways of the model that, if selectively constricted, could precisely match the size and anatomic location of ventilation defects imaged by PET. In data from six asthmatic subjects, these airways had diameters < 2.39 mm and mostly < 0.44 mm. After isolating and effectively closing airways in the model associated with these ventilation defects, we imposed constriction with various means and standard deviations to the remaining airways to match the measured lung resistance and elastance from the same subject. Our results show that matching both the degree of mechanical impairment and the size and location of the PET ventilation defects requires either constriction of airways < 2.4 mm alone, or a simultaneous constriction of small and large airways, but not just large airways alone. Also, whereas larger airway constriction may contribute to mechanical dysfunction during asthma, degradation in ventilation function requires heterogeneous distribution of near closures confined to small airways. C1 Boston Univ, Dept Biomed Engn, Boston, MA 02215 USA. Univ Auckland, Bioengn Inst, Auckland 1, New Zealand. Massachusetts Gen Hosp, Dept Anesthesia & Crit Care, Pulm & Crit Care Unit, Boston, MA 02114 USA. Massachusetts Gen Hosp, Dept Radiol, Pulm & Crit Care Unit, Boston, MA 02114 USA. Massachusetts Gen Hosp, Dept Med, Pulm & Crit Care Unit, Boston, MA 02114 USA. RP Lutchen, KR (reprint author), Boston Univ, Dept Biomed Engn, 44 Cummington St, Boston, MA 02215 USA. EM klutch@bu.edu OI Tawhai, Merryn/0000-0002-3211-6337 FU NHLBI NIH HHS [HL-076778, HL-68011] NR 25 TC 91 Z9 95 U1 0 U2 4 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA SN 8750-7587 J9 J APPL PHYSIOL JI J. Appl. Physiol. PD DEC PY 2005 VL 99 IS 6 BP 2388 EP 2397 DI 10.1152/japplphysiol.00391.2005 PG 10 WC Physiology; Sport Sciences SC Physiology; Sport Sciences GA 984QH UT WOS:000233318900044 PM 16081622 ER PT J AU Williams, DL Goldstein, G Carpenter, PA Minshew, NJ AF Williams, DL Goldstein, G Carpenter, PA Minshew, NJ TI Verbal spatial working memory in autism SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism; working memory; information processing ID HIGH-FUNCTIONING AUTISM; EXECUTIVE FUNCTION; DIAGNOSTIC INTERVIEW; NEOCORTICAL SYSTEMS; INDIVIDUALS; INTACT; MIND; COMPREHENSION; DYSFUNCTION; DISORDERS AB Verbal and spatial working memory were examined in high-functioning children, adolescents, and adults with autism compared to age and cognitive-matched controls. No deficit was found in verbal working memory in the individuals with autism using an N-back letter task and standardized measures. The distinction between the N-back task and others used previously to infer a working memory deficit in autism is that this task does not involve a complex cognitive demand. Deficits were found in spatial working memory. Understanding the basis for the dissociation between intact verbal working memory and impaired spatial working memory and the breakdown that occurs in verbal working memory as information processing demands are increased will likely provide valuable insights into the neural basis of autism. C1 Univ Pittsburgh, Sch Med, Pittsburgh, PA 15213 USA. Univ Pittsburgh, VA Pittsburgh Healthcare Syst, Sch Med, Pittsburgh, PA 15213 USA. Carnegie Mellon Univ, Pittsburgh, PA 15213 USA. RP Minshew, NJ (reprint author), Univ Pittsburgh, Sch Med, Webster Hall,Suite 300,3811 OHara St, Pittsburgh, PA 15213 USA. EM minshewnj@upmc.edu FU NICHD NIH HHS [HD35469]; NIMH NIH HHS [T32-MH18951] NR 48 TC 83 Z9 84 U1 4 U2 27 PU SPRINGER/PLENUM PUBLISHERS PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA SN 0162-3257 J9 J AUTISM DEV DISORD JI J. Autism Dev. Disord. PD DEC PY 2005 VL 35 IS 6 BP 747 EP 756 DI 10.1007/s10803-005-0021-x PG 10 WC Psychology, Developmental SC Psychology GA 003AG UT WOS:000234653400006 PM 16267641 ER PT J AU Gianni, D Chan, J Gwathmey, JK del Monte, F Hajjar, RJ AF Gianni, D Chan, J Gwathmey, JK del Monte, F Hajjar, RJ TI SERCA2a in heart failure: Role and therapeutic prospects SO JOURNAL OF BIOENERGETICS AND BIOMEMBRANES LA English DT Article DE heart failure; SERCA; gene therapy; sarcoplasmic reticulum ID MUSCLE SARCOPLASMIC-RETICULUM; NUCLEOTIDE-BINDING DOMAIN; ADENOVIRAL GENE-TRANSFER; FUNCTIONAL CONSEQUENCES; SKELETAL-MUSCLE; AMINO-ACIDS; CA2+ ATPASE; CARDIAC MYOCYTES; IN-VIVO; VENTRICULAR MYOCYTES AB Ca2+ is a key molecule controlling several cellular processes, from fertilization to cell death, in all cell types. In excitable and contracting cells, such as cardiac myocytes, Ca2+ controls Muscle contractility. The spatial and temporal segregation of Ca2+ concentrations are central to maintain its concentration gradients across the cells and thee Cellular compartments for proper function. SERCA2a is a cornerstone irioleCiAle for maintaining a balanced concentration of Ca2+ during the cardiac cycle, since it controls the transport of Ca2+ to the sarcoplasmic reticulum (SR) during relaxation. Alterations of the activity of this pump have been widely investigated, emphasizing its central role in the control of Ca2+ homeostasis and consequently in the pathogenesis of the contractile defect seen with heart failure. This review focuses on the molecular characteristics of the pump, its role during the cardiac cycle and the prospects derived from the Manipulation of SERCA2a for heart failure treatment. C1 Massachusetts Gen Hosp, Cardiovasc Res Ctr, Heart Failure Ctr, Boston, MA 02129 USA. Univ London Imperial Coll Sci Technol & Med, London, England. Gwathmey Inc, Cambridge, MA USA. Harvard Univ, Sch Med, Boston, MA USA. RP del Monte, F (reprint author), Massachusetts Gen Hosp, Cardiovasc Res Ctr, Heart Failure Ctr, 149 13th St,Rm 4217, Boston, MA 02129 USA. EM fdelmonte@partners.org NR 68 TC 25 Z9 31 U1 0 U2 2 PU SPRINGER/PLENUM PUBLISHERS PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA SN 0145-479X J9 J BIOENERG BIOMEMBR JI J. Bioenerg. Biomembr. PD DEC PY 2005 VL 37 IS 6 BP 375 EP 380 DI 10.1007/s10863-005-9474-z PG 6 WC Biophysics; Cell Biology SC Biophysics; Cell Biology GA 029EJ UT WOS:000236541600005 PM 16691468 ER PT J AU Arystarkhova, E Sweadner, KJ AF Arystarkhova, E Sweadner, KJ TI Splice variants of the gamma subunit (FXYD2) and their significance in regulation of the Na,K-ATPase in kidney SO JOURNAL OF BIOENERGETICS AND BIOMEMBRANES LA English DT Article DE FXYD family; endogenous inibitor; post-translational modification; stress response; growth control ID RENAL NA,K-ATPASE; NA+; ASSOCIATION; EXPRESSION; AFFINITY AB The recent discovery of a family of single-span membrane proteins (the FXYD proteins) introduced a new direction to the rather complicated area Of regulation of Na,K-ATPase. At least six members of the family have been shown to associate with the Na,K-ATPase in a cell- and tissue-specific manner, While four of them, namely the gamma subunit (FXYD2), CHIF (FXYD4), phospholemman (FXYD1), and dysadherin (FXYD5) have been identified in kidney. All four exhibited different effects oil the properties Of the PUMP ill heterologous expression systems. Taken along with their non-overlapping expression patterns in the nephron, this provides a potential structural basis for the segment-specific properties of the Na,K-ATPase that had been reported in a number of papers oil kidney physiology. This brief review summarizes our own contributions oil structure/functional Characterization of one of the family members, the gamma subunit (FXYD2). The focus is on splice variants of gamma, their structural similarity and yet distinct effects conferred to Na,K-ATPase. C1 Massachusetts Gen Hosp, Lab Membrane Biol, Boston, MA 02114 USA. Harvard Univ, Sch Med, Boston, MA 02114 USA. RP Arystarkhova, E (reprint author), Massachusetts Gen Hosp, Lab Membrane Biol, 415 Thier Wellman Res Bldg,55 Fruit St, Boston, MA 02114 USA. FU NHLBI NIH HHS [HL036271] NR 11 TC 19 Z9 20 U1 0 U2 2 PU SPRINGER/PLENUM PUBLISHERS PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA SN 0145-479X J9 J BIOENERG BIOMEMBR JI J. Bioenerg. Biomembr. PD DEC PY 2005 VL 37 IS 6 BP 381 EP 386 DI 10.1007/s10863-005-9475-y PG 6 WC Biophysics; Cell Biology SC Biophysics; Cell Biology GA 029EJ UT WOS:000236541600006 PM 16691469 ER PT J AU Sodha, S Ring, D Zurakowski, D Jupiter, JB AF Sodha, S Ring, D Zurakowski, D Jupiter, JB TI Prevalence of osteoarthrosis of the trapeziometacarpal joint SO JOURNAL OF BONE AND JOINT SURGERY-AMERICAN VOLUME LA English DT Article ID IDIOPATHIC ARM PAIN; POSTMENOPAUSAL WOMEN; HAND OSTEOARTHRITIS; DISABILITY; THUMB; ARTHRITIS; STRENGTH; GRIP; BASE AB Background: The age and gender-related prevalence of arthrosis of the trapeziometacarpal joint has been incompletely defined. Methods: The radiographs of 615 consecutive patients who had presented with an isolated fracture of the distal part of the radius over a two-year period were evaluated for evidence of trapeziometacarpal arthrosis. We used. a simple three-grade rating system suitable for standard wrist radiographs. Grade I indicated no or nearly no arthrosis; grade II, obvious arthrosis; and grade III, a totally destroyed joint. This rating system was demonstrated to have adequate intraobserver reliability (average kappa of 0.72, p < 0.001) and interobserver reliability (average kappa of 0.56, p < 0.001). The number of patients with each grade of arthrosis was analyzed according to age and gender. Results: The overall radiographic prevalence of trapeziometacarpal arthrosis in patients with a distal radial fracture increased steadily from the age of forty-one years onward and reached a prevalence of 91% in patients older than eighty years of age. The prevalence increased more rapidly in women than in men; it reached 94% in women who were older than eighty years of age compared with 85% in men who were older than eighty years of age. The prevalence of grade-III trapeziometacarpal arthrosis (a totally destroyed joint) was much greater in women than in men at all age levels; it reached a prevalence of 66% in women older than eighty years of age compared with 23% in men,older than eighty years of age. Conclusions: The radiographic prevalence of trapeziometacarpal arthrosis in patients presenting for treatment of a distal radial fracture is age-related, and trapeziometacarpal arthrosis is more likely to lead to complete joint destruction in women than it is in men. C1 Hand & Upper Extrem Surg, Crystal Run Healthcare, Middletown, NY 10941 USA. Massachusetts Gen Hosp, Dept Orthopaed Surg, Hand & Upper Extrem Serv, Boston, MA 02114 USA. Childrens Hosp, Dept Biostat, Boston, MA 02115 USA. RP Sodha, S (reprint author), Hand & Upper Extrem Surg, Crystal Run Healthcare, 155 Crystal Run Rd, Middletown, NY 10941 USA. EM dring@partners.org NR 29 TC 45 Z9 46 U1 0 U2 2 PU JOURNAL BONE JOINT SURGERY INC PI NEEDHAM PA 20 PICKERING ST, NEEDHAM, MA 02192 USA SN 0021-9355 J9 J BONE JOINT SURG AM JI J. Bone Joint Surg.-Am. Vol. PD DEC PY 2005 VL 87A IS 12 BP 2614 EP 2618 DI 10.2106/JBJS.E.00104 PG 5 WC Orthopedics; Surgery SC Orthopedics; Surgery GA 991JW UT WOS:000233811300003 PM 16322609 ER PT J AU Tsuji, T Del Monte, F Yoshikawa, Y Abe, T Taniguchi, S Takaki, M Hajjar, R AF Tsuji, T Del Monte, F Yoshikawa, Y Abe, T Taniguchi, S Takaki, M Hajjar, R TI Rescue of Ca2+ overload-induced left ventricle dysfunction by targeted ablation of phospholamban SO JOURNAL OF CARDIAC FAILURE LA English DT Meeting Abstract CT 9th Annual Scientific Meeting of the Japanese-Heart-Failure-Society CY OCT 20-22, 2005 CL Yamaguchi, JAPAN SP Japanese Heart Failure Soc C1 Nara Med Univ, Sch Med, Dept Thorac & Cardiovasc Surg, Kashihara, Nara 634, Japan. Nara Med Univ, Sch Med, Dept Physiol 2, Kashihara, Nara 634, Japan. Massachusetts Gen Hosp, Cardiovasc Res Ctr, Boston, MA 02114 USA. Harvard Univ, Sch Med, Boston, MA USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU CHURCHILL LIVINGSTONE INC MEDICAL PUBLISHERS PI PHILADELPHIA PA CURTIS CENTER, INDEPENDENCE SQUARE WEST, PHILADELPHIA, PA 19106-3399 USA SN 1071-9164 J9 J CARD FAIL JI J. Card. Fail. PD DEC PY 2005 VL 11 IS 9 SU S BP S323 EP S323 DI 10.1016/j.cardfail.2005.08.343 PG 1 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA 005FK UT WOS:000234807800262 ER PT J AU Zareba, W Moss, AJ Hall, WJ Wilber, DJ Ruskin, JN McNitt, S Brown, M Wang, HY AF Zareba, W Moss, AJ Hall, WJ Wilber, DJ Ruskin, JN McNitt, S Brown, M Wang, HY CA MADIT II Investigators TI Clinical course and implantable cardioverter defibrillator therapy in postinfarction women with severe left ventricular dysfunction SO JOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY LA English DT Article DE implantable cardioverter defibrillator; women; gender; prognosis; heart failure ID CORONARY-ARTERY-DISEASE; UNSUSTAINED TACHYCARDIA TRIAL; CARDIAC-ARREST; HEART-FAILURE; MYOCARDIAL-INFARCTION; EJECTION FRACTION; UNITED-STATES; DEATH; GENDER; MEN AB Implantable Cardioverter Defibrillator in Women. Background: There are limited data regarding implantable cardioverter defibrillator (ICD) therapy in postinfarction women with severe left ventricular dysfunction. The aim of this study was to evaluate the risk of cardiac events and effects of ICD therapy in women as compared to men enrolled in the Multicenter Automatic Defibrillator Implantation Trial II (MADIT II). Methods and Results: Among 1,232 patients enrolled in MADIT II, there were 192 (16%) women and 1,040 (84%) men. When compared to men, women had an increased frequency of NYHA class >= II (70 vs 63%; P = 0.067), hypertension (60% vs 52%; P = 0.047), diabetes (42% vs 34%; P = 0.027), and LBBB (25% vs 17%; P = 0.011), and less frequent CABG surgery (42% vs 60%; P < 0.001). The 2-year cumulative mortality in patients randomized to conventional therapy was not significantly different in women and men (30% and 20%, respectively; P = 0.19). Adjusting for relevant clinical covariates, the hazard ratios for ICD effectiveness were similar in women (0.57; 95% CI = 0.28-1.18; P = 0.132) and men (0.66; 95% CI = 0.48-0.91; P = 0.011). The risk of appropriate ICD therapy for VT/VF was lower in women than in men (hazard ratio = 0.60 for female vs male gender; 95% CI = 0.37-0.98; P = 0.039). Conclusions: MADIT II women had similar mortality and similar ICD effectiveness when compared to men. MADIT II women with ICDs had a lower risk of arrhythmic events with fewer episodes of ventricular tachycardia than men. C1 Univ Rochester, Med Ctr, Heart Res Follow Program, Cardiol Unit,Dept Med, Rochester, NY 14642 USA. Univ Rochester, Med Ctr, Dept Biostat & Computat Biol, Rochester, NY 14642 USA. Loyola Univ, Med Ctr, Cardiol Unit, Maywood, IL 60153 USA. Massachusetts Gen Hosp, Cardiac Arrhythmia Serv, Boston, MA 02114 USA. RP Zareba, W (reprint author), Univ Rochester, Med Ctr, Heart Res Follow Program, Cardiol Unit,Dept Med, Box 653, Rochester, NY 14642 USA. EM wojciech_zareba@urmc.rochester.edu NR 22 TC 57 Z9 57 U1 0 U2 0 PU BLACKWELL PUBLISHING PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DQ, OXON, ENGLAND SN 1045-3873 J9 J CARDIOVASC ELECTR JI J. Cardiovasc. Electrophysiol. PD DEC PY 2005 VL 16 IS 12 BP 1265 EP 1270 DI 10.1111/j.1540-8167.2005.00224.x PG 6 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA 991IV UT WOS:000233807600001 PM 16403053 ER PT J AU Ebrahimi, R Lincoff, AM Bittl, JA Chew, D Wolski, K Wadhan, N Toggart, EJ Topol, EJ AF Ebrahimi, R Lincoff, AM Bittl, JA Chew, D Wolski, K Wadhan, N Toggart, EJ Topol, EJ TI Bivalirudin vs heparin in percutaneous coronary intervention: A pooled analysis SO JOURNAL OF CARDIOVASCULAR PHARMACOLOGY AND THERAPEUTICS LA English DT Review DE anticoagulation; percutaneous coronary intervention; bivalirudin ID GLYCOPROTEIN IIB/IIIA INHIBITION; REPLACE-2 RANDOMIZED-TRIAL; DIRECT THROMBIN INHIBITORS; LOW-DOSE HEPARIN; DIABETES-MELLITUS; HEART-ASSOCIATION; DYNAMIC REGISTRY; ANGIOPLASTY; OUTCOMES; REVASCULARIZATION AB Objective: This study evaluates Outcomes With bivalirudin vs heparin in various patient subgroups and the overall population during percutaneous coronary interventions (PCI). Background: Recent data suggest that bivalirudin, a reversible direct thrombin inhibitor, provides ischemic protection superior to heparin and comparable to heparin plus glycoprotein (GP) IIb/IIIa inhibitors but with significantly fewer bleeding complications. Whether this advantage persists in different subgroups has not been fully defined. To our knowledge, this is the largest pooled analysis of bivalirudin to date. Methods: Four randomized controlled trials were identified that compared bivalirudin to heparin (with or without GP IIb/IIIa inhibitors) in PCI. The incidence of death, myocardial infarction (MI), revascularization, and major bleeding at 48 hours was compared between these two agents overall and in patients with and without diabetes mellitus, hypertension, renal insufficiency, and advanced age. Results: The trials consisted of 11,638 patients (bivalirudin, 5,861; heparin, 5,777). There were no significant differences in patient characteristics between the two groups. At 48 hours, the incidence of death, MI, revascularization, and major bleeding was significantly reduced in the bivalirudin group (7.8% vs 1.08%, P <.001); individual ischemic end points were significantly reduced for death (0.01% vs 0.02%, P =.049) and revascularization (2.0% vs 2.7%, P =.02). with similar reductions for major bleeding (2.7% vs 5.8%, P <.001). Subgroup analysis was generally consistent with the overall findings. Conclusion: This analysis further supports the superiority of bivalirudin compared with heparin. Bivalirudin provides excellent ischemic protection with a significant reduction of bleeding complications, even in high-risk subgroups. C1 Univ Calif Los Angeles, Sch Med, Dept Med, Cardiol Sect 111E,GLAVA,W Los Angeles VA, Los Angeles, CA 90073 USA. Cleveland Clin Fdn, Cleveland, OH 44195 USA. Ocala Heart & Vasc Inst, Munroe Reg Med Ctr, Ocala, FL USA. Flinders Med Ctr, Bedford Pk, SA, Australia. RP Ebrahimi, R (reprint author), Univ Calif Los Angeles, Sch Med, Dept Med, Cardiol Sect 111E,GLAVA,W Los Angeles VA, 11301 Wilshire Blvd, Los Angeles, CA 90073 USA. EM ramin.ebrahimi@med.va.gov OI Topol, Eric/0000-0002-1478-4729 NR 31 TC 21 Z9 22 U1 0 U2 0 PU WESTMINSTER PUBL INC PI GLEN HEAD PA 708 GLEN COVE AVE, GLEN HEAD, NY 11545 USA SN 1074-2484 J9 J CARDIOVASC PHARM T JI J. Cardiovasc. Pharmacol. Ther. PD DEC PY 2005 VL 10 IS 4 BP 209 EP 216 DI 10.1177/107424840501000401 PG 8 WC Cardiac & Cardiovascular Systems; Pharmacology & Pharmacy SC Cardiovascular System & Cardiology; Pharmacology & Pharmacy GA 996LH UT WOS:000234174900001 PM 16382257 ER PT J AU Bangs, ME Emslie, GJ Spencer, TJ Ramsey, JL Detke, HC Allen, AJ Sumner, CR AF Bangs, ME Emslie, GJ Spencer, TJ Ramsey, JL Detke, HC Allen, AJ Sumner, CR TI A study of atomoxetine in adolescents with ADHD and comorbid depression SO JOURNAL OF CHILD AND ADOLESCENT PSYCHOPHARMACOLOGY LA English DT Meeting Abstract CT 45th Annual Meeting of the New-Clinical-Drug-Evaluation-Unit CY JUN 06-09, 2005 CL Boca Raton, FL SP NIMH, New Clin Drug Evaluat Unit C1 Lilly Res Labs, Indianapolis, IN USA. Univ Texas, SW Med Ctr, Dallas, TX USA. Massachusetts Gen Hosp, Boston, MA 02114 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PI NEW ROCHELLE PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA SN 1044-5463 J9 J CHILD ADOL PSYCHOP JI J. Child Adolesc. Psychopharmacol. PD DEC PY 2005 VL 15 IS 6 BP 848 EP 849 PG 2 WC Pediatrics; Pharmacology & Pharmacy; Psychiatry SC Pediatrics; Pharmacology & Pharmacy; Psychiatry GA 000EC UT WOS:000234442700006 ER PT J AU Greenhill, LL Biederman, J Boellner, SW Rugino, TA Sangal, RB Swanson, JM AF Greenhill, LL Biederman, J Boellner, SW Rugino, TA Sangal, RB Swanson, JM TI Modafinil film-coated tablets significantly improve symptoms on ADHD Rating Scale-IV School and Home and overall clinical condition in children and adolescents with attention-deficit/hyperactivity disorder SO JOURNAL OF CHILD AND ADOLESCENT PSYCHOPHARMACOLOGY LA English DT Meeting Abstract CT 45th Annual Meeting of the New-Clinical-Drug-Evaluation-Unit CY JUN 06-09, 2005 CL Boca Raton, FL SP NIMH, New Clin Drug Evaluat Unit C1 New York State Psychiat Inst & Hosp, New York, NY 10032 USA. Massachusetts Gen Hosp, Boston, MA 02114 USA. Neurol & Clin Study Ctr, Little Rock, AR USA. Childrens Specialized Hosp, Toms River, NJ USA. Clin Neurophysiol Serv PC, Troy, MI USA. Univ Calif Irvine, Child Dev Ctr, Irvine, CA USA. NR 0 TC 1 Z9 1 U1 0 U2 1 PU MARY ANN LIEBERT INC PI NEW ROCHELLE PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA SN 1044-5463 J9 J CHILD ADOL PSYCHOP JI J. Child Adolesc. Psychopharmacol. PD DEC PY 2005 VL 15 IS 6 BP 849 EP 850 PG 2 WC Pediatrics; Pharmacology & Pharmacy; Psychiatry SC Pediatrics; Pharmacology & Pharmacy; Psychiatry GA 000EC UT WOS:000234442700008 ER PT J AU Biederman, J Swanson, JM Wigal, SB Kratochvil, CJ Boellner, SW Greenhill, LL AF Biederman, J Swanson, JM Wigal, SB Kratochvil, CJ Boellner, SW Greenhill, LL TI Safety and efficacy of modafinil film-coated tablets in children and adolescents with attention-deficit/hyperactivity SO JOURNAL OF CHILD AND ADOLESCENT PSYCHOPHARMACOLOGY LA English DT Meeting Abstract CT 45th Annual Meeting of the New-Clinical-Drug-Evaluation-Unit CY JUN 06-09, 2005 CL Boca Raton, FL SP NIMH, New Clin Drug Evaluat Unit C1 Massachusetts Gen Hosp, Boston, MA 02114 USA. Univ Calif Irvine, Child Dev Ctr, Irvine, CA USA. Univ Nebraska Med Ctr, Omaha, NE USA. Neurol & Clin Study Ctr, Little Rock, AR USA. New York State Psychiat Inst & Hosp, New York, NY 10032 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PI NEW ROCHELLE PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA SN 1044-5463 J9 J CHILD ADOL PSYCHOP JI J. Child Adolesc. Psychopharmacol. PD DEC PY 2005 VL 15 IS 6 BP 852 EP 853 PG 2 WC Pediatrics; Pharmacology & Pharmacy; Psychiatry SC Pediatrics; Pharmacology & Pharmacy; Psychiatry GA 000EC UT WOS:000234442700013 ER PT J AU Swanson, JM Greenhill, LL Lopez, FA Sedillo, A Biederman, J AF Swanson, JM Greenhill, LL Lopez, FA Sedillo, A Biederman, J TI Modafinil film-coated tablets demonstrate early efficacy in pediatric attentiondeficit/hyperactivity disorder and were not associated with withdrawal or discontinuation SO JOURNAL OF CHILD AND ADOLESCENT PSYCHOPHARMACOLOGY LA English DT Meeting Abstract CT 45th Annual Meeting of the New-Clinical-Drug-Evaluation-Unit CY JUN 06-09, 2005 CL Boca Raton, FL SP NIMH, New Clin Drug Evaluat Unit C1 Univ Calif Irvine, Child Dev Ctr, Irvine, CA USA. New York State Psychiat Inst & Hosp, New York, NY 10032 USA. Childrens Dev Ctr PA, Maitland, FL USA. Pedia Res LLC, Owensboro, KY USA. Massachusetts Gen Hosp, Boston, MA 02114 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PI NEW ROCHELLE PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA SN 1044-5463 J9 J CHILD ADOL PSYCHOP JI J. Child Adolesc. Psychopharmacol. PD DEC PY 2005 VL 15 IS 6 BP 852 EP 852 PG 1 WC Pediatrics; Pharmacology & Pharmacy; Psychiatry SC Pediatrics; Pharmacology & Pharmacy; Psychiatry GA 000EC UT WOS:000234442700012 ER PT J AU Albers, LJ Ozdemir, V Marder, SR Leeder, JS Raggi, MA Aravagiri, M Pearce, RE Reist, C AF Albers, LJ Ozdemir, V Marder, SR Leeder, JS Raggi, MA Aravagiri, M Pearce, RE Reist, C TI A focus on CYP1A2 activity and N-desmethylolanzapine - Is there a potential role for olanzapine-induced metabolic syndrome? SO JOURNAL OF CHILD AND ADOLESCENT PSYCHOPHARMACOLOGY LA English DT Meeting Abstract CT 45th Annual Meeting of the New-Clinical-Drug-Evaluation-Unit CY JUN 06-09, 2005 CL Boca Raton, FL SP NIMH, New Clin Drug Evaluat Unit C1 Univ Calif Irvine, Dept Psychiat & Human Behav, Vet Adm Long Beach Healthcare Syst, Irvine, CA 92717 USA. Univ Calif Los Angeles, Vet Adm Greater Los Angeles Healthcare Syst, Los Angeles, CA USA. Childrens Mercy Hosp, Div Pediat Clin Pharmacol & Med Toxicol, Kansas City, MO USA. Univ Bologna, Dept Pharmaceut Sci, I-40126 Bologna, Italy. RI Raggi, Maria Augusta/A-4545-2011 NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PI NEW ROCHELLE PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA SN 1044-5463 J9 J CHILD ADOL PSYCHOP JI J. Child Adolesc. Psychopharmacol. PD DEC PY 2005 VL 15 IS 6 BP 862 EP 863 PG 2 WC Pediatrics; Pharmacology & Pharmacy; Psychiatry SC Pediatrics; Pharmacology & Pharmacy; Psychiatry GA 000EC UT WOS:000234442700031 ER PT J AU Biederman, J Mick, E Wozniak, J Spencer, TJ AF Biederman, J Mick, E Wozniak, J Spencer, TJ TI A long-term, open-label trial of risperidone in children with bipolar disorder and comorbid attention-deficit/hyperactivity disorder SO JOURNAL OF CHILD AND ADOLESCENT PSYCHOPHARMACOLOGY LA English DT Meeting Abstract CT 45th Annual Meeting of the New-Clinical-Drug-Evaluation-Unit CY JUN 06-09, 2005 CL Boca Raton, FL SP NIMH, New Clin Drug Evaluat Unit C1 Massachusetts Gen Hosp, Boston, MA 02114 USA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU MARY ANN LIEBERT INC PI NEW ROCHELLE PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA SN 1044-5463 J9 J CHILD ADOL PSYCHOP JI J. Child Adolesc. Psychopharmacol. PD DEC PY 2005 VL 15 IS 6 BP 864 EP 864 PG 1 WC Pediatrics; Pharmacology & Pharmacy; Psychiatry SC Pediatrics; Pharmacology & Pharmacy; Psychiatry GA 000EC UT WOS:000234442700033 ER PT J AU Stevens, JR Kymissis, PI Baker, AJL AF Stevens, JR Kymissis, PI Baker, AJL TI Elevated prolactin levels in male youths treated with risperidone and quetiapine SO JOURNAL OF CHILD AND ADOLESCENT PSYCHOPHARMACOLOGY LA English DT Article ID LONG-TERM; ATYPICAL ANTIPSYCHOTICS; YOUNG-CHILDREN; OPEN-LABEL; ADOLESCENTS; TOLERABILITY; HYPERPROLACTINEMIA; SCHIZOPHRENIA; DISORDERS; EFFICACY AB The aim of this study was to report on the serum prolactin levels in 70 male youths at a residential treatment center who were treated with either risperidone or quetiapine. This is a cross-sectional retrospective medical chart review of 50 males (mean age, 13.5 +/- 2.8 years) treated with risperidone (mean dose, 2.4 +/- 1.6 mg/day) and 20 males (mean age, 13.5 2.4 years) treated with quetiapine (mean dose, 317.5 +/- 238 mg/day). Serum prolactin levels were drawn according to a protocol, after at least 6 weeks of treatment. Prolactin was above the upper limit of normal for 68% of the patients on risperidone and 20% of the patients on quetiapine (chi(2) analysis: R > Q; p < 0.001). Both risperidone and quetiapine produced dose-related increases in serum prolactin levels (R, r = 0.34, p = 0.017; Q, r = 0.45, p = 0.05). No correlation was found between duration of treatment and prolactin levels. Given that hyperprolactinemia secondary to antipsychotic treatment may result in reproductive and growth irregularities, periodic long-term monitoring during treatment with these two atypical antipsychotics (and perhaps others as well) may be warranted. C1 Dept Psychiat, Dobbs Ferry, NY 10522 USA. Massachusetts Gen Hosp, McLean Hosp, Adult Psychiat Residency, Boston, MA 02114 USA. Ctr Child Welf Res, Dobbs Ferry, NY USA. RP Kymissis, PI (reprint author), Dept Psychiat, Childrens Village, Dobbs Ferry, NY 10522 USA. EM pkymissis@childrensvillage.org NR 26 TC 24 Z9 25 U1 2 U2 3 PU MARY ANN LIEBERT INC PI NEW ROCHELLE PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA SN 1044-5463 J9 J CHILD ADOL PSYCHOP JI J. Child Adolesc. Psychopharmacol. PD DEC PY 2005 VL 15 IS 6 BP 893 EP 900 DI 10.1089/cap.2005.15.893 PG 8 WC Pediatrics; Pharmacology & Pharmacy; Psychiatry SC Pediatrics; Pharmacology & Pharmacy; Psychiatry GA 000EC UT WOS:000234442700039 PM 16379509 ER PT J AU Wilens, TE Waxmonsky, J Scott, M Swezey, A Kwon, A Spencer, TJ Biederman, J AF Wilens, TE Waxmonsky, J Scott, M Swezey, A Kwon, A Spencer, TJ Biederman, J TI An open trial of adjunctive donepezil in attention-deficit/hyperactivity disorder SO JOURNAL OF CHILD AND ADOLESCENT PSYCHOPHARMACOLOGY LA English DT Article ID DEFICIT-HYPERACTIVITY DISORDER; CONTROLLED CLINICAL-TRIAL; DOUBLE-BLIND; EXECUTIVE FUNCTIONS; ALZHEIMERS-DISEASE; ADULTS; CHILDREN; ADOLESCENTS; NICOTINE; PLACEBO AB Objective: Despite available pharmacotherapeutics, a number of youths with attention-deficit/hyperactivity disorder (ADHD) continue to experience residual symptoms and prominent executive function (EF) deficits resulting in impairment in multiple domains. We sought to determine if donepezil, used adjunctively to stimulant medication, would improve residual symptoms of ADHD and EF deficits. Methods: In a 12-week open trial, we treated 7 children and 6 adults who had ADHD and evidence of further EF deficits with adjunctive donepezil. All subjects were stabilized on stimulants, at which time donepezil was initiated at 2.5 mg daily and increased to a maximum of 10 mg over the 12-week trial. Results: Of 13 subjects receiving medication, 7 completed the trial. There was no clinically or statistically significant improvement in the ADHD Rating Scale and the Executive Function Checklist, our primary outcome measures. A majority of individuals experienced nonserious adverse events. Conclusions: Results of this small open study suggest that donepezil augmentation of stimulants is not well tolerated and does not appear useful for the treatment of residual ADHD and/or EF deficits. C1 Massachusetts Gen Hosp, Pediat Psychopharmacol Unit, Yawkey Ctr Outpatient Care, Boston, MA 02114 USA. Harvard Med Sch, Boston, MA USA. RP Wilens, TE (reprint author), Massachusetts Gen Hosp, Pediat Psychopharmacol Unit, Yawkey Ctr Outpatient Care, YAW-6A,32 Fruit St, Boston, MA 02114 USA. EM twilens@partners.org FU NIDA NIH HHS [DA11929] NR 49 TC 19 Z9 19 U1 1 U2 6 PU MARY ANN LIEBERT INC PI NEW ROCHELLE PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA SN 1044-5463 J9 J CHILD ADOL PSYCHOP JI J. Child Adolesc. Psychopharmacol. PD DEC PY 2005 VL 15 IS 6 BP 947 EP 955 DI 10.1089/cap.2005.15.947 PG 9 WC Pediatrics; Pharmacology & Pharmacy; Psychiatry SC Pediatrics; Pharmacology & Pharmacy; Psychiatry GA 000EC UT WOS:000234442700045 PM 16379515 ER PT J AU Stewart, SE Ceranoglu, TA O'Hanley, T Geller, DA AF Stewart, SE Ceranoglu, TA O'Hanley, T Geller, DA TI Performance of clinician versus self-report measures to identify obsessive-compulsive disorder in children and adolescents SO JOURNAL OF CHILD AND ADOLESCENT PSYCHOPHARMACOLOGY LA English DT Article ID STRUCTURED INTERVIEW; RELIABILITY; SCALE; VALIDITY; PHENOMENOLOGY; AGREEMENT; DIAGNOSIS; SYMPTOMS; VERSION; TRIALS AB Objective: The aim of this study was to study agreement between clinician-rated measures and self-report measures previously used in epidemiologic studies to identify obsessive-compulsive disorder (OCD) in youth and to determine the adequacy of self-report measures as screening instruments. Method: Leyton Obsessional Inventory-Child Version (LOI-CV) survey form self-report and Children's Yale-Brown Obsessive Compulsive Scale (CY-BOCS) clinician-report measures were compared in a sample of 81 OCD-affected youths diagnosed using structured diagnostic interviews and the best-estimate method. Sensitivities and agreement between tests are determined for different cutoff scores. Results: The LOI-CV survey form total (item + interference) score is correlated with K-SADS-E OCD severity (r = 0.37, p = 0.001) but not clinician-rated GAF scores (r = -0.18, p = 0.12). LOI-CV survey form sensitivities at cutoff scores of 15, 20, 25, and 30 are 55%, 36%, 28%, and 19%, respectively. CY-BOCS scores are correlated with subject-rated interview severity (p < 0.001) and clinician-rated GAF scores (p <= 0.05). CY-BOCS sensitivities at cutoff scores of 8, 10, 12, and 14 are 100%, 99%, 98%, and 90%. The cutoff scores required for greater than 95% sensitivity of the LOI-CV survey form and the CY-BOCS, respectively, are 2 and 12. LOI-CV survey form total scores do not correlate with CY-BOCS total or obsession subscores (p >= 0.03), but correlate with the CY-BOCS compulsion subscore. Conclusions: The clinician-rated CY-BOCS measure using parent and child reporting performs superiorly to the subject-rated LOI-CV measure using child reporting to identify pediatric OCD in a clinically referred population. Because self-report measures have been used in epidemiological studies, youth OCD prevalence rates may be higher than previously reported. C1 Massachusetts Gen Hosp, Boston, MA 02114 USA. Harvard Univ, Sch Med, McLean Hosp, Boston, MA USA. RP Geller, DA (reprint author), Pediat Psychopharmacol Res Program, 185 Alewife Brook Pkwy,Suite 2000, Cambridge, MA 02138 USA. EM dageller@partners.org RI Stewart, Evelyn/K-6961-2014; OI Stewart, S. Evelyn/0000-0002-0994-6383 FU NIMH NIH HHS [K08 MH01481] NR 30 TC 16 Z9 16 U1 3 U2 9 PU MARY ANN LIEBERT INC PI NEW ROCHELLE PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA SN 1044-5463 J9 J CHILD ADOL PSYCHOP JI J. Child Adolesc. Psychopharmacol. PD DEC PY 2005 VL 15 IS 6 BP 956 EP 963 DI 10.1089/cap.2005.15.956 PG 8 WC Pediatrics; Pharmacology & Pharmacy; Psychiatry SC Pediatrics; Pharmacology & Pharmacy; Psychiatry GA 000EC UT WOS:000234442700046 PM 16379516 ER PT J AU Fitzsimons, MG Baker, KH Peralta, R AF Fitzsimons, MG Baker, KH Peralta, R TI Anesthetic implications of traumatic pulmonary hernia repair SO JOURNAL OF CLINICAL ANESTHESIA LA English DT Article DE pulmonary herniation; anesthesia ID LUNG HERNIATION AB Traumatic pulmonary herniation involves the protrusion of lung parenchyma beyond the normal borders of the thoracic cage through a defect in the musculoskeletal wall. Anesthetic management involves airway protection, lung isolation, and avoidance of distension of the herniated segment. We report the successful anesthetic management during surgical management of pulmonary herniation. (c) 2005 Elsevier Inc. All rights reserved. C1 Massachusetts Gen Hosp, Dept Anesthesia & Crit Care, Boston, MA 02114 USA. Massachusetts Gen Hosp, Dept Surg, Boston, MA 02114 USA. RP Fitzsimons, MG (reprint author), Massachusetts Gen Hosp, Dept Anesthesia & Crit Care, Boston, MA 02114 USA. EM mfitzsimons@partners.org; khbaker@partners.org; rperalta@partners.org NR 14 TC 1 Z9 2 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0952-8180 J9 J CLIN ANESTH JI J. Clin. Anesth. PD DEC PY 2005 VL 17 IS 8 BP 627 EP 629 DI 10.1016/j.jclinane.2005.03.008 PG 3 WC Anesthesiology SC Anesthesiology GA 000XW UT WOS:000234496700012 PM 16427536 ER PT J AU Seton, M Jackson, V Lasser, KE Doppelt, S Pierre-Jacques, M Connelly, M AF Seton, M Jackson, V Lasser, KE Doppelt, S Pierre-Jacques, M Connelly, M TI Low 25-hydroxyvitamin D and osteopenia are prevalent in persons >= 55 yr with fracture at any site - A prospective, observational study of persons fracturing in the community SO JOURNAL OF CLINICAL DENSITOMETRY LA English DT Article DE community study; ambulatory; fracture; postmenopausal women ID BONE-MINERAL DENSITY; OSTEOPOROSIS RISK-ASSESSMENT; POSTMENOPAUSAL WOMEN; HIP FRACTURE; PERIMENOPAUSAL FRACTURES; VERTEBRAL FRACTURE; HYPOVITAMINOSIS-D; ANKLE FRACTURES; ELDERLY-WOMEN; EPIDEMIOLOGY AB Ethnic diversity and lower socioeconomic populations are poorly captured in most studies of osteoporosis and fracture risk. This article describes a prospective, observational study designed to analyze risk factors for fracture in an ambulatory, ethnically diverse, urban population aged >= 55 yr. The goal of the study was to determine the number of fractures associated with hypovitaminosis D (<= 15 ng/mL serum 25-hydroxyvitamin D) and osteopenia (T-score <-1.5) by bone mineral density (BMD). From January I to July 31, 2001, we identified 262 persons who fractured in our community 83 chose to enroll in the study. Enrolled patients had a BMD examination at two sites, their blood was drawn for 25-hydroxyvitamin D (25VitD), calcium, phosphorus, albumin, and alkaline phosphatase. At the completion of the study a letter was sent to the patients detailing the findings, and a copy sent to their physician. Of the 83 persons enrolled, 73 (88%) had evidence of osteopenia or osteoporosis (T-score <-1.5) and/or low 25VitD. All fractures in the community in person 2 >= 55 yr, with or without a history of antecedent trauma, should be assessed with BMD and screening for 25VitD. C1 Cambridge Hlth Alliance, Rheumatol Arthrit & Osteoporosis Ctr, Cambridge, MA 02139 USA. Massachusetts Gen Hosp, Boston, MA 02114 USA. Harvard Univ, Sch Med, Boston, MA USA. RP Seton, M (reprint author), Cambridge Hlth Alliance, Rheumatol Arthrit & Osteoporosis Ctr, 1493 Cambridge St, Cambridge, MA 02139 USA. EM Margaret_seton@hms.harvard.edu NR 44 TC 5 Z9 5 U1 1 U2 1 PU HUMANA PRESS INC PI TOTOWA PA 999 RIVERVIEW DRIVE SUITE 208, TOTOWA, NJ 07512 USA SN 1094-6950 J9 J CLIN DENSITOM JI J. Clin. Densitom. PD WIN PY 2005 VL 8 IS 4 BP 454 EP 460 DI 10.1385/JCD:8:4:454 PG 7 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA 990GH UT WOS:000233730700012 PM 16311431 ER PT J AU Hoffman, AR Biller, BMK Cook, D Baptista, J Silverman, BL Dao, L Attie, KM Fielder, P Maneatis, T Lippe, B AF Hoffman, AR Biller, BMK Cook, D Baptista, J Silverman, BL Dao, L Attie, KM Fielder, P Maneatis, T Lippe, B CA Genentech Adult Growth Hormone Grp TI Efficacy of a long-acting growth hormone (GH) preparation in patients with adult GH deficiency SO JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM LA English DT Article ID REPLACEMENT THERAPY; INSULIN SENSITIVITY; BODY-COMPOSITION; HYPOPITUITARY ADULTS; METABOLISM; SECRETION; MEN; MULTICENTER; MODULATION; GLUCOSE AB Context: Treatment of adult GH deficiency (AGHD) with daily injections ofGHresults in decreased adipose mass, increased lean body mass (LBM), increased bone mineral density, and improved quality of life. Objective: This study seeks to determine whether a depot preparation of GH given every 14 d would lead to comparable decreases in trunk adipose tissue as daily GH. Design: This open-label, randomized study compares subjects receiving depot GH, daily GH, or no therapy. Setting: The study was performed at 23 university or local referral endocrine centers. Patients or Other Participants: One hundred thirty-five adults with AGHD syndrome participated in the study. Intervention: Subjects were randomized to receive depot GH (n = 51), daily GH (n = 53), or no treatment (n = 31) for 32 wk. The dose of GH was titrated so that IGF-I was less than or equal to +2 SD of the age-adjusted normal range. M ain Outcome Measure: Trunk adipose tissue was the main outcome measure as measured by dual energy x-ray absorptiometry. Results: The percentage of the trunk region that is fat increased by 0.4 in the no treatment group, but decreased by 3.2 (P = 0.001 vs. untreated) in the GH depot group and by 2.5 (P < 0.004 vs. untreated) in the daily GH group. Visceral adipose tissue area decreased by 9.1% in the GH depot group and by 6.8% in the daily GH group. LBM and high-density lipoprotein increased in both treatment groups. Side effect profiles were similar. Three subjects receiving GH experienced serious episodes of adrenal insufficiency. Conclusions: GH diminishes trunk and visceral adipose tissue and increases LBM in AGHD. A depot form of GH that is administered every 14 d is as safe and effective as daily GH injections. C1 Dept Vet Affairs Palo Alto Hlth Care Syst, Palo Alto, CA 94304 USA. Stanford Univ, Palo Alto, CA 94304 USA. Harvard Univ, Sch Med, Boston, MA 02114 USA. Massachusetts Gen Hosp, Boston, MA 02114 USA. Oregon Hlth Sci Univ, Portland, OR 97201 USA. Genentech Inc, Med Affairs, San Francisco, CA 94080 USA. Alkermes Inc, Cambridge, MA 02139 USA. RP Hoffman, AR (reprint author), Dept Vet Affairs Palo Alto Hlth Care Syst, Bldg 100,Room D4-132,3801 Miranda Ave, Palo Alto, CA 94304 USA. EM arhoffman@stanford.edu NR 42 TC 44 Z9 45 U1 0 U2 0 PU ENDOCRINE SOC PI CHEVY CHASE PA 8401 CONNECTICUT AVE, SUITE 900, CHEVY CHASE, MD 20815-5817 USA SN 0021-972X J9 J CLIN ENDOCR METAB JI J. Clin. Endocrinol. Metab. PD DEC PY 2005 VL 90 IS 12 BP 6431 EP 6440 DI 10.1210/jc.2005-0928 PG 10 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA 990OV UT WOS:000233754000015 PM 16159930 ER PT J AU Florez, JC AF Florez, JC TI Editorial: Genetic susceptibility for polycystic ovary syndrome on chromosome 19: Advances in the genetic dissection of complex reproductive traits SO JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM LA English DT Editorial Material ID ASSOCIATION; VARIANTS; REPLICATION; FOLLISTATIN; RECEPTOR; LINKAGE; DISEASE; REGION; LOCUS C1 Massachusetts Gen Hosp, Diabet Unit, Boston, MA 02114 USA. Massachusetts Gen Hosp, Dept Med, Boston, MA 02114 USA. Massachusetts Gen Hosp, Dept Biol Mol, Boston, MA 02114 USA. Harvard Univ, Program Med & Populat Genet, Broad Inst, Cambridge, MA 02141 USA. MIT, Cambridge, MA 02141 USA. Harvard Univ, Sch Med, Dept Med, Boston, MA 02115 USA. RP Florez, JC (reprint author), Massachusetts Gen Hosp, Diabet Unit, 185 Cambridge St,Simches Res Ctr 6720, Boston, MA 02114 USA. EM jcflorez@partners.org FU NIDDK NIH HHS [1 K23 DK65978-02] NR 20 TC 0 Z9 0 U1 0 U2 1 PU ENDOCRINE SOC PI CHEVY CHASE PA 8401 CONNECTICUT AVE, SUITE 900, CHEVY CHASE, MD 20815-5817 USA SN 0021-972X J9 J CLIN ENDOCR METAB JI J. Clin. Endocrinol. Metab. PD DEC PY 2005 VL 90 IS 12 BP 6732 EP 6734 DI 10.1210/jc.2005-2204 PG 3 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA 990OV UT WOS:000233754000060 PM 16330807 ER PT J AU Seminara, SB AF Seminara, SB TI Editorial: We all remember our first kiss: Kisspeptin and the male gonadal axis SO JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM LA English DT Editorial Material ID METASTASIS SUPPRESSOR GENE; PROTEIN-COUPLED RECEPTOR; HYPOGONADOTROPIC HYPOGONADISM; KALLMANN-SYNDROME; GPR54; PEPTIDE; RAT; ENCODES; OBESITY; LIGAND C1 Massachusetts Gen Hosp, Reprod Endocrinol Unit, Boston, MA 02114 USA. RP Seminara, SB (reprint author), Massachusetts Gen Hosp, Reprod Endocrinol Unit, Bartlett Hall,Extens 505,55 Fruit St, Boston, MA 02114 USA. EM seminara.stephanie@mgh.harvard.edu FU NICHD NIH HHS [R01 HD043341, U54 HD028138] NR 28 TC 6 Z9 8 U1 0 U2 1 PU ENDOCRINE SOC PI CHEVY CHASE PA 8401 CONNECTICUT AVE, SUITE 900, CHEVY CHASE, MD 20815-5817 USA SN 0021-972X J9 J CLIN ENDOCR METAB JI J. Clin. Endocrinol. Metab. PD DEC PY 2005 VL 90 IS 12 BP 6738 EP 6740 DI 10.1210/jc.2005-2246 PG 3 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA 990OV UT WOS:000233754000062 PM 16330809 ER PT J AU Minneci, PC Deans, KJ Zhi, H Yuen, PST Star, RA Banks, SM Schechter, AN Natanson, C Gladwin, MT Solomon, SB AF Minneci, PC Deans, KJ Zhi, H Yuen, PST Star, RA Banks, SM Schechter, AN Natanson, C Gladwin, MT Solomon, SB TI Hemolysis-associated endothelial dysfunction mediated by accelerated NO inactivation by decompartmentalized oxyhemoglobin SO JOURNAL OF CLINICAL INVESTIGATION LA English DT Article ID CROSS-LINKED HEMOGLOBIN; CELL-FREE HEMOGLOBIN; NITRIC-OXIDE BIOAVAILABILITY; BETA-THALASSEMIA MAJOR; PULMONARY-HYPERTENSION; RELAXING FACTOR; CARDIOPULMONARY BYPASS; DEPENDENT RELAXATION; BIOLOGICAL-ACTIVITY; BLOOD SUBSTITUTES AB During intravascular hemolysis in human disease, vasomotor tone and organ perfusion may be impaired by the increased reactivity of cell-free plasma hemoglobin (Hb) with NO. We experimentally produced acute intravascular hemolysis in a canine model. in order to test the hypothesis that low levels of decompartmentalized or cell-free plasma Hb will severely reduce NO bioavailability and produce vasomotor instability. Importantly, in this model the total intravascular Hb level is unchanged; only the compartmentalization of Hb within the erythrocyte membrane is disrupted. Using a full-factorial design, we demonstrate that free water-induced intravascular hemolysis produces dose-dependent systemic vasoconstriction and impairs renal function. We find that these physiologic changes are secondary to the stoichiometric oxidation of endogenous NO by cell-free plasma oxyhemoglobin. In this model, 80 ppm of inhaled NO gas oxidized 85-90% of plasma oxyhemoglobin to methemoglobin, thereby inhibiting endogenous NO scavenging by cell-free Hb. As a result, the vasoconstriction caused by acute hemolysis was attenuated and the responsiveness to systemically infused NO donors was restored. These observations confirm that the acute toxicity of intravascular hemolysis occurs secondarily to the accelerated dioxygenation reaction of plasma oxyhemoglobin with endothelium-derived NO to form bioinactive nitrate. These biochemical and physiological studies demonstrate a major role for the intact erythrocyte in NO homeostasis and provide mechanistic support for the existence of a human syndrome of hemolysis-associated NO dysregulation, which may contribute to the vasculopathy of hereditary, acquired, and iatrogenic hemolytic states. C1 NHLBI, Vasc Med Branch, Crit Med Dept, Clin Ctr,NIH,Clin Res Ctr, Bethesda, MD 20892 USA. NIDDK, Mol Med Branch, NIH, Bethesda, MD 20892 USA. Massachusetts Gen Hosp, Dept Surg, Boston, MA 02114 USA. NIDDK, Renal Diagnost & Therapeut Unit, NIH, Bethesda, MD USA. RP Gladwin, MT (reprint author), NHLBI, Vasc Med Branch, Crit Med Dept, Clin Ctr,NIH,Clin Res Ctr, Bldg 10 CRC,Room 5-5140, Bethesda, MD 20892 USA. EM mgladwin@nih.gov RI Yuen, Peter/B-1954-2008; OI Yuen, Peter/0000-0001-9557-3909; Schechter, Alan N/0000-0002-5235-9408 FU Intramural NIH HHS NR 56 TC 151 Z9 152 U1 0 U2 4 PU AMER SOC CLINICAL INVESTIGATION INC PI ANN ARBOR PA 35 RESEARCH DR, STE 300, ANN ARBOR, MI 48103 USA SN 0021-9738 J9 J CLIN INVEST JI J. Clin. Invest. PD DEC PY 2005 VL 115 IS 12 BP 3409 EP 3417 DI 10.1172/JCI25040 PG 9 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA 990SL UT WOS:000233763400019 PM 16294219 ER PT J AU Knauf, C Cani, PD Perrin, C Iglesias, MA Maury, JF Bernard, E Benhamed, F Gremeaux, T Drucker, DJ Kahn, CR Girard, J Tanti, JF Delzenne, NM Postic, C Burcelin, R AF Knauf, C Cani, PD Perrin, C Iglesias, MA Maury, JF Bernard, E Benhamed, F Gremeaux, T Drucker, DJ Kahn, CR Girard, J Tanti, JF Delzenne, NM Postic, C Burcelin, R TI Brain glucagon-like peptide-1 increases insulin secretion and muscle insulin resistance to favor hepatic glycogen storage SO JOURNAL OF CLINICAL INVESTIGATION LA English DT Article ID GLUCOSE-METABOLISM; RAT-BRAIN; MESSENGER-RNA; SYMPATHOADRENAL RESPONSE; SKELETAL-MUSCLE; GENE-EXPRESSION; NERVOUS-SYSTEM; GLP-1 RECEPTOR; BINDING-SITES; MICE LACKING AB Intestinal glucagon-like peptide-1 (GLP-1) is a hormone released into the hepatoportal circulation that stimulates pancreatic insulin secretion. GLP-1 also acts as a neuropeptide to control food intake and cardiovascular functions, but its neural role in glucose homeostasis is unknown. We show that brain GLP-1 controlled whole-body glucose fate during hyperglycemic conditions. In mice undergoing a hyperglycemic hyperinsulinemic clamp, icv administration of the specific GLP-1 receptor antagonist exendin 9-39 (Ex9) increased muscle glucose utilization and glycogen content. This effect did not require muscle insulin action, as it also occurred in muscle insulin receptor KO mice. Conversely, icv infusion of the GLP-1 receptor agonist exendin 4 (Ex4) reduced insulin-stimulated muscle glucose utilization. In hyperglycemia achieved by i.v. infusion of glucose, icv Ex4, but not Ex9, caused a 4-fold increase in insulin secretion and enhanced liver glycogen storage. However, when glucose was infused intragastrically, icv Ex9 infusion lowered insulin secretion and hepatic glycogen levels, whereas no effects of icv Ex4 were observed. In diabetic mice fed a high-fat diet, a 1-month chronic i.p. Ex9 treatment improved glucose tolerance and fasting glycemia. Our data show that during hyperglycemia, brain GLP-1 inhibited muscle glucose utilization and increased insulin secretion to favor hepatic glycogen stores, preparing efficiently for the next fasting state. C1 Univ Toulouse 3, UMR 5018, IFR31, F-31062 Toulouse, France. Univ Catholique Louvain, Unite Pharmacocinet Metabol Nutr & Toxicol, B-1200 Brussels, Belgium. Univ Paris 05, Inst Cochin, INSERM, U567,UMR 8104,Dept Endocrinol, Paris, France. INSERM, Fac Med, IFR 50, Nice, France. Univ Toronto, Toronto Gen Hosp, Dept Med, Banting & Best Diabet Ctr, Toronto, ON M5G 1L7, Canada. Joslin Inst, Boston, MA USA. RP Burcelin, R (reprint author), Univ Toulouse 3, UMR 5018, IFR31, F-31062 Toulouse, France. EM burcelin@toulouse.inserm.fr RI Drucker, Daniel/A-4092-2010; burcelin, remy/M-6013-2014; OI Cani, Patrice D./0000-0003-2040-2448 NR 62 TC 184 Z9 191 U1 1 U2 5 PU AMER SOC CLINICAL INVESTIGATION INC PI ANN ARBOR PA 35 RESEARCH DR, STE 300, ANN ARBOR, MI 48103 USA SN 0021-9738 J9 J CLIN INVEST JI J. Clin. Invest. PD DEC PY 2005 VL 115 IS 12 BP 3554 EP 3563 DI 10.1172/JC125764 PG 10 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA 990SL UT WOS:000233763400033 PM 16322793 ER PT J AU Zigman, JM Nakano, Y Coppari, R Balthasar, N Marcus, JN Lee, CE Jones, JE Deysher, AE Waxman, AR White, RD Williams, TD Lachey, JL Seeley, RJ Lowell, BB Elmquist, JK AF Zigman, JM Nakano, Y Coppari, R Balthasar, N Marcus, JN Lee, CE Jones, JE Deysher, AE Waxman, AR White, RD Williams, TD Lachey, JL Seeley, RJ Lowell, BB Elmquist, JK TI Mice lacking ghrelin receptors resist the development of diet-induced obesity SO JOURNAL OF CLINICAL INVESTIGATION LA English DT Article ID GROWTH-HORMONE SECRETAGOGUE; AGOUTI-RELATED PROTEIN; FA/FA ZUCKER RATS; FOOD-INTAKE; FAT MASS; INSULIN; EXPRESSION; SECRETION; APPETITE; STOMACH AB Ghrelin is the endogenous ligand for the growth hormone secretagogue receptor (GHSR; ghrelin receptor). Since its discovery, accumulating evidence has suggested that ghrelin may play a role in signaling and reversing states of energy insufficiency. For example, ghrelin levels rise following food deprivation, and ghrelin administration stimulates feeding and increases body weight and adiposity. However, recent loss-of-function studies have raised questions regarding the physiological significance of ghrelin in regulating these processes. Here, we present results of a study using a novel GHSR-null mouse model, in which ghrelin administration fails to acutely stimulate food intake or activate arcuate nucleus neurons. We show that when fed a high-fat diet, both female and male GHSR-null mice eat less food, store less of their consumed calories, preferentially utilize fat as an energy substrate, and accumulate less body weight and adiposity than control mice. Similar effects on body weight and adiposity were also observed in female, but not male, GHSR-null mice fed standard chow. GHSR deletion also affected locomotor activity and levels of glycemia. These findings support the hypothesis that ghrelin-responsive pathways are an important component of coordinated body weight control. Moreover, our data suggest that ghrelin signaling is required for development of the full phenotype of diet-induced obesity. C1 Harvard Univ, Sch Med, Dept Med, Div Endocrinol Diabet & Metab,Beth Israel Deacone, Boston, MA 02115 USA. Univ Cincinnati, Dept Psychiat, Cincinnati, OH USA. Harvard Univ, Sch Med, Dept Neurol, BIDMC, Boston, MA 02115 USA. Harvard Univ, Sch Med, Program Neurosci, Boston, MA 02115 USA. RP Elmquist, JK (reprint author), Harvard Univ, Sch Med, Dept Med, Div Endocrinol Diabet & Metab,Beth Israel Deacone, Boston, MA 02115 USA. EM jelmquis@bidmc.harvard.edu RI Coppari, Roberto/B-4799-2014 FU NIDDK NIH HHS [DK56116, 1F32DK64564-01, 5T32DK07516, DK53301, DK59630, F32 DK064564, P01 DK056116, P30 DK057521, P30DK57521, R01 DK053301, R37 DK053301, T32 DK007516, U24 DK059630] NR 35 TC 345 Z9 351 U1 0 U2 23 PU AMER SOC CLINICAL INVESTIGATION INC PI ANN ARBOR PA 35 RESEARCH DR, STE 300, ANN ARBOR, MI 48103 USA SN 0021-9738 J9 J CLIN INVEST JI J. Clin. Invest. PD DEC PY 2005 VL 115 IS 12 BP 3564 EP 3572 DI 10.1172/JC126002 PG 9 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA 990SL UT WOS:000233763400034 PM 16322794 ER PT J AU Larson, PS Schlechter, BL de las Morenas, A Garber, JE Cupples, LA Rosenberg, CL AF Larson, PS Schlechter, BL de las Morenas, A Garber, JE Cupples, LA Rosenberg, CL TI Allele imbalance, or loss of heterozygosity, in normal breast epithelium of sporadic breast cancer cases and BRCA1 gene mutation carriers is increased compared with reduction mammoplasty tissues SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Article; Proceedings Paper CT 96th Annual Meeting of the American-Association-for-Cancer-Research CY APR 16-20, 2005 CL Anaheim, CA SP Amer Assoc Canc Res ID PROGESTERONE-RECEPTOR; HUMAN GENOME; CARCINOMAS; P53; EXPRESSION; ADJACENT; LESIONS; OCCURS AB Purpose Normal-appearing breast epithelium can contain genetic abnormalities, including allele imbalance (Al), also referred to as loss of heterozygosity. Whether abnormalities are associated with cancer or cancer risk is unknown. Patients and Methods We performed a miniallelotype, using 20 microsatellites, on each of 460 histologically normal, microdissected breast terminal ducto-lobular units (TDLUs) from three groups of women: sporadic breast cancer patients (SP; n = 18), BRCA1 gene mutation carriers (BRCA1; n = 16), and controls undergoing reduction mammoplasty (RM; n = 18). We analyzed the results using Fisher's exact tests, logistic regression, and generalized estimating equations. Results Al was increased three-fold in SP and BRCA1 groups compared with RM. Both the number of TDLUs with Al increased (eight [5%] of 162 in the RM group compared with 24 [15%] of 162 in the SP and 22 [16%] of 136 in the BRCA1 groups; P = .0150), and the proportion of patients with Al increased (five [28%] of 18 in the RM group compared with 15 [83%] of 18 in the SP and 13 [81%] of 16 in the BRCA1 groups; P = .0007). The adjusted odds ratios (OR) for Al in TDLU increased in SP (OR = 15.5) and BRCA1 (OR = 13.7) patients compared with RM (P = .0025). This result was particularly evident on chromosome 17q (P = .0393), where more Al was seen in BRCA1 (OR = 12.4) than in SP (OR = 4.9) patients or RM controls. Conclusion Increased prevalence of Al in normal-appearing epithelium is associated with breast cancer and increased breast cancer risk. The increased prevalence may reflect dysregulation, even in normal-appearing epithelium, of genomic processes contributing to cancer development. The clinical significance of genetic alterations in the subset of controls remains to be determined. C1 Boston Univ, Med Ctr, Dept Pathol & Lab Med, Sch Med, Boston, MA 02118 USA. Boston Univ, Sch Med, Dept Med, Boston, MA 02118 USA. Boston Univ, Sch Publ Hlth, Boston Med Ctr, Boston, MA 02118 USA. Boston Univ, Sch Publ Hlth, Dept Biostat, Boston, MA 02118 USA. Dana Farber Canc Inst, Dept Adult Oncol, Boston, MA 02115 USA. RP Rosenberg, CL (reprint author), Boston Univ, Med Ctr, Dept Pathol & Lab Med, Sch Med, 650 Albany St,EBRC 4, Boston, MA 02118 USA. EM crosenbe@bu.edu OI De Las Morenas, Antonio/0000-0001-9908-4096; Cupples, L. Adrienne/0000-0003-0273-7965 FU NCI NIH HHS [CA81078] NR 30 TC 25 Z9 25 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 DEC 1 PY 2005 VL 23 IS 34 BP 8613 EP 8619 DI 10.1200/JCO.2005.02.1451 PG 7 WC Oncology SC Oncology GA 989RA UT WOS:000233690200012 PM 16314623 ER PT J AU Burtness, B Goldwasser, MA Flood, W Mattar, B Forastiere, AA AF Burtness, B Goldwasser, MA Flood, W Mattar, B Forastiere, AA TI Phase III randomized trial of cisplatin plus placebo compared with cisplatin plus cetuximab in metastatic/recurrent head and neck cancer: An eastern cooperative oncology group study SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Article; Proceedings Paper CT 6th Annual Scientific Meeting of the Heart-Failure-Society-of-America CY SEP 23, 2002 CL BOCA RATON, FL SP Heart Failure Soc Amer ID GROWTH-FACTOR RECEPTOR; SQUAMOUS-CELL CARCINOMA; ANTIBODY CETUXIMAB; COLORECTAL-CANCER; RECURRENT; COMBINATION; EXPRESSION; SURVIVAL; C225; MULTICENTER AB Purpose Therapy of recurrent/metastatic squamous cell carcinoma of the head and neck results in median progression-free survival (PFS) of 2 months. These cancers are rich in epidermal growth factor receptor (EGFR). We wished to determine whether the addition of cetuximab, which inhibits activation of EGFR, would improve PFS. Patients and Methods Patients with recurrent/metastatic squamous cell carcinoma of the head and neck were randomly assigned to receive cisplatin every 4 weeks, with weekly: cetuximab (arm A) or placebo (arm 3). Tumor tissue was assayed for EGFR expression by immunohistochemistry. The primary end point was PFS. Secondary end points of interest were response rate, toxicity, overall survival, and correlation of EGFR with clinical end points. Results There were 117 analyzable patients enrolled. Median PFS was 2.7 months for arm B and 4.2 months for arm A. The hazard ratio for progression of arm A to arm B was 0.78 (95% CI, 0.54 to 1.12). Median overall survival was 8.0 months for arm B and 9.2 months for arm A (P = .21). The hazard ratio for survival by skin toxicity in cetuximab-treated patients was 0.42 (95% CI, 0.21 to 0.86). Objective response rate was 10% for arm A and 26% for arm B (P =.03). Enhancement of response was greater for patients with EGFR staining present in less than 80% of cells. Conclusion Addition of cetuximab to cisplatin significantly improves response rate. There was a survival advantage for the development of rash. Progression-free and overall survival were not significantly improved by the addition of cetuximab in this study. C1 Yale Univ, Sch Med, Dept Internal Med, New Haven, CT 06510 USA. Harvard Univ, Sch Publ Hlth, Dana Farber Canc Inst, Dept Biostat & Computat Biol, Boston, MA 02115 USA. Harvard Univ, Sch Publ Hlth, Dept Biostat, Boston, MA 02115 USA. Penn State Univ, Milton S Hershey Med Ctr, Div Hematol Oncol, Hershey, PA 17033 USA. Canc Ctr Kansas, Wichita, KS USA. Johns Hopkins Univ, Sidney Kimmel Canc Ctr, Baltimore, MD USA. RP Burtness, B (reprint author), Fox Chase Canc Ctr, 333 Cottman Ave, Philadelphia, PA 19111 USA. EM barbara.burtness@fccc.edu FU NCI NIH HHS [CA66636, CA07190, CA16116, CA21115, CA23318] NR 20 TC 510 Z9 532 U1 1 U2 12 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 DEC 1 PY 2005 VL 23 IS 34 BP 8646 EP 8654 DI 10.1200/JCO.2005.02A646 PG 9 WC Oncology SC Oncology GA 989RA UT WOS:000233690200016 PM 16314626 ER PT J AU Haller, DG Catalano, PJ Macdonald, JS O'Rourke, MA Frontiera, MS Jackson, DV Mayer, RJ AF Haller, DG Catalano, PJ Macdonald, JS O'Rourke, MA Frontiera, MS Jackson, DV Mayer, RJ TI Phase III study of fluorouracil, leucovorin, and levamisole in high-risk stage II and III colon cancer: Final report of Intergroup 0089 SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Article ID SURGICAL ADJUVANT THERAPY; COLORECTAL-CANCER; POOLED ANALYSIS; PLUS LEVAMISOLE; CLINICAL-TRIALS; RECTAL-CANCER; FOLINIC ACID; CHEMOTHERAPY; CARCINOMA; OUTCOMES AB Purpose In 1990, fluorouracil (FU) plus levamisole for 1 year became standard adjuvant treatment for patients with high-risk stages II and III colon cancer. Intergroup (INT) 0089 assessed the relative contributions of leucovorin and levamisole in such patients. Patients and Methods From 1988 to 1992, 3,794 patients were randomly assigned. Experimental treatment consisted of one of three chemotherapy regimens: the low-dose leucovorin plus FU (Mayo Clinic; LDLV) regimen, the high-dose leucovorin plus FU (Roswell Park; HDLV) regimen, and the low-dose leucovorin plus levamisole plus FU (LDLV plus LEV) regimen, each administered for 30 to 32 weeks. The control arm was levamisole plus FU (LEV) for 1 year. Results After a median follow-up of 10 years, of 3,561 eligible patients, 1,691 (47%) have died and 1,330 (37%) have experienced disease recurrence; 137 (10%) of those experiencing recurrence are still alive. A total of 481 patients (13%) died without evidence of recurrence, and 1,723 (48%) are alive and disease free. Although there were toxicity differences among the four arms, none was statistically superior in disease-free or overall survival. Conclusion The 6- to 8-month regimens of LDLV and HDLV without levamisole used in this trial, rather than the previous standard regimen of 12 months of LEV, have become widely used. INT-0089 has long-term follow-up of the largest clinical trial of patients with high-risk colon cancer, documenting not only the durability of the treatment effects, but also the natural history of patients with high-risk colon cancer, and analyses of treatment based on age, race, and comorbid conditions such as obesity, diabetes, and second primary cancers. C1 Univ Penn, Philadelphia, PA 19104 USA. Dana Farber Canc Inst, Dept Biostat, Boston, MA 02115 USA. St Vincents Hosp & Med Ctr, New York, NY 10011 USA. Canc Ctr Carolinas Eastside, Greenville, SC USA. Dean Med Ctr, Madison, WI USA. Ashville Hematol & Oncol, Asheville, NC USA. RP Haller, DG (reprint author), 16 Penn Tower,3400 Spruce St, Philadelphia, PA 19104 USA. EM daniel.haller@uphs.upenn.edu FU NCI NIH HHS [CA15488, CA21115, CA23318, CA32291, CA66636] NR 32 TC 185 Z9 191 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 DEC 1 PY 2005 VL 23 IS 34 BP 8671 EP 8678 DI 10.1200/JCO.2004.00.5686 PG 8 WC Oncology SC Oncology GA 989RA UT WOS:000233690200019 PM 16314627 ER PT J AU Bagatell, R Rumcheva, P London, WB Cohn, SL Look, AT Brodeur, GM Frantz, C Joshi, V Thorner, P Rao, PV Castleberry, R Bowman, LC AF Bagatell, R Rumcheva, P London, WB Cohn, SL Look, AT Brodeur, GM Frantz, C Joshi, V Thorner, P Rao, PV Castleberry, R Bowman, LC TI Outcomes of children with intermediate-risk neuroblastoma after treatment stratified by MYCN status and tumor cell ploidy SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Article ID PEDIATRIC-ONCOLOGY-GROUP; NEURO-BLASTOMA; N-MYC; METASTATIC NEUROBLASTOMA; INTENSIVE CHEMOTHERAPY; CYTOTOXIC THERAPY; NATURAL-HISTORY; STAGE; CANCER; INFANTS AB Purpose The goal of Pediatric Oncology Group 9243 was to improve outcomes for children with intermediate-risk neuroblastoma (NB). Patients and Methods Patients were assigned to treatments on the basis of age, tumor MYCN status, and tumor cell ploidy. Children in the less intensive arm A received cyclophosphamide/doxorubicin and. surgery. Patients not in complete remission postoperatively were treated with cisplatin/etoposide, cyclophosphamide/doxorubicin, and additional surgery. Patients with less favorable features were assigned to arm B, which consisted of carboplatin, etoposide, ifosfamide, and surgery. Survival rates were determined using an intent-to-treat approach. Results For arm-A patients, the 6-year event-free survival (EFS) was 86% with an SE of 3%. For arm-B patients, the 6-year EFS was 46% with an SE of 7%. MYCN status was the only statistically significant prognostic variable. Among patients whose tumors were MYCN nonamplified, a trend toward improved EFS was seen in children with hyperdiploid versus diploid tumors. However, many of these children responded well to salvage therapy, and overall survival rates did not differ on the basis of ploidy. Six-year EFS rates for arm B were patients with MYCN nonamplified, hyperdiploid tumors, 86% with an SE of 3%; patients with MYCN nonamplified, diploid tumors, 74% with an SE of 10%; patients with MYCN-amplified, hyperdiploid tumors, 46% with an SE of 15%; and patients with MYCN-amplified, diploid tumors, 22% with an SE of 10%. Conclusion Outcomes for patients with MYCN-nonamplified, hyperdiploid tumors were excellent. Therapy reductions for these patients merit study. A trend toward less favorable outcomes for patients with MYCN-nonamplified, diploid tumors was observed; more children may need. to be evaluated before therapy is reduced for this subgroup. For patients with MYCN-amplified tumors, new strategies are needed. C1 Univ Arizona, Dept Pediat, Tucson, AZ 85724 USA. Univ Arizona, Steele Childrens Res Ctr, Tucson, AZ 85724 USA. Univ Florida, Childrens Oncol Grp, Gainesville, FL 32611 USA. Northwestern Univ, Feinberg Sch Med, Chicago, IL 60611 USA. Harvard Univ, Sch Med, Dana Farber Canc Inst, Boston, MA 02115 USA. Univ Penn, Philadelphia, PA 19104 USA. Childrens Hosp Philadelphia, Philadelphia, PA 19104 USA. AI DuPont Hosp Children, Wilmington, DE USA. Hartford Hosp, Dept Pathol, Hartford, CT 06115 USA. Univ Toronto, Hosp Sick Children, Dept Lab Med, Toronto, ON M5G 1X8, Canada. Univ Alabama, Birmingham, AL 35233 USA. Emory Univ, Childrens Healthcare Atlanta, Atlanta, GA 30322 USA. RP Bagatell, R (reprint author), Univ Arizona, Arizona Hlth Sci Ctr, Dept Pediat Pediat Hematol Oncol, Room 5341,1501 N Campbell Ave, Tucson, AZ 85724 USA. EM bagatell@peds.afi7ona.edu OI Cohn, Susan/0000-0001-5749-7650 FU NCI NIH HHS [CA104605, CA39771, CA98543, U10 CA29139, U10 CA98413-01] NR 27 TC 42 Z9 44 U1 0 U2 2 PU AMER SOC CLINICAL ONCOLOGY PI ALEXANDRIA PA 330 JOHN CARLYLE ST, STE 300, ALEXANDRIA, VA 22314 USA SN 0732-183X J9 J CLIN ONCOL JI J. Clin. Oncol. PD DEC 1 PY 2005 VL 23 IS 34 BP 8819 EP 8827 DI 10.1200/JCO.2004.00.2931 PG 9 WC Oncology SC Oncology GA 989RA UT WOS:000233690200037 PM 16314642 ER PT J AU Manon, R O'Neill, A Knisely, J Werner-Wasik, M Lazarus, HM Wagner, H Gilbert, M Mehta, M AF Manon, R O'Neill, A Knisely, J Werner-Wasik, M Lazarus, HM Wagner, H Gilbert, M Mehta, M TI Phase II trial of radiosurgery for one to three newly diagnosed brain metastases from renal cell carcinoma, melanoma, and sarcoma: An eastern cooperative oncology group study (E 6397) SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Article; Proceedings Paper CT 40th Annual Meeting of the American-Society-of-Clinical-Oncology CY JUN 05-08, 2004 CL New Orleans, LA SP Amer Soc Clin Oncol ID RADIATION-THERAPY; STEREOTACTIC RADIOSURGERY; RANDOMIZED-TRIAL; MOTEXAFIN GADOLINIUM; RADIOTHERAPY; MANAGEMENT; SURVIVAL; DISEASE; CANCER AB Purpose Long-term brain metastases survivors are at risk for neurologic morbidity after whole-brain radiotherapy (WBRT). Retrospective radiosurgery (RS) reports found no survival difference when compared with WBRT. Before RS alone was evaluated with delayed WBRT in a phase III trial, the feasibility of RS alone was tested prospectively. Patients and Methods Patients with renal cell carcinoma, melanoma, or sarcoma; one to three brain metastases; and performance status of 0 to 2 were enrolled. Exclusion criteria were leptomeningeal disease; metastases in medulla, pons, or midbrain; or liver metastases. On the basis of tumor size, patients received 24, 18, or 15 Gy RS. At recurrence, management was discretionary. The primary end point was 3- and 6-month intracranial progression. Results Between July 1998 and August 2003, 36 patients were accrued; 31 were eligible. Median follow-up was 32.7 months and the median survival was 8.3 months (95% CI, 7.4 to 12.2). Three- and 6-month intracranial failure with RS alone was 25.8% and 48.3%. Failure within and outside the RS volume, when in-field and distant intracranial failures were scored independently, was 19.3% and 16.2% (3 months) and 32.2% and 32.2% (6 months), respectively. Approximately 38% of patients experienced death attributable to neurologic cause. There were three grade 3 toxicities related to RS. Conclusion Intracranial failure rates without WBRT were 25.8% and 48.3% at 3 and 6 months, respectively. Delaying WBRT may be appropriate for some subgroups of patients with radioresistant tumors, but routine avoidance of WBRT should be approached judiciously. C1 Univ Wisconsin, Madison, WI 53706 USA. Dana Farber Canc Inst, Boston, MA 02115 USA. Yale Univ, New Haven, CT 06520 USA. Thomas Jefferson Univ Hosp, Philadelphia, PA 19107 USA. Univ Hosp Cleveland, Cleveland, OH 44106 USA. Penn State Canc Inst, Hershey, PA USA. Univ Texas, MD Anderson Canc Ctr, Houston, TX 77030 USA. RP Mehta, M (reprint author), K4-B3,600 Highland Ave, Madison, WI 53792 USA. EM mehta@humonc.wisc.edu OI mehta, minesh/0000-0002-4812-5713 NR 29 TC 105 Z9 108 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 DEC 1 PY 2005 VL 23 IS 34 BP 8870 EP 8876 DI 10.1200/JCO.2005.01.8747 PG 7 WC Oncology SC Oncology GA 989RA UT WOS:000233690200043 PM 16314647 ER PT J AU Choudry, RB Cudkowicz, ME AF Choudry, RB Cudkowicz, ME TI Clinical trials in amyotrophic lateral sclerosis: The tenuous past and the promising future SO JOURNAL OF CLINICAL PHARMACOLOGY LA English DT Review DE amyotrophic lateral sclerosis; clinical trials; drug trials ID PLACEBO-CONTROLLED TRIAL; MOTOR-NEURON DISEASE; NEUROTROPHIC FACTOR PREVENTS; SUPEROXIDE-DISMUTASE; TRANSGENIC MODEL; GROWTH-FACTOR; ANIMAL-MODEL; DOUBLE-BLIND; SPINAL-CORD; MOUSE MODEL AB The post decade of research in amyotrophic lateral sclerosis has contributed to a greater understanding of the disease-process, the development of relevant animal models, and the identification of several therapeutic approaches that may delay disease progression. Completed and ongoing clinical trials and the process of selecting drugs for clinical trials are presented. C1 Massachusetts Gen Hosp, Neurol Clin Trials Unit, Dept Neurol, Boston, MA 02114 USA. RP Choudry, RB (reprint author), Massachusetts Gen Hosp, Neurol Clin Trials Unit, Dept Neurol, 55 Fruit St,GRB 1256, Boston, MA 02114 USA. EM rchoudry@partners.org NR 78 TC 10 Z9 14 U1 0 U2 2 PU SAGE PUBLICATIONS INC PI THOUSAND OAKS PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA SN 0091-2700 J9 J CLIN PHARMACOL JI J. Clin. Pharmacol. PD DEC PY 2005 VL 45 IS 12 BP 1334 EP 1344 DI 10.1177/0091270005282631 PG 11 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA 984KH UT WOS:000233303300001 PM 16291708 ER PT J AU Wohlreich, MM Martinez, JM Mallinckrodt, CH Prakash, A Watkin, JG Fava, M AF Wohlreich, MM Martinez, JM Mallinckrodt, CH Prakash, A Watkin, JG Fava, M TI An open-label study of duloxetine for the treatment of major depressive disorder - Comparison of switching versus initiating treatment approaches SO JOURNAL OF CLINICAL PSYCHOPHARMACOLOGY LA English DT Article ID TREATMENT-RESISTANT DEPRESSION; SEROTONIN REUPTAKE INHIBITORS; DOUBLE-BLIND; AUGMENTATION STRATEGIES; CLINICAL RELEVANCE; WORK PRODUCTIVITY; PARTIAL REMISSION; PRIMARY-CARE; VENLAFAXINE; TRIAL AB This study compared the stabilized duloxetine dose through approximately 12 weeks of treatment in patients initiating duloxetine therapy with that in patients switching to duloxetine from selective serotonin reuptake inhibitors or venlafaxine. All patients met Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition criteria for major depressive disorder. Patients (n = 112) exhibiting suboptimal response or poor tolerability to their current antidepressant medication (citalopram, escitalopram, fluvoxamine, paroxetine, sertraline, or venlafaxine) were switched to duloxetine 60 mg once daily (QD) without intermediate tapering or titration ("switching" group). A comparator group (n = 137), comprising patients not currently receiving antidepressant medication, was randomized to receive duloxetine 30 or 60 mg QD ("initiating" group). At the end of week 1, patients receiving 30 mg QD had their dose increased to 60 mg QD. During the remainder of the study, each patient's duloxetine dose could be titrated on the basis of degree of response within a range from 60 to 120 mg QD, with 90 mg QD as an intermediate dose. At the study end point, approximately one third of the patients in each treatment group were stabilized at each of the 3 studied duloxetine doses (60, 90, and 120 mg QD), and the distribution of stabilized doses among patients initiating duloxetine therapy did not differ significantly from that observed in patients switching to duloxetine. The efficacy of duloxetine in patients switching from selective serotonin reuptake inhibitor/ venlafaxine did not differ significantly from that observed in untreated patients initiating duloxetine therapy (baseline-to-end point mean changes: 17-Item Hamilton Rating Scale for Depression total score, -13.1 vs. -13.5; Hamilton Rating Scale for Anxiety, -10.6 vs. -10.3; and Clinical Global Impression of Severity, -2.22 vs. -2.38, respectively). The rate of discontinuation caused by adverse events among patients switched to duloxetine was significantly lower than that in patients initiating duloxetine therapy (6.3% vs. 16.1%, P = 0.018). Treatment-emergent adverse events occurring in more than 10% of patients in both treatment groups were nausea, headache, dry mouth, insomnia, diarrhea, and constipation. In the first week of therapy, patients switched to duloxetine reported significantly lower rates of headache and fatigue compared with patients initiating duloxetine. Thus, the efficacy of duloxetine in switched patients was comparable to that observed in patients initiating duloxetine therapy. Immediate switching from a selective serotonin reuptake inhibitor or venlafaxine to duloxetine (60 mg QD) was well tolerated. C1 Eli Lilly & Co, Lilly Corp Ctr, Lilly Res Labs, Indianapolis, IN 46285 USA. Baylor Coll Med, Dept Psychiat, Houston, TX 77030 USA. VISN 16 MIRECC, Dept Vet Affairs, Houston, TX USA. Massachusetts Gen Hosp, Dept Psychiat, Depress Clin & Res Program, Boston, MA 02114 USA. RP Wohlreich, MM (reprint author), Eli Lilly & Co, Lilly Corp Ctr, Lilly Res Labs, Indianapolis, IN 46285 USA. EM mwmd@lilly.com NR 34 TC 19 Z9 20 U1 4 U2 5 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3261 USA SN 0271-0749 J9 J CLIN PSYCHOPHARM JI J. Clin. Psychopharmacol. PD DEC PY 2005 VL 25 IS 6 BP 552 EP 560 DI 10.1097/01.jcp.0000185429.10053.c8 PG 9 WC Pharmacology & Pharmacy; Psychiatry SC Pharmacology & Pharmacy; Psychiatry GA 988VC UT WOS:000233628200008 PM 16282837 ER PT J AU Hermos, JA Young, MM Lawler, EV Stedman, MR Gagnon, DR Fiore, LD AF Hermos, JA Young, MM Lawler, EV Stedman, MR Gagnon, DR Fiore, LD TI Characterizations of long-term anxiolytic benzodiazepine - Prescriptions in veteran patients SO JOURNAL OF CLINICAL PSYCHOPHARMACOLOGY LA English DT Article ID POSTTRAUMATIC-STRESS-DISORDER; ANXIETY DISORDERS; SUBSTANCE-ABUSE; DRUGS AB To characterize long-term prescriptions for commonly prescribed anxiolytic benzodiazepines to veteran patients and to identify factors associated with high daily doses, we analyzed the linked pharmacy and administrative databases from New England Veterans Healthcare System (VISN 1), We analyzed treatment episodes of 3 months or longer with the 4 most commonly prescribed agents: alprazolam, clonazepam, diazepam, and lorazepam. Descriptive statistics and univariate and multivariate analyses described the sample and tested associations of pharmacological and clinical variables for patients prescribed the top 5% of average daily doses ("high-dose" prescriptions). From 16,630 full or partial treatment episodes for all 4 agents analyzed within a 42-month window, average daily doses were predominantly moderate, age-sensitive, and stable; refill lag intervals were short. Patients on "high-dose" prescriptions for the 4 agents combined, compared with "middle quartile" dose prescriptions, in adjusted analyses, were younger, more likely to have posttraumatic stress disorder (odds ratio [OR], 2.6-1 95% confidence interval [Cl], 2.17-3.13), substance abuse (OR, 1.50; 95% CI, 1.25-1.80), and anxiety (OR, 1.33; 95% Cl, 1.11-1.60) and were more likely to be receiving concurrent oxycodone/acetaminophen (OR, 2.05; 95% Cl, 1.642.56), anxiolytic benzodiazepine (OR, 1.51;(.)95% Cl, 1.12-2.03), antidepressant (OR, 2.15; 95% CI, 1.80-2.58), and neuroleptic (OR, 2.03; 95% Cl, 1.69-2.44) prescriptions. These results indicate that veteran patients prescribed anxiolytic benzodiazepines typically receive modest, nonincreasing doses over long-term treatment episodes. However, those on the highest average daily doses, typically more than recommended guidelines, are more likely to have clinical diagnoses and concurrent prescriptions for psychoaclive medications indicative of more complex and, perhaps, problematic management. C1 Massachusetts Vet Epidemiol Res & Informat Ctr, VA 151MAV, Boston Healthcare Syst, Pharmacoepidemiol Res Grp, Boston, MA 02130 USA. Boston Univ, Sch Publ Hlth, Boston, MA USA. RP Hermos, JA (reprint author), Massachusetts Vet Epidemiol Res & Informat Ctr, VA 151MAV, Boston Healthcare Syst, Pharmacoepidemiol Res Grp, 150 S Huntington Ave, Boston, MA 02130 USA. EM jhermos@bu.edu; melissa.young2@med.va.gov OI Gagnon, David/0000-0002-6367-3179; Stedman, Margaret/0000-0001-9271-8332 NR 23 TC 8 Z9 8 U1 0 U2 2 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3261 USA SN 0271-0749 J9 J CLIN PSYCHOPHARM JI J. Clin. Psychopharmacol. PD DEC PY 2005 VL 25 IS 6 BP 600 EP 604 DI 10.1097/01.jcp.0000185430.10053.1e PG 5 WC Pharmacology & Pharmacy; Psychiatry SC Pharmacology & Pharmacy; Psychiatry GA 988VC UT WOS:000233628200019 PM 16282847 ER PT J AU Johnson, SC Schmitz, TW Kawahara-Baccus, TN Rowley, HA Alexander, AL Lee, JH Davidson, RJ AF Johnson, SC Schmitz, TW Kawahara-Baccus, TN Rowley, HA Alexander, AL Lee, JH Davidson, RJ TI The cerebral response during subjective choice with and without self-reference SO JOURNAL OF COGNITIVE NEUROSCIENCE LA English DT Article ID POSTERIOR CINGULATE CORTEX; MEDIAL PREFRONTAL CORTEX; TRAUMATIC BRAIN-INJURY; EVENT-RELATED FMRI; ALZHEIMERS-DISEASE; FRONTAL LOBES; DEFAULT-MODE; PHYSIOLOGICAL CONDITION; IMPAIRED AWARENESS; NEURAL MECHANISMS AB The anterior medial prefrontal (AMPFC) and retrosplenial (RSC) cortices are active during self-referential decision-making tasks such as when participants appraise traits and abilities, or current affect. Other appraisal tasks requiring an evaluative decision or mental representation, such as theory of mind and perspective-taking tasks, also involve these regions. In many instances, these types of decisions involve a subjective opinion or preference, but also a degree of ambiguity in the decision, rather than a strictly, veridical response. However, this ambiguity is generally not controlled for in studies that examine self-referential decision-making. In this functional magnetic resonance imaging experiment with 17 healthy adults, we examined neural processes associated with subjective decision-making with and without an overt self-referential component. The task required subjective decisions about colors-regarding self-preference (internal subjective decision) or color similarity (external subjective decision) under conditions where there was no objectively correct response. Results indicated greater activation in the AMPFC, RSC, and caudate nucleus during internal subjective decision-making. The findings suggest that self-referential processing, rather than subjective judgments among ambiguous response alternatives, accounted for the AMPFC and RSC response. C1 William S Middleton Mem Vet Adm Med Ctr, Madison, WI 53705 USA. Univ Wisconsin, Madison, WI USA. RP Johnson, SC (reprint author), William S Middleton Mem Vet Adm Med Ctr, 2500 Overlook Terrace, Madison, WI 53705 USA. EM scj@medicine.wisc.edu FU NIMH NIH HHS [MH65723, R01 MH065723, R01 MH065723-03, R01 MH065723-04] NR 66 TC 61 Z9 63 U1 4 U2 8 PU M I T PRESS PI CAMBRIDGE PA 238 MAIN STREET, STE 500, CAMBRIDGE, MA 02142-1046 USA SN 0898-929X J9 J COGNITIVE NEUROSCI JI J. Cogn. Neurosci. PD DEC PY 2005 VL 17 IS 12 BP 1897 EP 1906 DI 10.1162/089892905775008607 PG 10 WC Neurosciences; Psychology, Experimental SC Neurosciences & Neurology; Psychology GA 993WW UT WOS:000233988600007 PM 16356327 ER PT J AU Adams, BM Banks, HT Davidian, M Kwon, HD Tran, HT Wynne, SN Rosenberg, ES AF Adams, BM Banks, HT Davidian, M Kwon, HD Tran, HT Wynne, SN Rosenberg, ES TI HIV dynamics: Modeling, data analysis, and optimal treatment protocols SO JOURNAL OF COMPUTATIONAL AND APPLIED MATHEMATICS LA English DT Article DE HIV models; parameter estimation; data and model reduction; structured treatment interruptions; optimal control ID ACTIVE ANTIRETROVIRAL THERAPY; CYTOTOXIC T-LYMPHOCYTES; VIRAL SUPPRESSION; IN-VIVO; HIV-1-INFECTED PATIENTS; TREATMENT INTERRUPTION; 1-INFECTED PATIENTS; COHERENT STRUCTURES; TYPE-1 REPLICATION; CELL RESPONSES AB We present an overview of some concepts and methodologies we believe useful in modeling HIV pathogenesis. After a brief discussion of motivation for and previous efforts in the development of mathematical models for progression of HIV infection and treatment, we discuss mathematical and statistical ideas relevant to Structured Treatment Interruptions (STI). Among these are model development and validation procedures including parameter estimation, data reduction and representation, and optimal control relative to STI. Results from initial attempts in each of these areas by an interdisciplinary team of applied mathematicians, statisticians and clinicians are presented. (c) 2005 Elsevier B.V. All rights reserved. C1 Harvard Univ, Sch Med, Massachusetts Gen Hosp, Boston, MA 02114 USA. Inha Univ, Dept Math, Inchon, South Korea. RP Banks, HT (reprint author), N Carolina State Univ, Ctr Res Sci Comp, Box 8205, Raleigh, NC 27695 USA. EM bmadams3@unity.ncsu.edu; htbanks@unity.ncsu.edu; davidian@unity.ncsu.edu; tran@math.ncsu.edu; snwynne@unity.ncsu.edu; erosenberg1@partners.org NR 70 TC 87 Z9 91 U1 0 U2 9 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0377-0427 EI 1879-1778 J9 J COMPUT APPL MATH JI J. Comput. Appl. Math. PD DEC 1 PY 2005 VL 184 IS 1 BP 10 EP 49 DI 10.1016/j.cam.2005.02.004 PG 40 WC Mathematics, Applied SC Mathematics GA 959UH UT WOS:000231544300003 ER PT J AU Collier, A Yohnson, KR Delamere, F Leonard, T Dellavalle, RP Williams, H AF Collier, Avanta Yohnson, Kathryn R. Delamere, Finola Leonard, Tina Dellavalle, Robert P. Williams, Hywel TI The cochrane skin group: Promoting the best evidence SO JOURNAL OF CUTANEOUS MEDICINE AND SURGERY LA English DT Article ID SYSTEMATIC REVIEWS; DERMATOLOGY AB Background. The international Cochrane Skin group, established in 1997, organizes, writes and disseminates systematic reviews of therapeutic interventions in dermatology. Objective To introduce the Cochrane Skin Group and what it offers to cutaneous medicine and surgery providers. Methods. Descriptive review of the structure and output of the Cochrane Collaboration Library and the Cochrane Skin Group. Results: Systematic reviews of randomized controlled trials produced through the Cochrane Skin Group provide a benchmark for evidence summaries for informing clinical decisions in dermatology. Conclusion: The work performed by the Cochrane Skin Group is an important component for informing the evidence base for the clinical practice of cutaneous and surgical dermatology. C1 Univ Colorado, Hlth Sci Ctr, Dept Dermatol, Denver, CO 80262 USA. Denver VA Med Ctr, Denver, CO USA. Univ Nottingham, Queens Med Ctr, Nottingham NG7 2RD, England. RP Dellavalle, RP (reprint author), Univ Colorado, Hlth Sci Ctr, Dept Dermatol, Denver, CO 80262 USA. EM roberr.dellavalle@uchsc.edu RI Dellavalle, Robert/L-2020-2013 OI Dellavalle, Robert/0000-0001-8132-088X FU NCI NIH HHS [CA92550]; NIAMS NIH HHS [T32 AR07411] NR 18 TC 6 Z9 6 U1 0 U2 0 PU SPRINGER PI NEW YORK PA 233 SPRING STREET, NEW YORK, NY 10013 USA SN 1203-4754 J9 J CUTAN MED SURG JI J. Cutan. Med. Surg. PD DEC PY 2005 VL 9 IS 6 BP 324 EP 331 DI 10.1007/s10227-005-0120-5 PG 8 WC Dermatology SC Dermatology GA 069OR UT WOS:000239458600008 PM 16699901 ER PT J AU Lin, JJ Hanten, WP Olson, SL Roddey, TS Soto-quijano, DA Lim, HK Sherwood, AM AF Lin, JJ Hanten, WP Olson, SL Roddey, TS Soto-quijano, DA Lim, HK Sherwood, AM TI Functional activity characteristics of individuals with shoulder dysfunctions SO JOURNAL OF ELECTROMYOGRAPHY AND KINESIOLOGY LA English DT Article DE electromyography; kinematics; shoulder; reliability; motion analysis ID SPINAL-CORD INJURY; IMPINGEMENT SYNDROME; UPPER EXTREMITY; MUSCLE-ACTIVITY; RELIABILITY; KINEMATICS; MOVEMENT; PAIN; ORIENTATION; MOTION AB Shoulder-related dysfunction affects individuals' ability to function independently and thus decreases quality of life. Functional task assessment is a key concern for a clinician in diagnostic assessment, outcome measurement, and planning of treatment programs. The purpose of this study was to test the reliability of the FASTRAK 3-dimensional (3-D) motion analysis and surface electromyography (sEMG) systems to analyze 3-D shoulder complex movements during functional tasks and compare motion patterns between subjects with and without shoulder dysfunctions (SDs). For the test, sEMG and 3-D motion analysis systems were used to characterize the functional tasks. Twenty-five asymptomatic male subjects and 21 male subjects with right shoulder disorders performed four functional tasks which involved arm reaching and raising activities with their dominant arms. Reliability was estimated by the intraclass correlation coefficient (ICC). Motion pattern was compared between two groups using mixed analysis of variances (ANOVAs). Shoulder complex kinematics and associated muscular activities during functional tasks were reliably quantified (ICC = 0.83-0.99) from the means of three trials. Relative to the group without SDs, the group with SDs showed significant alteration in shoulder complex kinematics (3 degrees-40 degrees) and associated muscular activities (3-10% maximum). Scapular tipping, scapular elevation, upper trapezius muscle function, and serratus anterior muscle function may have implications in the rehabilitation of patients with SDs. (c) 2005 Elsevier Ltd. All rights reserved. C1 Natl Taiwan Univ, Coll Med, Sch Phys Therapy, Taipei, Taiwan. Natl Taiwan Univ, Coll Med, Grad Inst Phys Therapy, Taipei, Taiwan. Texas Womans Univ, Sch Phys Therapy, Denton, TX 76204 USA. Baylor Coll Med, Dept Phys Med & Rehabil, Houston, TX 77030 USA. Michael E DeBakey Vet Affairs Med Ctr, Houston, TX USA. RP Lin, JJ (reprint author), Natl Taiwan Univ, Coll Med, Sch Phys Therapy, Taipei, Taiwan. EM lxjst@ha.mc.ntu.edu.tw RI lin, jiu jenq/H-4604-2014; OI lin, jiu jenq/0000-0001-9070-7939; Sherwood, Arthur/0000-0002-0110-4317 NR 44 TC 83 Z9 89 U1 0 U2 11 PU ELSEVIER SCI LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND SN 1050-6411 J9 J ELECTROMYOGR KINES JI J. Electromyogr. Kinesiol. PD DEC PY 2005 VL 15 IS 6 BP 576 EP 586 DI 10.1016/j.jelekin.2005.01.006 PG 11 WC Neurosciences; Physiology; Rehabilitation; Sport Sciences SC Neurosciences & Neurology; Physiology; Rehabilitation; Sport Sciences GA 982HU UT WOS:000233149500006 PM 16179197 ER PT J AU Potts, JT AF Potts, JT TI Parathyroid hormone: past and present SO JOURNAL OF ENDOCRINOLOGY LA English DT Review ID AMINO-ACID-SEQUENCE; CHICKEN PREPROPARATHYROID HORMONE; NUCLEOTIDE-SEQUENCE; POSTMENOPAUSAL WOMEN; BONE MASS; RECEPTOR; OSTEOPOROSIS; PEPTIDE; BOVINE; CALCIUM AB Research oil parathyroid hormone (PTH) has undergone four rather distinctive phases, beginning just before the turn of the 20th Century. Early debates about the function of the parathyroids were resolved by 1925, when understanding the role of PTH led to comprehending the action of the glands in calcium physiology. Elucidation of the pathophysiology of hormone excess (severe bone loss) and deficiency (hypocalcemia) continued over the following decades. With the advent of advances in chemical and molecular biology, the structure of PTH and its principal receptor (PTHrP-receptor [PTHR1]) were established. Tests with purified hormonal peptide in human led to the surprising, even paradoxical, finding that PTH call be used pharmacologically to build bone, providing a dramatic therapeutic impact oil osteoporosis. These developments have stimulated the field of calcium and bone biology and posed new questions about the role of PTH as well as possible new directions in therapy. C1 Massachusetts Gen Hosp, Dept Med, Endocrine Unit, Boston, MA 02114 USA. Harvard Univ, Sch Med, Boston, MA 02114 USA. RP Potts, JT (reprint author), Massachusetts Gen Hosp, Dept Med, Endocrine Unit, 149 13th St,Room 4013, Boston, MA 02114 USA. EM potts.john@mgh.harvard.edu NR 71 TC 133 Z9 145 U1 0 U2 8 PU SOC ENDOCRINOLOGY PI BRISTOL PA 22 APEX COURT, WOODLANDS, BRADLEY STOKE, BRISTOL BS32 4JT, ENGLAND SN 0022-0795 J9 J ENDOCRINOL JI J. Endocrinol. PD DEC PY 2005 VL 187 IS 3 BP 311 EP 325 DI 10.1677/joe.1.06057 PG 15 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA 996XV UT WOS:000234210200001 PM 16423810 ER PT J AU Pirani, C Chersoni, S Foschi, F Piana, G Loushine, RJ Tay, FR Prati, C AF Pirani, C Chersoni, S Foschi, F Piana, G Loushine, RJ Tay, FR Prati, C TI Does hybridization of intraradicular dentin really improve fiber post retention in endodontically treated teeth? SO JOURNAL OF ENDODONTICS LA English DT Article DE hybrid layer; resin tag; adhesion; fiber posts; SEM ID ROOT-CANAL DENTIN; POLYMERIZATION CONTRACTION STRESS; RESIN COMPOSITE LAYERS; BOND STRENGTHS; MICROLEAKAGE; CEMENTS; CURE; MICROTENSILE; ADHESIVES; SURFACE AB This study tested the hypothesis that hybridization of intraradicular dentin eliminates interfacial gaps, thereby improving the coronal seal and retention of teeth restored with fiber posts. Post spaces were bonded with two types of fiber posts, usingthe corresponding etch-and-rinse adhesives and dual-cured resin cements. Longitudinal sections of the interfaces were examined for dentin hybridization in the coronal- and middle thirds of the root canals. Resin replicas of these sections were evaluated for interfacial gap formation. Although intraradicualr dentin hybridization was not compromised irrespective of whether the adhesives were light-cured before cementation, the universal occurence of interfacial gaps along the hybrid layer surface or the post-cement interface reflects the challenge in bonding to postspaces with low compliance and high C-factors. The clinical success associated with bonded fiber posts is probably due to predominantly to frictional retention. C1 Univ Bologna, Alma Mater Studiorum, Dept Dent Sci, Endodont Unit, Bologna, Italy. Forsyth Inst, Dept Cytokine Biol, Boston, MA USA. Med Coll Georgia, Sch Dent, Dept Endodont, Augusta, GA 30912 USA. Univ Hong Kong, Fac Dent, Hong Kong, Hong Kong, Peoples R China. RP Tay, FR (reprint author), Univ Hong Kong, Prince Philip Dent Hosp, 34 Hosp Rd, Hong Kong, Hong Kong, Peoples R China. EM kfctay@netvigator.com RI Foschi, Federico /E-7531-2012; OI Prati, Carlo/0000-0001-8163-8628 NR 35 TC 64 Z9 70 U1 0 U2 2 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3261 USA SN 0099-2399 J9 J ENDODONT JI J. Endod. PD DEC PY 2005 VL 31 IS 12 BP 891 EP 894 DI 10.1097/01.don.0000164853.92310.e7 PG 4 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA 991RE UT WOS:000233830500011 PM 16306825 ER PT J AU Hsieh, MH Goodman, HM AF Hsieh, MH Goodman, HM TI A novel gene family in Arabidopsis encoding putative heptahelical transmembrane proteins homologous to human adiponectin receptors and progestin receptors SO JOURNAL OF EXPERIMENTAL BOTANY LA English DT Article DE Arabidopsis thaliana; G protein-coupled receptors; plant hormones; seven-transmembrane proteins; signal transduction ID FATTY-ACID OXIDATION; COUPLED RECEPTOR; INSULIN-RESISTANCE; BACILLUS-CEREUS; MLO FAMILY; CLONING; GCR1; METABOLISM; THALIANA; GLUCOSE AB A novel seven-transmembrane receptor family, that is comprised of human adiponectin receptors (AdipoRs) and membrane progestin receptors (mPRs) that share little sequence homology with all known G protein-coupled receptors (GPCRs), has been identified recently. Although a fish mPR has been suggested to be a GPCR, human AdipoRs seem to be structurally and functionally distinct from all known GPCRs. The identification of a novel gene family, the (h) under bar epta (h) under bar elical (p) under bar rotein (HHP) gene family, encoding proteins in Arabidopsis predicted to have a heptahelical transmembrane topology is reported here. There are at least five HHP genes in Arabidopsis whose encoded amino acid sequences have significant similarities to human AdipoRs and mPRs.The expression and regulation of the Arabidopsis HHP gene family has been studied here. The expression of the HHP gene family is differentially regulated by plant hormones. Steady-state levels of HHP1 mRNA are increased by treatments with abscisic acid and gibberellic acid, whereas levels of HHP2 mRNA are increased by abscisic acid and benzyladenine treatments. In addition, the expression of the HHP gene family is up-regulated by the presence of sucrose in the medium. Temperature and salt stress treatments also differentially affect the expression of the HHP genes. These novel seven-transmembrane proteins previously described in yeast and animals, and now identified in plants, may represent a new class of receptors that are highly conserved across kingdoms. C1 Acad Sinica, Inst Plant & Microbial Biol, Taipei 11529, Taiwan. Harvard Univ, Sch Med, Dept Genet, Boston, MA 02114 USA. Massachusetts Gen Hosp, Dept Mol Biol, Boston, MA 02114 USA. RP Hsieh, MH (reprint author), Acad Sinica, Inst Plant & Microbial Biol, Taipei 11529, Taiwan. EM ming@gate.sinica.edu.tw NR 52 TC 18 Z9 25 U1 0 U2 3 PU OXFORD UNIV PRESS PI OXFORD PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND SN 0022-0957 J9 J EXP BOT JI J. Exp. Bot. PD DEC PY 2005 VL 56 IS 422 BP 3137 EP 3147 DI 10.1093/jxb/eri311 PG 11 WC Plant Sciences SC Plant Sciences GA 987AR UT WOS:000233491300013 PM 16263907 ER PT J AU Rosow, DE Sahani, D Strobel, O Kalva, S Mino-Kenudson, M Holalkere, NS Alsfasser, G Saini, S Lee, SI Mueller, PR Fernandez-del Castillo, C Warshaw, AL Thayer, SP AF Rosow, DE Sahani, D Strobel, O Kalva, S Mino-Kenudson, M Holalkere, NS Alsfasser, G Saini, S Lee, SI Mueller, PR Fernandez-del Castillo, C Warshaw, AL Thayer, SP TI Imaging of acute mesenteric ischemia using multidetector CT and CT angiography in a porcine model SO JOURNAL OF GASTROINTESTINAL SURGERY LA English DT Article; Proceedings Paper CT 46th Annual Meeting of the Society-for-Surgery-of-the-Alimentary-Tract CY MAY 14-18, 2005 CL Chicago, IL SP Soc Surg Alimentary Tract DE mesenteric ischemia; computed tomography; angiography; animal model ID MAXIMUM INTENSITY PROJECTION; BOWEL ISCHEMIA; ACUTE ABDOMEN; DIAGNOSIS; ARTERY AB Acute mesenteric ischemia, a frequently lethal disease, requires prompt diagnosis and intervention for favorable clinical outcomes. This goal remains elusive due, in part, to lack of a noninvasive and accurate imaging study. Traditional angiography is the diagnostic gold standard but is invasive and costly. Computed tomography (CT) is readily available and noninvasive but has shown variable success in diagnosing this disease. The faster scanning time of multidetector row CT (M.D.CT) greatly facilitates the use of CT angiography (CTA) in the clinical setting. We sought to determine whether M.D.CT-CTA could accurately demonstrate vascular anatomy and capture the earliest stages of mesenteric ischemia in a porcine model. Pigs underwent embolization of branches of the superior mesenteric artery, then imaging by M.D.CT-CTA with three-dimensional reconstruction protocols. After scanning, diseased bowel segments were surgically resected and pathologically examined. Multidetector row CT and CT angiography reliably defined normal and occluded mesenteric vessels in the pig. It detected early changes of ischemia including poor arterial enhancement and venous dilatation, which were seen in all ischemic animals. The radiographic findings- compared with pathologic diagnoses- predicted ischemia, with a positive predictive value of 92%. These results indicate that M.D.CT-CTA holds great promise for the early detection necessary for successful treatment of acute mesenteric ischemia. C1 Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Surg, Boston, MA 02114 USA. Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Radiol, Boston, MA 02114 USA. Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Pathol, Boston, MA 02114 USA. RP Thayer, SP (reprint author), Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Surg, 15 Parkman St,WACC 464, Boston, MA 02114 USA. EM thayer@partners.org OI Holalkere, Nagaraj/0000-0001-6324-7682 FU NIDDK NIH HHS [K08 DK071329] NR 23 TC 13 Z9 17 U1 0 U2 2 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 2005 VL 9 IS 9 BP 1262 EP 1274 DI 10.1016/j.gassur.2005.07.034 PG 13 WC Gastroenterology & Hepatology; Surgery SC Gastroenterology & Hepatology; Surgery GA 998RF UT WOS:000234336100017 PM 16332482 ER PT J AU Meneghetti, AT Safadi, B Stewart, L Way, LW AF Meneghetti, AT Safadi, B Stewart, L Way, LW TI Local resection of ampullary tumors SO JOURNAL OF GASTROINTESTINAL SURGERY LA English DT Article; Proceedings Paper CT 46th Annual Meeting of the Society-for-Surgery-of-the-Alimentary-Tract CY MAY 14-18, 2005 CL Chicago, IL SP Soc Surg Alimentary Tract DE ampullary tumors; duodenal adenoma; periampullarv adenoma; ampullary adenoma; ampullary carcinoma; transduodenal resection; local resection ID ENDOSCOPIC SNARE EXCISION; MAJOR DUODENAL PAPILLA; VILLOUS TUMORS; PROGNOSTIC-FACTORS; FOLLOW-UP; VATER; ADENOMAS; CARCINOMA; MANAGEMENT; NEOPLASMS AB There is no consensus on the appropriateness of local resection for ampullary tumors, because malignant recurrence of what were thought to be benign tumors has been reported. This study examined the role of local resection in the management of ampullary tumors. Thirty patients (mean age 66 years) had transduodenal local resections performed at UCSF-Moffitt Hospital or the San Francisco VA Medical Center (February, 1992 to March, 2004). Mean follow-up time was 5.8 years. Preoperative biopsies (obtained in all patients) showed 18 adenomas, four adenomas with dysplasia, five adenomas with atypia, one adenoma with dysplasia and focal adenocarcinoma, and two tumors seen on endoscopy, whose biopsies showed only duodenal mucosa. In comparison with the final pathology findings, the results of frozen section examin- ations for malignancy in 20 patients, during the operation, were false-negative in three cases. The final pathologic diagnosis was 23 villous adenomas, six adenocarcinomas, and one paraganglioma. On preoperative biopsies, all patients who had high-grade dysplasia and one of five patients with atypia turned out to have invasive adenocarcinoma when the entire specimen was examined postoperatively. Two (33%) adenocarcinomas recurred at a mean of 4 years-, both had negative margins at the initial resection. Among the 23 adenomas, three (13%) recurred (all as adenomas) at a mean of 3.2 years; in only one of these cases was the margin positive at the time of resection. Tumor size did not influence recurrence rate. Ampullary tumors with high-grade dysplasia on preoperative biopsy should be treated by pancreaticoduodenectomy because they usually harbor malignancy. Recurrence is too common and unpredictable after local resection of malignant lesions for this to be considered an acceptable alternative to pancreaticoduodenectomy. Ampullary adenomas can be resected locally with good results, but the recurrence rate was 13 %, so endoscopic surveillance is indicated postoperatively. Frozen sections were obtained during the operation, but they were less reliable than expected. No adenomas recurred as carcinomas, suggesting that local resection is appropriate for these tumors in the absence of dysplasia or atypia on preoperative biopsies. C1 Univ Calif San Francisco, VAMC, San Francisco, CA 94121 USA. Univ Calif San Francisco, Dept Surg, San Francisco, CA 94143 USA. San Francisco VA Med Ctr, San Francisco, CA 94143 USA. RP Stewart, L (reprint author), Univ Calif San Francisco, VAMC, Box 112, San Francisco, CA 94121 USA. EM lygia.stewart@med.va.gov NR 26 TC 23 Z9 26 U1 0 U2 1 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 1091-255X J9 J GASTROINTEST SURG JI J. Gastrointest. Surg. PD DEC PY 2005 VL 9 IS 9 BP 1300 EP 1306 DI 10.1016/j.gassur.2005.08.031 PG 7 WC Gastroenterology & Hepatology; Surgery SC Gastroenterology & Hepatology; Surgery GA 998RF UT WOS:000234336100023 PM 16332486 ER PT J AU DeSalvo, KB Gregg, J Kleinpeter, M Pedersen, BR Stepter, A Peabody, J AF DeSalvo, KB Gregg, J Kleinpeter, M Pedersen, BR Stepter, A Peabody, J TI Cardiac risk underestimation in urban, black women SO JOURNAL OF GENERAL INTERNAL MEDICINE LA English DT Article; Proceedings Paper CT Regional Meeting of the Southern-Society-of-General-Internal-Medicine CY FEB 13, 2004 CL New Orleans, LA SP SO Soc Gen Internal Med DE women; cardiac risk factors; perceived risk; minority; stress ID CARDIOVASCULAR-DISEASE RISK; CORONARY HEART-DISEASE; PSYCHOSOCIAL STRESS; AFRICAN-AMERICANS; MENTAL STRESS; HEALTH; HYPERTENSION; DISPARITIES; ACCURACY; REVASCULARIZATION AB BACKGROUND: Black women have a disproportionately higher incidence of cardiovascular disease mortality than other groups and the reason for this health disparity is incompletely understood. Underestimation of personal cardiac risk may play a role. OBJECTIVE: We investigated the personal characteristics associated with underestimating cardiovascular disease in black women. DESIGN, SETTING, PARTICIPANTS: Trained surveyors interviewed 128 black women during the baseline evaluation for a randomized controlled trial in an urban, academic continuity clinic affiliated with a public hospital system. They provided information on the presence of cardiac risk factors and demographic and psychosocial characteristics. These self-report data were supplemented with medical record abstraction for weight. MEASUREMENTS AND MAIN RESULTS: The main outcome measure was the accurate perception of cardiac risk. Objective risk was determined by a simple count of major cardiac risk factors and perceived risk by respondent's answer to a survey question about personal cardiac risk. The burden of cardiac risk factors was high in this population: 77% were obese; 72% had hypertension; 48% had high cholesterol; 49% had a family history of heart disease; 31% had diabetes, and 22% currently used tobacco. Seventy-nine percent had 3 or more cardiac risk factors. Among those with 3 or more risk factors ("high risk"), 63% did not perceive themselves to be at risk for heart disease. Among all patients, objective and perceived cardiac risk was poorly correlated (kappa =0. 026). In a multivariable model, increased perceived personal stress and lower income were significant correlates of underestimating cardiac risk. CONCLUSIONS: Urban, disadvantaged black women in this study had many cardiac risk factors, yet routinely underestimated their risk of heart disease. We found that the strongest correlates of underestimation were perceived stress and lower personal income. C1 Tulane Univ, Hlth Sci Ctr, Sect Gen Internal Med & Geriatr, Dept Med, New Orleans, LA 70112 USA. Tulane Univ, Hlth Sci Ctr, Nephrol Sect, Dept Med, New Orleans, LA 70112 USA. Univ Calif San Francisco, Inst Global Hlth, San Francisco, CA 94143 USA. Univ Calif San Francisco, San Francisco Vet Affairs Med Ctr, San Francisco, CA 94143 USA. Amgen Inc, Thousand Oaks, CA USA. RP DeSalvo, KB (reprint author), Tulane Univ, Hlth Sci Ctr, Sect Gen Internal Med & Geriatr, Dept Med, 1430 Tulane Ave,SL-16, New Orleans, LA 70112 USA. EM kdesalv@tulane.edu NR 39 TC 23 Z9 23 U1 1 U2 4 PU BLACKWELL PUBLISHING PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DQ, OXON, ENGLAND SN 0884-8734 J9 J GEN INTERN MED JI J. Gen. Intern. Med. PD DEC PY 2005 VL 20 IS 12 BP 1127 EP 1131 DI 10.1111/j.1525-1497.2005.0252.x PG 5 WC Health Care Sciences & Services; Medicine, General & Internal SC Health Care Sciences & Services; General & Internal Medicine GA 997OG UT WOS:000234254700009 PM 16423102 ER PT J AU Crothers, K Griffith, TA McGinnis, KA Rodriguez-Barradas, MC Leaf, DA Weissman, S Gibert, CL Butt, AA Justice, AC AF Crothers, K Griffith, TA McGinnis, KA Rodriguez-Barradas, MC Leaf, DA Weissman, S Gibert, CL Butt, AA Justice, AC TI The impact of cigarette smoking on mortality, quality of life, and comorbid illness among HIV-positive veterans SO JOURNAL OF GENERAL INTERNAL MEDICINE LA English DT Article DE HIV; AIDS; smoking; mortality; health-related quality of life ID HUMAN-IMMUNODEFICIENCY-VIRUS; AGING COHORT 3-SITE; BACTERIAL PNEUMONIA; HEALTH SURVEY; INFECTION; INDIVIDUALS; ASSOCIATION; AIDS AB BACKGROUND: The impact of smoking on outcomes among those with HIV infection has not been determined in the era of highly active; retroviral therapy (HAART). STUDY OBJECTIVE: Determine the impact of smoking on morbidity and mortality in HFV-positive patients post-HAART. DESIGN: Prospective observational study. PARTICIPANTS: Eight hundred and sixty-seven HIV-positive veterans enrolled in the Veterans Aging Cohort 3 Site Study. MEASUREMENTS: Clinical data were collected through patient questionnaire, International Classification of Diseases-9th edition codes, and standardized chart extraction, and laboratory and mortality data through the national VA database. Quality of life was assessed with the physical component summary (PCS) of the Short-Form 12. RESULTS: Current smokers had increased respiratory symptoms, chronic obstructive pulmonary disease (COPD), and bacterial pneumonia. In analyses adjusted for age, race/ethnicity, CD4 cell count, HIV RNA level, hemoglobin, illegal drug and alcohol use, quality of life was substantially decreased (beta = -3.3, 95% confidence interval [CI] -5.3 to -1.4) and mortality was significantly increased (hazard ratio 1.99, 95% CI 1.03 to 3.86) in current smokers compared with never smokers. CONCLUSIONS: HIV-positive patients who currently smoke have increased mortality and decreased quality of life, as well as increased respiratory symptoms, COPD, and bacterial pneumonia. These findings suggest that smoking cessation should be emphasized for HIV-infected patients. C1 VA Connecticut Healthcare Syst, Dept Internal Med, West Haven, CT 06516 USA. Yale Univ, Sch Med, Dept Internal Med, New Haven, CT USA. Univ Pittsburgh, Ctr Social & Urban Res, Pittsburgh, PA USA. VA Pittsburgh Healthcare Syst, Ctr Hlth Equit Res & Promot, Pittsburgh, PA USA. Baylor Coll Med, Dept Med, Houston, TX 77030 USA. Michael E DeBakey VA Med Ctr, Houston, TX USA. Univ Calif Los Angeles, Dept Internal Med, Los Angeles, CA USA. Greater Los Angeles VA Med Ctr, Los Angeles, CA USA. Hosp St Raphael, Dept Internal Med, New Haven, CT USA. George Washington Univ, Dept Med, Washington, DC 20052 USA. VA Med Ctr, Infect Dis Sect, Washington, DC USA. Univ Pittsburgh, Sch Med, Dept Internal Med, Pittsburgh, PA USA. RP Justice, AC (reprint author), VA Connecticut Healthcare Syst, Dept Internal Med, 950 Campbell Ave,Mailstop 11 ASCLG, West Haven, CT 06516 USA. EM amy.justice2@med.va.gov OI Crothers, Kristina/0000-0001-9702-0371 FU NIA NIH HHS [K23 AG00826]; NIAAA NIH HHS [3U01 AA 13566, U01 AA013566] NR 19 TC 134 Z9 137 U1 2 U2 9 PU BLACKWELL PUBLISHING PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DQ, OXON, ENGLAND SN 0884-8734 J9 J GEN INTERN MED JI J. Gen. Intern. Med. PD DEC PY 2005 VL 20 IS 12 BP 1142 EP 1145 DI 10.1111/j.1525-1497.2005.0255.x PG 4 WC Health Care Sciences & Services; Medicine, General & Internal SC Health Care Sciences & Services; General & Internal Medicine GA 997OG UT WOS:000234254700013 PM 16423106 ER PT J AU Tierney, WM Gerrity, MS AF Tierney, WM Gerrity, MS TI The best of JGIM SO JOURNAL OF GENERAL INTERNAL MEDICINE LA English DT Editorial Material C1 Indiana Univ, Sch Med, Indianapolis, IN 46204 USA. Regenstrief Inst Inc, Indianapolis, IN USA. Oregon Hlth Sci Univ, Portland, OR 97201 USA. Portland VA Med Ctr, Portland, OR USA. RP Tierney, WM (reprint author), Indiana Univ, Sch Med, Indianapolis, IN 46204 USA. NR 6 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL PUBLISHING PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DQ, OXON, ENGLAND SN 0884-8734 J9 J GEN INTERN MED JI J. Gen. Intern. Med. PD DEC PY 2005 VL 20 IS 12 BP 1191 EP 1195 DI 10.1111/j.1525-1497.2005.00275.x PG 5 WC Health Care Sciences & Services; Medicine, General & Internal SC Health Care Sciences & Services; General & Internal Medicine GA 997OG UT WOS:000234254700022 ER PT J AU Jarvik, LF La Rue, A Gokhman, I Harrison, T Holt, L Steh, B Harker, J Larson, S Yaralian, P Matsuyama, S Rasgon, N Geschwind, D Freimer, N Jimenez, E Schaeffer, J AF Jarvik, LF La Rue, A Gokhman, I Harrison, T Holt, L Steh, B Harker, J Larson, S Yaralian, P Matsuyama, S Rasgon, N Geschwind, D Freimer, N Jimenez, E Schaeffer, J TI Middle-aged children of Alzheimer parents, a pilot study: Stable neurocognitive performance at 20-year follow-up SO JOURNAL OF GERIATRIC PSYCHIATRY AND NEUROLOGY LA English DT Article; Proceedings Paper CT Workshop on Children of Alzheimer Parent CY MAR 06-07, 2005 CL San Diego, CA SP Natl Inst Hlth DE Alzheimer's disease; offspring; longitudinal; neurocognitive ID 1ST-DEGREE RELATIVES; LATE-LIFE; DISEASE; RISK; DIAGNOSIS AB The objective of this pilot study on a convenience sample of 25 offspring of Alzheimer patients (mean age 61.5 +/- 8.8 years; range, 50-82) was the early detection of neurocognitive decline. This preliminary report appears to be the first one dealing with 20-year follow-up of neurocognitive data of Alzheimer's disease (AD) children. Digit symbol (Wechsler Adult Intelligence Scale) was the only of 11 neurocognitive measures with a significant decline. And that decline between first and last testing (mean = 19.98 +/- 0.30 years) was on raw scores, not scaled scores. Neither parents' age at onset of AD nor autopsy confirmation or offspring APOE-e4 status influenced neurocognitive results. More robust data than currently available are needed to confirm the findings of this first pilot study and to determine both the trajectory of neurocognitive decline in AD and the risks of developing AD faced by children whose parent had the disease. C1 Univ Calif Los Angeles, Neuropsychiat Inst & Hosp, Los Angeles, CA 90095 USA. Univ Calif Los Angeles, Dept Psychiat & Biobehav Sci, Los Angeles, CA 90095 USA. VA Greater Los Angeles Healthcare Syst, Los Angeles, CA USA. Univ Wisconsin, Wisconsin Alzheimers Inst, Dept Med, Madison, WI USA. Charles R Drew Univ, Dept Psychiat & Human Behav, Los Angeles, CA USA. Stanford Univ, Sch Med, Dept Psychiat & Behav Sci, Palo Alto, CA 94304 USA. Univ Calif Los Angeles, Dept Psychiat & Behav Sci, Los Angeles, CA 90024 USA. Univ Calif Los Angeles, Dept Neurol, Los Angeles, CA 90024 USA. Univ Calif Los Angeles, Dept Psychiat, Los Angeles, CA USA. Univ Calif Los Angeles, Dept Biobehav Sci & Human Genet, Los Angeles, CA USA. RP Jarvik, LF (reprint author), Univ Calif Los Angeles, Neuropsychiat Inst & Hosp, 760 Westwood Pl, Los Angeles, CA 90095 USA. EM ljarvik@ucla.edu NR 34 TC 8 Z9 8 U1 0 U2 0 PU SAGE PUBLICATIONS INC PI THOUSAND OAKS PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA SN 0891-9887 J9 J GERIATR PSYCH NEUR JI J. Geriatr. Psychiatry Neurol. PD DEC PY 2005 VL 18 IS 4 BP 187 EP 191 DI 10.1177/0891988705281862 PG 5 WC Geriatrics & Gerontology; Clinical Neurology; Psychiatry SC Geriatrics & Gerontology; Neurosciences & Neurology; Psychiatry GA 986EO UT WOS:000233433100002 PM 16306237 ER PT J AU Ercoli, L Siddarth, P Harrison, T Jimenez, E Jarvik, LF AF Ercoli, L Siddarth, P Harrison, T Jimenez, E Jarvik, LF TI Similar neurocognitive performance of adults with and without a history of parental Alzheimer's disease: A pilot study SO JOURNAL OF GERIATRIC PSYCHIATRY AND NEUROLOGY LA English DT Article; Proceedings Paper CT Workshop on Children of Alzheimer Parent CY MAR 06-07, 2005 CL San Diego, CA SP Natl Inst Hlth DE Alzheimer's disease; neurocognitive; Mini-Mental State Examination (MMSE); offspring; parent; family history ID MINI-MENTAL-STATE; IMMEDIATE VISUAL MEMORY; COGNITIVE DECLINE; GENETIC RISK; DEPRESSION; NORMS; AGE; IMPAIRMENT; RELATIVES AB The first reported 20-year prospective follow-up of middle-aged children of Alzheimer patients failed to find statistically significant neurocognitive decline. Because that report did not include a comparison group, the current study compared the 20-year follow-up scores with scores obtained on the same 8 measures by an age-comparable sample of healthy adults without a family history of Alzheimer's disease. Both were convenience samples (n = 24). Statistical analyses (correcting for age) yielded no significant group differences in neurocognitive scores but did show a significantly higher mean score for the comparison group on the Mini-Mental State Examination (29.5 vs 28.8, P = .003, controlling for age). Even though this finding suggests that adult children of a parent with Alzheimer's disease performed well on a limited neurocognitive battery and on the Mini-Mental State Examination, the findings are preliminary and require confirmation on large representative samples with appropriate controls and long-term follow-up. C1 Univ Calif Los Angeles, Dept Psychiat & Biobehav Sci, Los Angeles, CA USA. Univ Calif Los Angeles, Neuropsychiat Inst & Hosp, Los Angeles, CA USA. VA Greater Los Angeles Healthcare Syst, Los Angeles, CA USA. RP Ercoli, L (reprint author), Semel Inst Neurosci & Human Behav, 760 Westwood Pl,Suite 88-201, Los Angeles, CA 90024 USA. EM lercoli@mednet.ucla.edu FU CSR NIH HHS [RG2-96-051]; NCRR NIH HHS [M01RR00865]; NIA NIH HHS [AG13308, AG11268, AG100784, AG10123, AG05128, AG16570]; NIMH NIH HHS [MH52453]; NINDS NIH HHS [NS31153, NS26630] NR 30 TC 5 Z9 5 U1 3 U2 3 PU SAGE PUBLICATIONS INC PI THOUSAND OAKS PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA SN 0891-9887 J9 J GERIATR PSYCH NEUR JI J. Geriatr. Psychiatry Neurol. PD DEC PY 2005 VL 18 IS 4 BP 208 EP 212 DI 10.1177/0891988705281866 PG 5 WC Geriatrics & Gerontology; Clinical Neurology; Psychiatry SC Geriatrics & Gerontology; Neurosciences & Neurology; Psychiatry GA 986EO UT WOS:000233433100006 PM 16306241 ER PT J AU Tallaj, JA Franco, V Rayburn, BK Pinderski, L Benza, RL Pamboukian, S Foley, B Bourge, RC AF Tallaj, JA Franco, V Rayburn, BK Pinderski, L Benza, RL Pamboukian, S Foley, B Bourge, RC TI Response of doxorubicin-induced cardiomyopathy to the current management strategy of heart failure SO JOURNAL OF HEART AND LUNG TRANSPLANTATION LA English DT Article ID LEFT-VENTRICULAR DYSFUNCTION; CARDIOTOXICITY; MORTALITY; TRANSPLANTATION; CARVEDILOL; METOPROLOL; ENALAPRIL; MORBIDITY; BLOCKADE AB Background: Doxorubicin (D) (Adriamycin) is a potent and efficacious chemotherapeutic agent in the treatment of various forms of cancer, but its use has been limited by the development of cardiac toxicity. Historically, D-induced cardiomyopathy (CMP) has been refractory to therapy. We report our experience with this form of CMP at the University of Alabama at Birmingham. Methods: Twenty-five patients (20 women, 5 men) with a clinical diagnosis of D-CMP were referred to our program from 1990 to 2003. Patient data were extracted from office charts. Results: Patients were followed-up for 71 +/- 58 months. On presentation, the average left ventricular ejection fraction (LVEF) was 26 +/- 9.2%, and 88% of patients were New York Heart Association (NYHA) Class III or W. Patients were treated with angiotensin-converting enzyme inhibitors (ACEi; n = 23) or angiotensin-receptor blocker (ARB; n = 2), and 15 were treated with a combination of ACEi and beta-blockers (BB). With medical therapy, LVEF improved significantly (26 +/- 9.2% vs 35 +/- 16.5%, p = 0.022), as did the NYHA class (p < 0.003). All survivors (n = 19) were NYHA Class I or 11 with medical therapy, with 10 (53%) being Class I. In the group of patients treated with ACEi + BB, there was a statistically significant improvement in LVEF (26 +/- 10.0% vs 37 +/- 17.6%, p = 0.028), which not seen in the ACEi group, with a strong trend toward normalization of LV function (47% vs 10%, p = 0.054). Conclusions: In the current era of management of heart failure, D-CMP carries a better prognosis than previously described. Early addition of BB may further improve LVEF. C1 Univ Alabama, Div Cardiovasc Dis, Dept Med, Birmingham, AL 35294 USA. Univ Alabama, Birmingham VA Med Ctr, Dept Med, Birmingham, AL 35294 USA. RP Tallaj, JA (reprint author), Univ Alabama, Div Cardiovasc Dis, Dept Med, THT 338,1900 Univ Blvd, Birmingham, AL 35294 USA. EM jtallaj@uab.edu RI Franco, Veronica/E-3080-2011 NR 21 TC 51 Z9 53 U1 0 U2 4 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 1053-2498 J9 J HEART LUNG TRANSPL JI J. Heart Lung Transplant. PD DEC PY 2005 VL 24 IS 12 BP 2196 EP 2201 DI 10.1016/j.healun.2004.12.108 PG 6 WC Cardiac & Cardiovascular Systems; Respiratory System; Surgery; Transplantation SC Cardiovascular System & Cardiology; Respiratory System; Surgery; Transplantation GA 998HH UT WOS:000234308700030 PM 16364871 ER PT J AU Xiang, ZM Nesterov, EE Skoch, J Lin, T Hyman, BT Swager, TM Bacskai, BJ Reeves, SA AF Xiang, ZM Nesterov, EE Skoch, J Lin, T Hyman, BT Swager, TM Bacskai, BJ Reeves, SA TI Detection of myelination using a novel histological probe SO JOURNAL OF HISTOCHEMISTRY & CYTOCHEMISTRY LA English DT Article DE myelin; near-infrared; dye; fluorescence ID SQUARYLIUM DYES; TISSUE; STAIN AB Current methods for myelin staining in tissue sections include both histological and immunohistochemical techniques. Fluorescence immunohistochemistry, which uses antibodies against myelin components such as myelin basic protein, is often used because of the convenience for multiple labeling. To facilitate studies on myelin, this paper describes a quick and easy method for direct myelin staining in rodent and human tissues using novel near-infrared myelin (NIM) dyes that are comparable to other well-characterized histochemical reagents. The near-infrared fluorescence spectra of these probes allow fluorescent staining of tissue sections in multiple channels using visible light fluorophores commonly used in immunocytochemistry. These dyes have been used successfully to detect normal myelin structure and myelin loss in a mouse model of demyelination disease. C1 Harvard Univ, Sch Med, Massachusetts Gen Hosp, MIND, Charlestown, MA USA. MIT, Dept Chem, Cambridge, MA 02139 USA. MIT, Inst Soldier Nanotechnol, Cambridge, MA 02139 USA. RP Bacskai, BJ (reprint author), MIND, Bldg 114,16th St, Charlestown, MA 02129 USA. EM bbacskai@partners.org RI Swager, Timothy/H-7459-2012 OI Swager, Timothy/0000-0002-3577-0510 FU NIA NIH HHS [AG-08487, R01 AG008487]; NIBIB NIH HHS [EB-00768, R01 EB000768]; NINDS NIH HHS [NS-35996, R01 NS035996] NR 13 TC 38 Z9 38 U1 3 U2 7 PU HISTOCHEMICAL SOC INC PI SEATTLE PA UNIV WASHINGTON, DEPT BIOSTRUCTURE, BOX 357420, SEATTLE, WA 98195 USA SN 0022-1554 J9 J HISTOCHEM CYTOCHEM JI J. Histochem. Cytochem. PD DEC PY 2005 VL 53 IS 12 BP 1511 EP 1516 DI 10.1369/jhc.5A6704.2005 PG 6 WC Cell Biology SC Cell Biology GA 989DI UT WOS:000233652700009 PM 16046669 ER PT J AU von Boehmer, H AF von Boehmer, H TI Shaping the T cell repertoire SO JOURNAL OF IMMUNOLOGY LA English DT Editorial Material ID LY ANTIGENS; LYMPHOCYTES; THYMUS C1 Harvard Univ, Sch Med, Dana Farber Canc Inst, Boston, MA 02115 USA. RP von Boehmer, H (reprint author), Harvard Univ, Sch Med, Dana Farber Canc Inst, 44 Binney St, Boston, MA 02115 USA. EM harald_von_boehmer@dfci.harvard.edu NR 6 TC 3 Z9 3 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 2005 VL 175 IS 11 BP 7067 EP 7068 PG 2 WC Immunology SC Immunology GA 987UZ UT WOS:000233544200001 PM 16301607 ER PT J AU Keir, ME Latchman, YE Freeman, GJ Sharpe, AH AF Keir, ME Latchman, YE Freeman, GJ Sharpe, AH TI Programmed death-1 (PD-1): PD-ligand 1 interactions inhibit TCR-mediated positive selection of thymocytes SO JOURNAL OF IMMUNOLOGY LA English DT Article ID T-CELL-ACTIVATION; NEGATIVE SELECTION; TRANSGENIC MICE; B7 FAMILY; EXPRESSION; RECEPTOR; PROTEIN; MEMBER; DEATH; IMMUNORECEPTOR AB Positive selection during thymocyte development-is driven by the affinity and avidity of the TCR for MHC-peptide complexes expressed in the thymus. In this study, we show that programmed death-1 (PD-1), a member of the B7/CD28 family of costimulatory receptors, inhibits TCR-mediated positive selection through PD-1 ligand 1 (PD-L1):PD-1 interactions. Transgenic mice that constitutively overexpress PD-1 on CD4(+)CD8(+) thymocytes display defects in positive selection in vivo. Using an in vitro model system, we find that PD-1 is up-regulated following TCR engagement on CD4(+)CD8(+) murine thymocytes. Coligation of TCR and PD-1 on CD4(+)CD8(+) thymocytes with a novel PD-1 agonistic mAb inhibits the activation of ERK and up-regulation of bcl-2, both of which are downstream mediators essential for positive selection. Inhibitory signals through PD-1 can overcome the ability of positive costimulators, such as CD2 and CD28, to facilitate positive selection. Finally, defects in positive selection that result from PD-1 overexpression in thymocytes resolve upon elimination of PD-L1, but not PD-1 ligand 2, expression. PD-L1-deficient mice have increased numbers of CD4(+)CD8(+) and CD4(+) thymocytes, indicating that PD-L1 is involved in normal thymic selection. These data demonstrate that PD-1:PD-L1 interactions are critical to positive selection and play a role in shaping the T cell repertoire. C1 Harvard Univ, Brigham & Womens Hosp, Sch Med, Dept Pathol, Boston, MA 02115 USA. Harvard Univ, Dana Farber Canc Inst, Sch Med, Dept Med Oncol,Dept Med, Boston, MA 02115 USA. RP Sharpe, AH (reprint author), Harvard Univ, Brigham & Womens Hosp, Sch Med, Dept Pathol, 77 Ave Louis Pasteur,NRB-837, Boston, MA 02115 USA. EM asharpe@rics.bwh.harvard.edu FU NCI NIH HHS [CA84500, R01 CA084500]; NIAID NIH HHS [P01 AI039671, AI056299, AI39671, AI40614, P01 AI056299, P01 AI056299-03, R01 AI040614, R01 AI040614-09, R37 AI038310] NR 35 TC 64 Z9 66 U1 1 U2 7 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 2005 VL 175 IS 11 BP 7372 EP 7379 PG 8 WC Immunology SC Immunology GA 987UZ UT WOS:000233544200038 PM 16301644 ER PT J AU Rhatigan, DL Street, AE AF Rhatigan, DL Street, AE TI The impact of intimate partner violence on decisions to leave dating relationships - A test of the investment model SO JOURNAL OF INTERPERSONAL VIOLENCE LA English DT Article DE dating violence; relationship termination; stay-leave decisions ID ABUSIVE RELATIONSHIP; WOMEN; STAY; SATISFACTION; COMMITMENT; CONFLICT; SCALES AB This study explored the impact of violence exposure on investment-model constructs within a sample of college women involved in heterosexual dating relationships. Results generally supported the "common sense" hypothesis, suggesting that violence negatively impacts satisfaction for and commitment to one's relationship and is positively associated with intentions to leave. Exposure to psychological abuse uniquely impacted intentions to leave relationships above and beyond other model factors, suggesting that this may be a particularly important factor in determining college women's decisions. In a series of analyses examining the investment model within each of two groups (e.g., those exposed or not exposed to physical violence), results showed that the model predicted victimized women's decisions to leave as well as it predicted nonvictimized women's decisions. Taken together, results of this study suggest that victimized women base their relationship termination decisions on the same information as nonvictimized women do. C1 Univ Houston Downtown, Houston, TX USA. VA Boston Healthcare Syst, Natl Ctr Postraumat Stress Disorder, Boston, MA USA. Boston Univ, Sch Med, Boston, MA 02118 USA. RP Rhatigan, DL (reprint author), Univ Houston Downtown, Houston, TX USA. NR 30 TC 30 Z9 31 U1 1 U2 10 PU SAGE PUBLICATIONS INC PI THOUSAND OAKS PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA SN 0886-2605 J9 J INTERPERS VIOLENCE JI J. Interpers. Violence PD DEC PY 2005 VL 20 IS 12 BP 1580 EP 1597 DI 10.1177/0886260505280344 PG 18 WC Criminology & Penology; Family Studies; Psychology, Applied SC Criminology & Penology; Family Studies; Psychology GA 981JW UT WOS:000233085900004 PM 16246918 ER PT J AU Tsao, H AF Tsao, H TI The SNPs of RAF SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Editorial Material ID MALIGNANT-MELANOMA; GENE POLYMORPHISM; EGF GENE; BRAF; SUSCEPTIBILITY; MUTATIONS; RISK C1 Massachusetts Gen Hosp, Dept Dermatol, Boston, MA 02114 USA. RP Tsao, H (reprint author), Massachusetts Gen Hosp, Dept Dermatol, Boston, MA 02114 USA. NR 11 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL PUBLISHING PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DQ, OXON, ENGLAND SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD DEC PY 2005 VL 125 IS 6 BP XIV EP XV DI 10.1111/j.0022-202X.2005.23967.x PG 2 WC Dermatology SC Dermatology GA 991OS UT WOS:000233823900004 PM 16354174 ER PT J AU Chamlin, SL Cella, D Frieden, IJ Williams, ML Mancini, AJ Lai, JS Chren, MM AF Chamlin, SL Cella, D Frieden, IJ Williams, ML Mancini, AJ Lai, JS Chren, MM TI Development of the childhood atopic dermatitis impact scale: Initial validation of a quality-of-life measure for young children with atopic dermatitis and their families SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Article DE atopic dermatitis; quality of life; sleep disorder; validity ID ECZEMA; INDEX AB To measure the effects of atopic dermatitis (AD) on the quality of life of affected young children and their families, we developed a prototype 62-item instrument, the Childhood Atopic Dermatitis Impact Scale (CADIS). The prototype CADIS was developed from a comprehensive conceptual framework based on data from parents and clinicians. The instrument had eight subscales (four each for child and parent): physical health, emotional health, physical functioning, and social functioning. The goal of this work was to test the validity of and to refine the prototype of CADIS. Two hundred seventy parents of children under the age of 6 y with AD responded to the instrument. Content validity was demonstrated by expert and parent reviews of the drafted and refined instrument, and by analyzing parents' responses to open-ended questions about their children's skin disease. Construct validity was assessed in exploratory factor analyses which supported a refinement in the conceptual framework to consist of two dimensions with five domains: child dimensions (symptoms and activity limitation/behavior), and parent dimensions (family/social function, sleep, and emotions). Seventeen items were eliminated, yielding a 45-item refined version of CADIS (score 0-180) with evidence of content and construct validity and suggested use in clinical research. C1 Childrens Mem Hosp, Div Pediat Dermatol, Chicago, IL 60614 USA. Evanston NW Healthcare, Ctr Outcomes Res & Educ, Chicago, IL USA. NW Feinberg Sch Med, Chicago, IL USA. Univ Calif San Francisco, Dept Dermatol & Pediat, San Francisco, CA 94143 USA. Univ Calif San Francisco, Dept Pediat, San Francisco, CA 94143 USA. San Francisco Vet Affairs Med Ctr, Serv Dermatol, San Francisco, CA USA. RP Chamlin, SL (reprint author), Childrens Mem Hosp, Div Pediat Dermatol, Chicago, IL 60614 USA. EM schamlin@childrensmemorial.org OI Frieden, Ilona/0000-0001-7305-5940 FU NIAMS NIH HHS [K02 AR 02203-01] NR 16 TC 47 Z9 49 U1 0 U2 5 PU BLACKWELL PUBLISHING PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DQ, OXON, ENGLAND SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD DEC PY 2005 VL 125 IS 6 BP 1106 EP 1111 DI 10.1111/j.0022-202X.2005.23911.x PG 6 WC Dermatology SC Dermatology GA 991OS UT WOS:000233823900009 PM 16354179 ER PT J AU Yang, GA Rajadurai, A Tsao, H AF Yang, GA Rajadurai, A Tsao, H TI Recurrent patterns of dual RB and p53 pathway inactivation in melanoma SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Article DE CDK4; CDKN2A; genetics; melanoma; p53 ID SPORADIC PRIMARY MELANOMAS; CELL LINES; IN-VIVO; MUTATIONS; GENE; CDKN2A; LOCUS; P16(INK4A); P14(ARF); P19(ARF) AB Two growth inhibitory hurdles that must be overcome by the evolving cancer cell include pathways regulated by RB and p53. In human melanoma cells, inactivation of a single locus, CDKN2A, can lead to abrogation of both RB and p53 functionality through loss of the two CDKN2A cognate transcripts-p16 and p14ARF, respectively. We thus set out to assess how recurrent patterns of genetic injury at three critical human melanoma loci-CDKN2A, TP53, and CDK4-cooperate to disrupt both RB and p53 pathways. Overall, 77.8% of the melanoma cell lines analyzed showed genetic evidence of dual RB and p53 pathway compromise; this percentage is even higher if protein expression loss is considered. Although homozygous deletion of all three critical CDKN2-A exons (exons 1 beta, 1 alpha, and 2) represent the most common mechanism, concurrent loss of CDKN2A(Exon1 alpha) and CDKN2A(Exon1 beta) and simultaneous point mutagenesis of CDK4 and TP53 reflect alternative cassettes of dual inactivation. In cell lines with isolated CDKN2A(Exon2) mutations, coincident alterations in TP53 or deletion of CDKN2A(Exon1 beta) suggest that p16 transcript may be preferentially targeted over the p14ARF transcript as additional p53 pathway lesions are recruited. Moreover, predictive modeling of CDKN2A(Exon2) MiSSense mutations further suggests that the amino acid substitutions in this region negatively impact p16 to a greater extent than p14ARF. Taken together, our data point to a clear need in human melanoma cell lines, as in its murine counterpart, to disrupt both RB and p53 pathways and recurrent mechanisms may play into the unique genetic vulnerabilities of this tumor type. C1 Massachusetts Gen Hosp, Wellman Ctr Photomed, Boston, MA 02114 USA. Massachusetts Gen Hosp, Dept Dermatol, Boston, MA 02114 USA. RP Tsao, H (reprint author), Massachusetts Gen Hosp, Wellman Ctr Photomed, Boston, MA 02114 USA. EM htsao@partners.org FU NCI NIH HHS [K08 CA095532] NR 30 TC 32 Z9 32 U1 0 U2 4 PU BLACKWELL PUBLISHING PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DQ, OXON, ENGLAND SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD DEC PY 2005 VL 125 IS 6 BP 1242 EP 1251 DI 10.1111/j.0022-202X.2005.23931.x PG 10 WC Dermatology SC Dermatology GA 991OS UT WOS:000233823900025 PM 16354195 ER PT J AU Turisco, F Keogh, D Stubbs, C Glaser, J Crowley, WF AF Turisco, F Keogh, D Stubbs, C Glaser, J Crowley, WF TI Current status of integrating information technologies into the clinical research enterprise within US academic health centers: Strategic value and opportunities for investment SO JOURNAL OF INVESTIGATIVE MEDICINE LA English DT Article DE clinical research; information technology; human research; academic health centers; medical research AB Little information exists about the incorporation of information technologies (ITs) into clinical research processes within US academic health centers (AHCs). Therefore, we queried a group of 37 leading AHCs regarding their current status and future plans in clinical research IT. The survey specifically inquired about the presence or absence of basic infrastructure and IT support requirements; individual applications needed to support study preparation, study conduct, and its administrative support; and integration of data from basic research, clinical trials, and the clinical information systems increasingly used in health care delivery. Of the 37 AHCs, 78% responded. All strongly agreed that a "state-of-the-art" clinical research IT program would be ideal today and will be essential tomorrow. Nonetheless, no AHC currently has an IT solution that even approached this ideal. No AHC reported having all of the essential management foundations (ie, a coherent vision, an overall strategy, a governance structure, and a dedicated budget) necessary to launch and sustain a truly successful implementation of a cohesive clinical research IT platform. Many had achieved breakthroughs in individual aspects of clinical research IT, for example, adverse event reporting systems or consent form templates. However, overall implementation of IT to support clinical research is uneven and insufficient. These data document a substantial gap in clinical research IT investments in leading US AHCs. Linking the clinical research IT enterprise with its clinical operations in a meaningful fashion remains a crucial strategic goal of AHCs. If they are to continue to serve as the "translational research engines" that our society expects, AHCs must recognize this gap and allocate substantial resource deployment to remedying this situation. C1 Emerging Practice 1st Consulting Grp, Boston, MA USA. Partners Healthcare Inc, Corp Informat Technol Serv Dept, Boston, MA USA. Massachusetts Gen Hosp, Clin Res Program, Dept Med, Boston, MA 02114 USA. RP Crowley, WF (reprint author), Massachusetts Gen Hosp, Director Clin Res, Bartlett Hall Extens Bldg,Room 511,55 Fruit St, Boston, MA 02114 USA. NR 2 TC 14 Z9 14 U1 0 U2 2 PU B C DECKER INC PI HAMILTON PA 20 HUGHSON ST SOUTH, PO BOX 620, L C D 1, HAMILTON, ONTARIO L8N 3K7, CANADA SN 1081-5589 J9 J INVEST MED JI J. Invest. Med. PD DEC PY 2005 VL 53 IS 8 BP 425 EP 433 DI 10.2310/6650.2005.53806 PG 9 WC Medicine, General & Internal; Medicine, Research & Experimental SC General & Internal Medicine; Research & Experimental Medicine GA 999TL UT WOS:000234413300014 PM 16354581 ER PT J AU Kieran, MW AF Kieran, MW TI Anti-angiogenic therapy in pediatric neuro-oncology SO JOURNAL OF NEURO-ONCOLOGY LA English DT Article DE angiogenesis; anti-angiogenesis; biologic therapy; brain tumor; pediatric; VEGF ID ENDOTHELIAL GROWTH-FACTOR; MALIGNANT BRAIN-TUMORS; CENTRAL-NERVOUS-SYSTEM; LOW-GRADE ASTROCYTOMAS; PHASE-II TRIAL; ANTIANGIOGENIC THERAPY; GLIOBLASTOMA-MULTIFORME; METRONOMIC CHEMOTHERAPY; MICROVESSEL DENSITY; FACTOR EXPRESSION AB In order to grow, tissues require additional nutrients and oxygen as well as removal of waste products. Tumors achieve this by up-regulating angiogenic cytokines and/or down-regulating natural inhibitory proteins that allow neovascularization to proceed. Brain tumors continue to account for significant morbidity and mortality, in spite of significant advances in neurosurgical and radiation techniques and new chemotherapy combinations. As such, there is a real and immediate need for novel biologic therapies that can target these tumors. A number of new drugs that target different aspects of the angiogenic cascade have been identified and are now in clinical trials in children with primary brain tumors. In many of these pre-clinical and clinical studies, anti-angiogenic therapy has been well tolerated, has lacked many of the traditional toxicities of radiation and chemotherapy, does not require blood-brain barrier penetration, and targets a critical pathway in central nervous system tumor development. This review will discuss what angiogenesis is, how pediatric brain tumors regulate angiogenesis to obtain a vascular supply, what types of inhibitors are available, how different classes of inhibitors work, the types of resistance possible, how rapidly these inhibitors may work, and what surrogate markers of activity are available to follow response. C1 Dana Farber Canc Inst, Boston, MA 02115 USA. Harvard Univ, Sch Med, Boston, MA 02115 USA. Childrens Hosp, Boston, MA 02115 USA. RP Kieran, MW (reprint author), Dana Farber Canc Inst, 44 Binney St,Rm SW331, Boston, MA 02115 USA. EM mark_kier-an@dfci.harvard.edu OI Kieran, Mark/0000-0003-2184-7692 NR 97 TC 11 Z9 11 U1 0 U2 0 PU SPRINGER PI NEW YORK PA 233 SPRING STREET, NEW YORK, NY 10013 USA SN 0167-594X J9 J NEURO-ONCOL JI J. Neuro-Oncol. PD DEC PY 2005 VL 75 IS 3 BP 327 EP 334 DI 10.1007/s11060-005-6764-6 PG 8 WC Oncology; Clinical Neurology SC Oncology; Neurosciences & Neurology GA 988VX UT WOS:000233630500012 PM 16195797 ER PT J AU Mazarati, AM Baldwin, RA Shinmei, S Sankar, R AF Mazarati, AM Baldwin, RA Shinmei, S Sankar, R TI In vivo interaction between serotonin and galanin receptors types 1 and 2 in the dorsal raphe: implication for limbic seizures SO JOURNAL OF NEUROCHEMISTRY LA English DT Article DE dorsal raphe; galanin receptor; hippocampus; seizures; serotonin ID STATUS EPILEPTICUS; HIPPOCAMPAL GALANIN; 5-HT1A RECEPTORS; RAT HIPPOCAMPUS; MESSENGER-RNA; GALR1; EXPRESSION; SUBTYPES; BRAIN; MICE AB The neuropeptide galanin suppresses seizure activity in the hippocampus by inhibiting glutamatergic neurotransmission. Galanin may also modulate limbic seizures through interaction with other neurotransmitters in neuronal populations that project to the hippocampus. We examined the role of galanin receptors types 1 and 2 in the dorsal raphe (DR) in the regulation of serotonergic transmission and limbic seizures. Infusion of a mixed agonist of galanin receptors types 1 and 2 [galanin (1 - 29)] into the DR augmented the severity of limbic seizures in both rats and wild- type mice and concurrently reduced serotonin concentration in the DR and hippocampus as measured by immunofluorescence or HPLC. In contrast, injection of the galanin receptor type 2 agonist galanin (2 - 11) mitigated the severity of seizures in both species and increased serotonin concentration in both areas. Injection of both galanin fragments into the DR of galanin receptor type 1 knockout mice exerted anticonvulsant effects. Both the proconvulsant activity of galanin (1 - 29) and seizure suppression by galanin (2 - 11) were abolished in serotonin- depleted animals. Our data indicate that, in the DR, galanin receptors types 1 and 2 modulate serotonergic transmission in a negative and a positive fashion, respectively, and that these effects translate into either facilitation or inhibition of limbic seizures. C1 Univ Calif Los Angeles, Dept Pediat, Div Pediat Neurol, D Geffen Sch Med, Los Angeles, CA 90095 USA. W Los Angeles VA Med Ctr, Los Angeles, CA USA. RP Mazarati, AM (reprint author), Univ Calif Los Angeles, Dept Pediat, Div Pediat Neurol, D Geffen Sch Med, Box 951752,22-474 MDCC, Los Angeles, CA 90095 USA. EM mazarati@ucla.edu FU NINDS NIH HHS [NS043409, NS046516, R01 NS043409, R01 NS046516] NR 44 TC 40 Z9 41 U1 0 U2 0 PU BLACKWELL PUBLISHING PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DQ, OXON, ENGLAND SN 0022-3042 J9 J NEUROCHEM JI J. Neurochem. PD DEC PY 2005 VL 95 IS 5 BP 1495 EP 1503 DI 10.1111/j.1471-4159.2005.03498.x PG 9 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA 982NZ UT WOS:000233170200025 PM 16219029 ER PT J AU Ickenstein, GW Stein, J Ambrosi, D Goldstein, R Horn, M Bogdahn, U AF Ickenstein, GW Stein, J Ambrosi, D Goldstein, R Horn, M Bogdahn, U TI Predictors of survival after severe dysphagic stroke SO JOURNAL OF NEUROLOGY LA English DT Article DE stroke; dysphagia; neurorehabilitation; stroke outcome; feeding tubes ID ASPIRATION; COMPLICATIONS; GASTROSTOMY; RISK AB Background and Purpose Dysphagia is estimated to occur in up to 50% of the stroke neurorehabilitation population. Those patients with severe neurogenic oropharyngeal dysphagia (NOD) may receive feeding gastrostomy tubes (FGT) if non-invasive therapies prove ineffective in eliminating aspiration or sustaining adequate nutritional intake. Our aim was to quantify the recovery of swallowing function, and to identify variables predictive of survival after dysphagic stroke requiring FGT placement. Methods We identified consecutive stroke patients with severe dysphagic stroke requiring FGT placement admitted to a rehabilitation hospital between May 1998 and October 2001. The medical records were reviewed, and demographic, clinical, videofluoroscopic (VSS) and neuroimaging information were abstracted. A follow-up telephone interview was performed to determine whether the FGT was still in use, had been removed, or if the patient had died. State death certificate records were reviewed to ascertain date of death for subjects who had expired by the time of follow-up. Univariate and multivariate analyses were performed. Results 11.6% (77/664) of stroke patients admitted during the study period had severe dysphagic stroke with FGT insertion. Follow-up was available for 66 (85.7%) of these individuals at a mean of two years after acute stroke. On follow-up 64% (42/66) of the patients were alive and 45% had had the FGT removed and resumed oral diets. On univariate analysis patients who were alive at the time of follow-up had received FGT feeding for a shorter period of time (p < 0.0003), showed no signs of aspiration on the Clinical Assessment of Feeding & Swallowing (CAFS, p < 0.020) and on the Videofluoroscopic Swallowing Study (VSS, 0.001), had a better discharge FIM-Score (Functional Independence Measure) for eating (p < 0.0002) and cognitive function (p < 0.002) as well as better discharge FCM-Score (Functional Communication Measure) for swallowing (p < 0.0001). On multi-variate analysis we developed a model consisting of FGT removal at discharge from the rehabilitation hospital (p < 0.011) and non-aspiration during VSS (p < 0.040) that was significantly associated with longer survival time during follow-up. Conclusions Severe dysphagia requiring FGT is common in patients with stroke referred for neurorehabilitation. Patients who had a FGT in place at the time of discharge from the stroke rehabilitation unit or aspirated during VSS were substantially more likely to have died by the time of follow-up compared to those who had had the FGT removed and had no signs of aspiration on VSS. However functional outcome measurements (FIM, FCM) including the cognitive function (attention, concentration etc.) could play an important role for prediction of swallowing regeneration and survival in neurorehabilitation. These findings may have practical utility in guiding physicians and speech language pathologists when advising patients and families about prognosis in stroke survivors with severe dysphagia. C1 Univ Regensburg, Dept Neurol, D-93053 Regensburg, Germany. Harvard Univ, Massachusetts Gen Hosp, Stroke Program SRH, Boston, MA 02115 USA. Harvard Univ, Sch Med, Dept Phys Med & Rehabil, Boston, MA 02115 USA. RP Ickenstein, GW (reprint author), Univ Regensburg, Dept Neurol, Univ Str 84, D-93053 Regensburg, Germany. EM guntram.ickenstein@medbo.de NR 28 TC 41 Z9 47 U1 2 U2 5 PU DR DIETRICH STEINKOPFF VERLAG PI DARMSTADT PA PO BOX 10 04 62, D-64204 DARMSTADT, GERMANY SN 0340-5354 J9 J NEUROL JI J. Neurol. PD DEC PY 2005 VL 252 IS 12 BP 1510 EP 1516 DI 10.1007/s00415-005-0906-9 PG 7 WC Clinical Neurology SC Neurosciences & Neurology GA 994UJ UT WOS:000234056400013 PM 16136260 ER PT J AU Cantuti-Castelvetri, I Klucken, J Ingelsson, M Ramasamy, K McLean, PJ Frosch, MP Hyman, BT Standaert, DG AF Cantuti-Castelvetri, I Klucken, J Ingelsson, M Ramasamy, K McLean, PJ Frosch, MP Hyman, BT Standaert, DG TI Alpha-synuclein and chaperones in dementia with Lewy bodies SO JOURNAL OF NEUROPATHOLOGY AND EXPERIMENTAL NEUROLOGY LA English DT Article DE alpha-synuclein; dementia with Lewy bodies; molecular chaperone; real-time PCR; temporal cortex ID FAMILIAL PARKINSONS-DISEASE; ALZHEIMERS-DISEASE; MESSENGER-RNA; CONSENSUS RECOMMENDATIONS; POSTMORTEM DIAGNOSIS; NATIONAL-INSTITUTE; GENE TRIPLICATION; FIBRIL FORMATION; EXPRESSION; MUTATION AB The protein alpha-synuclein (ASYN) is thought to be involved in the development of dementia with Lewy bodies (DLB). Overexpression of ASYN has been linked to cellular toxicity and human disease, and in experimental models, chaperones such as heat shock proteins (HSPs) are protective against ASYN toxicity We have assessed the abundance of mRNA for ASYN and chaperones and the abundance and solubility of the encoded proteins in temporal cortex from sporadic human DLB. We found a reduction of ASYN mRNA in DLB (44.9% of control). The abundance of the Triton-soluble fraction (bioavailable protein) was not altered, but there was an increase of the Triton-in soluble component (likely representing aggregates). We evaluated 3 chaperones: HSP70, HSP90, and HDJ1. HSP70 mRNA was increased in DLB, whereas the mRNAs for HSP90 and HDJ1 were unchanged. HSP70 accumulated in the Triton-soluble fraction, whereas HSP90 and HDJ1 proteins accumulated in the Triton-insoluble fraction. These observations suggest that sporadic DLB is not associated with overexpression of ASYN. Rather, the persistence of normal soluble ASYN protein levels, despite the reduction of its mRNA, suggests a primary defect in clearance of the protein. However, this reduced clearance cannot be attributed to a failure of chaperone expression, because their mRNA is unchanged or increased in the DLB brain. C1 Massachusetts Gen Hosp, Massachusetts Gen Inst Neurodegenerat Dis, Charlestown, MA 02129 USA. Massachusetts Gen Hosp, CS Kubik Lab Neuropathol, Boston, MA 02114 USA. RP Standaert, DG (reprint author), Massachusetts Gen Hosp, Massachusetts Gen Inst Neurodegenerat Dis, 114 16th St,CNY114-2004, Charlestown, MA 02129 USA. EM standaert@helix.mgh.harvard.edu OI Standaert, David/0000-0003-2921-8348 FU NIA NIH HHS [AG005134]; NICHD NIH HHS [N01-HD-4-3368]; NIMH NIH HHS [R24-MH 068855]; NINDS NIH HHS [NS38372] NR 68 TC 30 Z9 33 U1 0 U2 2 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3261 USA SN 0022-3069 J9 J NEUROPATH EXP NEUR JI J. Neuropathol. Exp. Neurol. PD DEC PY 2005 VL 64 IS 12 BP 1058 EP 1066 DI 10.1097/01.jnen.0000190063.90440.69 PG 9 WC Clinical Neurology; Neurosciences; Pathology SC Neurosciences & Neurology; Pathology GA 992XE UT WOS:000233916500004 PM 16319716 ER PT J AU Cook, DG Li, XF Cherry, SD Cantrell, AR AF Cook, DG Li, XF Cherry, SD Cantrell, AR TI Presenilin 1 deficiency alters the activity of voltage-gated Ca2+ channels in cultured cortical neurons SO JOURNAL OF NEUROPHYSIOLOGY LA English DT Article ID FAMILIAL ALZHEIMERS-DISEASE; AMYLOID-BETA-PEPTIDE; KNOCK-IN MICE; CAPACITATIVE CALCIUM-ENTRY; GAMMA-SECRETASE CLEAVAGE; LONG-TERM POTENTIATION; HIPPOCAMPAL-NEURONS; INCREASED VULNERABILITY; INTRACELLULAR DOMAIN; MUTANT PRESENILIN-1 AB Cook, David G., Xiaofan Li, Sheree D. Cherry, and Angela R. Cantrell. Presenilin 1 deficiency alters the activity of voltage-gated Ca2+ channels in cultured cortical neurons. J Neurophysiol 94: 4421-4429, 2005. First published September 7, 2005; doi: 10.1152/jn.00745.2005. Presenilins 1 and 2 (PS1 and PS2, respectively) play a critical role in mediating gamma-secretase cleavage of the amyloid precursor protein (APP). Numerous mutations in the presenilins are known to cause early-onset familial Alzheimer's disease ( FAD). In addition, it is well established that PS1 deficiency leads to altered intracellular Ca2+ homeostasis involving endoplasmic reticulum Ca2+ stores. However, there has been little evidence suggesting Ca2+ signals from extracellular sources are influenced by PS1. Here we report that the Ca2+ currents carried by voltage-dependent Ca2+ channels are increased in PS1-deficient cortical neurons. This increase is mediated by a significant increase in the contributions of L- and P- type Ca2+ channels to the total voltage-mediated Ca2+ conductance in PS1 (-/-) neurons. In addition, chelating intracellular Ca2+ with 1,2-bis-(o-aminophenoxy) ethane-N,N,N' ,N' -tetraacetic acid (BAPTA) produced an increase in Ca2+ current amplitude that was comparable to the increase caused by PS1 deficiency. In contrast to this, BAPTA had no effect on voltage-dependent Ca2+ conductances in PS1-deficient neurons. These data suggest that PS1 deficiency may influence voltage-gated Ca2+ channel function by means that involve intracellular Ca2+ signaling. These findings reveal that PS1 functions at multiple levels to regulate and stabilize intracellular Ca2+ levels that ultimately control neuronal firing behavior and influence synaptic transmission. C1 Univ Tennessee, Hlth Sci Ctr, Dept Anat & Neurobiol, Memphis, TN 38163 USA. GRECC, Vet Affairs Puget Sound Hlth Care Syst, Seattle, WA USA. Univ Washington, Sch Med, Div Gerontol & Geriatr Med, Dept Med, Seattle, WA 98195 USA. RP Cantrell, AR (reprint author), Univ Tennessee, Hlth Sci Ctr, Dept Anat & Neurobiol, 855 Monroe Ave,Link 515, Memphis, TN 38163 USA. EM acantrell@utmem.edu FU NIA NIH HHS [AG-05136]; NIMH NIH HHS [K01 MH-01669] NR 68 TC 7 Z9 7 U1 0 U2 2 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA SN 0022-3077 J9 J NEUROPHYSIOL JI J. Neurophysiol. PD DEC PY 2005 VL 94 IS 6 BP 4421 EP 4429 DI 10.1152/jn.00745.2005 PG 9 WC Neurosciences; Physiology SC Neurosciences & Neurology; Physiology GA 984PP UT WOS:000233317100069 PM 16148264 ER PT J AU Weaver, F Follett, K Hur, K Ippolito, D Stern, M AF Weaver, F Follett, K Hur, K Ippolito, D Stern, M TI Deep brain stimulation in Parkinson disease: a metaanalysis of patient outcomes SO JOURNAL OF NEUROSURGERY LA English DT Article DE Parkinson disease; deep brain stimulation; subthalamic nucleus; globus pallidus internus ID SUBTHALAMIC NUCLEUS STIMULATION; HIGH-FREQUENCY STIMULATION; QUALITY-OF-LIFE; GLOBUS-PALLIDUS INTERNUS; 2-YEAR FOLLOW-UP; BILATERAL STIMULATION; ELECTRICAL-STIMULATION; MOTOR FLUCTUATIONS; PARS INTERNA; PALLIDOTOMY AB Object. Deep brain stimulation (DBS) to treat advanced Parkinson disease (PD) has been focused on one of two anatomical targets: the subthalamic nucleus (STN) and the globus pallidus internus (GPI). Authors of more than 65 articles have reported on bilateral DBS outcomes. With one exception, these studies involved pre- and postintervention comparisons of a single target. Despite the paucity of data directly comparing STN and GPI DBS, many clinicians already consider the STN to be the preferred target site. In this study the authors conducted a metaanalysis of the existing literature on patient outcomes following DBS of the STN and the GPI. Methods. This metaanalysis includes 31 STN and 14 GPI studies. Motor function improved significantly following stimulation (54% in patients whose STN was targeted and 40% in those whose GPI was stimulated), with effect sizes (ESs) of 2.59 and 2.04, respectively. After controlling for participant and study characteristics, patients who had undergone either STN or GPI DBS experienced comparable improved motor function following surgery (p = 0.094). The performance of activities of daily living improved significantly in patients with either target (40%). Medication requirements were significantly reduced following stimulation of the STN (ES = 1.51) but did not change when the GPI was stimulated (ES = -0.02). Conclusions. In this analysis the authors highlight the need for uniform, detailed reporting of comprehensive motor and nonmotor DBS outcomes at multiple time points and for a randomized trial of bilateral STN and GPI DBS. C1 Hines VAMC, Midwest Ctr Hlth Serv & Policy Res, Hines, IL 60141 USA. VA Iowa City Hlth Care Syst, Iowa City, IA USA. Univ Iowa, Iowa City, IA USA. Edward Hines Jr VA Hosp, Cooperat Studies Program Coordinating Ctr, Hines, IL USA. Philadelphia VA Med Ctr, Philadelphia, PA USA. Univ Penn, Philadelphia, PA 19104 USA. RP Weaver, F (reprint author), Hines VAMC, Midwest Ctr Hlth Serv & Policy Res, POB 5000 151H, Hines, IL 60141 USA. EM Frances.Weaver@va.gov NR 83 TC 86 Z9 88 U1 1 U2 3 PU AMER ASSOC NEUROLOGICAL SURGEONS PI CHARLOTTESVILLE PA UNIV VIRGINIA, 1224 WEST MAIN ST, STE 450, CHARLOTTESVILLE, VA 22903 USA SN 0022-3085 J9 J NEUROSURG JI J. Neurosurg. PD DEC PY 2005 VL 103 IS 6 BP 956 EP 967 DI 10.3171/jns.2005.103.6.0956 PG 12 WC Clinical Neurology; Surgery SC Neurosciences & Neurology; Surgery GA 990PT UT WOS:000233756400002 PM 16381181 ER PT J AU Matulonis, UA Seiden, MV Roche, M Krasner, C Fuller, AF Atkinson, T Kornblith, A Penson, R AF Matulonis, UA Seiden, MV Roche, M Krasner, C Fuller, AF Atkinson, T Kornblith, A Penson, R TI Long-acting octreotide for the treatment and symptomatic relief of bowel obstruction in advanced ovarian cancer SO JOURNAL OF PAIN AND SYMPTOM MANAGEMENT LA English DT Article DE long-acting octreotide; ovarian cancer; bowel obstruction ID QUALITY-OF-LIFE; INTESTINAL-OBSTRUCTION; CLINICAL-TRIALS; SOMATOSTATIN; MANAGEMENT; ABSORPTION; CARCINOMA; DISEASE; ANALOGS AB Symptoms of malignant bowel obstruction in patients with recurrent ovarian cancer lead to a poor quality of life. Sandostatin LAR (R) Depot (LAR) (Novartis Pharmaceuticals Corp., East Hanover, NJ) is an intramuscular, monthly administered, long-acting form of octreolide. LARs safety and utility were evaluated in a pilot study enrolling 15 advanced ovarian cancer patients with bowel dysfunction. Once safety with subcutaneous (SQ) octreotide was assessed, patients were given 30 mg LAR on Day 1 and octreotide SQ for 2 weeks. Of 13 evaluable patients, three patients had a major response to LAR treatment with reduction in bowel obstruction symptoms, two had a minor response, four had no response, and four had progressive symptoms. Three patients remained on LAR for more than 9 months. No significant toxicities were attributable to octreolide or LAR. Because three patients received nine or more monthly injections of LAR, possible direct antitumor effects Of LAR or synergy with chemotherapy needs to be explored. C1 Dana Farber Canc Inst, Div Med Oncol, Boston, MA 02115 USA. Massachusetts Gen Hosp, Div Hematol & Oncol, Boston, MA 02114 USA. Massachusetts Gen Hosp, Div Gynecol Oncol, Boston, MA 02114 USA. RP Matulonis, UA (reprint author), Dana Farber Canc Inst, Div Med Oncol, 44 Binney St, Boston, MA 02115 USA. NR 28 TC 26 Z9 29 U1 0 U2 2 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 2005 VL 30 IS 6 BP 563 EP 569 DI 10.1016/j.jpainsymman.2005.05.018 PG 7 WC Health Care Sciences & Services; Medicine, General & Internal; Clinical Neurology SC Health Care Sciences & Services; General & Internal Medicine; Neurosciences & Neurology GA 002IP UT WOS:000234605300010 PM 16376743 ER PT J AU Morrison, RS Maroney-Galin, C Kralovec, PD Meier, DE AF Morrison, RS Maroney-Galin, C Kralovec, PD Meier, DE TI The growth of palliative care programs in United States hospitals SO JOURNAL OF PALLIATIVE MEDICINE LA English DT Article ID OF-LIFE CARE; END; OLDER; CONSULTATIONS; IMPACT; PLACE; COSTS AB Background: Palliative care programs are becoming increasingly common in U.S. hospitals. Objective: To quantify the growth of hospital based palliative care programs from 2000-2003 and identify hospital characteristics associated with the development of a palliative care program. Design and measurements: Data were obtained from the 2001-2004 American Hospital Association Annual Surveys which covered calendar years 2000-2003. We identified all programs that self-reported the presence of a hospital-owned palliative care program and acute medical and surgical beds. Multivariate logistic regression was used to identify characteristics significantly associated with the presence of a palliative care program in the 2003 survey data. Results: Overall, the number of programs increased linearly from 632 (15% of hospitals) in 2000 to 1027 (25% of hospitals) in 2003. Significant predictors associated with an increased likelihood of having a palliative care program included greater numbers of hospital beds and critical care beds, geographic region, and being an academic medical center. Compared to not-for-profit hospitals, VA hospitals were significantly more likely to have a palliative care program and city, county or state and for-profit hospitals were significantly less likely to have a program. Hospitals operated by the Catholic Church, and hospitals that owned their own hospice program were significantly more likely to have a palliative care program than non-Catholic Church-operated hospitals and hospitals without hospice programs respectively. Conclusions: Our data suggest that although growth in palliative care programs has occurred throughout the nation's hospitals, larger hospitals, academic medical centers, not-for-profit hospitals, and VA hospitals are significantly more likely to develop a program compared to other hospitals. C1 CUNY Mt Sinai Sch Med, Brookdale Dept Geriatr, Hertzberg Palliat Care Inst, New York, NY 10029 USA. CUNY Mt Sinai Sch Med, Ctr Advance Palliat Care, New York, NY 10029 USA. Bronx Vet Adm Med Ctr, Ctr Geriatr Res Educ & Clin, Bronx, NY USA. Amer Hosp Assoc, Hlth Care Data Ctr, Chicago, IL USA. RP Morrison, RS (reprint author), CUNY Mt Sinai Sch Med, Brookdale Dept Geriatr, Hertzberg Palliat Care Inst, New York, NY 10029 USA. EM sean.morrison@mssm.edu FU NIA NIH HHS [K07 AG00903, K24 AG022345] NR 38 TC 128 Z9 130 U1 6 U2 8 PU MARY ANN LIEBERT INC PI NEW ROCHELLE PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA SN 1096-6218 J9 J PALLIAT MED JI J. Palliat. Med. PD DEC PY 2005 VL 8 IS 6 BP 1127 EP 1134 DI 10.1089/jpm.2005.8.1127 PG 8 WC Health Care Sciences & Services SC Health Care Sciences & Services GA 045XS UT WOS:000237776600011 PM 16351525 ER PT J AU Carlson, B Simopolous, N Goy, ER Jackson, A Ganzini, L AF Carlson, B Simopolous, N Goy, ER Jackson, A Ganzini, L TI Oregon hospice chaplains' experiences with patients requesting physician-assisted suicide SO JOURNAL OF PALLIATIVE MEDICINE LA English DT Article ID SOCIAL-WORKERS; TERMINALLY ILL; DIGNITY ACT; ATTITUDES; DEATH; EUTHANASIA; NURSES; DESIRE; CARE AB Background: Oregon's Death with Dignity Act (ODDA), which legalized physician-assisted suicide (PAS) for terminally ill individuals, was enacted in 1997. Eighty-six percent of the 171 patients who have died by PAS were enrolled in hospice. Objective: To survey hospice chaplains regarding their views on the ODDA and experiences working with patients who request PAS. Design: Single, anonymous, mailed survey. Subjects: All chaplains affiliated with one of Oregon's 50 hospices. Results: Fifty of 77 hospice chaplains whom we identified (65%) returned the survey. Forty-two percent of respondents opposed the ODDA and 40% supported it. Over half of respondents had, in the previous 3 years, worked with a patient who had made an explicit request for assisted suicide. Conversation with patients around PAS focused on the role of faith and spirituality in this decision, reasons for wanting hastened death, and family concerns or reactions to PAS. Chaplains did not feel that they had a strong influence on the patient's decisions about PAS (mean score of 4 on a 0-10 scale), though three chaplains reported a patient who withdrew their request for PAS because of the chaplain's involvement. Chaplains reported provision of a nonjudgmental presence helped the relationship with the patient. Conclusion: Oregon hospice chaplains are divided in their views on legalized PAS, but primarily see their role to deliver support to patients no matter what the patient's final decision regarding PAS. C1 Portland Vet Affairs Med Ctr, Div Mental Hlth, Portland, OR 97239 USA. Oregon Hlth & Sci Univ, Dept Psychiat, Portland, OR USA. Oregon Hospice Assoc, Portland, OR USA. RP Ganzini, L (reprint author), Portland Vet Affairs Med Ctr, Div Mental Hlth, P3MHDC,3710 SW US Vet Hosp Rd, Portland, OR 97239 USA. EM ganzinil@ohsu.edu NR 15 TC 13 Z9 13 U1 0 U2 2 PU MARY ANN LIEBERT INC PI NEW ROCHELLE PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA SN 1096-6218 J9 J PALLIAT MED JI J. Palliat. Med. PD DEC PY 2005 VL 8 IS 6 BP 1160 EP 1166 DI 10.1089/jpm.2005.8.1160 PG 7 WC Health Care Sciences & Services SC Health Care Sciences & Services GA 045XS UT WOS:000237776600015 PM 16351529 ER PT J AU Cherlin, E Fried, T Prigerson, HG Schulman-Green, D Johnson-Hurzeler, R Bradley, EH AF Cherlin, E Fried, T Prigerson, HG Schulman-Green, D Johnson-Hurzeler, R Bradley, EH TI Communication between physicians and family caregivers about care at the end of life: When do discussions occur and what is said? SO JOURNAL OF PALLIATIVE MEDICINE LA English DT Article; Proceedings Paper CT 57th Annual Meeting of the Gerontological-Society-of-America CY NOV 19-23, 2004 CL Washington, DC SP Gerontol Soc Amer ID HOSPICE ENROLLMENT; DECISION-MAKING; CLINICIAN; PROGNOSIS; DEATH; PERSPECTIVES; PREFERENCES; QUALITY; CANCER AB Background: Few studies have examined physician-family caregiver communication at the end of life, despite the important role families have in end-of-life care decisions. We examined family caregiver reports of physician communication about incurable illness, life expectancy, and hospice; the timing of these discussions; and subsequent family understanding of these issues. Design: Mixed methods study using a closed-ended survey of 206 family caregivers and open-ended, in-depth interviews with 12 additional family caregivers. Setting/Subjects: Two hundred eighteen primary family caregivers of patients with cancer enrolled with hospice between October 1999 and June 2002 Measurements: Family caregiver reports provided at the time of hospice enrollment of physician discussions of incurable illness, life expectancy, and hospice. Results: Many family caregivers reported that a physician never told them the patient's illness could not be cured (20.8%), never provided life expectancy (40% of those reportedly told illness was incurable), and never discussed using hospice (32.2%). Caregivers reported the first discussion of the illness being incurable and of hospice as a possibility occurred within 1 month of the patient's death in many cases (23.5% and 41.1%, respectively). In open-ended interviews, however, family caregivers expressed ambivalence about what they wanted to know, and their difficulty comprehending and accepting "bad news" was apparent in both qualitative and quantitative data. Conclusion: Our findings suggest that ineffective communication about end-of-life issues likely results from both physician's lack of discussion and family caregiver's difficulty hearing the news. Future studies should examine strategies for optimal physician-family caregiver communication about incurable illness, so that families and patients can begin the physical, emotional, and spiritual work that can lead to acceptance of the irreversible condition. C1 Yale Univ, Sch Med, Dept Epidemiol & Publ Hlth, New Haven, CT 06520 USA. Yale Univ, Sch Med, Dept Internal Med, New Haven, CT 06510 USA. VA Connecticut Healthcare Syst, CERC, West Haven, CT USA. Harvard Univ, Sch Med, Brigham & Womens Hosp, Dept Psychiat,Dana Farber Canc Inst,Ctr Psychonco, Boston, MA USA. Yale Univ, Sch Nursing, New Haven, CT 06536 USA. Connecticut Hospice, Branford, CT USA. John D Thompson Hospice Inst Educ Training & Res, Branford, CT USA. RP Bradley, EH (reprint author), Yale Univ, Sch Med, Dept Epidemiol & Publ Hlth, 60 Coll St, New Haven, CT 06520 USA. EM Elizabeth.bradley@yale.edu FU NCI NIH HHS [CA106370, R01 CA106370]; NIA NIH HHS [P30 AG021342, P30AG21342]; NIMH NIH HHS [R01 MH056529, MH63892, R01 MH063892] NR 34 TC 117 Z9 119 U1 4 U2 25 PU MARY ANN LIEBERT INC PI NEW ROCHELLE PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA SN 1096-6218 J9 J PALLIAT MED JI J. Palliat. Med. PD DEC PY 2005 VL 8 IS 6 BP 1176 EP 1185 DI 10.1089/jpm.2005.8.1176 PG 10 WC Health Care Sciences & Services SC Health Care Sciences & Services GA 045XS UT WOS:000237776600017 PM 16351531 ER PT J AU Rappaport, N Prince, JB Bostic, JQ AF Rappaport, N Prince, JB Bostic, JQ TI Lost in the black box: Juvenile depression, suicide, and the FDA's black box SO JOURNAL OF PEDIATRICS LA English DT Editorial Material ID ADOLESCENTS; DISORDER; CHILDREN; RISK C1 Cambridge Hlth Alliance, Cambridge, MA USA. Massachusetts Gen Hosp, Boston, MA 02114 USA. RP Rappaport, N (reprint author), 1493 Cambridge St, Cambridge, MA 02139 USA. EM nrappaport@comcast.net NR 19 TC 3 Z9 3 U1 2 U2 2 PU MOSBY-ELSEVIER PI NEW YORK PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA SN 0022-3476 EI 1097-6833 J9 J PEDIATR-US JI J. Pediatr. PD DEC PY 2005 VL 147 IS 6 BP 719 EP 720 DI 10.1016/j.jpeds.2005.08.037 PG 2 WC Pediatrics SC Pediatrics GA 994XX UT WOS:000234065600001 PM 16356415 ER PT J AU Choi, HK Seeger, JD AF Choi, HK Seeger, JD TI Lipid profiles among US elderly with untreated rheumatoid arthritis - The Third National Health and Nutrition Examination Survey SO JOURNAL OF RHEUMATOLOGY LA English DT Article DE rheumatoid arthritis; lipid profiles; apolipoprotein A-I; high density lipoprotein-cholesterol; NHANES III ID ACUTE-PHASE RESPONSE; SYSTEMIC-LUPUS-ERYTHEMATOSUS; DENSITY-LIPOPROTEIN CHOLESTEROL; HDL-CHOLESTEROL; CARDIOVASCULAR MORBIDITY; RISK-FACTORS; MORTALITY; CYTOKINES; DISEASE; ATHEROSCLEROSIS AB Objective. Recent studies suggest that patients with active rheumatoid arthritis (RA) have adverse serum lipid profiles. We examined lipid profiles among individuals with RA in a national sample of persons aged 60 years and older. Methods. Using data from 4862 participants (2379 men and 2483 women) aged 60 years and older in the Third National Health and Nutrition Examination Survey (1988-94), we examined lipid profiles among participants with RA who met the American College of Rheumatology (ACR) 1987 criteria and who were not taking glucocorticoids or disease modifying antirheumatic drugs (DMARD). Results. Participants with RA had lower high density lipoprotein cholesterol (HDL-C) and apolipoprotein A-I concentrations than those without RA. After adjusting for age and sex, the differences in HDL-C level between those with and those without RA were 2.5 mg/dl (95% CI 0.8 to 4.9) using;2: 3 of the ACR criteria (n of RA cases = 104) and 8.8 mg/dl (95% CI 3.2 to 14.3) using >= 4 criteria (n of RA cases = 26). Adjusting for age, sex, race, education, smoking status, body mass index, alcohol consumption, physical activity, dietary factors, and other potential confounders attenuated the differences slightly. The multivariate difference in serum apolipoprotein A-1 levels between those with and those without RA was 4.5 mg/dl (95% CI -0.8 to 9.8) using a 3 ACR criteria and 13.6 mg/dI (95% CI 3.2 to 24.1) using;2: 4 criteria. All individual RA disease activity measures tended to have inverse relations with HDL-C levels, but significant inverse associations were present only with the following variables: C-reactive protein [CRP; multivariate difference per I mg/dI of CRP, -1.3 mg/dI (95% CI -2.0 to -0.5)], presence of hand arthritis [-2.6 mg/dI (95% Cl -5.0 to -0.2)], and positive rheumatoid factor [-3.4 mg/dI (95% Cl-5.5 to -1. 3)]. Conclusion. These national survey data indicate that RA not treated with DMARD or glucocorticoids is associated with adverse lipid profiles characterized by lower HDL-C and apolipoprotein AI levels in persons aged >= 60 years. C1 Harvard Univ, Rheumatol Unit, Dept Med, Massachusetts Gen Hosp,Sch Med, Boston, MA 02114 USA. Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA. Ingenix Res & Data Solut, Auburndale, MA USA. RP Choi, HK (reprint author), Harvard Univ, Rheumatol Unit, Dept Med, Massachusetts Gen Hosp,Sch Med, Bulfinch 165,55 Fruit St, Boston, MA 02114 USA. EM hchoi@partners.org NR 50 TC 61 Z9 68 U1 0 U2 2 PU J RHEUMATOL PUBL CO PI TORONTO PA 920 YONGE ST, SUITE 115, TORONTO, ONTARIO M4W 3C7, CANADA SN 0315-162X J9 J RHEUMATOL JI J. Rheumatol. PD DEC PY 2005 VL 32 IS 12 BP 2311 EP 2316 PG 6 WC Rheumatology SC Rheumatology GA 992AZ UT WOS:000233857500008 PM 16331755 ER PT J AU Strangman, G Thompson, JH Strauss, MM Marshburn, TH Sutton, JP AF Strangman, G Thompson, JH Strauss, MM Marshburn, TH Sutton, JP TI Functional brain imaging of a complex navigation task following one night of total sleep deprivation: a preliminary study SO JOURNAL OF SLEEP RESEARCH LA English DT Article DE flight docking task; functional magnetic resonance imaging; hemodynamics; spacedock; total sleep deprivation ID ATTENTION; PERFORMANCE; HUMANS; MRI AB Several neuroimaging studies have demonstrated compensatory cerebral responses consequent to sleep deprivation (SD), but all have focused on simple tasks with limited behavioral response options. We assessed the cerebral effects associated with SD during the performance of a complex, open-ended, dual-joystick, 3D navigation task (simulated orbital docking) in a cross-over protocol, with counterbalanced orders of normal sleep (NS) and a single night of total SD (similar to 27 h). Behavioral performance on multiple measures was comparable in the two sleep conditions. Functional magnetic resonance imaging revealed multiple compensatory SD > NS cerebral responses, including the posterior superior temporal sulcus [Brodmann area (BA) 39/22/37], prefrontal cortex (BA 9), lateral temporal cortex (BA 22/21), and right substantia nigra. Right posterior cingulate cortex (BA 31) exhibited NS > SD activity. Our findings extend the compensatory cerebral response hypothesis to complex, open-ended tasks. C1 Harvard Univ, Sch Med, Massachusetts Gen Hosp, Dept Psychiat,Neural Syst Grp, Charlestown, MA 02129 USA. Harvard Univ, Sch Med, Massachusetts Gen Hosp, Athinoula A Martinos Ctr, Charlestown, MA USA. NASA, Lyndon B Johnson Space Ctr, Houston, TX 77058 USA. Natl Space Biomed Res Inst, Houston, TX USA. RP Strangman, G (reprint author), Harvard Univ, Sch Med, Massachusetts Gen Hosp, Dept Psychiat,Neural Syst Grp, 149 13th St Psychiat Rm 2651, Charlestown, MA 02129 USA. EM strang@nmr.mgh.harvard.edu RI Sanguansri, Luz/B-6630-2011 OI Sanguansri, Luz/0000-0003-1908-7604 FU NCRR NIH HHS [P41-RR014075]; NINDS NIH HHS [K25-NS046554] NR 22 TC 15 Z9 15 U1 0 U2 2 PU BLACKWELL PUBLISHING PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DQ, OXON, ENGLAND SN 0962-1105 J9 J SLEEP RES JI J. Sleep Res. PD DEC PY 2005 VL 14 IS 4 BP 369 EP 375 DI 10.1111/j.1365-2869.2005.00488.x PG 7 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA 990AI UT WOS:000233715200005 PM 16364137 ER PT J AU Doyle, PJ Hula, WD McNeil, MR Mikolic, JM Matthews, C AF Doyle, PJ Hula, WD McNeil, MR Mikolic, JM Matthews, C TI An application of Rasch analysis to the measurement of communicative functioning SO JOURNAL OF SPEECH LANGUAGE AND HEARING RESEARCH LA English DT Article; Proceedings Paper CT 34th Annual Clinical Aphasiology Conference CY 2004 CL Park City, UT DE communicative functioning; outcomes; Rasch analysis; measurement ID ITEM RESPONSE THEORY; STROKE IMPACT SCALE; RELIABILITY; SURVIVORS; VALIDITY; BURDEN; BOSS AB Purpose: The purposes of this investigation were to examine the construct dimensionality and range of ability effectively measured by 28 assessment items L obtained from 3 different patient-reported scales of communicative functioning, and to provide a demonstration of how the Rasch approach to measurement may contribute to the definition of latent constructs and the development of instruments to measure them. Method: Item responses obtained from 421 stroke survivors with and without communication disorders were examined using the Rasch partial credit model. The dimensionality of the item pool was evaluated by (a) examining correlations of Rasck person ability scores obtained separately from each of the 3 scales,. (b) iteratively excluding items exceeding mean square model fit criteria, and (c) using principal-components analysis of Rasch model residuals. The range of ability effectively measured by the item pool was examined by comparing item difficulty and category threshold calibrations to the distribution of person ability scores and by plotting the modeled standard error of person ability estimates as a function of person ability level. Results: The results indicate that most assessment items fit a unidimensional measurement model, with the notable exception of items relating to the use of written communication. The results also suggest that the range of ability that could be reliably measured by the current item pool was restricted relative to the range of ability observed in the patient sample. Conclusions: It is concluded that (a) a mature understanding of communicative functioning as a measurement construct will require further research, (b) patients with stroke-related communication disorders will be better served by the development of instruments measuring a wider range of communicative functioning ability, and (c) the theoretical and methodological tools provided by the Rasch family of measurement models may be productively applied to these efforts. C1 VA Pittsburgh Healthcare Syst, Pittsburgh, PA 15206 USA. Univ Pittsburgh, Pittsburgh, PA 15260 USA. VA Pittsburgh Healthcare Syst, Geriatr Res Educ & Clin Ctr, Pittsburgh, PA USA. RP Doyle, PJ (reprint author), VA Pittsburgh Healthcare Syst, 7180 Highland Dr,132A-H, Pittsburgh, PA 15206 USA. EM patrick.doyle@med.va.gov NR 52 TC 15 Z9 15 U1 0 U2 1 PU AMER SPEECH-LANGUAGE-HEARING ASSOC PI ROCKVILLE PA 10801 ROCKVILLE PIKE, ROCKVILLE, MD 20852-3279 USA SN 1092-4388 J9 J SPEECH LANG HEAR R JI J. Speech Lang. Hear. Res. PD DEC PY 2005 VL 48 IS 6 BP 1412 EP 1428 DI 10.1044/1092-4388(2005/098) PG 17 WC Audiology & Speech-Language Pathology; Linguistics; Rehabilitation SC Audiology & Speech-Language Pathology; Linguistics; Rehabilitation GA 022KY UT WOS:000236055900013 PM 16478380 ER PT J AU Walters, ST Matson, SA Baer, JS Ziedonis, DM AF Walters, ST Matson, SA Baer, JS Ziedonis, DM TI Effectiveness of workshop training for psychosocial addiction treatments: A systematic review SO JOURNAL OF SUBSTANCE ABUSE TREATMENT LA English DT Review DE workshop; training; clinicians; substance abuse; addiction ID COGNITIVE-BEHAVIORAL THERAPY; SUBSTANCE-ABUSE; EDUCATIONAL INTERVENTIONS; INTERVIEWING SKILLS; NETWORK THERAPY; CLINICAL-TRIALS; PRIMARY-CARE; ALCOHOL-USE; DISSEMINATION; PROGRAM AB Workshop training for psychosocial substance abuse treatment has been an important part of the transfer of evidence-based approaches into larger practice. Although they are widely used, training methods such as self-study reading, internet-based courses, and educational workshops have not traditionally been the focus of empirical investigations. Based on electronic and manual searches of the literature, we summarize 17 evaluations of workshop training that describe the training program and the educational outcomes. In general, training tends to improve attendees' knowledge, attitudes, and confidence in working with clients who have substance abuse problems. Some skill improvements, when measured, are usually seen immediately after training but are less often maintained over a longer time. Extended contact, through follow-up consultation, supervision, or feedback, appears to be necessary for the long-term adoption of skills. There are also a number of institutional factors that may influence the extent to which providers adopt new practices. Given the popularity of this training format, the role of workshop training needs to be a focus of future evaluative research. (c) 2005 Elsevier Inc. All rights reserved. C1 Univ Texas, Sch Publ Hlth, Dallas, TX 75390 USA. Univ Washington, Dept Psychol, Seattle, WA 98195 USA. Vet Affairs Puget Sound Healthcare Syst, Seattle, WA USA. Univ Med & Dent New Jersey, Robert Wood Johnson Med Sch, Dept Psychiat, Piscataway, NJ 08854 USA. RP Walters, ST (reprint author), Univ Texas, Sch Publ Hlth, V-8,Room 112,5323 Harry Hines Blvd, Dallas, TX 75390 USA. EM scott.walters@utsouthwestern.edu NR 41 TC 84 Z9 84 U1 2 U2 19 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND SN 0740-5472 J9 J SUBST ABUSE TREAT JI J. Subst. Abus. Treat. PD DEC PY 2005 VL 29 IS 4 BP 283 EP 293 DI 10.1016/j.jsat.2005.08.006 PG 11 WC Psychology, Clinical; Substance Abuse SC Psychology; Substance Abuse GA 994YE UT WOS:000234066300007 PM 16311181 ER PT J AU Shireman, PK Quinones, MP AF Shireman, PK Quinones, MP TI Differential necrosis despite similar perfusion in mouse strains after ischemia SO JOURNAL OF SURGICAL RESEARCH LA English DT Article DE collateral circulation; laser Doppler imaging; arteriogenesis; hind limb ischemia ID ENDOTHELIAL PROGENITOR CELLS; ARTERY GROWTH ARTERIOGENESIS; CONVERTING ENZYME-INHIBITION; MURINE SKELETAL-MUSCLE; CRITICAL LIMB ISCHEMIA; INDUCED ANGIOGENESIS; COLLATERAL GROWTH; T-CELL; REPERFUSION INJURY; HINDLIMB ISCHEMIA AB Background. Numerous mouse models have been used to study the tissue response to ischemia, but multiple technical differences make comparisons difficult. We have comprehensively characterized the mouse hind limb ischemia model and determined how different genetic backgrounds of mice affect recovery. Materials and methods. Severity of tissue necrosis and restoration of perfusion after femoral artery excision or femoral artery transection, using five different surgical procedures, were evaluated using laser Doppler imaging in a mouse model of hind limb ischemia. Severity of necrosis was concurrently measured using a five-point scale. Results. Significant differences were observed depending upon the surgical procedure used to initiate ischemia as well as the strain of mouse used. First, a progressively delayed and incomplete recovery of vascular perfusion occurred in relation to the anatomical position and extent of the arterial defect. Second, among mouse strains, the severity of tissue necrosis varied despite similar restoration of perfusion. Thus, DBA/1J mice had significantly increased severity and incidence of tissue loss as compared with either C57BI/6J (P = 0.01) or BALB/c (P = 0.01) mice. Finally, contrary to previous reports, T-cell-mediated immune events did not modify ischemia-induced hind limb perfusion and necrosis as responses in nude mice were not different than controls on either BALB/c or C57BI/6J backgrounds. Conclusions. Surgical approach, mouse strain, and measures of hind limb perfusion and tissue injury are crucial considerations in the study of ischemia. Understanding how different genetic backgrounds in mice can affect necrosis may provide insights into the diverse healing responses observed in humans. (c) 2005 Elsevier Inc. All rights reserved. C1 S Texas Vet Hlth Care Syst, San Antonio, TX USA. Barshop Inst Longev & Aging Studies, Dept Med, San Antonio, TX USA. Barshop Inst Longev & Aging Studies, Dept Surg, San Antonio, TX USA. Univ Texas, Hlth Sci Ctr, Dept Med, San Antonio, TX 78284 USA. Univ Texas, Hlth Sci Ctr, Dept Radiol, San Antonio, TX 78284 USA. RP Shireman, PK (reprint author), Univ Texas, Hlth Sci Ctr, Dept Surg, Div Vasc Surg, MSC 7741,7703 Floyd Curl Dr, San Antonio, TX 78229 USA. EM shireman@uthscsa.edu FU NHLBI NIH HHS [HL070158, HL074236] NR 53 TC 39 Z9 39 U1 0 U2 3 PU ACADEMIC PRESS INC ELSEVIER SCIENCE PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA SN 0022-4804 J9 J SURG RES JI J. Surg. Res. PD DEC PY 2005 VL 129 IS 2 BP 242 EP 250 DI 10.1016/j.jss.2005.06.013 PG 9 WC Surgery SC Surgery GA 995WJ UT WOS:000234135000010 PM 16051277 ER PT J AU Rotunda, AM Ablon, G Kolodney, MS AF Rotunda, AM Ablon, G Kolodney, MS TI Lipomas treated with subcutaneous deoxycholate injections SO JOURNAL OF THE AMERICAN ACADEMY OF DERMATOLOGY LA English DT Article ID MIXED MICELLES; FAT PADS; PHOSPHATIDYLCHOLINE; SOLUBILIZATION; MESOTHERAPY AB Background: Lipomas are benign neoplasms of mature fat cells. Current treatments are invasive and carry the risk of scarring. Injections of phosphatidylcholine solubilized with deoxycholate, a bile salt, have been used to reduce unwanted accumulations of fat. Recent in vitro and ex vivo investigations indicate that deoxycholate alone causes adipocyte lysis. Objective: We sought to report our experience treating lipomas subcutaneous deoxycholate injections. Methods: A total of 6 patients presenting with 12 lipomas were treated with intralesional injections of sodium deoxycholate (1.0%, 2.5% and 5.0%) at intervals of 2 to 20 weeks. Tumor size, cutaneous reactions, and patients' subjective responses were recorded before and after treatment. Results: All lipomas decreased in size (mean area reduction, 75%, range, 37%-100%) as determined by clinical measurement (with ultrasound in one lipoma) after an average of 2.2 treatments. Several lipomas fragmented or because softer in addition to decreasing in volume. Adverse effects, including transient burning, erythema, and local swelling, were associated with higher deoxycholate concentations but resolved without intervention. There was no clear association between deoxycholate concentration and efficacy. Conclusions: Our clinical experience supports our laboratory investigations demonstrating that deoxycholate, rather than phosphatidylcholine, is the active ingredient in subcutaneously injected formulas used to treat adipose tissue. this small series suggests that low concentration deoxycholate may be a relatively safe and effective treatment for small collections of fat. However, controlled clinical trials will ne necessary to substantiate these observations. C1 Univ Calif Los Angeles, David Geffen Sch Med, Div Dermatol, Los Angeles, CA 90024 USA. Harbor UCLA Med Ctr, W Los Angeles Vet Adm Med Ctr, Dept Dermatol, Torrance, CA 90509 USA. Harbor UCLA Med Ctr, Dept Med, Div Dermatol, Torrance, CA 90509 USA. Biomed Res Inst, Torrance, CA USA. RP Rotunda, AM (reprint author), Bennett Surg Ctr, St Johns Med Plaza,Suite 590, Santa Monica, CA 90404 USA. EM arotunda@hotmail.com NR 19 TC 45 Z9 47 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 2005 VL 53 IS 6 BP 973 EP 978 DI 10.1016/j.jaad.2005.07.068 PG 6 WC Dermatology SC Dermatology GA 990PQ UT WOS:000233756100005 PM 16310057 ER PT J AU Astner, S Gonzalez, E Cheung, A Rius-Diaz, F Gonzalez, S AF Astner, S Gonzalez, E Cheung, A Rius-Diaz, F Gonzalez, S TI Pilot study on the sensitivity and specificity of in vivo reflectance confocal microscopy in the diagnosis of allergic contact dermatitis SO JOURNAL OF THE AMERICAN ACADEMY OF DERMATOLOGY LA English DT Article ID SCANNING LASER MICROSCOPY; BASAL-CELL CARCINOMA; HUMAN SKIN; MULTICENTER; HISTOLOGY AB The validity, reproducibility, and specificity of patch-testing in the diagnosis of allergic contact dermatitis (ACD) have repeatedly been addressed. in vivo reflectance confocal microscopy (RCM) has been used for rela-time evaluation of the histopathologic features of ACD. This pilot study was designed to determine the sensitivity and specificity of KM in diagnosing ACD in reference to patch-testing. Sixteen participants were patch tested with allergens and control substances. Clinical scoring, digital photography and RCM evaluation were performed at 72 hours, and RCM images were subjected to blinded evaluation. RCM evaluation parameters included stratum corneum (SC) disruption, parakeratosis, stratum spinosum (SS) and stratum granulosum (SG) spongiosis, and exocytosis. Overall, there was high specificity for all RCM features, ranging from 95.8% to 100%. Sensitivity ranged from 51.9% to 96.3%. Significant parameters with high sensitivity and specificity included spongiosis and exocytosis at the level of SS. Logistic regression analysis was performed on significant variables; P values were determined promising noninvasive technology for the evaluation of ACD. SC changes are not helpful in the diagnosis of ACD, although the presence of SG spongiosis and SS spongiosis shows high sensitivity in diagnosing ACD. Larger sensitivity and specificity studies are needed and the identification of ACD has to be based on a defined diagnostic algorithm. A limitation of this study is the small sample size, larger sensitivity and specificity studies are needed to confirm these findings. In addition, individual allergens have to be subjected to further evaluations in order to demonstrate the applicability of our findings for other contact allergens. In that regard, RCM may be considered as an adjunctive tool, rather than a substitute, to clinical evaluation. C1 Mem Sloan Kettering Canc Ctr, Serv Dermatol, New York, NY 10022 USA. Harvard Univ, Massachusetts Gen Hosp, Sch Med, Wellman Ctr Photomed,Dept Dermatol, Boston, MA 02115 USA. Massachusetts Gen Hosp, Dept Dermatol, Contact Dermatitis Unit, Boston, MA 02114 USA. RP Gonzalez, S (reprint author), Mem Sloan Kettering Canc Ctr, Serv Dermatol, 2nd Floor,Rockefeller Outpatient Pavil,160 E 53rd, New York, NY 10022 USA. EM gonzals6@mskcc.org NR 25 TC 42 Z9 46 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 2005 VL 53 IS 6 BP 986 EP 992 DI 10.1016/j.jaad.2005.08.026 PG 7 WC Dermatology SC Dermatology GA 990PQ UT WOS:000233756100007 PM 16310059 ER PT J AU Oaklander, AL Siegel, SM AF Oaklander, AL Siegel, SM TI Cutaneous innervation: Form and function SO JOURNAL OF THE AMERICAN ACADEMY OF DERMATOLOGY LA English DT Review ID EPIDERMAL NERVE-FIBERS; GENE-RELATED PEPTIDE; HUMAN-SKIN; NOTALGIA-PARESTHETICA; SENSORY NEUROPATHY; POSTHERPETIC NEURALGIA; DIABETIC NEUROPATHY; PERIPHERAL-NERVE; IMMUNE CELLS; TRP CHANNEL AB It is useful for dermatologists to know about the innervation of the skin because dysfunction of cutaneous neurons can cause symptoms-such as itching, pain, and paresthesias-that are evaluated by dermatologists. We review the innervation of the skin and update readers about recent neuroscientific discoveries. C1 Massachusetts Gen Hosp, Dept Anesthesiol, Nerve Injury Unit, Boston, MA 02114 USA. Massachusetts Gen Hosp, Dept Neurol, Nerve Injury Unit, Boston, MA 02114 USA. Massachusetts Gen Hosp, Dept Neuropathol, Nerve Injury Unit, Boston, MA 02114 USA. RP Oaklander, AL (reprint author), Massachusetts Gen Hosp, Dept Anesthesiol, Nerve Injury Unit, 55 Fuit St,Clin 3, Boston, MA 02114 USA. EM aoaklander@partners.org FU NINDS NIH HHS [R01NS42866] NR 100 TC 23 Z9 25 U1 1 U2 5 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 2005 VL 53 IS 6 BP 1027 EP 1037 DI 10.1016/j.jaad.2005.08.049 PG 11 WC Dermatology SC Dermatology GA 990PQ UT WOS:000233756100012 PM 16310064 ER PT J AU Raffetto, JD Montgomery, JE Eberhardt, RT LaMorte, WW Menzoian, JO AF Raffetto, JD Montgomery, JE Eberhardt, RT LaMorte, WW Menzoian, JO TI Differences on risk factors for lower extremity arterial occlusive disease SO JOURNAL OF THE AMERICAN COLLEGE OF SURGEONS LA English DT Article ID STAGE RENAL-DISEASE; CARDIOVASCULAR-DISEASE; ENDOTHELIAL FUNCTION; REVASCULARIZATION; ARTERIOSCLEROSIS AB BACKGROUND: Patients undergoing lower extremity revascularization have associated cardiovascular risks: smoking, hypertension, dyslipidemia, and diabetes. This study evaluated the impact of cardiovascular risk factors on proximal versus distal arterial occlusive disease in patients undergoing lower extremity revascularization as adjusted to a control group without vascular disease. STUDY DESIGN: We performed a retrospective, case-control study that included 151 patients undergoing lower extremity revascularization and 229 patients undergoing knee and hip replacement (controls). Risk factors were determined for each of three separate groups undergoing revascularization for different levels of occlusive disease: aortoiliac, superficial femoral, and popliteal-tibial. Comparisons to controls were tested using t-tests or chi-square tests and multiple logistic regression. RESULTS: Dyslipidemia was associated with a significant risk of aortoiliac (odds ratio [OR] = 3.4; p = 0.0006) and superficial femoral occlusion (OR = 2.8; p = 0.01) but was less strongly associated with popliteal-tibial Occlusion (OR = 2.1; p = 0.09). Smoking was strongly associated with aortoiliac (OR = 4.5; p = 0.004) and superficial femoral disease (OR = 4.6; p = 0.0007) but not popliteal-tibial disease (OR = 1.3; p = 0.53). In contrast, diabetes mellitus and chronic renal insufficiency were strong risk factors for popliteal-tibial occlusion (OR = 5.4, p = 0.0002; OR = 3.9, p = 0.01, respectively), but were not significant risk factors for aortoiliac or superficial femoral occlusion. CONCLUSIONS: These data, which use revascularization level as a surrogate marker for lower extremity arterial disease, suggest that the risk factor profile for proximal disease differs from that of distal disease. These findings may reflect differences in the biology of disease and indicate that different risk factors have various anatomic influences on arterial disease formation. C1 VA Boston Healthcare Syst, Dept Surg, W Roxbury, MA 02132 USA. RP Raffetto, JD (reprint author), VA Boston Healthcare Syst, Dept Surg, 112,1400 VFW Pkwy, W Roxbury, MA 02132 USA. NR 24 TC 3 Z9 4 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 1072-7515 J9 J AM COLL SURGEONS JI J. Am. Coll. Surg. PD DEC PY 2005 VL 201 IS 6 BP 918 EP 924 DI 10.1016/j.jamcollsurg.2005.07.004 PG 7 WC Surgery SC Surgery GA 990IV UT WOS:000233737300013 PM 16310696 ER PT J AU Ganz, DA Higashi, T Rubenstein, LZ AF Ganz, DA Higashi, T Rubenstein, LZ TI Monitoring falls in cohort studies of community-dwelling older people: Effect of the recall interval SO JOURNAL OF THE AMERICAN GERIATRICS SOCIETY LA English DT Article DE mental recall; falls; systematic review; bias; reproducibility of results ID RISK-FACTORS; EPIDEMIOLOGY AB OBJECTIVES: To determine whether the interval over which patients are asked to remember their falls affects fall reporting. DESIGN: Systematic literature review. SETTING: Community. PARTICIPANTS: Individuals being monitored for falls in prospective studies that asked participants to recall falls over varying intervals. MEASUREMENTS: Sensitivity and specificity of retrospective recall compared with a criterion-standard prospective assessment using some form of ongoing fall monitoring. RESULTS: Six studies met the inclusion criteria. Recall of falls in the previous year was specific (specificity 91-95%) but less sensitive (sensitivity 80-89%) than the criterion standard of ongoing prospective collection of fall data using fall calendars or postcards. Patients with injurious falls were more likely to recall their falls. Lower Mini-Mental State Examination score was associated with poorer recall of falls in the one study addressing this issue. CONCLUSION: Whenever accurate data on all falls are critical, such as with interventions to decrease the rate of falls, researchers should gather information on falls every week or every month from study participants. The optimal method of fall monitoring-postcard, calendar, diary, telephone, or some combination of these-remains unknown. C1 Robert Wood Johnson Clin Scholars Program, Los Angeles, CA 90024 USA. Vet Affairs Greater Los Angeles Hlth Care Syst, Los Angeles, CA USA. Univ Calif Los Angeles, Mulicampus Program Geriatr Med & Gerontol, Los Angeles, CA USA. Univ Calif Los Angeles, Specialty Training & Adv Res Program, Los Angeles, CA USA. Kyoto Univ, Dept Epidemiol & Hlth Care Res, Kyoto, Japan. RP Ganz, DA (reprint author), Robert Wood Johnson Clin Scholars Program, 911 Broxton Pl,3rd Floor, Los Angeles, CA 90024 USA. EM dganz@mednet.ucla.edu NR 13 TC 171 Z9 174 U1 1 U2 6 PU BLACKWELL PUBLISHING PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DQ, OXON, ENGLAND SN 0002-8614 J9 J AM GERIATR SOC JI J. Am. Geriatr. Soc. PD DEC PY 2005 VL 53 IS 12 BP 2190 EP 2194 DI 10.1111/j.1532-5415.2005.00509.x PG 5 WC Geriatrics & Gerontology; Gerontology SC Geriatrics & Gerontology GA 987PL UT WOS:000233529700022 PM 16398908 ER PT J AU Moody-Ayers, SY Stewart, AL Covinsky, KE Inouye, SK AF Moody-Ayers, SY Stewart, AL Covinsky, KE Inouye, SK TI Prevalence and correlates of perceived societal racism in older African-American adults with type 2 diabetes mellitus SO JOURNAL OF THE AMERICAN GERIATRICS SOCIETY LA English DT Article DE perceived racism; racial or ethnic bias; discrimination; diabetes mellitus; African American ID SELF-RATED HEALTH; WHITE ADULTS; DISCRIMINATION; MORTALITY; PERCEPTIONS; COMMUNITY; RACE AB Although experiences of racism in day-to-day life may affect minority patients' interaction with the health system and may influence health outcomes, little is known about these experiences in patients with chronic diseases. The goal of this study was to explore the frequency and correlates of perceived societal racism in 42 African Americans aged 50 and older with type 2 diabetes mellitus. Twenty-seven items of the McNeilly Perceived Racism Scale were used to assess exposure to racist incidents in employment and public domains and emotional and coping responses to perceived racism in general. Mean age was 62, 71% were women, and more than half rated their health as fair/poor (55%). Overall, 95.2% of the participants reported at least some exposure to perceived societal racism. Higher mean lifetime exposure to societal racism, based on summary scores on the perceived racism scale, was reported by men (35.0 +/- 19.1) than women (19.7 +/- 14.4) (P <.01) and by those with higher household income (30.7 +/- 17.3) than those with lower household income (18.6 +/- 15.1) (P <.05). Greater passive coping (e.g., "avoiding it," "ignoring it") was associated with being female and having lower household income and fair/poor self-rated health. The findings that perception of racism and a range of emotional and coping responses were common in older African-American patients attending two diabetes clinics suggest that physicians and other healthcare providers may need to be more aware of patients' day-to-day experiences of societal racism and the influence these experiences may have on patient trust in the medical system and their adherence to medical advice or engagement in self-management of their chronic conditions. C1 San Francisco VA Med Ctr, San Francisco, CA 94121 USA. Univ Calif San Francisco, Dept Med, Div Geriatr, Inst Hlth & Aging, San Francisco, CA 94143 USA. Univ Calif San Francisco, Ctr Aging Diverse Communities, Med Effectiveness Res Ctr Diverse Populat, Inst Hlth & Aging, San Francisco, CA 94143 USA. Yale Univ, Sch Med, Dept Med, New Haven, CT USA. RP Moody-Ayers, SY (reprint author), San Francisco VA Med Ctr, 4150 Clement St, San Francisco, CA 94121 USA. EM sandra.moody@med.va.gov FU AHRQ HHS [K02HS000006-01]; NIA NIH HHS [R01AG12551, 1R01AG019827-01, K24AG00949, P30-AG15272, P30AG21342] NR 29 TC 35 Z9 35 U1 0 U2 4 PU BLACKWELL PUBLISHING PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DQ, OXON, ENGLAND SN 0002-8614 J9 J AM GERIATR SOC JI J. Am. Geriatr. Soc. PD DEC PY 2005 VL 53 IS 12 BP 2202 EP 2208 DI 10.1111/J.1532-5415.2005.00501.x PG 7 WC Geriatrics & Gerontology; Gerontology SC Geriatrics & Gerontology GA 987PL UT WOS:000233529700024 PM 16398910 ER PT J AU Lang, RM Bierig, M Devereux, RB Flachskampf, FA Foster, E Pellikka, PA Picard, MH Roman, MJ Seward, J Shanewise, JS Solomon, SD Spencer, KT Sutton, MS Stewart, WJ AF Lang, RM Bierig, M Devereux, RB Flachskampf, FA Foster, E Pellikka, PA Picard, MH Roman, MJ Seward, J Shanewise, JS Solomon, SD Spencer, KT Sutton, MS Stewart, WJ CA Chamber Quantification Writing Grp TI Recommendations for chamber quantification: A report from the American Society of Echocardiography's guidelines and standards committee and the chamber quantification writing group, developed in conjunction with the European Association of Echocardiography, a branch of the European Society of Cardiology SO JOURNAL OF THE AMERICAN SOCIETY OF ECHOCARDIOGRAPHY LA English DT Review ID LEFT ATRIAL VOLUME; TWO-DIMENSIONAL ECHOCARDIOGRAPHY; LEFT-VENTRICULAR MASS; ACUTE MYOCARDIAL-INFARCTION; INFERIOR VENA-CAVA; CROSS-SECTIONAL ECHOCARDIOGRAPHY; IN-VIVO VALIDATION; TIME 3-DIMENSIONAL ECHOCARDIOGRAPHY; CINE-COMPUTED-TOMOGRAPHY; NORMAL ADULT-POPULATION C1 Univ Chicago Hosp, Chicago, IL 60637 USA. St Louis Univ, Hlth Sci Ctr, St Louis, MO 63103 USA. Cornell Univ, Weill Med Coll, New York, NY USA. Univ Erlangen Nurnberg, Erlangen, Germany. Univ Calif San Francisco, San Francisco, CA 94143 USA. Mayo Clin Rochester, Rochester, MN USA. Massachusetts Gen Hosp, Boston, MA 02114 USA. Columbia Univ, New York, NY USA. Bringham & Womens Univ, Boston, MA USA. Univ Penn, Philadelphia, PA 19104 USA. Cleveland Clin Fdn, Cleveland, OH 44195 USA. RP Lang, RM (reprint author), Amer Soc Echocardiog, 1500 Sunday Dr,Suite 102, Raleigh, NC 27607 USA. RI Solomon, Scott/I-5789-2013 NR 140 TC 6228 Z9 6420 U1 18 U2 114 PU MOSBY, INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 USA SN 0894-7317 J9 J AM SOC ECHOCARDIOG JI J. Am. Soc. Echocardiogr. PD DEC PY 2005 VL 18 IS 12 BP 1440 EP 1463 DI 10.1016/j.echo.2005.10.005 PG 24 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA 997QI UT WOS:000234261300033 PM 16376782 ER PT J AU Seliger, SL Longstreth, WT Katz, R Manolio, T Fried, LF Shlipak, M Stehman-Breen, CO Newman, A Sarnak, M Gillen, DL Bleyer, A Siscovick, DS AF Seliger, SL Longstreth, WT Katz, R Manolio, T Fried, LF Shlipak, M Stehman-Breen, CO Newman, A Sarnak, M Gillen, DL Bleyer, A Siscovick, DS TI Cystatin C and subclinical brain infarction SO JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY LA English DT Article; Proceedings Paper CT 37th Annual Meeting of the American-Society-of-Nephrology CY OCT 27-NOV 01, 2004 CL St Louis, MO SP Amer Soc Nephrol ID STAGE RENAL-DISEASE; CARDIOVASCULAR-HEALTH; SERUM CREATININE; ELDERLY-PEOPLE; ROTTERDAM SCAN; OLDER-ADULTS; RISK; STROKE; ATHEROSCLEROSIS; INSUFFICIENCY AB Subclinical brain infarcts (SBI) are common in the elderly and are associated with covert neurologic and cognitive impairment. Although renal impairment is associated with accelerated cerebrovascular disease and an increased risk for clinically apparent brain infarct, few studies have examined the relationship between renal function and SBI, and these m ay have been limited by the inaccuracy of creatinine as a renal function marker. A cross-sectional study was performed among older adults in the Cardiovascular Health Study to examine associations between SBI and two serum markers of renal function: Serum creatinine (SCr) and cystatin C (CysC). Patients had cranial magnetic resonance imaging and renal markers measured in 1992 to 1993. Logistic regression was used to estimate the associations between renal function (estimated by 1/SCr and 1/CysC) and SBI, controlling for potential confounding factors. SBI were present in 789 (28.7%) of 2784 participants. A linear association with SBI was observed for 1/CysC (per 1-SD decrement; odds ratio [OR] 1.20; 95% confidence interval [CI] 1.09 to 1.32; P < 0.001) but not for 1/SCr (OR 1.08; 95% CI 0.98 to 1.19; P = 0.14), for which a quadratic U-shaped association was;suggested (P = 0.004). In a model with both markers, 1/CysC was linearly associated with SBI (OR 1.26; P < 0.001), whereas 1/SCr was not (OR 1.06; P = 0.3). The prevalence of SBI was directly associated with quintile of CysC, whereas the association 'between SCr and SBI was U-shaped, with greater prevalence at high and low levels. Compared with creatinine, CysC, a novel marker of renal function, has a stronger and more direct association with SBI in the elderly. C1 Univ Maryland, Div Nephrol, Baltimore, MD 21201 USA. Univ Washington, Dept Neurol, Seattle, WA 98195 USA. Univ Washington, Dept Biostat, Seattle, WA 98195 USA. Univ Washington, Dept Epidemiol & Med, Seattle, WA 98195 USA. NHLBI, Div Epidemiol & Clin Applicat, Bethesda, MD 20892 USA. Pittsburgh VA Med Ctr, Div Nephrol, Pittsburgh, PA USA. San Francisco VA Med Ctr, Div Gen Internal Med, San Francisco, CA USA. Amgen Inc, Thousand Oaks, CA 91320 USA. Univ Pittsburgh, Grad Sch Publ Hlth, Dept Epidemiol, Pittsburgh, PA USA. Tufts Univ New England Med Ctr, Div Nephrol, Boston, MA 02111 USA. Univ Chicago, Dept Hlth Studies, Chicago, IL 60637 USA. Wake Forest Univ, Div Nephrol, Winston Salem, NC 27109 USA. RP Seliger, SL (reprint author), Univ Maryland, Div Nephrol, N3W143,22 S Greene St, Baltimore, MD 21201 USA. EM sseliger@medicine.umaryland.edu RI Newman, Anne/C-6408-2013 OI Newman, Anne/0000-0002-0106-1150 FU NHLBI NIH HHS [N01-HC-15103, N01-HC-35129, N01-HC-85079, N01-HC-85086]; NIDDK NIH HHS [K23-DK063079] NR 31 TC 83 Z9 96 U1 1 U2 5 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3261 USA SN 1046-6673 J9 J AM SOC NEPHROL JI J. Am. Soc. Nephrol. PD DEC PY 2005 VL 16 IS 12 BP 3721 EP 3727 DI 10.1681/ASN.2005010006 PG 7 WC Urology & Nephrology SC Urology & Nephrology GA 992ON UT WOS:000233893600033 PM 16236809 ER PT J AU Fried, LF Katz, R Sarnak, MJ Shlipak, MG Chaves, PHM Jenny, NS Stehman-Breen, C Gillen, D Bleyer, AJ Hirsch, C Siscovick, D Newman, AB AF Fried, LF Katz, R Sarnak, MJ Shlipak, MG Chaves, PHM Jenny, NS Stehman-Breen, C Gillen, D Bleyer, AJ Hirsch, C Siscovick, D Newman, AB TI Kidney function as a predictor of noncardiovascular mortality SO JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY LA English DT Article ID SERUM CYSTATIN-C; GLOMERULAR-FILTRATION-RATE; CARDIOVASCULAR-DISEASE RISK; CHRONIC RENAL-INSUFFICIENCY; ELDERLY PERSONS; US ADULTS; MARKER; CREATININE; HEALTH; DEATH AB Chronic kidney disease is associated with a higher risk for cardiovascular mortality, as well as all-cause mortality. Whether chronic kidney disease is a predictor of noncardiovascular mortality is less clear. To further explore the latter, the association of kidney function with total noncardiovascular mortality and cause-specific mortality was assessed in the Cardiovascular Health Study, a community-based cohort of older individuals. Kidney disease was assessed using cystatin C and estimated GFR in 4637 participants in 1992 to 1993. Participants were followed until June 30, 2001. Deaths were adjudicated as cardiovascular or noncardiovascular disease by committee, and an underlying cause of death was assigned. The associations of kidney function with total noncardiovascular mortality and cause-specific mortality were analyzed by proportional hazards regression. Noncardiovascular mortality rates increased with higher cystatin C quartiles (16.8, 17.1, 21.6, and 50.0 per 1000 person-years). The association of cystatin C with noncardiovascular mortality persisted after adjustment for demographic factors; the presence of diabetes, C-reactive protein, hemoglobin, and prevalent cardiovascular disease; and measures of atherosclerosis (hazard ratio 1.69; 95% confidence interval 1.33 to 2.15, for the fourth quartile versus the first quartile). Results for estimated GFR were similar. The risk for noncardiac deaths attributed to pulmonary disease, infection, cancer, and other causes was similarly associated with cystatin C levels. Kidney function predicts noncardiovascular mortality from multiple causes in the elderly. Further research is needed to understand the mechanisms and evaluate interventions to reduce the high mortality rate in chronic kidney disease. C1 VA Pittsburgh Healthcare Syst, Pittsburgh, PA 15240 USA. Univ Pittsburgh, Sch Med, Div Renal & Electrolyte, Pittsburgh, PA 15240 USA. Univ Washington, Collaborat Hlth Studies Coordinating Ctr, Seattle, WA 98195 USA. Tufts Univ, New England Med Ctr, Dept Med, Div Nephrol, Boston, MA 02111 USA. Vet Affairs Med Ctr, Gen Internal Med Sect, San Francisco, CA USA. Univ Calif San Francisco, Dept Med, San Francisco, CA 94143 USA. Univ Calif San Francisco, Dept Epidemiol, San Francisco, CA 94143 USA. Univ Calif San Francisco, Dept Biostat, San Francisco, CA 94143 USA. Johns Hopkins Univ, Dept Med, Baltimore, MD USA. Johns Hopkins Univ, Dept Epidemiol, Baltimore, MD USA. Univ Vermont, Dept Pathol, Coll Med, Burlington, VT USA. Amgen Inc, Thousand Oaks, CA 91320 USA. Univ Calif Irvine, Dept Stat, Irvine, CA USA. Wake Forest Univ, Sch Med, Nephrol Sect, Winston Salem, NC 27109 USA. Univ Calif Davis, Med Ctr, Dept Med, Sacramento, CA 95817 USA. Univ Calif Davis, Med Ctr, Dept Publ Hlth Sci, Sacramento, CA 95817 USA. Univ Washington, Dept Med Epidemiol & Hlth Serv, Seattle, WA 98195 USA. Univ Pittsburgh, Sch Med, Div Geriatr Med, Pittsburgh, PA USA. Univ Pittsburgh, Grad Sch Publ Hlth, Dept Epidemiol, Pittsburgh, PA USA. RP Fried, LF (reprint author), VA Pittsburgh Healthcare Syst, 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-15103, N01-HC-35129, N01-HC-85079, N01-HC-85086] NR 40 TC 175 Z9 178 U1 1 U2 3 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3261 USA SN 1046-6673 J9 J AM SOC NEPHROL JI J. Am. Soc. Nephrol. PD DEC PY 2005 VL 16 IS 12 BP 3728 EP 3735 DI 10.1681/ASN.2005040384 PG 8 WC Urology & Nephrology SC Urology & Nephrology GA 992ON UT WOS:000233893600034 PM 16251239 ER PT J AU Jang, IK Pettigrew, V Picard, MH Kowey, PR Demmel, V Zile, MR Tatsuno, J Wackers, FJT Hibberd, M AF Jang, IK Pettigrew, V Picard, MH Kowey, PR Demmel, V Zile, MR Tatsuno, J Wackers, FJT Hibberd, M TI A randomized, double-blind, placebo-controlled study of the safety and efficacy of intravenous MCC-135 as an adjunct to primary percutaneous coronary intervention in patients with acute myocardial infarction: Rationale and design of the Evaluation of MCC-135 for Left Ventricular Salvage in Acute MI (EVOLVE) study SO JOURNAL OF THROMBOSIS AND THROMBOLYSIS LA English DT Article DE left ventricular function; percutaneous coronary intervention; single photon emission computed tomography; ST elevation myocardial infarction ID GLYCOPROTEIN-IIB/IIIA BLOCKADE; ANTI-C5 COMPLEMENT ANTIBODY; CONTROLLED-TRIAL; THROMBOLYTIC THERAPY; PRIMARY ANGIOPLASTY; INHIBITION; REPERFUSION; COMPLICATIONS; PEXELIZUMAB; MULTICENTER AB As a consequence of acute ischemia and reperfusion in patients with acute ST elevation myocardial infarction, calcium overload inside myocytes not only affects myocardial contraction, relaxation, and myocyte recovery following reperfusion, but also may be related to myocyte necrosis and fatal arrhythmia. MCC-135 is the first in a new class of agents that reduce intracellular calcium overload. Pre-clinical and early clinical studies yielded promising results for patients with ST elevation myocardial infarction. The Evaluation of MCC-135 for Left Ventricular Salvage in Acute MI (EVOLVE) study is a Phase 2a, multicenter, randomized, double-blind, placebo-controlled clinical trial of 2 new doses of MCC-135 (4.5 mg/kg/48 hours and 9.0 mg/kg/48 hours) as adjunct therapy for preservation of left ventricular function and reduction of infarct size in patients undergoing primary percutaneous coronary intervention (PCI) for electrocardiographically moderate-large ST elevation myocardial infarction. The primary endpoint will be left ventricular ejection fraction on Day 5 post myocardial infarction as determined by single photon emission computed tomography (SPECT). Secondary endpoints will include SPECT and echocardiographic assessments, serum cardiac markers, clinical outcomes, and safety measures at specific time points through Day 30 post myocardial infarction. Follow-up clinical and safety assessments will be continued until Day 180. The rationale, design, and methods of the EVOLVE study are described in this paper, along with 2 sub-studies, involving a comparison of pre- and post-PCI measurements with either SPECT or echocardiography, to examine myocardial salvage and the time course of changes in myocardial infarction size and left ventricular function. C1 Massachusetts Gen Hosp, Div Cardiol, Boston, MA 02114 USA. Harvard Univ, Sch Med, Boston, MA USA. Mitsubishi Pharma Amer Inc, Warren, NJ USA. Main Line Hlth Heart Ctr, Wynnewood, PA USA. Nabios, Munich, Germany. Med Univ S Carolina, Charleston, SC 29425 USA. RHJ Dept Vet Affairs Med Ctr, Charleston, SC USA. Mitsubishi Pharma Corp, Osaka, Japan. Yale Univ, Yale Univ Radionuclide CORE Lab, New Haven, CT USA. Cardiocorp Cardiovasc Clin Res, Lexington, MA USA. RP Jang, IK (reprint author), Massachusetts Gen Hosp, Div Cardiol, Gray Bigelow 800,55 Fruit St, Boston, MA 02114 USA. EM ijang@partners.org NR 26 TC 8 Z9 8 U1 0 U2 1 PU SPRINGER PI DORDRECHT PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS SN 0929-5305 J9 J THROMB THROMBOLYS JI J. Thromb. Thrombolysis PD DEC PY 2005 VL 20 IS 3 BP 147 EP 153 DI 10.1007/s11239-005-3267-4 PG 7 WC Hematology; Peripheral Vascular Disease SC Hematology; Cardiovascular System & Cardiology GA 980AO UT WOS:000232986500001 PM 16261287 ER PT J AU Velmahos, GC AF Velmahos, GC TI Abdominal insufflation decreases blood loss and mortality after porcine liver injury - 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 Velmahos, GC (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 1079-6061 J9 J TRAUMA JI J. Trauma-Injury Infect. Crit. Care PD DEC PY 2005 VL 59 IS 6 BP 1308 EP 1308 PG 1 WC Critical Care Medicine; Surgery SC General & Internal Medicine; Surgery GA 001DP UT WOS:000234514100007 ER PT J AU Sheridan, RL AF Sheridan, RL TI Determinants of quality of life and role-related disability after injury: Impact of acute psychological responses - Editorial comments SO JOURNAL OF TRAUMA-INJURY INFECTION AND CRITICAL CARE LA English DT Editorial Material ID CHILDREN; BURNS C1 Massachusetts Gen Hosp, Boston, MA 02114 USA. RP Sheridan, RL (reprint author), Massachusetts Gen Hosp, Boston, MA 02114 USA. NR 3 TC 0 Z9 0 U1 3 U2 5 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 1079-6061 J9 J TRAUMA JI J. Trauma-Injury Infect. Crit. Care PD DEC PY 2005 VL 59 IS 6 BP 1334 EP 1335 PG 2 WC Critical Care Medicine; Surgery SC General & Internal Medicine; Surgery GA 001DP UT WOS:000234514100013 ER PT J AU Kapur, GB Hutson, HR Davis, MA Rice, PL AF Kapur, GB Hutson, HR Davis, MA Rice, PL TI The United States twenty-year experience with bombing incidents: Implications for terrorism preparedness and medical response SO JOURNAL OF TRAUMA-INJURY INFECTION AND CRITICAL CARE LA English DT Article DE trauma; emergency medicine; prehospital care; emergency medical services; terrorism; blast injury; bombings; violence prevention; public health ID LARGE IMPROVISED BOMBS; AMMONIUM NITRATE/SUGAR; BLAST INJURIES; MANAGEMENT; HEALTH; EXPLOSIONS; CASUALTIES; FIRINGS; THREAT AB Background: Terrorist bombings remain a significant threat in the United States. However, minimal longitudinal data exists regarding the medical and public health impact because of bombings. Methods: We conducted a retrospective analysis of the number of incidents, injuries, and deaths because of explosive, incendiary, premature, and attempted bombings from January 1983 to December 2002. Morbidity and mortality by motives, target locations, and materials used were evaluated. Results: In the United States, 36,110 bombing incidents, 5,931 injuries, and 699 deaths were reported. There were 21,237 (58.8%) explosive bombings, 6,185 (17.1%) incendiary bombings, 1,107 (3.1%) premature bombings, and 7,581 (21.0%) attempted bombings. For explosive bombings with known motives, 72.9% of injuries and 73.8% of deaths were because of homicide. For incendiary bombings with known motives, 68.2% of injuries were because of extortion and revenge, and 53.5% of deaths were due to homicide. Private residences accounted for 29.0% of incidents, 31.5% of injuries, and 55.5% of deaths. Government installations accounted for 4.4% of incidents but were the site of 12.7% of injuries and 25.5% of deaths. In bombings with known materials, nitrate-based fertilizers accounted for 36.2% of injuries and 30.4% of deaths, and smokeless powder and black powder accounted for 33.2% of injuries and 27.1% of deaths. Conclusions: Illegal bombings and related injuries commonly occur in the United States. Because of the easy availability of bombing materials, government agencies and healthcare providers should prepare for potential mass-casualty bombings. C1 Brigham & Womens Hosp, Inst Int Emergency Med & Hlth, Boston, MA 02115 USA. Brigham & Womens Hosp, Dept Emergency Med, Boston, MA 02115 USA. Harvard Univ, Sch Med, Massachusetts Gen Hosp, Dept Emergency Med, Boston, MA USA. RP Kapur, GB (reprint author), George Washington Univ, 2150 Penn Ave NW,Suite 2B-417, Washington, DC 20037 USA. EM kapur@gwu.edu NR 41 TC 23 Z9 23 U1 2 U2 14 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 1079-6061 J9 J TRAUMA JI J. Trauma-Injury Infect. Crit. Care PD DEC PY 2005 VL 59 IS 6 BP 1436 EP 1444 DI 10.1097/01.ta.0000197853.49084.3c PG 9 WC Critical Care Medicine; Surgery SC General & Internal Medicine; Surgery GA 001DP UT WOS:000234514100036 PM 16394919 ER PT J AU Sheridan, RL AF Sheridan, RL TI Photoacoustic diagnosis of burns in rats - 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 Sheridan, RL (reprint author), Massachusetts Gen Hosp, Boston, MA 02114 USA. NR 3 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 1079-6061 J9 J TRAUMA JI J. Trauma-Injury Infect. Crit. Care PD DEC PY 2005 VL 59 IS 6 BP 1455 EP 1456 PG 2 WC Critical Care Medicine; Surgery SC General & Internal Medicine; Surgery GA 001DP UT WOS:000234514100039 ER PT J AU Hinton, DE Chhean, D Pich, V Safren, SA Hofmann, SG Pollack, MH AF Hinton, DE Chhean, D Pich, V Safren, SA Hofmann, SG Pollack, MH TI A Randomized controlled trial of cognitive-behavior therapy for Cambodian refugees with treatment-resistant PTSD and panic attacks: A cross-over design SO JOURNAL OF TRAUMATIC STRESS LA English DT Article ID POSTTRAUMATIC-STRESS-DISORDER; GENERALIZED ANXIETY DISORDER; SOUTHEAST-ASIAN REFUGEES; APPLIED RELAXATION; EXPOSURE THERAPY; EMOTIONAL DISORDERS; VIETNAMESE REFUGEES; INTRUSIVE MEMORIES; TRAUMA; METAANALYSIS AB We examined the therapeutic efficacy of a culturally adapted cognitive-behavior therapy for Cambodian refugees with treatment-resistant posttraumatic stress disorder (PTSD) and comordid panic attacks. We used a cross-over design, with 20 patients in the initial treatment (IT) condition and 20 in delayed treatment (DT). Repeated measures MANOVA, Group & times; Time ANOVAs, and planned contrasts indicated significantly greater improvement in the IT condition, with large effect sizes (Cohen's d) for all outcome measures: Anxiety Sensitivity Index (d = 3.78), Clinician-Administered PTSD Scale (d = 2.17), and Symptom Checklist 90-R subscales (d = 2.77). Likewise, the severity of (culturally related) neck-focused and orthostasis-cued panic attacks, including flashbacks associated with these subtypes, improved across treatment. C1 Massachusetts Gen Hosp, Dept Psychiat, Boston, MA 02114 USA. Harvard Univ, Sch Med, Cambridge, England. Arbour Counseling Serv, SE Asian Clin, Lowell, MA USA. Boston Univ, Ctr Anxiety Disorders, Boston, MA 02215 USA. RP Hinton, DE (reprint author), Massachusetts Gen Hosp, Dept Psychiat, 15 Parkman St,WACC 812, Boston, MA 02114 USA. EM devon_hinton@hms.harvard.edu RI Hofmann, Stefan/B-8769-2014 OI Hofmann, Stefan/0000-0002-3548-9681 NR 80 TC 107 Z9 111 U1 7 U2 19 PU JOHN WILEY & SONS INC PI HOBOKEN PA 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 0894-9867 J9 J TRAUMA STRESS JI J. Trauma Stress PD DEC PY 2005 VL 18 IS 6 BP 617 EP 629 DI 10.1002/jts.20070 PG 13 WC Psychology, Clinical; Psychiatry SC Psychology; Psychiatry GA 001KV UT WOS:000234532900004 PM 16382423 ER PT J AU Benacerraf, BR Benson, CB Abuhamad, AZ Copel, JA Abramowicz, JS DeVore, GR Doubilet, PM Lee, W Lev-Toaff, AS Merz, E Nelson, TR O'Neill, MJ Parsons, AK Platt, LD Pretorius, DH Timor-Tritsch, IE AF Benacerraf, BR Benson, CB Abuhamad, AZ Copel, JA Abramowicz, JS DeVore, GR Doubilet, PM Lee, W Lev-Toaff, AS Merz, E Nelson, TR O'Neill, MJ Parsons, AK Platt, LD Pretorius, DH Timor-Tritsch, IE TI Three- and 4-dimensional ultrasound in obstetrics and gynecology - Proceedings of the American Institute of Ultrasound in Medicine Consensus Conference SO JOURNAL OF ULTRASOUND IN MEDICINE LA English DT Article DE fetal ultrasound; gynecologic ultrasound; obstetric ultrasound; 3-dimensional ultrasound; ultrasound technology ID SPATIOTEMPORAL IMAGE CORRELATION; FETAL LUNG-VOLUME; CONGENITAL UTERINE ANOMALIES; COMPLEX ADNEXAL MASSES; POWER-DOPPLER; TRANSVAGINAL ULTRASOUND; PRENATAL-DIAGNOSIS; SONOGRAPHIC ASSESSMENT; CLINICAL-APPLICATIONS; OVARIAN-CANCER AB The American Institute of Ultrasound in Medicine convened a panel of physicians and scientists with interest and expertise in 3-dimensional (3D) ultrasound in obstetrics and gynecology to discuss the current diagnostic benefits and technical limitations in obstetrics and gynecology and consider the utility and role of this type of imaging in clinical practice now and in the future. This conference was held in Orlando, Florida, June 16 and 17, 2005. Discussions considered state-of-the-art applications of 3D ultrasound, specific clinical situations in which it has been found to be helpful, the role of 3D volume acquisition for improving diagnostic efficiency and patient throughput, and recommendations for future investigations related to the utility of volume sonography in obstetrics and gynecology. C1 Harvard Univ, Sch Med, Brigham & Womens Hosp, Dept Radiol, Boston, MA 02115 USA. Harvard Univ, Sch Med, Brigham & Womens Hosp, Dept Obstet & Gynecol, Boston, MA 02115 USA. Eastern Virginia Med Sch, Dept Obstet & Gynecol, Norfolk, VA 23501 USA. Yale Univ, Sch Med, Dept Obstet Gynecol & Reprod Sci, New Haven, CT USA. Rush Univ, Dept Obstet & Gynecol, Chicago, IL 60612 USA. Fetal Diagnost Ctr, Pasadena, CA USA. William Beaumont Hosp, Dept Obstet & Gynecol, Royal Oak, MI 48072 USA. Thomas Jefferson Univ, Ctr Med, Dept Radiol, Philadelphia, PA 19107 USA. Krankenhaus Nordw, Dept Obstet & Gynecol, Frankfurt, Germany. Univ Calif San Diego, Dept Radiol, San Diego, CA 92103 USA. Massachusetts Gen Hosp, Dept Radiol, Boston, MA 02114 USA. Univ S Florida, Dept Obstet & Gynecol, Tampa, FL 33620 USA. Ctr Fetal Med & Womens Ultrasound, Los Angeles, CA USA. NYU, Dept Obstet & Gynecol, New York, NY 10016 USA. RP Benacerraf, BR (reprint author), 333 Longwood Ave,Suite 400, Boston, MA 02115 USA. NR 83 TC 69 Z9 71 U1 0 U2 6 PU AMER INST ULTRASOUND MEDICINE PI LAUREL PA SUBSCRIPTION DEPT, 14750 SWEITZER LANE, STE 100, LAUREL, MD 20707-5906 USA SN 0278-4297 J9 J ULTRAS MED JI J. Ultrasound Med. PD DEC PY 2005 VL 24 IS 12 BP 1587 EP 1597 PG 11 WC Acoustics; Radiology, Nuclear Medicine & Medical Imaging SC Acoustics; Radiology, Nuclear Medicine & Medical Imaging GA 994XM UT WOS:000234064500001 PM 16301716 ER PT J AU McDougal, WS AF McDougal, WS TI Phallic preserving surgery in patients with invasive squamous cell carcinoma of the penis SO JOURNAL OF UROLOGY LA English DT Article DE penis; reconstructive procedures; surgical; carcinoma; squamous cell; neoplasm invasiveness ID FOLLOW-UP; SPREAD; CANCER; FLAP AB Purpose: Standard surgical methods to eradicate invasive squamous cell carcinoma of the penis often result in significant deformities. Wide local excision with skin grafting in select cases results in the preservation of normal phallic appearance and function. Materials and Methods: Seven patients with invasive squamous cell carcinoma of the penis were treated with wide excision and resurfaced by 1 of 3 methods, namely 1) a split-thickness graft, 2) a full-thickness graft or 3) shaft skin advancement. Results: At 1 to 5 years of followup there was 1 local recurrence proximal to the original resection site. Local excision of recurrence resulted in no evidence of disease at 2 years of followup following repeat excision. All other patients had no local recurrence. Conclusions: In select cases wide local excision with grafting or skin advancement results in a normal phallic appearance without jeopardizing cancer control. C1 Massachusetts Gen Hosp, Dept Urol, Boston, MA 02114 USA. Harvard Univ, Sch Med, Boston, MA USA. RP McDougal, WS (reprint author), Massachusetts Gen Hosp, Dept Urol, 55 Fruit St,GRB 1102, Boston, MA 02114 USA. EM wmcdougal@partners.org NR 9 TC 18 Z9 18 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3261 USA SN 0022-5347 J9 J UROLOGY JI J. Urol. PD DEC PY 2005 VL 174 IS 6 BP 2218 EP 2220 DI 10.1097/01.ju.0000181225.31468.82 PG 3 WC Urology & Nephrology SC Urology & Nephrology GA 984HN UT WOS:000233293700039 PM 16280767 ER PT J AU Vedantham, S Rundback, JH Comerota, AJ Hunter, DW Meissner, MH Hofmann, LV Horne, M Gloviczki, P Andrews, RT Fan, CM Hume, KM Goldhaber, SK Tapson, VF Razavi, MK Min, RJ AF Vedantham, S Rundback, JH Comerota, AJ Hunter, DW Meissner, MH Hofmann, LV Horne, M Gloviczki, P Andrews, RT Fan, CM Hume, KM Goldhaber, SK Tapson, VF Razavi, MK Min, RJ TI Development of a research agenda for endovascular treatment of venous thromboembolism: Proceedings from a multidisciplinary consensus panel SO JOURNAL OF VASCULAR AND INTERVENTIONAL RADIOLOGY LA English DT Article ID DEEP-VEIN THROMBOSIS; CATHETER-DIRECTED THROMBOLYSIS; QUALITY-OF-LIFE; LOWER-EXTREMITY; STREPTOKINASE; THERAPY; HEPARIN; DISEASE; TRIAL C1 Washington Univ, Dept Radiol, Mallinckrodt Inst Radiol, Sch Med, St Louis, MO 63110 USA. Cornell Univ, Dept Vasc & Intervent Radiol, Columbia Presbyterian Med Ctr, New York, NY USA. Cornell Univ, Dept Radiol, Weill Med Coll, New York, NY USA. Univ Michigan, Jobst Vasc Ctr, Toledo, OH USA. Univ Minnesota, Dept Radiol, Minneapolis, MN 55455 USA. Mayo Clin, Coll Med, Div Vasc Surg, Rochester, MN USA. Univ Washington, Sch Med, Seattle, WA 98195 USA. Univ Washington, Sch Med, Seattle, WA 98195 USA. Univ Washington, Dept Vasc & Intervent Radiol, Seattle, WA 98195 USA. Johns Hopkins Univ Hosp, Div Intervent Radiol, Baltimore, MD 21287 USA. NIH, Bethesda, MD 20892 USA. Massachusetts Gen Hosp, Dept Vasc Radiol, Boston, MA 02114 USA. Brigham & Womens Hosp, Div Cardiovasc, Boston, MA 02115 USA. Soc Intervent Radiol Fdn, Fairfax, VA USA. Duke Univ, Med Ctr, Dept Med, Durham, NC 27710 USA. St Joseph Vasc Inst, Orange, CA USA. RP Vedantham, S (reprint author), Washington Univ, Dept Radiol, Mallinckrodt Inst Radiol, Sch Med, 510 S Kingshighway Blvd, St Louis, MO 63110 USA. EM vedanthams@mir.wustl.edu NR 32 TC 5 Z9 5 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3261 USA SN 1051-0443 J9 J VASC INTERV RADIOL JI J. Vasc. Interv. Radiol. PD DEC PY 2005 VL 16 IS 12 BP 1567 EP 1573 PG 7 WC Radiology, Nuclear Medicine & Medical Imaging; Peripheral Vascular Disease SC Radiology, Nuclear Medicine & Medical Imaging; Cardiovascular System & Cardiology GA 997CE UT WOS:000234221800001 PM 16371519 ER PT J AU Vedantham, S Rundback, JH Khilnani, NM Gloviczki, P Andrews, RT Sadick, NS Fan, CM Meissner, MH Comerota, AJ Hume, KM Chrisman, HB Pavcnik, D Kaufman, JA Min, RJ AF Vedantham, S Rundback, JH Khilnani, NM Gloviczki, P Andrews, RT Sadick, NS Fan, CM Meissner, MH Comerota, AJ Hume, KM Chrisman, HB Pavcnik, D Kaufman, JA Min, RJ TI Development of a research agenda for endovenous treatment of lower-extremity venous reflux: Proceedings from a multidisciplinary consensus panel SO JOURNAL OF VASCULAR AND INTERVENTIONAL RADIOLOGY LA English DT Article ID RADIOFREQUENCY OBLITERATION CLOSURE; QUALITY-OF-LIFE; LASER TREATMENT; VARICOSE-VEINS; LIGATION; EVOLVES C1 Washington Univ, Sch Med, Mallinckrodt Inst Radiol, St Louis, MO 63110 USA. Cornell Univ, Dept Vasc & Intervent Radiol, Columbia Presbyterian Med Ctr, New York, NY USA. Cornell Univ, Dept Radiol, Weill Med Coll, New York, NY USA. Mayo Clin, Coll Med, Div Vasc Surg, Rochester, MN USA. Univ Washington, Dept Vasc & Intervent Radiol, Seattle, WA 98195 USA. Univ Washington, Seattle, WA 98195 USA. Massachusetts Gen Hosp, Dept Vasc Radiol, Boston, MA 02114 USA. Univ Michigan, Jobst Vasc Ctr, Toledo, OH USA. Soc Intervent Radiol Fdn, Fairfax, VA USA. Northwestern Univ, Sch Med, Dept Radiol, Chicago, IL 60611 USA. Oregon Hlth Sci Univ, Dotter Intervent Inst, Portland, OR 97201 USA. RP Vedantham, S (reprint author), Washington Univ, Sch Med, Mallinckrodt Inst Radiol, 510 S Kingshighway Blvd, St Louis, MO 63110 USA. EM vedanthams@mir.wustl.edu NR 13 TC 7 Z9 7 U1 0 U2 1 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3261 USA SN 1051-0443 J9 J VASC INTERV RADIOL JI J. Vasc. Interv. Radiol. PD DEC PY 2005 VL 16 IS 12 BP 1575 EP 1579 DI 10.1097/01.RVI.0000183869.53626.69 PG 5 WC Radiology, Nuclear Medicine & Medical Imaging; Peripheral Vascular Disease SC Radiology, Nuclear Medicine & Medical Imaging; Cardiovascular System & Cardiology GA 997CE UT WOS:000234221800002 PM 16371520 ER PT J AU Gould, LH Sui, JU Foellmer, H Oliphant, T Wang, T Ledizet, M Murakami, A Noonan, K Lambeth, C Kar, K Anderson, JF de Silva, AM Diamond, MS Koski, RA Marasco, WA Fikrig, E AF Gould, LH Sui, JU Foellmer, H Oliphant, T Wang, T Ledizet, M Murakami, A Noonan, K Lambeth, C Kar, K Anderson, JF de Silva, AM Diamond, MS Koski, RA Marasco, WA Fikrig, E TI Protective and therapeutic capacity of human single-chain Fv-Fc fusion proteins against West Nile virus SO JOURNAL OF VIROLOGY LA English DT Article ID RECOMBINANT ENVELOPE PROTEIN; ANTIBODY PROPHYLAXIS; TYPE-2 VIRUSES; DENGUE TYPE-1; ENCEPHALITIS; INFECTION; IMMUNOGLOBULIN; GLYCOPROTEIN; NEUTRALIZATION; IMMUNIZATION AB West Nile virus has spread rapidly across the United States, and there is currently no approved human vaccine or therapy to prevent or treat disease. Passive immunization with antibodies against the envelope protein represents a promising means to provide short-term prophylaxis and treatment for West Nile virus infection. In this study, we identified a panel of 11 unique human single-chain variable region antibody fragments (scFvs) that bind the envelope protein of West Nile virus. Selected scFvs were converted to Fc fusion proteins (scFv-Fcs) and were tested in mice for their ability to prevent lethal West Nile virus infection. Five of these scFv-Fcs, 11, 15, 71, 85, and 95, protected 100% of mice from death when given prior to infection with virus. Two of them, 11 and 15, protected 80% of mice when given at days 1 and 4 after infection. In addition, four of the scFv-Fcs cross-neutralized dengue virus, serotype 2. Binding assays using yeast surface display demonstrated that all of our scFvs bind to sites within domains I and II of West Nile virus envelope protein. These recombinant human scFvs are potential candidates for immunoprophylaxis and therapy of flavivirus infections. C1 Yale Univ, Sch Med, Dept Internal Med, Rheumatol Sect,Anlyan Ctr Med Res, New Haven, CT 06520 USA. Yale Univ, Sch Med, Dept Epidemiol & Publ Hlth, New Haven, CT 06520 USA. Dana Farber Canc Inst, Dept Canc Immunol & AIDS, Boston, MA 02115 USA. Washington Univ, Sch Med, Dept Mol Microbiol, St Louis, MO USA. L2 Diagnost, New Haven, CT USA. Univ N Carolina, Dept Microbiol & Immunol, Chapel Hill, NC USA. Connecticut Agr Expt Stn, New Haven, CT 06504 USA. RP Fikrig, E (reprint author), Yale Univ, Sch Med, Dept Internal Med, Rheumatol Sect,Anlyan Ctr Med Res, Room S525A,300 Cedar St, New Haven, CT 06520 USA. EM erol.fikrig@yale.edu OI SUI, JIANHUA/0000-0002-1272-9662 NR 32 TC 82 Z9 91 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 2005 VL 79 IS 23 BP 14606 EP 14613 DI 10.1128/JVI.79.23.14606-14613.2005 PG 8 WC Virology SC Virology GA 984CE UT WOS:000233279300015 PM 16282460 ER PT J AU Choi, WT Tian, SM Dong, CZ Kumar, S Liu, DX Madani, N An, J Sodroski, JG Huang, ZW AF Choi, WT Tian, SM Dong, CZ Kumar, S Liu, DX Madani, N An, J Sodroski, JG Huang, ZW TI Unique ligand binding sites on CXCR4 probed by a chemical biology approach: Implications for the design of selective human immunodeficiency virus type 1 inhibitors SO JOURNAL OF VIROLOGY LA English DT Article ID CHEMOKINE RECEPTOR CXCR4; CORECEPTOR ACTIVITY; HIV-1 CORECEPTOR; DOMAINS; ENTRY; INTERNALIZATION; LESTR/FUSIN; MUTAGENESIS; INFECTION; FUSION AB The chemokine receptor CXCR4 plays an important role as the receptor for the normal physiological function of stromal cell-derived factor 1 alpha (SDF-1 alpha) and the coreceptor for the entry of human immunodeficiency virus type 1 (HIV-1) into the cell. In a recent work (S. Tian et al., J. Virol. 79:12667-12673, 2005), we found that many residues throughout CXCR4 transmembrane (TM) and extracellular loop 2 domains are specifically involved in interaction with HIV-1 gp120, as most of these sites did not play a role in either SDF-1 alpha binding or signaling. These results provided direct experimental evidence for the distinct functional sites on CXCR4 for HIV-1 and the normal ligand SDF-1 alpha. To further understand the CXCR4-ligand interaction and to develop new CXCR4 inhibitors to block HIV-1 entry, we have recently generated a new family of unnatural chemokines, termed synthetically and modularly modified (SMM) chemokines, derived from the native sequence of SDF-1 alpha or viral macrophage inflammatory protein II (vMIP-II). These SMM chemokines contain various de novo-designed sequence replacements and substitutions by D-amino acids and display more enhanced CXCR4 selectivity, binding affinities, and/or anti-HIV activities than natural chemokines. Using these novel CXCR4-targeting SMM chemokines as receptor probes, we conducted ligand binding site mapping experiments on a panel of site-directed mutants of CXCR4. Here, we provide the first experimental evidence demonstrating that SMM chemokines interact with many residues on CXCR4 TM and extracellular domains that are important for HIV-1 entry, but not SDF-1 alpha binding or signaling. The preferential overlapping in the CXCR4 binding residues of SMM chemokines with HIV-1 over SDF-1 alpha illustrates a mechanism for the potent HIV-1 inhibition by these SMM chemokines. The discovery of distinct functional sites or conformational states influenced by these receptor sites mediating different functions of the natural ligand versus the viral or synthetic ligands has important implications for drug discovery, since the sites shared by SMM chemokines and HIV-1 but not by SDF-1 alpha can be targeted for the development of selective HIV-1 inhibitors devoid of interference with normal SDF-1 alpha function. C1 Univ Illinois, Dept Biochem, Urbana, IL 61801 USA. Univ Illinois, Dept Chem, Urbana, IL 61801 USA. Harvard Univ, Sch Med, Dana Farber Canc Inst, Dept Canc Immunol & AIDS, Boston, MA 02115 USA. Raylight Chemokine Pharmaceut Inc, La Jolla, CA 92037 USA. RP Huang, ZW (reprint author), Burnham Inst, 10901 N Torrey Pines Rd, La Jolla, CA 92037 USA. EM ziweihuang@burnham.org FU NHLBI NIH HHS [HL16059]; NIGMS NIH HHS [GM57761, R01 GM057761] NR 20 TC 44 Z9 44 U1 0 U2 4 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 2005 VL 79 IS 24 BP 15398 EP 15404 DI 10.1128/JVI.79.24.15398-15404.2005 PG 7 WC Virology SC Virology GA 997VK UT WOS:000234276700041 PM 16306611 ER PT J AU Ikeno, Y Hubbard, GB Lee, S Richardson, A Strong, R Diaz, V Nelson, JF AF Ikeno, Y Hubbard, GB Lee, S Richardson, A Strong, R Diaz, V Nelson, JF TI Housing density does not influence the longevity effect of calorie restriction SO JOURNALS OF GERONTOLOGY SERIES A-BIOLOGICAL SCIENCES AND MEDICAL SCIENCES LA English DT Article ID GROWTH-FACTOR-I; LIFE-SPAN; FOOD RESTRICTION; DIETARY RESTRICTION; FISCHER-344 RATS; MICE; INSULIN; AGE; PATHOGENESIS; RETARDATION AB This study examined the effect of housing density on the longevity-extending and disease-delaying actions of calorie restriction (CR). Singly or multiply housed (four per cage) mice were either fed ad libitum (AL) or were on CR beginning at 2 months. All CR mice were fed 40% less food than were multiply housed AL mice. CR increased median longevity by 19%, and housing density had no effect on this increase. CR also reduced neoplastic lesions in both housing groups, but lymphoma, the most common neoplasm, was reduced more in singly than in multiply housed mice. Singly housed AL mice ate 40% more food than did multiply housed AL mice, but weighed the same and lived as long as multiply housed AL mice. These results indicate that CR can extend life span as effectively in multiply as in singly housed mice, even though housing density can differentially affect the cancer-reducing effect of CR. C1 UTHSCSA, Dept Physiol, San Antonio, TX 78229 USA. UTHSCSA, Dept Cellular & Struct Biol, San Antonio, TX 78229 USA. UTHSCSA, Dept Pharmacol, San Antonio, TX 78229 USA. UTHSCSA, Barshop Ctr Longev & Aging Studies, San Antonio, TX 78229 USA. S Texas Vet Hlth Care Syst, Geriatr Res Educ & Clin Ctr, San Antonio, TX USA. S Texas Vet Hlth Care Syst, Res Serv, San Antonio, TX USA. SW Fdn Biomed Res, Dept Lab Anim Med, San Antonio, TX USA. RP Nelson, JF (reprint author), UTHSCSA, Dept Physiol, 7703 Floyd Curl Dr, San Antonio, TX 78229 USA. EM nelsonj@uthscsa.edu FU NIA NIH HHS [AG19899, 1P30-AG13319] NR 40 TC 50 Z9 50 U1 4 U2 5 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 2005 VL 60 IS 12 BP 1510 EP 1517 PG 8 WC Geriatrics & Gerontology; Gerontology SC Geriatrics & Gerontology GA 005RK UT WOS:000234841300003 PM 16424282 ER PT J AU Hamanishi, S Koike, T Chien, W Ravicz, ME Rosowski, JJ Merchant, SN Kobayashi, T Wada, H AF Hamanishi, S Koike, T Chien, W Ravicz, ME Rosowski, JJ Merchant, SN Kobayashi, T Wada, H TI Experimental assessment of the performance of an electromagnetic hearing aid in human temporal bones SO JSME INTERNATIONAL JOURNAL SERIES C-MECHANICAL SYSTEMS MACHINE ELEMENTS AND MANUFACTURING LA English DT Article DE electromagnetic; hearing aid; middle ear; tympanic membrane; human temporal bone ID INPUT IMPEDANCE; EAR; TRANSDUCER; STAPES AB To circumvent some of the problems inherent in conventional hearing aids such as low gain at high frequencies due to acoustic feedback, discomfort in occlusion of the external ear canal and so on, implantable hearing aids have been developed over the past two decades. The most prominent feature of implantable hearing aids is that a transducer is directly coupled to the one of the middle-ear ossicles. However, since invasive surgery is necessary for implantation of these hearing aids, they have not as yet been widely employed. We therefore constructed a prototype of a non-implantable hearing aid which is mainly composed of a microphone amplifier system and an electromagnetic transducer developed in our previous study. It can generate an excitation force to vibrate the ossicles by a coil adhered to the tympanic membrane. In this study, the excitation force generated by this hearing aid was evaluated using human temporal bones. The best result of experiments using three bones indicates that the newly developed hearing aid can generate an excitation force of more than 80 dB SPL in terms of sound pressure at frequencies between 0.8 and 3.2 kHz. C1 Tohoku Univ, Dept Bioengn & Robot, Sendai, Miyagi 9808579, Japan. Univ Electrocommun, Dept Mech Engn & Intelligent Syst, Chofu, Tokyo 1828585, Japan. Massachusetts Eye & Ear Infirm, Eaton Peabody Lab, Boston, MA 02114 USA. Tohoku Univ, Dept Otorhinolaryngol Head & Neck Surg, Sendai, Miyagi 9808579, Japan. RP Hamanishi, S (reprint author), Tohoku Univ, Dept Bioengn & Robot, 6-6-01 Aobayama, Sendai, Miyagi 9808579, Japan. EM hama@wadalab.mech.tohoku.ac.jp NR 19 TC 0 Z9 0 U1 0 U2 2 PU JAPAN SOC MECHANICAL ENGINEERS PI TOKYO PA SHINANOMACHI-RENGAKAN BLDG, SHINANOMACHI 35, SHINJUKU-KU, TOKYO, 160-0016, JAPAN SN 1344-7653 J9 JSME INT J C-MECH SY JI JSME Int. J. Ser. C-Mech. Syst. Mach. Elem. Manuf. PD DEC PY 2005 VL 48 IS 4 BP 529 EP 536 DI 10.1299/jsmec.48.529 PG 8 WC Engineering, Manufacturing; Engineering, Mechanical SC Engineering GA 008EA UT WOS:000235021800018 ER PT J AU Little, MO Moczynski, WV Richardson, PG Joffe, S AF Little, MO Moczynski, WV Richardson, PG Joffe, S TI Dana-Farber Cancer Institute ethics rounds: Life-threatening illness and the desire to adopt SO KENNEDY INSTITUTE OF ETHICS JOURNAL LA English DT Article AB Originally presented during Ethic Rounds at the Dana-Farber Cancer Institute, this commentary on the case of a patient treated for life-threatening cancer explores the responsibilities of health care providers when addressing the patient's desire to adopt a child. C1 Georgetown Univ, Dept Philosophy, Washington, DC 20057 USA. Georgetown Univ, Kennedy Inst Eth, Washington, DC 20057 USA. Dana Farber Canc Inst, Dept Pastoral Care, Boston, MA 02115 USA. Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02115 USA. Brigham & Womens Hosp, Dept Med, Boston, MA 02115 USA. Harvard Univ, Sch Med, Boston, MA 02115 USA. Dana Farber Canc Inst, Dept Pediat Oncol, Boston, MA 02115 USA. Childrens Hosp, Dept Med, Boston, MA 02115 USA. RP Little, MO (reprint author), Georgetown Univ, Dept Philosophy, Washington, DC 20057 USA. OI Joffe, Steven/0000-0002-0667-7384 NR 4 TC 1 Z9 2 U1 0 U2 0 PU JOHNS HOPKINS UNIV PRESS PI BALTIMORE PA JOURNALS PUBLISHING DIVISION, 2715 NORTH CHARLES ST, BALTIMORE, MD 21218-4363 USA SN 1054-6863 J9 KENNEDY INST ETHIC J JI Kennedy Inst. Ethics J. PD DEC PY 2005 VL 15 IS 4 BP 385 EP 393 DI 10.1353/ken.2005.0029 PG 9 WC Ethics; Philosophy; Social Issues SC Social Sciences - Other Topics; Philosophy; Social Issues GA 994OT UT WOS:000234041800004 PM 16453961 ER PT J AU Danda, RS Habiba, NM Rincon-Choles, H Bhandari, BK Barnes, JL Abboud, HE Pergola, PE AF Danda, RS Habiba, NM Rincon-Choles, H Bhandari, BK Barnes, JL Abboud, HE Pergola, PE TI Kidney involvement in a nongenetic rat model of type 2 diabetes SO KIDNEY INTERNATIONAL LA English DT Article DE nephropathy; insulin; streptozotocin; obesity; high fat diet; type 2 diabetes ID GROWTH-FACTOR-BETA; DIET-INDUCED OBESITY; RENAL EXPRESSION; BLOOD-PRESSURE; NEPHROPATHY; STREPTOZOTOCIN; HYPERTENSION; MELLITUS; INJURY; HYPERCHOLESTEROLEMIA AB Background. Rats fed a high fat diet and given a low dose of streptozotocin (STZ) (35 mg/kg) develop type 2 diabetes with insulin resistance, hyperinsulinemia, moderate hyperglycemia, hyperlipidemia, and salt-sensitive hypertension. We postulated that rats with noninsulinopenic (type 2) diabetes develop lesions of diabetic nephropathy significantly more prominent than those seen in classic insulinopenic (type 1) diabetic rats. Methods. Rats were fed regular chow or high fat diet (60% calories from fat and 70% animal fat). After 5 weeks, rats fed regular chow received vehicle (controls) or 55 mg/kg STZ (type 1 diabetes mellitus). Rats fed high fat diet received vehicle (high fat) or low dose STZ, 35 mg/kg (type 2 diabetes mellitus). Rats were sacrificed 14 weeks after STZ/vehicle injection. Results. Blood glucose, systolic blood pressure, and urinary protein excretion were significantly higher in both diabetes groups than in controls. Serum insulin levels (ng/mL) were higher in type 2 diabetes than in type 1 diabetes groups (0.49 +/- 0.12 vs. 0.07 +/- 0.07) (P = 0.01). Percentage of sclerosed glomeruli was significantly higher in type 2 diabetes group than in control and type 1 diabetes groups. Fibronectin expression was significantly increased in high fat, type 1 and type 2 diabetes groups compared to controls. The expression of type IV collagen, connective tissue growth factor (CTGF), and transforming growth factor-beta (TGF-beta) was significantly increased in high fat and type 2 diabetes groups compared to controls. Conclusion. Rats fed a high fat diet and given a low dose of STZ developed diabetes (with normal/high insulin levels), hypertension, and proteinuria. Kidney lesions in this type 2 model appear to be more pronounced than in type 1 diabetic rats despite lower blood glucose levels and proteinuria. We present a nongenetic rat model of type 2 diabetes mellitus and nephropathy. C1 Univ Texas, Hlth Sci Ctr, Dept Med, Div Nephrol, San Antonio, TX 78229 USA. S Texas Vet Hlth Care Syst, Audie L Murphy Div, San Antonio, TX USA. RP Pergola, PE (reprint author), Univ Texas, Hlth Sci Ctr, Dept Med, Div Nephrol, Mail Code 7882,7703 Floyd Curl Dr, San Antonio, TX 78229 USA. EM pergola@uthscsa.edu FU NHLBI NIH HHS [T32 HL07446] NR 34 TC 66 Z9 79 U1 0 U2 11 PU BLACKWELL PUBLISHING PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DQ, OXON, ENGLAND SN 0085-2538 J9 KIDNEY INT JI Kidney Int. PD DEC PY 2005 VL 68 IS 6 BP 2562 EP 2571 DI 10.1111/j.1523-1755.2005.00727.x PG 10 WC Urology & Nephrology SC Urology & Nephrology GA 983AU UT WOS:000233204300011 PM 16316331 ER PT J AU Oates, JC Varghese, S Bland, AM Taylor, TP Self, SE Stanislaus, R Almeida, JS Arthur, JM AF Oates, JC Varghese, S Bland, AM Taylor, TP Self, SE Stanislaus, R Almeida, JS Arthur, JM TI Prediction of urinary protein markers in lupus nephritis SO KIDNEY INTERNATIONAL LA English DT Article DE lupus nephritis; biomarkers; urine; electrophoresis; two-dimensional gel ID RENAL-ALLOGRAFT REJECTION; GEL-ELECTROPHORESIS; ERYTHEMATOSUS; PROTEOMICS; IDENTIFICATION; GLOMERULONEPHRITIS AB Background. Lupus nephritis is divided into six classes and scored according to activity and chronicity indices based on histologic findings. Treatment differs based on the pathologic findings. Renal biopsy is currently the only way to accurately predict class and activity and chronicity indices. We propose to use patterns of abundance of urine proteins to identify class and disease indices. Methods. Urine was collected from 20 consecutive patients immediately prior to biopsy for evaluation of lupus nephritis. The International Society of Nephrology/Renal Pathology Society (ISN/RPS) class of lupus nephritis, activity, and chronicity indices were determined by a renal pathologist. Proteins were separated by two-dimensional gel electrophoresis. Artificial neural networks were trained on normalized spot abundance values. Results. Biopsy specimens were classified in the database according to ISN/RPS class, activity, and chronicity. Nine samples had characteristics of more than one class present. Receiver operating characteristic (ROC) curves of the trained networks demonstrated areas under the curve ranging from 0.85 to 0.95. The sensitivity and specificity for the ISN/RPS classes were class II 100%, 100%; III 86%, 100%; IV 100%, 92%; and V 92%, 50%. Activity and chronicity indices had r values of 0.77 and 0.87, respectively. A list of spots was obtained that provided diagnostic sensitivity to the analysis. Conclusion. We have identified a list of protein spots that can be used to develop a clinical assay to predict ISN/RPS class and chronicity for patients with lupus nephritis. An assay based on antibodies against these spots could eliminate the need for renal biopsy, allow frequent evaluation of disease status, and begin specific therapy for patients with lupus nephritis. C1 Med Univ S Carolina, Dept Med, Charleston, SC 29425 USA. Med Univ S Carolina, Dept Pathol & Lab Med, Charleston, SC 29425 USA. Med Univ S Carolina, Dept Biostat Bioinformat & Epidemiol, Charleston, SC 29425 USA. Ralph H Johnson VA Med Ctr, Charleston, SC 29425 USA. RP Arthur, JM (reprint author), Med Univ S Carolina, Dept Med, 829 CSB,96 Jonathon Lucas Dr, Charleston, SC 29425 USA. EM arthurj@musc.edu FU NCRR NIH HHS [M01 RR001070, M01 RR001070-30A15172, M01 RR001070-315791, RR01070]; NHLBI NIH HHS [N01HV28181, N01-HV-28181]; NIAMS NIH HHS [R21 AR051719, R21 AR051719-01, R21 AR051719-02, R21AR051719] NR 26 TC 45 Z9 46 U1 0 U2 0 PU BLACKWELL PUBLISHING PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DQ, OXON, ENGLAND SN 0085-2538 J9 KIDNEY INT JI Kidney Int. PD DEC PY 2005 VL 68 IS 6 BP 2588 EP 2592 DI 10.1111/j.1523-1755.2005.00730.x PG 5 WC Urology & Nephrology SC Urology & Nephrology GA 983AU UT WOS:000233204300014 PM 16316334 ER PT J AU Jiang, T Liebman, SE Lucia, MS Li, JP Levi, M AF Jiang, T Liebman, SE Lucia, MS Li, JP Levi, M TI Role of altered renal lipid metabolism and the sterol regulatory element binding proteins in the pathogenesis of age-related renal disease SO KIDNEY INTERNATIONAL LA English DT Article DE SREBPs; cholesterol; triglycerides; nephropathy; glomerular basement membrane thickness; podocyte width ID LOW-DENSITY-LIPOPROTEIN; FATTY-ACID SYNTHESIS; MESANGIAL CELLS; DIABETIC-NEPHROPATHY; COLORIMETRIC DETERMINATION; CHOLESTEROL TRANSPORT; REPLACEMENT THERAPY; INSULIN-RESISTANCE; GLOMERULAR INJURY; GENE-EXPRESSION AB RBackground. There are well-known changes in age-related renal function and structure, including glomerulosclerosis and decline in glomerular filtration rate (GFR). The purpose of this study was to identify a potential role for lipids in mediating age-related renal disease. Methods. Mice of five different age groups (3, 6, 12, 19, and 23 months old) were studied. Results. We have found that in C57BL/6 mice there was a progressive increase in age-related glomerulosclerosis [increase in periodic acid-Schiff (PAS) staining and accumulation of extracellular matrix proteins including type IV collagen and fibronectin], increased glomerular basement thickness and podocyte width and effacement, and increased proteinuria. These changes were associated with age-related increase in lipid accumulation as determined by increased Oil Red O staining in kidney sections. Biochemical analysis indicated that these lipid deposits corresponded to significant increases in renal triglyceride and cholesterol content. We have also found significant age-related increases in the nuclear transcription factors, sterol regulatory element-binding proteins (SREBP-1 and SREBP-2), protein abundance and increased expression or activity of their target enzymes that play an important role in lipid synthesis. Conclusion. Our results indicated that there was an age-related increase in renal expression of SREBP-1 and SREBP-2 with resultant increases in lipid synthesis and triglyceride and cholesterol accumulation in the kidney. Because we have previously shown that increased expression of SREBPs in the kidney per se results in glomerulosclerosis and proteinuria, our data suggested that increased SREBPs' expression resulting in increased renal lipid accumulation may play an important role in age-related nephropathy. C1 Univ Colorado, Hlth Sci Ctr, Dept Med, Div Renal Dis & Hypertens, Denver, CO 80262 USA. Univ Colorado, Hlth Sci Ctr, Dept Pathol, Denver, CO USA. Univ Colorado, Hlth Sci Ctr, Dept Physiol & Biophys, Denver, CO USA. Denver VA Med Ctr, Denver, CO USA. RP Levi, M (reprint author), Univ Colorado, Hlth Sci Ctr, Dept Med, Div Renal Dis & Hypertens, 4200 E 9th Ave,C281, Denver, CO 80262 USA. EM Moshe.Levi@UCHSC.edu OI Levi, Moshe/0000-0002-6225-946X FU NIA NIH HHS [7R03 AG20361-02]; NIDDK NIH HHS [1F32 DK065407-01, 5R01 DK062209-02] NR 71 TC 53 Z9 56 U1 0 U2 3 PU BLACKWELL PUBLISHING PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DQ, OXON, ENGLAND SN 0085-2538 J9 KIDNEY INT JI Kidney Int. PD DEC PY 2005 VL 68 IS 6 BP 2608 EP 2620 DI 10.1111/j.1523-1755.2005.00733.x PG 13 WC Urology & Nephrology SC Urology & Nephrology GA 983AU UT WOS:000233204300017 PM 16316337 ER PT J AU Holbrook, EH Leopold, DA Schwob, JE AF Holbrook, EH Leopold, DA Schwob, JE TI Abnormalities of axon growth in human olfactory mucosa SO LARYNGOSCOPE LA English DT Article DE olfactory biopsies; olfactory nerve; neuroma; dysosmia; nervefibrosis; respiratory metaplasia ID TRAUMATIC ANOSMIA; SENSORY NEURONS; EPITHELIUM; RECONSTITUTION; LESION AB Objectives/Hypothesis. Random biopsies of the human adult olfactory mucosa often demonstrate degenerative changes in the olfactory epithelium (OE) in both dysosmic and normosmic patients and, consequently, have limited diagnostic usefulness. However, detailed analysis of the subepithelial tissue with specific attention to the fascicles of the olfactory nerve and abnormalities of axonal growth may improve the correlation of histopathology with sensory function. Study Design: Retrospective review of human OE biopsies. Methods. Mucosal biopsies from the olfactory area obtained from 27 subjects were examined by light and electron microscopy, with particular attention to the olfactory nerve fascicles; results were correlated with clinical status. Immunohistochemical analysis was used to characterize the extent of axonal depletion, relative maturity of the parent population, and aberrant axonal growth. Results: As expected, there are areas of respiratory metaplasia and neuronal depletion in normosmic as well as dysosmic patients. The degree of axon degeneration within the fascicles correlates better with individual olfactory status. Immature neurons predominate, and re-entrant neuromas develop in patients with olfactory loss caused by disconnection from the olfactory bulb. Individuals with olfactory loss caused by epithelial damage as with chronic rhinosinusitis display evidence of nerve fascicle degeneration and intraepithelial neuromas. Conclusion. The status of olfactory axons provides useful information on the overall condition of the olfactory periphery and improves the diagnostic usefulness of mucosal biopsies. In addition to an assessment of the epithelium per se, the fascicles of the olfactory nerve need to be characterized for a complete analysis of the olfactory mucosa. C1 Massachusetts Eye & Ear Infirm, Dept Otolaryngol, Boston, MA 02114 USA. Harvard Univ, Sch Med, Dept Otol & Laryngol, Boston, MA 02115 USA. Univ Nebraska, Med Ctr, Dept Otolaryngol Head & Neck Surg, Omaha, NE USA. Tufts Univ, Sch Med, Dept Anat & Cellular Biol, Boston, MA 02111 USA. RP Holbrook, EH (reprint author), Massachusetts Eye & Ear Infirm, Dept Otolaryngol, 243 Charles St, Boston, MA 02114 USA. EM eric_holbrook@meei.harvard.edu FU NIDCD NIH HHS [P01 DC000220, R01 DC000467] NR 22 TC 23 Z9 24 U1 1 U2 3 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3261 USA SN 0023-852X J9 LARYNGOSCOPE JI Laryngoscope PD DEC PY 2005 VL 115 IS 12 BP 2144 EP 2154 DI 10.1097/01.MLG.0000181493.83661.CE PG 11 WC Medicine, Research & Experimental; Otorhinolaryngology SC Research & Experimental Medicine; Otorhinolaryngology GA 996SX UT WOS:000234196100011 PM 16369158 ER PT J AU Ravindranath, Y Chang, M Steuber, CP Becton, D Dahl, G Civin, C Camitta, B Carroll, A Raimondi, SC Weinstein, HJ AF Ravindranath, Y Chang, M Steuber, CP Becton, D Dahl, G Civin, C Camitta, B Carroll, A Raimondi, SC Weinstein, HJ CA Pediat Oncology Grp TI Pediatric Oncology Group (POG) studies of acute myeloid leukemia (AML): a review of four consecutive childhood AML trials conducted between 1981 and 2000 SO LEUKEMIA LA English DT Review DE AML; childhood; treatment; bone marrow transplantation; daunorubicin dosing; high-dose cytarabine ID BONE-MARROW-TRANSPLANTATION; CHILDRENS CANCER GROUP; DOWN-SYNDROME CHILDREN; HIGH-DOSE CYTARABINE; EVENT-FREE SURVIVAL; CHROMOSOMAL-ABNORMALITIES; CYTOSINE-ARABINOSIDE; CHEMOTHERAPY; THERAPY; RISK AB From 1981 to 2000, a total of 1823 children with acute myeloid leukemia (AML) enrolled on four consecutive Pediatric Oncology Group (POG) clinical trials. POG 8101 demonstrated that the induction rate associated with the 3 + 7 + 7 combination of daunorubicin, Ara-C, and 6-thioguanine (DAT) was greater than that associated with an induction regimen used to treat acute lymphoblastic leukemia (82 vs 61%; P = 0.02). Designed as a pilot study to determine the feasibility of administration of noncross-resistant drug pairs and later modified to assess the effect of dose intensification of Ara-C during the second induction course, POG 8498 confirmed the high initial rate of response to DAT (84.2%) and showed that dose intensification of Ara-C during the second induction course resulted in a trend toward higher event-free survival (EFS) estimates than did standard-dose DAT (2 + 5) during the second induction course (5-year EFS estimates, 22 vs 27%; P = 0.33). Age < 2 years and leukocyte count < 100000/mm(3) emerged as significantly good prognostic factors. The most significant observation made in the POG 8498 study was the markedly superior outcome of children with Down's syndrome who were treated on the high-dose Ara-C regimen. POG 8821 compared the efficacy of autologous bone marrow transplantation (BMT) with that of intensive consolidation chemotherapy. Intent-to-treat analysis revealed similar 5year EFS estimates for the group that underwent autologous BMT (36 +/- 4.7%) and for the group that received only intensive chemotherapy (35 +/- 4.5%) (P = 0.25). There was a high rate of treatment-related mortality in the autologous transplantation group. The study demonstrated superior results of allogeneic BMT for patients with histocompatible related donors (5-year EFS estimate 6375.4%) and of children with Down's syndrome (5- year EFS estimate, 66 +/- 8.6%). The POG 9421 AML study evaluated high-dose Ara- C as part of the first induction course and the use of the multidrug resistance modulator cyclosporine. Preliminary results showed that patients receiving both highdose Ara- C for remission induction and the MDR modulator for consolidation had a superior outcome ( 5- year EFS estimate, 42 +/- 8.2%) than did patients receiving other treatment; however, the difference was not statistically significant. These four studies demonstrate the importance of dose intensification of Ara- C in the treatment of childhood AML; cytogenetics as the single most prognostic factor and the unique curability of AML in children with Down's syndrome. C1 Wayne State Univ, Detroit, MI 48201 USA. Childrens Hosp Michigan, Dept Pediat, Detroit, MI 48201 USA. Univ Florida, Dept Stat, Gainesville, FL 32611 USA. Baylor Coll Med, Dept Pediat, Houston, TX 77030 USA. Univ Arkansas Med Sci, Dept Pediat, Little Rock, AR 72205 USA. Stanford Univ, Sch Med, Dept Pediat, Stanford, CA 94305 USA. Johns Hopkins Univ, Sch Med, Dept Pediat, Baltimore, MD 21205 USA. Midw Childrens Hosp, Dept Pediat, Milwaukee, WI USA. Med Coll Wisconsin, Milwaukee, WI 53226 USA. Univ Alabama Birmingham, Dept Genet, Birmingham, AL USA. St Jude Childrens Res Hosp, Dept Pathol, Memphis, TN 38101 USA. Massachusetts Gen Hosp, Div Pediat Oncol, Boston, MA 02114 USA. Harvard Univ, Sch Med, Boston, MA 02115 USA. RP Ravindranath, Y (reprint author), Wayne State Univ, Childrens Hosp Michigan, Georgie Ginopolis Chair Pediat Canc & Hematol, Sch Med, 2M34,3901 Beaubien Blvd, Detroit, MI 48201 USA. EM ravi@med.wayne.edu FU NCI NIH HHS [CA-41573, CA-33587, CA-28439, CA-20549, CA-69428, CA-03161, CA-25408, CA-29293, CA-32053, CA-11233, CA-05587, CA-33625, CA-15898, CA-28383, CA-07431, CA-28476, CA-29139, CA-29691, CA-33603, CA-69177, CA-15525] NR 36 TC 102 Z9 110 U1 0 U2 3 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 2005 VL 19 IS 12 BP 2101 EP 2116 DI 10.1038/sj.leu.2403927 PG 16 WC Oncology; Hematology SC Oncology; Hematology GA 986PN UT WOS:000233462300009 PM 16136167 ER PT J AU Stone, ME AF Stone, ME TI Fragile innocence: A father's memoir of his daughter's courageous journey. SO LIBRARY JOURNAL LA English DT Book Review C1 Massachusetts Gen Hosp Lib, Boston, MA 02114 USA. RP Stone, ME (reprint author), Massachusetts Gen Hosp Lib, Boston, MA 02114 USA. NR 1 TC 0 Z9 0 U1 0 U2 0 PU BOWKER MAGAZINE GROUP CAHNERS MAGAZINE DIVISION PI NEW YORK PA 249 W 17TH ST, NEW YORK, NY 10011 USA SN 0363-0277 J9 LIBR J JI Libr. J. PD DEC PY 2005 VL 130 IS 20 BP 155 EP 155 PG 1 WC Information Science & Library Science SC Information Science & Library Science GA 992ZX UT WOS:000233923600283 ER PT J AU McGuire, BM Bonkovsky, HL Carithers, RL Chung, RT Goldstein, LI Lake, JR Lok, AS Potter, CJ Rand, E Voigt, MD Davis, PR Bloomer, JR AF McGuire, BM Bonkovsky, HL Carithers, RL Chung, RT Goldstein, LI Lake, JR Lok, AS Potter, CJ Rand, E Voigt, MD Davis, PR Bloomer, JR TI Liver transplantation for erythropoietic protoporphyria liver disease SO LIVER TRANSPLANTATION LA English DT Article ID BONE-MARROW-TRANSPLANTATION; INTRAVENOUS HEME-ALBUMIN; PERFUSED-RAT-LIVER; COMPLICATIONS; PATIENT; PHOTOSENSITIVITY; PLASMAPHERESIS; POLYNEUROPATHY; FERROCHELATASE; DYSFUNCTION AB In erythropoietic protoporphyria (EPP), there is excessive production of protoporphyrin, primarily in the bone marrow, resulting in increased biliary excretion of this heme precursor. Some patients will develop progressive liver disease that may ultimately require liver transplantation. However, excessive production of protoporphyrin by the bone marrow continues after transplantation, which may cause recurrent disease in the allograft. This study was performed to define post-transplant survival, the risk of recurrent disease, and specific management issues in patients transplanted for EPP liver disease. The patients studied consisted of twelve males and eight females, with an average age of 31 (range, 13-56) years at the time of transplantation. The estimated maximum MELD score prior to transplant was 21 (range, 15-29). Unique complications in the perioperative period were light induced tissue damage in four patients and neuropathy in six, requiring prolonged mechanical ventilation in four. Patient and graft survival rates were 85% at 1 year, 69% at 5 years, and 47% at 10 years. Recurrent EPP liver disease occurred in 11 of 17 patients (65%) who survived more than 2 months. Three patients were retransplanted at 1.8, 12.6, and 14.5 years after the initial transplant for recurrent EPP liver disease. In conclusion, the 5-year patient survival rate in patients transplanted for EPP liver disease is good, but the recurrence of EPP liver disease appears to diminish long term graft and patient survival. C1 Univ Alabama, Dept Med, Birmingham, AL 35294 USA. Univ Connecticut, Dept Med, Farmington, CT 06032 USA. Univ Washington, Dept Med, Seattle, WA 98195 USA. Massachusetts Gen Hosp, Dept Med, Boston, MA 02114 USA. Univ Calif Los Angeles, Dept Surg, Los Angeles, CA 90024 USA. Univ Minnesota, Dept Med, Minneapolis, MN 55455 USA. Univ Michigan, Dept Med, Ann Arbor, MI 48109 USA. Ohio State Univ, Dept Pediat, Columbus, OH 43210 USA. Childrens Hosp Philadelphia, Dept Pediat, Philadelphia, PA 19104 USA. Univ Iowa, Dept Med, Iowa City, IA 52242 USA. RP McGuire, BM (reprint author), Univ Alabama, Dept Med, 1530 3rd Ave S,MCLM 262A, Birmingham, AL 35294 USA. EM bmcguire@uab.edu RI Lok, Anna /B-8292-2009; OI Yang, Shuman/0000-0002-9638-0890 FU NCRR NIH HHS [M01 RR 01693]; NIDDK NIH HHS [DK 026466, N01 DK 92326, R01 DK 038825, R01 DK 918825, U01 DK 065193] NR 39 TC 60 Z9 61 U1 0 U2 0 PU JOHN WILEY & SONS INC PI HOBOKEN PA 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 1527-6465 J9 LIVER TRANSPLANT JI Liver Transplant. PD DEC PY 2005 VL 11 IS 12 BP 1590 EP 1596 DI 10.1002/lt.20620 PG 7 WC Gastroenterology & Hepatology; Surgery; Transplantation SC Gastroenterology & Hepatology; Surgery; Transplantation GA 991MB UT WOS:000233817000020 PM 16315313 ER PT J AU Lynch, T Kim, E AF Lynch, T Kim, E TI Optimizing chemotherapy and targeted agent combinations in NSCLC SO LUNG CANCER LA English DT Article; Proceedings Paper CT 11th World Conference on Lung Cancer CY JUL 03-06, 2005 CL Barcelona, SPAIN DE targeted therapy; docetaxel; non-small cell lung cancer; bevacizumab; epidermal growth factor receptor (EGFR); vascular endothelial growth factor (VEGF) ID CELL LUNG-CANCER; PHASE-II TRIAL; PREVIOUSLY TREATED PATIENTS; PLUS CARBOPLATIN; RANDOMIZED-TRIAL; PACLITAXEL; GEFITINIB; ERLOTINIB; INHIBITOR; DOCETAXEL AB Chemotherapy extends life and provides symptom palliation for patients with advanced non-small cell lung cancer (NSCLC). Numerous trials have been conducted that evaluate a variety of doublet regimens, but the majority of trials have found equal efficacy among the treatment arms. Indeed, a plateau appears to have been reached with respect to survival associated with traditional cytotoxic drug regimens. It was initially hoped that the addition of novel targeted agents to conventional chemotherapy would produce significant survival benefits for patients with advanced NSCLC; however, most trials have failed to show such a benefit. There is no survival benefit associated with adding erlotinib or gefitinib to a chemotherapy regimen, although there is a significant improvement in survival associated with erlotinib monotherapy in the second- and third-line advanced disease setting. In contrast, the results of E4599 clearly demonstrate that the addition of bevacizumab to paclitaxel-carboplatin chemotherapy extends survival in a select group of patients with non-squamous cell NSCLC. E4599 also represents a rational approach to drug development that could be modeled in other trials, namely, the use of a large, well designed, randomized trial prior to beginning a traditional phase 11 approach. This strategy can lead to the identification of subgroups most likely to benefit, as well as those that might experience increased toxicity, such as patients with squamous cell carcinoma treated with bevacizumab. Another approach to optimizing targeted therapy involves selecting a chemotherapy regimen with the greatest potential for synergy based on preclinical modeling. Because docetaxel has been shown to prolong survival in second-line treament, a number of novel agents have been combined with docetaxel in order to improve efficacy. Alternatively, investigators have sought to combine novel agents with either carboplatin-paclitaxel or cisplatin-gemcitabine in firstline treatment. A number of trials are underway that combine these agents with inhibitors of the epidermal growth factor receptor (EGFR), Vascular endothetial growth factor (VEGF), and the proteasome, as well as COX2 inhibitors, and novel immunomodulators. (c) 2005 Elsevier Science Ltd. C1 Univ Texas, MD Anderson Canc Ctr, Houston, TX 77030 USA. Massachusetts Gen Hosp, Boston, MA 02114 USA. RP Kim, E (reprint author), Univ Texas, MD Anderson Canc Ctr, 1515 Holcombe Blvd,Box 432, Houston, TX 77030 USA. EM tlynch@partners.org; edkim@mdanderson.org NR 37 TC 11 Z9 14 U1 0 U2 0 PU ELSEVIER IRELAND LTD PI CLARE PA ELSEVIER HOUSE, BROOKVALE PLAZA, EAST PARK SHANNON, CO, CLARE, 00000, IRELAND SN 0169-5002 J9 LUNG CANCER-J IASLC JI Lung Cancer PD DEC PY 2005 VL 50 SU 2 BP S25 EP S32 DI 10.1016/S0169-5002(05)81570-3 PG 8 WC Oncology; Respiratory System SC Oncology; Respiratory System GA 009BO UT WOS:000235086300005 PM 16557671 ER PT J AU Liu, CL Zaslavsky, AM Ganz, ML Perrin, J Gortmaker, S McCormick, MC AF Liu, CL Zaslavsky, AM Ganz, ML Perrin, J Gortmaker, S McCormick, MC TI Continuity of health insurance coverage for children with special health care needs SO MATERNAL AND CHILD HEALTH JOURNAL LA English DT Article DE CSHCN; health insurance; continuity; MEPS ID MEDICAID-ELIGIBLE CHILDREN; IDENTIFYING CHILDREN; WELFARE-REFORM; PARENTAL EMPLOYMENT; ACCESS; DEFINITION; IMPACT; ENROLLMENT; FAMILIES; MANDATES AB Objectives: To assess the continuity of health insurance coverage and its associated factors for children with special health care needs (CSHCN). Methods: Logistic regression and proportional hazard models were estimated on monthly insurance enrollment for 5594 children in the 1996 Medical Expenditure Panel Survey. CSHCN were identified using a non-categorical approach. Stratified analyses were conducted to determine whether any characteristics differentiated the effects of CSHCN status on children's coverage. Results: In 1996, more than 8% of CSHCN were uninsured for the entire year. For those who were insured in January 1996, 14% lost their coverage by December 1996. CSHCN were more likely than other children to be insured (92% vs. 89%), mainly due to their better access to public insurance (35% vs. 23%). Conversely, CSHCN were less likely than other children to stay insured if they were school-aged, non-Hispanic White, from working, low-income families or the US Midwest region. Higher parental education improved health insurance enrollment for CSHCN, whereas higher family income or having activity limitations protected them from losing coverage. Regardless of CSHCN status, being publicly insured was associated with a higher risk of losing coverage for children. Conclusions: Despite increased health care needs, a considerable proportion of CSHCN is unable to access or maintain coverage. Compared to other children, CSHCN are more likely to have coverage but no more likely to stay insured. Improving continuity of coverage for publicly insured children is needed, especially CSHCN who are more likely to obtain their coverage through public programs. C1 Harvard Univ, Sch Publ Hlth, Dept Soc, Boston, MA 02115 USA. Harvard Univ, Sch Med, Dept Hlth Care Policy, Boston, MA 02115 USA. Massachusetts Gen Hosp, Child & Adolescent Hlth Policy, Boston, MA 02114 USA. RP Liu, CL (reprint author), 2 N Park St, Watertown, MA 02472 USA. EM liu_chialing@yahoo.com OI Ganz, Michael/0000-0002-9702-2999; McCormmick, Marie/0000-0002-3938-1707 NR 45 TC 10 Z9 10 U1 0 U2 1 PU SPRINGER/PLENUM PUBLISHERS PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA SN 1092-7875 J9 MATERN CHILD HLTH J JI Matern. Child Health J. PD DEC PY 2005 VL 9 IS 4 BP 363 EP 375 DI 10.1007/s10995-005-0019-1 PG 13 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA 997HW UT WOS:000234237200003 PM 16328707 ER PT J AU Engelsman, M Kooy, HM AF Engelsman, M Kooy, HM TI Target volume dose considerations in proton beam treatment planning for lung tumors SO MEDICAL PHYSICS LA English DT Article ID CANCER; THERAPY; MOTION; DISTRIBUTIONS; RADIOTHERAPY AB We performed a treatment planning study in order to gather basic insight in the effect of setup errors and breathing motion on the cumulative proton dose to a lung tumor. We used a simplified geometry that simulates a 50 mm diameter gross tumor volume (GTV) located centrally inside lung tissue. The GTV was expanded with a uniform 5 mm margin into a clinical target volume (CTV) and into a variety of planning target volume (PTV's). Proton beam apertures were designed to conform the prescribed dose laterally to the PTV while the range compensator was designed to provide distal coverage of the CTV. Different smearing distances were applied to the range compensators, and the cumulative dose in the CTV was evaluated for different combinations of breathing motion and systematic setup errors. Evaluation parameters were the dose to 99% of the CTV (D99) and the equivalent uniform dose (EUD), with a surviving fraction at 2 Gy of SF2=0.5. For a single proton field designed to a 15 mm expansion of the CTV and without smearing applied to the range compensator, D99 of the CTV reduced from 96% for no tumor displacement to 41% and 13% for systematic setup errors of 5 and 10 mm, respectively. For a representative clinical combination, of 5 mm systematic error and 10 mm breathing amplitude, the EUD of the CTV was about 40 Gy (prescribed dose 70 Gy) regardless the CTV to PTV margin, and without smearing. Smearing the range compensator increases the dose to the CTV substantially with a lateral margin and smearing distance of 7.5 mm providing ample tumor coverage. In this latter case, D99 of the target volume increased to 87% for a single field treatment plan. Smearing does, however, lead to an increase in dose to normal tissues distal to the clinical target volume. Next to countering geometric mismatches due to patient setup, smearing can also be used to counter the detrimental effects of breathing motion on the dose to the clinical target volume. We show that the lateral margin and smearing distance can be substantially smaller than the maximum tumor displacement due to setup errors and patient breathing, as measured by the D99 and the EUD. (c) 2005 American Association of Physicists in Medicine. C1 Massachusetts Gen Hosp, NE Proton Therapy Ctr, Boston, MA 02114 USA. Harvard Univ, Sch Med, Dept Radiat Oncol, Boston, MA 02114 USA. RP Kooy, HM (reprint author), Massachusetts Gen Hosp, NE Proton Therapy Ctr, Fruit St, Boston, MA 02114 USA. EM hkooy@partners.org FU NCI NIH HHS [5 PO1 CA21239-24] NR 17 TC 45 Z9 45 U1 0 U2 2 PU AMER ASSOC PHYSICISTS MEDICINE AMER INST PHYSICS PI MELVILLE PA STE 1 NO 1, 2 HUNTINGTON QUADRANGLE, MELVILLE, NY 11747-4502 USA SN 0094-2405 J9 MED PHYS JI Med. Phys. PD DEC PY 2005 VL 32 IS 12 BP 3549 EP 3557 DI 10.1118/1.2126187 PG 9 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA 002WV UT WOS:000234643700005 PM 16475753 ER PT J AU Pereira, RI Draznin, B AF Pereira, RI Draznin, B TI Inhibition of the phosphatidylinositol 3 '-kinase signaling pathway leads to decreased insulin-stimulated adiponectin secretion from 3T3-L1 adipocytes SO METABOLISM-CLINICAL AND EXPERIMENTAL LA English DT Article ID CORONARY-ARTERY-DISEASE; PROTEIN-ADIPONECTIN; PLASMA-CONCENTRATIONS; ADIPOSE-TISSUE; PHOSPHOINOSITIDE 3-KINASE; SKELETAL-MUSCLE; GENE-EXPRESSION; DEFICIENT MICE; RESISTANCE; KINASE AB Adiponectin is a protein secreted by adipocytes, which modulates insulin resistance and is thought to confer protection from atherosclerosis. Decreased circulating adiponectin is seen in states of insulin resistance, yet the cause of this decrease remains unclear. We investigated the role of insulin in adiponectin secretion and the effect of selective insulin resistance on insulin-stimulated adiponectin secretion by 3T3-L1 adipocytes. Inhibition of the phosphatidylinositol 3'-kinase (PI3K) insulin-signaling pathway was induced with wortmannin (WT) or with a kinase-inactive Akt adenoviral construct (Akt-KD), and inhibition of the mitogen-activated protein kinase pathway was induced with PD98059 or with a dominant-negative ras adenoviral construct (DNras). The PI3K pathway was activated with a constitutively active Akt adenoviral construct (Akt-myr). Adiponectin was measured by Western blot, and adiponectin messenger RNA (mRNA) levels were determined by real-time reverse transcription-polymerase chain reaction. Insulin treatment increased adiponectin secretion and decreased intracellular adiponectin. Treatment with 100 nmol/L insulin for 24 hours resulted in a 78% increase in secreted adiponectin (P < .05). Insulin had no effect on adiponectin mRNA. WT or Akt-KD, but not PD98059 or DNras, inhibited insulin-stimulated adiponectin secretion (P < .05). Activation of the PI3K pathway resulted in increased insulin-independent adiponectin secretion. Inhibition of the PI3K- or mitogen-activated protein kinase-dependent pathway decreased adiponectin mRNA by 50% (P < .01). We demonstrate a decrease in insulin-stimulated adiponectin secretion with selective inhibition of the PI3K pathway. These results suggest a mechanism for the observed decreased adiponectin levels associated with insulin resistance, when defects in the PI3K-dependent insulin-signaling pathway lead to decreased adiponectin production, inadequate adiponectin secretion, and therefore low circulating adiponectin levels. (c) 2005 Elsevier Inc. All rights reserved. C1 Denver Vet Affairs Med Ctr, Res Serv, Denver, CO 80220 USA. Univ Colorado, Dept Med, Denver, CO 80262 USA. Hlth Sci Ctr, Denver, CO 80262 USA. RP Draznin, B (reprint author), Denver Vet Affairs Med Ctr, Res Serv, Denver, CO 80220 USA. EM boris.draznin@med.va.gov NR 57 TC 35 Z9 37 U1 0 U2 2 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0026-0495 J9 METABOLISM JI Metab.-Clin. Exp. PD DEC PY 2005 VL 54 IS 12 BP 1636 EP 1643 DI 10.1016/j.metabol.2005.07.002 PG 8 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA 995TU UT WOS:000234127800013 PM 16311098 ER PT J AU Wolfe, J Turner, K Caulfield, M Newton, TL Melia, K Martin, J Goldstein, J AF Wolfe, J Turner, K Caulfield, M Newton, TL Melia, K Martin, J Goldstein, J TI Gender and trauma as predictors of military attrition: A study of Marine Corps recruits SO MILITARY MEDICINE LA English DT Article ID POSTTRAUMATIC-STRESS-DISORDER; SEXUAL ABUSE; VIETNAM VETERANS; AGGRESSION; FEMALE; REVICTIMIZATION; VICTIMIZATION; PREVALENCE; EVENTS; SAMPLE AB Recent studies have shown high rates of premilitary trauma exposure among U.S. military enlistees. Given the association of trauma with later stressor vulnerability, it is important to examine the role of premilitary stress and trauma in adaptation to the stress of recruit training. U.S. Marine Corps recruits (N = 1,530) were surveyed for premilitary histories of interpersonal trauma to examine the relationship between premilitary trauma and attrition from recruit training. The majority of the recruits (47.5% of men and 68.1% of women) reported experiencing at least one interpersonal trauma before entering the Marine Corps. Individuals with a history of interpersonal trauma were at significantly greater risk for attrition; they were 1.5 times more likely to drop out of recruit training than were individuals without a trauma history. These findings suggest that developing interventions to bolster recruits' coping skills may improve adaptation to the recruit training environment and thus decrease attrition. C1 VA Boston Healthcare Syst, Natl Ctr PTSD, Boston, MA 02130 USA. Bryn Mawr Coll, Grad Sch Social Work & Social Res, Bryn Mawr, PA 19010 USA. Harvard Univ, Sch Med, Boston, MA 02115 USA. RP Wolfe, J (reprint author), VA Boston Healthcare Syst, Natl Ctr PTSD, Boston, MA 02130 USA. NR 35 TC 20 Z9 20 U1 1 U2 2 PU ASSN MILITARY SURG US PI BETHESDA PA 9320 OLD GEORGETOWN RD, BETHESDA, MD 20814 USA SN 0026-4075 J9 MIL MED JI Milit. Med. PD DEC PY 2005 VL 170 IS 12 BP 1037 EP 1043 PG 7 WC Medicine, General & Internal SC General & Internal Medicine GA 019JU UT WOS:000235832200013 PM 16491944 ER PT J AU Wang, SA Rahemtullah, A Faquin, WC Roepke, J Harris, NL Hasserjian, RP AF Wang, SA Rahemtullah, A Faquin, WC Roepke, J Harris, NL Hasserjian, RP TI Hodgkin's lymphoma of the thyroid: a clinicopathologic study of five cases and review of the literature SO MODERN PATHOLOGY LA English DT Review DE thyroid; Hodgkin's; lymphoma; nodular sclerosis; thyroiditis ID FINE-NEEDLE ASPIRATION; MALIGNANT-LYMPHOMA; DISEASE; GLAND; NODULE; MANIFESTATION; DIAGNOSIS; TUMOR AB Hodgkin's lymphoma rarely involves the thyroid gland. We report the clinical and pathologic features of five cases of Hodgkin's lymphoma that presented as thyroid lesions. All five patients were females, aged 29-59 years. Three patients had a history of chronic thyroiditis and hypothyroidism and two were euthyroid. One patient had a remote history of Hodgkin's lymphoma. Imaging studies showed a `cold' nodule (three cases) or a diffusely enlarged thyroid gland, resembling goiter or fibrosclerosing thyroiditis (two cases). Thyroid fine-needle aspiration was performed before thyroidectomy in all cases; three of these cases contained some atypical cells, raising the possibility of Hodgkin's lymphoma. Histologically, all cases were classical Hodgkin's lymphoma, nodular sclerosis subtype. The four patients with primary thyroid lymphoma had Stage IIE disease. All patients were treated with surgical excision and chemotherapy, with or without radiation therapy, and were alive after 2 months to 7 years of follow-up. A review of the English literature between 1962 and 2005 revealed 16 cases of thyroid Hodgkin's lymphoma, with a female preponderance and generally favorable outcome similar to the cases in our series. Hodgkin's lymphoma of the thyroid is rare and can mimic a primary thyroid epithelial tumor or thyroiditis clinically. Histologic diagnosis may be difficult due to marked fibrosis. Hodgkin's lymphoma should be considered in the differential diagnosis of thyroid neoplasms. C1 Harvard Univ, Sch Med, Massachusetts Gen Hosp, Dept Pathol, Boston, MA USA. E Cent Indiana Pathol PC, Muncie, IN USA. RP Hasserjian, RP (reprint author), Massachusetts Gen Hosp, Dept Pathol, 55 Fruit St, Boston, MA 02114 USA. EM rhasserjian@partners.org NR 44 TC 16 Z9 19 U1 0 U2 0 PU NATURE PUBLISHING GROUP PI NEW YORK PA 345 PARK AVENUE SOUTH, NEW YORK, NY 10010-1707 USA SN 0893-3952 J9 MODERN PATHOL JI Mod. Pathol. PD DEC PY 2005 VL 18 IS 12 BP 1577 EP 1584 DI 10.1038/modpathol.3800501 PG 8 WC Pathology SC Pathology GA 985IZ UT WOS:000233372100007 PM 16258502 ER PT J AU Liu, E Sinha, S Williams, C Cyrille, M Heller, E Snapper, SB Georgopoulos, K St-Arnaud, R Force, T Dedhar, S Gerszten, RE AF Liu, E Sinha, S Williams, C Cyrille, M Heller, E Snapper, SB Georgopoulos, K St-Arnaud, R Force, T Dedhar, S Gerszten, RE TI Targeted deletion of integrin-linked kinase reveals a role in T-cell chemotaxis and survival SO MOLECULAR AND CELLULAR BIOLOGY LA English DT Article ID PROTEIN-KINASE; PHOSPHOINOSITIDE 3-KINASE; SIGNAL-TRANSDUCTION; ADHESION; ACTIVATION; PROLIFERATION; INFLAMMATION; PI3K-GAMMA; MIGRATION/; B/AKT AB Integrin-linked kinase (ILK) is a serine/threonine kinase that is important in cell-matrix interactions and cell signaling. To examine the role of ILK in leukocyte trafficking and survival, we generated T cell-specific ILK knockouts by breeding ILKflor/flox mice to transgenic mice expressing Cre recombinase under control of the Lck proximal promoter. Thymic T cells from Lck-Cre(+)/ILKflox/flox mice had a marked reduction (> 95%) in ILK protein levels. Thymic cellularity was comparable in 3- to 4-week-old mice, but a threefold diminution of thymic T cells became evident by 6 to 8 weeks of age in the T cell-specific ILK knockout mice due to increased cell death of double-positive (DP) T cells. Analysis of peripheral T cells by quantitative PCR and by breeding Lck-Cre(+)/ILKflow/flow mice to a YFP-transgenic reporter strain demonstrated an approximate 20-fold enrichment of ILK-competent cells, suggesting these cells have a competitive advantage in trafficking to and/or survival in peripheral lymphatic organs. We explored mechanisms related to altered cell trafficking and survival that might explain the decreases in thymic cellularity and enrichment for ILK-competent cells in the spleen and lymph nodes. We observed a > 50% reduction in chemotaxis of ILK-deficient T cells to the chemokines CXCL12 (stromal cell-derived factor [SDF]-1 alpha) and CCL19 (macrophage inflammatory protein [MIP]-3 beta), as well as enhanced apoptosis of ILK-deficient cells upon stress. Signaling studies in ILK-deficient T cells demonstrated diminished phosphorylation of Akt on the activating phosphorylation site, Ser 473, and a concordant decrease in Akt kinase activity following stimulation with the chemokine SDF-1. Rac1 activation was also markedly diminished in ILK-deficient T cells following chemokine stimulation. These data extend the role of ILK to immune-cell trafficking and survival via modulation of Akt- and Rac-dependent substrates, and have implications for cell recruitment in both homeostatic and pathological processes. C1 Massachusetts Gen Hosp, Ctr Immunol & Inflammatory Dis, Charlestown, MA USA. Massachusetts Gen Hosp, Div Cardiol, Charlestown, MA USA. Harvard Univ, Sch Med, Boston, MA 02115 USA. Massachusetts Gen Hosp, Cutaneous Biol Res Ctr, Charlestown, MA USA. Massachusetts Gen Hosp, Gastrointestinal Unit, Charlestown, MA USA. Shriners Hosp Crippled Children, Montreal, PQ, Canada. McGill Univ, Montreal, PQ, Canada. Tufts Univ, Sch Med, New England Med Ctr, Mol Cardiol Res Inst, Boston, MA 02111 USA. Univ British Columbia, Dept Biochem & Mol Biol, Vancouver, BC V5Z 1M9, Canada. Vancouver Gen Hosp, Jack Bell Canc Ctr, Vancouver, BC, Canada. Hlth Sci Ctr, Vancouver, BC, Canada. RP Gerszten, RE (reprint author), Massachusetts Gen Hosp E 8307, Ctr Immunol & Inflammatory Dis, 149 13th St, Charlestown, MA 02129 USA. EM rgerszten@partners.org OI Force, Thomas/0000-0002-0450-8659 NR 32 TC 34 Z9 36 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 2005 VL 25 IS 24 BP 11145 EP 11155 DI 10.1128/MCB.25.24.11145-11155.2005 PG 11 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA 990RZ UT WOS:000233762200041 PM 16314534 ER PT J AU Knudsen, GM Medzihradszky, KF Lim, KC Hansell, E McKerrow, JH AF Knudsen, GM Medzihradszky, KF Lim, KC Hansell, E McKerrow, JH TI Proteomic analysis of Schistosoma mansoni cercarial secretions SO MOLECULAR & CELLULAR PROTEOMICS LA English DT Article ID IN-GEL DIGESTION; PROTEIN IDENTIFICATION; SERINE-PROTEASE; LIFE-CYCLE; CLONING; SKIN; ANTIGENS; TEGUMENT; IMMUNOGENICITY; PENETRATION AB Schistosomiasis is a global health problem caused by several species of schistosome blood flukes. The initial stage of infection is invasion of human skin by a multicellular larva, the cercaria. We identified proteins released by cercariae when they are experimentally induced to exhibit invasive behavior. Comparison of the proteome obtained from skin lipid-induced cercariae (the natural activator), a cleaner mechanical induction procedure, and an uninduced proteomic control allowed identification of protein groups contained in cercarial acetabular gland secretion versus other sources. These included a group of proteins involved in calcium binding, calcium regulation, and calcium-activated functions; two proteins (paramyosin and SPO-1) implicated in immune evasion; and protease isoforms implicated in degradation of host skin barriers. Several other protein families, traditionally found as cytosolic proteins, appeared concentrated in secretory cells. These included proteins with chaperone activity such as HSP70, -86, and -60. Comparison of the three experimental proteomes also allowed identification of protein contaminants from the environment that were identified because of the high sensitivity of the MS/MS system used. These included proteins from the intermediate host snail in which cercariae develop, the investigator, and the laboratory environment. Identification of proteins secreted by invasive larvae provides important new information for validation of models of skin invasion and immune evasion and aids in rational development of an anti-schistosome vaccine. C1 Univ Calif San Francisco, Dept Pathol, San Francisco, CA 94143 USA. Univ Calif San Francisco, Sandler Ctr, San Francisco, CA 94143 USA. Univ Calif San Francisco, Ctr Liver, San Francisco, CA 94143 USA. Univ Calif San Francisco, Mass Spectrometry Facil, Dept Pharmaceut Chem, San Francisco, CA 94143 USA. San Francisco Vet Affairs Med Ctr, San Francisco, CA 94121 USA. RP McKerrow, JH (reprint author), Univ Calif San Francisco, Dept Pathol, QB3,Box 2550,McKerrow 508B, San Francisco, CA 94143 USA. EM jmck@cgl.ucsf.edu FU NCRR NIH HHS [RR001614, RR012961, RR015804]; NIGMS NIH HHS [P41 GM103481] NR 42 TC 123 Z9 130 U1 3 U2 19 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA SN 1535-9476 J9 MOL CELL PROTEOMICS JI Mol. Cell. Proteomics PD DEC PY 2005 VL 4 IS 12 BP 1862 EP 1875 DI 10.1074/mcp.M500097-MCP200 PG 14 WC Biochemical Research Methods SC Biochemistry & Molecular Biology GA 990WP UT WOS:000233774200003 PM 16112986 ER PT J AU Petryshen, TL Middleton, FA Tahl, AR Rockwell, GN Purcell, S Aldinger, KA Kirby, A Morley, CP McGann, L Gentile, KL Waggoner, SG Medeiros, HM Carvalho, C Macedo, A Albus, M Maier, W Trixler, M Eichhammer, P Schwab, SG Wildenauer, DB Azevedo, MH Pato, MT Pato, CN Daly, MJ Sklar, P AF Petryshen, TL Middleton, FA Tahl, AR Rockwell, GN Purcell, S Aldinger, KA Kirby, A Morley, CP McGann, L Gentile, KL Waggoner, SG Medeiros, HM Carvalho, C Macedo, A Albus, M Maier, W Trixler, M Eichhammer, P Schwab, SG Wildenauer, DB Azevedo, MH Pato, MT Pato, CN Daly, MJ Sklar, P TI Genetic investigation of chromosome 5q GABA(A) receptor subunit genes in schizophrenia SO MOLECULAR PSYCHIATRY LA English DT Review DE linkage disequilibrium; haplotypes; single nucleotide polymorphisms; oligonucleotide array sequence analysis; gene expression ID GENOME-WIDE SCAN; FAMILY-BASED ASSOCIATION; AT-RISK HAPLOTYPE; SUSCEPTIBILITY LOCI; PREFRONTAL CORTEX; BIPOLAR DISORDER; MESSENGER-RNAS; LINKAGE ANALYSIS; POPULATION STRATIFICATION; MICROARRAY ANALYSIS AB We previously performed a genome- wide linkage scan in Portuguese schizophrenia families that identified a risk locus on chromosome 5q31 - q35. This finding was supported by meta-analysis of 20 other schizophrenia genome- wide scans that identified 5q23.2 - q34 as the second most compelling susceptibility locus in the genome. In the present report, we took a two- stage candidate gene association approach to investigate a group of gamma- aminobutyric acid ( GABA) A receptor subunit genes ( GABRA1, GABRA6, GABRB2, GABRG2, and GABRP) within our linkage peak. These genes are plausible candidates based on prior evidence for GABA system involvement in schizophrenia. In the first stage, associations were detected in a Portuguese patient sample with single nucleotide polymorphisms ( SNPs) and haplotypes in GABRA1 ( P = 0.00062 - 0.048), GABRP ( P = 0.0024 - 0.042), and GABRA6 ( P = 0.0065 - 0.0088). The GABRA1 and GABRP findings were replicated in the second stage in an independent German family- based sample ( P = 0.0015 - 0.043). Supportive evidence for association was also obtained for a previously reported GABRB2 risk haplotype. Exploratory analyses of the effects of associated GABRA1 haplotypes on transcript levels found altered expression of GABRA6 and coexpressed genes of GABRA1 and GABRB2. Comparison of transcript levels in schizophrenia patients and unaffected siblings found lower patient expression of GABRA6 and coexpressed genes of GABRA1. Interestingly, the GABRA1 coexpressed genes include synaptic and vesicle- associated genes previously found altered in schizophrenia prefrontal cortex. Taken together, these results support the involvement of the chromosome 5q GABA(A) receptor gene cluster in schizophrenia, and suggest that schizophrenia- associated haplotypes may alter expression of GABA- related genes. C1 Harvard Univ, Broad Inst, Program Med & Populat Genet, Cambridge, MA 02138 USA. MIT, Cambridge, MA 02139 USA. Ctr Human Genet Res, Psychiat & Neurodev Genet Unit, Boston, MA 02114 USA. Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Psychiat, Boston, MA USA. SUNY Syracuse, Ctr Neuropsychiat Genet, Syracuse, NY USA. SUNY Syracuse, Dept Psychiat, Syracuse, NY USA. SUNY Syracuse, Dept Neurosci & Physiol, Syracuse, NY USA. Massachusetts Gen Hosp, Ctr Human Genet Res, Boston, MA 02114 USA. Georgetown Univ, Dept Psychiat, Washington, DC USA. Univ Coimbra, Coimbra, Portugal. Mental State Hosp, Haar, Germany. Univ Bonn, Dept Psychiat, D-5300 Bonn, Germany. Univ Med Sch Pecs, Dept Psychiat, Pecs, Hungary. Univ Regensburg, Dept Psychiat, D-8400 Regensburg, Germany. Univ Western Australia, Western Australian Inst Med Res, Crawley, WA, Australia. Univ Western Australia, Med Res Ctr, Crawley, WA, Australia. Univ Western Australia, Sch Psychiat & Clin Neurosci, Crawley, WA, Australia. Vet Adm Med Ctr, Washington, DC 20422 USA. RP Sklar, P (reprint author), Ctr Human Genet Res, Psychiat & Neurodev Genet Unit, 185 Cambridge St,6th Floor, Boston, MA 02114 USA. EM sklar@psych.mgh.harvard.edu RI macedo santos, antonio/M-5737-2013; Morley, Christopher P/K-1907-2014; OI macedo santos, antonio/0000-0003-2180-2718; Morley, Christopher P/0000-0003-0185-7148; de Oliveira Barreto Coimbra Carvalho, Celia Maria/0000-0003-4453-8139 FU NIMH NIH HHS [MH058693, MH52618] NR 110 TC 69 Z9 73 U1 2 U2 5 PU NATURE PUBLISHING GROUP PI LONDON PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND SN 1359-4184 J9 MOL PSYCHIATR JI Mol. Psychiatr. PD DEC PY 2005 VL 10 IS 12 BP 1074 EP 1088 DI 10.1038/sj.mp.4001739 PG 15 WC Biochemistry & Molecular Biology; Neurosciences; Psychiatry SC Biochemistry & Molecular Biology; Neurosciences & Neurology; Psychiatry GA 986QA UT WOS:000233463600004 PM 16172613 ER PT J AU Devlin, B Cook, EH Coon, H Dawson, G Grigorenko, EL McMahon, W Minshew, N Pauls, D Smith, M Spence, MA Rodier, PM Stodgell, C Schellenberg, GD AF Devlin, B Cook, EH Coon, H Dawson, G Grigorenko, EL McMahon, W Minshew, N Pauls, D Smith, M Spence, MA Rodier, PM Stodgell, C Schellenberg, GD CA CPEA Genetics Network TI Autism and the serotonin transporter: the long and short of it SO MOLECULAR PSYCHIATRY LA English DT Article DE autism; serotonin transporter; heterogeneity; genetic association; autistic disorder ID FAMILY-BASED ASSOCIATION; GENE PROMOTER VARIANTS; LINKAGE DISEQUILIBRIUM; GENOMEWIDE SCREEN; PERSONALITY-TRAITS; GENOMIC SCREEN; DISORDER; SLC6A4; REGION; POLYMORPHISM AB Autism is a neurodevelopmental disorder manifesting early in childhood. Some symptoms of autism are alleviated by treatment with selective serotonin reuptake inhibitors, which are known to interact with the serotonin transporter. Moreover, variation in the gene that encodes the transporter ( SLC6A4), especially the HTTLPR locus, is known to modulate its expression. It is natural, therefore, to evaluate whether this variation plays a role in liability to autism. We investigated the impact of alleles at HTTLPR and three other loci in SLC6A4 by using a large, independent family- based sample ( 390 families, 1528 individuals) from the NIH Collaborative Programs of Excellence in Autism ( CPEA) network. Allele transmissions to individuals diagnosed with autism were biased only for HTTLPR, both for the narrow diagnosis of autism ( P = 0.035) and for the broader diagnosis of autism spectrum ( P = 0.007). The short allele of HTTLPR was significantly overtransmitted. Investigation of haplotype transmissions suggested that, in our data, biased transmission was only due to HTTLPR. With respect to this locus, there are now seven of 12 studies reporting significant transmission bias of HTTLPR alleles, a noteworthy result in itself. However, the studies with significant findings are almost equally divided between overtransmission of short and overtransmission of long alleles. We place our results within this extremely heterogeneous field of studies. Determining the factors influencing the relationship between autism phenotypes and HTTLPR variation, as well as other loci in SLC6A4, could be an important advance in our understanding of this complex disorder. C1 Vet Affairs Med Ctr, Seattle, WA 98108 USA. Univ Pittsburgh, Dept Psychiat, Pittsburgh, PA USA. Univ Illinois, Inst Juvenile Res, Dept Psychiat, Chicago, IL USA. Univ Utah, Dept Psychiat, Div Child & Adolescent Psychiat, Salt Lake City, UT USA. Univ Washington, Dept Psychol, Seattle, WA 98195 USA. Yale Univ, Sch Med, Ctr Child Study, New Haven, CT 06510 USA. Yale Univ, Sch Med, Dept Psychol, New Haven, CT 06510 USA. Harvard Univ, Sch Med, Massachusetts Gen Hosp, Unit Psychiat & Neurodev Genet, Charlestown, MA USA. Univ Calif Irvine, Dept Pediat, Irvine, CA 92717 USA. Univ Rochester, Med Ctr, Dept OB GYN, Rochester, NY 14642 USA. Univ Washington, Dept Med, Seattle, WA USA. Univ Washington, Dept Neurol, Seattle, WA USA. Univ Washington, Dept Pharmacol, Seattle, WA 98195 USA. RP Schellenberg, GD (reprint author), Vet Affairs Med Ctr, 182B,1660 S Columbian Rd, Seattle, WA 98108 USA. EM zachdad@u.washington.edu RI Stodgell, Christopher/A-1161-2007; OI Stodgell, Christopher/0000-0002-1666-5299 FU NCRR NIH HHS [M01-RR00064, M01-RR00044]; NICHD NIH HHS [P01 HD35476, U19 HD035465, U19 HD035466, U19 HD035469, U19 HD35482]; NIMH NIH HHS [MH057881, R01 MH057881] NR 44 TC 118 Z9 125 U1 6 U2 12 PU NATURE PUBLISHING GROUP PI LONDON PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND SN 1359-4184 J9 MOL PSYCHIATR JI Mol. Psychiatr. PD DEC PY 2005 VL 10 IS 12 BP 1110 EP 1116 DI 10.1038/sj.mp.4001724 PG 7 WC Biochemistry & Molecular Biology; Neurosciences; Psychiatry SC Biochemistry & Molecular Biology; Neurosciences & Neurology; Psychiatry GA 986QA UT WOS:000233463600008 PM 16103890 ER PT J AU Aghi, M Chiocca, EA AF Aghi, M Chiocca, EA TI Contribution of bone marrow-derived cells to blood vessels in ischemic tissues and tumors SO MOLECULAR THERAPY LA English DT Review DE endothelial progenitor cells; vasculogenesis; angiogenesis; bone marrow; neoplasms; ischemia; blood vessels; gene therapy ID ENDOTHELIAL PROGENITOR CELLS; DOSE METRONOMIC CHEMOTHERAPY; HEMATOPOIETIC STEM-CELLS; IN-VIVO; INDUCED ANGIOGENESIS; PRECURSOR CELLS; MURINE TUMORS; CD34(+) CELLS; GROWTH-FACTOR; NEOVASCULARIZATION AB Vessels are formed during embryonic development through three distinct processes. Angiogenesis and arteriogenesis involve the remodeling of established capillary networks and arterioles, while vasculogenesis involves the differentiation of mesodermal progenitor cells called angioblasts into mature endothelial cells. Until recently, postnatal vessel development was felt to occur exclusively through angiogenesis or arteriogenesis. However, recent studies using experimental tumor and ischemia models have raised controversy regarding whether vasculogenesis occurs in postnatal vessel development, with some studies suggesting the possibility and others refuting it. Here, we summarize the process of embryonic vessel development and review studies investigating the role of postnatal vasculogenesis in vessel formation in adult ischemia and tumors. We then focus on studies in which wild-type and genetically modified vascular progenitor cells have been investigated as possible cellular therapies for tumors or ischemia. We also take note of key issues that will need to be understood about the biology of vasculogenesis before cellular therapies utilizing vascular progenitor cells can be finally taken from the bench to the bedside. C1 Massachusetts Gen Hosp, Dept Neurosurg, Boston, MA 02114 USA. Harvard Univ, Sch Med, Boston, MA 02114 USA. Ohio State Univ, Med Ctr, Dept Neurosurg, Columbus, OH 43210 USA. RP Aghi, M (reprint author), Massachusetts Gen Hosp, Dept Neurosurg, White Bldg Room 502,55 Fruit St, Boston, MA 02114 USA. EM maghi@partners.org NR 64 TC 53 Z9 57 U1 1 U2 4 PU NATURE PUBLISHING GROUP PI NEW YORK PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA SN 1525-0016 J9 MOL THER JI Mol. Ther. PD DEC PY 2005 VL 12 IS 6 BP 994 EP 1005 DI 10.1016/j.ymthe.2005.07.693 PG 12 WC Biotechnology & Applied Microbiology; Genetics & Heredity; Medicine, Research & Experimental SC Biotechnology & Applied Microbiology; Genetics & Heredity; Research & Experimental Medicine GA 992DN UT WOS:000233864700002 PM 16137927 ER PT J AU Braun, SE Wong, FE Connole, M Qiu, G Lee, L Gillis, J Lu, XB Humeau, L Slepushkin, V Binder, GK Dropulic, B Johnson, RP AF Braun, SE Wong, FE Connole, M Qiu, G Lee, L Gillis, J Lu, XB Humeau, L Slepushkin, V Binder, GK Dropulic, B Johnson, RP TI Inhibition of simian/human immunodeficiency virus replication in CD4(+) T cells derived from lentiviral-transduced CD34(+) hematopoietic cells SO MOLECULAR THERAPY LA English DT Article DE HIV-1; SHIV; gene therapy; lentiviral vectors; hematopoietic stem cells; nonhuman primates ID NOD/SCID REPOPULATING CELLS; GENE-THERAPY; STEM-CELLS; VECTOR TRANSDUCTION; HIV-1 REPLICATION; PROGENITOR CELLS; INSERTIONAL MUTAGENESIS; TYPE-1 REPLICATION; MEDIATED TRANSFER; INFECTED PATIENTS AB We examined the ability of a HIV-1-based vector (VRX494) encoding a 937-bp antisense HIV-1 envelope sequence to inhibit the replication of chimeric SIV/HIV-1 viruses encoding the HIV-1 envelope. Challenge of VRX494-transduced CEMx174 cells resulted in potent inhibition of HIV-1 and several SHIV strains. To evaluate the potential efficacy of the VRX494 vector for stem cell gene therapy, rhesus CD34(+) bone marrow cells were transduced with VRX494 and then cultured on thymus stroma to induce T cell differentiation. Transduction conditions for CD34(+) cells were optimized to yield high transduction efficiency with minimal effective multiplicity of infection. Purified CD4(+) GFP(+) T cells derived from VRX494-transduced CD34(+) cells strongly inhibited SHIV HXBC2P 3.2 and SHIV 89.6P replication compared to controls. Southern blot analysis of VRX494-transduced T cell clones revealed a subset of cells with multiple proviral copies per cell. Expression of GFP and the antisense inhibitor in VRX494-transduced cells was upregulated by Tat. Analysis of HIV-1 envelope sequences in VRX494-transduced cells revealed modifications consistent with those mediated by double-stranded RNA-dependent adenosine deaminase. These results indicate that the macaque/SHIV model should serve as a useful preclinical model to evaluate this lentiviral vector expressing an HIV-1 antisense inhibitor for stem cell gene therapy for AIDS. C1 Harvard Univ, Sch Med, Div Immunol, New England Reg Primate Res Ctr, Southborough, MA 01772 USA. VIRxSYS Corp, Gaithersburg, MD 20877 USA. Johns Hopkins Univ, Sch Med, Sydney Kimmel Comprehens Canc Ctr, Baltimore, MD 21231 USA. Massachusetts Gen Hosp, Partners AIDS Res Ctr, Boston, MA 02129 USA. Massachusetts Gen Hosp, Infect Dis Unit, Boston, MA 02129 USA. RP Braun, SE (reprint author), Harvard Univ, Sch Med, Div Immunol, New England Reg Primate Res Ctr, 1 Pine Hill Dr, Southborough, MA 01772 USA. EM stephen_braun@hms.harvard.edu FU NCI NIH HHS [CA 73473]; NCRR NIH HHS [RR 00168]; NIAID NIH HHS [AI 42851] NR 52 TC 8 Z9 10 U1 1 U2 2 PU ACADEMIC PRESS INC ELSEVIER SCIENCE PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA SN 1525-0016 J9 MOL THER JI Mol. Ther. PD DEC PY 2005 VL 12 IS 6 BP 1157 EP 1167 DI 10.1016/j.ymthe.2005.07.698 PG 11 WC Biotechnology & Applied Microbiology; Genetics & Heredity; Medicine, Research & Experimental SC Biotechnology & Applied Microbiology; Genetics & Heredity; Research & Experimental Medicine GA 992DN UT WOS:000233864700019 PM 16168713 ER PT J AU Nishimura, RN Sharp, FR AF Nishimura, RN Sharp, FR TI Heat shock proteins and neuromuscular disease SO MUSCLE & NERVE LA English DT Review DE amyotrophic lateral sclerosis; cell injury; chaperones; heat shock proteins; inflammatory myopathy; motor neuron disease; muscle; muscular dystrophy; neuromuscular diseases; neuropathy; stress proteins ID ALPHA-B-CRYSTALLIN; HUMAN SKELETAL-MUSCLE; AMYOTROPHIC-LATERAL-SCLEROSIS; BULBAR MUSCULAR-ATROPHY; RAT HINDLIMB MUSCLES; CONTINUOUS CONTRACTILE ACTIVITY; ENDOPLASMIC-RETICULUM STRESS; ANDROGEN RECEPTOR PROTEIN; DESMIN-RELATED MYOPATHY; HSP72 GENE-EXPRESSION AB The heat shock proteins are families of proteins with known activities that include chaperoning nascent peptides within the cell and cytoprotection. Most work on the nervous system has related to the role of heat shock proteins in neuroprotection from either hypoxic-ischemic or traumatic injury. The role of these proteins during normal physiological activity and injury is still under investigation. Heat shock proteins in neuromuscular disease have been investigated to some extent but were largely neglected until recently. The goal of this review is to summarize the evidence linking heat shock proteins with neuromuscular disease and to provide some insight into the roles or functions of these proteins in disease states. C1 Vet Affairs Greater Los Angeles Healthcare Syst, Dept Neurol, Sepulveda, CA 91343 USA. Univ Calif Los Angeles, David Geffen Sch Med, Dept Neurol, Los Angeles, CA USA. Univ Calif Davis, MIND Inst, Sacramento, CA 95817 USA. Univ Calif Davis, Dept Neurol, Sacramento, CA 95817 USA. RP Nishimura, RN (reprint author), Vet Affairs Greater Los Angeles Healthcare Syst, Dept Neurol, 16111 Plummer St, Sepulveda, CA 91343 USA. EM rnishimu@ucla.edu NR 169 TC 28 Z9 28 U1 0 U2 1 PU JOHN WILEY & SONS INC PI HOBOKEN PA 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 0148-639X J9 MUSCLE NERVE JI Muscle Nerve PD DEC PY 2005 VL 32 IS 6 BP 693 EP 709 DI 10.1002/mus.20373 PG 17 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA 990HP UT WOS:000233734100001 PM 15962334 ER PT J AU McCarthy Jr Perez, JM Bruckner, C Weissleder, R AF McCarthy, JR Perez, JM Bruckner, C Weissleder, R TI Polymeric nanoparticle preparation that eradicates tumors SO NANO LETTERS LA English DT Article ID SINGLET OXYGEN PRODUCTION; PHOTODYNAMIC THERAPY; QUANTUM YIELDS; IN-VIVO; DELIVERY; CANCER; DRUG; PHOTOSENSITIZERS; DERIVATIVES; METASTASES AB We report the production of poly(lactic-co-glycolic acid) nanoparticles that encapsulate the photosensitizer meso-tetraphenylporpholactol. These nanoparticles are stable and nonphototoxic upon systemic administration. Upon cellular internalization, the photosensitizer is released from the nanoparticle and becomes highly phototoxic. Irradiation with visible light results in cell-specific killing of several cancer cell lines. Importantly, in vivo experiments show complete eradication of cancers in mouse models. The concept of photosensitizers with selective phototoxicity should have widespread applications in cancer therapy. C1 Harvard Univ, Sch Med, Massachusetts Gen Hosp, Ctr Mol Imaging Res, Charlestown, MA 02129 USA. Univ Connecticut, Dept Chem, Storrs, CT 06269 USA. RP Weissleder, R (reprint author), Harvard Univ, Sch Med, Massachusetts Gen Hosp, Ctr Mol Imaging Res, Bldg 149,13th St,Room 5403, Charlestown, MA 02129 USA. OI Bruckner, Christian/0000-0002-1560-7345 FU NCI NIH HHS [CA 101078 1, P50 CA 86355, T32 CA 79443]; NHLBI NIH HHS [R01 HL 080731] NR 34 TC 128 Z9 134 U1 1 U2 29 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 2005 VL 5 IS 12 BP 2552 EP 2556 DI 10.1021/nl0519229 PG 5 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 998YY UT WOS:000234357000040 PM 16351214 ER PT J AU Mukherjee, A Veraksa, A Bauer, A Rosse, C Camonis, J Artavanis-Tsakonas, S AF Mukherjee, A Veraksa, A Bauer, A Rosse, C Camonis, J Artavanis-Tsakonas, S TI Regulation of notch signalling by non-visual beta-arrestin SO NATURE CELL BIOLOGY LA English DT Article ID FACTOR-I RECEPTOR; DROSOPHILA-MELANOGASTER; ANKYRIN REPEATS; DOWN-REGULATION; PROTEIN; DELTEX; PATHWAY; ENDOCYTOSIS; BETA-ARRESTIN-2; UBIQUITINATION AB Signalling activity of the Notch receptor, which plays a fundamental role in metazoan cell fate determination, is controlled at multiple levels. We uncovered a Notch signal-controlling mechanism that depends on the ability of the non-visual P-arrestin, Kurtz (Krz), to influence the degradation and, consequently, the function of the Notch receptor. We identified Krz as a binding partner of a known Notch-pathway modulator, Deltex (Dx), and demonstrated the existence of a trimeric Notch-Dx-Krz protein complex. This complex mediates the degradation of the Notch receptor through a ubiquitination-dependent pathway. Our results establish a novel mode of regulation of Notch signalling and define a new function for non-visual beta-arrestins. C1 Harvard Univ, Massachusetts Gen Hosp, Sch Med, Canc Ctr,Dept Cell Biol, Charlestown, MA 02129 USA. Inst Curie, F-75248 Paris, France. Cellzome AG, D-69117 Heidelberg, Germany. Coll France, F-75231 Paris, France. RP Artavanis-Tsakonas, S (reprint author), Harvard Univ, Massachusetts Gen Hosp, Sch Med, Canc Ctr,Dept Cell Biol, Charlestown, MA 02129 USA. EM tsakonas@helix.mgh.harvard.edu FU NCI NIH HHS [CA098402]; NIGMS NIH HHS [GM62931]; NINDS NIH HHS [NS26084] NR 50 TC 121 Z9 122 U1 0 U2 2 PU NATURE PUBLISHING GROUP PI LONDON PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND SN 1465-7392 J9 NAT CELL BIOL JI Nat. Cell Biol. PD DEC PY 2005 VL 7 IS 12 BP 1191 EP 1201 DI 10.1038/ncb1327 PG 11 WC Cell Biology SC Cell Biology GA 990MW UT WOS:000233748900012 PM 16284625 ER PT J AU Stern, HM Murphey, RD Shepard, JL Amatruda, JF Straub, CT Pfaff, KL Weber, G Tallarico, JA King, RW Zon, LI AF Stern, HM Murphey, RD Shepard, JL Amatruda, JF Straub, CT Pfaff, KL Weber, G Tallarico, JA King, RW Zon, LI TI Small molecules that delay S phase suppress a zebrafish bmyb mutant SO NATURE CHEMICAL BIOLOGY LA English DT Article ID DNA-REPLICATION; CHECKPOINT; TRANSCRIPTION; DISCOVERY; MUTATION; CANCER; DAMAGE; ATR; ACTIVATION; EXPRESSION AB Bmyb is a ubiquitously expressed transcription factor involved in cellular proliferation and cancer(1-4). Loss of bmyb function in the zebrafish mutant crash&burn (crb) results in decreased cyclin B1 expression, mitotic arrest and genome instability(5). These phenotypic observations in crb mutants could be attributed to the decreased expression of cyclin B1, a cell-cycle regulatory protein that is responsible for driving cell progression from G2 through mitosis. To identify small molecules that interact with the bmyb pathway, we developed an embryo-based suppressor screening strategy. In 16 weeks we screened a diverse similar to 16,000 compound library, and discovered one previously unknown compound, persynthamide (psy, 1), that suppressed bmyb-dependent mitotic defects. Psytreated embryos showed an S-phase delay, and knockdown of the cell-cycle checkpoint regulator ataxia telangiectasia-and Rad-related kinase (ATR) abrogated the suppression of crb. The DNA synthesis inhibitors aphidicolin (2) and hydroxyurea (3) also suppressed crb. S-phase inhibition upregulated cyclin B1 mRNA, promoting the progression of cells through mitosis. Our study demonstrates that chemical suppressor screening in zebrafish can identify compounds with cell-cycle activity and can be used to identify pathways that interact with specific cell-cycle phenotypes. C1 Brigham & Womens Hosp, Dept Pathol, Boston, MA 02115 USA. Childrens Hosp, Dana Farber Canc Inst, Howard Hughes Med Inst, Stem Cell Program, Boston, MA 02115 USA. Childrens Hosp, Dana Farber Canc Inst, Howard Hughes Med Inst, Div Hematol & Oncol, Boston, MA 02115 USA. Harvard Univ, Sch Med, Boston, MA 02115 USA. Harvard Univ, Sch Med, Inst Chem & Cell Biol, Boston, MA 02115 USA. RP Zon, LI (reprint author), Brigham & Womens Hosp, Dept Pathol, 75 Francis St, Boston, MA 02115 USA. EM zon@enders.tch.harvard.edu OI King, Randall/0000-0001-7882-8180 FU NIDDK NIH HHS [5K08 DK061849, 1R01 DK55381] NR 28 TC 111 Z9 116 U1 0 U2 14 PU NATURE PUBLISHING GROUP PI NEW YORK PA 345 PARK AVENUE SOUTH, NEW YORK, NY 10010-1707 USA SN 1552-4450 J9 NAT CHEM BIOL JI Nat. Chem. Biol. PD DEC PY 2005 VL 1 IS 7 BP 366 EP 370 DI 10.1038/nchembio749 PG 5 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA 986KE UT WOS:000233447700007 PM 16372403 ER PT J AU Ryan, PD Goss, PE AF Ryan, PD Goss, PE TI The evolving role of aromatase inhibitors in the treatment of early-stage breast cancer SO NATURE CLINICAL PRACTICE ONCOLOGY LA English DT Editorial Material ID POSTMENOPAUSAL WOMEN; TAMOXIFEN THERAPY; RANDOMIZED-TRIAL; RECURRENCE C1 Massachusetts Gen Hosp, Breast & Ovarian Canc Genet Clin, Boston, MA 02114 USA. Harvard Univ, Sch Med, Cambridge, MA 02138 USA. RP Ryan, PD (reprint author), Massachusetts Gen Hosp, Ctr Canc, 100 Blossom St,Cox 640, Boston, MA 02114 USA. EM pdryan@partners.org NR 10 TC 2 Z9 2 U1 0 U2 1 PU NATURE PUBLISHING GROUP PI NEW YORK PA 345 PARK AVENUE SOUTH, NEW YORK, NY 10010-1707 USA SN 1743-4254 J9 NAT CLIN PRACT ONCOL JI Nat. Clin. Pract. Oncol. PD DEC PY 2005 VL 2 IS 12 BP 596 EP 597 DI 10.1038/ncponc0360 PG 2 WC Oncology SC Oncology GA 989BF UT WOS:000233647200002 PM 16341095 ER PT J AU Smith, MR AF Smith, MR TI Therapy insight: osteoporosis during hormone therapy for prostate cancer SO NATURE CLINICAL PRACTICE UROLOGY LA English DT Review DE fracture; GnRH agonist; osteoporosis; prostate cancer ID BONE-MINERAL DENSITY; ANDROGEN-DEPRIVATION THERAPY; X-RAY ABSORPTIOMETRY; RANDOMIZED CONTROLLED-TRIAL; POSTMENOPAUSAL WOMEN; VITAMIN-D; OLDER MEN; ZOLEDRONIC ACID; HIP-FRACTURES; SEX STEROIDS AB The intended therapeutic effect of gonadotropin-releasing-hormone (GnRH) agonists is hypogonadism, which is a leading cause of osteoporosis in men. Observations are consistent with this effect: GnRH agonists decrease bone mineral density and increase fracture risk in men with prostate cancer. Estrogens play a central role in homeostasis of the normal male skeleton and evidence suggests that estrogen deficiency is primarily responsible for the adverse skeletal effects of GnRH agonists. The mechanism of treatment-related bone loss involves acceleration of physiologic bone turnover. In small, randomized, controlled trials, bisphosphonates (pamidronate, zoledronic acid) and selective estrogen-receptor modulators (raloxifene, toremifene) increased bone mineral density in GnRH-agonist-treated men. Two ongoing large, randomized, placebo-controlled studies will prospectively define fracture outcomes in men with prostate cancer and assess the efficacy of novel pharmacologic interventions (AMG 162, toremifene) in GnRH-agonist-treated men. C1 Massachusetts Gen Hosp, Div Hematol & Oncol, Boston, MA 02114 USA. Harvard Univ, Sch Med, Boston, MA USA. RP Smith, MR (reprint author), Massachusetts Gen Hosp, Div Hematol & Oncol, Cox 640,100 Blossom St, Boston, MA 02114 USA. EM smith.matthew@mgh.harvard.edu NR 66 TC 8 Z9 10 U1 0 U2 0 PU NATURE PUBLISHING GROUP PI NEW YORK PA 345 PARK AVENUE SOUTH, NEW YORK, NY 10010-1707 USA SN 1743-4270 J9 NAT CLIN PRACT UROL JI Nat. Clin. Pract. Urol. PD DEC PY 2005 VL 2 IS 12 BP 608 EP 615 DI 10.1038/nopuro0326 PG 8 WC Urology & Nephrology SC Urology & Nephrology GA 990GN UT WOS:000233731300011 PM 16474548 ER PT J AU Bell, DW Gore, I Okimoto, RA Godin-Heymann, N Sordella, R Mulloy, R Sharma, SV Brannigan, BW Mohapatra, G Settleman, J Haber, DA AF Bell, DW Gore, I Okimoto, RA Godin-Heymann, N Sordella, R Mulloy, R Sharma, SV Brannigan, BW Mohapatra, G Settleman, J Haber, DA TI Inherited susceptibility to lung cancer may be associated with the T790M drug resistance mutation in EGFR SO NATURE GENETICS LA English DT Article ID ACQUIRED-RESISTANCE; KINASE INHIBITORS; TYROSINE KINASE; RECEPTOR GENE; GEFITINIB; SENSITIVITY; ERLOTINIB AB Somatic activating mutations in EGFR identify a subset of non-small cell lung cancer that respond to tyrosine kinase inhibitors. Acquisition of drug resistance is linked to a specific secondary somatic mutation, EGFR T790M. Here we describe a family with multiple cases of non-small cell lung cancer associated with germline transmission of this mutation. Four of six tumors analyzed showed a secondary somatic activating EGFR mutation, arising in cis with the germline EGFR mutation T790M. These observations implicate altered EGFR signaling in genetic susceptibility to lung cancer. C1 Harvard Univ, Sch Med, Massachusetts Gen Hosp, Ctr Canc, Charlestown, MA 02129 USA. St Vincents Hosp, Bruno Canc Ctr, Birmingham, AL 35205 USA. Harvard Univ, Sch Med, Massachusetts Gen Hosp, Dept Pathol, Charlestown, MA 02129 USA. RP Haber, DA (reprint author), Harvard Univ, Sch Med, Massachusetts Gen Hosp, Ctr Canc, 13th St, Charlestown, MA 02129 USA. EM haber@helix.mgh.harvard.edu NR 15 TC 218 Z9 235 U1 1 U2 16 PU NATURE PUBLISHING GROUP PI NEW YORK PA 345 PARK AVENUE SOUTH, NEW YORK, NY 10010-1707 USA SN 1061-4036 J9 NAT GENET JI Nature Genet. PD DEC PY 2005 VL 37 IS 12 BP 1315 EP 1316 DI 10.1038/ng1671 PG 2 WC Genetics & Heredity SC Genetics & Heredity GA 989FC UT WOS:000233657300008 PM 16258541 ER PT J AU Monsuur, AJ de Bakker, PIW Alizadeh, BZ Zhernakova, A Bevova, MR Strengman, E Franke, L van't Slot, R van Belzen, MJ Lavrijsen, ICM Diosdado, B Daly, MJ Mulder, CJJ Mearin, ML Meijer, JWR Meijer, GA van Oort, E Wapenaar, MC Koeleman, BPC Wijmenga, C AF Monsuur, AJ de Bakker, PIW Alizadeh, BZ Zhernakova, A Bevova, MR Strengman, E Franke, L van't Slot, R van Belzen, MJ Lavrijsen, ICM Diosdado, B Daly, MJ Mulder, CJJ Mearin, ML Meijer, JWR Meijer, GA van Oort, E Wapenaar, MC Koeleman, BPC Wijmenga, C TI Myosin IXB variant increases the risk of celiac disease and points toward a primary intestinal barrier defect SO NATURE GENETICS LA English DT Article ID EPITHELIAL BARRIER; PREVALENCE; MAPS AB Celiac disease is probably the best-understood immune-related disorder. The disease presents in the small intestine and results from the interplay between multiple genes and gluten, the triggering environmental factor(1). Although HLA class II genes explain 40% of the heritable risk, non-HLA genes accounting for most of the familial clustering have not yet been identified. Here we report significant and replicable association (P = 2.1 x 10(-6)) to a common variant located in intron 28 of the gene myosin IXB (MYO9B), which encodes an unconventional myosin molecule that has a role in actin remodeling of epithelial enterocytes(2,3). Individuals homozygous with respect to the at-risk allele have a 2.3-times higher risk of celiac disease ( P = 1.55 x 10(-5)). This result is suggestive of a primary impairment of the intestinal barrier in the etiology of celiac disease, which may explain why immunogenic gluten peptides are able to pass through the epithelial barrier. C1 Univ Med Ctr Utrecht, DBG Dept Med Genet, Complex Genet Sect, NL-3584 CG Utrecht, Netherlands. Harvard Univ, Broad Inst, Cambridge, MA 02141 USA. MIT, Broad Inst, Cambridge, MA 02141 USA. Massachusetts Gen Hosp, Ctr Human Genet Res, Boston, MA 02114 USA. VU Univ Med Ctr, Dept Gastroenterol, NL-1007 MB Amsterdam, Netherlands. Leiden Univ, Med Ctr, Dept Pediat, NL-2300 RC Leiden, Netherlands. Rijnstate Hosp, Dept Pathol, NL-6800 TA Arnhem, Netherlands. VU Univ Med ctr, Dept Pathol, NL-1007 MB Amsterdam, Netherlands. RP Wijmenga, C (reprint author), Univ Med Ctr Utrecht, DBG Dept Med Genet, Complex Genet Sect, Univ Weg 100, NL-3584 CG Utrecht, Netherlands. EM t.n.wijmenga@med.uu.nl RI de Bakker, Paul/B-8730-2009; Wijmenga, Cisca/D-2173-2009; OI de Bakker, Paul/0000-0001-7735-7858; Franke, Lude/0000-0002-5159-8802; Zhernakova, Alexandra/0000-0002-4574-0841; Wijmenga, Cisca/0000-0002-5635-1614; Ziad Alizadeh, Behrooz/0000-0002-1415-8007 NR 24 TC 153 Z9 161 U1 1 U2 8 PU NATURE PUBLISHING GROUP PI NEW YORK PA 345 PARK AVENUE SOUTH, NEW YORK, NY 10010-1707 USA SN 1061-4036 J9 NAT GENET JI Nature Genet. PD DEC PY 2005 VL 37 IS 12 BP 1341 EP 1344 DI 10.1038/ng1680 PG 4 WC Genetics & Heredity SC Genetics & Heredity GA 989FC UT WOS:000233657300013 PM 16282976 ER PT J AU Luster, AD Alon, R von Andrian, UH AF Luster, AD Alon, R von Andrian, UH TI Immune cell migration in inflammation: present and future therapeutic targets SO NATURE IMMUNOLOGY LA English DT Review ID CD8(+) T-CELLS; IN-VIVO; DENDRITIC CELLS; L-SELECTIN; INTEGRIN ACTIVATION; EXTRACELLULAR-MATRIX; PERIPHERAL-TISSUES; ENDOTHELIAL-CELLS; LYMPHOID-TISSUES; INFLAMED TISSUES AB The burgeoning field of leukocyte trafficking has created new and exciting opportunities in the clinic. Trafficking signals are being defined that finely control the movement of distinct subsets of immune cells into and out of specific tissues. Because the accumulation of leukocytes in tissues contributes to a wide variety of diseases, these 'molecular codes' have provided new targets for inhibiting tissue-specific inflammation, which have been confirmed in the clinic. However, immune cell migration is also critically important for the delivery of protective immune responses to tissues. Thus, the challenge for the future will be to identify the trafficking molecules that will most specifically inhibit the key subsets of cells that drive disease processes without affecting the migration and function of leukocytes required for protective immunity. C1 Harvard Univ, Sch Med, Massachusetts Gen Hosp,Ctr Immunol & Inflammatory, Dept Med,Div Rheumatol Allergy & Immunol, Boston, MA 02114 USA. Weizmann Inst Sci, Dept Immunol, IL-76100 Rehovot, Israel. Harvard Univ, Sch Med, CBR Inst Biomed Res, Boston, MA 02115 USA. Harvard Univ, Sch Med, Dept Pathol, Boston, MA 02115 USA. RP Luster, AD (reprint author), Harvard Univ, Sch Med, Massachusetts Gen Hosp,Ctr Immunol & Inflammatory, Dept Med,Div Rheumatol Allergy & Immunol, Boston, MA 02114 USA. EM luster.andrew@mgh.harvard.edu; ronen.alon@weizmann.ac.il; uva@cbr.med.harvard.edu RI von Andrian, Ulrich/A-5775-2008 NR 97 TC 629 Z9 643 U1 5 U2 56 PU NATURE PUBLISHING GROUP PI NEW YORK PA 345 PARK AVENUE SOUTH, NEW YORK, NY 10010-1707 USA SN 1529-2908 J9 NAT IMMUNOL JI Nat. Immunol. PD DEC PY 2005 VL 6 IS 12 BP 1182 EP 1190 DI 10.1038/ni1275 PG 9 WC Immunology SC Immunology GA 985IX UT WOS:000233371900003 PM 16369557 ER PT J AU Kretschmer, K Apostolou, I Hawiger, D Khazaie, K Nussenzweig, MC von Boehmer, H AF Kretschmer, K Apostolou, I Hawiger, D Khazaie, K Nussenzweig, MC von Boehmer, H TI Inducing and expanding regulatory T cell populations by foreign antigen SO NATURE IMMUNOLOGY LA English DT Article ID TRANSCRIPTION FACTOR FOXP3; IN-VIVO EXPANSION; DENDRITIC CELLS; AUTOIMMUNE-DISEASE; CUTTING EDGE; INDUCTION; EXPRESSION; TOLERANCE; THYMUS; UNRESPONSIVENESS AB Evidence suggests that regulatory T cells expressing the transcription factor Foxp3 develop extrathymically and intrathymically. Mechanisms of extrathymic induction require further scrutiny, especially as proliferation and/or phenotypic changes of preexisting suppressor cells must be distinguished from true de novo generation. Here we report the conversion of truly naive CD4(+) T cells into suppressor cells expressing Foxp3 by targeting of peptide-agonist ligands to dendritic cells and by analysis of Foxp3 expression at the level of single cells. We show that conversion was achieved by minute antigen doses with suboptimal dendritic cell activation. The addition of transforming growth factor-beta or the absence of interleukin 2 production, which reduces proliferation, enhanced the conversion rate. In addition, regulatory T cell populations induced in subimmunogenic conditions could subsequently be expanded by delivery of antigen in immunogenic conditions. The extrathymic generation and proliferation of regulatory T cells may contribute to self-tolerance as well as the poor immunogenicity of tumors and may be exploited clinically to prevent or reverse unwanted immunity. C1 Harvard Univ, Sch Med, Dana Farber Canc Inst, Dept Pathol, Boston, MA 02115 USA. Yale Univ, Sch Med, Immunol Sect, New Haven, CT 06520 USA. Rockefeller Univ, Lab Mol Immunol, New York, NY 10021 USA. Howard Hughes Med Inst, New York, NY 10021 USA. RP von Boehmer, H (reprint author), Harvard Univ, Sch Med, Dana Farber Canc Inst, Dept Pathol, Boston, MA 02115 USA. EM harald_von_boehmer@dfci.harvard.edu RI Kretschmer, Karsten/E-8174-2010 FU NIAID NIH HHS [R37 AI53102] NR 31 TC 778 Z9 814 U1 2 U2 25 PU NATURE PUBLISHING GROUP PI NEW YORK PA 345 PARK AVENUE SOUTH, NEW YORK, NY 10010-1707 USA SN 1529-2908 J9 NAT IMMUNOL JI Nat. Immunol. PD DEC PY 2005 VL 6 IS 12 BP 1219 EP 1227 DI 10.1038/ni1265 PG 9 WC Immunology SC Immunology GA 985IX UT WOS:000233371900009 PM 16244650 ER PT J AU Intlekofer, AM Takemoto, N Wherry, EJ Longworth, SA Northrup, JT Palanivel, VR Mullen, AC Gasink, CR Kaech, SM Miller, JD Gapin, L Ryan, K Russ, AP Lindsten, T Orange, JS Goldrath, AW Ahmed, R Reiner, SL AF Intlekofer, AM Takemoto, N Wherry, EJ Longworth, SA Northrup, JT Palanivel, VR Mullen, AC Gasink, CR Kaech, SM Miller, JD Gapin, L Ryan, K Russ, AP Lindsten, T Orange, JS Goldrath, AW Ahmed, R Reiner, SL TI Effector and memory CD8(+) T cell fate coupled by T-bet and eomesodermin SO NATURE IMMUNOLOGY LA English DT Article ID INTERLEUKIN-2 RECEPTOR-BETA; MARROW-DERIVED CELLS; IFN-GAMMA PRODUCTION; LINEAGE COMMITMENT; NATURAL-KILLER; CUTTING EDGE; HOMEOSTATIC PROLIFERATION; TRANSCRIPTION FACTOR; PROTECTIVE IMMUNITY; CD8-T-CELL MEMORY AB Two seemingly unrelated hallmarks of memory CD8(+) T cells are cytokine-driven proliferative renewal after pathogen clearance and a latent effector program in anticipation of rechallenge. Memory CD8(+) T cells and natural killer cells share cytotoxic potential and dependence on the growth factor interleukin 15. We now show that mice with compound mutations of the genes encoding the transcription factors T-bet and eomesodermin were nearly devoid of several lineages dependent on interleukin 15, including memory CD8(+) T cells and mature natural killer cells, and that their cells had defective cytotoxic effector programming. Moreover, T-bet and eomesodermin were responsible for inducing enhanced expression of CD122, the receptor specifying interleukin 15 responsiveness. Therefore, these key transcription factors link the long-term renewal of memory CD8(+) T cells to their characteristic effector potency. C1 Univ Penn, Abramson Familly Canc Res Inst, Philadelphia, PA 19104 USA. Univ Penn, Dept Med, Philadelphia, PA 19104 USA. Univ Penn, Dept Pediat, Philadelphia, PA 19104 USA. Univ Penn, Dept Pathol & Lab Med, Philadelphia, PA 19104 USA. Emory Univ, Sch Med, Emory Vaccine Ctr, Atlanta, GA 30322 USA. Emory Univ, Sch Med, Dept Microbiol & Immunol, Atlanta, GA 30322 USA. Univ Colorado, Hlth Sci Ctr, Natl Jewish Med & Res Ctr, Integrated Dept Immunol, Denver, CO 80206 USA. Univ Oxford, Dept Biochem, Genet Unit, Oxford OX1 3QU, England. Harvard Univ, Sch Med, Brigham & Womens Hosp, Joslin Diabet Ctr,Sect Immunol & Immunogenet, Boston, MA 02215 USA. Harvard Univ, Sch Med, Brigham & Womens Hosp, Dept Med, Boston, MA 02215 USA. RP Reiner, SL (reprint author), Univ Penn, Abramson Familly Canc Res Inst, Philadelphia, PA 19104 USA. EM sreiner@mail.med.upenn.edu RI Orange, Jordan/D-5239-2009; OI orange, jordan/0000-0001-7117-7725 FU NIAID NIH HHS [AI007532, AI042370, AI061699, T32 AI055428] NR 47 TC 522 Z9 527 U1 2 U2 16 PU NATURE PUBLISHING GROUP PI NEW YORK PA 345 PARK AVENUE SOUTH, NEW YORK, NY 10010-1707 USA SN 1529-2908 J9 NAT IMMUNOL JI Nat. Immunol. PD DEC PY 2005 VL 6 IS 12 BP 1236 EP 1244 DI 10.1038/ni1268 PG 9 WC Immunology SC Immunology GA 985IX UT WOS:000233371900011 PM 16273099 ER PT J AU Gao, XJ Bashirova, A Iversen, AKN Phair, J Goedert, JJ Buchbinder, S Hoots, K Vlahov, D Altfeld, M O'Brien, SJ Carrington, M AF Gao, XJ Bashirova, A Iversen, AKN Phair, J Goedert, JJ Buchbinder, S Hoots, K Vlahov, D Altfeld, M O'Brien, SJ Carrington, M TI AIDS restriction HLA allotypes target distinct intervals of HIV-1 pathogenesis SO NATURE MEDICINE LA English DT Article ID VIRUS TYPE-1 INFECTION; T-LYMPHOCYTE RESPONSE; ESCAPE MUTATION; TRANSMISSION; GAG; REVERSION; EVOLUTION AB An effective acquired immune response to infectious agents mediated by HLA-restricted T-cell recognition can target different stages of disease pathogenesis. We show here that three distinct HLA alleles known to alter the overall rate of AIDS progression act during distinct intervals after HIV-1 infection. The discrete timing of HLA allele influence suggests alternative functional mechanisms in immune defense against this dynamic and chronic immunosuppressive disease. C1 NCI, Lab Genom Divers, SAIC Frederick, Basic Res Program, Frederick, MD 21702 USA. Johns Hopkins Univ, Sch Med, Baltimore, MD 21231 USA. Univ Oxford, John Radcliffe Hosp, Weatherall Inst Mol Med, MRC Human Immunol Unit, Oxford OX3 9DS, England. Northwestern Univ, Howard Brown Hlth Ctr, Chicago, IL 60611 USA. Northwestern Univ, Fineberg Sch Med, Chicago, IL 60611 USA. NCI, Viral Epidemiol Branch, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA. San Francisco Dept Publ Hlth, San Francisco, CA 94102 USA. Univ Texas, Hlth Sci Ctr, Gulf States Hemophilia Ctr, Houston, TX 77030 USA. New York Acad Med, Ctr Urban Epidemiol Studies, New York, NY 10029 USA. Massachusetts Gen Hosp, Partners AIDS Res Ctr, Charlestown, MA 02129 USA. NCI, Lab Genom Divers, Frederick, MD 21702 USA. RP Carrington, M (reprint author), NCI, Lab Genom Divers, SAIC Frederick, Basic Res Program, POB B, Frederick, MD 21702 USA. EM carringt@ncifcrf.gov FU Intramural NIH HHS; NCI NIH HHS [N01-CO-12400]; NIDA NIH HHS [DA 04334] NR 15 TC 134 Z9 137 U1 0 U2 7 PU NATURE PUBLISHING GROUP PI NEW YORK PA 345 PARK AVENUE SOUTH, NEW YORK, NY 10010-1707 USA SN 1078-8956 J9 NAT MED JI Nat. Med. PD DEC PY 2005 VL 11 IS 12 BP 1290 EP 1292 DI 10.1038/nm1333 PG 3 WC Biochemistry & Molecular Biology; Cell Biology; Medicine, Research & Experimental SC Biochemistry & Molecular Biology; Cell Biology; Research & Experimental Medicine GA 990WR UT WOS:000233774400025 PM 16288280 ER PT J AU Karlamangla, AS Singer, BH Chodosh, J McEwen, BS Seeman, TE AF Karlamangla, AS Singer, BH Chodosh, J McEwen, BS Seeman, TE TI Urinary cortisol excretion as a predictor of incident cognitive impairment SO NEUROBIOLOGY OF AGING LA English DT Article; Proceedings Paper CT SPARK Workshop 2004 CY JUL, 2004 CL Bar Harbor, ME DE urine cortisol; resting cortisol levels; incident cognitive impairment; cognitive decline; longitudinal study; prospective cohort ID MENTAL STATUS QUESTIONNAIRE; ALZHEIMERS-DISEASE; PLASMA-CORTISOL; DEHYDROEPIANDROSTERONE-SULFATE; VASCULAR DEMENTIA; MACARTHUR; BRAIN; CORTICOSTEROIDS; STRESS; WOMEN AB Elevated glucocorticoid levels have been associated with cognitive impairment, including dementia. However, few longitudinal studies have examined the association between resting cortisol levels and the incidence of cognitive impairment. We measured overnight urinary excretion of cortisol in 538 high-functioning men and women, 70-79 years of age, in 1988, and assessed their cognitive functioning in 1988, 199 1, and 1995 using the short portable mental status questionnaire (SPMSQ). Compared to participants in the bottom quartile of urinary cortisol at baseline, those in the top three quartiles had higher risk of incident cognitive impairment over the 7-year follow up (i.e., decline in SPMSQ score to below six out of nine). This association was not affected by adjustment for age, gender, education level, ethnicity, smoking, prevalent cardiovascular disease, and blood pressure (adjusted odds ratio for the highest quartile 2.34, 95% confidence interval, 1.07-5.14). There was no effect modification by gender; the association was equally strong in men and women. We conclude that urinary excretion of cortisol predicts incident cognitive impairment in older men and women. (c) 2005 Elsevier Inc. All rights reserved. C1 Univ Calif Los Angeles, David Geffen Sch Med, Div Geriatr, Los Angeles, CA 90095 USA. Princeton Univ, Off Populat Res, Princeton, NJ 08544 USA. VA Greater Los Angeles Hlth Syst, Hlth Serv Res, Los Angeles, CA USA. Rockefeller Univ, Neuroendocrinol Lab, New York, NY 10021 USA. RP Karlamangla, AS (reprint author), Univ Calif Los Angeles, David Geffen Sch Med, Div Geriatr, 10945 Le Conte 2339, Los Angeles, CA 90095 USA. EM akarlamangla@mednet.ucla.edu OI Chodosh, Joshua/0000-0001-7784-4306 NR 36 TC 15 Z9 15 U1 5 U2 8 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0197-4580 J9 NEUROBIOL AGING JI Neurobiol. Aging PD DEC PY 2005 VL 26 SU 1 BP S80 EP S84 DI 10.1016/j.neurobiolaging.2005.09.037 PG 5 WC Geriatrics & Gerontology; Neurosciences SC Geriatrics & Gerontology; Neurosciences & Neurology GA 995SF UT WOS:000234123400018 ER PT J AU Pontikis, CC Cotman, SL MacDonald, ME Cooper, JD AF Pontikis, CC Cotman, SL MacDonald, ME Cooper, JD TI Thalamocortical neuron loss and localized astrocytosis in the Cln3(triangle ex7/8) knock-in mouse model of Batten disease SO NEUROBIOLOGY OF DISEASE LA English DT Article DE Batten disease; juvenile neuronal ceroid lipofuscinosis; JNCL; CLN3; thalamocortical degeneration; astrocytosis; lysosomal storage disorder ID CEROID-LIPOFUSCINOSIS; INFANTILE TYPE; TARGETED DISRUPTION; EVOKED-POTENTIALS; GLIAL ACTIVATION; JUVENILE; CLN3; PATHOLOGY; PROTEIN; BRAIN AB Juvenile neuronal ceroid lipofuscinosis (JNCL) is the result of mutations in the Cln3 gene. The Cln(3) knock-in mouse (Cln(3)(Delta ex7/8)) reproduces the most common Cln3 mutation and we have now characterized the CNS of these mice at 12 months of age. With the exception of the thalamus, Cln3(Delta ex7/8) homozygotes displayed no significant regional atrophy, but a range of changes in individual laminar thickness that resulted in variable cortical thinning across subfields. Stereological analysis revealed a pronounced loss of. neurons within individual laminae of somatosensory cortex of affected mice and the novel finding of a loss of sensory relay thalamic neurons. These affected mice also exhibited profound astrocytic reactions that were most pronounced in the neocorlex and thalamus, but diminished in other brain regions. These data provide the first direct evidence for neurodegenerative and reactive changes in the thalamocortical system in JNCL and emphasize the localized nature of these events. (c) 2005 Elsevier Inc. All rights reserved. C1 Univ London Kings Coll, Inst Psychiat, MRC,Pediat Storage Disorders Lab, Social Genet & Dev Psychiat Ctr,Dept Neurosci, London SE5 8AF, England. Massachusetts Gen Hosp East, Mol Neurogenet Unit, Ctr Human Genet Res, Boston, MA 02129 USA. RP Cooper, JD (reprint author), Univ London Kings Coll, Inst Psychiat, MRC,Pediat Storage Disorders Lab, Social Genet & Dev Psychiat Ctr,Dept Neurosci, Box P040,De Crespigny Pk, London SE5 8AF, England. EM j.cooper@iop.kcl.ac.uk RI Cooper, Jonathan/C-8117-2009 OI Cooper, Jonathan/0000-0003-1339-4750 FU NINDS NIH HHS [NS33648, NS41930, R01 NS033648] NR 55 TC 56 Z9 56 U1 0 U2 1 PU ACADEMIC PRESS INC ELSEVIER SCIENCE PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA SN 0969-9961 J9 NEUROBIOL DIS JI Neurobiol. Dis. PD DEC PY 2005 VL 20 IS 3 BP 823 EP 836 DI 10.1016/j.nbd.2005.05.018 PG 14 WC Neurosciences SC Neurosciences & Neurology GA 990JN UT WOS:000233739100021 PM 16006136 ER PT J AU Long, CJ Brown, EN Triantafyllou, C Aharon, I Wald, LL Solo, V AF Long, CJ Brown, EN Triantafyllou, C Aharon, I Wald, LL Solo, V TI Nonstationary noise estimation in functional MRI SO NEUROIMAGE LA English DT Article DE functional MRI; time-varying models; Functional Data Analysis ID TEMPORAL AUTOCORRELATION; DENSITY-ESTIMATION; FMRI DATA; INFERENCE; MODELS AB An important issue in functional MRI analysis is accurate characterisation of the noise processes present in the data. Whilst conventional fMRI noise representations often assume stationarity (or time-invariance) in the noise generating sources, such approaches may serve to suppress important dynamic information about brain function. As an alternative to these fixed temporal assumptions, we present in this paper two time-varying procedures for examining nonstationary noise structure in fMRI data. In the first procedure, we approximate nonstationary behaviour by means of a collection of simple but numerous time-varying parametric models. This is accomplished through the derivation of a locally parametric AutoRegressive (AR) plus drift model which tracks temporal covariance by allowing the model parameters to evolve over time. Before exploring time variation in these parameters, window-widths (bandwidths) that are well suited to the latent time-varying noise structure must be determined. To do this, we employ a bandwidth selection mechanism based on Stein's Unbiased Risk Estimator (SURE) criterion. In the second procedure, we describe the fMRI noise using a nonparametric method based on Functional Data Analysis (FDA). This process generates well-conditioned nonstationary covariance estimates that reflect temporal continuity in the underlying data structure whilst penalizing effective model dimension. We demonstrate both methods on simulated data and investigate the presence of nonstationary noise in resting fMRI data using the whitening capabilities of the locally parametric procedure. We evaluate the comparative behaviour of the stationary and nonstationary AR-based methods on data acquired at 1.5, 3 and 7 T magnetic field strengths and show that incorporation of time variation in the AR parameters leads to an overall decrease in the level of residual structure in the data. The FDA noise modelling technique is formulated within an activation mapping procedure and compared to the SPM (Statistical Parametric Mapping) toolbox on a cognitive face recognition task. Both the SPM and FDA methods show good sensitivity on this task, but we find that inclusion of the nonstationary FDA noise model seems to improve detection power in important task-related medial temporal regions. (c) 2005 Elsevier Inc. All rights reserved. C1 MGH, MIT, HMS, Martinos Ctr Biomed Imaging, Charlestown, MA 02129 USA. Massachusetts Gen Hosp, Dept Anesthesia & Crit Care, Boston, MA 02129 USA. Harvard MIT, Div Hlth Sci & Technol, Boston, MA 02132 USA. Univ Michigan, Dept Elect Engn & Comp Sci, Ann Arbor, MI 48109 USA. Univ Michigan, Dept Stat, Ann Arbor, MI 48109 USA. RP Long, CJ (reprint author), MGH, MIT, HMS, Martinos Ctr Biomed Imaging, Charlestown, MA 02129 USA. EM cjl@nmr.mgh.harvard.edu RI Triantafyllou, Christina/E-7724-2011; Wald, Lawrence/D-4151-2009 FU NCRR NIH HHS [P41 RR14705]; NIBIB NIH HHS [R01 EB0522]; NIMH NIH HHS [K02 MH61637] NR 54 TC 25 Z9 25 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 1053-8119 J9 NEUROIMAGE JI Neuroimage PD DEC PY 2005 VL 28 IS 4 BP 890 EP 903 DI 10.1016/j.neuroimage.2005.06.043 PG 14 WC Neurosciences; Neuroimaging; Radiology, Nuclear Medicine & Medical Imaging SC Neurosciences & Neurology; Radiology, Nuclear Medicine & Medical Imaging GA 994FC UT WOS:000234015300015 PM 16129625 ER PT J AU Floren, A Sollenberg, U Lundstrom, L Zorko, M Stojan, J Budihna, M Wheatley, M Martin, NP Kilk, K Mazarati, A Bartfai, T Lindgren, M Langel, U AF Floren, A Sollenberg, U Lundstrom, L Zorko, M Stojan, J Budihna, M Wheatley, M Martin, NP Kilk, K Mazarati, A Bartfai, T Lindgren, M Langel, U TI Multiple interaction sites of galnon trigger its biological effects SO NEUROPEPTIDES LA English DT Article DE galanin; galnon; G-protein; receptor; signaling ID GALANIN-RECEPTOR AGONIST; BETA-ADRENERGIC-RECEPTOR; HIPPOCAMPAL GALANIN; STATUS EPILEPTICUS; HIGH-AFFINITY; PEPTIDES; PROTEINS; LIGANDS; BRAIN; STIMULATION AB Galnon was first reported as a low molecular weight non-peptide agonist at galanin receptors [Saar et al. (2002) Proc. Natl. Acad. Sci. USA 99, 7136-7141]. Following its systemic administration, this synthetic ligand affected a range of important physiological processes including appetite, seizures and pain. Physiological activity of galnon could not be explained solely by the activation of the three known galanin receptors, GalR1, GalR2 and GalR3. Consequently, it was possible that galnon generates its manifold effects by interacting with other signaling pathway components, in addition to via GalR1-3. In this report, we establish that galnon: (i) can penetrate across the plasma membrane of cells, (ii) can activate intracellular G-proteins directly independent of receptor activation thereby triggering downstream signaling, (iii) demonstrates selectivity for different G-proteins, and (iiii) is a ligand to other G-protein coupled receptors (GPCRs) in addition to via GalR1-3. We conclude that galnon has multiple sites of interaction within the GPCR signaling cascade which mediate its physiological effects. (c) 2005 Elsevier Ltd. All rights reserved. C1 Univ Stockholm, Dept Neurochem, SE-10691 Stockholm, Sweden. Univ Ljubljana, Fac Med, Inst Biochem, Ljubljana 1000, Slovenia. Univ Ljubljana, Fac Med, Inst Pharmacol & Expt Toxicol, Ljubljana 1000, Slovenia. Univ Birmingham, Sch Biosci, Birmingham B15 2TT, W Midlands, England. Duke Univ, Med Ctr, Howard Hughes Med Inst, Durham, NC 27710 USA. Univ Tartu, Ctr Mol & Clin Med, EE-51014 Tartu, Estonia. Univ Calif Los Angeles, Dept Neurol, W Los Angeles Vet Adm Med Ctr, Los Angeles, CA 90073 USA. Scripps Res Inst, Dept Neuropharmacol, La Jolla, CA 92037 USA. RP Langel, U (reprint author), Univ Stockholm, Dept Neurochem, S Arrheniusv 21 A, SE-10691 Stockholm, Sweden. EM ulo@neurochem.su.se OI Martin, Negin/0000-0003-3166-8989 FU NINDS NIH HHS [NS043409] NR 38 TC 24 Z9 25 U1 0 U2 1 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 2005 VL 39 IS 6 BP 547 EP 558 DI 10.1016/j.npep.2005.09.005 PG 12 WC Endocrinology & Metabolism; Neurosciences SC Endocrinology & Metabolism; Neurosciences & Neurology GA 993NF UT WOS:000233960100002 PM 16297447 ER PT J AU Evans, K Wright, CI Wedig, MM Pollack, MH Rauch, SL AF Evans, K Wright, CI Wedig, MM Pollack, MH Rauch, SL TI Schematic faces evoke exaggerated regional activation within the amygdala in social anxiety disorder SO NEUROPSYCHOPHARMACOLOGY LA English DT Meeting Abstract CT 44th Annual Meeting of the American-College-Neuropsychopharmacology CY DEC 11-15, 2005 CL Waikoloa, HI SP Vanderbilt Univ Sch Med Dept Psychiat C1 Massachusetts Gen Hosp, Div Psychiat Neurosci, Charlestown, MA USA. NR 0 TC 1 Z9 1 U1 1 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 2005 VL 30 SU 1 BP S164 EP S164 PG 1 WC Neurosciences; Pharmacology & Pharmacy; Psychiatry SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry GA 986IA UT WOS:000233442100431 ER PT J AU Evins, AE Alpert, JE Pava, J Petersen, TJ Farabaugh, AH Fava, M AF Evins, AE Alpert, JE Pava, J Petersen, TJ Farabaugh, AH Fava, M TI A double blind placebo controlled trial of bupropion added to nicotine patch and cognitive behavioral therapy in smokers with current or past unipolar depressive disorder SO NEUROPSYCHOPHARMACOLOGY LA English DT Meeting Abstract CT 44th Annual Meeting of the American-College-Neuropsychopharmacology CY DEC 11-15, 2005 CL Waikoloa, HI SP Vanderbilt Univ Sch Med Dept Psychiat ID SMOKING-CESSATION; MAJOR DEPRESSION; MOOD; HISTORY C1 Massachusetts Gen Hosp, Boston, MA 02114 USA. NR 7 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 2005 VL 30 SU 1 BP S91 EP S91 PG 1 WC Neurosciences; Pharmacology & Pharmacy; Psychiatry SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry GA 986IA UT WOS:000233442100248 ER PT J AU Henderson, DC Cagliero, E Copeland, PM Louie, PM Borba, CP Goff, DC AF Henderson, DC Cagliero, E Copeland, PM Louie, PM Borba, CP Goff, DC TI Schizophrenia, diabetic ketoacidosis and atypical antipsychotic agents SO NEUROPSYCHOPHARMACOLOGY LA English DT Meeting Abstract CT 44th Annual Meeting of the American-College-Neuropsychopharmacology CY DEC 11-15, 2005 CL Waikoloa, HI SP Vanderbilt Univ Sch Med Dept Psychiat C1 Harvard Univ, Sch Med, Massachusetts Gen Hosp, 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 2005 VL 30 SU 1 BP S190 EP S190 PG 1 WC Neurosciences; Pharmacology & Pharmacy; Psychiatry SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry GA 986IA UT WOS:000233442100495 ER PT J AU Nierenberg, AA Greist, JH Mallinckrodt, CH Prakash, A Watkin, JG Sambunaris, A Tollefson, GD Wohlreich, MM AF Nierenberg, AA Greist, JH Mallinckrodt, CH Prakash, A Watkin, JG Sambunaris, A Tollefson, GD Wohlreich, MM TI Onset of antidepressant action and acute efficacy and safety of duloxetine versus escitalopram and placebo in the treatment of major depressive disorder SO NEUROPSYCHOPHARMACOLOGY LA English DT Meeting Abstract CT 44th Annual Meeting of the American-College-Neuropsychopharmacology CY DEC 11-15, 2005 CL Waikoloa, HI SP Vanderbilt Univ Sch Med Dept Psychiat C1 Massachusetts Gen Hosp, Boston, MA 02114 USA. NR 0 TC 5 Z9 5 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 2005 VL 30 SU 1 BP S142 EP S142 PG 1 WC Neurosciences; Pharmacology & Pharmacy; Psychiatry SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry GA 986IA UT WOS:000233442100377 ER PT J AU Olson, V AF Olson, V TI Norepinephrine in opiate reward, locomotion, and withdrawal: Evidence for distinct contributions by the locus coeruleus and the nucleus tractus solitarius SO NEUROPSYCHOPHARMACOLOGY LA English DT Meeting Abstract CT 44th Annual Meeting of the American-College-Neuropsychopharmacology CY DEC 11-15, 2005 CL Waikoloa, HI SP Vanderbilt Univ Sch Med Dept Psychiat C1 Univ Washington, VA Puget Sound Hlth Care Syst, Seattle, WA 98195 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 2005 VL 30 SU 1 BP S2 EP S2 PG 1 WC Neurosciences; Pharmacology & Pharmacy; Psychiatry SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry GA 986IA UT WOS:000233442100005 ER PT J AU Papakostas, GI Nutt, DJ Tucker, VL Krishen, A Fava, M AF Papakostas, GI Nutt, DJ Tucker, VL Krishen, A Fava, M TI Resolution of sleepiness and fatigue in the treatment of major depressive disorder: A comparison of bupropion and the selective serotonin reuptake inhibitors SO NEUROPSYCHOPHARMACOLOGY LA English DT Meeting Abstract CT 44th Annual Meeting of the American-College-Neuropsychopharmacology CY DEC 11-15, 2005 CL Waikoloa, HI SP Vanderbilt Univ Sch Med Dept Psychiat C1 Harvard Univ, Sch Med, Massachusetts Gen Hosp, Depress Clin & Res Program, Boston, MA 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 2005 VL 30 SU 1 BP S186 EP S187 PG 2 WC Neurosciences; Pharmacology & Pharmacy; Psychiatry SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry GA 986IA UT WOS:000233442100488 ER PT J AU Pierre, JM Peloian, JH Wirshing, DA Wirshing, WC Marder, SR AF Pierre, JM Peloian, JH Wirshing, DA Wirshing, WC Marder, SR TI A double-blind placebo controlled trial of modafinil for negative symptoms in schizophrenia SO NEUROPSYCHOPHARMACOLOGY LA English DT Meeting Abstract CT 44th Annual Meeting of the American-College-Neuropsychopharmacology CY DEC 11-15, 2005 CL Waikoloa, HI SP Vanderbilt Univ Sch Med Dept Psychiat C1 VA Greater Los Angeles Healthcare Syst, Dept Psychiat, Los Angeles, CA 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 2005 VL 30 SU 1 BP S207 EP S207 PG 1 WC Neurosciences; Pharmacology & Pharmacy; Psychiatry SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry GA 986IA UT WOS:000233442100538 ER PT J AU Rauch, SL Milad, MR Orr, SP Pitman, RK AF Rauch, SL Milad, MR Orr, SP Pitman, RK TI Magnetic resonance imaging studies of extinction retention in human subjects SO NEUROPSYCHOPHARMACOLOGY LA English DT Meeting Abstract CT 44th Annual Meeting of the American-College-Neuropsychopharmacology CY DEC 11-15, 2005 CL Waikoloa, HI SP Vanderbilt Univ Sch Med Dept Psychiat 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 2005 VL 30 SU 1 BP S73 EP S73 PG 1 WC Neurosciences; Pharmacology & Pharmacy; Psychiatry SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry GA 986IA UT WOS:000233442100204 ER PT J AU Rauch, SL Whalen, PJ Shin, LM Pollack, MH AF Rauch, SL Whalen, PJ Shin, LM Pollack, MH TI Functional magnetic resonance imaging studies of amygdalo-cortical function in panic disorder SO NEUROPSYCHOPHARMACOLOGY LA English DT Meeting Abstract CT 44th Annual Meeting of the American-College-Neuropsychopharmacology CY DEC 11-15, 2005 CL Waikoloa, HI SP Vanderbilt Univ Sch Med Dept Psychiat C1 Massachusetts Gen Hosp, Charlestown, MA USA. NR 0 TC 0 Z9 0 U1 0 U2 3 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 2005 VL 30 SU 1 BP S20 EP S20 PG 1 WC Neurosciences; Pharmacology & Pharmacy; Psychiatry SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry GA 986IA UT WOS:000233442100060 ER PT J AU Weiss, AP Henderson, DC Weilburg, JB Goff, DC Meigs, JB Cagliero, E Grant, RW AF Weiss, AP Henderson, DC Weilburg, JB Goff, DC Meigs, JB Cagliero, E Grant, RW TI Treatment of cardiac risk factors in patients with schizophrenia and diabetes SO NEUROPSYCHOPHARMACOLOGY LA English DT Meeting Abstract CT 44th Annual Meeting of the American-College-Neuropsychopharmacology CY DEC 11-15, 2005 CL Waikoloa, HI SP Vanderbilt Univ Sch Med Dept Psychiat C1 Massachusetts Gen Hosp, Dept Psychiat, 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 2005 VL 30 SU 1 BP S261 EP S261 PG 1 WC Neurosciences; Pharmacology & Pharmacy; Psychiatry SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry GA 986IA UT WOS:000233442100678 ER PT J AU Greene, MF AF Greene, MF TI Fatal infections associated with mifepristone-induced abortion SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Editorial Material C1 Harvard Univ, Sch Med, Boston, MA 02115 USA. Massachusetts Gen Hosp, Boston, MA 02114 USA. RP Greene, MF (reprint author), Harvard Univ, Sch Med, Boston, MA 02115 USA. NR 2 TC 13 Z9 13 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 DEC 1 PY 2005 VL 353 IS 22 BP 2317 EP 2318 DI 10.1056/NEJMp058260 PG 2 WC Medicine, General & Internal SC General & Internal Medicine GA 988EO UT WOS:000233574600001 PM 16319378 ER PT J AU Flanz, J Doyle, B AF Flanz, J Doyle, B TI Janet M. Sisterson - Dedication SO NUCLEAR INSTRUMENTS & METHODS IN PHYSICS RESEARCH SECTION B-BEAM INTERACTIONS WITH MATERIALS AND ATOMS LA English DT Biographical-Item C1 Massachusetts Gen Hosp, Boston, MA 02114 USA. Sandia Natl Labs, Livermore, CA 94550 USA. RP Flanz, J (reprint author), Massachusetts Gen Hosp, Boston, MA 02114 USA. NR 1 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0168-583X J9 NUCL INSTRUM METH B JI Nucl. Instrum. Methods Phys. Res. Sect. B-Beam Interact. Mater. Atoms PD DEC PY 2005 VL 241 IS 1-4 BP XIV EP XV DI 10.1016/j.nimb.2005.07.212 PG 2 WC Instruments & Instrumentation; Nuclear Science & Technology; Physics, Atomic, Molecular & Chemical; Physics, Nuclear SC Instruments & Instrumentation; Nuclear Science & Technology; Physics GA 997PX UT WOS:000234260000004 ER PT J AU Sisterson, J AF Sisterson, J TI Ion beam therapy in 2004 SO NUCLEAR INSTRUMENTS & METHODS IN PHYSICS RESEARCH SECTION B-BEAM INTERACTIONS WITH MATERIALS AND ATOMS LA English DT Article; Proceedings Paper CT 18th International Conference on Application of Accelerators in Research and Industry (CAARI) CY OCT 10-15, 2004 CL Ft Worth, TX SP US DOE, Natl Sci Fdn, Int Atom Energy Agcy, Natl Canc Inst, Sadia Natl Lab, Oak Ridge Natl Lab, Oak Ridge Associated Univ, Los Alamos Natl Lab, Synergy Vaccum, Ft Worth Convent & Vistors Bureau, Elsevier B V, Univ N Texas DE radiation therapy; proton beams; carbon ion beams ID PROTON; RADIOTHERAPY AB From 1954 to July 2004, almost 40,000 patients have been treated with proton beams: from 1957 to 1992, heliumsilicon ion beams were used to treat similar to 2000 patients; and since 1994, -2000 patients have been treated with carbon ion beams. Now in 2004, there are 22 proton therapy facilities located throughout the world and many newer facilities are designed specifically for the hospital setting. In North America, Europe, Russia, Japan and the Southern Hemisphere there are 5, 7, 3, 6 and 1 proton therapy facilities respectively. In Japan, there are two carbon ion facilities and in Europe, one carbon ion facility. (c) 2005 Elsevier B.V. All rights reserved. C1 Massachusetts Gen Hosp, NE Proton Therapy Ctr, Boston, MA 02114 USA. RP Sisterson, J (reprint author), Massachusetts Gen Hosp, NE Proton Therapy Ctr, 30 Fruit St, Boston, MA 02114 USA. EM jsisterson@partners.org NR 13 TC 34 Z9 34 U1 0 U2 1 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0168-583X J9 NUCL INSTRUM METH B JI Nucl. Instrum. Methods Phys. Res. Sect. B-Beam Interact. Mater. Atoms PD DEC PY 2005 VL 241 IS 1-4 BP 713 EP 716 DI 10.1016/j.nimb.2005.07.121 PG 4 WC Instruments & Instrumentation; Nuclear Science & Technology; Physics, Atomic, Molecular & Chemical; Physics, Nuclear SC Instruments & Instrumentation; Nuclear Science & Technology; Physics GA 997PX UT WOS:000234260000149 ER PT J AU Smirnakis, KV Chasan-Taber, L Wolf, M Markenson, G Ecker, JL Thadhani, R AF Smirnakis, KV Chasan-Taber, L Wolf, M Markenson, G Ecker, JL Thadhani, R TI Postpartum diabetes screening in women with a history of gestational diabetes SO OBSTETRICS AND GYNECOLOGY LA English DT Article ID GLUCOSE-INTOLERANCE; FOLLOW-UP; MELLITUS; ASSOCIATION; PREDICTORS; RISK; COMPLICATIONS; POPULATION; PREVALENCE; MANAGEMENT AB OBJECTIVE: Women with a history of gestational diabetes mellitus (GDM) are at high risk for developing type 2 diabetes (diabetes mellitus, DM). The American Diabetes Association recommends regular postpartum diabetes screening for women with a history of GDM, but the American College of Obstetricians and Gynecologists (ACOG) is not as directive. We sought to examine postpartum glycemic testing in women diagnosed with GDM. METHODS: We conducted an observational cohort study of women diagnosed with GDM at one of two large academic medical centers between 2000 and 2001. Kaplan-Meier estimates of the time from delivery to the first postpartum DM screening tests were determined, and predictors of postpartum DM screening were examined using Cox proportional hazards testing. RESULTS: Only 37% of eligible women underwent the postpartum diabetes screening tests recommended by the American Diabetes Association (fasting glucose or oral glucose tolerance test [OGTT]), with a median time from delivery to the first such testing of 428 days. By comparison, 94% of women underwent postpartum cervical cancer screening using a Papanicolaou (Pap) test, with a median time from delivery to Pap testing of 49 days. Even when random glucose testing was included in a broad definition of postpartum DM screening (random or fasting glucose, glycosylated hemoglobin, or OGTT), only two thirds of women (67%) received a postpartum glycemic assessment. CONCLUSION: In the population studied, only 37% of women with a history of GDM were screened for postpartum DM according to guidelines published by the American Diabetes Association. Efforts to improve postpartum DM screening in this high-risk group are warranted. C1 Harvard Univ, Sch Med, Dept Med, Renal Unit,Massachusetts Gen Hosp, Boston, MA 02114 USA. Univ Massachusetts, Dept Biostat & Epidemiol, Sch Publ Hlth & Hlth Sci, Amherst, MA 01003 USA. Baystate Med Ctr, Dept Obstet & Gynecol, Springfield, MA USA. Harvard Univ, Sch Med, Dept Obstet & Gynecol, Massachusetts Gen Hosp, Boston, MA 02114 USA. RP Thadhani, R (reprint author), Harvard Univ, Sch Med, Dept Med, Renal Unit,Massachusetts Gen Hosp, Bulfinch 127,55 Fruit St, Boston, MA 02114 USA. EM rthadhani@partners.org FU NCRR NIH HHS [RR17376]; NICHD NIH HHS [HD 39223] NR 30 TC 77 Z9 80 U1 0 U2 8 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3261 USA SN 0029-7844 J9 OBSTET GYNECOL JI Obstet. Gynecol. PD DEC PY 2005 VL 106 IS 6 BP 1297 EP 1303 DI 10.1097/01.AOG.0000189081.46925.90 PG 7 WC Obstetrics & Gynecology SC Obstetrics & Gynecology GA 989SX UT WOS:000233695200013 PM 16319255 ER PT J AU Choopong, P Khan, N Sangwan, VS Zafirakis, P Rallatos, CL Rojas, B Baltatzis, S Foster, CS AF Choopong, P Khan, N Sangwan, VS Zafirakis, P Rallatos, CL Rojas, B Baltatzis, S Foster, CS TI Eosinophil activation in Wegener's granulomatosis: A harbinger of disease progression? SO OCULAR IMMUNOLOGY AND INFLAMMATION LA English DT Article DE eosinophil activation; eosinophil cationic protein; major basic protein; Wegener's granulomatosis ID OCULAR MANIFESTATIONS; LIMITED FORMS; DIAGNOSTIC-VALUE; INVOLVEMENT; EXPERIENCE; SCLERITIS; EYE AB Purpose: To investigate the relation between eosinophil activation in tissue from patients with an active, limited form of Wegener's granulomatosis (WG) affecting the eye and subsequent systemic disease activity. Methods: Analysis of ocular specimens obtained from 10 patients was performed. Sections were probed with antibodies to assess the presence of major basic protein (MBP) and eosinophil cationic protein (ECP). Results: Four of the 10 specimens demonstrated the presence of MBP and ECP. WG progressed to the complete form in two of these patients, who received no or inadequate treatment. The other two, treated with cyclophosphamide for one year, did not progress to the complete form of WG during observation after therapy. Conclusions: Activated eosinophils in sclera or conjunctiva of patients with ocular limited WG may predict progression to complete WG. C1 Massachusetts Eye & Ear Infirm, Dept Ophthalmol, Ocular Immunol & Uveitis Serv, Boston, MA 02114 USA. RP Foster, CS (reprint author), Massachusetts Eye & Ear Infirm, Dept Ophthalmol, Ocular Immunol & Uveitis Serv, 243 Charles St, Boston, MA 02114 USA. EM fosters@uveitis.org OI ROJAS LOPEZ, MARIA BLANCA/0000-0002-8980-4659; Sangwan, Virender/0000-0002-8229-4158 NR 32 TC 2 Z9 2 U1 1 U2 4 PU TAYLOR & FRANCIS INC PI PHILADELPHIA PA 325 CHESTNUT ST, SUITE 800, PHILADELPHIA, PA 19106 USA SN 0927-3948 J9 OCUL IMMUNOL INFLAMM JI Ocul. Immunol. Inflamm. PD DEC PY 2005 VL 13 IS 6 BP 439 EP 445 DI 10.1080/09273940591004250 PG 7 WC Ophthalmology SC Ophthalmology GA 990AV UT WOS:000233716500003 PM 16321888 ER PT J AU Papadaki, T Zacharopoulos, I Iaccheri, B Fiore, T Foster, CS AF Papadaki, T Zacharopoulos, I Iaccheri, B Fiore, T Foster, CS TI Somatostatin for uveitic cystoid macular edema (CME) SO OCULAR IMMUNOLOGY AND INFLAMMATION LA English DT Article DE cystoid macular edema; somatostatin; uveitis ID OCTREOTIDE AB Purpose: To report the favorable response of bilateral recalcitrant uveitic cystoid macular edema (CME) to treatment with a somatostatin analog. Methods: Medical ophthalmic history and the results of ophthalmic examinations were recorded. Fluorescein angiography (FA) studies were reviewed. Results: A 52-year-old white female with intermediate uveitis developed bilateral recalcitrant CME. Treatment with subcutaneous injections of the somatostatin analog octreotide resulted in partial resolution of the CME and improvement of visual acuity. Conclusions: Somatostatin may play a role in the treatment of CME secondary to uveitis. C1 Harvard Univ, Massachusetts Eye & Ear Infirm, Sch Med, Ocular Immunol & Uveitis Serv, Boston, MA 02114 USA. RP Foster, CS (reprint author), Harvard Univ, Massachusetts Eye & Ear Infirm, Sch Med, Ocular Immunol & Uveitis Serv, 243 Charles St, Boston, MA 02114 USA. EM fosters@uveitis.org NR 7 TC 17 Z9 17 U1 0 U2 0 PU TAYLOR & FRANCIS INC PI PHILADELPHIA PA 325 CHESTNUT ST, SUITE 800, PHILADELPHIA, PA 19106 USA SN 0927-3948 J9 OCUL IMMUNOL INFLAMM JI Ocul. Immunol. Inflamm. PD DEC PY 2005 VL 13 IS 6 BP 469 EP 470 DI 10.1080/09273940691001964 PG 2 WC Ophthalmology SC Ophthalmology GA 990AV UT WOS:000233716500008 PM 16321893 ER PT J AU Kafkala, C Daoud, YJ Paredes, I Foster, CS AF Kafkala, C Daoud, YJ Paredes, I Foster, CS TI Masquerade scleritis SO OCULAR IMMUNOLOGY AND INFLAMMATION LA English DT Article DE metastatic ocular carcinoma; scleritis; uveal melanoma ID CHOROIDAL MELANOMA; EYE; ORBIT AB Purpose: To report two cases in which malignancy masqueraded as scleritis, delaying the diagnosis. Methods: Two patients initially diagnosed and treated for unilateral scleritis were referred for management of persistent inflammation. Additional evaluation uncovered underlying malignant processes. Results: The first patient presented with scleritis initially responsive to systemic corticosteroids, with relapse one month later. Upon referral, peripheral fundus examination revealed elevated lesions. Additional studies confirmed the diagnosis of choroidal melanoma. The patient was treated with proton-beam irradiation. The second patient developed necrotizing scleritis unresponsive to systemic steroids, methotrexate, and cyclophosphamide. A scleral biopsy disclosed an undifferentiated high-grade carcinoma, likely metastatic. Exenteration was performed. Conclusions: Scleritis can present a diagnostic challenge. It is often the sole initial manifestation of an occult systemic problem. Treatment-resistant scleritis should raise the suspicion of an infectious or malignant masquerade. C1 Harvard Univ, Massachusetts Eye & Ear Infirm, Sch Med, Ocular Immunol & Uveitis Serv, Boston, MA USA. RP Foster, CS (reprint author), Massachusetts Eye & Ear Infirm, Immunol & Uveitis Serv, 243 Charles St, Boston, MA 02114 USA. EM fosters@uveitis.org NR 15 TC 8 Z9 8 U1 0 U2 1 PU TAYLOR & FRANCIS INC PI PHILADELPHIA PA 325 CHESTNUT ST, SUITE 800, PHILADELPHIA, PA 19106 USA SN 0927-3948 J9 OCUL IMMUNOL INFLAMM JI Ocul. Immunol. Inflamm. PD DEC PY 2005 VL 13 IS 6 BP 479 EP 482 DI 10.1080/09273940591004133 PG 4 WC Ophthalmology SC Ophthalmology GA 990AV UT WOS:000233716500011 PM 16321896 ER PT J AU Richardson, PG Schlossman, R Hideshima, T Anderson, KC AF Richardson, PG Schlossman, R Hideshima, T Anderson, KC TI New treatments for multiple myeloma SO ONCOLOGY-NEW YORK LA English DT Review ID PROTEASOME INHIBITOR PS-341; OVERCOMES DRUG-RESISTANCE; STEM-CELL TRANSPLANTATION; THALIDOMIDE PLUS DEXAMETHASONE; DEPENDENT KINASE INHIBITOR; COOPERATIVE-ONCOLOGY-GROUP; NEWLY-DIAGNOSED MYELOMA; HIGH-DOSE CHEMOTHERAPY; PHASE-II TRIAL; FACTOR-KAPPA-B AB In 2004, multiple myeloma was diagnosed in more than 15, 000 people in the United States and will account for approximately 20% of deaths due to hematologic malignancies. Although traditional therapies such as melphalan (Alkeran)/prednisone, combination chemotherapy with VAD (vincristine, doxorubicin [Adriamycin], and dexamethasone), and high-dose chemotherapy with stem cell transplantation have shown some success, median survival remains between 3 to 5 years. Treatment options for patients with multiple myeloma have increased in recent years, with the promise of improvement in survival. New agents, such as the proteasome inhibitor bortezomib (Velcade), the antiangiogenic and immunomodulator thalidomide (Thalomid) and its analogs, such as lenalidomide (Revlimid), together with other small molecules, including arsenic trioxide (Trisenox), and other targeted therapies, have been studied alone and in combination with other antineoplastic therapies, either as induction therapy prior to stem cell transplantation or in patients with relapsed disease. Bortezomib recently was approved in the United States for the treatment of multiple myeloma in patients who have received at least one prior therapy. The use of bortezomib-based regimens as front-line therapy as well as the use of other agents in multiple myeloma remain under investigation, and approvals for both thalidomide and lenalidomide are hoped for soon, with the overall prospect of patient outcome continuing to be increasingly positive. C1 Dana Farber Canc Inst, Div Hematol Oncol, Jerome Lipper Multiple Myeloma Ctr, Boston, MA 02115 USA. Harvard Univ, Sch Med, Cambridge, MA 02138 USA. RP Richardson, PG (reprint author), Dana Farber Canc Inst, Div Hematol Oncol, Jerome Lipper Multiple Myeloma Ctr, Dana 1B02 44 Binney St, Boston, MA 02115 USA. EM Paul_Richardson@dfci.harvard.edu NR 107 TC 17 Z9 18 U1 0 U2 0 PU P R R INC PI MELVILLE PA 48 SOUTH SERVICE RD, MELVILLE, NY 11747 USA SN 0890-9091 J9 ONCOLOGY-NY JI Oncology-NY PD DEC PY 2005 VL 19 IS 14 BP 1781 EP 1792 PG 12 WC Oncology SC Oncology GA 052EV UT WOS:000238215200005 PM 16506632 ER PT J AU Lee, MS Egan, RA Shults, WT Lessell, S AF Lee, MS Egan, RA Shults, WT Lessell, S TI Idiopathic repetitive oculomotor nerve palsies in otherwise normal patients SO OPHTHALMOLOGY LA English DT Article; Proceedings Paper CT 31st Annual North-American-Neuro-Ophthalmology-Society Meeting CY FEB 12-17, 2005 CL Copper Mt, CO SP N Amer Neuro Ophthalmol Soc ID VASCULAR COMPRESSION AB Objective: To describe a unique idiopathic disorder characterized by transient repetitive unilateral oculomotor pareses. Design: Retrospective observational case series. Participants: Three women presenting for tertiary neuro-ophthalmologic evaluation. Methods: Review of patient records. Main Outcome Measures: Historical information, clinical examination, neuroimaging, and laboratory evaluation for myasthenia gravis. Results: Three 44- to 69-year-old women had recurrent unilateral ptosis over the course of 2 to 4 years. Two had concurrent diplopia with ipsilateral limitation of adduction, and 2 also had a large poorly reactive pupil in the involved eye during the episodes. The attacks lasted between 30 seconds and 4 hours and occurred up to 6 times daily. None of the patients were migraineurs, nor had they received radiation therapy. Neuro-ophthalmologically normal between episodes, all patients had normal magnetic resonance imaging/angiography and testing for myasthenia gravis. Conclusion: Transient, recurrent, unilateral oculomotor nerve palsies may occur spontaneously in healthy individuals. The pathogenesis remains obscure, but the multiple recurrences without evident sequelae and the failure to develop any systemic or neurological disorder suggest that this phenomenon is not indicative of a serious underlying disorder. C1 Univ Minnesota, Dept Ophthalmol, Minneapolis, MN 55455 USA. Casey Eye Inst, Portland, OR USA. Massachusetts Eye & Ear Infirm, Boston, MA 02114 USA. RP Lee, MS (reprint author), Univ Minnesota, Dept Ophthalmol, 420 Delaware St SE,MMC 493, Minneapolis, MN 55455 USA. EM leex2679@umn.edu NR 13 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0161-6420 J9 OPHTHALMOLOGY JI Ophthalmology PD DEC PY 2005 VL 112 IS 12 BP 2225 EP 2226 DI 10.1016/j.ophtha.2005.09.008 PG 2 WC Ophthalmology SC Ophthalmology GA 991MS UT WOS:000233818700026 PM 16325713 ER PT J AU Oh, WY Yun, SH Tearney, GJ Bouma, BE AF Oh, WY Yun, SH Tearney, GJ Bouma, BE TI 115 kHz tuning repetition rate ultrahigh-speed wavelength-swept semiconductor laser SO OPTICS LETTERS LA English DT Article ID OPTICAL COHERENCE TOMOGRAPHY; FIBER LASER; FILTER AB We demonstrate an ultrahigh-speed wavelength-swept semiconductor laser using a polygon-based wavelength scanning filter. With a polygon rotational speed of 900 revolutions per second, a continuous wavelength tuning rate of 9200 nm/ms and a tuning repetition rate of 115 kHz were achieved. The wavelength tuning range of the laser was 80 nm centered at 1325 nm, and the average polarized output power was 23 mW. (c) 2005 Optical Society of America. C1 Harvard Univ, Sch Med, Boston, MA 02114 USA. Massachusetts Gen Hosp, Wellman Ctr Photomed, Boston, MA 02114 USA. RP Oh, WY (reprint author), Harvard Univ, Sch Med, 50 Blossom St,BAR 704, Boston, MA 02114 USA. EM woh1@partners.org RI Oh, Wang-Yuhl/C-2055-2011 FU NCI NIH HHS [R01 CA103769, R01 CA103769-03, R33 CA110130, R33 CA110130-02]; NHLBI NIH HHS [R01 HL076398, R01 HL076398-05] NR 10 TC 108 Z9 111 U1 1 U2 16 PU OPTICAL SOC AMER PI WASHINGTON PA 2010 MASSACHUSETTS AVE NW, WASHINGTON, DC 20036 USA SN 0146-9592 J9 OPT LETT JI Opt. Lett. PD DEC 1 PY 2005 VL 30 IS 23 BP 3159 EP 3161 DI 10.1364/OL.30.003159 PG 3 WC Optics SC Optics GA 985OL UT WOS:000233387300015 PM 16350273 ER PT J AU Leder, BZ Finkelstein, JS AF Leder, BZ Finkelstein, JS TI Effect of aromatase inhibition on bone metabolism in elderly hypogonadal men SO OSTEOPOROSIS INTERNATIONAL LA English DT Article DE androgen deficiency in the aging male (ADAM); andropause; aromatase inhibition; bone metabolism; hypogonadism; testosterone ID RANDOMIZED CONTROLLED-TRIAL; HEALTH INITIATIVE MEMORY; ANDROGEN INSENSITIVITY SYNDROME; CONJUGATED EQUINE ESTROGENS; GLOBAL COGNITIVE FUNCTION; LOW SERUM TESTOSTERONE; SEX-HORMONE LEVELS; MIDDLE-AGED MEN; ADULT MALE-MICE; MINERAL DENSITY AB Both estrogens and androgens play important roles in skeletal development and maintenance in men. The relative importance of estrogens and androgens in male bone metabolism, however, remains undefined. Anastrozole is an oral aromatase inhibitor that decreases estrogen production and increases androgen production in men. Currently, anastrozole is being investigated as a potential agent for the treatment of hypogonadism in aging men. Because anastrozole lowers estrogen levels and raises androgen levels, its effect on bone metabolism is difficult to predict. To assess the effects of anastrozole on bone turnover, we randomized 37 elderly (ages 62-74) mildly hypogonadal men (serum testosterone < 350 ng/dl) to receive either anastrozole 1 mg daily (n =12), anastrozole 1 mg twice weekly (n =11), or daily placebo (n =14) for 12 weeks. Serum gonadal steroid levels, serum and urine biochemical markers of bone turnover, serum osteoprotegerin, and total body bone mineral density were measured at baseline and week 12. Mean serum levels of total and bioavailable testosterone increased substantially in both treated groups. Specifically, mean +/- SD bioavailable testosterone levels increased from 99 +/- 31 ng/dl to 207 +/- 65 ng/dl in the group receiving 1 mg of anastrozole daily and from 115 +/- 37 ng/dl to 178 +/- 55 ng/dl in the subjects receiving 1 mg of anastrozole twice weekly (p < 0.001 vs placebo for both groups). Serum estradiol levels decreased modestly in both treated groups (from 26 +/- 8 pg/ml to 17 +/- 6 pg/ml in the daily treatment group and from 27 +/- 8 pg/ml to 17 +/- 5 pg/ml in the twice-weekly treatment group, p < 0.001 vs placebo for both groups). Despite these hormonal changes, no increases in biochemical markers of bone resorption were observed. Specifically, mean serum N-telopeptide and urinary deoxypyridinoline concentrations remained stable in both treated groups over the 12-week treatment period. Similarly, serum biochemical markers of bone formation (osteocalcin and amino-terminal propeptide of type 1 collagen), serum osteoprotegerin, and total body bone mineral density did not change. These data demonstrate that although short-term administration of anastrozole decreases serum estradiol levels in elderly men with mild hypogonadism, this intervention does not adversely affect bone metabolism over a 12-week period. This lack of an effect may be due to the concomitant increase in testosterone production, the relative modest effect on estradiol production, or a combination of both factors. These results suggest that anastrozole therapy is unlikely to have an adverse effect on bone metabolism when taken over extended periods and may prove to be a valuable method of normalizing testosterone production in older men. C1 Massachusetts Gen Hosp, Endocrine Unit, Dept Med, Boston, MA 02114 USA. RP Leder, BZ (reprint author), Massachusetts Gen Hosp, Endocrine Unit, Dept Med, Bulfinch 325,Fruit St, Boston, MA 02114 USA. EM bzleder@partners.org FU NCRR NIH HHS [K23-RR16310, RR-1066]; NIDDK NIH HHS [K24-DK002759] NR 76 TC 27 Z9 28 U1 0 U2 0 PU SPRINGER LONDON LTD PI GODALMING PA SWEETAPPLE HOUSE CATTESHALL ROAD, GODALMING GU7 3DJ, SURREY, ENGLAND SN 0937-941X J9 OSTEOPOROSIS INT JI Osteoporosis Int. PD DEC PY 2005 VL 16 IS 12 BP 1487 EP 1494 DI 10.1007/s00198-005-1890-8 PG 8 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA 993YZ UT WOS:000233997600004 PM 15856361 ER PT J AU Nassif, NA Armstrong, WB de Boer, JF Wong, BJF AF Nassif, NA Armstrong, WB de Boer, JF Wong, BJF TI Measurement of morphologic changes induced by trauma with the use of coherence tomography in porcine vocal cords SO OTOLARYNGOLOGY-HEAD AND NECK SURGERY LA English DT Article ID OPTICAL BIOPSY; GASTROINTESTINAL-TRACT; ORAL-CAVITY; HUMAN SKIN; DERMATOLOGY; SPEED AB BACKGROUND AND OBJECTIVE: To evaluate the ability of optical coherence tomography (OCT) (a noncontact, high-resolution imaging technique that generates detailed cross-sectional images of tissue structure) to image and document acute response to trauma in the larynx. MATERIALS AND METHODS: Porcine larynges were dissected to expose the vocal cords. Vocal cords were imaged with 1310 nanometer (nm) light source with a bandwidth of 75 nm at I frame/second (s). Vocal cord injuries were simulated by applying topical phenolic acid, injecting titanium dioxide into the submucosa, and carbon dioxide laser irradiation. RESULTS: The epithelium, basement membrane, and lamina propria were clearly delineated, and the effect of each intervention could be monitored as lesions progressed. The OCT image corresponded closely with histology. CONCLUSION: OCT is a powerful imaging tool with the potential for use in real time and has potential for multiple clinical applications in the larynx. C1 Univ Calif Irvine, Dept Otolaryngol Head & Neck Surg, Orange, CA 92868 USA. Univ Calif Irvine, Dept Phys & Astron, Orange, CA 92868 USA. Univ Calif Irvine, Beckman Laser Inst & Med Clin, Orange, CA 92868 USA. Univ Calif Irvine, Dept Biomed Engn, Orange, CA 92868 USA. Harvard Univ, Massachusetts Gen Hosp, Sch Med, Wellman Lab Photomed, Boston, MA USA. RP Armstrong, WB (reprint author), Univ Calif Irvine, Dept Otolaryngol Head & Neck Surg, 101 City Dr S,Bldg 56,Ste 511, Orange, CA 92868 USA. EM wbarmstr@uci.edu RI de Boer, Johannes/B-7590-2012 OI de Boer, Johannes/0000-0003-1253-4950 FU NEI NIH HHS [R24EY12877-01]; NIDCD NIH HHS [DC 00170-01]; NIGMS NIH HHS [GM 58785] NR 20 TC 10 Z9 10 U1 0 U2 0 PU MOSBY, INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 USA SN 0194-5998 J9 OTOLARYNG HEAD NECK JI Otolaryngol. Head Neck Surg. PD DEC PY 2005 VL 133 IS 6 BP 845 EP 850 DI 10.1016/j.otohns.2005.09.013 PG 6 WC Otorhinolaryngology; Surgery SC Otorhinolaryngology; Surgery GA 996MV UT WOS:000234179000006 PM 16360501 ER PT J AU Kristjanson, LJ Christakis, N AF Kristjanson, LJ Christakis, N TI Investigating euthanasia: methodological, ethical and clinical considerations SO PALLIATIVE MEDICINE LA English DT Editorial Material C1 Edith Cowan Univ, Canc Council Western Australia, Chair Palliat Care, Churchlands, WA 6018, Australia. Harvard Univ, Sch Med, Boston, MA USA. Massachusetts Gen Hosp, Boston, MA 02114 USA. RP Kristjanson, LJ (reprint author), Edith Cowan Univ, Canc Council Western Australia, Chair Palliat Care, Churchlands, WA 6018, Australia. RI Christakis, Nicholas/B-6690-2008; Christakis, Nicholas/C-3205-2009 NR 5 TC 1 Z9 1 U1 0 U2 0 PU HODDER ARNOLD, HODDER HEADLINE PLC PI LONDON PA 338 EUSTON ROAD, LONDON NW1 3BH, ENGLAND SN 0269-2163 J9 PALLIATIVE MED JI Palliat. Med. PD DEC PY 2005 VL 19 IS 8 BP 575 EP 577 DI 10.1191/0269216305pm1088xx PG 3 WC Health Care Sciences & Services; Public, Environmental & Occupational Health; Medicine, General & Internal SC Health Care Sciences & Services; Public, Environmental & Occupational Health; General & Internal Medicine GA 992ZL UT WOS:000233922400001 PM 16450873 ER PT J AU Grant, RW Meigs, JB AF Grant, RW Meigs, JB TI Management of the metabolic syndrome SO PANMINERVA MEDICA LA English DT Review DE metabolic syndrome; insulin resistance; diabetes mellitus; cardiovascular diseases ID TYPE-2 DIABETES-MELLITUS; CORONARY-HEART-DISEASE; IMPAIRED GLUCOSE-TOLERANCE; DENSITY-LIPOPROTEIN CHOLESTEROL; CARDIOVASCULAR RISK-FACTORS; LIFE-STYLE INTERVENTION; TREATMENT PANEL-III; INHIBITOR-KAPPA-B; INSULIN-RESISTANCE; UNITED-STATES AB The metabolic syndrome (MetS) represents the co-occurrence of insulin resistance, hypertension, central adiposity, atherogenic dyslipidemia, and a pro-inflammatory and pro-thrombotic state. Patients with this syndrome are at increased risk for the development of type 2 diabetes mellitus and cardiovascular disease. Epidemiologic studies reveal a prevalence of the MetS that increases with age and obesity. Patients with the MetS should be recognized as being at high risk for cardiovascular complications. Ongoing research focuses on the underlying pathophysiology of this disorder and the use of drug therapy to directly target insulin resistance and endothelial dysfunction. Currently, the standard of care includes active identification and aggressive management of traditional cardiovascular risk actors with an emphasis on healthy lifestyle changes to reduce weight and increase physical fitness. C1 Massachusetts Gen Hosp, Div Gen Med, Dept Med, Boston, MA 02114 USA. Harvard Univ, Sch Med, Boston, MA USA. RP Grant, RW (reprint author), Massachusetts Gen Hosp, Div Gen Med, Dept Med, 50 Staniford St,9th Floor, Boston, MA 02114 USA. EM rgrant@partners.org OI Grant, Richard/0000-0002-6164-8025 FU NIDDK NIH HHS [DK067452] NR 74 TC 6 Z9 6 U1 0 U2 0 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 2005 VL 47 IS 4 BP 219 EP 228 PG 10 WC Medicine, General & Internal SC General & Internal Medicine GA 027LQ UT WOS:000236417500003 PM 16489321 ER PT J AU Sallan, SE Lipshultz, SE AF Sallan, SE Lipshultz, SE TI Wise up: Do not do it without protection! SO PEDIATRIC BLOOD & CANCER LA English DT Editorial Material ID ACUTE LYMPHOBLASTIC-LEUKEMIA; DOXORUBICIN THERAPY; CHILDHOOD; DEXRAZOXANE C1 Dana Farber Canc Inst, Boston, MA 02115 USA. Harvard Univ, Sch Med, Boston, MA 02115 USA. Univ Miami, Miller Sch Med, Dept Pediat, Miami, FL 33152 USA. Sylvester Comprehens Canc Ctr, Miami, FL USA. RP Sallan, SE (reprint author), Dana Farber Canc Inst, 44 Binney St, Boston, MA 02115 USA. EM stephen_sallan@dfci.harvard.edu NR 8 TC 7 Z9 7 U1 0 U2 0 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 1545-5009 J9 PEDIATR BLOOD CANCER JI Pediatr. Blood Cancer PD DEC PY 2005 VL 45 IS 7 BP 872 EP 873 DI 10.1002/pbc.20568 PG 2 WC Oncology; Hematology; Pediatrics SC Oncology; Hematology; Pediatrics GA 977YU UT WOS:000232840200003 PM 16206201 ER PT J AU Jacobson-Dickman, E Levitsky, L AF Jacobson-Dickman, E Levitsky, L TI Oral agents in managing diabetes mellitus in children and adolescents SO PEDIATRIC CLINICS OF NORTH AMERICA LA English DT Article ID IMPROVES GLYCEMIC CONTROL; LONG-TERM COMPLICATIONS; BLOOD-GLUCOSE CONTROL; INSULIN THERAPY; CONTROLLED TRIAL; GENE-EXPRESSION; METFORMIN; MANAGEMENT; UKPDS; PROGRESSION AB Type 2 diabetes mellitus is a chronic disease with potentially devastating long-term complications. Despite the tremendous body of research and experience in the adult population, relatively little is established regarding this condition and its optimal management in children and adolescents. The pediatric community awaits results of ongoing trials as well as further study of optimal intervention in children, as they continue to extrapolate management practices from their adult counterparts. C1 Massachusetts Gen Hosp Children, Dept Pediat, Boston, MA 02115 USA. Harvard Univ, Sch Med, Boston, MA 02115 USA. Massachusetts Gen Hosp, Pediat Endocrine Unit, Boston, MA 02114 USA. RP Levitsky, L (reprint author), Massachusetts Gen Hosp, Pediat Endocrine Unit, BHX 410,55 Fruit St, Boston, MA 02114 USA. EM llevitsky@partners.org NR 44 TC 2 Z9 4 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 USA SN 0031-3955 J9 PEDIATR CLIN N AM JI Pediatr. Clin. N. Am. PD DEC PY 2005 VL 52 IS 6 BP 1689 EP + DI 10.1016/j.pcl.2005.07.008 PG 16 WC Pediatrics SC Pediatrics GA 994NS UT WOS:000234039100009 PM 16301089 ER PT J AU Ashraf, A Abdullatif, H Hardin, W Moates, JM AF Ashraf, A Abdullatif, H Hardin, W Moates, JM TI Unusual case of neonatal diabetes mellitus due to congenital pancreas agenesis SO PEDIATRIC DIABETES LA English DT Article DE gall bladder agenesis; Ipf-1; neonatal diabetes; pancreas agenesis; pancreas development ID INFLAMMATORY DEMYELINATING POLYNEUROPATHY; GUILLAIN-BARRE-SYNDROME; REGULATORY T-CELLS; SCHWANN-CELLS; SERUM LEVELS; NOD MICE; NEUROPATHY; POLYRADICULONEUROPATHY; SUSCEPTIBILITY; EXPRESSION AB Congenital absence of the pancreas is an extremely rare condition. We participated in the care of a patient with an unusual presentation of neonatal diabetes attributable to agenesis of the pancreas. Additional clinical features of the patient included cardiac septal defects, gall bladder agenesis and duodenal malrotation. Appropriate institution of insulin, exocrine pancreatic supplements and surgical repair of the cardiac and intestinal anomalies resulted in the infant's survival. Of the reported cases of congenital pancreas agenesis, two cases have been ascribed to mutations in the insulin promoter factor-1 (Ipf-1) gene. Deletion of the Ipf-1-homolog pdx-1 in mice results in the failure of pancreas to develop. Analysis of both exons of the Ipf-1 coding sequence from the presented patient's genomic DNA, however, did not identify a mutation. These results suggest that a congenital or genetic perturbation occurred in this infant most likely before the appearance of dorsal pancreatic bud in the 3 mm long embryonic stage, around the embryonic day 25 in human development, before the onset of Ipf-1 expression. C1 Childrens Hosp Alabama, Dept Pediat, Div Pediat Endocrinol & Metab, Birmingham, AL 35233 USA. Childrens Hosp Alabama, Dept Pediat Surg, Birmingham, AL 35233 USA. Univ Alabama, Sch Med, Dept Med, Div Endocrinol & Metab, Birmingham, AL USA. Birmingham Vet Affairs Med Ctr, Birmingham, AL USA. RP Ashraf, A (reprint author), Childrens Hosp Alabama, Dept Pediat, Div Pediat Endocrinol & Metab, 1600 7th Ave S, Birmingham, AL 35233 USA. EM aashraf@peds.uab.edu NR 30 TC 19 Z9 19 U1 0 U2 1 PU BLACKWELL PUBLISHING PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DQ, OXON, ENGLAND SN 1399-543X J9 PEDIATR DIABETES JI Pediatr. Diabetes PD DEC PY 2005 VL 6 IS 4 BP 239 EP 248 DI 10.1111/j.1399-543X.2005.00114.x PG 10 WC Endocrinology & Metabolism; Pediatrics SC Endocrinology & Metabolism; Pediatrics GA 001XK UT WOS:000234575800010 PM 16390394 ER PT J AU Chen, CC Louie, S Shi, HN Walker, WA AF Chen, CC Louie, S Shi, HN Walker, WA TI Preinoculation with the probiotic Lactobacillus acidophilus early in life effectively inhibits murine Citrobacter rodentium colitis SO PEDIATRIC RESEARCH LA English DT Article ID ENTEROPATHOGENIC ESCHERICHIA-COLI; INFLAMMATORY-BOWEL-DISEASE; GROWTH-FACTOR-BETA; IMMUNOGLOBULIN-A; COLONIC HYPERPLASIA; B-CELLS; MICE; INFECTION; BIFIDOBACTERIUM; RESPONSES AB Enteropathogenic Escherichia coli (EPEC) is a common pathogen in infantile diarrhea, Causing a characteristic histopathologic attaching and effacing (A/E) lesion in the intestinal mucosa. The mouse pathogen Citrobacter rodentium causes a similar A/E lesion in the murine intestine. Like EPEC, C. rodentium infection results in colonic crypt hyperplasia, goblet cell depletion, epithelial proliferation, and mucosal disruption. Using this murine model, we tested the hypothesis that preinoculation of murine gut with Lactobacillus acidophilus early in life can enhance host defense against enteric bacterial infection and attenuate bacteria-mediated colitis. Two-week old BALB/c mice were inoculated with L. acidophilus twice per week for 4 weeks before C. rodentium infection or concomitantly with the exposure to C. rodentium at 6-8 weeks of age. The probiotics were administered twice weekly thereafter. We observed that L. acidophilus inoculation in mice inhibits C. rodentium-induced colitis, which is associated with a decrease in C. rodentium colonization and translocation, an increase in its clearance, and a suppression of colonic myeloperoxidase (MPO) activity. Probiotic treatment also stimulates regulatory cytokine expression in the colon [transforming growth factor beta (TGF-beta), interleukin (IL)-10]. Preinoculation with L. acidophilus is more effective than concomitant use of probiotics in the induction of intestinal IgA secretion and in the downregulation of proinflammatory cytokine expression [tumor necrosis factor alpha (TNF-alpha), IL-6, and IL-12]. These observations suggest that inoculation with probiotics can effectively prevent bacteria-induced colitis by limiting enteric bacteria infection and promoting mucosal protective regulatory immune responses. This study may have ramifications for prevention of infectious diarrhea in human infants and children, particularly in developing countries. C1 Massachusetts Gen Hosp, Mucosal Immunol Lab, Charlestown, MA 02129 USA. Chang Gung Childrens Hosp, Taoyuan, Taiwan. Chang Gung Univ, Taoyuan, Taiwan. RP Walker, WA (reprint author), Massachusetts Gen Hosp, Mucosal Immunol Lab, 114 16th St,114-3503, Charlestown, MA 02129 USA. EM wwalker@partners.org FU NIDDK NIH HHS [P01-DK-33506, DK059996, P30-DK40561, R01-DK070260] NR 46 TC 60 Z9 67 U1 1 U2 6 PU INT PEDIATRIC RESEARCH FOUNDATION, INC PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 USA SN 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD DEC PY 2005 VL 58 IS 6 BP 1185 EP 1191 DI 10.1203/01.pdr.0000183660.39116.83 PG 7 WC Pediatrics SC Pediatrics GA 985ZB UT WOS:000233416500009 PM 16306191 ER PT J AU Antin, JH AF Antin, JH TI Approaches to graft-vs-host disease SO PEDIATRIC TRANSPLANTATION LA English DT Article; Proceedings Paper CT 8th Meeting on Stem Cell Transplantation in Children CY JAN 20-22, 2005 CL Scottsdale, AZ SP Amgen Inc, BioMartin Genzyme LLC DE graft-versus-host disease; stem cell transplantation ID STEM-CELL TRANSPLANTATION; INTERLEUKIN-1 RECEPTOR ANTAGONIST; BONE-MARROW TRANSPLANTATION; MYCOPHENOLATE-MOFETIL; PHASE-I/II; ANTITHYMOCYTE GLOBULIN; RETROSPECTIVE ANALYSIS; UNRELATED DONORS; CONTROLLED TRIAL; DOUBLE-BLIND AB Graft-vs-host disease (GVHD) is one of the most difficult problems in stem cell transplantation. It is best considered in the context of the normal immune response. The role of the immune system is to identify and eliminate foreign antigens. In the case of GVHD, the antigens are minor histocompatibility antigens (mHA) recognized in an inflammatory milieu. The immune system cannot reasonably be expected to selectively recognize microbial antigens and ignore mHA. This approach would require the generation of selective tolerance something that clearly occurs but which we have frustratingly little control over. While we can often treat and remit even life-threatening GVHD, the consequence has been the development of fatal opportunistic infections. The challenge is to change our style of thinking about GVHD to allow a transition from a 'nuclear winter' approach that controls GVHD at the price of infection, to a more selective patient approach that recognizes the limitations of immunosuppressive therapy. C1 Brigham & Womens Hosp, Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02115 USA. RP Antin, JH (reprint author), Dana Farber Canc Inst, 44 Binney St, Boston, MA 02115 USA. EM joseph_antin@dfci.harvard.edu FU NHLBI NIH HHS [U01 HL69249, P01 HL070149] NR 35 TC 7 Z9 7 U1 0 U2 0 PU BLACKWELL PUBLISHING PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DQ, OXON, ENGLAND SN 1397-3142 J9 PEDIATR TRANSPLANT JI Pediatr. Transplant. PD DEC PY 2005 VL 9 SU 7 BP 71 EP 75 DI 10.1111/j.1399-3046.2005.00441.x PG 5 WC Pediatrics; Transplantation SC Pediatrics; Transplantation GA 991HK UT WOS:000233802900009 PM 16305620 ER PT J AU Biederman, J Swanson, JM Wigal, SB Kratochvil, CJ Boellner, SW Earl, CQ Jiang, J Greenhill, L AF Biederman, J Swanson, JM Wigal, SB Kratochvil, CJ Boellner, SW Earl, CQ Jiang, J Greenhill, L TI Efficacy and safety of modafinil film-coated tablets in children and adolescents with attention-deficit/hyperactivity disorder: Results of a randomized, double-blind, placebo-controlled, flexible-dose study SO PEDIATRICS LA English DT Article DE modafinil; modafinil film-coated tablets; ADHD; efficacy; tolerability; clinical trial ID DEFICIT HYPERACTIVITY DISORDER; INDUCED WAKEFULNESS; AMPHETAMINE; ANXIETY; CONDUCT; BRAIN; ADHD AB Objective. Modafinil, which is structurally and pharmacologically different from other agents that are used for the treatment of children with attention-deficit/hyperactivity disorder (ADHD), selectively activates the cortex and has low potential for abuse. Initial studies of the use of modafinil to treat ADHD showed significant improvements in the core symptoms of the disorder, namely inattention, hyperactivity, and impulsivity. This study evaluated a new formulation of modafinil (modafinil film - coated tablets) in children and adolescents with ADHD. Methods. This 9-week, multicenter, randomized, double-blind, placebo-controlled, flexible- dose study evaluated the film-coated tablet formulation of modafinil, which was titrated to an optimal dose on the basis of efficacy and tolerability ( range: 170 - 425 mg once daily). Efficacy was assessed by clinicians who completed the Attention-Deficit/Hyperactivity Disorder Rating Scale-IV (ADHD-RS-IV) based on interviews with teachers School Version) and parents ( Home Version) and the Clinical Global Impression of Improvement scale. Safety evaluation was based on assessments of adverse event reports, laboratory tests, vital signs, and body weight. Results. A total of 248 subjects were randomly assigned in a 2: 1 ratio, and 246 were treated with modafinil (n = 164) or placebo (n = 82). Treatment groups were comparable with respect to demographics and baseline characteristics. Intention-to-treat analysis (ITT) showed that compared with placebo, treatment with modafinil significantly improved the core symptoms of ADHD as shown by greater reductions in the ADHD-RS-IV School Version total scores from baseline to final visit ( mean change [SD]: -15.0 [11.8] vs -7.3 [9.7]) (effect size: 0.69; 95% confidence interval: 0.57-0.82). Significant improvements were observed with modafinil treatment on the ADHD-RS-IV School Version at week 1, with improvements maintained throughout the study. Similar differences in symptom improvements were observed on the ADHD-RS-IV Home Version between modafinil-treated and placebo-treated patients. Treatment with modafinil also significantly reduced subscale scores for inattention and hyperactivity-impulsivity on both School and Home Versions compared with placebo. At the final visit, 48% of modafinil-treated patients were rated as "much" or "very much" improved in overall clinical condition compared with 17% of placebo-treated patients (Clinical Global Impression of Improvement). Most adverse events were mild to moderate in severity, and the majority resolved during treatment. The most commonly reported adverse events in the modafinil group were insomnia (29%), headache (20%), and decreased appetite (16%). Three percent of modafinil-treated patients and 4% of placebo-treated patients discontinued treatment because of adverse events. Conclusions. Modafinil film-coated tablets significantly improved ADHD symptoms at school and home as evaluated by clinicians, teachers, and parents. Treatment with once-daily modafinil was generally well tolerated, with few discontinuations as a result of adverse events. C1 Massachusetts Gen Hosp, Yawkey Ctr Outpatient Care, Pediat Psychopharmacol Res Unit, Dept Pediat Psychopharmacol, Boston, MA 02114 USA. Univ Calif Irvine, Child Dev Ctr, Irvine, CA 92717 USA. Univ Nebraska, Med Ctr, Omaha, NE 68182 USA. Neurol & Clin Study Ctr, Little Rock, AR USA. Cephalon Inc, W Chester, PA USA. New York State Psychiat Inst & Hosp, New York, NY 10032 USA. RP Biederman, J (reprint author), Massachusetts Gen Hosp, Yawkey Ctr Outpatient Care, Pediat Psychopharmacol Res Unit, Dept Pediat Psychopharmacol, YAW-6A-6900,32 Fruit St, Boston, MA 02114 USA. EM jbiederman@partners.org NR 31 TC 55 Z9 57 U1 1 U2 6 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 2005 VL 116 IS 6 BP E777 EP E784 DI 10.1542/peds.2005-0617 PG 8 WC Pediatrics SC Pediatrics GA 989JH UT WOS:000233668200079 PM 16322134 ER PT J AU O'Riordan, K Akilov, OE Hasan, T AF O'Riordan, Katie Akilov, Oleg E. Hasan, Tayyaba TI The potential for photodynamic therapy in the treatment of localized infections SO PHOTODIAGNOSIS AND PHOTODYNAMIC THERAPY LA English DT Review DE Photodynamic therapy; Photosensitizer; Local infection; Antimicrobial AB At the present time photodynamic therapy (PDT) is receiving considerable interest for its potential as an antimicrobial therapy. This treatment may be a valuable tool in achieving a rapid reduction of the microbial burden perhaps even in the management of localized infections that are resistant to standard antibiotic regimens. A variety of photosensitizers from different groups including porphyrins, chlorophyll derivatives, phthalocyanines and azines have been effective in the photokilling of many Gram-positive and Gram-negative bacterial pathogens in addition to parasites, fungi, and viruses. Much of the suggested antimicrobial uses of this therapy are based on results from in vitro studies. Only a limited number of animal models of infection or clinical studies have been employed to assess the effectiveness of PDT. These studies have reported moderate successes that have not quite achieved the expectations projected from the in vitro results. In order to fully validate the potential of PDT as an antimicrobial therapy considerably more effort is required in the area of appropriate experimental models to better understand the mechanisms of photodynamic destruction of bacteria. (C) 2005 Elsevier B.V. All rights reserved. C1 [Hasan, Tayyaba] Massachusetts Gen Hosp, Wellman Ctr Photomed, Boston, MA 02114 USA. Harvard Univ, Sch Med, Boston, MA 02114 USA. RP Hasan, T (reprint author), Massachusetts Gen Hosp, Wellman Ctr Photomed, Boston, MA 02114 USA. EM thasan@partners.org FU Department of Defense Medical Free Electron Laser Program [FA9550-04-1-0079] FX This work was founded by the Department of Defense Medical Free Electron Laser Program Grant No. FA9550-04-1-0079 NR 117 TC 77 Z9 80 U1 0 U2 16 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 1572-1000 J9 PHOTODIAGN PHOTODYN JI Photodiagnosis Photodyn. Ther. PD DEC PY 2005 VL 2 IS 4 BP 247 EP 262 DI 10.1016/S1572-1000(05)00099-2 PG 16 WC Oncology SC Oncology GA V27CK UT WOS:000208591100002 PM 25048867 ER PT J AU Pastor-Soler, N Pietrement, C Breton, S AF Pastor-Soler, N Pietrement, C Breton, S TI Role of acid/base transporters in the male reproductive tract and potential consequences of their malfunction SO PHYSIOLOGY LA English DT Review ID VACUOLAR H+-ATPASE; SECRETING EPITHELIAL-CELLS; RAT EPIDIDYMAL EPITHELIUM; BOUND CARBONIC-ANHYDRASE; KIDNEY COLLECTING DUCT; ACTIN-BINDING SITE; V-ATPASE; NA+/H+ EXCHANGER; CADMIUM CHLORIDE; LUMINAL ACIDIFICATION AB Acid/base transporters play a key role in establishing an acidic luminal environment for sperm maturation and storage in the male reproductive tract. Impairment of the acidification capacity of the epididymis, via either genetic mutations or exposure to environmental factors, may have profound consequences on male fertility. C1 Massachusetts Gen Hosp, Div Nephrol, Program Membrane Biol, Boston, MA 02114 USA. Harvard Univ, Sch Med, Boston, MA USA. RP Pastor-Soler, N (reprint author), Massachusetts Gen Hosp, Div Nephrol, Program Membrane Biol, Boston, MA 02114 USA. EM sbreton@partners.org FU NICHD NIH HHS [HD-40793, K08-HD-45524, R01 HD040793]; NIDDK NIH HHS [DK-38452, P01 DK038452] NR 140 TC 66 Z9 69 U1 0 U2 2 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA SN 1548-9213 J9 PHYSIOLOGY JI Physiology PD DEC PY 2005 VL 20 BP 417 EP 428 DI 10.1152/physiol.00036.2005 PG 12 WC Physiology SC Physiology GA 986XA UT WOS:000233481800007 PM 16287991 ER PT J AU Sachs, G Weeks, DL Wen, Y Marcus, EA Scott, DR Melchers, K AF Sachs, G Weeks, DL Wen, Y Marcus, EA Scott, DR Melchers, K TI Acid acclimation by Helicobacter pylori SO PHYSIOLOGY LA English DT Review ID PROTON MOTIVE FORCE; ESCHERICHIA-COLI; UREASE ACTIVITY; GASTRIC-MUCOSA; IN-VIVO; AGMATINE ANTIPORTER; VIBRIO-CHOLERAE; PH HOMEOSTASIS; GENES; RESISTANCE AB Helicobacter pylori is a Gram-negative neutralophile associated with peptic ulcers and gastric cancer. It has a unique ability to colonize the human stomach by acid acclimation. It uses the pH-gated urea channel, Urel, to enhance urea access to intrabacterial urease and a membrane-anchored periplasmic carbonic anhydrase to regulate periplasmic pH to similar to 6.1 in acidic media, whereas other neutralophiles cannot regulate periplasmic pH and thus only transit the stomach. C1 Univ Calif Los Angeles, David Geffen Sch Med, Lab Membrane Biol, Los Angeles, CA 90024 USA. Vet Affairs Greater Los Angeles Hlth Care Syst, Los Angeles, CA USA. Altana Res Inst, Boston, MA USA. RP Sachs, G (reprint author), Univ Calif Los Angeles, David Geffen Sch Med, Lab Membrane Biol, Los Angeles, CA 90024 USA. EM gsachs@ucla.edu FU NIDDK NIH HHS [DK-53462, DK-46917, DK-58333] NR 63 TC 66 Z9 69 U1 0 U2 3 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA SN 1548-9213 J9 PHYSIOLOGY JI Physiology PD DEC PY 2005 VL 20 BP 429 EP 438 DI 10.1152/physiol.00032.2005 PG 10 WC Physiology SC Physiology GA 986XA UT WOS:000233481800008 PM 16287992 ER PT J AU Xu, AW Kaelin, CB Morton, GJ Ogimoto, K Stanhope, K Graham, J Baskin, DG Havel, P Schwartz, MW Barsh, GS AF Xu, AW Kaelin, CB Morton, GJ Ogimoto, K Stanhope, K Graham, J Baskin, DG Havel, P Schwartz, MW Barsh, GS TI Effects of hypothalamic neurodegeneration on energy balance SO PLOS BIOLOGY LA English DT Article ID AGOUTI-RELATED PROTEIN; ARCUATE NUCLEUS; NEUROPEPTIDE-Y; GENE-EXPRESSION; FOOD-INTAKE; OB/OB MICE; NEURONS; PROOPIOMELANOCORTIN; LEPTIN; OBESITY AB Normal aging in humans and rodents is accompanied by a progressive increase in adiposity. To investigate the role of hypothalamic neuronal circuits in this process, we used a Cre-lox strategy to create mice with specific and progressive degeneration of hypothalamic neurons that express agouti-related protein (Agrp) or proopiomelanocortin (Pomc), neuropeptides that promote positive or negative energy balance, respectively, through their opposing effects on melanocortin receptor signaling. In previous studies, Pomc mutant mice became obese, but Agrp mutant mice were surprisingly normal, suggesting potential compensation by neuronal circuits or genetic redundancy. Here we find that Pomc-ablation mice develop obesity similar to that described for Pomc knockout mice, but also exhibit defects in compensatory hyperphagia similar to what occurs during normal aging. Agrp-ablation female mice exhibit reduced adiposity with normal compensatory hyperphagia, while animals ablated for both Pomc and Agrp neurons exhibit an additive interaction phenotype. These findings provide new insight into the roles of hypothalamic neurons in energy balance regulation, and provide a model for understanding defects in human energy balance associated with neurodegeneration and aging. C1 Stanford Univ, Sch Med, Dept Genet, Stanford, CA 94305 USA. Stanford Univ, Sch Med, Dept Pediat, Stanford, CA 94305 USA. Univ Washington, Harborview Med Ctr, Dept Med, Seattle, WA 98195 USA. Univ Calif Davis, Dept Nutr, Davis, CA 95616 USA. VA Puget Sound Hlth Care Syst, Seattle, WA 98195 USA. RP Barsh, GS (reprint author), Stanford Univ, Sch Med, Dept Genet, Stanford, CA 94305 USA. EM gbarsh@cmgm.stanford.edu RI Schwartz, Michael/H-9950-2012 FU NIDDK NIH HHS [DK48506, DK68384, P01 DK068384, R01 DK048506] NR 43 TC 99 Z9 99 U1 0 U2 5 PU PUBLIC LIBRARY SCIENCE PI SAN FRANCISCO PA 185 BERRY ST, STE 1300, SAN FRANCISCO, CA 94107 USA SN 1544-9173 J9 PLOS BIOL JI PLoS. Biol. PD DEC PY 2005 VL 3 IS 12 BP 2168 EP 2176 AR e415 DI 10.1371/journal.pbio.0030415 PG 9 WC Biochemistry & Molecular Biology; Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics GA 992SI UT WOS:000233903800012 PM 16296893 ER PT J AU Almaas, E Oltvai, ZN Barabasi, AL AF Almaas, Eivind Oltvai, Zoltan N. Barabasi, Albert-Laszlo TI The activity reaction core and plasticity of metabolic networks SO PLOS COMPUTATIONAL BIOLOGY LA English DT Article ID ESCHERICHIA-COLI MG1655; TRANSCRIPTIONAL REGULATION; GENOME; MODEL; ORGANIZATION; DEFINITION; PATHWAYS; PATTERNS; YEAST; K-12 AB Understanding the system-level adaptive changes taking place in an organism in response to variations in the environment is a key issue of contemporary biology. Current modeling approaches, such as constraint-based flux-balance analysis, have proved highly successful in analyzing the capabilities of cellular metabolism, including its capacity to predict deletion phenotypes, the ability to calculate the relative flux values of metabolic reactions, and the capability to identify properties of optimal growth states. Here, we use flux-balance analysis to thoroughly assess the activity of Escherichia coli, Helicobacter pylori, and Saccharomyces cerevisiae metabolism in 30,000 diverse simulated environments. We identify a set of metabolic reactions forming a connected metabolic core that carry non-zero fluxes under all growth conditions, and whose flux variations are highly correlated. Furthermore, we find that the enzymes catalyzing the core reactions display a considerably higher fraction of phenotypic essentiality and evolutionary conservation than those catalyzing noncore reactions. Cellular metabolism is characterized by a large number of species-specific conditionally active reactions organized around an evolutionary conserved, but always active, metabolic core. Finally, we find that most current antibiotics interfering with bacterial metabolism target the core enzymes, indicating that our findings may have important implications for antimicrobial drug- target discovery. C1 Univ Pittsburgh, Sch Med, Dept Pathol, Pittsburgh, PA 15260 USA. Lawrence Livermore Natl Lab, Biosci Directorate, Microbial Syst Div, Livermore, CA USA. Univ Notre Dame, Ctr Complex Network Res, Notre Dame, IN 46556 USA. Univ Notre Dame, Dept Phys, Notre Dame, IN 46556 USA. Harvard Univ, Dana Farber Canc Inst, Ctr Canc Syst Biol, Boston, MA 02115 USA. RP Oltvai, ZN (reprint author), Univ Pittsburgh, Sch Med, Dept Pathol, Pittsburgh, PA 15260 USA. EM oltvai@pitt.edu OI Almaas, Eivind/0000-0002-9125-326X NR 22 TC 70 Z9 72 U1 0 U2 1 PU PUBLIC LIBRARY SCIENCE PI SAN FRANCISCO PA 185 BERRY ST, STE 1300, SAN FRANCISCO, CA 94107 USA SN 1553-734X J9 PLOS COMPUT BIOL JI PLoS Comput. Biol. PD DEC PY 2005 VL 1 IS 7 BP 557 EP 563 AR e68 DI 10.1371/journal.pcbi.0010068 PG 7 WC Biochemical Research Methods; Mathematical & Computational Biology SC Biochemistry & Molecular Biology; Mathematical & Computational Biology GA 069WS UT WOS:000239480500004 PM 16362071 ER PT J AU Sonn, GA Aronson, W Litwin, MS AF Sonn, GA Aronson, W Litwin, MS TI Impact of diet on prostate cancer: a review SO PROSTATE CANCER AND PROSTATIC DISEASES LA English DT Review DE prostate cancer; diet; supplements ID HIGH-FAT DIET; VITAMIN-E; PROSPECTIVE COHORT; UNITED-STATES; GREEN TEA; ALPHA-TOCOPHEROL; LNCAP TUMORS; NETHERLANDS-COHORT; INDUCED APOPTOSIS; DECREASED GROWTH AB Epidemiological studies suggest that environmental factors may mediate the transformation of latent prostate cancer into clinically apparent tumors and that diet appears to influence this progression. Close correlations between average per capita fat intake and prostate cancer mortality internationally generated interest in underlying mechanisms for this link, such as through serum levels of androgens, free radicals, proinflammatory fatty acid metabolites, or insulin-like growth factor. Much interest currently lies in the potential of HMG-CoA reductase inhibitors (statins) to play a chemopreventative role in prostate cancer. Lycopene, a potent antioxidant found in tomatoes, may exert a protective effect in the prostate. Selenium and vitamin E have also been shown to decrease the risk of prostate cancer in some men. Calcium may support vitamin D-related antiproliferative effects in prostate cancer. Certain soy proteins, common in the Asian diet, have been shown to inhibit prostate cancer cell growth. Finally, green tea may also have a chemopreventive effect by inducing apoptosis. Despite confounding factors present in clinical studies assessing the effect of diet on cancer risk, the data remain compelling that a variety of nutrients may prevent the development and progression of prostate cancer. C1 Univ Calif Los Angeles, Dept Urol, David Geffen Sch Med, Los Angeles, CA 90095 USA. Univ Calif Los Angeles, Sch Publ Hlth, Dept Hlth Serv, Los Angeles, CA 90024 USA. Univ Calif Los Angeles, Jonsson Comprehens Canc Ctr, Los Angeles, CA 90024 USA. Vet Adm Greater Los Angeles Healthcare Syst, Los Angeles, CA USA. RP Litwin, MS (reprint author), Univ Calif Los Angeles, Dept Urol, David Geffen Sch Med, Box 951738, Los Angeles, CA 90095 USA. EM mlitwin@mednet.ucla.edu NR 93 TC 88 Z9 90 U1 4 U2 17 PU NATURE PUBLISHING GROUP PI LONDON PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND SN 1365-7852 J9 PROSTATE CANCER P D JI Prostate Cancer Prostatic Dis. PD DEC PY 2005 VL 8 IS 4 BP 304 EP 310 DI 10.1038/sj.pcan.4500825 PG 7 WC Oncology; Urology & Nephrology SC Oncology; Urology & Nephrology GA 999VE UT WOS:000234418000002 PM 16130015 ER PT J AU Ray, R Doyle, GA Crowley, JJ Buono, RJ Oslin, DW Patkar, AA Mannelli, P DeMaria, PA O'Brien, CP Berrettini, WH AF Ray, R Doyle, GA Crowley, JJ Buono, RJ Oslin, DW Patkar, AA Mannelli, P DeMaria, PA O'Brien, CP Berrettini, WH TI A functional prodynorphin promoter polymorphism and opioid dependence SO PSYCHIATRIC GENETICS LA English DT Article DE addiction and genetics; dynorphin; opioid; polymorphism ID GENE; SUPPRESSION; WITHDRAWAL; EXPRESSION; DYNORPHIN; COCAINE AB Objectives The prodynorphin gene (PDYN) promoter has a repeat polymorphism that is functionally important in association with substance abuse. We examined this polymorphism for association in our sample of 168 opioid-dependent patients and 122 ethnically and geographically matched controls. Methods Patients were selected from university-affiliated residential and non-residential addiction treatment programs in the Philadelphia area. A sample of blood was drawn from consenting individuals and genomic DNA was isolated. Polymerase chain reaction amplification of the PDYN promoter was performed and various genotypes were determined on the basis of differing sizes of the polymerase chain reaction products. The genotype and allele data were analyzed by Fisher's exact test. Result A significant difference in genotype (P < 0.0006) and allele (p < 10(-5)) frequencies was found between the African American and European American populations. We did not detect any significant difference in genotype or allele frequencies between the patients and controls within the European American ethnic group. However, we detected a weak association (P= 0.013) when we compared allele frequencies of patients and controls in the African American population. Conclusions These data suggest that the PDYN repeat polymorphism should be studied in additional opioid-dependent populations. Psychiatr Genet 15:295-298 (c) 2005 Lippincott Williams & Wilkins. C1 Univ Penn, Sch Med, Ctr Neurobiol & Behav, Dept Psychiat, Philadelphia, PA 19104 USA. Univ Penn, Dept Pharmacol, Philadelphia, PA 19104 USA. Vet Affairs Med Ctr, Philadelphia, PA USA. Jefferson Med Coll, Dept Psychiat & Human Behav, Philadelphia, PA USA. RP Berrettini, WH (reprint author), Univ Penn, Sch Med, Ctr Neurobiol & Behav, Dept Psychiat, Room 111,415 Curie Blvd, Philadelphia, PA 19104 USA. EM wadeb@mail.med.upenn.edu OI Crowley, James/0000-0001-9051-1557 FU PHS HHS [P60-05186] NR 10 TC 16 Z9 16 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3261 USA SN 0955-8829 J9 PSYCHIAT GENET JI Psychiatr. Genet. PD DEC PY 2005 VL 15 IS 4 BP 295 EP 298 DI 10.1097/00041444-200512000-00013 PG 4 WC Genetics & Heredity; Neurosciences SC Genetics & Heredity; Neurosciences & Neurology GA 993UB UT WOS:000233979500012 PM 16314761 ER PT J AU Goldberg, JF Allen, MH Miklowitz, DA Bowden, CL Endick, CJ Chessick, CA Wisniewski, SR Miyahara, S Sagduyu, K Thase, ME Calabrese, JR Sachs, GS AF Goldberg, JF Allen, MH Miklowitz, DA Bowden, CL Endick, CJ Chessick, CA Wisniewski, SR Miyahara, S Sagduyu, K Thase, ME Calabrese, JR Sachs, GS TI Suicidal ideation and pharmacotherapy among STEP-BD patients SO PSYCHIATRIC SERVICES LA English DT Article; Proceedings Paper CT 41st Annual Meeting of the American-College-of-Neuropsychopharmacology CY DEC 08-12, 2002 CL SAN JUAN, PR SP Amer Coll Neuropsychopharmacol ID BIPOLAR AFFECTIVE-DISORDER; MAJOR AFFECTIVE-DISORDERS; MOOD DISORDERS; I DISORDER; LITHIUM; RISK; SCHIZOPHRENIA; PREVENTION; GUIDELINES; MORTALITY AB Objective: Little is known about the effects of lithium on suicidal ideation or about the possible antisuicidal effects of divalproex, second-generation antipsychotics, or antidepressants among persons with bipolar disorder. Methods: Using a cross-sectional design, the authors examined patterns of psychotropic drug use relative to suicidal ideation among 1,000 patients with bipolar disorder in the National Institute of Mental Health's Systematic Treatment Enhancement Program for Bipolar Disorder (STEP-BD). Results: The presence of suicidal ideation was similar between patients who were taking any lithium and those who were not (22.2 percent and 25.8 percent, respectively) and between those who were taking any divalproex and those who were not (20.3 percent and 21.5 percent). Suicidal ideation was significantly more prevalent among patients who were taking a second-generation antipsychotic than those who were not (26 percent and 17 percent) and those who were taking an antidepressant and those who were not (25 percent and 14 percent). After other variables had been controlled for, lithium prescriptions were significantly more common among patients who had suicidal ideation. Conclusions: Among patients with bipolar disorder who have suicidal ideation, antidepressants and second-generation antipsychotics appear to be prescribed by community practitioners more often than other medications, with lithium reserved for those with more severe illness characteristics. C1 Silver Hill Hosp, New Canaan, CT 06840 USA. Univ Colorado, Sch Med, Dept Psychiat, Boulder, CO 80309 USA. Univ Colorado, Dept Psychol, Boulder, CO 80309 USA. Univ Texas, Hlth Sci Ctr, Dept Psychiat, San Antonio, TX 78285 USA. Northwestern Univ, Feinberg Sch Med, Dept Psychiat, Chicago, IL 60611 USA. Univ Pittsburgh, Sch Publ Hlth, Dept Epidemiol, Pittsburgh, PA 15260 USA. Univ Missouri, Sch Med, Kansas City, MO 64110 USA. Univ Pittsburgh, Western Psychiat Inst & Clin, Pittsburgh, PA 15260 USA. Case Western Reserve Univ, Dept Psychiat, Cleveland, OH 44106 USA. Massachusetts Gen Hosp, Dept Psychiat, Boston, MA 02114 USA. RP Goldberg, JF (reprint author), Silver Hill Hosp, 208 Valley Rd, New Canaan, CT 06840 USA. EM jfgoldberg@yahoo.com RI Allen, Michael/A-8776-2011; OI Wisniewski, Stephen/0000-0002-3877-9860 FU NIMH NIH HHS [K-23 MH-01936, N01-MH-80001] NR 34 TC 18 Z9 18 U1 1 U2 1 PU AMER PSYCHIATRIC PUBLISHING, INC PI ARLINGTON PA 1000 WILSON BOULEVARD, STE 1825, ARLINGTON, VA 22209-3901 USA SN 1075-2730 J9 PSYCHIAT SERV JI Psychiatr. Serv. PD DEC PY 2005 VL 56 IS 12 BP 1534 EP 1540 DI 10.1176/appi.ps.56.12.1534 PG 7 WC Health Policy & Services; Public, Environmental & Occupational Health; Psychiatry SC Health Care Sciences & Services; Public, Environmental & Occupational Health; Psychiatry GA 991OE UT WOS:000233822500007 PM 16339615 ER PT J AU Martinez, JM Marangell, LB Simon, NM Miyahara, S Wisniewski, SR Harrington, J Pollack, MH Sachs, GS Thase, ME AF Martinez, JM Marangell, LB Simon, NM Miyahara, S Wisniewski, SR Harrington, J Pollack, MH Sachs, GS Thase, ME TI Baseline predictors of serious adverse events at one year among patients with bipolar disorder in STEP-BD SO PSYCHIATRIC SERVICES LA English DT Article ID TREATMENT ENHANCEMENT PROGRAM; DEPRESSIVE SYMPTOMS; MYOCARDIAL-INFARCTION; RISK-FACTOR; REHOSPITALIZATION; HOSPITALIZATION; MORTALITY; SURGERY; ONSET; AGE AB Objective: Little is known about serious adverse events that occur in the context of clinical care for bipolar disorder. This study examined predictors of serious adverse events in a large cohort of patients with bipolar disorder. Methods: Types and frequency of serious adverse events were tabulated on the basis of data from the first 1,000 participants in the Systematic Treatment Enhancement Program for Bipolar Disorder (STEP-BD). STEP-BD follows a large cohort of patients longitudinally. Treatments are provided as deemed most appropriate by the treating psychiatrist. Logistic regression was used to identify variables present at study entry that were associated with the occurrence of a serious adverse event within one year. Results: A total of 161 serious adverse events were reported among 118 participants. The most frequent serious adverse event was hospitalization for suicidal ideation (44 participants, or 27 percent). A greater number of previous psychiatric medications was predictive of the occurrence of a psychiatric serious adverse event among participants who had less than one year of study follow-up data. A history of psychosis, current substance abuse, lower household income, and a fully syndromic baseline mood state were associated with the occurrence of a psychiatric serious adverse event among participants who had one full year of follow-up data. Conclusions: These data identify clinical and demographic factors that warrant closer clinical follow-up, because these factors may be predictive of poor outcomes in the following year, even in the context of expert care. C1 Baylor Coll Med, Mood Disorders Ctr, Meninger Dept Psychiat, Ben Taub Gen Hosp, Houston, TX 77030 USA. Massachusetts Gen Hosp, Ctr Anxiety & Traumat Stress Disorders, Boston, MA 02114 USA. Univ Pittsburgh, Grad Sch Publ Hlth, Epidemiol Data Ctr, Pittsburgh, PA 15260 USA. Harvard Univ, Sch Med, Partners Bipolar Disorder Treatment Ctr, Massachusetts Gen Hosp, Cambridge, MA 02138 USA. Univ Pittsburgh, Med Ctr, Dept Psychiat, Pittsburgh, PA 15260 USA. RP Martinez, JM (reprint author), Baylor Coll Med, Mood Disorders Ctr, Meninger Dept Psychiat, Ben Taub Gen Hosp, 6655 Travis St,Suite 560, Houston, TX 77030 USA. EM jmartine@bcm.tmc.edu OI Wisniewski, Stephen/0000-0002-3877-9860 FU NIMH NIH HHS [N01-MH-80001] NR 21 TC 17 Z9 17 U1 1 U2 1 PU AMER PSYCHIATRIC PUBLISHING, INC PI ARLINGTON PA 1000 WILSON BOULEVARD, STE 1825, ARLINGTON, VA 22209-3901 USA SN 1075-2730 J9 PSYCHIAT SERV JI Psychiatr. Serv. PD DEC PY 2005 VL 56 IS 12 BP 1541 EP 1548 DI 10.1176/appi.ps.56.12.1541 PG 8 WC Health Policy & Services; Public, Environmental & Occupational Health; Psychiatry SC Health Care Sciences & Services; Public, Environmental & Occupational Health; Psychiatry GA 991OE UT WOS:000233822500008 PM 16339616 ER PT J AU Pirl, WF Greer, JA Weissgarber, C Liverant, G Safren, SA AF Pirl, WF Greer, JA Weissgarber, C Liverant, G Safren, SA TI Screening for infectious diseases among patients in a state psychiatric hospital SO PSYCHIATRIC SERVICES LA English DT Article ID SEVERE MENTAL-ILLNESS; HUMAN-IMMUNODEFICIENCY-VIRUS; HEPATITIS-C; UNITED-STATES; PREVALENCE; PEOPLE; HIV AB This cross-sectional retrospective study examined the frequency of positive tests for infectious diseases among 655 patients who were admitted to a state psychiatric hospital from 1997 to 1999. Not all patients who were admitted to the hospital were tested for each disease. Rates of positive tuberculin (20.2 percent), hepatitis B (23.9 percent), and hepatitis C (21.5 percent) tests were all significantly greater than estimates for the U.S. general population. A minority of patients were tested for HIV, and 29.0 percent were positive. The rate of hepatitis A was similar to that in the general population (33.2 percent). Independent risk factors for markers of disease included age, immigrant status, homelessness, and history of substance use. These results confirm the importance of screening for infectious diseases among individuals with severe and persistent mental illness. C1 Massachusetts Gen Hosp, Dept Psychiat, Boston, MA 02114 USA. Erich Lindemann Mental Hlth Care, Boston, MA USA. Boston Univ, Dept Psychol, Boston, MA 02215 USA. RP Pirl, WF (reprint author), Massachusetts Gen Hosp, Dept Psychiat, Wang Ambulat Care Ctr 812,15 Parkman St, Boston, MA 02114 USA. EM wpirl@partners.org NR 10 TC 16 Z9 17 U1 0 U2 0 PU AMER PSYCHIATRIC PUBLISHING, INC PI ARLINGTON PA 1000 WILSON BOULEVARD, STE 1825, ARLINGTON, VA 22209-3901 USA SN 1075-2730 J9 PSYCHIAT SERV JI Psychiatr. Serv. PD DEC PY 2005 VL 56 IS 12 BP 1614 EP 1616 DI 10.1176/appi.ps.56.12.1614 PG 3 WC Health Policy & Services; Public, Environmental & Occupational Health; Psychiatry SC Health Care Sciences & Services; Public, Environmental & Occupational Health; Psychiatry GA 991OE UT WOS:000233822500022 PM 16339630 ER PT J AU Biederman, J Mick, E Fried, R Aleardi, M Potter, A Herzig, K AF Biederman, J Mick, E Fried, R Aleardi, M Potter, A Herzig, K TI A simulated workplace experience for nonmedicated adults with and without ADHD SO PSYCHIATRIC SERVICES LA English DT Article AB Eighteen nonmedicated adults with attention-deficit hyperactivity disorder (ADHD) and IS who did not have ADHD were evaluated in a full-day simulated workplace experience. It was hypothesized that adults with ADHD would evidence greater impairments on simulated tasks, off-task behavior, and self-reported ADHD symptoms than those without ADHD. Participants were compared on self-reported ADHD symptoms, objective observations, and performance on written tasks. Significant differences were noted in reading comprehension and math fluency as well as observer-rated and self-reported behavior, but not attention. The results of this study suggest that ADHD among adults is associated with significant deficits in performance of workplace tasks, internal experiences, and external observations of core symptoms of ADHD. C1 Massachusetts Gen Hosp, Boston, MA 02114 USA. RP Biederman, J (reprint author), Massachusetts Gen Hosp, ACC 7, Boston, MA 02114 USA. EM biedermann@helix.mgh.harvard.edu OI Mick, Eric/0000-0001-8505-8145 NR 10 TC 16 Z9 16 U1 2 U2 4 PU AMER PSYCHIATRIC PUBLISHING, INC PI ARLINGTON PA 1000 WILSON BOULEVARD, STE 1825, ARLINGTON, VA 22209-3901 USA SN 1075-2730 J9 PSYCHIAT SERV JI Psychiatr. Serv. PD DEC PY 2005 VL 56 IS 12 BP 1617 EP 1620 DI 10.1176/appi.ps.56.12.1617 PG 4 WC Health Policy & Services; Public, Environmental & Occupational Health; Psychiatry SC Health Care Sciences & Services; Public, Environmental & Occupational Health; Psychiatry GA 991OE UT WOS:000233822500023 PM 16339631 ER PT J AU Zou, KH Greve, DN Wang, M Pieper, SD Warfield, SK White, NS Manandhar, S Brown, GG Vangel, MG Kikinis, R Wells, WM AF Zou, KH Greve, DN Wang, M Pieper, SD Warfield, SK White, NS Manandhar, S Brown, GG Vangel, MG Kikinis, R Wells, WM CA FIRST BIRN Res Grp TI Reproducibility of functional MR imaging: Preliminary results of prospective multi-institutional study performed by biomedical informatics research network SO RADIOLOGY LA English DT Article ID TEST-RETEST RELIABILITY; SURFACE-BASED ANALYSIS; CORTICAL SURFACE; HEMODYNAMIC-RESPONSE; COORDINATE SYSTEM; WORKING-MEMORY; VARIABILITY; SEGMENTATION; VALIDATION; ACTIVATION AB PURPOSE: To prospectively investigate the factors-including subject, brain hemisphere, study site, field strength, imaging unit vendor, imaging run, and examination visit-affecting the reproducibility of functional magnetic resonance (MR) imaging activations based on a repeated sensory-motor (SM) task. MATERIALS AND METHODS: The institutional review boards of all participating sites approved this HIPAA-compliant study. All subjects gave informed consent. Functional MR imaging data were repeatedly acquired from five healthy men aged 20-29 years who performed the same SM task at 10 sites. Five 1.5-T MR imaging units, four 3.0-T units, and one 4.0-T unit were used. The subjects performed bilateral finger tapping on button boxes with a 3-Hz audio cue and a reversing checkerboard. In a block design, 15-second epochs of alternating baseline and tasks yielded 85 acquisitions per run. Functional MR images were acquired with block-design echo-planar or spiral gradient-echo sequences. Brain activation maps standardized in a unit-sphere for the left and right hemispheres of each subject were constructed. Areas under the receiver operating characteristic curve, intraclass correlation coefficients, multiple regression analysis, and paired Student t tests were used for statistical analyses. RESULTS: Significant factors were subject (P < .005), k-space (P < .005), and field strength (P = .02) for sensitivity and subject (P = .03) and k-space (P = .05) for specificity. At 1.5-T MR imaging, mean sensitivities ranged from 7% to 32% and mean specificities were higher than 99%. At 3.0 T, mean sensitivities and specificities ranged from 42% to 85% and from 96% to 99%, respectively. At 4.0 T, mean sensitivities and specificities ranged from 41% to 73% and from 95% to 99%, respectively. Mean areas under the receiver operating characteristic curve (+/- their standard errors) were 0.77 0.05 at 1.5 T, 0.90 +/- 0.09 at 3.0 T, and 0.95 +/- 0.02 at 4.0 T, with significant differences between the 1.5- and 3.0-T examinations and between the 1.5- and 4.0-T examinations (P < .01 for both comparisons). Intraclass correlation coefficients ranged from 0.49 to 0.71. CONCLUSION: MR imaging at 3.0- and 4.0-T yielded higher reproducibility across sites and significantly better results than 1.5-T imaging. The effects of subject, k-space, and field strength on examination reproducibility were significant. (c) RSNA, 2005. C1 Brigham & Womens Hosp, Surg Planning Lab, Dept Radiol, Boston, MA 02115 USA. Harvard Univ, Sch Med, Dept Hlth Care Policy, Boston, MA 02115 USA. Harvard Univ, Sch Med, Athinoula A Martinos Ctr Biomed Engn, Dept Radiol,Massachesetts Gen Hosp, Boston, MA 02115 USA. Isomics, Cambridge, MA USA. MIT, Comp Sci & Artificial Intelligence Lab, Cambridge, MA 02139 USA. Brigham & Womens Hosp, Computat Radiol Lab, Dept Radiol, Boston, MA 02115 USA. Childrens Hosp, Dept Radiol, Boston, MA 02115 USA. Univ Calif San Diego, Lab Cognit Imaging, Dept Psychiat, La Jolla, CA 92093 USA. Vet Affairs San Diego Hlth Care Syst, San Diego, CA USA. RP Zou, KH (reprint author), Brigham & Womens Hosp, Surg Planning Lab, Dept Radiol, 75 Francis St, Boston, MA 02115 USA. EM zou@bwh.harvard.edu RI Warfield, Simon/B-3352-2009; OI Warfield, Simon/0000-0002-7659-3880 FU AHRQ HHS [R03 HS013234, R03HS013234-01]; NCI NIH HHS [R21CA89449-01]; NCRR NIH HHS [P41RR13218, P41 RR013218, P41 RR014075, P41RR14075]; NIMH NIH HHS [R21 MH067054, R21MH67054]; NLM NIH HHS [R01 LM007861, R01 LM007861-03, R01LM007861-01A1] NR 30 TC 68 Z9 68 U1 0 U2 4 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 JAN PY 2005 VL 237 IS 3 BP 781 EP 789 DI 10.1148/radiol.2373041630 PG 9 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA 985LV UT WOS:000233380100004 PM 16304101 ER PT J AU Thrall, JH AF Thrall, JH TI Reinventing radiology in the digital age - Part III. Facilities, work processes, and job responsibilities SO RADIOLOGY LA English DT Editorial Material ID SPIRAL COMPUTED-TOMOGRAPHY; CT COLONOGRAPHY; LESIONS C1 Massachusetts Gen Hosp, Dept Radiol, Boston, MA 02114 USA. RP Thrall, JH (reprint author), Massachusetts Gen Hosp, Dept Radiol, MZ-FND 216,14 Fruit St, Boston, MA 02114 USA. EM thrall.james@mgh.harvard.edu NR 19 TC 10 Z9 10 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 JAN PY 2005 VL 237 IS 3 BP 790 EP 793 DI 10.1148/radiol.2373051296 PG 4 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA 985LV UT WOS:000233380100005 PM 16304102 ER PT J AU Chan, HP Wei, J Sahiner, B Rafferty, EA Wu, T Roubidoux, MA Moore, RH Kopans, DB Hadjiiski, LM Helvie, MA AF Chan, HP Wei, J Sahiner, B Rafferty, EA Wu, T Roubidoux, MA Moore, RH Kopans, DB Hadjiiski, LM Helvie, MA TI Computer-aided detection system for breast masses on digital tomosynthesis mammograms: Preliminary experience SO RADIOLOGY LA English DT Article ID FINITE-SAMPLE SIZE; SCREENING MAMMOGRAPHY; DEPTH-PERCEPTION; DIAGNOSIS; STEREOMAMMOGRAPHY; PERFORMANCE; MAGNIFICATION; CANCER; ROC AB The purpose of the study was to design a computer-aided detection (CAD) system for breast mass detection on digital breast tomosynthesis (DBT) mammograms and to perform a preliminary evaluation of the performance of this system. Twenty-six patients were imaged with a prototype DBT system. Institutional review board approval and written informed patient consent were obtained. Use of the data set in this study was HIPAA compliant. The CAD system first screened the three-dimensional volume of the mass candidates by means of gradient-field analysis. Each mass candidate was segmented from the structured background, and its image features were extracted. A feature classifier was designed to differentiate true masses from normal tissues. The CAD system was trained and tested by using a leave-one-case-out method. The classifier calculated a mean area under the test receiver operating characteristic curve of 0.91 +/- 0.03 (standard error of mean). The CAD system achieved a sensitivity of 85%, with 2.2 false-positive objects per case. The results demonstrate the feasibility of the authors' approach to the development of a CAD system for DBT mammography. (c) RSNA, 2005. C1 Univ Michigan, Dept Radiol, Ann Arbor, MI 48109 USA. Massachusetts Gen Hosp, Dept Radiol, Boston, MA 02114 USA. RP Chan, HP (reprint author), Univ Michigan, Dept Radiol, 1500 E Med Ctr Dr,UHB1F510B, Ann Arbor, MI 48109 USA. EM chanhp@umich.edu FU NCI NIH HHS [CA91713, CA95153, R01 CA091713, R01 CA091713-07, R01 CA095153, R01 CA095153-01A1] NR 20 TC 66 Z9 67 U1 0 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 JAN PY 2005 VL 237 IS 3 BP 1075 EP 1080 DI 10.1148/radiol.2373041657 PG 6 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA 985LV UT WOS:000233380100043 PM 16237141 ER PT J AU Wah, TM Arellano, RS Gervais, DA Saltallamacchia, CA Martino, J Halpern, EF Maher, M Mueller, PR AF Wah, TM Arellano, RS Gervais, DA Saltallamacchia, CA Martino, J Halpern, EF Maher, M Mueller, PR TI Image-guided percutaneous radiofrequency ablation and incidence of post-radiofrequency ablation syndrome: Prospective survey SO RADIOLOGY LA English DT Article ID HEPATOCELLULAR-CARCINOMA; HEPATIC-TUMORS; COMPLICATIONS; EMBOLIZATION; INHIBITOR AB PURPOSE: To evaluate prospectively the incidence of post-radiofrequency (RF) ablation syndrome and determine its impact on the quality of life in the 10 days after percutaneous RF ablation. MATERIALS AND METHODS: This study was approved by the institutional review board and was HIPAA compliant. Informed consent was obtained for this survey in all patients by the interventional nurse coordinators. Thirty-six patients (20 men, 16 women; mean age, 69.3 years; range, 40-88 years) underwent RF ablation for 26 liver tumors and 17 renal tumors. Twenty control patients (11 men, nine women; mean age, 60.8 years; range, 35-76 years) underwent biopsy of focal liver lesions or renal lesions. With a standardized questionnaire, a telephone survey was conducted on days 1, 3, 5, and 10 after RF ablation or biopsy. The symptoms and interference with lifestyle were documented prospectively with a numeric intensity scale by using grades 0-10. Statistical analysis with Fisher exact test and analysis of variance was performed. RESULTS: After RF ablation, 15 (42%) patients developed low-grade fever (P <.001), 29 (81%) had flulike symptoms (P <.001), and four were asymptomatic. Symptoms peaked on day 3 and mainly resolved by day 10. Twelve (33%) patients had complete post-RF ablation syndrome: fever and flulike symptoms (P =.005). Flulike symptoms were more prolonged when they were accompanied with fever, peaked on day 5, and resolved more quickly for patients with renal lesions than they did for patients with liver lesions. Four patients had persistent fever caused by pneumonia (n =2), pleural effusion and atelectasis (n =1), or liver abscess (n =1). No control patients developed both fever and flulike symptoms. Post-RF ablation patients with symptoms experienced significantly greater pain and interference with general and work activities, which peaked on day 1, than did control patients (P =.01 [pain], P <.001 [general and work activities]). CONCLUSION: Complete post-RF ablation syndrome occurs in approximately one-third of patients but is self-limiting within 10 days after the procedure. Persistent or late-onset fever may indicate concurrent infection elsewhere or possible abscess formation. (c) RSNA 2005. C1 Massachusetts Gen Hosp, Div Abdominal Imaging & Intervent Radiol, Boston, MA 02114 USA. Inst Technol Assessment, Dept Stat, Boston, MA USA. RP Mueller, PR (reprint author), Massachusetts Gen Hosp, Div Abdominal Imaging & Intervent Radiol, 55 Fruit St,White Bldg 270, Boston, MA 02114 USA. EM pmueller@partners.org NR 14 TC 34 Z9 36 U1 0 U2 5 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 JAN PY 2005 VL 237 IS 3 BP 1097 EP 1102 DI 10.1148/radiol.2373042008 PG 6 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA 985LV UT WOS:000233380100046 PM 16304121 ER PT J AU Yu, SY Viola, F Christoforidis, JB D'Amico, DJ AF Yu, SY Viola, F Christoforidis, JB D'Amico, DJ TI Dystrophic calcification of the fibrous capsule around a hydrogel explant 13 years after scleral buckling surgery: Capsular calcification of a hydrogel explant SO RETINA-THE JOURNAL OF RETINAL AND VITREOUS DISEASES LA English DT Article DE buckle; calcification; capsule; hydrogel; Miragel ID IMPLANT C1 Massachusetts Eye & Ear Infirm, Retina Serv, Boston, MA 02114 USA. Harvard Univ, Sch Med, Dept Ophthalmol, Boston, MA USA. RP D'Amico, DJ (reprint author), Massachusetts Eye & Ear Infirm, Retina Serv, 243 Charles St, Boston, MA 02114 USA. EM djdamico@meei.harvard.edu NR 8 TC 3 Z9 3 U1 0 U2 1 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3261 USA SN 0275-004X J9 RETINA-J RET VIT DIS JI Retin.-J. Retin. Vitr. Dis. PD DEC PY 2005 VL 25 IS 8 BP 1104 EP 1107 DI 10.1097/00006982-200512000-00025 PG 4 WC Ophthalmology SC Ophthalmology GA 008AQ UT WOS:000235013000025 PM 16340547 ER PT J AU Yu, JH Yang, WH Gulick, T Bloch, KD Bloch, DB AF Yu, JH Yang, WH Gulick, T Bloch, KD Bloch, DB TI Ge-1 is a central component of the mammalian cytoplasmic mRNA processing body SO RNA-A PUBLICATION OF THE RNA SOCIETY LA English DT Article DE mRNA processing body; mRNA decay; autoantigen ID NUCLEAR-LOCALIZATION SEQUENCE; STRESS GRANULES; GW BODIES; WD-REPEAT; PROTEIN; DEGRADATION; SITES; GW182; AUTOANTIBODIES; STABILITY AB The mRNA processing body (P-body) is a cellular structure that regulates gene expression by degrading cytoplasmic mRNA. The objective of this study was to identify and characterize novel components of the mammalian P-body. Approximately 5% of patients with the autoimmune disease primary biliary cirrhosis have antibodies directed against this structure. Serum from one of these patients was used to identify a cDNA encoding Ge-1, a 1401-amino-acid protein. Ge-1 contains an N-terminal WD40 motif and C-terminal domains characterized by a repeating psi(X2-3) motif. Ge-1 co-localized with previously identified P-body components, including proteins involved in mRNA decapping (DCP1a and DCP2) and the autoantigen GW182. The Ge-1 C-terminal domain was necessary and sufficient to target the protein to P-bodies. Following exposure of cells to oxidative stress, Ge-1-containing P-bodies were found adjacent to TIA-containing stress granules. During the recovery period, TIA returned to the nucleus while Ge-1-containing P-bodies localized to the perinuclear region. siRNA-mediated knock-down of Ge-1 resulted in loss of P-bodies containing Ge-1, DCP1a, and DCP2. In contrast, Ge-1-containing P-bodies persisted despite knock-down of DCP2. Taken together, the results of this study show that Ge-1 is a central component of P-bodies and suggest that Ge-1 may act prior to the 5-decapping step in mRNA degradation. C1 Harvard Univ, Sch Med, Dept Med, Ctr Immunol & Inflammat Dis, Boston, MA 02114 USA. Massachusetts Gen Hosp, Diabet Res Labs, Boston, MA USA. Massachusetts Gen Hosp, Cardiovasc Res Ctr, Gen Med Serv, Boston, MA 02114 USA. RP Bloch, DB (reprint author), Massachusetts Gen Hosp, CNY 8302,149 13th St, Charlestown, MA 02129 USA. EM bloch@helix.mgh.harvard.edu FU NHLBI NIH HHS [HL070896, R01 HL070896, R01 HL074352, HL074352]; NIDDK NIH HHS [DK051179] NR 25 TC 110 Z9 117 U1 0 U2 3 PU COLD SPRING HARBOR LAB PRESS, PUBLICATIONS DEPT PI WOODBURY PA 500 SUNNYSIDE BLVD, WOODBURY, NY 11797-2924 USA SN 1355-8382 J9 RNA JI RNA-Publ. RNA Soc. PD DEC PY 2005 VL 11 IS 12 BP 1795 EP 1802 DI 10.1261/rna.2142405 PG 8 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA 990QS UT WOS:000233758900007 PM 16314453 ER PT J AU Miller, DD McEvoy, JP Davis, SM Caroff, SN Saltz, BL Chakos, MH Swartz, MS Keefe, RSE Rosenheck, RA Stroup, TS Lieberman, JA AF Miller, DD McEvoy, JP Davis, SM Caroff, SN Saltz, BL Chakos, MH Swartz, MS Keefe, RSE Rosenheck, RA Stroup, TS Lieberman, JA TI Clinical correlates of tardive dyskinesia in schizophrenia: Baseline data from the CATIE schizophrenia trial SO SCHIZOPHRENIA RESEARCH LA English DT Article DE tardive dyskinesia; schizophrenia; antipsychotic adverse effects; clinical features ID ABNORMAL INVOLUNTARY MOVEMENTS; RISK-FACTORS; ANTIPSYCHOTIC TRIALS; NEGATIVE SYMPTOMS; OLDER PATIENTS; PSYCHIATRIC-PATIENTS; DRUG-ADDICTION; USE DISORDERS; PREVALENCE; ASSOCIATION AB Objective: To examine the clinical characteristics of individuals with schizophrenia that develop tardive dyskinesia (TD) associated with antipsychotic treatment. Methods: Baseline data on 1460 patients with schizophrenia were collected as part of the Clinical Antipsychotic, Trials of intervention Effectiveness schizophrenia study. Subjects who met Schooler-Kane criteria for probable TD were compared to those without TD. Multiple regression analyses were used to examine the relationship between TD and clinical variables. Results: 212 subjects met the Schooler-Kane criteria for probable TD and 1098 had no history or current evidence of TD. Subjects with TD were older, had a longer duration of receiving antipsychotic medication, and were more likely to have been receiving a conventional antipsychotic and an anticholinergic agent. After controlling for important baseline covariates, diabetes mellitus (DM) and hypertension did not predict TD, whereas substance abuse significantly predicted TD. Differences in cognitive functioning were not significantly different after controlling for baseline covariates. The. TD subjects also had higher ratings of psychopathology, EPSE, and akathisia. Conclusion: Our results confirm the established relationships between the presence of TD and age, duration of treatment with antipsychotics, treatment with a conventional antipsychotic, treatment with anticholinergics, the presence of EPS and akathisia, and substance abuse. Subjects with TD had higher ratings of psychopathology as measured by the PANSS. We found no support for DM or hypertension increasing the risk of TD, or for TD being associated with cognitive impairment. (c) 2005 Elsevier B.V. All rights reserved. C1 Univ Iowa, Carver Coll Med, Iowa City, IA 52242 USA. Duke Univ, Med Ctr, Durham, NC USA. Quintiles Inc, Res Triangle Pk, NC USA. Univ Penn, Sch Med, Philadelphia, PA 19104 USA. Dept Vet Affairs Med Ctr, Philadelphia, PA 19104 USA. Mental Hlth Advocates Inc, Boca Raton, FL USA. Suny Downstate Med Ctr, Brooklyn, NY 11203 USA. Yale Univ, Sch Med, West Haven, CT 06516 USA. Univ N Carolina, Sch Med, Neurosci Hosp, Chapel Hill, NC USA. RP Miller, DD (reprint author), Univ Iowa, Carver Coll Med, 2-105 MEB,500 Newton Rd, Iowa City, IA 52242 USA. EM del-miller@uiowa.edu RI Stroup, Thomas/F-9188-2014 OI Stroup, Thomas/0000-0002-3123-0672 FU NIMH NIH HHS [N01 MH90001] NR 64 TC 81 Z9 82 U1 3 U2 7 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 2005 VL 80 IS 1 BP 33 EP 43 DI 10.1016/j.schres.2005.07.034 PG 11 WC Psychiatry SC Psychiatry GA 002KU UT WOS:000234611100005 PM 16171976 ER PT J AU Goff, DC Sullivan, LM McEvoy, JP Meyer, JM Nasrallah, HA Daumit, GL Lamberti, S D'Agostino, RB Stroup, TS Davis, S Lieberman, JA AF Goff, DC Sullivan, LM McEvoy, JP Meyer, JM Nasrallah, HA Daumit, GL Lamberti, S D'Agostino, RB Stroup, TS Davis, S Lieberman, JA TI A comparison of ten-year cardiac risk estimates in schizophrenia patients from the CATIE study and matched controls SO SCHIZOPHRENIA RESEARCH LA English DT Article ID CORONARY-HEART-DISEASE; EXCESS MORTALITY; GLUCOSE-TOLERANCE; CIGARETTE-SMOKING; STOCKHOLM COUNTY; MOOD DISORDERS; MEDICAL-CARE; MORBIDITY; PEOPLE; INDIVIDUALS AB Objective: Standardized mortality rates are elevated in schizophrenia compared to the general population. The incidence of coronary heart disease (CHD) and the relative contribution of CHD to increased mortality in schizophrenia patients are not clear, despite recent concerns about metabolic complications of certain atypical antipsychotics. Method: Ten-year risk for CHD was calculated for 689 subjects who participated in the Clinical Trials of Antipsychotic Treatment Effectiveness (CATIE) Schizophrenia Trial at baseline using the Framingham CHD risk function and were compared with age-, race- and gender-matched controls from the National Health and Nutrition Examination Survey (NHANES) III. Results: Ten-year CHD risk was significantly elevated in male (9.4% vs. 7.0%) and female (6.3% vs. 4.2%) schizophrenia patients compared to controls (p=0.0001). Schizophrenia patients had significantly higher rates of smoking (69% vs. 35%), diabetes (13% vs. 3%), and hypertension (27% vs. 17%) and lower HDL cholesterol levels (43.7 vs. 49.3 mg/dl) compared to controls (p < 0.001). Only total cholesterol levels did not differ between groups. Ten-year CHD risk remained significantly elevated in schizophrenia patients after controlling for body mass index (p = 0.0001). Conclusions: These results are consistent with recent evidence of increased cardiac mortality in schizophrenia patients. While the impact of cigarette smoking is clear, the relative contributions to cardiac risk of specific antipsychotic agents, diet, exercise, and quality of medical care remain to be clarified. (c) 2005 Elsevier B.V. All rights reserved. C1 Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Psychiat, Boston, MA 02114 USA. RP Goff, DC (reprint author), Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Psychiat, 25 Staniford St, Boston, MA 02114 USA. EM goff@psych.mgh.harvard.edu RI Stroup, Thomas/F-9188-2014; OI Stroup, Thomas/0000-0002-3123-0672; Sullivan, Lisa/0000-0003-0726-7149 FU NIMH NIH HHS [N01MH90001] NR 43 TC 297 Z9 300 U1 3 U2 18 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 2005 VL 80 IS 1 BP 45 EP 53 DI 10.1016/j.schres.2005.08.010 PG 9 WC Psychiatry SC Psychiatry GA 002KU UT WOS:000234611100006 PM 16198088 ER PT J AU Ouellette, H Kassarjian, A Tretreault, P Palmer, W AF Ouellette, H Kassarjian, A Tretreault, P Palmer, W TI Imaging of the overhead throwing athlete SO SEMINARS IN MUSCULOSKELETAL RADIOLOGY LA English DT Article DE throwing; biomechanics; imaging; shoulder; elbow; magnetic resonance ID ULNAR COLLATERAL LIGAMENT; ROTATOR CUFF TEARS; CORACOID IMPINGEMENT SYNDROME; DISTAL BICEPS TENDON; MR ARTHROGRAPHY; OSTEOCHONDRITIS-DISSECANS; BASEBALL PLAYERS; COMPUTED-TOMOGRAPHY; GLENOID IMPINGEMENT; VALGUS STABILITY AB Knowledge of overhead throwing biomechanics is crucial to understand specific injuries encountered in throwing athletes on diagnostic imaging. Most specific injuries of overhead throwing athletes occur at the shoulder and elbow. Throwing athletes are susceptible to rotator cuff tears from tensile overload and external and internal impingement. The labrum is also commonly degenerated or torn secondary to overuse syndrome, internal impingement, and microtrauma. The elbow is typically injured secondary to excessive valgus forces during throwing. The ulnar collateral ligament, ulnar nerve, and common flexor tendon origin are all at increased risk of injury. Capitellar osteochondral injuries and loose intra-articular bodies are also frequent. Knowledge of injury pathophysiology is crucial to understanding the treatment rationale in throwing athletes. C1 Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Radiol, Boston, MA 02114 USA. Univ Montreal, CHUM Hop Notre Dame, Dept Orthoped Surg, Montreal, PQ, Canada. RP Ouellette, H (reprint author), Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Radiol, 55 Fruit St,Yawkey 6th Floor, Boston, MA 02114 USA. NR 83 TC 13 Z9 14 U1 3 U2 6 PU THIEME MEDICAL PUBL INC PI NEW YORK PA 333 SEVENTH AVE, NEW YORK, NY 10001 USA SN 1089-7860 J9 SEMIN MUSCULOSKEL R JI Semin. Musculoskelet. Radiol. PD DEC PY 2005 VL 9 IS 4 BP 316 EP 333 DI 10.1055/s-2005-923377 PG 18 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA 991CD UT WOS:000233788900005 PM 16315115 ER PT J AU Towfighi, A Greenberg, SM Rosand, J AF Towfighi, A Greenberg, SM Rosand, J TI Treatment and prevention of primary intracerebral hemorrhage SO SEMINARS IN NEUROLOGY LA English DT Review DE intracerebral hemorrhage; cerebral amyloid angiopathy; hypertension; warfarin ID CEREBRAL AMYLOID ANGIOPATHY; APOLIPOPROTEIN-E EPSILON-2; ACTIVATED FACTOR-VII; CYSTATIN-C GENE; ALZHEIMERS-DISEASE; INTRACRANIAL HEMORRHAGE; BRAIN EDEMA; BLOOD-FLOW; GRANULOMATOUS-ANGIITIS; PERIHEMATOMAL EDEMA AB Intracerebral hemorrhage (ICH), which constitutes 10 to 15% of all strokes and affects similar to 65,000 people each year in the United States, has the highest mortality rate of all stroke subtypes. Hypertension, cerebral amyloid anglopathy, and anticoagulation underlie the majority of cases of ICH. Warfarin not only increases the risk but also increases the severity of ICH by causing hematoma expansion. With the advent of gradient-echo magnetic resonance imaging, patients with underlying cerebral amyloid anglopathy or hypertensive vasculopathy can be identified, and measures can be taken to prevent ICH. Initiating an antihypertensive regimen in a patient with nonlobar microbleeds suggestive of hypertensive vasculopathy, and withholding warfarin in patients with lobar microbleeds suggestive of cerebral amyloid anglopathy, are emerging prevention strategies. Although a treatment for cerebral amyloid anglopathy does not exist, agents targeting beta-amyloid metabolism and bioactivity are promising candidates. Strategies for preventing warfarin-associated hemorrhage include strict monitoring of anticoagulation levels and using agents such as direct thrombin inhibitors. The future of ICH management lies in therapies targeted at the pathophysiological steps in ICH. Potential treatments include glutamate receptor antagonists for preventing glutamate excitotoxicity, matrix metalloproteinase and thrombin inhibitors for preventing perihematomal edema, and recombinant activated factor VII for preventing hematomal expansion. C1 Massachusetts Gen Hosp, Boston, MA 02114 USA. RP Rosand, J (reprint author), Neurol Clin Trials Unit, 15 Parkman St,ACC 836, Boston, MA 02114 USA. NR 102 TC 16 Z9 19 U1 1 U2 3 PU THIEME MEDICAL PUBL INC PI NEW YORK PA 333 SEVENTH AVE, NEW YORK, NY 10001 USA SN 0271-8235 J9 SEMIN NEUROL JI Semin. Neurol. PD DEC PY 2005 VL 25 IS 4 BP 445 EP 452 DI 10.1055/s-2005-923538 PG 8 WC Clinical Neurology SC Neurosciences & Neurology GA 995DW UT WOS:000234082000013 PM 16342000 ER PT J AU Janne, PA AF Janne, PA TI Ongoing first-line studies of epidermal growth factor receptor tyrosine kinase inhibitors in select patient populations SO SEMINARS IN ONCOLOGY LA English DT Review ID CELL LUNG-CANCER; PHASE-III TRIAL; ACTIVATING MUTATIONS; GEFITINIB ZD1839; RANDOMIZED-TRIAL; EGFR MUTATIONS; GENE-MUTATIONS; EXPRESSION; SURVIVAL; SENSITIVITY C1 Dana Farber Canc Inst, Dept Med Oncol, Lowe Ctr Thorac Oncol, Boston, MA 02115 USA. Brigham & Womens Hosp, Dept Med, Boston, MA 02115 USA. Harvard Univ, Sch Med, Boston, MA USA. RP Janne, PA (reprint author), Dana Farber Canc Inst, Dept Med Oncol, Lowe Ctr Thorac Oncol, D1234,44 Binney St, Boston, MA 02115 USA. EM pjanne@partners.org RI Mendez, Pedro /J-8955-2016 OI Mendez, Pedro /0000-0001-6713-7907 NR 54 TC 6 Z9 6 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC 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 2005 VL 32 IS 6 SU 10 BP S9 EP S15 DI 10.1053/j.seminoncol.2005.10.004 PG 7 WC Oncology SC Oncology GA 016YC UT WOS:000235659400003 PM 16459174 ER PT J AU Wesolowski, JR Lev, MH AF Wesolowski, JR Lev, MH TI CT: History, technology, and clinical aspects SO SEMINARS IN ULTRASOUND CT AND MRI LA English DT Article ID AXIAL SCANNING TOMOGRAPHY; NEURORADIOLOGY; PATIENT C1 Massachusetts Gen Hosp, Div Neuroradiol, Boston, MA 02114 USA. Harvard Univ, Sch Med, Boston, MA USA. RP Lev, MH (reprint author), Massachusetts Gen Hosp, Div Neuroradiol, GRB-285,55 Fruit St, Boston, MA 02114 USA. EM mlev@partners.org NR 23 TC 6 Z9 6 U1 0 U2 2 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 USA SN 0887-2171 J9 SEMIN ULTRASOUND CT JI Semin. Ultrasound CT MRI PD DEC PY 2005 VL 26 IS 6 BP 376 EP 379 DI 10.1053/j.sult.2005.07.007 PG 4 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA 994KB UT WOS:000234029600002 PM 16392657 ER PT J AU Vu, D Lev, MH AF Vu, D Lev, MH TI Noncontrast CT in acute stroke SO SEMINARS IN ULTRASOUND CT AND MRI LA English DT Article ID ACUTE ISCHEMIC-STROKE; TISSUE-PLASMINOGEN ACTIVATOR; CEREBRAL-ARTERY TERRITORY; COMPUTED TOMOGRAPHIC FINDINGS; COOPERATIVE ACUTE STROKE; ACUTE HEMISPHERIC STROKE; HEMORRHAGIC TRANSFORMATION; THROMBOLYTIC THERAPY; ECASS II; INTRAVENOUS THROMBOLYSIS C1 Massachusetts Gen Hosp, Neuroradiol Div, Boston, MA 02114 USA. Harvard Univ, Sch Med, Boston, MA USA. RP Lev, MH (reprint author), Massachusetts Gen Hosp, Neuroradiol Div, GRB 285,Fruit St, Boston, MA 02114 USA. EM mlev@partners.org NR 46 TC 9 Z9 9 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 USA SN 0887-2171 J9 SEMIN ULTRASOUND CT JI Semin. Ultrasound CT MRI PD DEC PY 2005 VL 26 IS 6 BP 380 EP 386 DI 10.1053/j.sult.2005.07.008 PG 7 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA 994KB UT WOS:000234029600003 PM 16392658 ER PT J AU Romero, JM AF Romero, JM TI CT angiography source image evaluation for stroke SO SEMINARS IN ULTRASOUND CT AND MRI LA English DT Article ID DOPPLER SONOGRAPHY; EMERGENCY; ISCHEMIA; RISK C1 Massachusetts Gen Hosp, Boston, MA 02114 USA. RP Romero, JM (reprint author), Massachusetts Gen Hosp, Neuroradiol White 2nd Floor, Boston, MA 02114 USA. EM jmromero@partners.org NR 25 TC 6 Z9 7 U1 0 U2 1 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 USA SN 0887-2171 J9 SEMIN ULTRASOUND CT JI Semin. Ultrasound CT MRI PD DEC PY 2005 VL 26 IS 6 BP 387 EP 393 DI 10.1053/j.sult.2005.07.010 PG 7 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA 994KB UT WOS:000234029600004 PM 16392659 ER PT J AU Mullins, ME AF Mullins, ME TI The hyperdense cerebral artery sign on head CT scan SO SEMINARS IN ULTRASOUND CT AND MRI LA English DT Article ID COMPUTED-TOMOGRAPHY; ACUTE STROKE; PROGNOSTIC VALUE; THROMBOLYTIC THERAPY; INCREASED DENSITY; INFARCTION; OCCLUSION; THROMBOSIS; ANGIOGRAPHY; EMERGENCY C1 Massachusetts Gen Hosp, Div Neuroradiol, Boston, MA 02114 USA. RP Mullins, ME (reprint author), Massachusetts Gen Hosp, Div Neuroradiol, GRB 285,55 Fruit St, Boston, MA 02114 USA. EM mmullins@partners.org NR 49 TC 9 Z9 10 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 USA SN 0887-2171 J9 SEMIN ULTRASOUND CT JI Semin. Ultrasound CT MRI PD DEC PY 2005 VL 26 IS 6 BP 394 EP 403 DI 10.1053/j.sult.2005.07.009 PG 10 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA 994KB UT WOS:000234029600005 PM 16392660 ER PT J AU Ay, H Koroshetz, WJ Vangel, M Benner, T Melinosky, C Zhu, MW Menezes, N Lopez, CJ Sorensen, AG AF Ay, H Koroshetz, WJ Vangel, M Benner, T Melinosky, C Zhu, MW Menezes, N Lopez, CJ Sorensen, AG TI Conversion of ischemic brain tissue into infarction increases with age SO STROKE LA English DT Article DE aging; cerebral ischemia; imaging, diffusion-weighted; magnetic resonance imaging; magnetic resonance imaging; perfusion-weighted; mitochondria; penumbra ID CEREBRAL-BLOOD-FLOW; HIGH-RESOLUTION MEASUREMENT; TRACER BOLUS PASSAGES; TIME-COURSE; HYPERACUTE STROKE; WEIGHTED MRI; DIFFUSION; PERFUSION; VOLUME; RAT AB Background and Purpose - Brain regions normal on diffusion-weighted imaging (DWI) but abnormal on mean transit time (MTT) maps represent tissue at risk of infarction, yet the fate of these regions is quite variable. The imperfect correlation between tissue outcome and initial imaging parameters suggests that each patient's brain may have different susceptibility to ischemic stress. We hypothesize that age is a marker for tissue susceptibility to ischemia and thus plays a role in determining tissue outcome in human stroke. Methods - Sixty patients with acute ischemic stroke and a region of DWI/MTT mismatch that was > 20% of the DWI volume were included. All patients were scanned twice, within 12 hours of symptom onset and on day 5 or later. The percentage mismatch lost (PML) was calculated as percentage of initial DWI/MTT mismatch volume that was infarcted on the follow-up MRI. The statistical analysis explored relationships among the covariates age, Trial of Org 10172 in Acute Stroke Treatment (TOAST) subtypes, time-to-MRI, and initial DWI, MTT volume, mean arterial blood pressure and blood glucose level at admission, and previous history of hypertension and diabetes mellitus. Results - Univariate comparisons showed that age (P = 0.003), hypertension (P = 0.009), and diabetes mellitus (P = 0.0002) were significantly associated with PML. Regression analyses showed age to be a significant covariate (P = 0.02). The regression model predicted a change in PML of approximate to 0.65% per year. The adjusted proportion of variance (R-2) in PML that could be explained by age alone was 14%. Conclusion - Age-dependent increase in conversion of ischemic tissue into infarction suggests that age is a biological marker for the variability in tissue outcome in acute human stroke. C1 Harvard Univ, Sch Med, Massachusetts Gen Hosp, AA Martinos Ctr,Dept Neurol, Boston, MA 02129 USA. RP Ay, H (reprint author), Harvard Univ, Sch Med, Massachusetts Gen Hosp, AA Martinos Ctr,Dept Neurol, 13th CNY149-2301 Charlestown, Boston, MA 02129 USA. EM ayhmgh@hotmail.com NR 35 TC 59 Z9 60 U1 1 U2 2 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3261 USA SN 0039-2499 J9 STROKE JI Stroke PD DEC PY 2005 VL 36 IS 12 BP 2632 EP 2636 DI 10.1161/01.STR.0000189991.23918.01 PG 5 WC Clinical Neurology; Peripheral Vascular Disease SC Neurosciences & Neurology; Cardiovascular System & Cardiology GA 986LZ UT WOS:000233452400031 PM 16269639 ER PT J AU Stephen, AE Milas, M Garner, CN Wagner, KE Siperstein, AE AF Stephen, AE Milas, M Garner, CN Wagner, KE Siperstein, AE TI Use of surgeon-performed office ultrasound and parathyroid fine needle aspiration for complex parathyroid localization SO SURGERY LA English DT Article ID SPORADIC PRIMARY HYPERPARATHYROIDISM; RECURRENT HYPERPARATHYROIDISM; PREOPERATIVE LOCALIZATION; ULTRASONOGRAPHY; REOPERATION; ADENOMAS; HORMONE; LESIONS; BIOPSY; PERSISTENT AB Background. This study investigates the utility of ultrasound guided parathyroid, fine needle aspiration (FNA) as a localizing technique in patients with hyperparathyroidism (HPT) undergoing re-operative neck surgery or with unusually appearing or ectopically located glands. Methods. Selected patients with HPT underwent surgeon-performed FNA with ultrasound guidance. Aspirate contents were sent for cytology and parathyroid hormone (PTH) levels. All patients subsequently underwent parathyroid exploration. Results. 54 patients underwent 5 7 ultrasound guided parathyroid biopsies. Indications for FNA included prior parathyroid (n = 29), thyroid (n = 11), or other neck surgery (n = 2), or unusual parathyroid appearance or location (n = 12). A true positive was defined as a site where the PTH aspirate was >40 pg/mL and a hypercellular gland was removed at surgery. Based on this, there were 44 true positives, 10 true negatives, and 3 false negatives; there were, no false Positives. The median PTH level in Positive aspirates was 11, 665 pg/mL. Cytology was primarily helpful in excluding other diagnoses. Conclusion. Ultrasound guided FNA is a highly specific localization test for parathyroid tumors. This procedure can be successfully performed by surgeons in the office setting and is extremely valuable for directing parathyroid exploration in challenging cases. We recommend incorporating ultrasound and FNA as a pre-operative localization strategy for selected patients with HPT. C1 Massachusetts Gen Hosp, Dept Surg Oncol, Div Surg Oncol, Boston, MA 02114 USA. Cleveland Clin Fdn, Dept Surg, Cleveland, OH 44195 USA. RP Stephen, AE (reprint author), Massachusetts Gen Hosp, Dept Surg Oncol, Div Surg Oncol, 55 Fruit St, Boston, MA 02114 USA. EM astephen@partners.org NR 25 TC 21 Z9 23 U1 0 U2 0 PU MOSBY, INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 USA SN 0039-6060 J9 SURGERY JI Surgery PD DEC PY 2005 VL 138 IS 6 BP 1143 EP 1150 DI 10.1016/j.surg.2005.08.030 PG 8 WC Surgery SC Surgery GA 998LB UT WOS:000234319000045 PM 16360402 ER PT J AU Milas, M Stephen, A Berber, E Wagner, K Miskulin, J Siperstein, A AF Milas, M Stephen, A Berber, E Wagner, K Miskulin, J Siperstein, A TI Ultrasonography for the endocrine surgeon: A valuable clinical tool that enhances diagnostic and therapeutic outcomes SO SURGERY LA English DT Article; Proceedings Paper CT 26th Annual Meeting of the American-Association-of-Endocrine-Surgeons CY APR, 2005 CL Cancun, MEXICO SP Amer Assoc Endocrine Surg ID PRIMARY HYPERPARATHYROIDISM; THYROID-CANCER; ULTRASOUND; ASSOCIATION; MALIGNANCY; MANAGEMENT; NODULES; DISEASE AB Background. Surgeon-performed ultrasonography (U/S) has revolutionized many subspecialties by broadening the diagnostic and interventional scope of practice. We report our experience on the impact of surgeon-performed U/S in an endocrine surgery practice. Methods. Prospectively maintained records of patients from November 1999 to November 2004 were reviewed to establish patterns and outcomes of U/S practice. Surgeon-performed neck U/S was done routinely at the initial clinic visit and incorporated into resident/fellow education. Results. A total of 5703 U/S were performed on endocrine patients with thyroid 42%, parathyroid 57%, and adrenal 1% disorders. Diagnostic fine-needle aspiration biopsy (FNA) was achieved with low sampling errors (< 7 %). When U/S identified thyroid nodules coexisting with hyperparathyroidism, preoperative FNA correctly established benign. thyroid diagnosis and minimized need, for thyroidectomy. U/S successfully imaged abnormal parathyroid glands when Tc-99-sestamibi scans were negative. U/S data significantly changed treatment plans in nearly two thirds of thyroid cancer patients. Surgical residents readily mastered essential U/S skills. Conclusions. Surgeon-performed U/S is a highly specific tool for identification of endocrine disease in the neck. It, is learned readily and performed accurately, and junctions as an informative extension of physical examination. Because it substantially benefits patient care and impacts surgical decision making, neck U/S is recommended highly (is a valuable adjunct to endocrine surgical practice. C1 Cleveland Clin Fdn, Dept Gen Surg, Cleveland, OH 44195 USA. Massachusetts Gen Hosp, Dept Surg, Boston, MA 02114 USA. Charlotte Surg Grp, Charlotte, NC USA. RP Milas, M (reprint author), Cleveland Clin Fdn, Dept Gen Surg, 9500 Euclid Ave A80, Cleveland, OH 44195 USA. EM milasm@ccf.org NR 25 TC 35 Z9 36 U1 0 U2 0 PU MOSBY, INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 USA SN 0039-6060 J9 SURGERY JI Surgery PD DEC PY 2005 VL 138 IS 6 BP 1193 EP 1200 DI 10.1016/j.surg.2005.08.032 PG 8 WC Surgery SC Surgery GA 998LB UT WOS:000234319000057 PM 16360408 ER PT J AU Joehl, RJ AF Joehl, RJ TI Preoperative evaluation: Pulmonary, cardiac, renal dysfunction and comorbidities SO SURGICAL CLINICS OF NORTH AMERICA LA English DT Article ID MAJOR NONCARDIAC SURGERY; ABDOMINAL-SURGERY; RISK-ASSESSMENT; PERIOPERATIVE COMPLICATIONS; PRACTICE GUIDELINES; VASCULAR-SURGERY; OBESE PATIENTS; SURGICAL RISK; TASK-FORCE; EVENTS AB This article reviews evidence supporting the exercise of risk assessment and demonstrates how it assists in determining which patients should undergo a planned invasive procedure. The article focuses on the preoperative functional assessment of three major organ systems-cardiac, pulmonary, and renal-and reviews guidelines for determining which patients need additional testing of organ system function. The article also discusses how to improve the condition of selected patients so that the surgeon can achieve the best possible result and outcome. C1 US Dept Vet Affairs, Vet Affairs Edward Hines Jr Hosp, Surg Serv 112, Hines, IL 60141 USA. Loyola Univ, Med Ctr, Maywood, IL 60153 USA. RP Joehl, RJ (reprint author), US Dept Vet Affairs, Vet Affairs Edward Hines Jr Hosp, Surg Serv 112, Roosevelt Rd & 5th Ave,POB 5000, Hines, IL 60141 USA. EM raymond.joel@med.va.gov NR 40 TC 8 Z9 8 U1 0 U2 3 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 USA SN 0039-6109 J9 SURG CLIN N AM JI Surg. Clin.-North Am. PD DEC PY 2005 VL 85 IS 6 BP 1061 EP + DI 10.1016/j.suc.2005.09.015 PG 14 WC Surgery SC Surgery GA 999JV UT WOS:000234386500003 PM 16326193 ER PT J AU Gibbs, VC AF Gibbs, VC TI Patient safety practices in the operating room: Correct-site surgery and nothing left behind SO SURGICAL CLINICS OF NORTH AMERICA LA English DT Article ID SURGICAL SPONGES AB Not until the late 1990s, after the publication of the National Academy of Medicine's treatise '' To Err Is Human,'' did safety standards specifically for patients begin to be considered in operating room practices. This report and other studies documented operating room mistakes including, for example, operations on the wrong hand or limb, operations on the wrong patient, and the performance of wrong procedures. Cases have also been documented of sponges or instruments being left by mistake inside patients following surgery. Poor communication is the most common root cause of errors. This article explores these issues and explains procedures and protocols developed to reduce surgical errors. C1 Univ Calif San Francisco, Dept Surg, QI Program, San Francisco, CA 94143 USA. San Francisco Vet Affairs Med Ctr, San Francisco, CA 94121 USA. RP Gibbs, VC (reprint author), Univ Calif San Francisco, Dept Surg, QI Program, 533 Parnassus Ave,U-157,Box 0617, San Francisco, CA 94143 USA. EM gibbsv@surgery.ucsf.edu NR 18 TC 27 Z9 27 U1 0 U2 3 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 USA SN 0039-6109 J9 SURG CLIN N AM JI Surg. Clin.-North Am. PD DEC PY 2005 VL 85 IS 6 BP 1307 EP + DI 10.1016/j.suc.2005.09.007 PG 14 WC Surgery SC Surgery GA 999JV UT WOS:000234386500021 PM 16326211 ER PT J AU Whited, JD Datta, SK Aiello, LM Aiello, LP Cavallerano, JD Conlin, PR Horton, MB Vigersky, RA Poropatich, RK Challa, P Darkins, AW Bursell, SE AF Whited, JD Datta, SK Aiello, LM Aiello, LP Cavallerano, JD Conlin, PR Horton, MB Vigersky, RA Poropatich, RK Challa, P Darkins, AW Bursell, SE TI A modeled economic analysis of a digital teleophthalmology system as used by three federal healthcare agencies for detecting proliferative diabetic retinopathy SO TELEMEDICINE JOURNAL AND E-HEALTH LA English DT Article AB The objective of this study was to compare, using a 12-month time frame, the cost-effectiveness of a nonmydriatic digital teleophthalmology system (Joslin Vision Network) versus traditional clinic-based ophthalmoscopy examinations with pupil dilation to detect proliferative diabetic retinopathy and its consequences. Decision analysis techniques, including Monte Carlo simulation, were used to model the use of the Joslin Vision Network versus conventional clinic-based ophthalmoscopy among the entire diabetic populations served by the Indian Health Service, the Department of Veterans Affairs, and the active duty Department of Defense. The economic perspective analyzed was that of each federal agency. Data sources for costs and outcomes included the published literature, epidemiologic data, administrative data, market prices, and expert opinion. Outcome measures included the number of true positive cases of proliferative diabetic retinopathy detected, the number of patients treated with panretinal laser photocoagulation, and the number of cases of severe vision loss averted. In the base-case analyses, the Joslin Vision Network was the dominant strategy in all but two of the nine modeled scenarios, meaning that it was both less costly and more effective. In the active duty Department of Defense population, the Joslin Vision Network would be more effective but cost an extra $1,618 per additional patient treated with panretinal laser photo-coagulation and an additional $13,748 per severe vision loss event averted. Based on our economic model, the Joslin Vision Network has the potential to be more effective than clinic-based ophthalmoscopy for detecting proliferative diabetic retinopathy and averting cases of severe vision loss, and may do so at lower cost. C1 Vet Adm Med Ctr, Ctr Hlth Serv Res Primary Care, Durham, NC 27705 USA. Duke Univ, Med Ctr, Div Gen Internal Med, Durham, NC 27710 USA. Harvard Univ, Sch Med, Joslin Diabet Ctr, Beetham Eye Inst, Boston, MA 02115 USA. Harvard Univ, Sch Med, Dept Ophthalmol, Boston, MA USA. Brigham & Womens Hosp, Div Endocrinol Diabet & Hypertens, Boston, MA 02115 USA. Vet Affairs Boston Healthcare Syst, Boston, MA USA. Indian Hlth Serv, Eye Dept, Phoenix Indian Med Ctr, Phoenix, AZ USA. Walter Reed Army Med Ctr, Serv Endocrinol, Washington, DC 20307 USA. Walter Reed Army Med Ctr, Telemed Directorate, Washington, DC 20307 USA. Duke Univ, Med Ctr, Dept Ophthalmol, Durham, NC 27710 USA. Vet Healthcare Adm Telemed Strateg Healthcare Grp, Washington, DC USA. RP Whited, JD (reprint author), Vet Adm Med Ctr, Ctr Hlth Serv Res Primary Care, 152,Bldg 6,508 Fulton St, Durham, NC 27705 USA. EM white046@mc.duke.edu FU NIDDK NIH HHS [K24DK63214] NR 24 TC 45 Z9 46 U1 0 U2 1 PU MARY ANN LIEBERT INC PI NEW ROCHELLE PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA SN 1530-5627 J9 TELEMED J E-HEALTH JI Telemed. J. e-Health PD DEC PY 2005 VL 11 IS 6 BP 641 EP 651 DI 10.1089/tmj.2005.11.641 PG 11 WC Health Care Sciences & Services SC Health Care Sciences & Services GA 011PF UT WOS:000235279900019 PM 16430383 ER PT J AU Balbach, ED Barbeau, EM AF Balbach, ED Barbeau, EM TI Beyond quagmires: the evolving quality of documents research SO TOBACCO CONTROL LA English DT Editorial Material ID TOBACCO INDUSTRY EFFORTS; HEALTH; SMOKE; LABOR C1 Tufts Univ, Community Hlth Program, Medford, MA 02155 USA. Dana Farber Canc Inst, Boston, MA 02115 USA. RP Balbach, ED (reprint author), Tufts Univ, Community Hlth Program, 112 Packard Ave, Medford, MA 02155 USA. EM edith.balbach@tufts.edu NR 18 TC 10 Z9 10 U1 0 U2 0 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 2005 VL 14 IS 6 BP 361 EP 362 DI 10.1136/tc.2005.014449 PG 2 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA 988QE UT WOS:000233614900001 PM 16319351 ER PT J AU Valeri, CR Ragno, G Khuri, S AF Valeri, CR Ragno, G Khuri, S TI Freezing human platelets with 6 percent dimethyl sulfoxide with removal of the supernatant solution before freezing and storage at-80 degrees C without postthaw processing SO TRANSFUSION LA English DT Article ID CRYOPRESERVED BABOON PLATELETS; CHILLED BLOOD-PLATELETS; PROCOAGULANT ACTIVITY; HEMOSTATIC FUNCTION; AUTOLOGOUS FRESH; P-SELECTIN; MICROPARTICLES; CLEARANCE; CIRCULATION; SURVIVAL AB BACKGROUND: Platelets (PLTs) can be frozen with 6 percent dimethyl sulfoxide (DMSO) at -80 degrees C for up to 2 years. This method has been modified by concentrating the PLTs and removing the supernatant before freezing. STUDY DESIGN AND METHODS: High-yield leukoreduced PLTs stored at 22 degrees C for up to 5 days were divided into three equal volumes: one was frozen with 6 percent DMSO at -80 degrees C, thawed, washed, and resuspended in plasma (old method with DMSO); the second was treated with 6 percent DMSO, concentrated to remove the supernatant DMSO, frozen at -80 degrees C, thawed, and diluted with 0.9 percent NaCl (new method with DMSO); and the third was treated with 0.9 percent NaCl without DMSO, concentrated to remove the supernatant solution, frozen at -80 degrees C, thawed, and diluted with 0.9 percent NaCl (new method without DMSO). RESULTS: Freeze-thaw-wash recovery of PLTs frozen by the old method with DMSO was 74 +/- 2 percent with 5 percent PLT microparticles. Freeze-thaw recovery was 94 +/- 2 percent with 7 percent PLT microparticles (new method with DMSO) and 69 +/- 9 percent with 15 percent PLT microparticles (new method without DMSO). Total DMSO in washed PLTs was 400 and 600 mg in PLTs concentrated before freezing. In vivo recovery of PLTs frozen by the new method with DMSO and transfused into normal volunteers was 30 percent and the life span was 7 days. CONCLUSION: Concentrating PLTs before freezing simplified the procedure by eliminating postthaw washing. PLTs frozen by this method had more PLTs with reduced GPIb and increased annexin V binding than those frozen by the old method. C1 USN, Blood Res Lab, Boston, MA 02118 USA. Boston VA Healthcare Syst, Dept Surg, W Roxbury Div, Boston, MA USA. RP Valeri, CR (reprint author), USN, Blood Res Lab, Boston, MA 02118 USA. EM navblood@nbrl.org NR 25 TC 34 Z9 36 U1 0 U2 1 PU BLACKWELL PUBLISHING PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DQ, OXON, ENGLAND SN 0041-1132 J9 TRANSFUSION JI Transfusion PD DEC PY 2005 VL 45 IS 12 BP 1890 EP 1898 DI 10.1111/j.1537-2995.2005.00647.x PG 9 WC Hematology SC Hematology GA 987PV UT WOS:000233530700009 PM 16371041 ER PT J AU Darabi, K Dzik, S AF Darabi, K Dzik, S TI Hyperhemolysis syndrome in anemia of chronic disease SO TRANSFUSION LA English DT Article ID HEMOLYTIC TRANSFUSION REACTIONS AB BACKGROUND: Occasional cases of delayed hemolytic transfusion reaction (DHTR) demonstrate severe and persistent hemolysis and are referred to as hyperhemolysis syndrome. This syndrome usually occurs in patients with sickle cell disease and possibly thalassemia who receive multiple transfusions. There are few such clinical reports in patients without hemoglobinopathies. CASE REPORT: A 67-year-old woman with anemia and a history of four previous transfusions was admitted with shortness of breath and a hematocrit (Hct) level of 27 percent. The patient was group O with a negative antibody screen. She received 1 unit of electronically cross-matched red blood cells (RBCs) and was discharged. Thirteen days later she returned to hospital with weakness and a Hct level of 23 percent. The antibody screen now demonstrated anti-K alloantibody. The direct antigloblulin test (DAT) was positive with both anti-immunoglobulin G and anti-complement (C3). Anti-K was recovered in the eluate. The previously transfused RBC unit was positive for presence of the K antigen. The patient's RBCs were negative for the presence of K antigen. Other laboratory data confirmed ongoing hemolysis, and a diagnosis of DHTR was made. She continued to display findings of active hemolysis for 9 more weeks requiring 19 units of RBCs. Thirty-four days after the original transfusion, her DAT remained positive and both the plasma sample and a RBC eluate demonstrated anti-K. CONCLUSION: The delayed hemolytic transfusion reaction with hyperhemolysis can occur among patients without hemoglobinopathies. C1 Massachusetts Gen Hosp, Blood Transfus Serv, Boston, MA 02114 USA. Harvard Univ, Joint Program Transfus Med, Boston, MA 02115 USA. RP Darabi, K (reprint author), Massachusetts Gen Hosp, Blood Transfus Serv, J-224,55 Fruit St, Boston, MA 02114 USA. EM kamrandarabi@yahoo.com NR 9 TC 22 Z9 23 U1 0 U2 0 PU BLACKWELL PUBLISHING PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DQ, OXON, ENGLAND SN 0041-1132 J9 TRANSFUSION JI Transfusion PD DEC PY 2005 VL 45 IS 12 BP 1930 EP 1933 DI 10.1111/j.1537-2995.2005.00608.x PG 4 WC Hematology SC Hematology GA 987PV UT WOS:000233530700014 PM 16371046 ER PT J AU Kaysen, D Morris, MK Rizvi, SL Resick, PA AF Kaysen, D Morris, MK Rizvi, SL Resick, PA TI Peritraumatic responses and their relationship to perceptions of threat in female crime victims SO VIOLENCE AGAINST WOMEN LA English DT Article DE crime victims; peritraumatic responses; resistance; sexual assault; victim reactions ID POSTTRAUMATIC-STRESS-DISORDER; SEXUAL ASSAULT VICTIMS; PTSD SYMPTOM SEVERITY; RAPE VICTIMS; TRAUMATIC EVENTS; DISSOCIATION; PREDICTORS; RESISTANCE; ATTRIBUTIONS; IMPACT AB Peritraumatic responses, aside front dissociation, have been understudied in acute trauma populations. Participants were 172 female rape, 68 assault, and 80 robbery victims recruited through formal reporting agencies and assessed 1 month after the crime. Despite substantial overlap across crimes, rape victims reported more emotional responses reflecting fear, detachment, shame, and more nonactive behavioral responses. Regression analysis examining the prediction of perceived threat by peritraumatic responses and crime variables indicated that increased duration of crimes; decreased calmness; increased fear; numbing, use of begging, pleading, and crying; and attempts to reason with the perpetrator(s) were all significantly associated with increased appraisal of threat. C1 VA Boston Healthcare Syst, Natl Ctr PTSD, Boston, MA USA. FU NIAAA NIH HHS [F32 AA014728]; NIMH NIH HHS [R01 MH046992] NR 51 TC 26 Z9 27 U1 1 U2 5 PU SAGE PUBLICATIONS INC PI THOUSAND OAKS PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA SN 1077-8012 J9 VIOLENCE AGAINST WOM JI Violence Against Women PD DEC PY 2005 VL 11 IS 12 BP 1515 EP 1535 DI 10.1177/1077801205280931 PG 21 WC Women's Studies SC Women's Studies GA 014GL UT WOS:000235467500004 PM 16247114 ER PT J AU Kuhtreiber, WM Kodama, S Burger, DE Dale, EA Faustman, DL AF Kuhtreiber, WM Kodama, S Burger, DE Dale, EA Faustman, DL TI Methods to characterize lymphoid apoptosis in a murine model of autoreactivity SO JOURNAL OF IMMUNOLOGICAL METHODS LA English DT Article DE apoptosis; cytokines; splenocytes; biomarkers; TNF-alpha ID SYSTEMIC-LUPUS-ERYTHEMATOSUS; NF-KAPPA-B; MULTIPLE-SCLEROSIS PATIENTS; IN-VITRO; DEFECTIVE APOPTOSIS; ETANERCEPT THERAPY; CROHNS-DISEASE; NOD MICE; LYMPHOCYTES; CELLS AB The immune system is shaped by the random generation of lymphocytes followed by apoptosis of self-reactive cells, a process termed negative selection. The survival of these pathogenic cells in the periphery can elicit autoreactivity. We describe the development of a biomarker assay for the detection of pathogenic subpopulations of lymphoid cells in adult non-obese diabetic (NOD) mice based on disease-specific alterations in spontaneous or triggered cell death. Utilizing improved methods of cell separations, two distinct lymphoid cell subpopulations with increased susceptibility to apoptosis were identified and quantified. A subpopulation of CD8(+) T cells that constitutes similar to 3-7% of the total CD8(+) T cell population underwent apoptosis on exposure to low concentrations of TNF-alpha. Such cells were exclusively detected only in NOD mice with histologic signs of active autoreactivity. The non-T cell compartment of NOD immune system, although resistant to TNF-alpha-induced apoptosis, contained a subpopulation of B cells with spontaneous death by culture alone. The refined detection of small numbers of lymphoid cell subsets with quantifiable differences in apoptosis provides a possible immune biomarker for monitoring disease activity or treatment interventions. (c) 2005 Elsevier B.V. All rights reserved. C1 Massachusetts Gen Hosp, Immunobiol Lab, Charlestown, MA 02139 USA. Harvard Univ, Sch Med, Charlestown, MA 02139 USA. RP Faustman, DL (reprint author), Massachusetts Gen Hosp, Immunobiol Lab, Bldg 149,13th St,CNY-3601, Charlestown, MA 02139 USA. EM faustman@helix.mgh.harvard.edu FU NIDDK NIH HHS [DK57521] NR 42 TC 4 Z9 4 U1 0 U2 2 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0022-1759 J9 J IMMUNOL METHODS JI J. Immunol. Methods PD NOV 30 PY 2005 VL 306 IS 1-2 BP 137 EP 150 DI 10.1016/j.jim.2005.08.008 PG 14 WC Biochemical Research Methods; Immunology SC Biochemistry & Molecular Biology; Immunology GA 996LD UT WOS:000234174500012 PM 16242708 ER PT J AU Lim, GW Wang, SX Zeng, Q Sung, B Yang, LL Mao, JR AF Lim, GW Wang, SX Zeng, Q Sung, B Yang, LL Mao, JR TI Expression of spinal NMDA receptor and PKC gamma after chronic morphine is regulated by spinal glucocorticoid receptor SO JOURNAL OF NEUROSCIENCE LA English DT Article DE glucocorticoid receptor; NMDA receptor; morphine tolerance; RU38486; protein kinase C; protein kinase A; adenylyl cyclase; cAMP response element-binding protein; CREB ID ELEMENT-BINDING PROTEIN; ABNORMAL PAIN SENSITIVITY; PERIPHERAL-NERVE INJURY; DORSAL HORN NEURONS; DOWN-REGULATION; KINASE-C; GLUTAMATE TRANSPORTERS; BASOLATERAL AMYGDALA; NEUROPATHIC PAIN; OPIOID THERAPY AB Spinal NMDA receptor (NMDAR), protein kinase C (PKC), and glucocorticoid receptor (GR) have all been implicated in the mechanisms of morphine tolerance; however, how these cellular elements interact after chronic morphine exposure remains unclear. Here we show that the expression of spinal NMDAR and PKC gamma after chronic morphine is regulated by spinal GR through a cAMP response element-binding protein (CREB)- dependent pathway. Chronic morphine (10 mu g, i.t.; twice daily for 6 d) induced a time- dependent upregulation of GR, the NR1 subunit of NMDAR, and PKC gamma within the rat's spinal cord dorsal horn. This NR1 and PKC gamma upregulation was significantly diminished by intrathecal coadministration of morphine with the GR antagonist RU38486 or a GR antisense oligodeoxynucleotide. Intrathecal coadministration of morphine with an adenylyl cyclase inhibitor (2', 5'-dideoxyadenosine) or a protein kinase A inhibitor (H89) also significantly attenuated morphine- induced NR1 and PKC gamma expression, whereas intrathecal treatment with an adenylyl cyclase activator (forskolin) alone mimicked morphine-induced expression of GR, NR1, and PKC gamma. Moreover, the expression of phosphorylated CREB was upregulated within the spinal cord dorsal horn after chronic morphine, and a CREB antisense oligodeoxynucleotide coadministered intrathecally with morphine prevented the upregulation of GR, NR1, and PKC gamma. These results indicate that spinal GR through the cAMP-CREB pathway played a significant role in NMDAR and PKC gamma expression after chronic morphine exposure. The data suggest that genomic interaction among spinal GR, NMDAR, and PKC gamma may be an important mechanism that contributes to the development of morphine tolerance. C1 Harvard Univ, Sch Med,Dept Anesthesia & Crit Care, Massachusetts Gen Hosp,Wang Ambulatory Care Ctr 3, Pain Res Grp,Div Pain Med, Boston, MA 02114 USA. RP Mao, JR (reprint author), Harvard Univ, Sch Med,Dept Anesthesia & Crit Care, Massachusetts Gen Hosp,Wang Ambulatory Care Ctr 3, Pain Res Grp,Div Pain Med, 15 Parkman St, Boston, MA 02114 USA. EM jmao@partners.org FU NIDA NIH HHS [R01 DA08835]; NINDS NIH HHS [R01 NS42661, R01 NS45681] NR 66 TC 60 Z9 71 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 30 PY 2005 VL 25 IS 48 BP 11145 EP 11154 DI 10.1523/JNEUROSCI.3768-05.2005 PG 10 WC Neurosciences SC Neurosciences & Neurology GA 988RD UT WOS:000233617500010 PM 16319314 ER PT J AU Cai, JM Hatsukami, TS Ferguson, MS Kerwin, WS Saam, T Chu, BC Takaya, N Polissar, NL Yuan, C AF Cai, JM Hatsukami, TS Ferguson, MS Kerwin, WS Saam, T Chu, BC Takaya, N Polissar, NL Yuan, C TI In vivo quantitative measurement of intact fibrous cap and lipid-rich necrotic core size in atherosclerotic carotid plaque - Comparison of high-resolution, contrast-enhanced magnetic resonance imaging and histology SO CIRCULATION LA English DT Article DE magnetic resonance imaging; carotid arteries; contrast media; atherosclerosis; lipids ID SUDDEN CORONARY DEATH; LESIONS; MRI; CLASSIFICATION; RUPTURE; INTRAPLAQUE; COMPONENTS; THICKNESS; ACCURACY; STENOSIS AB Background - Previous studies with contrast- enhanced magnetic resonance imaging ( CEMRI) have shown that the fibrous cap ( FC) in atherosclerotic carotid plaques enhances with gadolinium- based contrast agents. Conversely, the lipid- rich necrotic core ( LR- NC), lacking both vasculature and matrix, shows no or only slight enhancement. The goal of this study was to assess whether CEMRI can be used to accurately measure the dimensions of the intact FC and LR- NC. Methods and Results - Twenty- one patients scheduled for carotid endarterectomy were imaged with a 1.5- T scanner. Precontrast images and CEMRI were obtained. One hundred eight locations with an intact FC were matched between MRI and the excised histology specimens. Quantitative measurements of FC length along the lumen circumference, FC area, and LR- NC area were collected from CEMRI images and histology sections. Blinded comparison of corresponding MR images and histology slices showed moderate to good correlation for length ( r = 0.73, P < 0.001) and area ( r = 0.80, P < 0.001) of the intact FC. The mean percentage LR- NC areas ( LR- NC area/ wall area) measured by CEMRI and histology were 30.1% and 32.7%, respectively, and were strongly correlated across locations ( r = 0.87, P < 0.001). Conclusions - In vivo high- resolution CEMRI is capable of quantitatively measuring the dimensions of the intact FC and LR- NC. These new parameters may be useful to evaluate plaque vulnerability and provide continuous variables for characterizing the intact FC and LR- NC in progression and regression studies. C1 Univ Washington, Dept Radiol, Seattle, WA 98195 USA. Peoples Liberat Army Gen Hosp, Dept Radiol, Beijing, Peoples R China. Univ Washington, VA Puget Sound Hlth Care Syst, Seattle, WA 98195 USA. Univ Washington, Dept Surg, Seattle, WA 98195 USA. Mtn Whisper Light Stat Consulting, Seattle, WA USA. RP Yuan, C (reprint author), Univ Washington, Dept Radiol, 1959 NE Pacific St,Box 357115, Seattle, WA 98195 USA. EM cyuan@u.washington.edu FU NHLBI NIH HHS [R01 HL61816, R01 HL56874] NR 29 TC 248 Z9 280 U1 0 U2 22 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3261 USA SN 0009-7322 J9 CIRCULATION JI Circulation PD NOV 29 PY 2005 VL 112 IS 22 BP 3437 EP 3444 DI 10.1161/CIRCULATIONHA.104.528174 PG 8 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 988AC UT WOS:000233558300013 PM 16301346 ER PT J AU Cherepanov, P Ambrosio, ALB Rahman, S Ellenberger, T Engelman, A AF Cherepanov, P Ambrosio, ALB Rahman, S Ellenberger, T Engelman, A TI Structural basis for the recognition between HIV-1 integrase and transcriptional coactivator p75 SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE integration; structure; retrovirus; transcription; host factor ID VIRUS TYPE-1 INTEGRASE; SMALL-MOLECULE ANTAGONISTS; DNA-BINDING DOMAIN; CATALYTIC DOMAIN; NUCLEAR-LOCALIZATION; HUMAN-CELLS; MACROMOLECULAR STRUCTURES; CRYSTAL-STRUCTURE; TERMINAL DOMAIN; ZINC-BINDING AB Integrase (IN) is an essential retroviral enzyme, and human transcriptional coactivator p75, which is also referred to as lens epithelium-derived growth factor (LEDGF), is the dominant cellular binding partner of HIV-1 IN. Here, we report the crystal structure of the dimeric catalytic core domain of HIV-1 IN complexed to the IN-binding domain of LEDGF. Previously identified LEDGF hotspot residues anchor the protein to both monomers at the IN dinner interface. The principal structural features of IN that are recognized by the host factor are the backbone conformation of residues 168-171 from one monomer and a hydrophobic patch that is primarily comprised of a-helices 1 and 3 of the second IN monomer. inspection of diverse retroviral primary and secondary sequence elements helps to explain the apparent lentiviral tropism of the LEDGF-IN interaction. Because the lethal phenotypes of HIV-1 mutant viruses unable to interact with LEDGF indicate that IN function is highly sensitive to perturbations of the structure around the LEDGF-binding site, we propose that small molecule inhibitors of the protein-protein interaction might similarly disrupt HIV-1 replication. C1 Dana Farber Canc Inst, Dept Canc Immunol & AIDS, Boston, MA 02115 USA. Harvard Univ, Sch Med, Dept Pathol, Boston, MA 02115 USA. Harvard Univ, Sch Med, Dept Biol Chem & Mol Pharmacol, Boston, MA 02115 USA. Univ Sao Paulo, Ctr Biotecnol Mol Estrutural, Inst Fis Sao Carlos, BR-13560970 Sao Carlos, SP, Brazil. 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; Ambrosio, Andre/C-9089-2012; Sao Carlos Institute of Physics, IFSC/USP/M-2664-2016 OI Cherepanov, Peter/0000-0002-0634-538X; Ambrosio, Andre/0000-0002-9515-930X; FU NIAID NIH HHS [AI39394, AI62249, R01 AI039394, R21 AI062249, R37 AI039394]; NIGMS NIH HHS [GM59902, R01 GM059902] NR 56 TC 256 Z9 268 U1 0 U2 8 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 29 PY 2005 VL 102 IS 48 BP 17308 EP 17313 DI 10.1073/pnas.0506921402 PG 6 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA 990RX UT WOS:000233762000010 PM 16260736 ER PT J AU Michaelson, JS Cheongsiatmoy, JA Dewey, F Silverstein, MJ Sgroi, D Smith, B Tanabe, KK AF Michaelson, JS Cheongsiatmoy, JA Dewey, F Silverstein, MJ Sgroi, D Smith, B Tanabe, KK TI Spread of human cancer cells occurs with probabilities indicative of a nongenetic mechanism SO BRITISH JOURNAL OF CANCER LA English DT Article DE metastasis; probability; mutation ID BREAST-CANCER; NATURAL-HISTORY; TUMOR SIZE; METASTASIS; CARCINOMA; MORPHOMETRY; GENES AB There has been much uncertainty as to whether metastasis requires mutation at the time of spread. Here, we use clinical data to calculate the probability of the spread of melanoma and breast cancer cells. These calculations reveal that the probability of the spread of cancer cells is relatively high for small tumours (similar to 1 event of spread for every 500 cells for melanomas of 0.1 mm) and declines as tumours increase in size (similar to 1 event of spread for every 10(8) cells for melanomas of 12 mm). The probability of spread of breast cancer cells from the lymph nodes to the periphery is similar to 1 event of spread for every 10(8) cells in the nodal masses, which have a mean diameter of 5 mm, while the probability of spread of cancer cells from the breast to the periphery when the primary masses are 5mm is also similar to 1 event of spread for every 10(8) cells. Thus, the occurrence of an event of spread from the breast to the lymph nodes appears not to increase the propensity of the progeny of those cells to spread from the lymph nodes to the periphery. These values indicate that the spread of human breast cancer and melanoma cells is unlikely to occur by a mechanism requiring mutation at the time of spread. C1 Massachusetts Gen Hosp, Dept Pathol, Div Surg Oncol, Boston, MA 02114 USA. Massachusetts Gen Hosp, Dept Surg, Boston, MA 02114 USA. Harvard Univ, Sch Med, Dept Surg, Boston, MA 02115 USA. Harvard Univ, Sch Med, Dept Pathol, Boston, MA 02115 USA. Univ So Calif, Keck Sch Med, Dept Surg, Los Angeles, CA USA. RP Michaelson, JS (reprint author), Massachusetts Gen Hosp, Dept Pathol, Div Surg Oncol, Cox Bldg,Room 626,100 Blossom St, Boston, MA 02114 USA. EM michaelj@helix.mgh.harvard.edu NR 24 TC 25 Z9 25 U1 0 U2 0 PU NATURE PUBLISHING GROUP PI LONDON PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND SN 0007-0920 J9 BRIT J CANCER JI Br. J. Cancer PD NOV 28 PY 2005 VL 93 IS 11 BP 1244 EP 1249 DI 10.1038/sj.bjc.6602848 PG 6 WC Oncology SC Oncology GA 986PQ UT WOS:000233462600008 PM 16278668 ER PT J AU Lazar, SW Kerr, CE Wasserman, RH Gray, JR Greve, DN Treadway, MT McGarvey, M Quinn, BT Dusek, JA Benson, H Rauch, SL Moore, CI Fischl, B AF Lazar, SW Kerr, CE Wasserman, RH Gray, JR Greve, DN Treadway, MT McGarvey, M Quinn, BT Dusek, JA Benson, H Rauch, SL Moore, CI Fischl, B TI Meditation experience is associated with increased cortical thickness SO NEUROREPORT LA English DT Article DE insula; meditation; plasticity; prefrontal cortex ID CEREBRAL-CORTEX; PREFRONTAL CORTEX; BRAIN AB Previous research indicates that long-term meditation practice is associated with altered resting electroencephalogram patterns, suggestive of long lasting changes in brain activity. We hypothesized that meditation practice might also be associated with changes in the brain's physical structure. Magnetic resonance imaging was used to assess cortical thickness in 20 participants with extensive Insight meditation experience, which involves focused attention to internal experiences. Brain regions associated with attention, interoception and sensory processing were thicker in meditation participants than matched controls, including the prefrontal cortex and right anterior insula. Between-group differences in prefrontal cortical thickness were most pronounced in older participants, suggesting that meditation might offset age-related cortical thinning. Finally, the thickness of two regions correlated with meditation experience. These data provide the first structural evidence for experience-dependent cortical plasticity associated with meditation practice. C1 Massachusetts Gen Hosp, Pediat Neuroimaging Res Program, Boston, MA 02114 USA. Harvard Univ, Osher Inst, Sch Med, Boston, MA 02115 USA. Yale Univ, Dept Psychol, New Haven, CT 06520 USA. Massachusetts Gen Hosp, Athinoula A Martinos Ctr Biomed Imaging, Boston, MA 02114 USA. Harvard Univ, Grad Sch Educ, Cambridge, MA 02138 USA. Mind Body Med Inst, Chestnut Hill, MA USA. Harvard Univ, Sch Med, Beth Israel Deaconess Med Ctr, Dept Med, Boston, MA 02115 USA. MIT, Dept Brain & Cognit Sci, Cambridge, MA 02139 USA. MIT, McGovern Inst Brain Res, Cambridge, MA 02139 USA. MIT, CSAIL, Cambridge, MA 02139 USA. RP Lazar, SW (reprint author), Room 2609,149 13th St, Charlestown, MA 02129 USA. EM lazar@nmr.mgh.harvard.edu RI Gray, Jeremy/A-9719-2008; Moore, Christopher/C-5588-2009; Kerr, Catherine/D-3299-2009; Gray, Jeremy/A-2635-2013; Lazar, Sara/G-3809-2012 OI Lazar, Sara/0000-0003-1126-8363 FU NCCIH NIH HHS [R21 AT002860, K01 AT000694, K01AT00694-01, R21AT002860-02]; NCRR NIH HHS [P41 RR014075, P41RR14075]; ODCDC CDC HHS [H75/CCH 123424, H75/CCH119124] NR 25 TC 492 Z9 507 U1 17 U2 140 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3261 USA SN 0959-4965 J9 NEUROREPORT JI Neuroreport PD NOV 28 PY 2005 VL 16 IS 17 BP 1893 EP 1897 DI 10.1097/01.wnr.0000186598.66243.19 PG 5 WC Neurosciences SC Neurosciences & Neurology GA 987VS UT WOS:000233546200005 PM 16272874 ER PT J AU Rauch, SL Milad, MR Orr, SR Quinn, BT Fischl, B Pitman, RK AF Rauch, SL Milad, MR Orr, SR Quinn, BT Fischl, B Pitman, RK TI Orbitofrontal thickness, retention of fear extinction, and extraversion SO NEUROREPORT LA English DT Article DE fear conditioning; personality traits; skin conductance; ventral prefrontal cortex ID MEDIAL PREFRONTAL CORTEX; INDIVIDUAL-DIFFERENCES; AMYGDALA; HUMANS; PERSONALITY; NEURONS; MEMORY AB People differ in their personality traits and in their ability to modulate fear. Does our personality determine how well we extinguish conditioned fear responses? Or is the opposite true? Herein, we examine the relationships between personality traits, memory for fear extinction, and cortical thickness as a measure of brain structure. We found that in healthy humans, extinction retention and thickness of the medial orbitofrontal cortex are positively correlated with extraversion. Path analysis indicates that extinction retention mediates the relationship between the medial orbitofrontal cortex thickness and extraversion, thereby illustrating one path through which brain structure influences personality. C1 Massachusetts Gen Hosp, Dept Psychiat, Psychiat Neurosci Div, Charlestown, MA 02129 USA. Massachusetts Gen Hosp, Nucl Magnet Resonance Ctr, Charlestown, MA 02129 USA. Harvard Univ, Sch Med, Charlestown, MA USA. Dept Vet Affairs Med Ctr, Manchester, NH USA. RP Rauch, SL (reprint author), Massachusetts Gen Hosp, Dept Psychiat, Psychiat Neurosci Div, Bldg 149,13th St,2nd Floor, Charlestown, MA 02129 USA. EM rauch@psych.mgh.harvard.edu NR 25 TC 75 Z9 78 U1 1 U2 6 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3261 USA SN 0959-4965 J9 NEUROREPORT JI Neuroreport PD NOV 28 PY 2005 VL 16 IS 17 BP 1909 EP 1912 DI 10.1097/01.wnr.0000186599.66243.50 PG 4 WC Neurosciences SC Neurosciences & Neurology GA 987VS UT WOS:000233546200008 PM 16272877 ER PT J AU Bilenca, A Desjardins, A Bouma, BE Tearney, GJ AF Bilenca, A Desjardins, A Bouma, BE Tearney, GJ TI Multicanonical Monte-Carlo simulations of light propagation in biological media SO OPTICS EXPRESS LA English DT Article ID OPTICAL-PROPERTIES; DIFFUSION-THEORY; TISSUES; MODEL AB Monte-Carlo simulation is an important tool in the field of biomedical optics, but suffers from significant computational expense. In this paper, we present the multicanonical Monte-Carlo (MMC) method for improving the efficiency of classical Monte Carlo simulations of light propagation in biological media. The MMC is an adaptive importance sampling technique that iteratively equilibrates at the optimal importance distribution with little (if any) a priori knowledge of how to choose and bias the importance proposal distribution. We illustrate the efficiency of this method by evaluating the probability density function (pdf) for the radial distance of photons exiting from a semi-infinite homogeneous tissue as well as the pdf for the maximum penetration depth of photons propagating in an inhomogeneous tissue. The results agree very well with diffusion theory as well as classical Monte-Carlo simulations. A six to sevenfold improvement in computational time is achieved by the MMC algorithm in calculating pdf values as low as 10(-8). This result suggests that the MMC method can be useful in efficiently studying numerous applications of light propagation in complex biological media where the remitted photon yield is low. (c) 2005 Optical Society of America C1 Harvard Univ, Sch Med, Boston, MA 02114 USA. Massachusetts Gen Hosp, Wellman Ctr Photomed, Boston, MA 02114 USA. RP Bilenca, A (reprint author), Harvard Univ, Sch Med, 50 Blossom St,BAR 7, Boston, MA 02114 USA. EM abilenca@partners.com NR 15 TC 10 Z9 11 U1 0 U2 1 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 28 PY 2005 VL 13 IS 24 BP 9822 EP 9833 DI 10.1364/OPEX.13.009822 PG 12 WC Optics SC Optics GA 993QY UT WOS:000233971200023 PM 19503191 ER PT J AU Tseng, YL Kuwaki, K Dor, FJMF Shimizu, A Houser, S Hisashi, Y Yamada, K Robson, SC Awwad, M Schuurman, HJ Sachs, DH Cooper, DKC AF Tseng, YL Kuwaki, K Dor, FJMF Shimizu, A Houser, S Hisashi, Y Yamada, K Robson, SC Awwad, M Schuurman, HJ Sachs, DH Cooper, DKC TI alpha 1,3-Galactosyltransferase gene-knockout pig heart transplantation in baboons with survival approaching 6 months SO TRANSPLANTATION LA English DT Article DE alpha 1,3-galactosyltransferase gene-knockout; anti-CD154 monoclonal antibody; baboon; costimulatory blockade; heart transplantation; pig; xenotransplantation ID DISSEMINATED INTRAVASCULAR COAGULATION; HUMORAL XENOGRAFT REJECTION; KIDNEY-TRANSPLANTATION; MONOCLONAL-ANTIBODY; IN-VITRO; XENOTRANSPLANTATION; CELLS; ENDOTHELIUM; BLOCKADE; VIVO AB Background. The recent generation of alpha 1,3-galactosyltransferase gene-knockout (GalT-KO) pigs has allowed investigation of the survival of GalT-KO pig organs in nonhuman primates. Methods. Heterotopic heart transplantation from GalT-KO pigs was carried out in baboons (n=8) using a human antihuman CD154 monoclonal antibody-based immunosuppressive regimen. Results. In six of the eight cases, graft survival extended to between approximately 2 and 6 months. All grafts developed thrombotic microangiopathy (TM). In particular, the clinical course of one baboon in which the graft functioned for 179 days is summarized. This baboon received aspirin (40 mg on alternate days) from day 4 in addition to heparin, which may have been a factor in the delay of onset and progression of TM and in prolonged graft survival. Maintenance therapy with anti-CD154 mAb, mycophenolate mofetil, and methylprednisolone was associated with persistently low numbers of CD3(+)CD4(+) and CD3(+)CD8(+) cells. Despite persisting depletion of these cells, no infectious complications occurred. Conclusions. It remains to be established whether TM is related to a very low level of natural preformed or T-cell-induced antibody deposition on the graft, inducing endothelial activation and injury, or to molecular incompatibilities in the coagulation mechanisms between pig and baboon, or to both. However, function of a pig organ in a baboon for a period approaching six months, which has not been reported previously, lends encouragement that the barriers to xenotransplantation will eventually be overcome. C1 Harvard Univ, Sch Med, Massachusetts Gen Hosp, Transplantat Biol Res Ctr, Boston, MA 02115 USA. Harvard Univ, Sch Med, Massachusetts Gen Hosp, Dept Pathol, Boston, MA 02115 USA. Harvard Univ, Sch Med, Beth Israel Deaconess Med Ctr, Ctr Immunobiol, Boston, MA 02115 USA. Immerge BioTherapeut Inc, Cambridge, MA USA. Erasmus Univ, Med Ctr, Dept Surg, Rotterdam, Netherlands. RP Cooper, DKC (reprint author), Univ Pittsburgh, Med Ctr, Thomas E Starzl Transplantat Inst, Biomed Sci Tower E 1550A,200 Lothrop St, Pittsburgh, PA 15261 USA. EM cooperdk@upmc.edu RI Dor, Frank/E-1032-2013 OI Dor, Frank/0000-0001-7845-3075 FU PHS HHS [1P01 A145897] NR 25 TC 116 Z9 119 U1 0 U2 2 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3261 USA SN 0041-1337 J9 TRANSPLANTATION JI Transplantation PD NOV 27 PY 2005 VL 80 IS 10 BP 1493 EP 1500 DI 10.1097/01.tp.0000181397.41143.fa PG 8 WC Immunology; Surgery; Transplantation SC Immunology; Surgery; Transplantation GA 994YH UT WOS:000234066600022 PM 16340796 ER PT J AU Kourmouli, N Sun, YM van der Sar, S Singh, PB Brown, JP AF Kourmouli, N Sun, YM van der Sar, S Singh, PB Brown, JP TI Epigenetic regulation of mammalian pericentric heterochromatin in vivo by HP1 SO BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS LA English DT Article DE HP1; histone code; heterochromatin; epigenetics ID HISTONE H3; CONSTITUTIVE HETEROCHROMATIN; LYSINE-9 METHYLATION; SATELLITE REPEATS; PROTEIN-1 HP1; CHROMO DOMAIN; ANIMALS; METHYLTRANSFERASE; EUCHROMATIN; EXPRESSION AB We developed a model system whereby HP1 can be targeted to pericentric heterochromatin in ES cells lacking Suv(3)9h1/2 histone methyltransferase (HMTase) activities. HP1 so targeted can reconstitute tri-methylated lysine 9 of histone H3 (Me(3)K9143) and tri-methylated lysine 20 of histone H4 (Me(3)K20H4) at pericentric heterochromatin, indicating that HP1 can regulate the distribution of these histone modifications in vivo. Both homo- and hetero-typic interactions between the HP1 isotypes were demonstrated in vivo as were HP1 interactions with the ESET/SETDB1 HMTase and the ATRX chromatin remodelling enzyme. We conclude that HP1 not only "deciphers" the histone code but can also "encode it." (c) 2005 Elsevier Inc. All rights reserved. C1 Forschungszentrum Borstel, Dept Immunol & Cell Biol, Div Tumor Biol, D-23845 Borstel, Germany. Univ Leeds, Sch Biochem & Mol Biol, Leeds LS2 9JT, W Yorkshire, England. Univ Edinburgh, Wellcome Trust Ctr Cell & Mol Biol, Edinburgh EH9 3JR, Midlothian, Scotland. Massachusetts Gen Hosp, Cutaneous Biol Res Ctr, Charlestown, MA 02129 USA. RP Singh, PB (reprint author), Forschungszentrum Borstel, Dept Immunol & Cell Biol, Div Tumor Biol, D-23845 Borstel, Germany. EM psingh@fz-borstel.de RI Sun, Yuh-Man/N-1579-2014; Singh, Prim/G-1088-2014 NR 30 TC 42 Z9 43 U1 0 U2 6 PU ACADEMIC PRESS INC ELSEVIER SCIENCE PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA SN 0006-291X J9 BIOCHEM BIOPH RES CO JI Biochem. Biophys. Res. Commun. PD NOV 25 PY 2005 VL 337 IS 3 BP 901 EP 907 DI 10.1016/j.bbrc.2005.09.132 PG 7 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA 978YY UT WOS:000232910300022 PM 16213461 ER PT J AU Morissette, MR Cook, SA Rosenzweig, A AF Morissette, MR Cook, SA Rosenzweig, A TI Myostatin regulates cardiac hypertrophy through a novel p38-Akt mechanism SO CIRCULATION RESEARCH LA English DT Meeting Abstract CT Scientific Meeting of the American-Heart-Association CY NOV 13-16, 2005 CL Dallas, TX SP Amer Heart Assoc C1 Massachusetts Gen Hosp, Charlestown, MA USA. Hammersmith Hosp, MRC, Ctr Clin Sci, London, England. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3261 USA SN 0009-7330 J9 CIRC RES JI Circ.Res. PD NOV 25 PY 2005 VL 97 IS 11 MA 5015 BP 1203 EP 1203 PG 1 WC Cardiac & Cardiovascular Systems; Hematology; Peripheral Vascular Disease SC Cardiovascular System & Cardiology; Hematology GA 986OZ UT WOS:000233460900035 ER PT J AU Fujii, N Hirshman, MF Kane, EM Ho, RC Peter, LE Seifert, MM Goodyear, LJ AF Fujii, N Hirshman, MF Kane, EM Ho, RC Peter, LE Seifert, MM Goodyear, LJ TI AMP-activated protein kinase alpha 2 activity is not essential for contraction- and hyperosmolarity-induced glucose transport in skeletal muscle SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID ACTIVATED PROTEIN-KINASE; GAMMA-SUBUNIT ISOFORMS; ACETYL-COA CARBOXYLASE; CATALYTIC SUBUNIT; INSULIN; RAT; EXPRESSION; EXERCISE; STIMULATION; METABOLISM AB To examine the role of AMP-activated protein kinase ( AMPK) in muscle glucose transport, we generated muscle-specific transgenic mice (TG) carrying cDNAs of inactive alpha 2 (alpha 2i TG) and alpha 1 (alpha 1i TG) catalytic subunits. Extensor digitorum longus (EDL) muscles from wild type and TG mice were isolated and subjected to a series of in vitro incubation experiments. In alpha 2i TG mice basal alpha 2 activity was barely detectable, whereas basal alpha 1 activity was only partially reduced. Known AMPK stimuli including 5-aminoimidazole-4-carboxamide-1- beta-4-ribofuranoside (AICAR), rotenone ( a Complex I inhibitor), dinitrophenol ( a mitochondrial uncoupler), muscle contraction, and sorbitol ( producing hyperosmolar shock) did not increase AMPK alpha 2 activity in alpha 2i TG mice, whereas alpha 1 activation was attenuated by only 30 - 50%. Glucose transport was measured in vitro using isolated EDL muscles from alpha 2i TG mice. AICAR- and rotenone-stimulated glucose transport was fully inhibited in alpha 2iTG mice; however, the lack of AMPK alpha 2 activity had no effect on contraction or sorbitol-induced glucose transport. Similar to these observations in vitro, contraction-stimulated glucose transport, assessed in vivo by 2-deoxy-D-[H-3] glucose incorporation into EDL, tibialis anterior, and gastrocnemius muscles, was normal in alpha 2i TG mice. Thus, AMPK alpha 2 activation is essential for some, but not all, insulin-independent glucose transport. Muscle contraction- and hyperosmolarity-induced glucose transport may be regulated by a redundant mechanism in which AMPK alpha 2 is one of multiple signaling pathways. C1 Joslin Diabet Ctr, Div Res, Boston, MA 02215 USA. Brigham & Womens Hosp, Dept Med, Boston, MA 02115 USA. Harvard Univ, Sch Med, Boston, MA 02115 USA. RP Goodyear, LJ (reprint author), Joslin Diabet Ctr, Div Res, 1 Joslin Pl, Boston, MA 02215 USA. EM Laurie.Goodyear@joslin.harvard.edu RI Fujii, Nobuharu/J-2724-2014 OI Fujii, Nobuharu/0000-0002-0974-3033 FU NIAMS NIH HHS [AR42238, R01 AR45670, F32 AR049662]; NIDDK NIH HHS [DK36836] NR 47 TC 113 Z9 116 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 25 PY 2005 VL 280 IS 47 BP 39033 EP 39041 DI 10.1074/jbc.M504208200 PG 9 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA 985FL UT WOS:000233362200017 PM 16186119 ER PT J AU Gao, L Tse, SW Conrad, C Andreadis, A AF Gao, L Tse, SW Conrad, C Andreadis, A TI Saitohin, which is nested in the tau locus and confers allele-specific susceptibility to several neurodegenerative diseases, interacts with peroxiredoxin SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID NONSELENIUM GLUTATHIONE-PEROXIDASE; PROGRESSIVE SUPRANUCLEAR PALSY; ALZHEIMERS-DISEASE; OXIDATIVE STRESS; PARKINSONS-DISEASE; Q7R POLYMORPHISM; EXPRESSION PATTERNS; 1-CYS PEROXIREDOXIN; GENE POLYMORPHISM; HUMAN BRAIN AB Saitohin is a gene unique to humans and their closest relatives, the function of which is not yet known. Saitohin contains a single polymorphism (Q7R), and its Q and R alleles belong to the H1 and H2 tau haplotype, respectively. The Saitohin Q allele confers susceptibility to several neurodegenerative diseases. To get a handle on Saitohin function, we used it as a bait in a yeast two-hybrid screen. By this assay and subsequent co-immunoprecipitation and glutathione S-transferase pull-down assays, we discovered and confirmed that Saitohin interacts with peroxiredoxin 6, a unique member of that family that is bifunctional and the levels of which increase in Pick disease. The strength of the interaction appeared to be allele-specific, giving the first distinction between the two forms of Saitohin. C1 Univ Massachusetts, Shriver Ctr, Sch Med, Waltham, MA 02452 USA. Massachusetts Gen Hosp, Dept Neurol, Alzheimers Unit, Charlestown, MA 02129 USA. Univ Massachusetts, Med Ctr, Dept Cell Biol, Worcester, MA 01655 USA. RP Andreadis, A (reprint author), Univ Massachusetts, Shriver Ctr, Sch Med, 200 Trapelo Rd, Waltham, MA 02452 USA. EM athena.andreadis@umassmed.edu FU NIA NIH HHS [AG018486] NR 34 TC 19 Z9 22 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 25 PY 2005 VL 280 IS 47 BP 39268 EP 39272 DI 10.1074/jbc.M506116200 PG 5 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA 985FL UT WOS:000233362200044 PM 16186110 ER PT J AU Rattan, R Giri, S Singh, AK Singh, I AF Rattan, R Giri, S Singh, AK Singh, I TI 5-Aminoimidazole-4-carboxamide-1-beta-D-ribofuranoside inhibits cancer cell proliferation in vitro and in vivo via AMP-activated protein kinase SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID MTOR SIGNALING PATHWAY; PEUTZ-JEGHERS-SYNDROME; FATTY-ACID OXIDATION; N-TERMINAL KINASE; INDUCED APOPTOSIS; PERMEABLE ACTIVATOR; MAMMALIAN TARGET; RIBONUCLEOSIDE; SURVIVAL; GROWTH AB 5-Aminoimidazole-4-carboxamide-1-beta-4-ribofuranoside ( AICAR) is widely used as an AMP-kinase activator, which regulates energy homeostasis and response to metabolic stress. Here, we investigated the effect of AICAR, an AMPK activator, on proliferation of various cancer cells and observed that proliferation of all the examined cell lines was significantly inhibited by AICAR treatment due to arrest in S-phase accompanied with increased expression of p21, p27, and p53 proteins and inhibition of PI3K-Akt pathway. Inhibition in in vitro growth of cancer cells was mirrored in vivo with increased expression of p21, p27, and p53 and attenuation of Akt phosphorylation. Anti-proliferative effect of AICAR is mediated through activated AMP-activated protein kinase ( AMPK) as iodotubericidin and dominant-negative AMPK expression vector reversed the AICAR-mediated growth arrest. Moreover, constitutive active AMPK arrested the cells in S-phase by inducing the expression of p21, p27, and p53 proteins and inhibiting Akt phosphorylation, suggesting the involvement of AMPK. AICAR inhibited proliferation in both LKB and LKB knock-out mouse embryo fibroblasts to similar extent and arrested cells at S-phase when transfected with dominant negative expression vector of LKB. Altogether, these results indicate that AICAR can be utilized as a therapeutic drug to inhibit cancer, and AMPK can be a potential target for treatment of various cancers independent of the functional tumor suppressor gene, LKB. C1 Med Univ S Carolina, Childrens Res Inst, Dept Pediat, Charleston, SC 29425 USA. Ralph Johnson Vet Affairs Med Ctr, Dept Pathol & Lab Med, Charleston, SC 29425 USA. RP Singh, I (reprint author), Med Univ S Carolina, Childrens Res Inst, Dept Pediat, 173 Ashley Ave,5th Floor, Charleston, SC 29425 USA. EM singhi@musc.edu FU NINDS NIH HHS [NS-22576, NS-34741, NS-37766, NS-40144, NS-40810] NR 46 TC 251 Z9 260 U1 0 U2 11 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 25 PY 2005 VL 280 IS 47 BP 39582 EP 39593 DI 10.1074/jbc.M507443200 PG 12 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA 985FL UT WOS:000233362200081 PM 16176927 ER PT J AU Gorin, Y Block, K Hernandez, J Bhandari, B Wagner, B Barnes, JL Abboud, HE AF Gorin, Y Block, K Hernandez, J Bhandari, B Wagner, B Barnes, JL Abboud, HE TI Nox4 NAD(P)H oxidase mediates hypertrophy and fibronectin expression in the diabetic kidney SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID GLOMERULAR MESANGIAL CELLS; AKT/PROTEIN KINASE-B; ANGIOTENSIN-II; OXIDATIVE STRESS; NADPH OXIDASE; HIGH-GLUCOSE; EXTRACELLULAR-MATRIX; PROTEIN-SYNTHESIS; GENE-EXPRESSION; DNA-DAMAGE AB Renal hypertrophy and extracellular matrix accumulation are early features of diabetic nephropathy. We investigated the role of the NAD(P) H oxidase Nox4 in generation of reactive oxygen species (ROS), hypertrophy, and fibronectin expression in a rat model of type 1 diabetes induced by streptozotocin. Phosphorothioated antisense (AS) or sense oligonucleotides for Nox4 were administered for 2 weeks with an osmotic minipump 72 h after streptozotocin treatment. Nox4 protein expression was increased in diabetic kidney cortex compared with non-diabetic controls and was down-regulated in AS-treated animals. AS oligonucleotides inhibited NADPH-dependent ROS generation in renal cortical and glomerular homogenates. ROS generation by intact isolated glomeruli from diabetic animals was increased compared with glomeruli isolated from AS-treated animals. AS treatment reduced whole kidney and glomerular hypertrophy. Moreover, the increased expression of fibronectin protein was markedly reduced in renal cortex including glomeruli of AS-treated diabetic rats. Akt/protein kinase B and ERK1/2, two protein kinases critical for cell growth and hypertrophy, were activated in diabetes, and AS treatment almost abolished their activation. In cultured mesangial cells, high glucose increased NADPH oxidase activity and fibronectin expression, effects that were prevented in cells transfected with AS oligonucleotides. These data establish a role for Nox4 as the major source of ROS in the kidneys during early stages of diabetes and establish that Nox4-derived ROS mediate renal hypertrophy and increased fibronectin expression. C1 Univ Texas, Hlth Sci Ctr, Dept Med, Div Nephrol, San Antonio, TX 78229 USA. S Texas Vet Hlth Care Syst, Audie L Murphy Mem Hosp Div, San Antonio, TX 78229 USA. RP Abboud, HE (reprint author), Univ Texas, Hlth Sci Ctr, Dept Med, Div Nephrol, MC 7882,7703 Floyd Curl Dr, San Antonio, TX 78229 USA. EM abboud@uthsca.edu OI Gorin, Yves/0000-0003-4048-6925; Wagner, Brent/0000-0002-7063-0142 FU NIDDK NIH HHS [DK33665, DK43988] NR 62 TC 290 Z9 303 U1 2 U2 14 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 25 PY 2005 VL 280 IS 47 BP 39616 EP 39626 DI 10.1074/jbc.M502412200 PG 11 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA 985FL UT WOS:000233362200085 PM 16135519 ER PT J AU Okuhira, K Fitzgerald, ML Sarracino, DA Manning, JJ Bell, SA Goss, JL Freeman, MW AF Okuhira, K Fitzgerald, ML Sarracino, DA Manning, JJ Bell, SA Goss, JL Freeman, MW TI Purification of ATP-binding cassette transporter A1 and associated binding proteins reveals the importance of beta 1-syntrophin in cholesterol efflux SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID HIGH-DENSITY-LIPOPROTEIN; TANGIER-DISEASE; APOA-I; ABCA1 TRANSPORTER; HDL CHOLESTEROL; PEST SEQUENCE; ATHEROSCLEROSIS; PHOSPHORYLATION; MUTATIONS; DEGRADATION AB ATP-binding cassette transporter A1 ( ABCA1) plays a critical role in HDL cholesterol metabolism, but the mechanism by which it transports lipid across membranes is poorly understood. Because growing evidence implicates accessory proteins in this process, we developed a method by which proteins interacting with the intact transporter could be identified. cDNAs encoding wild-type ABCA1 and a mutant lacking the C-terminal PDZ binding motif of ABCA1 were transfected into 293 cells, and the expressed proteins were solubilized using detergent conditions ( 0.75% CHAPS, 1 mg/ml phosphatidylcholine) predicted to retain high affinity protein-protein interactions. Proteins that co-purified with ABCA1 on an antibody affinity column were identified by liquid chromatographymass spectrometric analysis. A novel interaction with the PDZ protein beta 1-syntrophin was identified using this approach, and this interaction was confirmed in human THP-1 macrophages and in mouse liver. Small interference RNA inhibition of beta 1-syntrophin expression reduced cholesterol efflux from primary skin fibroblasts by 50% while decreasing efflux 30% in bone marrow-derived macrophages. Inhibition of beta 1-syntrophin decreased ABCA1 protein levels, whereas overexpression of beta 1-syntrophin increased ABCA1 cell-surface expression and stimulated efflux to apolipoprotein A-I. These findings indicate that beta 1-syntrophin acts through a class-I PDZ interaction with the C terminus of ABCA1 to regulate the cellular distribution and activity of the transporter. The approach used to identify beta 1-syntrophin as an ABCA1-binding protein should prove useful in elucidating other protein interactions upon which ABCA1 function depends. C1 Harvard Univ, Lipid Metab Unit, Sch Med, Massachusetts Gen Hosp, Boston, MA 02114 USA. Harvard Univ, Partners Ctr Genet & Genom, Sch Med, Massachusetts Gen Hosp, Boston, MA 02114 USA. RP Fitzgerald, ML (reprint author), Harvard Univ, Lipid Metab Unit, Sch Med, Massachusetts Gen Hosp, Jackson 1321, Boston, MA 02114 USA. EM mfitzger@molbio.mgh.harvard.edu; freeman@molbio.mgh.harvard.edu FU NHLBI NIH HHS [HL074136, HL68988, HL45098, HL72358] NR 40 TC 47 Z9 47 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 25 PY 2005 VL 280 IS 47 BP 39653 EP 39664 DI 10.1074/jbc.M5101870200 PG 12 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA 985FL UT WOS:000233362200089 PM 16192269 ER PT J AU Basu, U Chaudhuri, J Alpert, C Dutt, S Ranganath, S Li, G Schrum, JP Manis, JP Alt, FW AF Basu, U Chaudhuri, J Alpert, C Dutt, S Ranganath, S Li, G Schrum, JP Manis, JP Alt, FW TI The AID antibody diversification enzyme is regulated by protein kinase A phosphorylation SO NATURE LA English DT Article ID CLASS-SWITCH RECOMBINATION; SINGLE-STRANDED-DNA; CYTIDINE DEAMINASE AID; SOMATIC HYPERMUTATION; B-CELLS; MECHANISM; TRANSCRIPTION; EXPRESSION; MYC AB Antibodies, which are produced by B-lineage cells, consist of immunoglobulin heavy (IgH) and light (IgL) chains that have amino-terminal variable regions and carboxy-terminal constant regions. In response to antigens, B cells undergo two types of genomic alterations to increase antibody diversity. Affinity for antigen can be increased by introduction of point mutations into IgH and IgL variable regions by somatic hypermutation. In addition, antibody effector functions can be altered by changing the expressed IgH constant region exons through IgH class switch recombination (CSR)(1-3). Somatic hypermutation and CSR both require the B-cell-specific activation-induced cytidine deaminase protein (AID)(4-6), which initiates these reactions through its single-stranded (ss)DNA-specific cytidine deaminase activity(7-11). In biochemical assays, replication protein A (RPA), a ssDNA-binding protein(12), associates with phosphorylated AID from activated B cells and enhances AID activity on transcribed double-stranded (ds)DNA containing somatic hypermutation or CSR target sequences. This AID-RPA association, which requires phosphorylation, may provide a mechanism for allowing AID to access dsDNA targets in activated B cells(13,14). Here we show that AID from B cells is phosphorylated on a consensus protein kinase A (PKA) site and that PKA is the physiological AID kinase. Thus, AID from non-lymphoid cells can be functionally phosphorylated by recombinant PKA to allow interaction with RPA and promote deamination of transcribed dsDNA substrates. Moreover, mutation of the major PKA phosphorylation site of AID preserves ssDNA deamination activity, but markedly reduces RPA-dependent dsDNA deamination activity and severely impairs the ability of AID to effect CSR in vivo. We conclude that PKA has a critical role in post-translational regulation of AID activity in B cells. 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. Harvard Univ, Sch Med, Childrens Hosp, Joint Program Transfus Med,Dept Pathol, Boston, MA 02115 USA. RP Harvard Univ, Sch Med, Howard Hughes Med Inst, Childrens Hosp,CBR Inst Biomed Res, Boston, MA 02115 USA. EM alt@enders.tch.harvard.edu NR 29 TC 167 Z9 171 U1 1 U2 10 PU NATURE PUBLISHING GROUP PI LONDON PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND SN 0028-0836 EI 1476-4687 J9 NATURE JI Nature PD NOV 24 PY 2005 VL 438 IS 7067 BP 508 EP 511 DI 10.1038/nature04255 PG 4 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA 986NY UT WOS:000233458200052 PM 16251902 ER PT J AU Hafler, DA Kent, SC Chen, YH Bregoli, L Clemmings, SM Hering, B Kenyon, NS Ricordi, C AF Hafler, DA Kent, SC Chen, YH Bregoli, L Clemmings, SM Hering, B Kenyon, NS Ricordi, C TI Immunology - Insulin auto-antigenicity in type 1 diabetes - Reply SO NATURE LA English DT Editorial Material ID MYELIN BASIC-PROTEIN; T-CELL-CLONES; EPITOPE C1 Brigham & Womens Hosp, Ctr Neurol Dis, Boston, MA 02115 USA. Harvard Univ, Sch Med, Boston, MA 02115 USA. Univ Minnesota, Dept Surg, Minneapolis, MN 55455 USA. Univ Miami, Diabet Res Inst, Cell Transplant Ctr, Miami, FL 33136 USA. RP Hafler, DA (reprint author), Brigham & Womens Hosp, Ctr Neurol Dis, Boston, MA 02115 USA. EM dhafler@rics.bwh.harvard.edu NR 8 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 0028-0836 J9 NATURE JI Nature PD NOV 24 PY 2005 VL 438 IS 7067 BP E5 EP E6 DI 10.1038/nature04424 PG 2 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA 986NY UT WOS:000233458200037 ER PT J AU Attiyeh, EF London, WB Mosse, YP Wang, Q Winter, C Khazi, D McGrady, PW Seeger, RC Look, AT Shimada, H Brodeur, GM Cohn, SL Matthay, KK Maris, JM AF Attiyeh, EF London, WB Mosse, YP Wang, Q Winter, C Khazi, D McGrady, PW Seeger, RC Look, AT Shimada, H Brodeur, GM Cohn, SL Matthay, KK Maris, JM CA Children's Oncology Grp TI Chromosome 1p and 11q deletions and outcome in neuroblastoma SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Article; Proceedings Paper CT 41st Annual Meeting of the American-Society-of-Clinical-Oncology CY MAY 13-17, 2005 CL Orlando, FL SP Amer Soc Clin Oncol ID PEDIATRIC-ONCOLOGY-GROUP; TUMOR-CELL PLOIDY; GENE AMPLIFICATION; ALLELIC DELETION; STAGE; HYBRIDIZATION; PROGRESSION; DEFINITION; ONCOGENE; THERAPY AB BACKGROUND Neuroblastoma is a childhood cancer with considerable morbidity and mortality. Tumor-derived biomarkers may improve risk stratification. METHODS We screened 915 samples of neuroblastoma for loss of heterozygosity (LOH) at chromosome bands 1p36 and 11q23. Additional analyses identified a subgroup of cases of 11q23 LOH with unbalanced 11q LOH (unb11q LOH; defined as loss of 11q with retention of 11p). The associations of LOH with relapse and survival were determined. RESULTS LOH at 1p36 was identified in 209 of 898 tumors (23 percent) and LOH at 11q23 in 307 of 913 (34 percent). Unb11q LOH was found in 151 of 307 tumors with 11q23 LOH (17 percent of the total cohort). There was a strong association of 1p36 LOH, 11q23 LOH, and unb11q LOH with most high-risk disease features (P<0.001). LOH at 1p36 was associated with amplification of the MYCN oncogene (P<0.001), but 11q23 LOH and unb11q LOH were not (P<0.001 and P=0.002, respectively). Cases with unb11q LOH were associated with three-year event-free and overall survival rates (+/-SE) of 50+/-5 percent and 66+/-5 percent, respectively, as compared with 74+/-2 percent and 83+/-2 percent among cases without unb11q LOH (P<0.001 for both comparisons). In a multivariate model, unb11q LOH was independently associated with decreased event-free survival (P=0.009) in the entire cohort, and both 1p36 LOH and unb11q LOH were independently associated with decreased progression-free survival in the subgroup of patients with features of low-risk and intermediate-risk disease (P=0.002 and P=0.02, respectively). CONCLUSIONS Unb11q LOH and 1p36 LOH are independently associated with a worse outcome in patients with neuroblastoma. C1 Univ Penn, Childrens Hosp Philadelphia, Sch Med, Philadelphia, PA 19104 USA. Abramson Family Canc Res Inst, Philadelphia, PA USA. Childrens Oncol Grp, Arcadia, CA USA. Univ Florida, Dept Stat, Gainesville, FL 32611 USA. Childrens Oncol Grp, Gainesville, FL USA. Childrens Hosp Los Angeles, Los Angeles, CA 90027 USA. Harvard Univ, Sch Med, Dana Farber Canc Inst, Boston, MA 02115 USA. Northwestern Univ, Feinberg Sch Med, Chicago, IL 60611 USA. Univ Calif San Francisco, Sch Med, San Francisco, CA USA. RP Maris, JM (reprint author), Childrens Hosp Philadelphia, Abramson Pediat Res Ctr 902A, Div Oncol, 3615 Civic Ctr Blvd, Philadelphia, PA 19104 USA. EM maris@email.chop.edu OI Cohn, Susan/0000-0001-5749-7650 FU NCI NIH HHS [R01-CA39771, R01-CA87847, U10-CA78966, U10-CA98543] NR 30 TC 250 Z9 258 U1 2 U2 9 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 24 PY 2005 VL 353 IS 21 BP 2243 EP 2253 DI 10.1056/NEJMoa052399 PG 11 WC Medicine, General & Internal SC General & Internal Medicine GA 986FC UT WOS:000233434500007 PM 16306521 ER PT J AU Dickerson, BC Holtzman, D Grant, PE Tian, D Walsh, R Harris, NL AF Dickerson, BC Holtzman, D Grant, PE Tian, D Walsh, R Harris, NL TI A woman with seizure, disturbed gait, and altered mental status - Mitochondrial encephalomyopathy, lactic acidosis, and stroke-like episodes (the MELAS syndrome). SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Editorial Material ID COMPLEX-I; MUTATION; DNA; ENCEPHALOPATHY; EPIDEMIOLOGY; DEMENTIA; DISEASE; GENE; MYOPATHIES; DISORDERS C1 Massachusetts Gen Hosp, Dept Neurol, Boston, MA 02114 USA. Massachusetts Gen Hosp, Dept Pediat, Boston, MA 02114 USA. Massachusetts Gen Hosp, Dept Radiol, Div Pediat Radiol, Boston, MA 02114 USA. Massachusetts Gen Hosp, Dept Pathol, Boston, MA 02114 USA. Brigham & Womens Hosp, Dept Neurol, Div Cognit & Behav Neurol, Boston, MA 02115 USA. Harvard Univ, Sch Med, Dept Neurol, Boston, MA 02115 USA. Harvard Univ, Sch Med, Dept Pediat, Boston, MA 02115 USA. Harvard Univ, Sch Med, Dept Radiol, Boston, MA 02115 USA. RP Dickerson, BC (reprint author), Massachusetts Gen Hosp, Dept Neurol, Boston, MA 02114 USA. NR 35 TC 11 Z9 14 U1 1 U2 2 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 24 PY 2005 VL 353 IS 21 BP 2271 EP 2280 PG 10 WC Medicine, General & Internal SC General & Internal Medicine GA 986FC UT WOS:000233434500012 PM 16306525 ER PT J AU Lee, BH Williams, IR Anastasiadou, E Boulton, CL Joseph, SW Amaral, SM Curley, DP Duclos, N Huntly, BJP Fabbro, D Griffin, JD Gilliland, DG AF Lee, BH Williams, IR Anastasiadou, E Boulton, CL Joseph, SW Amaral, SM Curley, DP Duclos, N Huntly, BJP Fabbro, D Griffin, JD Gilliland, DG TI FLT3 internal tandem duplication mutations induce myeloproliferative or lymphoid disease in a transgenic mouse model SO ONCOGENE LA English DT Article DE FLT3 tyrosine kinase; transgenic; mouse; leukemia ID ACUTE MYELOID-LEUKEMIA; RECEPTOR TYROSINE KINASE; HEMATOPOIETIC-CELLS; CONSTITUTIVE ACTIVATION; EXPRESSION; GENE; TRANSFORMATION; COMPARTMENT; PKC412; LIGAND AB Activating FMS-like tyrosine kinase 3 (FLT3) mutations have been identified in similar to 30% of patients with acute myelogenous leukemia (AML), and recently in a smaller subset of patients with acute lymphoblastic leukemia (ALL). To explore the in vivo consequences of an activating FLT3 internal tandem duplication mutation (FLT3-ITD), we created a transgenic mouse model in which FLT3-ITD was expressed under the control of the vav hematopoietic promoter. Five independent lines of vavFLT3-ITD transgenic mice developed a myeloproliferative disease with high penetrance and a disease latency of 6-12 months. The phenotype was characterized by splenomegaly, megakaryocytic hyperplasia, and marked thrombocythemia, but without leukocytosis, polycythemia, or marrow fibrosis, displaying features reminiscent of the human disease essential thrombocythemia (ET). Clonal immature B- or T-lymphoid disease was observed in two additional founder mice, respectively, that could be secondarily transplanted to recipient mice that rapidly developed lymphoid disease. Treatment of these mice with the FLT3 tyrosine kinase inhibitor, PKC412, resulted in suppression of disease and a statistically significant prolongation of survival. These results demonstrate that FLT3-ITD is capable of inducing myeloproliferative as well as lymphoid disease, and indicate that small-molecule tyrosine kinase inhibitors may be an effective treatment for lymphoid malignancies in humans that are associated with activating mutations in FLT3. C1 Brigham & Womens Hosp, Div Hematol, Dept Med, Boston, MA 02115 USA. Brigham & Womens Hosp, Dept Pathol, Boston, MA 02115 USA. Emory Univ, Dept Pathol, Atlanta, GA 30322 USA. Novartis Pharma AG, Basel, Switzerland. Harvard Univ, Sch Med, Dana Farber Canc Inst, Boston, MA 02115 USA. Harvard Univ, Sch Med, Howard Hughes Med Inst, Boston, MA 02115 USA. RP Gilliland, DG (reprint author), Brigham & Womens Hosp, Div Hematol, Dept Med, Childrens Hosp Res Bldg,1 Blackfan Circle,5th Flo, Boston, MA 02115 USA. EM ggilliland@rics.bwh.harvard.edu RI Williams, Ifor/D-3648-2011; huntly, brian/E-6725-2014 OI Williams, Ifor/0000-0002-8810-2911; huntly, brian/0000-0003-0312-161X FU NCI NIH HHS [CA66996]; NHLBI NIH HHS [5T32HL 07627-16]; NIDDK NIH HHS [DK50654] NR 33 TC 39 Z9 40 U1 0 U2 3 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 24 PY 2005 VL 24 IS 53 BP 7882 EP 7892 DI 10.1038/sj.onc.1208933 PG 11 WC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity GA 986PU UT WOS:000233463000007 PM 16116483 ER PT J AU Swap, CJ Nagurney, JT AF Swap, CJ Nagurney, JT TI Value and limitations of chest pain history in the evaluation of patients with suspected acute coronary syndromes SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION LA English DT Review ID ACUTE MYOCARDIAL-INFARCTION; NORMAL TROPONIN CONCENTRATIONS; ACUTE CARDIAC ISCHEMIA; CARE-UNIT ADMISSION; CLINICAL CHARACTERISTICS; EMERGENCY-DEPARTMENT; RISK STRATIFICATION; ARTERY-DISEASE; NONDIABETIC PATIENTS; SYMPTOM PRESENTATION AB Context The chest pain history, physical examination, determination of coronary artery disease (CAD) risk factors, and the initial electrocardiogram compose the information immediately available to clinicians to help determine the probability of acute myocardial infarction (AMI) or acute coronary syndrome (ACS) in patients with chest pain. However, conflicting data exist about the usefulness of the chest pain history and which components are most useful. Objective To identify the elements of the chest pain history that may be most helpful to the clinician in identifying ACS in patients presenting with chest pain. Evidence Acquisition MEDLINE and Ovid were searched from 1970 to September 2005 by using specific key words and Medical Subject Heading terms. Reference lists of these articles and current cardiology textbooks were also consulted. Evidence Synthesis Certain chest pain characteristics decrease the likelihood of ACS or AMI, namely, pain that is stabbing, pleuritic, positional, or reproducible by palpation (likelihood ratios [LRs] 0.2-0.3). Conversely, chest pain that radiates to one shoulder or both shoulders or arms or is precipitated by exertion is associated with LRs (2.3-4.7) that increase the likelihood of ACS. The chest pain history itself has not proven to be a powerful enough predictive tool to obviate the need for at least some diagnostic testing. Combinations of elements of the chest pain history with other initially available information, such as a history of CAD, have identified certain groups that may be safe for discharge without further evaluation, but further study is needed before such a recommendation can be considered reasonable. Conclusion Although certain elements of the chest pain history are associated with increased or decreased likelihoods of a diagnosis of ACS or AMI, none of them alone or in combination identify a group of patients that can be safely discharged without further diagnostic testing. C1 Massachusetts Gen Hosp, Boston, MA 02114 USA. RP Nagurney, JT (reprint author), Massachusetts Gen Hosp, 55 Fruit St,Clin 115, Boston, MA 02114 USA. EM jnagurney@partners.org NR 82 TC 155 Z9 164 U1 0 U2 11 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610-0946 USA SN 0098-7484 J9 JAMA-J AM MED ASSOC JI JAMA-J. Am. Med. Assoc. PD NOV 23 PY 2005 VL 294 IS 20 BP 2623 EP 2629 DI 10.1001/jama.294.20.2623 PG 7 WC Medicine, General & Internal SC General & Internal Medicine GA 986FT UT WOS:000233436200028 PM 16304077 ER PT J AU Pertin, M Ji, RR Berta, T Powell, AJ Karchewski, L Tate, SN Isom, LL Woolf, CJ Gilliard, N Spahn, DR Decosterd, I AF Pertin, M Ji, RR Berta, T Powell, AJ Karchewski, L Tate, SN Isom, LL Woolf, CJ Gilliard, N Spahn, DR Decosterd, I TI Upregulation of the voltage-gated sodium channel beta 2 subunit in neuropathic pain models: Characterization of expression in injured and non-injured primary sensory neurons SO JOURNAL OF NEUROSCIENCE LA English DT Article DE pain; neuropathic pain; sodium channel; beta subunit; nerve injury; animal model ID SPINAL NERVE LIGATION; DORSAL-ROOT GANGLION; PRIMARY AFFERENT NEURONS; ALPHA-SUBUNIT; BETA-SUBUNITS; AUXILIARY SUBUNIT; SCIATIC-NERVE; RAT-BRAIN; MECHANICAL ALLODYNIA; IONIC MECHANISMS AB The development of abnormal primary sensory neuron excitability and neuropathic pain symptoms after peripheral nerve injury is associated with altered expression of voltage-gated sodium channels ( VGSCs) and a modification of sodium currents. To investigate whether the beta 2 subunit of VGSCs participates in the generation of neuropathic pain, we used the spared nerve injury ( SNI) model in rats to examine beta 2 subunit expression in selectively injured ( tibial and common peroneal nerves) and uninjured ( sural nerve) afferents. Three days after SNI, immunohistochemistry and Western blot analysis reveal an increase in the beta 2 subunit in both the cell body and peripheral axons of injured neurons. The increase persists for > 4 weeks, although beta 2 subunit mRNA measured by real-time reverse transcription-PCR and in situ hybridization remains unchanged. Although injured neurons show the most marked upregulation, beta 2 subunit expression is also increased in neighboring non-injured neurons and a similar pattern of changes appears in the spinal nerve ligation model of neuropathic pain. That increased beta 2 subunit expression in sensory neurons after nerve injury is functionally significant, as demonstrated by our finding that the development of mechanical allodynia-like behavior in the SNI model is attenuated in beta 2 subunit null mutant mice. Through its role in regulating the density of mature VGSC complexes in the plasma membrane and modulating channel gating, the beta 2 subunit may play a key role in the development of ectopic activity in injured and non-injured sensory afferents and, thereby, neuropathic pain. C1 Univ Lausanne Hosp, Dept Anesthesiol, Anesthesiol Pain Res Grp, CH-1005 Lausanne, Switzerland. Univ Lausanne, Fac Biol & Med, Dept Cell Biol & Morphol, CH-1005 Lausanne, Switzerland. Brigham & Womens Hosp, Dept Anesthesiol, Pain Res Ctr, Boston, MA 02115 USA. Harvard Univ, Sch Med, Boston, MA 02115 USA. GlaxoSmith Kline Res & Dev, Gene Express & Prot Biochem Dept, Stevenage SG1 2NY, Herts, England. Univ Michigan, Dept Pharmacol, Ann Arbor, MI 48109 USA. Massachusetts Gen Hosp, Dept Anesthesia & Crit Care, Neural Plast Res Grp, Boston, MA 02121 USA. Harvard Univ, Sch Med, Boston, MA 02121 USA. RP Decosterd, I (reprint author), Univ Lausanne Hosp, Dept Anesthesiol, Anesthesiol Pain Res Grp, Bugnon 9, CH-1005 Lausanne, Switzerland. EM isabelle.decosterd@chuv.ch RI Berta, Temugin/A-6908-2016 OI Berta, Temugin/0000-0002-4486-8288 FU NINDS NIH HHS [NS040698, NS039518] NR 66 TC 71 Z9 73 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 23 PY 2005 VL 25 IS 47 BP 10970 EP 10980 DI 10.1523/JNEUROSCI.3066-05.2005 PG 11 WC Neurosciences SC Neurosciences & Neurology GA 986OU UT WOS:000233460400018 PM 16306410 ER PT J AU Morrow, DA Givertz, MM AF Morrow, DA Givertz, MM TI Modulation of myocardial energetics - Emerging evidence for a therapeutic target in cardiovascular disease SO CIRCULATION LA English DT Editorial Material DE editorials; angina; fatty acids; heart failure; ion channels ID HEART-FAILURE; RAT-HEART; DILATED CARDIOMYOPATHY; ANTIANGINAL AGENT; CLINICAL-TRIAL; PERHEXILINE; RANOLAZINE; TRIMETAZIDINE; ANGINA; DOGS C1 Harvard Univ, Brigham & Womens Hosp, Sch Med, TIMI Study Grp, Boston, MA 02115 USA. Harvard Univ, Brigham & Womens Hosp, Sch Med, Adv Heart Dis Program, Boston, MA 02115 USA. Harvard Univ, Brigham & Womens Hosp, Sch Med, Div Cardiovasc, Boston, MA 02115 USA. Harvard Univ, Brigham & Womens Hosp, Sch Med, Dept Med, Boston, MA 02115 USA. RP Morrow, DA (reprint author), TIMI Study Grp, 350 Longwood Ave,1st Floor, Boston, MA 02115 USA. EM dmorrow@partners.org NR 21 TC 22 Z9 25 U1 0 U2 3 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3261 USA SN 0009-7322 J9 CIRCULATION JI Circulation PD NOV 22 PY 2005 VL 112 IS 21 BP 3218 EP 3221 DI 10.1161/CIRCULATIONAHA.105.581819 PG 4 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 986CZ UT WOS:000233428200003 PM 16301353 ER PT J AU Albert, CM Oh, K Whang, W Manson, JE Chae, CU Stampfer, MJ Willett, WC Hu, FB AF Albert, CM Oh, K Whang, W Manson, JE Chae, CU Stampfer, MJ Willett, WC Hu, FB TI Dietary alpha-linolenic acid intake and risk of sudden cardiac death and coronary heart disease SO CIRCULATION LA English DT Article DE death, sudden; women; arrhythmia; nutrition; fatty acids ID POLYUNSATURATED FATTY-ACIDS; FISH CONSUMPTION; MYOCARDIAL-INFARCTION; UNITED-STATES; WOMEN; MEN; COHORT; METAANALYSIS; PREVENTION; MORTALITY AB Background - alpha-Linolenic acid, an intermediate-chain n-3 fatty acid found primarily in plants, may decrease the risk of fatal coronary heart disease (CHD) through a reduction in fatal ventricular arrhythmias and sudden cardiac death (SCD). Methods and Results - We prospectively examined the association between dietary intake of alpha-linolenic acid assessed via updated food-frequency questionnaires and the risk of SCD, other fatal CHD, and nonfatal myocardial infarction (MI) among 76 763 women participating in the Nurses' Health Study who were free from cancer and completed a dietary questionnaire at baseline in 1984. During 18 years of follow-up, we identified 206 SCDs, 641 other CHD deaths, and 1604 nonfatal MIs. After controlling for coronary risk factors and other fatty acids, including long-chain n-3 fatty acids, the intake of alpha-linolenic acid was inversely associated with the risk of SCD (P for trend, 0.02) but not with the risk of other fatal CHD or nonfatal MI. Compared with women in the lowest quintile of alpha-linolenic acid intake, those in the highest 2 quintiles had a 38% to 40% lower SCD risk. This inverse relation with SCD risk was linear and remained significant even among women with high intakes of long-chain n-3 fatty acids. Conclusions - These prospective data suggest that increasing dietary intake of alpha-linolenic acid may reduce the risk of SCD but not other types of fatal CHD or nonfatal MI in women. The specificity of the association between alpha-linolenic acid and SCD supports the hypothesis that these n-3 fatty acids may have antiarrhythmic properties. C1 Brigham & Womens Hosp, Div Prevent Med, Boston, MA 02215 USA. Brigham & Womens Hosp, Ctr Arrhythmia Prevent, Boston, MA 02215 USA. Brigham & Womens Hosp, Div Cardiovasc, Boston, MA 02215 USA. Brigham & Womens Hosp, Channing Lab, Boston, MA 02215 USA. Brigham & Womens Hosp, Dept Med, Boston, MA 02215 USA. Massachusetts Gen Hosp, Dept Med, Div Cardiol, Boston, MA 02114 USA. Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA. Harvard Univ, Sch Publ Hlth, Dept Nutr, Boston, MA 02115 USA. RP Albert, CM (reprint author), Brigham & Womens Hosp, Div Prevent Med, 900 Commonwealth Ave E, Boston, MA 02215 USA. EM calbert@partners.org FU NCI NIH HHS [CA-87969]; NHLBI NIH HHS [1-K08-HL-03783, HL-34594] NR 35 TC 117 Z9 127 U1 1 U2 15 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3261 USA SN 0009-7322 J9 CIRCULATION JI Circulation PD NOV 22 PY 2005 VL 112 IS 21 BP 3232 EP 3238 DI 10.1161/CIRCULATIONAHA.105.572008 PG 7 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 986CZ UT WOS:000233428200006 PM 16301356 ER PT J AU Koyama, S Sasaki, Y Andersen, GJ Tootell, RBH Matsuura, M Watanabe, T AF Koyama, S Sasaki, Y Andersen, GJ Tootell, RBH Matsuura, M Watanabe, T TI Separate processing of different global-motion structures in visual cortex is revealed by fMRI SO CURRENT BIOLOGY LA English DT Article ID OPTIC FLOW; AREA MT; DIRECTION; NEURONS; INTEGRATION; PERCEPTION; MECHANISMS; HUMANS; MONKEY; BRAIN AB The visual system has the remarkable ability to extract several types of meaningful global-motion signals, such as radial motion, translation motion, and rotation, for different visual functions and actions. In the monkey brain, different groups of cells in MST respond best to different types of global motion [1, 2], whereas in lower cortical areas including MT, no such differential responses have been found. Here, we show that an area (or areas) lower than MST in the human brain [3] responds to different types of global motion. A series of human functional magnetic resonance imaging (fMRI) experiments, in which attention was controlled for, indicated that the center of radial motion activates the corresponding location in the V3A representation, whereas translation motion activates mainly in a more peripheral representation of V3A. These results suggest that in the human brain, V3A is an area that differentially responds according to the type of global motion. C1 Boston Univ, Dept Psychol, Boston, MA 02215 USA. Massachusetts Gen Hosp, NMR Ctr, Charlestown, MA 02129 USA. Univ Calif Riverside, Dept Psychol, Riverside, CA 92521 USA. Tokyo Med & Dent Univ, Bunkyo Ku, Tokyo 1138510, Japan. RP Watanabe, T (reprint author), Boston Univ, Dept Psychol, 64 Cummington St, Boston, MA 02215 USA. EM takeo@bu.edu OI Koyama, Shinichi/0000-0001-6280-5750 FU NEI NIH HHS [EY R01-07980, R01EY015980-01]; NIA NIH HHS [2R01AG013419-06A2] NR 32 TC 39 Z9 39 U1 0 U2 6 PU CELL PRESS PI CAMBRIDGE PA 1100 MASSACHUSETTS AVE, CAMBRIDGE, MA 02138 USA SN 0960-9822 J9 CURR BIOL JI Curr. Biol. PD NOV 22 PY 2005 VL 15 IS 22 BP 2027 EP 2032 DI 10.1016/j.cub.2005.10.069 PG 6 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA 990VI UT WOS:000233770900024 PM 16303562 ER PT J AU Hefter, RL Manoach, DS Barton, JJS AF Hefter, RL Manoach, DS Barton, JJS TI Perception of facial expression and facial identity in subjects with social developmental disorders SO NEUROLOGY LA English DT Article ID EMOTIONAL PROCESSING DISORDER; AUTISM SPECTRUM DISORDER; HIGH-FUNCTIONING AUTISM; ASPERGER-SYNDROME; FACE RECOGNITION; LEARNING-DISABILITY; REVISED VERSION; YOUNG-CHILDREN; NORMAL ADULTS; INDIVIDUALS AB Background: It has been hypothesized that the social dysfunction in social developmental disorders (SDDs), such as autism, Asperger disorder, and the socioemotional processing disorder, impairs the acquisition of normal face-processing skills. The authors investigated whether this purported perceptual deficit was generalized to both facial expression and facial identity or whether these different types of facial perception were dissociated in SDDs. Methods: They studied 26 adults with a variety of SDD diagnoses, assessing their ability to discriminate famous from anonymous faces, their perception of emotional expression from facial and nonfacial cues, and the relationship between these abilities. They also compared the performance of two defined subgroups of subjects with SDDs on expression analysis: one with normal and one with impaired recognition of facial identity. Results: While perception of facial expression was related to the perception of nonfacial expression, the perception of facial identity was not related to either facial or nonfacial expression. Likewise, subjects with SDDs with impaired facial identity processing perceived facial expression as well as those with normal facial identity processing. Conclusion: The processing of facial identity and that of facial expression are dissociable in social developmental disorders. Deficits in perceiving facial expression may be related to emotional processing more than face processing. Dissociations between the perception of facial identity and facial emotion are consistent with current cognitive models of face processing. The results argue against hypotheses that the social dysfunction in social developmental disorder causes a generalized failure to acquire face-processing skills. C1 Beth Israel Deaconess Med Ctr, Dept Neurol, Boston, MA 02215 USA. Beth Israel Deaconess Med Ctr, Dept Ophthalmol, Boston, MA 02215 USA. Harvard Univ, Sch Med, Boston, MA 02115 USA. Massachusetts Gen Hosp, Dept Psychiat, Boston, MA 02114 USA. Harvard Univ, Sch Med, Athinoula A Martinos Ctr Biomed Imaging, Boston, MA 02115 USA. Univ British Columbia, Dept Neurol, Vancouver, BC V5Z 1M9, Canada. Univ British Columbia, Dept Ophthalmol & Visual Sci, Vancouver, BC V5Z 1M9, Canada. RP Barton, JJS (reprint author), VGH Eye Care Ctr, Neuroophthalmol Sect D, 2550 Willow St, Vancouver, BC V5Z 3N9, Canada. EM jasonbarton@shaw.ca RI Barton, Jason/A-6362-2012 FU NIMH NIH HHS [1R01 MH069898] NR 49 TC 28 Z9 30 U1 5 U2 11 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3261 USA SN 0028-3878 J9 NEUROLOGY JI Neurology PD NOV 22 PY 2005 VL 65 IS 10 BP 1620 EP 1625 DI 10.1212/01.wnl.0000184498.16959.c0 PG 6 WC Clinical Neurology SC Neurosciences & Neurology GA 986CY UT WOS:000233428100020 PM 16301491 ER PT J AU Wills, AM Plante, DT Dukkipati, SR Corcoran, CP Standaert, DG AF Wills, AM Plante, DT Dukkipati, SR Corcoran, CP Standaert, DG TI Pacemaker-induced tachycardia caused by inappropriate response to parkinsonian tremor SO NEUROLOGY LA English DT Editorial Material C1 Massachusetts Gen Hosp, Dept Neurol, Boston, MA 02129 USA. Massachusetts Gen Hosp, Dept Psychiat, Boston, MA 02129 USA. Massachusetts Gen Hosp, Dept Cardiol, Boston, MA 02129 USA. RP Wills, AM (reprint author), Massachusetts Gen Hosp, Dept Neurol, CNY 16 St,114-2001, Boston, MA 02129 USA. EM awills@partners.org OI Standaert, David/0000-0003-2921-8348 NR 1 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3261 USA SN 0028-3878 J9 NEUROLOGY JI Neurology PD NOV 22 PY 2005 VL 65 IS 10 BP 1676 EP 1677 DI 10.1212/01.wnl.0000184489.74795.b2 PG 2 WC Clinical Neurology SC Neurosciences & Neurology GA 986CY UT WOS:000233428100040 PM 16301511 ER PT J AU Shinohara, ML Jansson, M Hwang, ES Werneck, MBF Glimcher, LH Cantor, H AF Shinohara, ML Jansson, M Hwang, ES Werneck, MBF Glimcher, LH Cantor, H TI T-bet-dependent expression of osteopontin contributes to T cell polarization SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE genetic programming; T helper 1 development; type-1 immune response ID NITRIC-OXIDE SYNTHASE; IFN-GAMMA PROMOTER; MEDIATED-IMMUNITY; DENDRITIC CELLS; DEFICIENT MICE; DISEASE; ATHEROSCLEROSIS; INHIBITION; CYTOKINE; GATA-3 AB The osteopontin (Opn) glycoprotein has been implicated in diverse physiological processes, including vascularization, bone formation, and inflammatory responses. Studies of its role in immune responses has suggested that Opn can set the early stage of type-1 immune (cell-mediated) responses through differential regulation of IL-12 and IL-10 cytokine gene expression in macrophages. Although Opn has been suggested to play a role in the development of type-1 immunity, little is known about control of Opn gene expression. Here, we report that Opn gene expression in activated T cells, but not macrophages, is regulated by T-bet, a transcription factor that controls CD4(+) T helper (Th1) cell lineage commitment. We also find that T-bet-dependent expression of Opn in T cells is essential for efficient skewing of CD4(+) T and CD8(+) T cells toward the Th1 and type 1 CD8(+) T cells (Tc1) pathway, respectively. Taken together, these findings begin to delineate the genetic basis of Opn expression in T cells and further clarify the role of Opn in Th and Tc1 development. C1 Harvard Univ, Sch Publ Hlth, Dana Farber Canc Inst, Dept Canc Immunol & AIDS, Boston, MA 02115 USA. Harvard Univ, Sch Publ Hlth, Dept Immunol & Infect Dis, Boston, MA 02115 USA. Harvard Univ, Sch Med, Dept Pathol, Boston, MA 02115 USA. Harvard Univ, Sch Med, Dept Med, Boston, MA 02115 USA. RP Cantor, H (reprint author), Harvard Univ, Sch Publ Hlth, Dana Farber Canc Inst, Dept Canc Immunol & AIDS, 44 Binney St, Boston, MA 02115 USA. EM harvey_cantor@dfci.harvard.edu RI Werneck, Miriam/H-5802-2012 FU NCI NIH HHS [CA 48126, T32 CA 70083, T32 CA070083]; NIAID NIH HHS [AI 56296, AI 12184, AI 48125, P01 AI056296, R01 AI048125, R37 AI012184] NR 29 TC 91 Z9 95 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 22 PY 2005 VL 102 IS 47 BP 17101 EP 17106 DI 10.1073/pnas.0508666102 PG 6 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA 986PW UT WOS:000233463200036 PM 16286640 ER PT J AU Chen, ZB Herman, AE Matos, M Mathis, D Benoist, C AF Chen, ZB Herman, AE Matos, M Mathis, D Benoist, C TI Where CD4(+) CD25(+) T reg cells impinge on autoimmune diabetes SO JOURNAL OF EXPERIMENTAL MEDICINE LA English DT Article ID TRANSCRIPTION FACTOR FOXP3; DENDRITIC CELLS; IN-VIVO; IMMUNE PATHOLOGY; HOMEOSTASIS; EXPANSION; MICE; COSTIMULATION; PROLIFERATION; RECRUITMENT AB Foxp3 is required for the generation and activity of CD4(+)CD25(+) regulatory T (T reg) cells, which are important controllers of autoimmunity, including type-1 diabetes. To determine where T reg cells affect the diabetogenic cascade, we crossed the Foxp3 scurfy mutation, which eliminates T reg cells, with the BDC2.5 T cell receptor ( TCR) transgenic mouse line. In this model, the absence of T reg cells did not augment the initial activation or phenotypic characteristics of effector T cells in the draining lymph nodes, nor accelerate the onset of T cell infiltration of the pancreatic islets. However, this insulitis was immediately destructive, causing a dramatic progression to overt diabetes. Microarray analysis revealed that T reg cells in the insulitic lesion adopted a gene expression program different from that in lymph nodes, whereas T reg cells in draining or irrelevant lymph nodes appeared very similar. Thus, T reg cells primarily impinge on autoimmune diabetes by reining in destructive T cells inside the islets, more than during the initial activation in the draining lymph nodes. 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 Benoist, C (reprint author), Harvard Univ, Sch Med, Joslin Diabet Ctr, Sect Immunol & Immunogenet, Boston, MA 02215 USA. EM cbdm@joslin.harvard.edu FU NIAID NIH HHS [P01 AI039671, P01-AI139671-09] NR 41 TC 194 Z9 199 U1 1 U2 10 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 21 PY 2005 VL 202 IS 10 BP 1387 EP 1397 DI 10.1084/jem.20051409 PG 11 WC Immunology; Medicine, Research & Experimental SC Immunology; Research & Experimental Medicine GA 986DK UT WOS:000233429500009 PM 16301745 ER PT J AU Arroyo, JD Hahn, WC AF Arroyo, JD Hahn, WC TI Involvement of PP2A in viral and cellular transformation SO ONCOGENE LA English DT Review DE protein phosphatase 2A; SV40ST; transformation ID PROTEIN PHOSPHATASE 2A; SMALL-T-ANTIGEN; SMALL TUMOR-ANTIGEN; SV40 LARGE-T; SIMIAN-VIRUS-40 LARGE-T; ANCHORAGE-INDEPENDENT GROWTH; PPP2R1B GENE ALTERATIONS; REGULATORY-A-SUBUNIT; MAP KINASE PATHWAY; VIRUS 40 GENE AB Although the small DNA tumor virus SV40 ( simian virus 40) fails to replicate in human cells, understanding how SV40 transforms human and murine cells has and continues to provide important insights into cancer initiation and maintenance. The early region of SV40 encodes two oncoproteins: the large T ( LT) and small t ( ST) antigens. SV40 LT contributes to murine and human cell transformation in part by inactivating the p53 and retinoblastoma protein tumor suppressor proteins. SV40 ST inhibits the activity of the protein phosphatase 2A ( PP2A) family of serine-threonine phosphatases, and this interaction is required for SV40-mediated transformation of human cells. PP2A regulates multiple signaling pathways, suggesting many possible targets important for viral replication and cell transformation. Genetic manipulation of particular PP2A subunits has confirmed a role for specific complexes in transformation, and recent work implicates the perturbation of the phosphatidylinositol 3-kinase/Akt pathway and c-Myc stability in transformation by ST and PP2A. Mutations in PP2A subunits occur at low frequency in human tumors, suggesting that alterations of PP2A signaling play a role in both experimentally induced and spontaneously arising cancers. Unraveling the complexity of PP2A signaling will not only provide further insights into cancer development but may identify novel targets with promise for therapeutic manipulation. C1 Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02115 USA. Brigham & Womens Hosp, Dept Med, Boston, MA 02115 USA. Harvard Univ, Sch Med, Dept Pathol, Boston, MA 02115 USA. Harvard Univ, Sch Med, Dept Med, Boston, MA 02115 USA. MIT, Broad Inst, Cambridge, MA 02139 USA. Harvard Univ, Broad Inst, Cambridge, MA 02139 USA. RP Hahn, WC (reprint author), Dana Farber Canc Inst, Dept Med Oncol, 44 Binney St,Dana 710C, Boston, MA 02115 USA. EM william_hahn@dfci.harvard.edu OI Arroyo, Jason/0000-0002-5674-6739 FU NCI NIH HHS [K01 CA94223, P01 CA50661] NR 143 TC 148 Z9 158 U1 0 U2 8 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 21 PY 2005 VL 24 IS 52 BP 7746 EP 7755 DI 10.1038/sj.onc.1209038 PG 10 WC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity GA 985JD UT WOS:000233372600010 PM 16299534 ER PT J AU Aghi, M Martuza, RL AF Aghi, M Martuza, RL TI Oncolytic viral therapies - the clinical experience SO ONCOGENE LA English DT Review DE oncolytic virus; clinical trials; adenovirus; herpesvirus; vaccinia virus; Newcastle disease virus ID HERPES-SIMPLEX-VIRUS; REPLICATION-SELECTIVE ADENOVIRUS; PHASE-I TRIAL; RECURRENT PROSTATE-CANCER; NEWCASTLE-DISEASE VIRUS; SUICIDE GENE-THERAPY; LONG-TERM SURVIVAL; NECK-CANCER; ATTENUATED ADENOVIRUS; MALIGNANT GLIOMA AB It has been 9 years since the beginning of the first clinical trial in which an oncolytic virus was administered to cancer patients. Since then, oncolytic viruses from five different species have been taken to phase I and II clinical trials in over 300 cancer patients. While additional studies will be required to ascertain if the efficacy of any of these agents is high enough to warrant adding them to the existing therapeutic regimen, it has been reassuring that DNA viruses engineered to achieve tumor selectivity and RNA viruses with relative inherent natural tumor selectivity have proven reasonably safe at the wide range of doses that were tested. Here, we review the biology and clinical results of these five species of viruses and discuss lessons learned and challenges for the future. C1 Massachusetts Gen Hosp, Dept Neurosurg, Boston, MA 02114 USA. RP Aghi, M (reprint author), Massachusetts Gen Hosp, Dept Neurosurg, White Bldg Room 502,55 Fruit St, Boston, MA 02114 USA. EM maghi@partners.org NR 69 TC 186 Z9 188 U1 4 U2 19 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 21 PY 2005 VL 24 IS 52 BP 7802 EP 7816 DI 10.1038/sj.onc.1209037 PG 15 WC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity GA 985JD UT WOS:000233372600015 PM 16299539 ER PT J AU Newhauser, W Koch, N Hummel, S Ziegler, M Titt, U AF Newhauser, W Koch, N Hummel, S Ziegler, M Titt, U TI Monte Carlo simulations of a nozzle for the treatment of ocular tumours with high-energy proton beams SO PHYSICS IN MEDICINE AND BIOLOGY LA English DT Article ID NEUTRON DOSE-EQUIVALENT; SECONDARY NEUTRON; UVEAL MELANOMA; THERAPY; ALGORITHM; DOSIMETRY; FLUENCE; EYE; IMPLEMENTATION; IRRADIATION AB By the end of 2002, 33 398 patients worldwide had been treated with proton radiotherapy, 10829 for eye diseases. The dose prediction algorithms used today for Ocular proton therapy treatment planning rely on parameterizations of measured proton dose distributions, i.e., broad-beam and pencil-beam techniques, whose predictive capabilities are inherently limited by severe approximations and simplifications in modelling the radiation transport physics. In contrast, the Monte Carlo radiation transport technique can, in principle, provide accurate predictions of the proton treatment beams by taking into account all the physical processes involved, including coulombic energy loss, energy straggling, multiple Coulomb scattering, elastic and nonelastic nuclear interactions, and the transport of secondary particles. It has not been shown, however, whether it is possible to commission a proton treatment planning system by using data exclusively from Monte Carlo Simulations of the treatment apparatus and a phantom. In this work, we made benchmark comparisons between Monte Carlo predictions and measurements of an ocular proton treatment beamline. The maximum differences between absorbed dose profiles from simulations and measurements were 6% and 0.6 mm, while typical differences were less than 2% and 0.2 mm. The computation time for the entire virtual commissioning process is less than one day. The study revealed that, after a significant development effort, it Monte Carlo model of a proton therapy apparatus is sufficiently accurate and fast for commissioning a treatment planning system. C1 Univ Texas, MD Anderson Canc Ctr, Houston, TX 77030 USA. Univ Texas, Grad Sch Biomed Sci, Houston, TX 77030 USA. Univ Calif Los Angeles, Los Angeles, CA 90024 USA. Massachusetts Gen Hosp, Boston, MA 02114 USA. RP Newhauser, W (reprint author), Univ Texas, MD Anderson Canc Ctr, 1515 Holcombe Blvd, Houston, TX 77030 USA. EM wnewhaus@mdanderson.org NR 58 TC 54 Z9 54 U1 0 U2 3 PU IOP PUBLISHING LTD PI BRISTOL PA DIRAC HOUSE, TEMPLE BACK, BRISTOL BS1 6BE, ENGLAND SN 0031-9155 J9 PHYS MED BIOL JI Phys. Med. Biol. PD NOV 21 PY 2005 VL 50 IS 22 BP 5229 EP 5249 DI 10.1088/0031-9155/50/22/002 PG 21 WC Engineering, Biomedical; Radiology, Nuclear Medicine & Medical Imaging SC Engineering; Radiology, Nuclear Medicine & Medical Imaging GA 993RR UT WOS:000233973100003 PM 16264250 ER PT J AU Burstein, HJ Parker, LM Keshaviah, A Doherty, J Partridge, AH Schapira, L Ryan, PD Younger, J Harris, LN Moy, B Come, SE Schumer, ST Bunnell, CA Haldoupis, M Gelman, R Winer, EP AF Burstein, HJ Parker, LM Keshaviah, A Doherty, J Partridge, AH Schapira, L Ryan, PD Younger, J Harris, LN Moy, B Come, SE Schumer, ST Bunnell, CA Haldoupis, M Gelman, R Winer, EP TI Efficacy of pegfilgrastim and darbepoetin alfa as hematopoietic support for dose-dense every-2-week adjuvant breast cancer chemotherapy SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Article ID QUALITY-OF-LIFE; PATIENTS RECEIVING CHEMOTHERAPY; WEEKLY EPOETIN-ALPHA; INDUCED ANEMIA; DOUBLE-BLIND; TRIAL; DOXORUBICIN; PACLITAXEL; HEMOGLOBIN; THERAPY AB Purpose Dose-dense, every-2-week adjuvant chemotherapy using doxorubicin/cyclophosphamide (AC; 60/600 mg/m(2) every 2 weeks X four cycles) followed by paclitaxel (175 mg/m(2) every 2 weeks X four cycles), requiring filgrastim on days 3 through 10 of each cycle has been shown to improve survival compared with every-3-week treatment schedules but is associated with greater risk of BBC transfusion (13%). The role of long-acting hematopoietic growth factors in facilitating every-2-week chemotherapy and minimizing hematologic toxicity has not been established. Patients and Methods Women with stage I to III breast cancer received dose-dense AC -> paclitaxel as neoadjuvant or adjuvant chemotherapy. Patients received pegfilgrastim 6 mg subcutaneous (SQ) on day 2 of each cycle. Darbepoetin alfa was initiated at 200 mu g SO every 2 weeks for hemoglobin <= 12 g/dL, and administered thereafter, according to a preplanned algorithm. The primary end points were to evaluate the percentage of patients with febrile neutropenia and the percentage of patients requiring BBC transfusion. Results Among 135 women treated on this single arm study, there were two cases of febrile neutropenia (incidence 1.5%). No patients received BBC transfusion. Darbepoetin alfa therapy was initiated in 92% of patients. The modest leukocytosis seen during paclitaxel cycles was attributable, in part, to corticosteroid premedication. Other toxicity and dose-delivery were similar to dose-dense AC -> paclitaxel in Cancer and Leukemia Group B 9741. Conclusion Pegfilgrastim and darbepoetin alfa are effective and safe in facilitating every-2-week AC paclitaxel, minimizing rates of febrile neutropenia and BBC transfusion. C1 Dana Farber Canc Inst, Boston, MA 02115 USA. Brigham & Womens Hosp, Boston, MA 02115 USA. Massachusetts Gen Hosp, Boston, MA 02114 USA. Beth Israel Deaconess Med Ctr, Boston, MA 02215 USA. Harvard Univ, Sch Med, Boston, MA 02115 USA. RP Burstein, HJ (reprint author), Dana Farber Canc Inst, 44 Binney St, Boston, MA 02115 USA. EM hburstein@partners.org NR 19 TC 40 Z9 41 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 20 PY 2005 VL 23 IS 33 BP 8340 EP 8347 DI 10.1200/JCO.2005.02.8621 PG 8 WC Oncology SC Oncology GA 985XJ UT WOS:000233411700011 PM 16293865 ER PT J AU Meyerhardt, JA Heseltine, D Campos, H Holmes, MD Willett, WC Winer, EP Enzinger, PC Bunnell, CA Kulke, MH Fuchs, CS AF Meyerhardt, JA Heseltine, D Campos, H Holmes, MD Willett, WC Winer, EP Enzinger, PC Bunnell, CA Kulke, MH Fuchs, CS TI Assessment of a dietary questionnaire in cancer patients receiving cytotoxic chemotherapy SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Article ID FOOD-FREQUENCY QUESTIONNAIRE; VITAMIN-E INTAKE; ALPHA-TOCOPHEROL; BREAST-CANCER; PROSTATE-CANCER; CISPLATIN CHEMOTHERAPY; GAMMA-TOCOPHEROL; BETA-CAROTENE; COLON-CANCER; LUNG-CANCER AB Purpose Few studies have examined the influence of diet on survival and chemotherapy-associated toxicities in patients with cancer. Although several comprehensive dietary questionnaires have been validated and calibrated in healthy populations, similar studies have not been performed among cancer patients. Methods Two hundred patients with colorectal, breast, or neuroendocrine cancer undergoing treatment with cytotoxic chemotherapy completed a self-administered, 131-item, semiquantitative food frequency questionnaire. Using the questionnaire, we calculated dietary intakes of carotenoids, tocopherols, and fatty acids, and correlated these values with relevant biomarkers measured in simultaneously collected plasma specimens. Results The Pearson correlation coefficients for various carotenoids as measured by the questionnaire, with the corresponding measurements in plasma specimens, ranged from 0.33 to 0.44 (all P <.001), adjusted for total energy intake, body mass index, age, sex, smoking status, and total plasma cholesterol. Similarly, the adjusted correlation between self-reported total vitamin E intake and plasma alpha-tocopherol was 0.34 (P < .001). Correlations between questionnaire and plasma measurements of trans-fat, eicosapentaenoic acid, and docosahexaenoic acid were 0.55, 0.29, and 0.42 (all P < .001), respectively. These levels of correlation are consistent with those reported in similar studies of self-reported diet in otherwise healthy populations. Conclusion Among patients with cancer receiving cytotoxic chemotherapy, questionnaire-based measurements of various micronutrients and dietary factors appeared to predict meaningful differences in the corresponding measurements in plasma specimens. This dietary questionnaire could offer an informative and practical means for assessing the influence of diet in cancer patients receiving chemotherapy. C1 Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02115 USA. Harvard Univ, Sch Publ Hlth, Dept Nutr & Epidemiol, Boston, MA 02115 USA. Brigham & Womens Hosp, Channing Lab, Dept Med, Boston, MA 02115 USA. RP Meyerhardt, JA (reprint author), Dana Farber Canc Inst, Dept Med Oncol, 44 Binney St, Boston, MA 02115 USA. EM jmeyerhardt@partners.org FU NCI NIH HHS [K07CA097992] NR 62 TC 9 Z9 9 U1 2 U2 3 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 20 PY 2005 VL 23 IS 33 BP 8453 EP 8460 DI 10.1200/JCO.2005.02.5460 PG 8 WC Oncology SC Oncology GA 985XJ UT WOS:000233411700025 PM 16293876 ER PT J AU Malo, MS Pushpakaran, P Hodin, RA AF Malo, MS Pushpakaran, P Hodin, RA TI A 'Swinging Cradle' model for in vitro classification of different types of response elements of a nuclear receptor SO BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS LA English DT Article DE 3-4-5 rule; binding site; crystal structure; electrophoretic mobility shift assay; nuclear receptor; promoter; response elements; retinoic acid; thyroid hormone; vitamin D ID THYROID-HORMONE; DIRECT REPEATS; RETINOIC ACID; DNA-BINDING; GENE; DETERMINANTS; SPECIFICITY; SUPERFAMILY; MECHANISMS AB Nuclear receptors are hormone-activated transcription factors that bind to specific target sequences termed hormone-response element (HRE). A HRE usually consists of two half-sites (5'-AGGTCA-3' consensus sequence) arranged as a direct, everted or inverted repeat with variable spacer region. Assignment of a HRE as a direct, everted or inverted repeat is based on its homology to the consensus half-site, but minor variations can make such an assignment confusing. We hypothesize a 'Swinging Cradle' model for HRE classification, whereby the core HRE functions as the "sitting platform" for the NR, and the extra nucleotides at either end act as the "sling" of the Cradle. We show that in vitro binding of the thyroid hormone receptor and 9-cis retinoic acid receptor heterodimer to an everted repeat TRE follows the 'Swinging Cradle' model, whereas the other TREs do not. We also show that among these TREs, the everted repeat mediates the highest biological activity. (c) 2005 Elsevier Inc. All rights reserved. C1 Harvard Univ, Sch Med, Massachusetts Gen Hosp, Dept Surg, Boston, MA 02114 USA. RP Hodin, RA (reprint author), Harvard Univ, Sch Med, Massachusetts Gen Hosp, Dept Surg, Boston, MA 02114 USA. EM rhodin@partners.org RI pushpakaran, dr prem raj/D-3540-2009 OI pushpakaran, dr prem raj/0000-0002-2289-5277 FU NIDDK NIH HHS [DK47186, DK50623] NR 18 TC 1 Z9 1 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 0006-291X J9 BIOCHEM BIOPH RES CO JI Biochem. Biophys. Res. Commun. PD NOV 18 PY 2005 VL 337 IS 2 BP 490 EP 497 DI 10.1016/j.bbrc.2005.09.080 PG 8 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA 977ZF UT WOS:000232841300013 PM 16198314 ER PT J AU Lenz, G Avruch, J AF Lenz, G Avruch, J TI Glutamatergic regulation of the p70S6 kinase in primary mouse neurons SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID LONG-TERM POTENTIATION; LOCAL PROTEIN-SYNTHESIS; METHYL-D-ASPARTATE; HIPPOCAMPAL-NEURONS; SYNAPTIC PLASTICITY; CORTICAL-NEURONS; CA1 REGION; RECEPTOR; ACTIVATION; MEMORY AB Brief glutamatergic stimulation of neurons from fetal mice, cultured in vitro for 6 days, activates the mTOR-S6 kinase, ERK1/2 and Akt pathways, to an extent approaching that elicited by brain-derived neurotrophic factor. In contrast, sustained glutamatergic stimulation inhibits ERK, Akt, and S6K. Glutamatergic activation of S6K is calcium/calmodulin-dependent and is prevented by inhibitors of calcium/calmodulin-dependent protein kinase 2, phosphatidylinositol 3-OH-kinase and by rapamycin. 2-Amino-5- phosphonovaleric acid, an inhibitor of N'-methyl-D-aspartate receptors, abolishes glutamatergic activation of ERK1/2 but not the activation of mTOR-S6K; the latter is completely abolished by inhibitors of voltage-dependent calcium channels. Added singly, dopamine gives slight, and norepinephrine a more significant, activation of ERK and S6K; both catecholeamines, however, enhance glutamatergic activation of S6K but not ERK. After 12 days in culture, the response to direct glutamatergic activation is attenuated but can be uncovered by suppression of gamma-aminobutyric acid interneurons with bicuculline in the presence of the weak K+ channel blocker 4-aminopyridine (4-AP). This selective synaptic activation of mTOR-S6K is also resistant to APV and inhibited by Ca2+ channel blockers and higher concentrations of glutamate. Elongation factor 2 (EF2) is phosphorylated and inhibited by the eEF2 kinase (CaM kinase III); the latter is inhibited by the S6K or Rsk. Bicuculline/4-AP or KCl-induced depolarization reduces, whereas higher concentrations of glutamate increases, EF2 phosphorylation. Thus the mTOR-S6K pathway in neurons, a critical component of the late phase of LTP, is activated by glutamatergic stimulation in a calcium/calmodulin-dependent fashion through a calcium pool controlled by postsynaptic voltage-dependent calcium channels, whereas sustained stimulation of extrasynaptic glutamate receptors is inhibitory. C1 Massachusetts Gen Hosp, Dept Mol Biol, Boston, MA 02114 USA. Massachusetts Gen Hosp, Diabet Unit, Boston, MA 02114 USA. Massachusetts Gen Hosp, Med Serv, Boston, MA 02114 USA. Harvard Univ, Sch Med, Dept Med, Boston, MA 02114 USA. Univ Fed Rio Grande Sul, Dept Biophys, IB, BR-91501970 Porto Alegre, RS, Brazil. RP Avruch, J (reprint author), Dept Mol Biol, Richard B Simches Res Bldg,6th Floor,185 Cambridg, Boston, MA 02114 USA. EM avruch@molbio.mgh.harvard.edu RI Lenz, Guido/A-7618-2008 FU NCI NIH HHS [CA73818]; NIDDK NIH HHS [DK17776] NR 32 TC 94 Z9 97 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 18 PY 2005 VL 280 IS 46 BP 38121 EP 38124 DI 10.1074/jbc.C500363200 PG 4 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA 983NR UT WOS:000233239800003 PM 16183639 ER PT J AU Ijiri, K Zerbini, LF Peng, HB Correa, RG Lu, BF Walsh, N Zhao, YN Taniguchi, N Huang, XL Otu, H Wang, H Wang, JF Komiya, S Ducy, P Rahman, MU Flavell, RA Gravallese, EM Oettgen, P Libermann, TA Goldring, MB AF Ijiri, K Zerbini, LF Peng, HB Correa, RG Lu, BF Walsh, N Zhao, YN Taniguchi, N Huang, XL Otu, H Wang, H Wang, JF Komiya, S Ducy, P Rahman, MU Flavell, RA Gravallese, EM Oettgen, P Libermann, TA Goldring, MB TI A novel role for GADD45 beta as a mediator of MMP-13 gene expression during chondrocyte terminal differentiation SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID BONE MORPHOGENETIC PROTEIN-2; GROWTH-FACTOR-BETA; NF-KAPPA-B; X COLLAGEN GENE; TRANSCRIPTION FACTOR; IN-VIVO; HYPERTROPHIC CHONDROCYTES; ENDOCHONDRAL OSSIFICATION; SKELETAL MORPHOGENESIS; CBFA1-DEFICIENT MICE AB The growth arrest and DNA damage-inducible 45 beta(GADD45 beta) gene product has been implicated in the stress response, cell cycle arrest, and apoptosis. Here we demonstrated the unexpected expression of GADD45 beta in the embryonic growth plate and uncovered its novel role as an essential mediator of matrix metalloproteinase-13 (MMP-13) expression during terminal chondrocyte differentiation. We identified GADD45 beta as a prominent early response gene induced by bone morphogenetic protein-2 (BMP-2) through a Smad1/Runx2-dependent pathway. Because this pathway is involved in skeletal development, we examined mouse embryonic growth plates, and we observed expression of Gadd45 beta mRNA coincident with Runx2 protein in pre-hypertrophic chondrocytes, whereas GADD45 beta protein was localized prominently in the nucleus in late stage hypertrophic chondrocytes where Mmp-13 mRNA was expressed. In Gadd45 beta(-/-) mouse embryos, defective mineralization and decreased bone growth accompanied deficient Mmp-13 and Col10a1 gene expression in the hypertrophic zone. Transduction of small interfering RNA-GADD45 beta in epiphyseal chondrocytes in vitro blocked terminal differentiation and the associated expression of Mmp-13 and Col10a1 mRNA in vitro. Finally, GADD45 beta stimulated MMP-13 promoter activity in chondrocytes through the JNK-mediated phosphorylation of JunD, partnered with Fra2, in synergy with Runx2. These observations indicated that GADD45 beta plays an essential role during chondrocyte terminal differentiation. C1 Harvard Univ, Sch Med, Inst Med, Boston, MA 02115 USA. Beth Israel Deaconess Med Ctr, New England Baptist Bone & Joint Inst, Boston, MA 02115 USA. Beth Israel Deaconess Med Ctr, Genom Ctr, Boston, MA 02115 USA. Salk Inst Biol Studies, Genet Lab, La Jolla, CA 92037 USA. Univ Pittsburgh, Sch Med, Dept Immunol, Pittsburgh, PA 15261 USA. Kagoshima Univ, Grad Sch Med & Dent, Dept Neuromusculoskeletal Disorders, Kagoshima 8908520, Japan. Baylor Coll Med, Dept Mol & Human Genet, Houston, TX 77030 USA. Massachusetts Gen Hosp, Ctr Immunol & Inflammatory Dis, Boston, MA 02114 USA. Yale Univ, Sch Med, Howard Hughes Med Inst, New Haven, CT 06520 USA. RP Goldring, MB (reprint author), Harvard Univ, Sch Med, Inst Med, HIM 246,4 Blackfan Circle, Boston, MA 02115 USA. EM mgoldrin@bidmc.harvard.edu RI Libermann, Towia/F-9866-2010; Correa, Ricardo/G-7613-2012; Wang, Hong/H-6298-2012; Zhao, Yani/A-1968-2013; Zerbini, Luiz /B-7720-2015; OI Correa, Ricardo/0000-0001-6940-7034; Libermann, Towia/0000-0002-4006-8179; Otu, Hasan/0000-0002-9253-8152 FU NIA NIH HHS [R01 AG022021, R01-AG22021]; NIAID NIH HHS [R01 AI049527, R01-AI49527]; NIAMS NIH HHS [R01-AR45378] NR 90 TC 60 Z9 63 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 18 PY 2005 VL 280 IS 46 BP 38544 EP 38555 DI 10.1074/jbc.M504202200 PG 12 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA 983NR UT WOS:000233239800053 PM 16144844 ER PT J AU Muroyama, Y Fujiwara, Y Orkin, SH Rowitch, DH AF Muroyama, Y Fujiwara, Y Orkin, SH Rowitch, DH TI Specification of astrocytes by bHLH protein SCL in a restricted region of the neural tube SO NATURE LA English DT Article ID SPINAL-CORD; STEM-CELLS; MOTOR-NEURON; GENE-EXPRESSION; V2 INTERNEURONS; SCL/TAL-1; IDENTITY; DIFFERENTIATION; PRECURSORS AB Astrocytes are the most abundant and functionally diverse glial population in the vertebrate central nervous system (CNS)(1). However, the mechanisms underlying astrocyte specification are poorly understood. It is well established that cellular diversification of neurons in the embryo is generated by position-dependent extrinsic signals and combinatorial interactions of transcription factors that direct specific cell fates by suppressing alternative fates(2). It is unknown whether a comparable process determines embryonic astrocyte identity. Indeed, astrocyte development is generally thought to take place in a position-independent manner(3,4). Here we show multiple functions of Stem cell leukaemia (Scl, also known as Tal1), which encodes a basic helix-loop-helix (bHLH) transcription factor, in the regulation of both astrocyte versus oligodendrocyte cell fate acquisition and V2b versus V2a interneuron cell fate acquisition in the p2 domain of the developing vertebrate spinal cord. Our findings demonstrate a regionally restricted transcriptional programme necessary for astrocyte and V2b interneuron development, with striking parallels to the involvement of SCL in haematopoiesis. They further indicate that acquisition of embryonic glial subtype identity might be regulated by genetic interactions between SCL and the transcription factor Olig2 in the ventral neural tube. C1 Dana Farber Canc Inst, Dept Pediat Oncol, Boston, MA 02115 USA. Childrens Hosp, Howard Hughes Med Inst, Boston, MA 02115 USA. Childrens Hosp, Div Hematol, Boston, MA 02115 USA. Childrens Hosp, Div Newborn Med, Boston, MA 02115 USA. RP Dana Farber Canc Inst, Dept Pediat Oncol, 44 Binney St, Boston, MA 02115 USA. EM stuart_orkin@dfci.harvard.edu; david_rowitch@dfci.harvard.edu OI Muroyama, Yuko/0000-0002-6697-2123 NR 30 TC 98 Z9 99 U1 2 U2 11 PU NATURE PUBLISHING GROUP PI LONDON PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND SN 0028-0836 EI 1476-4687 J9 NATURE JI Nature PD NOV 17 PY 2005 VL 438 IS 7066 BP 360 EP 363 DI 10.1038/nature04139 PG 4 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA 984JR UT WOS:000233300200049 PM 16292311 ER PT J AU Smith, BL Kopans, DB Koerner, FC Morrow, M Davidson, NE Partridge, AH Harris, NL AF Smith, BL Kopans, DB Koerner, FC Morrow, M Davidson, NE Partridge, AH Harris, NL TI Case 35-2005: A 56-year-old woman with breast cancer and isolated tumor cells in a sentinel lymph node - Invasive ductal carcinoma of the breast with isolated tumor cells in a sentinel lymph node (T1b pN0 (i+)) SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Editorial Material ID NONSENTINEL AXILLARY NODES; ADJUVANT THERAPY; RANDOMIZED-TRIAL; FOLLOW-UP; POSTOPERATIVE RADIOTHERAPY; NATURAL-HISTORY; CLINICAL-TRIAL; DISSECTION; METASTASES; BIOPSY C1 Johns Hopkins Univ, Sch Med, Baltimore, MD 21218 USA. Fox Chase Canc Ctr, Philadelphia, PA 19111 USA. Massachusetts Gen Hosp, Dept Radiol, Boston, MA 02114 USA. Massachusetts Gen Hosp, Dept Pathol, Boston, MA 02114 USA. Harvard Univ, Sch Med, Boston, MA USA. RP Smith, BL (reprint author), Johns Hopkins Univ, Sch Med, Baltimore, MD 21218 USA. NR 53 TC 3 Z9 3 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 17 PY 2005 VL 353 IS 20 BP 2177 EP 2185 PG 9 WC Medicine, General & Internal SC General & Internal Medicine GA 984FT UT WOS:000233288600012 PM 16291988 ER PT J AU Tubman, VN Levine, JE Campagna, DR Fleming, MD Neufeld, EJ AF Tubman, VN Levine, JE Campagna, DR Fleming, MD Neufeld, EJ TI X-linked gray platelet syndrome due to a GATA1 Arg216GIn mutation. SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 Univ Penn, Sch Med, Philadelphia, PA 19104 USA. Harvard Univ, Childrens Hosp, Sch Med, Dana Farber Canc Inst, Boston, MA 02115 USA. RI Neufeld, Ellis/F-9331-2011 NR 0 TC 5 Z9 5 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 2005 VL 106 IS 11 MA 5 BP 6A EP 6A PN 1 PG 1 WC Hematology SC Hematology GA 986CF UT WOS:000233426000006 ER PT J AU Gorgun, G Holderried, TAW Ledieu, R Zahrieh, D Gribben, JG AF Gorgun, G Holderried, TAW Ledieu, R Zahrieh, D Gribben, JG TI CLL cells in TCL1 transgenic mice induce similar defects in CD4 and CD8 T cells to those observed in patients with CLL. SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 Dana Farber Canc Inst, CLL Res Consortium, Boston, MA 02115 USA. Barts & London Sch Med, CLL Res Consortium, Canc Res UK Med Oncol Unit, London, England. 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 2005 VL 106 IS 11 MA 50 BP 19A EP 19A PN 1 PG 1 WC Hematology SC Hematology GA 986CF UT WOS:000233426000051 ER PT J AU Mauerer, K Gorgun, G Zahrieh, D Gribben, JG AF Mauerer, K Gorgun, G Zahrieh, D Gribben, JG TI Successful generation of cytotoxic T-cells that kill CLL cells using heteroclitic peptides is independent of the native peptide binding affinity to HLA-A*0201. SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 Harvard Univ, Sch Med, Dana Farber Canc Inst, Boston, MA 02115 USA. Barts & London Sch Med, Inst Canc, CLL Res Corp, London, England. NR 0 TC 0 Z9 0 U1 0 U2 1 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2005 VL 106 IS 11 MA 54 BP 20A EP 21A PN 1 PG 2 WC Hematology SC Hematology GA 986CF UT WOS:000233426000055 ER PT J AU Ledieu, R Gorgun, G Gribben, JG AF Ledieu, R Gorgun, G Gribben, JG TI In vivo demonstration of donor idiotype specific T cells that kill primary CLL cells post allogeneic transplant. SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 St Bartholomews Hosp, CRUK Med Oncol Unit, London, England. 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 2005 VL 106 IS 11 MA 62 BP 23A EP 23A PN 1 PG 1 WC Hematology SC Hematology GA 986CF UT WOS:000233426000063 ER PT J AU Van Vlierberghe, P Meijerink, JPP Lee, C Ferrando, AA Look, AT van Wering, ER Beverloo, HB Aster, JC Pieters, R AF Van Vlierberghe, P Meijerink, JPP Lee, C Ferrando, AA Look, AT van Wering, ER Beverloo, HB Aster, JC Pieters, R TI A new recurrent 9q34 duplication in pediatric T-cell acute lymphoblastic leukemia. SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 Erasmus MC, Sophia Childrens Hosp, Dept Pediat Oncol Hematol, Rotterdam, Netherlands. Erasmus MC, Dept Clin Genet, Rotterdam, Netherlands. Harvard Univ, Brigham & Womens Hosp, Sch Med, Dept Pathol, Boston, MA 02115 USA. Dana Farber Canc Inst, Dept Pediat Oncol, Boston, MA 02115 USA. DCOG, The Hague, Netherlands. RI Van Vlierberghe, Pieter/G-8894-2013 OI Van Vlierberghe, Pieter/0000-0001-9063-7205 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 2005 VL 106 IS 11 MA 89 BP 30A EP 30A PN 1 PG 1 WC Hematology SC Hematology GA 986CF UT WOS:000233426000090 ER PT J AU Tissing, WJE den Boer, ML Meijerink, JPP Menezes, RX Swagemakers, S van der Spek, PJ Sallan, SE Armstrong, S Pieters, R AF Tissing, WJE den Boer, ML Meijerink, JPP Menezes, RX Swagemakers, S van der Spek, PJ Sallan, SE Armstrong, S Pieters, R TI Genome-wide identification of prednisolone-responsive genes in primary acute lymphoblastic leukemia cells. SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 Sophia Childrens Univ Hosp, Erasmus MC, Rotterdam, Netherlands. Univ Groningen, Med Ctr, Beatrix Children Clin, Groningen, Netherlands. Leiden Univ, Med Ctr, Leiden, Netherlands. Erasmus MC, Rotterdam, Netherlands. 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 2005 VL 106 IS 11 MA 103 BP 34A EP 35A PN 1 PG 2 WC Hematology SC Hematology GA 986CF UT WOS:000233426000104 ER PT J AU Armstrong, SA Wei, G Lamb, J Opferman, J Twomey, D Stam, R den Boer, M Sallan, SE Pieters, R Golub, TR AF Armstrong, SA Wei, G Lamb, J Opferman, J Twomey, D Stam, R den Boer, M Sallan, SE Pieters, R Golub, TR TI A gene expression connectivity map identifies rapamycin as a glucocorticoid resistance reversal agent in lymphoblastic leukemia. SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 Childrens Hosp, Boston, MA 02115 USA. Dana Farber Canc Inst, Boston, MA 02115 USA. St Jude Childrens Res Hosp, Memphis, TN USA. Sophia Childrens Univ Hosp, Rotterdam, Netherlands. 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 2005 VL 106 IS 11 MA 108 BP 36A EP 36A PN 1 PG 1 WC Hematology SC Hematology GA 986CF UT WOS:000233426000109 ER PT J AU Chauhan, D Velankar, M Hideshima, T Mitsiades, C Catley, L Raje, N Schlossman, R Richardson, P Anderson, KC AF Chauhan, D Velankar, M Hideshima, T Mitsiades, C Catley, L Raje, N Schlossman, R Richardson, P Anderson, KC TI Targeting Bcl-2 as therapy for multiple myeloma. SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 Dana Farber Canc Inst, Boston, MA 02115 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 2005 VL 106 IS 11 MA 109 BP 36A EP 36A PN 1 PG 1 WC Hematology SC Hematology GA 986CF UT WOS:000233426000110 ER PT J AU Wang, M Talpaz, M Jagannath, S Chanan-Khan, AA Alexanian, R Weber, DM Gavino, M Estrov, Z Harris, PJ Picker, D Schlossman, RL Tassone, P Anderson, KC Munshi, NC AF Wang, M Talpaz, M Jagannath, S Chanan-Khan, AA Alexanian, R Weber, DM Gavino, M Estrov, Z Harris, PJ Picker, D Schlossman, RL Tassone, P Anderson, KC Munshi, NC TI A phase 1, multi-center, dose escalation study of atiprimod in patients with refractory or relapsed multiple myeloma (MM). SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 Univ Texas, MD Anderson Canc Ctr, Houston, TX 77030 USA. St Vincents Comprehens Canc Ctr, New York, NY USA. Roswell Pk Canc Inst, Buffalo, NY 14263 USA. Callisto Pharmaceut, New York, NY 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 2005 VL 106 IS 11 MA 111 BP 36A EP 37A PN 1 PG 2 WC Hematology SC Hematology GA 986CF UT WOS:000233426000112 ER PT J AU Levine, RL Belisle, C Wadleigh, M Lee, SJ Chagnon, P Gilliland, DG Busque, L AF Levine, RL Belisle, C Wadleigh, M Lee, SJ Chagnon, P Gilliland, DG Busque, L TI X-linked clonality analysis and quantitative JAK2V617F assessment reveals a strong association between clonality and JAK2V617F in PV but not in ET/MMM, and identifies a subset of JAK2V617F negative ET and MMM patients with clonal hematopoiesis. SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 Brigham & Womens Hosp, Div Hematol, Boston, MA 02115 USA. Hop Maison Neuve Rosemont, Dept Hematol, Montreal, PQ H1T 2M4, Canada. Dana Farber Canc Inst, Div Med Oncol, Boston, MA 02115 USA. Harvard Univ, Sch Med, 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 2005 VL 106 IS 11 MA 117 BP 38A EP 38A PN 1 PG 1 WC Hematology SC Hematology GA 986CF UT WOS:000233426000118 ER PT J AU Berkofsky-Fessler, W McConnell, MJ Huang, K Bailey, ML Barber, DL Levine, RL Neuberg, DS Gilliland, DG Licht, JD AF Berkofsky-Fessler, W McConnell, MJ Huang, K Bailey, ML Barber, DL Levine, RL Neuberg, DS Gilliland, DG Licht, JD TI The transcriptional profile of PV displays limited similarity to EPO stimulated progenitor cells: Evidence that JAK2 V617F confers a novel program to malignant hematopoietic stem cells. SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 Mt Sinai Sch Med, New York, NY USA. Ontario Canc Inst, Toronto, ON M4X 1K9, 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 2005 VL 106 IS 11 MA 120 BP 39A EP 39A PN 1 PG 1 WC Hematology SC Hematology GA 986CF UT WOS:000233426000121 ER PT J AU Ebert, BL Levine, RL Wadleigh, M Brunet, JP Pretz, JL Buque, L Lee, SJ Gilliland, DG Golub, TR AF Ebert, BL Levine, RL Wadleigh, M Brunet, JP Pretz, JL Buque, L Lee, SJ Gilliland, DG Golub, TR TI Characterization of distinct molecular signatures in myeloproliferative diseases with the JAK2V617F mutation and wild type JAK2. SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 Dana Farber Canc Inst, Dept Med, Boston, MA 02115 USA. Dana Farber Canc Inst, Dept Pediat Oncol, Boston, MA 02115 USA. Broad Inst, Canc Gen Grp, Cambridge, MA USA. Brigham & Womens Hosp, Dept Hematol, Boston, MA 02115 USA. Hop Maison Neuve Rosemont, Dept Hematol, Montreal, ON, Canada. 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 2005 VL 106 IS 11 MA 119 BP 39A EP 39A PN 1 PG 1 WC Hematology SC Hematology GA 986CF UT WOS:000233426000120 ER PT J AU Chauhan, AK Kamath, AF Kisucka, J Dole, VS Loscalzo, J Handy, DE Wagner, DD AF Chauhan, AK Kamath, AF Kisucka, J Dole, VS Loscalzo, J Handy, DE Wagner, DD TI Elevated levels of homocysteine compromise blood-brain barrier integrity in mice. SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 CBR Inst Biomed Res, CBRI, Boston, MA USA. Harvard Univ, Sch Med, Dept Pathol, Boston, MA 02115 USA. Harvard Univ, Sch Med, Brigham & Womens Hosp, Dept Med,Cardiovasc Div, 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 2005 VL 106 IS 11 MA 3856 BP 45B EP 45B PN 2 PG 1 WC Hematology SC Hematology GA 986CG UT WOS:000233426100155 ER PT J AU Ballen, K Sobocinski, KA Zhang, MJ Arora, M Horowitz, MM Giralt, S AF Ballen, K Sobocinski, KA Zhang, MJ Arora, M Horowitz, MM Giralt, S CA Chronic Leukemia Working Comm TI Outcome of bone marrow transplantation for myelofibrosis. SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 Massachusetts Gen Hosp, Boston, MA 02114 USA. Med Coll Wisconsin, Ctr Int Blood & Marrow Transplant Res, Milwaukee, WI 53226 USA. Univ Minnesota, Minneapolis, MN USA. MD Anderson Canc Ctr, Houston, TX 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 2005 VL 106 IS 11 MA 170 BP 53A EP 53A PN 1 PG 1 WC Hematology SC Hematology GA 986CF UT WOS:000233426000171 ER PT J AU Margossian, SP Ho, G Kennedy, R D'Andrea, AD AF Margossian, SP Ho, G Kennedy, R D'Andrea, AD TI Functional interaction between FANCD2 and ATM in the DNA damage response. SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 Harvard Univ, Sch Med, Dept Pediat Oncol, Childrens Hosp, Boston, MA 02115 USA. Harvard Univ, Sch Med, Dana Farber Canc Inst, Boston, MA 02115 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2005 VL 106 IS 11 MA 181 BP 56A EP 56A PN 1 PG 1 WC Hematology SC Hematology GA 986CF UT WOS:000233426000182 ER PT J AU Yamagata, T Benoist, C Mathis, D AF Yamagata, T Benoist, C Mathis, D TI A shared gene-expression signature in innate-like lymphocytes. SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 Harvard Univ, Sch Med, Joslin Diabet Ctr, Sect Immunol & Immunogenet, Boston, MA 02115 USA. Dokkyo Univ, Sch Med, Dept Hematol, Mibu, Tochigi 32102, Japan. 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 2005 VL 106 IS 11 MA 3903 BP 56B EP 56B PN 2 PG 1 WC Hematology SC Hematology GA 986CG UT WOS:000233426100202 ER PT J AU Cretien, A Proust, A Gazda, H Meerpohl, J Niemeyer, CM Delaunay, J Tchernia, G Narla, M Da Costa, L AF Cretien, A Proust, A Gazda, H Meerpohl, J Niemeyer, CM Delaunay, J Tchernia, G Narla, M Da Costa, L TI Proteasome inhibitors restore to normal the decreased levels of protein expression and nucleolar localization of various mutant ribosomal S19 proteins identified in DBA patients. SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 Inst Gustave Roussy, INSERM, Unite 362, Villejuif, France. Ctr Reference Maladies Genet Erythrocyte & Erythr, Le Kremlin Bicetre, France. Dana Farber Canc Inst, Boston, MA 02115 USA. Univ Klinder Klin, Freiburg, Germany. New York Blood Ctr, New York, NY 10021 USA. RI Meerpohl, Joerg/J-4224-2013 OI Meerpohl, Joerg/0000-0002-1333-5403 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 2005 VL 106 IS 11 MA 185 BP 57A EP 57A PN 1 PG 1 WC Hematology SC Hematology GA 986CF UT WOS:000233426000186 ER PT J AU Bae, JE Tai, YT Hidesima, T Catley, L Li, XF Prabhala, RH Bachu, RB Bertheau, R Shammas, MA Samala, S Miller, J Anderson, KC Munshi, NC AF Bae, JE Tai, YT Hidesima, T Catley, L Li, XF Prabhala, RH Bachu, RB Bertheau, R Shammas, MA Samala, S Miller, J Anderson, KC Munshi, NC TI Proteasome inhibitor does not affect the function of human immune systems: Effects on dendritic cells, T lymphocytes and NK cells. SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 Harvard Univ, Sch Med, Dana Farber Canc Inst, Jerome Lipper Multiple Myeloma Ctr, Boston, MA 02115 USA. Univ Minnesota, Ctr Canc, Minneapolis, MN 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 2005 VL 106 IS 11 MA 3930 BP 62B EP 63B PN 2 PG 2 WC Hematology SC Hematology GA 986CG UT WOS:000233426100229 ER PT J AU Scheijen, B Ngo, HT Griffin, JD AF Scheijen, B Ngo, HT Griffin, JD TI FOXO transcription factors are negatively regulated by p38 map kinases downstream of FLT3 receptor signaling. SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 Dana Farber Canc Inst, Boston, MA 02115 USA. Brigham & Womens Hosp, Dept Med, Boston, MA 02115 USA. Harvard Univ, Sch Med, Boston, MA 02115 USA. RI Scheijen, Blanca/E-3523-2016 OI Scheijen, Blanca/0000-0001-8029-9230 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 2005 VL 106 IS 11 MA 203 BP 63A EP 63A PN 1 PG 1 WC Hematology SC Hematology GA 986CF UT WOS:000233426000204 ER PT J AU Bussel, JB Kuter, DJ George, JN Aledort, LM Lichtin, AE Lyons, RM Nieva, J Wasser, JS Bourgeois, E Kappers-Klunne, M LeFrere, F Schipperus, MR Kelly, R Christal, J Chen, CF Nichol, JL AF Bussel, JB Kuter, DJ George, JN Aledort, LM Lichtin, AE Lyons, RM Nieva, J Wasser, JS Bourgeois, E Kappers-Klunne, M LeFrere, F Schipperus, MR Kelly, R Christal, J Chen, CF Nichol, JL TI Long-term dosing of AMG 531 is effective and well tolerated in thrombocytopenic patients with immune thrombocytopenic purpura. SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 Cornell Med Ctr, New York, NY USA. Massachusetts Gen Hosp, Boston, MA 02114 USA. Univ Oklahoma, Hlth Sci Ctr, Oklahoma City, OK USA. Mt Sinai Hosp, New York, NY 10029 USA. Cleveland Clin Fdn, Cleveland, OH 44195 USA. Hematol Oncol Assoc So Tex, San Antonio, TX USA. Scripps Clin, La Jolla, CA USA. DeQuattro, Community Canc Ctr, Manchester, CT USA. CHRU Claude Huriet, Lille, France. Erasmus MC, Rotterdam, Netherlands. Hop Necker Enfants Malad, Paris, France. HagaZiekenhuis, The Hague, Netherlands. Amgen Inc, Global Dev, Thousand Oaks, CA 91320 USA. NR 0 TC 7 Z9 9 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2005 VL 106 IS 11 MA 220 BP 68A EP 68A PN 1 PG 1 WC Hematology SC Hematology GA 986CF UT WOS:000233426000221 ER PT J AU Friedberg, JW Cohen, P Cheson, BD Robinson, KS Forero-Torres, A Fayad, L La Casce, AS Bessudo, A Camacho, ES Williams, ME van der Jagt, RH Oliver, J Benaim, E AF Friedberg, JW Cohen, P Cheson, BD Robinson, KS Forero-Torres, A Fayad, L La Casce, AS Bessudo, A Camacho, ES Williams, ME van der Jagt, RH Oliver, J Benaim, E TI Bendamustine HCI (TREANDA (TM)) treatment results in high rates of objective response in patients with rituximab-refractory and alkylator-refractory indolent B-Cell non-hodgkin's lymphoma (NHL): Results from a phase II multicenter single-agent study (SDX-105-01). SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 Univ Rochester, Wilmot Canc Ctr, Rochester, NY USA. Georgetown Univ Hosp, Washington, DC 20007 USA. QE II Hlth Sci Ctr, Halifax, NS, Canada. Univ Alabama, Birmingham, AL USA. Univ Texas, MD Anderson Canc Ctr, Houston, TX 77030 USA. Dana Farber Canc Inst, Boston, MA 02115 USA. Pacific Oncol & Hematol Assoc Inc, Encinitas, CA USA. Desert Reg Med Ctr, Palm Springs, CA USA. Univ Virginia, Charlottesville, VA USA. Ottawa Hosp, Ottawa, ON, Canada. Salmedix Inc, Frazer, PA 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 2005 VL 106 IS 11 MA 229 BP 70A EP 70A PN 1 PG 1 WC Hematology SC Hematology GA 986CF UT WOS:000233426000230 ER PT J AU Negri, J Mitsiades, N Deng, QW Wen, ZQ Geer, DC McMullan, C Poulaki, V Hideshima, T Chauhan, D Meyer, T Munshi, NC Richardson, PG Kung, AL Anderson, KC Mitsiades, CS AF Negri, J Mitsiades, N Deng, QW Wen, ZQ Geer, DC McMullan, C Poulaki, V Hideshima, T Chauhan, D Meyer, T Munshi, NC Richardson, PG Kung, AL Anderson, KC Mitsiades, CS TI PKC412 is a multi-targeting kinase inhibitor with activity against multiple myeloma in vitro and in vivo. SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 Harvard Univ, Sch Med, Jerome Lipper Multiple Myeloma Ctr, Dept Med Oncol,Dana Farber Canc Inst, Boston, MA 02115 USA. Novartis Pharma, Novartis Inst BioMed Res, Basel, Switzerland. Harvard Univ, Sch Med, Dana Farber Canc Inst, Dept Pediat Oncol, 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 2005 VL 106 IS 11 MA 247 BP 75A EP 75A PN 1 PG 1 WC Hematology SC Hematology GA 986CF UT WOS:000233426000248 ER PT J AU Hideshima, T Catley, L Yasui, H Ishitsuka, K Raje, N Mitsiades, C Podar, K Munshi, NC Chauhan, D Richardson, PG Anderson, KC AF Hideshima, T Catley, L Yasui, H Ishitsuka, K Raje, N Mitsiades, C Podar, K Munshi, NC Chauhan, D Richardson, PG Anderson, KC TI Perifosine, an oral bioactive novel alkyl-phospholipid, inhibits akt and induces in vitro and in vivo cytotoxicity in human multiple myeloma (MM) SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA 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, 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 2005 VL 106 IS 11 MA 250 BP 76A EP 76A PN 1 PG 1 WC Hematology SC Hematology GA 986CF UT WOS:000233426000251 ER PT J AU Neri, P Tassone, P Shammas, MA Batchu, RB Blotta, S Samala, S Catley, L Hamasaki, M Hideshima, T Jacob, GS Picker, DH Venuta, S Anderson, KC Munshi, NC AF Neri, P Tassone, P Shammas, MA Batchu, RB Blotta, S Samala, S Catley, L Hamasaki, M Hideshima, T Jacob, GS Picker, DH Venuta, S Anderson, KC Munshi, NC TI In vivo anti-tumor activity of atiprimod on SCID models of multiple myeloma. SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 Dana Farber Canc Inst, Jerome Lipper Multiple Myeloma Ctr, Boston, MA 02115 USA. VA Boston Healthcare Syst, Boston, MA USA. Univ Magna Graecia, Catanzaro, Italy. Callisto Pharmaceut Inc, New York, NY 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 2005 VL 106 IS 11 MA 249 BP 76A EP 76A PN 1 PG 1 WC Hematology SC Hematology GA 986CF UT WOS:000233426000250 ER PT J AU Wolanskyj, AP Lasho, TL Schwager, SM McClure, RF Wadleigh, M Lee, SJ Gilliland, DG Tefferi, A AF Wolanskyj, AP Lasho, TL Schwager, SM McClure, RF Wadleigh, M Lee, SJ Gilliland, DG Tefferi, A TI JAK2 V617F mutation in essential thrombocythemia: Clinical associations and long-term prognostic relevance. SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 Mayo Clin, Rochester, MN USA. Harvard Univ, Sch Med, Dana Farber Canc Inst, Boston, MA 02115 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2005 VL 106 IS 11 MA 254 BP 77A EP 78A PN 1 PG 2 WC Hematology SC Hematology GA 986CF UT WOS:000233426000255 ER PT J AU Tefferi, A Sirhan, S Lasho, TL Schwager, SM Strand, JS Elliott, MA Mesa, RA Wolanskyj, AP Steensma, DP Li, CY Wadleigh, M Lee, SJ Gilliland, DG AF Tefferi, A Sirhan, S Lasho, TL Schwager, SM Strand, JS Elliott, MA Mesa, RA Wolanskyj, AP Steensma, DP Li, CY Wadleigh, M Lee, SJ Gilliland, DG TI The clinical and PRV-1 expression phenotype of wild-type, heterozygous, and homozygous JAK2 V617F in polycythemia vera. SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 Mayo Clin, Rochester, MN USA. Harvard Univ, Sch Med, Dana Farber Canc Inst, Boston, MA 02115 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2005 VL 106 IS 11 MA 255 BP 78A EP 78A PN 1 PG 1 WC Hematology SC Hematology GA 986CF UT WOS:000233426000256 ER PT J AU Haining, WN Ebert, B Subramanian, A Kaech, S Nadler, L Wherry, EJ Golub, T AF Haining, WN Ebert, B Subramanian, A Kaech, S Nadler, L Wherry, EJ Golub, T TI Transcriptional mapping of T cell memory reveals that chronic viral infection arrests memory differentiation. SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 Dana Farber Canc Inst, Boston, MA 02115 USA. Harvard Univ, Broad Inst, Cambridge, MA 02138 USA. MIT, Cambridge, MA 02138 USA. Wistar Inst Anat & Biol, Philadelphia, PA 19104 USA. Yale Univ, New Haven, CT 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 2005 VL 106 IS 11 MA 328 BP 99A EP 99A PN 1 PG 1 WC Hematology SC Hematology GA 986CF UT WOS:000233426000329 ER PT J AU Klein, U Casola, S Cattoretti, G Shen, Q Lia, M Mo, TW Ludwig, T Rajewsky, K Dalla-Favera, R AF Klein, U Casola, S Cattoretti, G Shen, Q Lia, M Mo, TW Ludwig, T Rajewsky, K Dalla-Favera, R TI IRF-4/MUM-1 expression is a critical switch in the generation of plasma cells versus memory B-cells. SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 Columbia Univ, Ctr Comprehens Canc, Inst Canc Genet & Herbert Irving, New York, NY 10032 USA. Harvard Univ, Sch Med, CBR Inst Biomed Res, Boston, MA 02115 USA. RI Cattoretti, Giorgio/H-2340-2011 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 2005 VL 106 IS 11 MA 337 BP 102A EP 102A PN 1 PG 1 WC Hematology SC Hematology GA 986CF UT WOS:000233426000338 ER PT J AU Tzachanis, D Lafuente, EM Li, LQ Berezovskaya, A Freeman, GJ Boussiotis, VA AF Tzachanis, D Lafuente, EM Li, LQ Berezovskaya, A Freeman, GJ Boussiotis, VA TI Twisted gastrulation (Tsg), an evolutionarily conserved, secreted, morphogenetic protein enhances TGF-b signaling in T lymphocytes. SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 Beth Israel Deaconess Hosp, Boston, MA USA. Massachusetts Gen Hosp, TBRC, Boston, MA 02114 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 2005 VL 106 IS 11 MA 341 BP 103A EP 103A PN 1 PG 1 WC Hematology SC Hematology GA 986CF UT WOS:000233426000342 ER PT J AU Hochster, HS Weller, E Gascoyne, RD Ryan, TS Habermann, TM Gordon, LI Frankel, SR Horning, SJ AF Hochster, HS Weller, E Gascoyne, RD Ryan, TS Habermann, TM Gordon, LI Frankel, SR Horning, SJ TI Maintenance rituximab after CVP results in superior clinical outcome in advanced follicular lymphoma (FL): Results of the E1496 phase III trial from the Eastern cooperative oncology group and the cancer and leukemia group SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 Stanford Univ, Sch Med, Stanford, CA 94305 USA. Dana Farber Canc Inst, Boston, MA 02115 USA. British Columbia Canc Control Agcy, Vancouver, BC, Canada. Mayo Clin, Rochester, MN USA. Northwestern Univ, Chicago, IL 60611 USA. Univ Maryland, Baltimore, MD 21201 USA. NYU, Sch Med, New York, NY USA. NR 0 TC 54 Z9 54 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 2005 VL 106 IS 11 MA 349 BP 106A EP 106A PN 1 PG 1 WC Hematology SC Hematology GA 986CF UT WOS:000233426000350 ER PT J AU Marango, J Shimoyama, M Leibovitch, BA Zhou, MM Martinez, Y Sirulnik, A Chesi, M Bergsagel, PL Licht, JD AF Marango, J Shimoyama, M Leibovitch, BA Zhou, MM Martinez, Y Sirulnik, A Chesi, M Bergsagel, PL Licht, JD TI The multiple myeloma SET domain (MMSET) protein is a histone H3 and H4 methyltransferase with properties of a transcriptional co-repressor. SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 Mt Sinai Sch Med, Div Hematol Oncol, New York, NY USA. Mt Sinai Sch Med, Struct Biol Program, New York, NY USA. Dana Farber Canc Inst, Boston, MA 02115 USA. Mayo Clin, Dept Hematol Oncol, 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 2005 VL 106 IS 11 MA 358 BP 108A EP 108A PN 1 PG 1 WC Hematology SC Hematology GA 986CF UT WOS:000233426000359 ER PT J AU Carrasco, RD Sukhdeo, K Protopopova, M German, M Henderson, J Anderson, KC DePinho, RA AF Carrasco, RD Sukhdeo, K Protopopova, M German, M Henderson, J Anderson, KC DePinho, RA TI Targeted overexpression of the transcription factor XBP-1 in B cells promotes plasma cell and lymph oplasmacytic neoplasms in transgenic mice. SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 Harvard Univ, Sch Med, Dana Farber Canc Inst, Boston, MA 02115 USA. Brigham & Womens Hosp, Dept Pathol, 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 2005 VL 106 IS 11 MA 359 BP 109A EP 109A PN 1 PG 1 WC Hematology SC Hematology GA 986CF UT WOS:000233426000360 ER PT J AU Chanan-Khan, AA Richardson, PG Alsina, M Carroll, M Lonial, S Krishnan, A Albitar, M Zhou, Y Mitsiades, C Cropp, G Hannah, AL Anderson, KC AF Chanan-Khan, AA Richardson, PG Alsina, M Carroll, M Lonial, S Krishnan, A Albitar, M Zhou, Y Mitsiades, C Cropp, G Hannah, AL Anderson, KC TI Phase 1 clinical trial of KOS-953+Bortezomib (BZ) in relapsed refractory multiple myeloma (MM) SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 Roswell Pk Canc Inst, Dept Med, Buffalo, NY 14263 USA. Dana Farber Canc Inst, Boston, MA 02115 USA. Univ S Florida, H Lee Moffitt Canc Ctr, Tampa, FL 33682 USA. Arizona Canc Ctr, Tucson, AZ USA. Emory Univ, Atlanta, GA 30322 USA. City Hope Natl Med Ctr, Duarte, CA 91010 USA. Nichols Inst, San Juan Capistrano, CA USA. Kosan Biosci, Hayward, CA USA. NR 0 TC 8 Z9 8 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2005 VL 106 IS 11 MA 362 BP 109A EP 110A PN 1 PG 2 WC Hematology SC Hematology GA 986CF UT WOS:000233426000363 ER PT J AU Richardson, PG Chanan-Khan, AA Alsina, M Doss, D Landrigan, B Kettner, D Albitar, M Mitsiades, C Cropp, GF Johnson, RG Hannah, AL Anderson, KC AF Richardson, PG Chanan-Khan, AA Alsina, M Doss, D Landrigan, B Kettner, D Albitar, M Mitsiades, C Cropp, GF Johnson, RG Hannah, AL Anderson, KC TI Safety and activity of KOS-953 in patients with relapsed refractory multiple myeloma (MM): Interim results of a phase 1 trial. SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 Dana Farber Canc Inst, Boston, MA 02115 USA. Roswell Pk Canc Inst, Buffalo, NY 14263 USA. Univ S Florida, H Lee Moffitt Canc Ctr, Tampa, FL 33682 USA. Nichols Inst, San Juan Capistrano, CA USA. Kosan Biosci, Hayward, CA USA. NR 0 TC 19 Z9 19 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2005 VL 106 IS 11 MA 361 BP 109A EP 109A PN 1 PG 1 WC Hematology SC Hematology GA 986CF UT WOS:000233426000362 ER PT J AU Richardson, P Schlossman, R Munshi, N Avigan, D Jagannath, S Alsina, M Doss, D McKenney, M Hande, K Farrell, M Gorelik, S Colson, K Warren, D Lunde, L Michelle, R Cole, G Mitsiades, C Hideshima, T Myers, T Knight, R Anderson, K AF Richardson, P Schlossman, R Munshi, N Avigan, D Jagannath, S Alsina, M Doss, D McKenney, M Hande, K Farrell, M Gorelik, S Colson, K Warren, D Lunde, L Michelle, R Cole, G Mitsiades, C Hideshima, T Myers, T Knight, R Anderson, K TI A phase 1 trial of lenalidomide (REVLIMID (R)) with bortezomib (VELCADE (R)) in relapsed and refractory multiple myeloma. SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 Dana Farber Canc Inst, Boston, MA 02115 USA. Beth Israel Deaconess Med Ctr, Boston, MA 02215 USA. H Lee Moffitt Canc Ctr, Tampa, FL USA. NR 0 TC 16 Z9 16 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2005 VL 106 IS 11 MA 365 BP 110A EP 111A PN 1 PG 2 WC Hematology SC Hematology GA 986CF UT WOS:000233426000366 ER PT J AU San Miguel, JF Richardson, P Sonneveld, P Schuster, M Irwin, D Stadtmauer, E Facon, T Harousseau, J Ben-Yehuda, D Lonial, S Goldschmidt, H Reece, D Blade, J Boccadoro, M Cavenagh, J Dalton, W Boral, A Schenkein, D Anderson, K AF San Miguel, JF Richardson, P Sonneveld, P Schuster, M Irwin, D Stadtmauer, E Facon, T Harousseau, J Ben-Yehuda, D Lonial, S Goldschmidt, H Reece, D Blade, J Boccadoro, M Cavenagh, J Dalton, W Boral, A Schenkein, D Anderson, K TI Frequency, characteristics, and reversibility of peripheral neuropathy (PN) in the APEX trial. SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 Hosp Univ Salamanca, Salamanca, Spain. Dana Farber Canc Inst, Boston, MA 02115 USA. Univ Rotterdam Hosp, Rotterdam, Netherlands. NY Presbyterian Hosp, New York, NY 10021 USA. Univ Penn, Ctr Canc, Philadelphia, PA 19104 USA. Hadassah Univ Hosp, Jerusalem, Israel. Emory Univ, Atlanta, GA 30322 USA. Univ Heidelberg, Heidelberg, Germany. Univ Barcelona, Barcelona, Spain. H Lee Moffitt Canc Ctr, Tampa, FL USA. RI FACON, THIERRY/M-9736-2014 OI FACON, THIERRY/0000-0001-7705-8460 NR 0 TC 18 Z9 18 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2005 VL 106 IS 11 MA 366 BP 111A EP 111A PN 1 PG 1 WC Hematology SC Hematology GA 986CF UT WOS:000233426000367 ER PT J AU Grabowski, EF Buonanno, FS Doody, D Van Cott, EM Grant, PE Jones, RM Whalen, M Nowiski, N AF Grabowski, EF Buonanno, FS Doody, D Van Cott, EM Grant, PE Jones, RM Whalen, M Nowiski, N TI Two cases of pediatric hit requiring unusually high doses of direct thrombin inhibitors: Does a subset of such patients exist? SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 Harvard Univ, Sch Med, Massachusetts Gen Hosp, Stroke Serv, 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 2005 VL 106 IS 11 MA 4161 BP 120B EP 121B PN 2 PG 2 WC Hematology SC Hematology GA 986CG UT WOS:000233426100460 ER PT J AU Richardson, PG Soiffer, RJ Antin, JH Jin, Z Kurtzberg, J Martin, PL Hockenbery, D Murray, KF Vogelsang, GB Chen, A Krishnan, A Kernan, NA Avigan, D Spitzer, TR Warren, D Momtaz, P Revta, C Wei, LJ Iacobelli, M McDonald, GB Guinan, EC AF Richardson, PG Soiffer, RJ Antin, JH Jin, Z Kurtzberg, J Martin, PL Hockenbery, D Murray, KF Vogelsang, GB Chen, A Krishnan, A Kernan, NA Avigan, D Spitzer, TR Warren, D Momtaz, P Revta, C Wei, LJ Iacobelli, M McDonald, GB Guinan, EC TI Defibrotide (DF) for the treatment of Veno-Occlusive Disease (VOD) and multi-system organ failure (MOF) post SCT: Analysis of response and survival according to degree and type of MOV. SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dana Farber Canc Inst,BIDMC,Childrens Hosp, Boston, MA USA. Duke Univ, Med Ctr, Durham, NC 27706 USA. Mem Sloan Kettering Canc Ctr, New York, NY 10021 USA. Columbia Univ, New York, NY 10027 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 2005 VL 106 IS 11 MA 399 BP 120A EP 120A PN 1 PG 1 WC Hematology SC Hematology GA 986CF UT WOS:000233426000400 ER PT J AU Ruutu, T Barosi, G Benjamin, RJ Clark, RE George, JN Gratwohl, A Holler, E Iacobelli, M Kentouche, K Lammle, B Moake, JL Richardson, P Socie, G Zeigler, Z Niederwieser, D Barbui, T AF Ruutu, T Barosi, G Benjamin, RJ Clark, RE George, JN Gratwohl, A Holler, E Iacobelli, M Kentouche, K Lammle, B Moake, JL Richardson, P Socie, G Zeigler, Z Niederwieser, D Barbui, T TI Diagnostic criteria for hematopoietic stem cell transplantation-associated microangiopathy (TAM): Results of a consensus process by an international working group. SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 Helsinki Univ Hosp, Dept Med, Helsinki, Finland. IRCCS, Policlin San Matteo, Pavia, Italy. Amer Red Cross, Dedham, MA USA. Royal Liverpool Univ Hosp, Liverpool, Merseyside, England. Univ Oklahoma, Norman, OK 73019 USA. Univ Basel Hosp, CH-4031 Basel, Switzerland. Univ Regensburg, D-8400 Regensburg, Germany. Gentium, Como, Italy. Univ Jena, D-6900 Jena, Germany. Univ Hosp Bern, CH-3010 Bern, Switzerland. Baylor Coll Med, Houston, TX 77030 USA. Harvard Univ, Sch Med, Boston, MA 02115 USA. Dana Farber Canc Inst, Boston, MA 02115 USA. Hop St Louis, Paris, France. Inst Transfus Med, Pittsburgh, PA USA. Univ Leipzig, D-7010 Leipzig, Germany. Osped Riuniti Bergamo, I-24100 Bergamo, Italy. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2005 VL 106 IS 11 MA 400 BP 120A EP 120A PN 1 PG 1 WC Hematology SC Hematology GA 986CF UT WOS:000233426000401 ER PT J AU Stone, RM Fischer, T Paquette, R Schiller, G Schiffer, CA Ehninger, G Cortes, J Kantarjian, H DeAngelo, DA Yu, R Zhang, L Cohen, PS Wang, YF Phillips, P Giles, F AF Stone, RM Fischer, T Paquette, R Schiller, G Schiffer, CA Ehninger, G Cortes, J Kantarjian, H DeAngelo, DA Yu, R Zhang, L Cohen, PS Wang, YF Phillips, P Giles, F TI Phase IB study of PKC412, an oral FLT3 kinase inhibitor, in sequential and simultaneous combinations with daunorubicin and cytarabine (DA) induction and high-dose cytarabine consolidation in newly diagnosed patients with AML. SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 Dana Farber Canc Inst, Boston, MA 02115 USA. Univ Mainz Klinikum, Mainz, Germany. Univ Calif Los Angeles, Med Ctr, Los Angeles, CA USA. Karmanos Canc Inst, Detroit, MI USA. Univ Klinikum Carl Gustav Carus, Dresden, Germany. Univ Texas, MD Anderson Canc Ctr, Houston, TX 77030 USA. Novartis Oncol, E Hanover, NJ USA. NR 0 TC 23 Z9 25 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 2005 VL 106 IS 11 MA 404 BP 121A EP 122A PN 1 PG 2 WC Hematology SC Hematology GA 986CF UT WOS:000233426000405 ER PT J AU Chauhan, AK Motto, DG Lamb, CB Dockal, M Scheiflinger, F Ginsburg, D Wagner, DD AF Chauhan, AK Motto, DG Lamb, CB Dockal, M Scheiflinger, F Ginsburg, D Wagner, DD TI The metalloprotease ADAMTS13 is a natural anti-thrombotic. SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 Biomed Res Inst, CBRI, CBR, Boston, MA USA. Harvard Univ, Sch Med, Dept Pathol, Boston, MA 02115 USA. Univ Michigan, Dept Pediat, Ann Arbor, MI 48109 USA. Baxter Biosci, Vienna, Austria. Univ Michigan, Howard Hughes Med Inst, Dept Internal Med, Ann Arbor, MI 48109 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2005 VL 106 IS 11 MA 409 BP 123A EP 123A PN 1 PG 1 WC Hematology SC Hematology GA 986CF UT WOS:000233426000410 ER PT J AU Takahashi, H Feuerhake, F Kutok, JL Monti, S Dal Cin, PS Neuberg, D Aster, JC Shipp, MA AF Takahashi, H Feuerhake, F Kutok, JL Monti, S Dal Cin, PS Neuberg, D Aster, JC Shipp, MA TI FAS death domain deletions and increased c-FLIPlong expression occur in different subtypes of diffuse large B-cell lymphoma. SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA 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. Broad Inst, Cambridge, MA USA. Dana Farber Canc Inst, Dept Biotechnol, 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 2005 VL 106 IS 11 MA 416 BP 125A EP 125A PN 1 PG 1 WC Hematology SC Hematology GA 986CF UT WOS:000233426000417 ER PT J AU Saito, Y Healy, B Kaufman, RM Dzik, WH AF Saito, Y Healy, B Kaufman, RM Dzik, WH TI Off-label use of recombinant FVIIa: Clinical characteristics that may influence outcomes. SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 Massachusetts Gen Hosp, Boston, MA 02114 USA. Harvard Univ, Sch Publ Hlth, 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 2005 VL 106 IS 11 MA 431 BP 130A EP 130A PN 1 PG 1 WC Hematology SC Hematology GA 986CF UT WOS:000233426000432 ER PT J AU Prall, WC Czibere, A Grall, F Zerbini, LF Jaeger, M Spentzos, D Libermann, TA Gattermann, N Aivado, M Haas, R AF Prall, WC Czibere, A Grall, F Zerbini, LF Jaeger, M Spentzos, D Libermann, TA Gattermann, N Aivado, M Haas, R TI Age-related transcription levels of KU70 and BIK in CD34+hematopoietic stem and progenitor cells SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 Univ Dusseldorf, Dept Hematol Oncol & Clin Immunol, D-4000 Dusseldorf, NRW, Germany. Univ Dusseldorf, Dept Orthoped Surg, D-4000 Dusseldorf, NRW, Germany. Harvard Univ, Sch Med, Beth Israel Deaconess Med Ctr, BIDMC Genom Ctr, Boston, MA USA. RI Zerbini, Luiz /B-7720-2015 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 2005 VL 106 IS 11 MA 4205 BP 132B EP 132B PN 2 PG 1 WC Hematology SC Hematology GA 986CG UT WOS:000233426100504 ER PT J AU Krivstov, AV Twomey, D Feng, ZH Stubbs, MC Golub, TR Armstrong, SA AF Krivstov, AV Twomey, D Feng, ZH Stubbs, MC Golub, TR Armstrong, SA TI MLL-Fusion proteins induce a stem cell program in committed progenitors to generate leukemia stem cells. SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 Childrens Hosp, 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 2005 VL 106 IS 11 MA 465 BP 140A EP 140A PN 1 PG 1 WC Hematology SC Hematology GA 986CF UT WOS:000233426000466 ER PT J AU Leonard, JP Furman, RR Cheung, YKK Feldman, EJ Cho, HJ Vose, JM Nichols, G Glynn, PW Joyce, MA Ketas, J Ruan, J Carew, J Niesvizky, R LaCasce, A Chadburn, A Cesarman, E Coleman, M AF Leonard, JP Furman, RR Cheung, YKK Feldman, EJ Cho, HJ Vose, JM Nichols, G Glynn, PW Joyce, MA Ketas, J Ruan, J Carew, J Niesvizky, R LaCasce, A Chadburn, A Cesarman, E Coleman, M TI Phase I/II trial of bortezomib plus CHOP-Rituximab in diffuse large B cell (DLBCL) and mantle cell lymphoma (MCL): Phase I results. SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 Cornell Univ, Weill Med Coll, Ctr Lymphoma & Myeloma, New York, NY USA. New York Presbyterian Hosp, New York, NY USA. Columbia Univ, Herbert Irving Comprehens Canc Ctr, New York, NY USA. Univ Nebraska, Med Ctr, Omaha, NE USA. Dana Farber Canc Inst, Boston, MA 02115 USA. NR 0 TC 17 Z9 17 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2005 VL 106 IS 11 MA 491 BP 147A EP 147A PN 1 PG 1 WC Hematology SC Hematology GA 986CF UT WOS:000233426000492 ER PT J AU Treon, S Hunter, ZR Matous, J Badros, A Joyce, RM Mannion, B Advani, R Cook, D Songer, J Hill, J Kaden, BR Sharon, D Steiss, R Branagan, AR Patterson, CJ AF Treon, S Hunter, ZR Matous, J Badros, A Joyce, RM Mannion, B Advani, R Cook, D Songer, J Hill, J Kaden, BR Sharon, D Steiss, R Branagan, AR Patterson, CJ TI Phase II study of bortezomib in Waldenstrom's Macroglobulinemia: Results of WMCTG trial 03-248. SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 Harvard Univ, Sch Med, Dana Farber Canc Inst, Bing Ctr Waldenstroms Macroglobilinemia, Boston, MA 02115 USA. Rocky Mt Canc Ctr, Denver, CO USA. Univ Maryland, Greenbaum Canc Ctr, Baltimore, MD 21201 USA. Beth Israel Deaconess Med Ctr, Boston, MA 02215 USA. St Elizabeths Med Ctr, Crestview Hills, KY USA. Stanford Univ, Med Ctr, Palo Alto, CA 94304 USA. Bay Reg Med Ctr, Bay City, MI USA. Ball Canc Ctr, Muncie, IN USA. Hendersonville Hematol & Oncol, Hendersonville, NC USA. NW Med Specialists, Niles, IL USA. Monmouth Hematol & Oncol Associates, Long Branch, NJ USA. Atlanta Canc Care, Roswell, GA 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 2005 VL 106 IS 11 MA 490 BP 147A EP 147A PN 1 PG 1 WC Hematology SC Hematology GA 986CF UT WOS:000233426000491 ER PT J AU Ray, A Cowan-Jacob, S Manley, PW Mestan, J Griffin, JD AF Ray, A Cowan-Jacob, S Manley, PW Mestan, J Griffin, JD TI Identification of Bcr/Abl point mutations conferring resistance to the Abel kinase inhibitor AMN107 by a random mutagenesis study. SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 Dana Farber Canc Inst, Boston, MA 02115 USA. Novartis Inst Biomed Res, Basel, Switzerland. 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 2005 VL 106 IS 11 MA 494 BP 148A EP 148A PN 1 PG 1 WC Hematology SC Hematology GA 986CF UT WOS:000233426000495 ER PT J AU Alsayed, Y Timm, M Leontovich, A Santos, D Ho, A Singha, U Francis, L Huston, A Lu, GW Lentzsch, S Roodman, GD Xavier, L Treon, S Ghobrial, IM AF Alsayed, Y Timm, M Leontovich, A Santos, D Ho, A Singha, U Francis, L Huston, A Lu, GW Lentzsch, S Roodman, GD Xavier, L Treon, S Ghobrial, IM TI Proteomic analysis of Waldenstrom Macroglobulinemia (WM) using nanoscale protein micorarray techniques. SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 Univ Pittsburgh, Pittsburgh, PA USA. Mayo Clin, Med Ctr, Rochester, MN 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 2005 VL 106 IS 11 MA 504 BP 150A EP 151A PN 1 PG 2 WC Hematology SC Hematology GA 986CF UT WOS:000233426000505 ER PT J AU Van Ness, B Crowley, J Ramos, C Grindle, S Rasmussen, E Blood, E Hoering, A Barlogie, B Greipp, P Durie, B AF Van Ness, B Crowley, J Ramos, C Grindle, S Rasmussen, E Blood, E Hoering, A Barlogie, B Greipp, P Durie, B TI Incidence, outcomes, and SNP genotypes show different ethnic association in patients with myeloma, assessed in SWOG and ECOG clinical trials S9321 and E9486: From the bank on a cure. SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 Univ Minnesota, Ctr Canc, Minneapolis, MN USA. Canc Res & Biostat, Seattle, WA USA. Dana Farber Canc Inst, Boston, MA 02115 USA. Univ Arkansas Med Sci, Little Rock, AR 72205 USA. Mayo Clin, Rochester, MN USA. Cedars Sinai Med Ctr, Los Angeles, CA 90048 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 2005 VL 106 IS 11 MA 506 BP 151A EP 151A PN 1 PG 1 WC Hematology SC Hematology GA 986CF UT WOS:000233426000507 ER PT J AU Kumar, S Greipp, PR Haug, J Kline, M Chng, WJ Blood, E Bergsagel, L Lust, JA Gertz, MA Fonseca, R Rajkumar, SV AF Kumar, S Greipp, PR Haug, J Kline, M Chng, WJ Blood, E Bergsagel, L Lust, JA Gertz, MA Fonseca, R Rajkumar, SV TI Gene expression profiling of myeloma cells at diagnosis can predict response to therapy with thalidomide and dexamethasone combination. SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 Mayo Clin, Rochester, MN USA. Mayo Clin, Scottsdale, AZ USA. Ctr Stat, ECOG, Dana Farber Canc Inst, Boston, MA 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 2005 VL 106 IS 11 MA 508 BP 152A EP 152A PN 1 PG 1 WC Hematology SC Hematology GA 986CF UT WOS:000233426000509 ER PT J AU Zangari, M Najarian, KB Esseltine, DL Lee, CK Barlogie, B Elice, F Burns, MJ Yaccoby, S Richardson, P Sonneveld, P AF Zangari, M Najarian, KB Esseltine, DL Lee, CK Barlogie, B Elice, F Burns, MJ Yaccoby, S Richardson, P Sonneveld, P TI The anti-myeloma effect of bortezomib is associated with osteoblastic activity. SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 Univ Arkansas Med Sci, Myeloma Inst Res & Therapy, Little Rock, AR 72205 USA. Millennium Pharmaceut Co, Cambridge, MA USA. Dana Farber Canc Inst, Boston, MA 02115 USA. Univ Rotterdam Hosp, Rotterdam, Netherlands. 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 2005 VL 106 IS 11 MA 510 BP 152A EP 153A PN 1 PG 2 WC Hematology SC Hematology GA 986CF UT WOS:000233426000511 ER PT J AU Huang, FW Babitt, JL Wrighting, DM Samad, TA Xia, Y Sidis, Y Campagna, JA Chung, RT Schneyer, AL Woolf, CJ Andrews, NC Lin, HY AF Huang, FW Babitt, JL Wrighting, DM Samad, TA Xia, Y Sidis, Y Campagna, JA Chung, RT Schneyer, AL Woolf, CJ Andrews, NC Lin, HY TI Hemojuvelin acts as a bone morphogenetic protein co-receptor to regulate hepcidin expression. SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 Massachusetts Gen Hosp, Boston, MA 02114 USA. Harvard Univ, Sch Med, Boston, MA USA. Childrens Hosp, Boston, MA 02115 USA. Howard Hughes Med Inst, Boston, MA 02115 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 2005 VL 106 IS 11 MA 511 BP 153A EP 153A PN 1 PG 1 WC Hematology SC Hematology GA 986CF UT WOS:000233426000512 ER PT J AU Brown, JR Li, SL Kim, H Fisher, DC Cutler, C Ho, V Lee, SJ Ritz, J Antin, JH Soiffer, RJ Gribben, JG Alyea, EP AF Brown, JR Li, SL Kim, H Fisher, DC Cutler, C Ho, V Lee, SJ Ritz, J Antin, JH Soiffer, RJ Gribben, JG Alyea, EP TI High levels of early donor chimerism and treatment-responsive disease predict improved progression-free survival following non-myeloablative transplantation for advanced CLL. SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 Dana Farber Canc Inst, Boston, MA 02115 USA. Harvard Univ, Sch 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 2005 VL 106 IS 11 MA 560 BP 166A EP 167A PN 1 PG 2 WC Hematology SC Hematology GA 986CF UT WOS:000233426001029 ER PT J AU Guinan, EC Gribben, JG Brennan, LL Nadler, LM AF Guinan, EC Gribben, JG Brennan, LL Nadler, LM TI Patients (Pts) surviving haploidentical stem cell transplantation (SCT) after ex vivo costimulatory blockade to induce anergy experience few long-term complications. SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 Dana Farber Canc Inst, Boston, MA 02115 USA. Childrens Hosp, Boston, MA 02115 USA. Barts & London Sch Med, Canc Res UK Med Oncol Unit, London, England. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2005 VL 106 IS 11 MA 599 BP 178A EP 178A PN 1 PG 1 WC Hematology SC Hematology GA 986CF UT WOS:000233426001068 ER PT J AU Feuerhake, F Monti, S Blank, J Wu, EX Chen, W Golub, TR Shipp, MA AF Feuerhake, F Monti, S Blank, J Wu, EX Chen, W Golub, TR Shipp, MA TI Signatures of response to the proteasome inhibitor bortezomib in diffuse large B-cell lymphoma. SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 Dana Farber Canc Inst, Boston, MA 02115 USA. Broad Inst, Cambridge, MA USA. Millennium 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 2005 VL 106 IS 11 MA 608 BP 181A EP 181A PN 1 PG 1 WC Hematology SC Hematology GA 986CF UT WOS:000233426001077 ER PT J AU Tai, YT Li, XF Coffey, R Breitkreutz, I Catley, L Podar, K Hideshima, T Chauhan, D Raje, N Schlossman, R Richardson, P Munshi, NC Anderson, KC AF Tai, YT Li, XF Coffey, R Breitkreutz, I Catley, L Podar, K Hideshima, T Chauhan, D Raje, N Schlossman, R Richardson, P Munshi, NC Anderson, KC TI Role of BAFF in adhesion and growth of human multiple myeloma cells in the bone marrow microenvironment. SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 Dana Farber Canc Inst, Boston, MA 02115 USA. RI Catley, Laurence/E-5313-2013 NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2005 VL 106 IS 11 MA 627 BP 186A EP 186A PN 1 PG 1 WC Hematology SC Hematology GA 986CF UT WOS:000233426001096 ER PT J AU Arinobu, Y Iwasaki, H Gurish, MF Mizuno, SI Shigematsu, H Ozawa, H Tenen, DG Austen, FK Akashi, K AF Arinobu, Y Iwasaki, H Gurish, MF Mizuno, SI Shigematsu, H Ozawa, H Tenen, DG Austen, FK Akashi, K TI Identification of bipotent basophil/mast cell progenitors in adult murine hematopoiesis. SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 Harvard Univ, Sch Med, Dana Farber Canc Inst, Dept Canc Immunol & AIDS, Boston, MA 02115 USA. Kyushu Univ Hosp, Ctr Cellular & Mol Med, Fukuoka 812, Japan. Brigham & Womens Hosp, Dept Med, Div Rheumatol Allergy & Immunol, Boston, MA 02115 USA. Harvard Univ, Sch Med, Harvard Inst Med, 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 2005 VL 106 IS 11 MA 633 BP 188A EP 188A PN 1 PG 1 WC Hematology SC Hematology GA 986CF UT WOS:000233426001102 ER PT J AU Shammas, MA Koley, H Tassone, P Neri, P Protopopov, A Gryaznov, S Chin, A Bertheau, RC Mitsiades, C Anderson, KC Munshi, NC AF Shammas, MA Koley, H Tassone, P Neri, P Protopopov, A Gryaznov, S Chin, A Bertheau, RC Mitsiades, C Anderson, KC Munshi, NC TI GRN163L, a novel and potent telomerase inhibitor, inhibits myeloma cell growth in vitro and in vivo. SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 VA Boston Hlth Care Syst, Res & Dev, W Roxbury, MA USA. Dana Farber Canc Inst, 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 2005 VL 106 IS 11 MA 639 BP 189A EP 190A PN 1 PG 2 WC Hematology SC Hematology GA 986CF UT WOS:000233426001108 ER PT J AU Chauhan, D Chao, TH He, DL Hideshima, T Catley, L Suh, YG Schlossman, R Neuteboom, S Palladino, MA Anderson, KC AF Chauhan, D Chao, TH He, DL Hideshima, T Catley, L Suh, YG Schlossman, R Neuteboom, S Palladino, MA Anderson, KC TI Targeting therapy for resistant multiple myeloma with a novel inhibitor of NF-KB, NPI-1387. SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 Dana Farber Canc Inst, Boston, MA 02115 USA. Nereus Pharmaceut Inc, San Diego, CA USA. Seoul Natl Univ, Seoul, South Korea. 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 2005 VL 106 IS 11 MA 640 BP 190A EP 190A PN 1 PG 1 WC Hematology SC Hematology GA 986CF UT WOS:000233426001109 ER PT J AU Chauhan, D Chang, Y He, DL Hideshima, T Podar, K Tao, F Neri, P Schlossman, R Schindler, J Carver, B Richardson, P Anderson, KC AF Chauhan, D Chang, Y He, DL Hideshima, T Podar, K Tao, F Neri, P Schlossman, R Schindler, J Carver, B Richardson, P Anderson, KC TI Expression and modulation of carbohydrate-binding protein galectin-3 in multiple myeloma cells by combined treatment with GCS-100 and dexamethasone. SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 Harvard Univ, Sch Med, Dana Farber Canc Inst, Boston, MA 02115 USA. GlycoGenesys Inc, 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 2005 VL 106 IS 11 MA 4447 BP 190B EP 190B PN 2 PG 1 WC Hematology SC Hematology GA 986CG UT WOS:000233426101150 ER PT J AU Shigematsu, H Mizuno, SI Iwasaki, H Arinobu, Y Ozawa, H Sternberg, DW Huntly, B Gilliland, DG Akashi, K AF Shigematsu, H Mizuno, SI Iwasaki, H Arinobu, Y Ozawa, H Sternberg, DW Huntly, B Gilliland, DG Akashi, K TI Lineage instruction by oncogenic tyrosine kinase fusions. SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 Harvard Univ, Sch Med, Dept Canc Immunol & AIDS, Dana Farber Canc Inst, Boston, MA 02115 USA. Kyushu Univ Hosp, Ctr Cellular & Mol Med, Fukuoka 812, Japan. Mt Sinai Sch Med, Dept Hematol Oncol, New York, NY USA. Brigham & Womens Hosp, Div 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 2005 VL 106 IS 11 MA 643 BP 191A EP 191A PN 1 PG 1 WC Hematology SC Hematology GA 986CF UT WOS:000233426001112 ER PT J AU Dubois, C Panicot-Dubois, L Furie, BC Furie, B AF Dubois, C Panicot-Dubois, L Furie, BC Furie, B TI Dynamics of calcium mobilization in platelets during thrombus formation in a living mouse SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 BIDMC, Div Hemostasis & Thrombosis, Boston, MA 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 2005 VL 106 IS 11 MA 649 BP 192A EP 192A PN 1 PG 1 WC Hematology SC Hematology GA 986CF UT WOS:000233426001118 ER PT J AU Sandmaier, BM Maris, MB Maloney, DG Gooley, TA Shizuru, JA Niederwieser, DW Chauncey, TR Sahebi, F Agura, E Maziarz, RT Bruno, B Pulsipher, M Langston, AA Wade, J McSweeney, PA Epner, E Bethge, W Forman, SJ Blume, KG Storb, R AF Sandmaier, BM Maris, MB Maloney, DG Gooley, TA Shizuru, JA Niederwieser, DW Chauncey, TR Sahebi, F Agura, E Maziarz, RT Bruno, B Pulsipher, M Langston, AA Wade, J McSweeney, PA Epner, E Bethge, W Forman, SJ Blume, KG Storb, R TI Hematopoietic cell transplants (HCT) from HLA-matched related (MRD) and unrelated (URD) donors for patients with hematologic malignancies using low-dose TBI conditioning. SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 Fred Hutchinson Canc Res Ctr, Seattle, WA 98104 USA. Univ Washington, Seattle, WA 98195 USA. Stanford Univ, Stanford, CA 94305 USA. Univ Leipzig, D-7010 Leipzig, Germany. City Hope Natl Med Ctr, Duarte, CA 91010 USA. VA Puget Sound Hlth Care Syst, Seattle, WA USA. Univ Turin, Turin, Italy. Baylor Univ, Dallas, TX USA. Rocky Mt Blood & Marrow Transplantat, Denver, CO USA. Oregon Hlth Sci Univ, Portland, OR 97201 USA. Univ Utah, Salt Lake City, UT USA. Emory Univ, Atlanta, GA 30322 USA. Med Coll Wisconsin, Milwaukee, WI 53226 USA. Univ Tubingen, Tubingen, Germany. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2005 VL 106 IS 11 MA 655 BP 194A EP 194A PN 1 PG 1 WC Hematology SC Hematology GA 986CF UT WOS:000233426001124 ER PT J AU Griffin, JD Weisberg, EL AF Griffin, JD Weisberg, EL TI Simultaneous administration of AMN107 and imatinib in the treatment of imatinib-sensitive and imatinib-resistant chronic myeloid leukemia. SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 Dana Farber Canc Inst, Boston, MA 02115 USA. NR 0 TC 4 Z9 4 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2005 VL 106 IS 11 MA 694 BP 205A EP 205A PN 1 PG 1 WC Hematology SC Hematology GA 986CF UT WOS:000233426001163 ER PT J AU Krause, DS von Andrian, UH Van Etten, RA AF Krause, DS von Andrian, UH Van Etten, RA TI Selectins and their ligands are required for homing and engraftment of BCR-ABL plus leukemia-initiating cells. SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 Tufts New England Med Ctr, Mol Oncol Res Inst, Boston, MA USA. Harvard Univ, Sch Med, CBR Inst Biomed Res, Boston, MA 02115 USA. Massachusetts Gen Hosp, Dept Pathol, Boston, MA 02114 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 2005 VL 106 IS 11 MA 697 BP 206A EP 206A PN 1 PG 1 WC Hematology SC Hematology GA 986CF UT WOS:000233426001166 ER PT J AU Motto, DG Chauhan, AK Zhu, GJ Homeister, J Lamb, CB Desch, KC Tsai, HM Wagner, DD Ginsburg, D AF Motto, DG Chauhan, AK Zhu, GJ Homeister, J Lamb, CB Desch, KC Tsai, HM Wagner, DD Ginsburg, D TI Shigatoxin triggers thrombotic thrombocytopenic purpura in genetically susceptible ADAMTS13-deficient mice. SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 Univ Michigan, Ann Arbor, MI 48109 USA. Harvard Univ, CBR Inst Biomed Res, Boston, MA 02115 USA. Albert Einstein Coll Med, Bronx, NY 10467 USA. Howard Hughes Med Inst, Coconut Grove, FL 33133 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 2005 VL 106 IS 11 MA 723 BP 214A EP 215A PN 1 PG 2 WC Hematology SC Hematology GA 986CF UT WOS:000233426001192 ER PT J AU Schulze, H Korpal, M Hurov, J Kim, SW Zhang, J Cantley, LC Graf, T Shivdasani, RA AF Schulze, H Korpal, M Hurov, J Kim, SW Zhang, J Cantley, LC Graf, T Shivdasani, RA TI Phosphatidyl inositol (4,5)P2 marks megakaryocyte internal membranes and is associated with megakaryocyte maturation and platelet release. SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 Dana Farber Canc Inst, Boston, MA 02115 USA. Harvard Univ, Sch Med, Boston, MA 02115 USA. Beth Israel Deaconess Med Ctr, Boston, MA 02215 USA. Albert Einstein Coll Med, New York, NY USA. RI Cantley, Lewis/D-1800-2014 OI Cantley, Lewis/0000-0002-1298-7653 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 2005 VL 106 IS 11 MA 732 BP 217A EP 217A PN 1 PG 1 WC Hematology SC Hematology GA 986CF UT WOS:000233426001201 ER PT J AU Schulze, H Dose, M Korpal, M Italiano, JE Shivdasani, RA AF Schulze, H Dose, M Korpal, M Italiano, JE Shivdasani, RA TI RanBP10 is a cytoplasmic GDP/GTP exchange factor that modulates microtubule dynamics in late megakaryocytes. SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 Dana Farber Canc Inst, Boston, MA 02115 USA. Brigham & Womens Hosp, Boston, MA 02115 USA. Harvard Univ, Sch Med, 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 2005 VL 106 IS 11 MA 738 BP 218A EP 218A PN 1 PG 1 WC Hematology SC Hematology GA 986CF UT WOS:000233426001207 ER PT J AU Palomero, T Odom, DT Margolin, A Aster, J Califano, A Young, RA Look, AT Ferrando, AA AF Palomero, T Odom, DT Margolin, A Aster, J Califano, A Young, RA Look, AT Ferrando, AA TI Transcriptional regulatory networks downstream of NOTCH1 in T-cell acute lymphoblastic leukemia. SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 Columbia Univ, Inst Canc Genet, New York, NY USA. Whitehead Inst Biomed Res, Cambridge, MA 02142 USA. Columbia Univ, Dept Biomed Informat, New York, NY USA. Brigham & Womens Hosp, Boston, MA 02115 USA. Dana Farber Canc Inst, Boston, MA 02115 USA. RI Young, Richard/F-6495-2012; Califano, Andrea/F-7239-2012 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 2005 VL 106 IS 11 MA 740 BP 219A EP 219A PN 1 PG 1 WC Hematology SC Hematology GA 986CF UT WOS:000233426001209 ER PT J AU Li, LQ Berezovskaya, A Boussiotis, VA AF Li, LQ Berezovskaya, A Boussiotis, VA TI The cyclin-dependent kinase inhibitor p27(KIP1) is mandatory for tolerance induction in vivo. SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 Massachusetts Gen Hosp, TBRC, Boston, MA 02114 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 2005 VL 106 IS 11 MA 769 BP 227A EP 227A PN 1 PG 1 WC Hematology SC Hematology GA 986CF UT WOS:000233426001238 ER PT J AU Hatjiharissi, E Santos, DD Xu, L Verselis, S Modica, M Leleu, X Hunter, Z Ho, AW Manning, R Patterson, C Anderson, KC Fox, E Treon, SP AF Hatjiharissi, E Santos, DD Xu, L Verselis, S Modica, M Leleu, X Hunter, Z Ho, AW Manning, R Patterson, C Anderson, KC Fox, E Treon, SP TI Individuals expressing Fc gamma RIIIA-158 V/V and V/F show increased NK cell surface expression of FcgRIIIA (CD16), rituximab binding, and demonstrate higher levels of ADCC activity in response to rituximab. SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 Dana Farber Canc Inst, Bing Ctr Waldenstroms Macroglobulinaemia, Boston, MA 02115 USA. Harvard Univ, Sch Med, Boston, MA 02115 USA. Dana Farber Canc Inst, Jerome Lipper Multiple Myeloma Ctr, Boston, MA 02115 USA. Mol Diagnost Lab, Boston, MA USA. RI Hunter, Zachary/H-3018-2013 OI Hunter, Zachary/0000-0002-1689-1691 NR 0 TC 2 Z9 3 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2005 VL 106 IS 11 MA 776 BP 229A EP 229A PN 1 PG 1 WC Hematology SC Hematology GA 986CF UT WOS:000233426001245 ER PT J AU Kerbauy, F Maris, M Storer, B Maloney, D Niederwieser, D Agura, E Pulsipher, M Chauncey, T Maziarz, R Forman, S Langston, A Wade, J Scott, B Deeg, J Storb, R Sandmaier, BM AF Kerbauy, F Maris, M Storer, B Maloney, D Niederwieser, D Agura, E Pulsipher, M Chauncey, T Maziarz, R Forman, S Langston, A Wade, J Scott, B Deeg, J Storb, R Sandmaier, BM TI Efficacy of nonmyeloablative hematopoietic cell transplant (HCT) in secondary myelodysplastic syndrome (MDS) and its impact on the primary disease. SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 Fred Hutchinson Canc Res Ctr, CRD, Seattle, WA 98104 USA. Univ Washington, Seattle, WA 98195 USA. Univ Leipzig, D-7010 Leipzig, Germany. Baylor Univ, Dallas, TX USA. Univ Utah, Salt Lake City, UT USA. VA Puget Sound Hlth Care Syst, Seattle, WA USA. Oregon Hlth Sci Univ, Portland, OR 97201 USA. City Hope Natl Med Ctr, Duarte, CA 91010 USA. Emory Univ, Atlanta, GA 30322 USA. Med Coll Wisconsin, 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 2005 VL 106 IS 11 MA 792 BP 234A EP 234A PN 1 PG 1 WC Hematology SC Hematology GA 986CF UT WOS:000233426001261 ER PT J AU Yang, G Huang, SC Benz, EJ AF Yang, G Huang, SC Benz, EJ TI A novel splicing factor RBM-9 regulates protein 4.1R exon 16 splicing. SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA 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 2005 VL 106 IS 11 MA 805 BP 237A EP 237A PN 1 PG 1 WC Hematology SC Hematology GA 986CF UT WOS:000233426001274 ER PT J AU Korsgren, C Birkenmeier, CS Barker, JE Peters, LL Lux, SE AF Korsgren, C Birkenmeier, CS Barker, JE Peters, LL Lux, SE TI The C-terminus of alpha spectrin binds protein 4.2 and is necessary for optimal spectrin-actin binding. SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 Childrens Hosp, Boston, MA 02115 USA. Dana Farber Canc Inst, Boston, MA 02115 USA. Jackson Lab, Bar Harbor, ME 04609 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 2005 VL 106 IS 11 MA 810 BP 239A EP 239A PN 1 PG 1 WC Hematology SC Hematology GA 986CF UT WOS:000233426001279 ER PT J AU Filippi, MD Szczur, K Xu, HM Zheng, Y Settleman, J Williams, DA AF Filippi, MD Szczur, K Xu, HM Zheng, Y Settleman, J Williams, DA TI Regulation of the Rho GTPase, RhoA, activity is critical for erythropoiesis during embryo development. SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 Cincinnati Childrens Res Fdn, Cincinnati, OH USA. Massachusetts Gen Hosp, Ctr Canc, Charlestown, MA USA. Harvard Univ, Sch Med, Charlestown, 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 2005 VL 106 IS 11 MA 829 BP 244A EP 244A PN 1 PG 1 WC Hematology SC Hematology GA 986CF UT WOS:000233426001298 ER PT J AU Woo, AJ Moron, TB Choe, SK Schindler, YL Sullivan, MR Fujiwara, Y Paw, BH Cantor, AB AF Woo, AJ Moron, TB Choe, SK Schindler, YL Sullivan, MR Fujiwara, Y Paw, BH Cantor, AB TI Identification of zfp148 (ZBP-89) as a novel GATA-1 associated transcription factor involved in megakaryopoiesis and definitive erythropoiesis. SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 Harvard Univ, Sch Med, Dana Farber Canc Inst, Div Pediat Hematol Oncol,Childrens Hosp, Boston, MA 02115 USA. Harvard Univ, Sch Med, Brigham & Womens Hosp, Div 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 2005 VL 106 IS 11 MA 828 BP 244A EP 244A PN 1 PG 1 WC Hematology SC Hematology GA 986CF UT WOS:000233426001297 ER PT J AU Ho, VT Kim, HT Windawi, S Liney, D Milford, E Gribben, J Cutler, C Lee, SJ Antin, JH Soiffer, RJ Alyea, EP AF Ho, VT Kim, HT Windawi, S Liney, D Milford, E Gribben, J Cutler, C Lee, SJ Antin, JH Soiffer, RJ Alyea, EP TI HLA-C mismatch is associated with inferior outcome after unrelated donor non-myeloablative hematopoietic stem cell transplantation. SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA 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 2005 VL 106 IS 11 MA 835 BP 246A EP 246A PN 1 PG 1 WC Hematology SC Hematology GA 986CF UT WOS:000233426001304 ER PT J AU Akahane, K Inukai, T Inaba, T Kurosawa, H Endo, M Goto, H Kiyokawa, N Look, AT Goi, K Sugita, K Nakazawa, S AF Akahane, K Inukai, T Inaba, T Kurosawa, H Endo, M Goto, H Kiyokawa, N Look, AT Goi, K Sugita, K Nakazawa, S TI Induction of CD33 expression in B-precursor ALL by E2A-HLF fusion transcription factor derived from t(17;19). SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 Univ Yamanashi, Sch Med, Yamanashi, Japan. Hiroshima Univ, Res Inst Radiat Biol & Med, Hiroshima, Japan. Iwate Med Univ, Morioka, Iwate, Japan. Yokohama City Univ, Sch Med, Yokohama, Kanagawa 232, Japan. Natl Res Inst Child Hlth & Dev, Tokyo, Japan. Dana Farber Canc Inst, Boston, MA 02115 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2005 VL 106 IS 11 MA 851 BP 251A EP 251A PN 1 PG 1 WC Hematology SC Hematology GA 986CF UT WOS:000233426001320 ER PT J AU Leleu, X O'Connor, K Ho, A Santos, DD Manning, R Xu, L Hatjiharissi, E Tournilhac, O Chemaly, M Branagan, AR Hunter, ZR Patterson, CJ Anderson, KC Treon, S AF Leleu, X O'Connor, K Ho, A Santos, DD Manning, R Xu, L Hatjiharissi, E Tournilhac, O Chemaly, M Branagan, AR Hunter, ZR Patterson, CJ Anderson, KC Treon, S TI Hepatitis C viral infection is not associated with Waldenstrom's macroglobulinemia. SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 Ctr Hosp Reg & Univ Lille, Fac Med Lille, Immunol Lab, F-59037 Lille, France. Ctr Hosp Reg & Univ Lille, Fac Med Lille, Serv Malad Sang, F-59037 Lille, France. Dana Farber Canc Inst, Jerome Lipper Multiple Myeloma Ctr, Boston, MA 02115 USA. Dana Farber Canc Inst, Bing Ctr Waldenstroms Macroglobulinemia, 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 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2005 VL 106 IS 11 MA 4693 BP 253B EP 253B PN 2 PG 1 WC Hematology SC Hematology GA 986CG UT WOS:000233426101395 ER PT J AU Ho, AW Leleu, X Hatjiharissi, E Tournilhac, O Xu, L O'Connor, K Manning, R Santos, D Chemaly, M Branagan, A Hunter, Z Patterson, C Anderson, KC Treon, SP AF Ho, AW Leleu, X Hatjiharissi, E Tournilhac, O Xu, L O'Connor, K Manning, R Santos, D Chemaly, M Branagan, A Hunter, Z Patterson, C Anderson, KC Treon, SP TI A novel functional role for soluble CD27 in the pathogenesis of Waldenstrom's macroglobulinemia. SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 Dana Farber Canc Inst, Bing Ctr Waldenstroms Macroglobulinemia, Boston, MA 02115 USA. Dana Farber Canc Inst, Jerome Lipper Multiple Myeloma Ctr, 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 2005 VL 106 IS 11 MA 4701 BP 255B EP 255B PN 2 PG 1 WC Hematology SC Hematology GA 986CG UT WOS:000233426101403 ER PT J AU Friedberg, JW Ciminello, L Kelly, J Clawson, S Hoelzer, D Holte, H LaCasce, AS Mead, G Thomas, D van Imhoff, GW Cheson, B Magrath, IT Fisher, RI AF Friedberg, JW Ciminello, L Kelly, J Clawson, S Hoelzer, D Holte, H LaCasce, AS Mead, G Thomas, D van Imhoff, GW Cheson, B Magrath, IT Fisher, RI TI Outcome of patients > age 40 with Burkitt lymphoma (BL) treated with aggressive chemotherapuetic regimens: Results from the international Burkitt lymphoma collaborative group SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 Univ Rochester, James P Wilmot Canc Ctr, Rochester, NY 14627 USA. INCTR, Brussels, Belgium. Inst Pasteur, B-1040 Brussels, Belgium. Univ Frankfurt, D-6000 Frankfurt, Germany. Dana Farber Canc Inst, Boston, MA 02115 USA. Univ Texas, MD Anderson Canc Ctr, Houston, TX 77030 USA. Acad Hosp Groningen, Groningen, Netherlands. Georgetown Univ, Washington, DC 20057 USA. Univ Oslo, Rikshosp, Radium Hosp Trust, N-0027 Oslo, Norway. Royal S Hants Hosp, Southampton SO9 4PE, Hants, England. 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 2005 VL 106 IS 11 MA 928 BP 273A EP 273A PN 1 PG 1 WC Hematology SC Hematology GA 986CF UT WOS:000233426001397 ER PT J AU Robertson, M Kahl, B Vose, J de Vos, S Laughlin, M Flynn, P Rowland, K Cruz, J Goldberg, S Darnstein, C Enas, N Neuberg, D Savage, K Thornton, D Slapak, C Shipp, M AF Robertson, M Kahl, B Vose, J de Vos, S Laughlin, M Flynn, P Rowland, K Cruz, J Goldberg, S Darnstein, C Enas, N Neuberg, D Savage, K Thornton, D Slapak, C Shipp, M TI A phase II study of enzastaurin, a protein kinase C-beta (PKC beta) inhibitor, in the treatment of relapsed diffuse large B-cell lymphoma (DLBCL) SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 Indiana Univ, Med Ctr, Indianapolis, IN 46204 USA. Univ Wisconsin, Madison, WI 53706 USA. Univ Nebraska, Med Ctr, Lincoln, NE 68583 USA. Univ Calif Los Angeles, Los Angeles, CA 90024 USA. Case Western Reserve Univ, Cleveland, OH 44106 USA. Carle Clin Assoc, Ctr Canc, Urbana, IL USA. Joe Arrington Res Ctr, Lubbock, TX USA. Hackensack Univ, Med Ctr, Ctr Canc, Hackensack, NJ USA. Eli Lilly & Co, Indianapolis, IN 46285 USA. Dana Farber Canc Inst, Boston, MA 02115 USA. British Columbia Canc Agcy, Vancouver, BC V5Z 4E6, Canada. 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 2005 VL 106 IS 11 MA 934 BP 275A EP 275A PN 1 PG 1 WC Hematology SC Hematology GA 986CF UT WOS:000233426001403 ER PT J AU Santos, DD Ho, AW Tournilhac, O Leleu X Hatjiharrisi, E Xu, L Tassone, P Neri, P Hunter, Z Chemaly, MAZ Branagan, A Manning, R Patterson, C Adamia, S Kriangkum, J Kutok, JL Pilarski, L Anderson, KC Munshi, N Treon, SP AF Santos, DD Ho, AW Tournilhac, O Leleu, X Hatjiharrisi, E Xu, L Tassone, P Neri, P Hunter, Z Chemaly, MAZ Branagan, A Manning, R Patterson, C Adamia, S Kriangkum, J Kutok, JL Pilarski, L Anderson, KC Munshi, N Treon, SP TI Establishment of a Waldenstrom's Macroglobulinemia cell line (BCWM.1) with productive in vivo engraftment in SCID-hu mice SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 Dana Farber Canc Inst, Bing Ctr Waldenstroms Macroglubulinemia, Boston, MA 02115 USA. Harvard Univ, Sch Med, Dept Med, Boston, MA 02115 USA. VA Boston Healthcare Syst, Boston, MA USA. Magna Graecia Univ Catanzaro, Sch Med, Catanzaro, Italy. Ctr Canc, Catanzaro, Italy. Univ Alberta, Cross Canc Inst, Dept Oncol, Edmonton, AB, Canada. RI Hunter, Zachary/H-3018-2013 OI Hunter, Zachary/0000-0002-1689-1691 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 2005 VL 106 IS 11 MA 979 BP 288A EP 288A PN 1 PG 1 WC Hematology SC Hematology GA 986CF UT WOS:000233426001448 ER PT J AU Santos, DD Chemaly, MZA Tournilhac, O OConnor, KE Hatjiharissi, E Leleu X Xu, L Branagan, AR Manning, RJ Patterson, C Ho, AW Hunter, ZR Tai, YT You, JM Kutok, JL Anderson, KC Munshi, N Treon, SP AF Santos, DD Chemaly, MZA Tournilhac, O OConnor, KE Hatjiharissi, E Leleu, X Xu, L Branagan, AR Manning, RJ Patterson, C Ho, AW Hunter, ZR Tai, YT You, JM Kutok, JL Anderson, KC Munshi, N Treon, SP TI Bone marrow mast cells are significantly increased in patients with Waldenstrom's Macroglobulinemia, and their number following therapeutic intervention is dependent on extent of response SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 Dana Farber Canc Inst, Bing Ctr Waldenstroms Macroglobulinemia, Boston, MA 02115 USA. Harvard Univ, Sch Med, Dept Med, Boston, MA 02115 USA. Brigham & Womens Hosp, Dept Pathol, Boston, MA 02115 USA. Dana Farber Canc Inst, Jerome Lipper Multiple Myeloma Ctr, 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 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 2005 VL 106 IS 11 MA 980 BP 288A EP 288A PN 1 PG 1 WC Hematology SC Hematology GA 986CF UT WOS:000233426001449 ER PT J AU Hunter, ZR Leleu, X Santos, DD Hamilton, S Verselis, S Fox, EA Grewal, I Treon, S AF Hunter, ZR Leleu, X Santos, DD Hamilton, S Verselis, S Fox, EA Grewal, I Treon, S TI Sequence analysis in the BLYS and APRIL receptor TACI reveals novel variants with a potential pathogenetic role in Waldenstrom's Macroglobulinemia (WM) SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 Dana Farber Canc Inst, Bing Ctr Waldenstroms Macroglobulinemia, Boston, MA 02115 USA. Dana Farber Canc Inst, Mol Diagnost Lab, Boston, MA 02115 USA. Genentech BioOncol, San Francisco, CA 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 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 2005 VL 106 IS 11 MA 991 BP 291A EP 291A PN 1 PG 1 WC Hematology SC Hematology GA 986CF UT WOS:000233426001460 ER PT J AU Leleu, X Xu, L Santos, DD Ho, AW Hunter, ZR O'Connor, K Manning, RJ Tournilhac, O Chemaly, M Branagan, AR Patterson, CJ Anderson, KC Treon, S AF Leleu, X Xu, L Santos, DD Ho, AW Hunter, ZR O'Connor, K Manning, RJ Tournilhac, O Chemaly, M Branagan, AR Patterson, CJ Anderson, KC Treon, S TI The unfolded protein response is a determinant of disease actvity in Waldenstrom's Macroglobulinemia (WM) SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 Dana Farber Canc Inst, Bing Waldenstroms Macroglobulinemia Ctr, Boston, MA 02115 USA. Harvard Univ, Sch Med, Boston, MA 02115 USA. Dana Farber Canc Inst, Jerome Lipper Multiple Myeloma Ctr, Boston, MA 02115 USA. CHRU Lille, Fac Med, Immunol Lab, Lille, France. CHRU Lille, Fac Med, Serv Malad Sang, Lille, France. 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 2005 VL 106 IS 11 MA 996 BP 292A EP 292A PN 1 PG 1 WC Hematology SC Hematology GA 986CF UT WOS:000233426001465 ER PT J AU Xu, L Leleu, X Hunter, ZR Santos, DD Ho, AW Hatjiharissi, E O'Connor, K Manning, RJ Chemaly, M Branagan, AR Patterson, CJ Verselis, S Fox, E Anderson, KC Treon, S AF Xu, L Leleu, X Hunter, ZR Santos, DD Ho, AW Hatjiharissi, E O'Connor, K Manning, RJ Chemaly, M Branagan, AR Patterson, CJ Verselis, S Fox, E Anderson, KC Treon, S TI Abnormal expression of the plasma cell differentiation factor XBox protein 1 (Xbp-1) in Waldenstrom's Macroglobulinemia SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 Bing Waldenstroms Macroglobulinemia Ctr, Dana Farber Canc Inst, Boston, MA USA. Harvard Univ, Sch Med, Boston, MA USA. Jerome Lipper Multiple Myeloma Ctr, Dana Farber Canc Inst, Boston, MA USA. CHRU, Lab Immunol, Lille, France. CHRU, Serv Malad Sang, Fac Med Lille, Lille, France. 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 2005 VL 106 IS 11 MA 1003 BP 294A EP 294A PN 1 PG 1 WC Hematology SC Hematology GA 986CF UT WOS:000233426001472 ER PT J AU Letai, A Certo, M Brown, JR Moore, V AF Letai, A Certo, M Brown, JR Moore, V TI The molecular basis for BCL-2 oncogene addiction in CLL. SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA 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 2005 VL 106 IS 11 MA 5008 BP 333B EP 333B PN 2 PG 1 WC Hematology SC Hematology GA 986CG UT WOS:000233426102110 ER PT J AU Cook, RJ Coleman, RE Major, P Lipton, A Brown, JE Lee, KA Smith, M Saad, F Chen, YM Hei, YJ AF Cook, RJ Coleman, RE Major, P Lipton, A Brown, JE Lee, KA Smith, M Saad, F Chen, YM Hei, YJ TI Prognostic significance of biochemical markers of bone metabolism in patients with bone lesions from multiple myeloma (MM). SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 Univ Waterloo, Waterloo, ON N2L 3G1, Canada. Weston Pk Hosp, Ctr Canc Res, Yorkshire Canc Res Acad Unit Clin Oncol, Dept Oncol, Sheffield, S Yorkshire, England. McMaster Univ, Juravinski Canc Ctr, Dept Oncol, Hamilton, ON, Canada. Penn State Univ, Milton S Hershey Med Ctr, Dept Oncol, Hershey, PA 17033 USA. Massachusetts Gen Hosp, Dept Hematol Oncol, Boston, MA 02114 USA. Ctr Hosp Univ Montreal, Hop Notre Dame, Dept Oncol, Montreal, PQ, Canada. Novartis Pharmaceut Corp, Novartis Oncol, E Hanover, NJ USA. NR 0 TC 0 Z9 0 U1 0 U2 2 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2005 VL 106 IS 11 MA 5015 BP 335B EP 335B PN 2 PG 1 WC Hematology SC Hematology GA 986CG UT WOS:000233426102117 ER PT J AU Gribben, J Stephans, K Marshal, B AF Gribben, J Stephans, K Marshal, B TI Fludarabine and alemtuzumab versus fludarabine and rituximab in the treatment of relapsed B-cell chronic lymphocytic leukemia: Results from a phase II study. SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 Harvard Univ, Sch Med, Dana Farber Canc Inst, Boston, MA 02115 USA. Barts & London Sch Med, Canc Res UK Med Oncol Unit, London, England. 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 2005 VL 106 IS 11 MA 5046 BP 343B EP 343B PN 2 PG 1 WC Hematology SC Hematology GA 986CG UT WOS:000233426102148 ER PT J AU Chiaretti, S Tavolaro, S Ghia, E Ariola, C Matteucci, C Maggio, R Vitale, A Ritz, J Mecucci, C Guarini, A Foa, R AF Chiaretti, S Tavolaro, S Ghia, E Ariola, C Matteucci, C Maggio, R Vitale, A Ritz, J Mecucci, C Guarini, A Foa, R TI Detection of the NUP214-ABL rearrangement in T-ALL by high-density oligonucleotide arrays: Evidence of the value of this approach in the identification of gene amplifications SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 Univ Roma La Sapienza, Div Hematol, Dept Cellular Biotechnol & Hematol, Rome, Italy. Univ Perugia, Hematol & 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 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2005 VL 106 IS 11 MA 1211 BP 353A EP 353A PN 1 PG 1 WC Hematology SC Hematology GA 986CF UT WOS:000233426002146 ER PT J AU Zom, E Nelson, EA Mohseni, M Litsa, D Kim, H Bellucci, R Porcheray, F Canning, C Soiffer, RJ Ritz, J AF Zom, E Nelson, EA Mohseni, M Litsa, D Kim, H Bellucci, R Porcheray, F Canning, C Soiffer, RJ Ritz, J TI IL-2 therapy promotes the expansion of human CD4+ CD25+ regulatory T cells and selectively upregulates the expression of FOXP3 in T cells in vivo. SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA 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 2005 VL 106 IS 11 MA 1257 BP 366A EP 366A PN 1 PG 1 WC Hematology SC Hematology GA 986CF UT WOS:000233426002192 ER PT J AU Yoshida, S Ishikawa, F Yasukawa, M Miyamoto, T Yoshimoto, G Kawano, N Shimoda, K Akashi, K Shultz, LD Harada, M AF Yoshida, S Ishikawa, F Yasukawa, M Miyamoto, T Yoshimoto, G Kawano, N Shimoda, K Akashi, K Shultz, LD Harada, M TI Long-term engraftment and self-renewal of AML stem cells in the newborn NOD-scid/IL2rgmll immumodeficient mouse model. SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 Kyushu Univ, Grad Sch Med Sci, Dept Med & Biosystem Sci, Fukuoka 812, Japan. Ehime Univ, Sch Med, Dept Med 1, Toon, Japan. Kyushu Univ Hosp, Ctr Cellular & Mol Med, Fukuoka 812, Japan. Dana Farber Canc Inst, Dept Canc Immunol & AIDS, Boston, MA 02115 USA. Jackson Lab, Bar Harbor, ME 04609 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 2005 VL 106 IS 11 MA 1261 BP 367A EP 367A PN 1 PG 1 WC Hematology SC Hematology GA 986CF UT WOS:000233426002196 ER PT J AU Tai, YT Catley, L Li, XF Coffey, R Breitkreutz, I Bae, J Podar, K Hideshima, T Chauhan, D Schlossman, R Richardson, P Treon, SP Grewal, IS Munshi, NC Anderson, KC AF Tai, YT Catley, L Li, XF Coffey, R Breitkreutz, I Bae, J Podar, K Hideshima, T Chauhan, D Schlossman, R Richardson, P Treon, SP Grewal, IS Munshi, NC Anderson, KC TI Immunomodulatory drug lenalidomide (CC-5013, IMiD3) augments anti-CD40 SGN-40-induced cytotoxicity in human multiple myeloma: Clinical implications. SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 Dana Farber Canc Inst, Boston, MA 02115 USA. RI Catley, Laurence/E-5313-2013 NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2005 VL 106 IS 11 MA 5150 BP 370B EP 370B PN 2 PG 1 WC Hematology SC Hematology GA 986CG UT WOS:000233426102252 ER PT J AU Raje, N Kumar, S Hideshima, T Ishitsuka, K Yasui, H Shiraishi, N Kiziltepe, T Chhetri, S Munshi, NC Anderson, KC AF Raje, N Kumar, S Hideshima, T Ishitsuka, K Yasui, H Shiraishi, N Kiziltepe, T Chhetri, S Munshi, NC Anderson, KC TI Didox induced apoptosis occurs by inhibiting DNA synthesis and repair via down-regulation of ribonucleotide reductase M1 in multiple myeloma (MM). SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 Dana Farber Canc Inst, Boston, MA 02115 USA. Massachusetts Gen Hosp, Boston, MA 02114 USA. Mayo Clin, Div Hematol, 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 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2005 VL 106 IS 11 MA 5153 BP 371B EP 371B PN 2 PG 1 WC Hematology SC Hematology GA 986CG UT WOS:000233426102255 ER PT J AU Song, WH van der Vliet, HJJ Wang, RJ Prabhala, R Podar, K Tai, YT Catley, L Shammas, M Anderson, KC Balk, SP Exley, MA Munshi, NC AF Song, WH van der Vliet, HJJ Wang, RJ Prabhala, R Podar, K Tai, YT Catley, L Shammas, M Anderson, KC Balk, SP Exley, MA Munshi, NC TI In vitro generation of highly-purified functional invariant NKT cells: A strategy for immunotherapy in multiple myeloma. SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA 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, Beth Israel Deaconess Med Ctr, Boston, MA USA. RI van der Vliet, Hans/B-1176-2013; 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 2005 VL 106 IS 11 MA 5183 BP 379B EP 379B PN 2 PG 1 WC Hematology SC Hematology GA 986CG UT WOS:000233426102285 ER PT J AU Saito, TI Sykes, M AF Saito, TI Sykes, M TI Long-lasting anti-tumor immunity induced by the rejection of donor hematopoietic cells in mixed bone marrow chimeras. SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 Harvard Univ, Massachusetts Gen Hosp, Sch Med, 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 2005 VL 106 IS 11 MA 1319 BP 383A EP 383A PN 1 PG 1 WC Hematology SC Hematology GA 986CF UT WOS:000233426002254 ER PT J AU Rodriguez, MA Czuczman, MS Friedberg, JW Kho, ME LaCasce, AS Millenson, M Auayporn, N Niland, J Ter Veer, A Zelenetz, AD Weeks, JC AF Rodriguez, MA Czuczman, MS Friedberg, JW Kho, ME LaCasce, AS Millenson, M Auayporn, N Niland, J Ter Veer, A Zelenetz, AD Weeks, JC TI Age significantly influences presentation and patterns of care in patients with newly diagnosed diffuse large cell lymphoma (DLCL): Collective data from 5 centers participating in the National Comprehensive Center Network (NCCN) NHL Outcomes Project. SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 Univ Texas, MD Anderson Canc Ctr, Lymphoma Myeloma Dept, Houston, TX 77030 USA. Roswell Pk Canc Inst, Buffalo, NY 14263 USA. Univ Rochester, James P Wilmot Canc Ctr, Rochester, NY USA. Dana Farber Canc Inst, Boston, MA 02115 USA. Fox Chase Canc Ctr, Philadelphia, PA 19111 USA. City Hope Natl Med Ctr, Duarte, CA 91010 USA. Mem Sloan Kettering Canc Ctr, New York, NY 10021 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2005 VL 106 IS 11 MA 1335 BP 388A EP 388A PN 1 PG 1 WC Hematology SC Hematology GA 986CF UT WOS:000233426002270 ER PT J AU Passegue, E Wagers, AJ Giuriato, S Anderson, WC Weissman, IL AF Passegue, E Wagers, AJ Giuriato, S Anderson, WC Weissman, IL TI Cell cycle regulation and cell fate decisions in hematopoietic stem cells. SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 Stanford Univ, Dept Pathol, Sch Med, Div Oncol, Stanford, CA 94305 USA. Joslin Diabet Ctr, Sect Dev & Stem Cell Biol, Boston, MA 02215 USA. Stanford Univ, Sch Med, Dept Med, Div Oncol, Stanford, CA 94305 USA. RI Giuriato, Sylvie/A-9113-2010 OI Giuriato, Sylvie/0000-0003-3274-3397 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 2005 VL 106 IS 11 MA 1349 BP 391A EP 391A PN 1 PG 1 WC Hematology SC Hematology GA 986CF UT WOS:000233426002284 ER PT J AU Armistead, P Mohseni, M Gerwin, R Zhang, WD Iravani, M Ghavamzadeh, A Ritz, J Wu, C AF Armistead, P Mohseni, M Gerwin, R Zhang, WD Iravani, M Ghavamzadeh, A Ritz, J Wu, C TI Post-transplant monitoring of erythroid lineage specific chimerism SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 Dana Farber Canc Inst, Ctr Hematol Oncol, Boston, MA 02115 USA. Shariati Hosp, Div Transplantat, Tehran, Iran. Harvard Univ, Sch Med, Dept 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 2005 VL 106 IS 11 MA 5233 BP 392B EP 392B PN 2 PG 1 WC Hematology SC Hematology GA 986CG UT WOS:000233426102335 ER PT J AU Tothova, Z Kollipara, R DePinho, RA Gilliland, DG AF Tothova, Z Kollipara, R DePinho, RA Gilliland, DG TI The role of forkhead transcription factors FoxO1, FoxO3 and FoxO4 in hematopoiesis and leukemogenesis. SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 Harvard Univ, Sch Med, Dept Genet, Boston, MA 02115 USA. Brigham & Womens Hosp, Div Hematol, Dept Med, Boston, MA 02115 USA. Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02115 USA. NR 0 TC 0 Z9 0 U1 1 U2 1 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2005 VL 106 IS 11 MA 1350 BP 392A EP 392A PN 1 PG 1 WC Hematology SC Hematology GA 986CF UT WOS:000233426002285 ER PT J AU Yusuf, RZ McAfee, S Dey, BR Yeap, B Spitzer, TR Ballen, KK AF Yusuf, RZ McAfee, S Dey, BR Yeap, B Spitzer, TR Ballen, KK TI Successful autologous stem cell transplantation in patients with non-Hodgkin's lymphoma over the age of 70 years SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA 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 2005 VL 106 IS 11 MA 5290 BP 407B EP 407B PN 2 PG 1 WC Hematology SC Hematology GA 986CG UT WOS:000233426102391 ER PT J AU Zhang, XF Wang, JF Kunos, G Goopman, JE AF Zhang, XF Wang, JF Kunos, G Goopman, JE TI The potential role of delta(9)-tetrahydrocannabinol in the pathogenesis of Kaposi's sarcoma. SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 Harvard Univ, Sch Med, Beth Israel Deaconess Med Ctr, Div Expt Med, Boston, MA 02115 USA. Harvard Univ, Sch Med, Dept Surg, BIDMC, Boston, MA 02115 USA. NIAAA, NIH, Bethesda, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2005 VL 106 IS 11 MA 1429 BP 413A EP 413A PN 1 PG 1 WC Hematology SC Hematology GA 986CF UT WOS:000233426002364 ER PT J AU Winter, SS Khawaja, H Jiang, Z Kooperberg, C Ferrando, A Look, T Larson, RS AF Winter, SS Khawaja, H Jiang, Z Kooperberg, C Ferrando, A Look, T Larson, RS TI Microarray analyses in a case-control cohort of T-ALL samples identifies gene signature of potential prognostic significance. SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 Univ New Mexico, Hlth Sci Ctr, Albuquerque, NM USA. Fred Hutchinson Canc Ctr, Div Publ Hlth Sci, Seattle, WA USA. Columbia Univ, Inst Canc Genet, 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 2005 VL 106 IS 11 MA 1448 BP 418A EP 418A PN 1 PG 1 WC Hematology SC Hematology GA 986CF UT WOS:000233426002383 ER PT J AU Chng, WJ Van Wier, S Ahmann, G Santana-Davila, R Jalal, S Ketterling, R Bergsagel, PL Chesi, M Trendle, M Oken, M Blood, E Henderson, K Kyle, R Gertz, M Lacy, M Dispenzieri, A Greipp, P Fonseca, R AF Chng, WJ Van Wier, S Ahmann, G Santana-Davila, R Jalal, S Ketterling, R Bergsagel, PL Chesi, M Trendle, M Oken, M Blood, E Henderson, K Kyle, R Gertz, M Lacy, M Dispenzieri, A Greipp, P Fonseca, R TI Compendium of karyotypic abnormalities and their clinical implications in hyperdiploid multiple myeloma (H-MM). SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 Mayo Clin Scottsdale, Scottsdale, AZ USA. Mayo Clin, Pathol & Lab Med, Rochester, MN USA. Missouri Canc Associates, Columbia, MO USA. N Mem Med Ctr, Robbinsdale, MN USA. ECOG Stat Ctr, Dana Faber Canc Inst, Boston, MA USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2005 VL 106 IS 11 MA 1539 BP 442A EP 442A PN 1 PG 1 WC Hematology SC Hematology GA 986CF UT WOS:000233426002474 ER PT J AU Spitzer, TR McAfee, SL Bimalangshu, DR Ballen, K Attar, E Colby, C Preffer, F Saidman, S Shaffer, J Sachs, DH Sykes, M AF Spitzer, TR McAfee, SL Bimalangshu, DR Ballen, K Attar, E Colby, C Preffer, F Saidman, S Shaffer, J Sachs, DH Sykes, M TI In vivo and ex vivo T-cell depleted (TCD) nonmyeloablativehaploidentical stem cell transplantation (NSCT) for hematologic malignancy (HM). SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 Massachusetts Gen Hosp, Dept Med, Boston, MA 02114 USA. Massachusetts Gen Hosp, Dept Pathol, Boston, MA 02114 USA. Transplantat Biol Res Ctr, Charlestown, 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 2005 VL 106 IS 11 MA 5431 BP 444B EP 444B PN 2 PG 1 WC Hematology SC Hematology GA 986CG UT WOS:000233426102532 ER PT J AU Tai, YT Li, C Coffey, R Breitkreutz, I Li, XF Catley, LL Schlossman, RL Richardson, PG Anderson, KC Munshi, NC AF Tai, YT Li, C Coffey, R Breitkreutz, I Li, XF Catley, LL Schlossman, RL Richardson, PG Anderson, KC Munshi, NC TI Chromosomal deletions and amplifications in multiple myeloma detected by 500K single nucleotide polymorphism array analysis. SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 Dana Farber Canc Inst, Boston, MA 02115 USA. Harvard Univ, Sch Publ Hlth, 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 2005 VL 106 IS 11 MA 1551 BP 445A EP 445A PN 1 PG 1 WC Hematology SC Hematology GA 986CF UT WOS:000233426002486 ER PT J AU Kutnar, S Greipp, PR Haug, JL Kline, M Chng, WJ Blood, E Lust, JA Bergsagel, L Gertz, MA Fonseca, R Rajkumar, SV AF Kutnar, S Greipp, PR Haug, JL Kline, M Chng, WJ Blood, E Lust, JA Bergsagel, L Gertz, MA Fonseca, R Rajkumar, SV TI Comparison of newly diagnosed and relapsed refractory multiple myeloma using transcriptional profiling of myeloma cells. SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 Mayo Clin, Rochester, MN USA. Mayo Clin, Scottsdale, AZ USA. Dana Farber Canc Inst, Stat Ctr, Eastern Cooperat Oncol Grp, 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 2005 VL 106 IS 11 MA 1555 BP 446A EP 446A PN 1 PG 1 WC Hematology SC Hematology GA 986CF UT WOS:000233426002490 ER PT J AU Adamia, S Treon, S Santos, D Hunter, Z Mant, MJ Reiman, T Belch, AR Pilarski, LM AF Adamia, S Treon, S Santos, D Hunter, Z Mant, MJ Reiman, T Belch, AR Pilarski, LM TI Single nucleotide polymorphisms (SNPs) and recurrent mutations in the hyaluronan synthase 1 (HASI) gene may predispose to multiple myeloma (MM) and Waldenstrom's macroglobulinemia (WM). SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 Univ Alberta & Cross Canc Inst, Edmonton, AB, Canada. Harvard Univ, Sch Med, Boston, MA USA. Dana Farber Canc Inst, Boston, MA USA. Univ Alberta, Edmonton, AB, Canada. RI Hunter, Zachary/H-3018-2013 OI Hunter, Zachary/0000-0002-1689-1691 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 2005 VL 106 IS 11 MA 1558 BP 447A EP 447A PN 1 PG 1 WC Hematology SC Hematology GA 986CF UT WOS:000233426002493 ER PT J AU Shammas, MA Koley, H Neri, P Tassone, P Batchu, RB Bertheau, R Reis, RJS Munshi, NC AF Shammas, MA Koley, H Neri, P Tassone, P Batchu, RB Bertheau, R Reis, RJS Munshi, NC TI Molecular basis of genomic instability and progression in multiple myeloma: Potential role of apurinic (apyrimidinic) endonuclease. SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 Dana Farber Canc Inst, Jerome Lipper Multiple Myeloma Ctr, Boston, MA USA. VA Boston Hlth Care, Roxbury, MA USA. Harvard Univ, Sch Med, Boston, MA USA. Univ Arkansas Med Sci, Little Rock, AR USA. Cent Arkansas Vet Healthcare Syst, Little Rock, AR 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 2005 VL 106 IS 11 MA 1561 BP 448A EP 448A PN 1 PG 1 WC Hematology SC Hematology GA 986CF UT WOS:000233426002496 ER PT J AU Richardson, P Jagannath, S Hussein, M Berenson, J Singhal, S Irwin, D Williams, SF Bensinger, W Badros, AZ Vescio, R Kenvin, L Yu, ZN Olesnyckyj, M Faleck, H Zeldis, J Knight, R Anderson, KC AF Richardson, P Jagannath, S Hussein, M Berenson, J Singhal, S Irwin, D Williams, SF Bensinger, W Badros, AZ Vescio, R Kenvin, L Yu, ZN Olesnyckyj, M Faleck, H Zeldis, J Knight, R Anderson, KC TI A multicenter, single-arm, open-label study to evaluate the efficacy and safety of single-agent lenalidomide in patients with relapsed and refractory multiple myeloma; Prelininary results. SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 Dana Farber Canc Inst, Boston, MA 02115 USA. St Vincents Comprehens Canc Ctr, New York, NY USA. Cleveland Clin Fdn, Cleveland, OH USA. Inst Myeloma & Bone Canc Res, W Hollywood, CA USA. Robert H Lurie Canc Ctr, Chicago, IL USA. Alta Bates Canc Ctr, Berkeley, CA USA. Midwest Canc Res Grp, Skokie, IL USA. Fred Hutchinson Canc Res Ctr, Seattle, WA USA. Univ Maryland, Greenebaum Canc Ctr, Baltimore, MD USA. Cedars Sinai Med Ctr, Los Angeles, CA 90048 USA. Celgnene Corp, Summit, NJ USA. NR 0 TC 10 Z9 10 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2005 VL 106 IS 11 MA 1565 BP 449A EP 449A PN 1 PG 1 WC Hematology SC Hematology GA 986CF UT WOS:000233426002500 ER PT J AU Hideshima, T Bradner, JE Wong, J Chauhan, D Richardson, PG Schreiber, SL Anderson, KC AF Hideshima, T Bradner, JE Wong, J Chauhan, D Richardson, PG Schreiber, SL Anderson, KC TI Small molecule inhibition of proteasome and aggresome function induces synergistic anti-tumor activity in multiple myeloma. SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 Dana Farber Canc Inst, Boston, MA USA. Harvard Univ, Med Sch, Boston, MA USA. Harvard Univ, Broad Inst, Cambridge, MA USA. MIT, Cambridge, MA USA. Harvard Univ, Howard Hughes Med Inst, Cambridge, MA 02138 USA. NR 0 TC 0 Z9 0 U1 0 U2 2 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2005 VL 106 IS 11 MA 1570 BP 450A EP 451A PN 1 PG 2 WC Hematology SC Hematology GA 986CF UT WOS:000233426002505 ER PT J AU Catley, L Tai, YT Hideshima, T Chauhan, D Weisberg, E Kiziltepe, T Neri, P Tassone, P Versace, R Atadja, P Munshi, NC Anderson, KC AF Catley, L Tai, YT Hideshima, T Chauhan, D Weisberg, E Kiziltepe, T Neri, P Tassone, P Versace, R Atadja, P Munshi, NC Anderson, KC TI Novel hydroxamic acid-derived HDAC inhibitor LBH589 potently activates intrinsic and extrinsic apoptotic pathways, and induces tubulin hyperacetylation in multiple myeloma. SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 Dana Farber Canc Inst, Boston, MA USA. VA Hosp, Boston, MA USA. Novartis, Cambridge, 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 2005 VL 106 IS 11 MA 1578 BP 453A EP 453A PN 1 PG 1 WC Hematology SC Hematology GA 986CF UT WOS:000233426002513 ER PT J AU Catley, L Hideshima, T Chauhan, D Neri, P Tassone, P Tai, YT Song, WH Carrasco, DR Munshi, NC Anderson, KC AF Catley, L Hideshima, T Chauhan, D Neri, P Tassone, P Tai, YT Song, WH Carrasco, DR Munshi, NC Anderson, KC TI Alkylphosphocholine perifosine inhibits myeloma cell growth while inducing myeloid hyperplasia in a marine myeloma model. SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 Dana Farber Canc Inst, Boston, MA USA. VA, 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 2005 VL 106 IS 11 MA 1579 BP 453A EP 453A PN 1 PG 1 WC Hematology SC Hematology GA 986CF UT WOS:000233426002514 ER PT J AU Podar, K Tonon, G Raab, MS Sattler, M Abtahi, D Tai, YT LeGouill, S Ishitsuka, K Yasui, H Depinho, RA Hideshima, T Chauhan, D Anderson, KC AF Podar, K Tonon, G Raab, MS Sattler, M Abtahi, D Tai, YT LeGouill, S Ishitsuka, K Yasui, H Depinho, RA Hideshima, T Chauhan, D Anderson, KC TI Up-regulation of c-Jun contributes to induction of apoptosis by Adaphostin in human multiple myeloma cells. SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 Dana Farber Canc Inst, Boston, MA USA. Univ Nantes, Hotel Dieu Ctr Hosp, Inst Biol, INSERM U0601,, Nantes, France. Univ Nantes, Hotel Dieu Ctr Hosp, Serv Hematol, 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 2005 VL 106 IS 11 MA 1585 BP 454A EP 454A PN 1 PG 1 WC Hematology SC Hematology GA 986CF UT WOS:000233426002520 ER PT J AU Podar, K Tai, YT Abtahi, D Raab, MS Yasui, H Ishitsuka, K Shiraishi, N Catley, LR Sattler, M Raje, N Hideshima, T Chauhan, D AF Podar, K Tai, YT Abtahi, D Raab, MS Yasui, H Ishitsuka, K Shiraishi, N Catley, LR Sattler, M Raje, N Hideshima, T Chauhan, D TI Targeting Src-family kinase activation and downstream molecular events to overcome MM cell growth, survival, and drug-resistance. SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 Dana Farber Canc Inst, Jerome Lipper Multiple Myeloma Ctr, Boston, MA 02115 USA. RI Catley, Laurence/E-5313-2013 NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2005 VL 106 IS 11 MA 1583 BP 454A EP 454A PN 1 PG 1 WC Hematology SC Hematology GA 986CF UT WOS:000233426002518 ER PT J AU Podar, K Raab, MS Abtahi, D Tai, YT Lin, B Munshi, NC Hideshima, T Chauhan, D Anderson, KC AF Podar, K Raab, MS Abtahi, D Tai, YT Lin, B Munshi, NC Hideshima, T Chauhan, D Anderson, KC TI The PKC-inhibitor enzastaurin inhibits MM cell growth, survival and migration in the bone marrow microenvironment. SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 Dana Farber Canc Inst, Jerome Lipper Multiple Myeloma Ctr, Boston, MA 02115 USA. Eli Lilly & Co, Lilly Corp Ctr, Indianapolis, IN 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 2005 VL 106 IS 11 MA 1584 BP 454A EP 454A PN 1 PG 1 WC Hematology SC Hematology GA 986CF UT WOS:000233426002519 ER PT J AU Kiziltepe, T Ishitsuka, K Hideshima, T Raje, N Shiraishi, N Yasui, H Catley, L Chauhan, D Saavedra, JE Keefer, LK Shami, PJ Anderson, KC AF Kiziltepe, T Ishitsuka, K Hideshima, T Raje, N Shiraishi, N Yasui, H Catley, L Chauhan, D Saavedra, JE Keefer, LK Shami, PJ Anderson, KC TI JS-K, a GST-activated nitric oxide generator, induces apoptosis and overcomes in vitro drug resistance in multiple myeloma cells. SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA 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. SAIC, Frederick, MD USA. NCI, Comparat Carcinogenesis Lab, NIH, Frederick, MD 21701 USA. Univ Utah, Div Med Oncol, Salt Lake City, UT USA. Salt Lake City Vet Adm Med Ctr, Salt Lake City, UT USA. RI Catley, Laurence/E-5313-2013; Keefer, Larry/N-3247-2014 OI Keefer, Larry/0000-0001-7489-9555 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 2005 VL 106 IS 11 MA 1593 BP 456A EP 456A PN 1 PG 1 WC Hematology SC Hematology GA 986CF UT WOS:000233426002528 ER PT J AU McEarchern, JA McDonagh, C Ho, A Tai, YT Francisco, L Klussman, K Morris-Tilden, C Gordon, K Oflazoglu, E Kissler, K Munshi, N Anderson, KC Treon, SP Carter, P Wahl, AF Grewal, LS Law, CL AF McEarchern, JA McDonagh, C Ho, A Tai, YT Francisco, L Klussman, K Morris-Tilden, C Gordon, K Oflazoglu, E Kissler, K Munshi, N Anderson, KC Treon, SP Carter, P Wahl, AF Grewal, LS Law, CL TI A humanized anti-CD70 monoclonal antibody targets CD70-expressing multiple myeloma. SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 Seattle Genet, Pre Clin Therapeut, Bothell, WA USA. Seattle Genet, Antibody Technol, Bothell, WA USA. Dana Farber Canc Inst, Boston, MA 02115 USA. Seattle Genet, Bioproc Dev, Bothell, WA 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 2005 VL 106 IS 11 MA 1591 BP 456A EP 456A PN 1 PG 1 WC Hematology SC Hematology GA 986CF UT WOS:000233426002526 ER PT J AU Shammas, MA Batchu, RB Koley, H Bertheau, RC Neri, P Goyal, R Anderson, KC Munshi, NC AF Shammas, MA Batchu, RB Koley, H Bertheau, RC Neri, P Goyal, R Anderson, KC Munshi, NC TI A green tea polyphenol, epigallocatechin-3-gallate, induces selective apoptosis in multiple myeloma cells: Mechanism of action and therapeutic potential. SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 Dana Farber Canc Inst, Jerome Lipper Multiple Myeloma Ctr, Boston, MA USA. VA Boston Hlth Care, Res & Dev, Boston, MA USA. Harvard Univ, Med Sch, 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 2005 VL 106 IS 11 MA 1590 BP 456A EP 456A PN 1 PG 1 WC Hematology SC Hematology GA 986CF UT WOS:000233426002525 ER PT J AU Bae, J Carrasco, R Sukhdeo, K Tassone, P Neri, P Tai, YT Li, XF Coffey, R Prabhala, R Anderson, K Munshi, N AF Bae, J Carrasco, R Sukhdeo, K Tassone, P Neri, P Tai, YT Li, XF Coffey, R Prabhala, R Anderson, K Munshi, N TI XBP-1 a selective and specific target for immunotherapy in myeloma. SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 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 2005 VL 106 IS 11 MA 1594 BP 457A EP 457A PN 1 PG 1 WC Hematology SC Hematology GA 986CF UT WOS:000233426002529 ER PT J AU Dayyani, F Zhang, YT Zaidi, ST Sweetser, DA AF Dayyani, F Zhang, YT Zaidi, ST Sweetser, DA TI TLE corepressors as novel candidate AML tumor suppressor genes that regulate Wnt signaling, cell cycle progression, and myeloid differentiation. SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 Harvard Univ, Massachusetts Gen Hosp, Sch Med, Boston, MA USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2005 VL 106 IS 11 MA 1601 BP 458A EP 458A PN 1 PG 1 WC Hematology SC Hematology GA 986CF UT WOS:000233426002536 ER PT J AU Stubbs, MC Krivtsov, A Kim, YM Wright, RD Feng, ZH Agarwal, J Kung, AL Armstrong, SA AF Stubbs, MC Krivtsov, A Kim, YM Wright, RD Feng, ZH Agarwal, J Kung, AL Armstrong, SA TI MLL-AF9 and FLT3 cooperation during myeloid leukemogenesis: Development of a model for rapid testing of new therapeutics. SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 Childrens Hosp, Div Hematol Oncol, Boston, MA 02115 USA. Dana Farber Canc Inst, Dept Pediat 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 2005 VL 106 IS 11 MA 1605 BP 459A EP 459A PN 1 PG 1 WC Hematology SC Hematology GA 986CF UT WOS:000233426002540 ER PT J AU Heinrichs, S Schoch, C Neuberg, DS Look, AT AF Heinrichs, S Schoch, C Neuberg, DS Look, AT TI HOXB9 is aberrantly expressed in blast cells in a subset of acute myeloid leukemia patients and supports proliferation of AML cell lines. SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 Dana Farber Canc Inst, Dept Pediat Oncol, Boston, MA 02115 USA. LMU Grosshadern, Lab Leukemia Diagnost, Munich, Germany. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2005 VL 106 IS 11 MA 1613 BP 461A EP 462A PN 1 PG 2 WC Hematology SC Hematology GA 986CF UT WOS:000233426002548 ER PT J AU Johnson, DC Grindle, S Davies, F Gonzalez, D Ramos, C Hawkins, K Bell, S Kesby, H Rajkumar, SV Rassmusen, E Crowley, J Blood, E Child, JA Durie, BGM Van Ness, BG Morgan, GJ AF Johnson, DC Grindle, S Davies, F Gonzalez, D Ramos, C Hawkins, K Bell, S Kesby, H Rajkumar, SV Rassmusen, E Crowley, J Blood, E Child, JA Durie, BGM Van Ness, BG Morgan, GJ TI Inherited genetic variation and the risk of developing venous thrombosis with thalidomide treatment in myeloma patients. SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 Inst Canc Res, Sect Haematooncol, Surrey, England. Univ Minnesota, Acad Unit Oncol & Haematol, Minneapolis, MN USA. Univ Leeds, Clin Trials Res Unit, Leeds, W Yorkshire, England. Univ Leeds, Acad Dept Haematol & Oncol, Leeds, W Yorkshire, England. Mayo Clin, Div Hematol, Rochester, MN USA. Canc Res & Biostat, Seattle, WA USA. Dana Farber Canc Inst, Dept Biostat Sci, Boston, MA USA. Sinai Comprehens Canc Ctr, Los Angeles, CA USA. RI Johnson, David/A-3907-2011 OI Johnson, David/0000-0003-0887-3343 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 2005 VL 106 IS 11 MA 1624 BP 464A EP 464A PN 1 PG 1 WC Hematology SC Hematology GA 986CF UT WOS:000233426002559 ER PT J AU Shi, JL Pipe, SW Rasmussen, JT Heegaard, CW Gilbert, GE AF Shi, JL Pipe, SW Rasmussen, JT Heegaard, CW Gilbert, GE TI Regulated phosphatidylserine exposure on platelets mediates fibrin formation in hemostasis and thrombosis. SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 VA Boston Healthcare Syst, Boston, MA USA. Brigham & Womens Hosp, Boston, MA 02115 USA. Harvard Univ, Sch Med, Boston, MA USA. Univ Michigan, Ann Arbor, MI 48109 USA. Aarhus Univ, Dept Mol Biol, DK-8000 Aarhus, Denmark. 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 2005 VL 106 IS 11 MA 1645 BP 470A EP 470A PN 1 PG 1 WC Hematology SC Hematology GA 986CF UT WOS:000233426003007 ER PT J AU Italiano, JE Richardson, JL Schulze, H Drabek, K Bulinski, C Galjart, N Shivdasani, RA Hartwig, JH Patel, SR AF Italiano, JE Richardson, JL Schulze, H Drabek, K Bulinski, C Galjart, N Shivdasani, RA Hartwig, JH Patel, SR TI The marginal microtubule coil in the resting blood platelet is a dynamic bipolar array. SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 Brigham & Womens Hosp, Div Hematol, Boston, MA 02115 USA. Dana Farber Canc Inst, Dept Adult Oncol & Canc Biol, Boston, MA 02115 USA. Harvard Univ, Sch Med, Dept Med, Boston, MA 02115 USA. Erasmus Univ, Dept Cell Biol & Genet, NL-3000 DR Rotterdam, Netherlands. Columbia Univ, Dept Biol Sci, New York, NY 10027 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 2005 VL 106 IS 11 MA 1653 BP 472A EP 472A PN 1 PG 1 WC Hematology SC Hematology GA 986CF UT WOS:000233426003015 ER PT J AU Huang, SC Norton, SM Liu, ES Zhou, AY Guang, Y Benz, EJ AF Huang, SC Norton, SM Liu, ES Zhou, AY Guang, Y Benz, EJ TI Regulation of exon 2'/2 of protein 4.1R by coordinated transcription and splicing. SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA 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 2005 VL 106 IS 11 MA 1663 BP 474A EP 475A PN 1 PG 2 WC Hematology SC Hematology GA 986CF UT WOS:000233426003025 ER PT J AU Robledo, RF Lambert, AJ Gwynn, B Rowe, LB Gilligan, DM Lux, SE Peters, LL AF Robledo, RF Lambert, AJ Gwynn, B Rowe, LB Gilligan, DM Lux, SE Peters, LL TI Two new recessive mouse mutations cause severe hemolytic anemia and reveal unexpected interactions in the C-terminus of alpha-spectrin. SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 Jackson Lab, Bar Harbor, ME 04609 USA. Childrens Hosp, Div Hematol Oncol, Boston, MA 02115 USA. Harvard Univ, Sch Med, Dana Farber Canc Inst, Boston, MA 02115 USA. Univ Washington, Sch Med, Puget Sound Blood Ctr, Seattle, WA 98195 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 2005 VL 106 IS 11 MA 1662 BP 474A EP 474A PN 1 PG 1 WC Hematology SC Hematology GA 986CF UT WOS:000233426003024 ER PT J AU Fukata, M Ishikawa, F Shimazu, I Ito, H Shimoda, K Akashi, K Shultz, LD Harada, M AF Fukata, M Ishikawa, F Shimazu, I Ito, H Shimoda, K Akashi, K Shultz, LD Harada, M TI Purified murine hematopoietic stem cells contribute to the generation of cardiomyocytes via cell fusion. SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 Kyushu Univ, Grad Sch Med Sci, Dept Med & Biosyst Sci, Fukuoka 812, Japan. Kyushu Univ Hosp, Ctr Cellular & Mol Med, Fukuoka 812, Japan. Dana Farber Canc Inst, Dept Canc Immunol & AIDS, Boston, MA USA. Jackson Lab, Bar Harbor, ME 04609 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 2005 VL 106 IS 11 MA 1700 BP 485A EP 485A PN 1 PG 1 WC Hematology SC Hematology GA 986CF UT WOS:000233426003062 ER PT J AU Janzen, V Fleming, H Reynolds, G Waring, M Scadden, DT AF Janzen, V Fleming, H Reynolds, G Waring, M Scadden, DT TI Caspase-3 has apoptotic and non-apoptotic functions in regulating the fate of hematopoietic stem cells. SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 Harvard Univ, Massachusetts Gen Hosp, Sch Med, Ctr Regenerat Med & Technol, Boston, MA USA. Harvard Stem Cell Inst, 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 2005 VL 106 IS 11 MA 1717 BP 489A EP 489A PN 1 PG 1 WC Hematology SC Hematology GA 986CF UT WOS:000233426003079 ER PT J AU Saito, AM Cutler, C Zahrieh, D Soiffer, RJ Ho, VT Alyea, EP Antin, JH Lee, SJ AF Saito, AM Cutler, C Zahrieh, D Soiffer, RJ Ho, VT Alyea, EP Antin, JH Lee, SJ TI Comparison of methotrexate- versus sirolimus-containing graft-versus-host disease prophylaxis regimens after myeloablative stem cell transplantation. SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA 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 2005 VL 106 IS 11 MA 1797 BP 511A EP 511A PN 1 PG 1 WC Hematology SC Hematology GA 986CF UT WOS:000233426003159 ER PT J AU Silverman, LR McKenzie, DR Peterson, BL Stone, RM Powell, BL Mayo, C Backstrom, JT Larson, RA AF Silverman, LR McKenzie, DR Peterson, BL Stone, RM Powell, BL Mayo, C Backstrom, JT Larson, RA CA Canc Leukemia Grp B (CALGB) TI Response rates in patients with acute myeloid leukemia (AML), treated with azacitidine, using WHO and international working group (IWG) criteria for myelodysplastic syndrome (MDS). SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 Mt Sinai Sch Med, New York, NY USA. Pharm Corp, Overland Pk, KS USA. Duke Univ, Med Ctr, Durham, NC USA. Dana Farber Canc Inst, Boston, MA 02115 USA. Wake Forest Univ, Baptist Med Ctr, Winston Salem, NC 27109 USA. Univ Chicago, Chicago, IL 60637 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 2005 VL 106 IS 11 MA 1848 BP 525A EP 526A PN 1 PG 2 WC Hematology SC Hematology GA 986CF UT WOS:000233426003210 ER PT J AU Ballen, KK Shpall, EJ Avigan, D Yeap, B McAfee, S Dey, BR Attar, E Kronenberg, H Antin, JH Spitzer, TR AF Ballen, KK Shpall, EJ Avigan, D Yeap, B McAfee, S Dey, BR Attar, E Kronenberg, H Antin, JH Spitzer, TR TI Parathyroid hormone may improve autologous stem cell mobilization via the stem cell niche SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 Massachusetts Gen Hosp, Boston, MA 02114 USA. MD Anderson Canc Ctr, Houston, TX USA. 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 2005 VL 106 IS 11 MA 1968 BP 557A EP 557A PN 1 PG 1 WC Hematology SC Hematology GA 986CF UT WOS:000233426003330 ER PT J AU Bashey, A Medina, B Corringham, S Pasek, M Carrier, E Streicher, H Lowy, I Mason, J Soiffer, RJ Ball, ED AF Bashey, A Medina, B Corringham, S Pasek, M Carrier, E Streicher, H Lowy, I Mason, J Soiffer, RJ Ball, ED TI Phase I study of a neutralizing monoclonal anti-CTLA4 antibody (MDX-010) in patients with relapse of malignancy after allogeneic hematopoietic stem cell transplantation SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 Univ Calif San Diego, Blood & Marrow Transplantat Program, Moores Canc Ctr, La Jolla, CA 92093 USA. NCI, Pharmaceut Management Branch, Bethesda, MD 20892 USA. Medarex Inc, Bloomsbury, NJ USA. Scripps Clin, BMT, La Jolla, CA 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 2005 VL 106 IS 11 MA 2017 BP 571A EP 571A PN 1 PG 1 WC Hematology SC Hematology GA 986CF UT WOS:000233426003379 ER PT J AU Ganti, AK Lee, SJ Armitage, JO Bierman, PJ Bociek, G Devetten, MP Maness, LJ Reed, EC Vose, JM Loberiza, F AF Ganti, AK Lee, SJ Armitage, JO Bierman, PJ Bociek, G Devetten, MP Maness, LJ Reed, EC Vose, JM Loberiza, F TI Outcomes following hematopoietic stem cell transplantation for hematologic malignancies in patients with or without advanced care planning SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 Univ Nebraska, Med Ctr, Omaha, NE USA. 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 2005 VL 106 IS 11 MA 2025 BP 573A EP 573A PN 1 PG 1 WC Hematology SC Hematology GA 986CF UT WOS:000233426003387 ER PT J AU Ballen, KK Spitzer, TR Yeap, B Steve, M Dey, BR Attar, E Alyea, E Cutler, C Ho, V Lee, S Soiffer, R Antin, JH AF Ballen, KK Spitzer, TR Yeap, B Steve, M Dey, BR Attar, E Alyea, E Cutler, C Ho, V Lee, S Soiffer, R Antin, JH TI Excellent disease-free survival after double cord blood transplantation using a reduced intensity chemotherapy only conditioning regimen in a diverse adult population. SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA 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 7 Z9 7 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2005 VL 106 IS 11 MA 2048 BP 579A EP 580A PN 1 PG 2 WC Hematology SC Hematology GA 986CF UT WOS:000233426003410 ER PT J AU Cutler, C Li, SL Kim, HT Macdonell, R Ho, V Alyea, E Lee, SJ Soiffer, RJ Antin, JH AF Cutler, C Li, SL Kim, HT Macdonell, R Ho, V Alyea, E Lee, SJ Soiffer, RJ Antin, JH TI Sirolimus and tacrolimus without methotrexate as graft-vs-host disease prophylaxis after matched, unrelated peripheral blood stem cell transplantation: Excellent GVHD control with low transplant-related morbidity and mortality. SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02115 USA. Dana Farber Canc Inst, Dept Biostat & Computat Biol, 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 2005 VL 106 IS 11 MA 2051 BP 580A EP 580A PN 1 PG 1 WC Hematology SC Hematology GA 986CF UT WOS:000233426003413 ER PT J AU Khan, KD O'Brien, S Rai, KR Brown, JR Cook, P Maddox, AM Duarte, AM Haltom, EJ Uprichard, MJ AF Khan, KD O'Brien, S Rai, KR Brown, JR Cook, P Maddox, AM Duarte, AM Haltom, EJ Uprichard, MJ TI Phase 2 study of talabostat and rituximab in patients with advanced chronic lymphoctyic leukemia (CLL) previously treated with a rituximab/fludarabine regimen. SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 Indiana Oncol Hematol Consultants, Indianapolis, IN USA. Univ Texas, MD Anderson Canc Ctr, Houston, TX 77030 USA. Long Isl Jewish Med Ctr, New Hyde Pk, NY 11042 USA. Dana Farber Canc Inst, Boston, MA 02115 USA. NYU, Ctr Med, New York, NY USA. Univ Arkansas Med Sci, Little Rock, AR 72205 USA. Point Therapeut, Clin Dev, 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 2005 VL 106 IS 11 MA 2125 BP 601A EP 601A PN 1 PG 1 WC Hematology SC Hematology GA 986CF UT WOS:000233426003487 ER PT J AU Grabowski, EF Nestoridi, E Garcia, A Fox, JG Ingelfinger, JR AF Grabowski, EF Nestoridi, E Garcia, A Fox, JG Ingelfinger, JR TI Tissue factor-driven enhanced platelet aggregation in flowing blood in a rabbit model of childhood hemolytic uremic syndrome. SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 Harvard Univ, Sch Med, Massachusetts Gen Hosp, Boston, MA 02115 USA. MIT, 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 2005 VL 106 IS 11 MA 2166 BP 612A EP 612A PN 1 PG 1 WC Hematology SC Hematology GA 986CF UT WOS:000233426004014 ER PT J AU Renfroe, JL Forbes, P Braunstein, J Neufeld, EJ AF Renfroe, JL Forbes, P Braunstein, J Neufeld, EJ TI Relationship of transfusion and iron-related complications to cost of care in thalassemia. SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 Childrens Hosp, Clin Res Program, Boston, MA 02115 USA. Dana Farber Canc Inst, Boston, MA 02115 USA. RI Neufeld, Ellis/F-9331-2011 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 2005 VL 106 IS 11 MA 2240 BP 631A EP 631A PN 1 PG 1 WC Hematology SC Hematology GA 986CF UT WOS:000233426004087 ER PT J AU Kratz, A Rubattu, L Maier-Redelsperger, M Amendola, G Danise, P d'Onofrio, G Zini, G van Duijnhoven, H Siguret, V Gouin-Thibault, I Gioia, M Cillari, E Ermens, A Carandina, G Cynober, T Fossat, C Lesesve, JF Sylvain, S AF Kratz, A Rubattu, L Maier-Redelsperger, M Amendola, G Danise, P d'Onofrio, G Zini, G van Duijnhoven, H Siguret, V Gouin-Thibault, I Gioia, M Cillari, E Ermens, A Carandina, G Cynober, T Fossat, C Lesesve, JF Sylvain, S TI Automated pre-classification of anemia based on the results of a routine automated hematology system. SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 Massachusetts Gen Hosp, Boston, MA 02114 USA. Azienda Osped SS Annunziata, Sassari, Italy. Tenon Hosp, Paris, France. Osped Umberto 1, Salerno, Italy. Univ Sacred Heart, I-00168 Rome, Italy. Elkerliek Hosp, Helmond, Netherlands. Charles Foiz Jean Rostand Hosp, Ivry, France. Azienda Osped V Cervello, Palermo, Italy. Amphia Hosp, Breda, Netherlands. Azienda USL Ferrara, Cento, Italy. CHU Bicetre, Le Kremlin Bicetre, France. Hosp Timone, Marseille, France. Nancy Univ Hosp, Vandoeuvre Les Nancy, France. RI Zini, Gina/C-1760-2016 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 2005 VL 106 IS 11 MA 2253 BP 635A EP 635A PN 1 PG 1 WC Hematology SC Hematology GA 986CF UT WOS:000233426004100 ER PT J AU Ishikawa, F Lino, T Niiro, H Yoshida, S Miyamoto, T Shigematsu, H Shultz, LD Harada, M Akashi, K AF Ishikawa, F Lino, T Niiro, H Yoshida, S Miyamoto, T Shigematsu, H Shultz, LD Harada, M Akashi, K TI Human conventional and plasmacytoid dendritic cells can originate from both lymphoid and myeloid progenitors in a new humanized mouse system. SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 Kyushu Univ, Grad Sch Med Sci, Dept Med & Biosystem Sci, Fukuoka, Japan. Kyushu Univ Hosp, Ctr Cellular & Mol Med, Fukuoka, Japan. Dana Farber Canc Inst, Dept Canc Immunol & AIDS, Boston, MA USA. Jackson Lab, Bar Harbor, ME 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 2005 VL 106 IS 11 MA 2273 BP 640A EP 641A PN 1 PG 2 WC Hematology SC Hematology GA 986CF UT WOS:000233426004120 ER PT J AU Wu, CJ Krishnamurti, L Gladwin, MT Biernacki, M Rogers, SA Wang, XD Zahrieh, D Antin, JH Ritz, J AF Wu, CJ Krishnamurti, L Gladwin, MT Biernacki, M Rogers, SA Wang, XD Zahrieh, D Antin, JH Ritz, J TI Mixed hematopoietic chimerism for sickle cell disease prevents intravascular hemolysis and corrects biomarkers of endothelial function. SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 Dana Farber Canc Inst, Dept Hematol Neoplasia, Boston, MA USA. Brigham & Womens Hosp, Dept Med, Boston, MA USA. Childrens Hosp Pittsburgh, Pittsburgh, PA USA. NHLBI, Cardiovasc Branch, Vasc Therapeut Sect, NIH, Bethesda, MD 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 2005 VL 106 IS 11 MA 2333 BP 656A EP 656A PN 1 PG 1 WC Hematology SC Hematology GA 986CF UT WOS:000233426004180 ER PT J AU Vance, GH Kim, H Hicks, G Cherry, A Higgins, R Tallman, MS Fernandez, HF Dewald, G AF Vance, GH Kim, H Hicks, G Cherry, A Higgins, R Tallman, MS Fernandez, HF Dewald, G TI Utility of interphase FISH to stratify patients into cytogenetic risk categories at diagnosis of AML in an ECOG clinical trial (E1900). SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 Indiana Univ, Sch Med, Indianapolis, IN 46204 USA. Dana Farber Canc Inst, Boston, MA 02115 USA. Mayo Clin, Rochester, MN USA. Stanford Hlth Serv, Stanford, CA USA. Abbott NW Hosp, Minneapolis, MN 55407 USA. Northwestern Univ, Feinberg Sch Med, Chicago, IL 60611 USA. Florida Int Univ, Miami, FL 33199 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 2005 VL 106 IS 11 MA 2377 BP 669A EP 669A PN 1 PG 1 WC Hematology SC Hematology GA 986CF UT WOS:000233426004224 ER PT J AU Aguiar, RCT Takeyama, K He, CY Kreinbrink, K Shipp, MA AF Aguiar, RCT Takeyama, K He, CY Kreinbrink, K Shipp, MA TI B-aggressive lymphoma (BAL) family proteins have unique domains which modulate transcription and exhibit PARP activity. SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 Dana Farber Canc Inst, Div Hematol Malignancies, 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 2005 VL 106 IS 11 MA 2400 BP 675A EP 675A PN 1 PG 1 WC Hematology SC Hematology GA 986CF UT WOS:000233426004247 ER PT J AU Bae, J Mitsiades, C Yu-Tzu, T Martinson, J Batchu, RB Bertheau, R Li, C Prabhala, R Masood, S Hideshima, T Catley, L Anderson, K Munshi, N AF Bae, J Mitsiades, C Yu-Tzu, T Martinson, J Batchu, RB Bertheau, R Li, C Prabhala, R Masood, S Hideshima, T Catley, L Anderson, K Munshi, N TI Hsp90 is critical for the regulation of phenotype and functionality of human dendritic cells. SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 Harvard Univ, Med Ctr, Dana Farber Canc Inst, Boston, MA 02115 USA. Rush Univ, Med Ctr, Chicago, IL 60612 USA. Harvard Univ, Med Ctr, Dana Farber Canc Inst, Boston, MA 02115 USA. RI Catley, Laurence/E-5313-2013 NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2005 VL 106 IS 11 MA 2401 BP 675A EP 676A PN 1 PG 2 WC Hematology SC Hematology GA 986CF UT WOS:000233426004248 ER PT J AU Friedberg, JW Kelly, J Kutok, JL Salloum, R Brenn, T Fisher, DC Ronan, E McCauley, M Rich, L Marquis, D Rothberg, PG Liesveld, J Fisher, RI Coffman, R Mosmann, T Freedman, AS AF Friedberg, JW Kelly, J Kutok, JL Salloum, R Brenn, T Fisher, DC Ronan, E McCauley, M Rich, L Marquis, D Rothberg, PG Liesveld, J Fisher, RI Coffman, R Mosmann, T Freedman, AS TI CpG oligonucleotide (1018 ISS) may overcome rituximab (R) resistance in follicular lymphoma (FL) through enhanced ADCC, T cell expansion, and alteration of tumor microenvironment. SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 Univ Rochester, James P Wilmot Canc Ctr, Rochester, NY USA. Brigham & Womens Hosp, Boston, MA 02115 USA. Dana Farber Canc Inst, Boston, MA 02115 USA. Dynavax Technol, Berkeley, 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 2005 VL 106 IS 11 MA 2434 BP 684A EP 685A PN 1 PG 2 WC Hematology SC Hematology GA 986CF UT WOS:000233426004281 ER PT J AU Hatjiharissi, E Hansen, M Verselis, S Santos, DD Xu, L Manning, R Hunter, Z Leleu, X Ho, AW Patterson, CJ Fox, E Treon, SP AF Hatjiharissi, E Hansen, M Verselis, S Santos, DD Xu, L Manning, R Hunter, Z Leleu, X Ho, AW Patterson, CJ Fox, E Treon, SP TI Polymorphisms in Fc gamma RIIIA are genetically linked to Fc gamma RIIA and may account for the primary predictive role ascribed to polymorphisms in Fc gamma RIIIA-158 in determining rituximab responses. SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 Dana Farber Canc Inst, Bing Ctr Waldenstroms Macroglobulinemia, Boston, MA 02115 USA. Harvard Univ, Sch Med, Boston, MA 02115 USA. Dana Farber Canc Inst, Mol Diagnost Lab, Boston, MA 02115 USA. RI Hunter, Zachary/H-3018-2013 OI Hunter, Zachary/0000-0002-1689-1691 NR 0 TC 0 Z9 1 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2005 VL 106 IS 11 MA 2433 BP 684A EP 684A PN 1 PG 1 WC Hematology SC Hematology GA 986CF UT WOS:000233426004280 ER PT J AU Friedberg, JW Leonard, JP Younes, A Fisher, DC Gordon, LI Moore, JO Czucznan, MS Miller, TP Stiff, PJ Cheson, BD Forero-Torres, A Finucane, DM Leigh, BR Molina, A AF Friedberg, JW Leonard, JP Younes, A Fisher, DC Gordon, LI Moore, JO Czucznan, MS Miller, TP Stiff, PJ Cheson, BD Forero-Torres, A Finucane, DM Leigh, BR Molina, A TI Updated results from a phase II study of galiximab (anti-CD80) in combination with rituximab for relapsed or refractory, follicular NHL. SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 Univ Rochester, Med Ctr, Rochester, NY 14642 USA. Weill Cornell Med Ctr, New York, NY USA. Univ Texas, MD Anderson Canc Ctr, Houston, TX 77030 USA. Dana Farber Canc Inst, Boston, MA 02115 USA. Northwestern Univ, Feinberg Sch Med, Chicago, IL 60611 USA. Duke Univ, Med Ctr, Durham, NC USA. Roswell Pk Canc Inst, Buffalo, NY 14263 USA. Univ Arizona, Tucson, AZ USA. Loyola Univ, Med Ctr, Chicago, IL 60611 USA. Georgetown Univ, Washington, DC USA. Univ Alabama, Birmingham, AL USA. Biogen Idec, San Diego, CA USA. NR 0 TC 9 Z9 9 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2005 VL 106 IS 11 MA 2435 BP 685A EP 685A PN 1 PG 1 WC Hematology SC Hematology GA 986CF UT WOS:000233426004282 ER PT J AU Treon, SP Hunter, Z Patterson, CJ Branagan, AR AF Treon, SP Hunter, Z Patterson, CJ Branagan, AR TI Thalidomide in combination with rituximab is active in Waldenstrom's macroglobulinemia and may overcome poor response determinants associated with rituximab monotherapy. SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 Dana Farber Canc Inst, Bing Ctr Waldenstroms Macroglobulinemia, Boston, MA 02115 USA. RI Hunter, Zachary/H-3018-2013 OI Hunter, Zachary/0000-0002-1689-1691 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 2005 VL 106 IS 11 MA 2442 BP 686A EP 687A PN 1 PG 2 WC Hematology SC Hematology GA 986CF UT WOS:000233426004289 ER PT J AU Treon, SP Patterson, CJ Hunter, ZR Branagan, AR AF Treon, SP Patterson, CJ Hunter, ZR Branagan, AR TI Phase II study of CC-5013 (revlimid) and rituximab in Waldenstrom's macroglobulinemia: Preliminary safety and efficacy results. SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 Dana Farber Canc Inst, Bing Ctr Waldenstroms Macroglobulinemia, 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 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2005 VL 106 IS 11 MA 2443 BP 687A EP 687A PN 1 PG 1 WC Hematology SC Hematology GA 986CF UT WOS:000233426004290 ER PT J AU Bradner, J Shen, JP Greenberg, E Hideshima, T Anderson, KC Schreiber, SL AF Bradner, J Shen, JP Greenberg, E Hideshima, T Anderson, KC Schreiber, SL TI Targeting the protein degradation pathway in multiple myeloma with synergistic, selective small molecules. SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 Broad Inst Harvard, Chem Biol Grp, Cambridge, MA USA. MIT, Cambridge, MA 02139 USA. Jerome Lipper Multiple Myeloma Ctr, Dana Farber Canc Inst, Boston, MA USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2005 VL 106 IS 11 MA 2471 BP 694A EP 694A PN 1 PG 1 WC Hematology SC Hematology GA 986CF UT WOS:000233426004318 ER PT J AU Neri, P Tassone, P Shammas, MA Carrasco, DR Burger, R Mitsdiades, CS Blotta, S Prabhala, RH Catley, L Venuta, S Anderson, KC Munshi, NC AF Neri, P Tassone, P Shammas, MA Carrasco, DR Burger, R Mitsdiades, CS Blotta, S Prabhala, RH Catley, L Venuta, S Anderson, KC Munshi, NC TI Novel model to evaluate changes in gene expression profile of Myeloma cells in vivo following interaction with human BM microenvironment. SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 Jerome Lipper Multiple Myeloma Ctr, Dana Farber Canc Inst, Boston, MA USA. VA Boston Healthcare Syst, Boston, MA USA. Univ Magna Graecia, Catanzaro, Italy. 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 2005 VL 106 IS 11 MA 2490 BP 699A EP 700A PN 1 PG 2 WC Hematology SC Hematology GA 986CF UT WOS:000233426004337 ER PT J AU Dispenzieri, A Blood, E Vesole, D Fonseca, R Callander, N Greipp, PR AF Dispenzieri, A Blood, E Vesole, D Fonseca, R Callander, N Greipp, PR TI A phase II study of PS-341 for patients with high risk, newly diagnosed multiple myeloma: A trial of the Eastern Cooperative Oncology Group (E2A02). SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 Mayo Clin, Rochester, MN USA. Dana Farber Canc Inst, Boston, MA 02115 USA. St Vincents Comprehens Canc Ctr, New York, NY USA. Univ Wisconsin, Madison, WI USA. Mayo Clin, Scottsdale, AZ 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 2005 VL 106 IS 11 MA 2546 BP 715A EP 715A PN 1 PG 1 WC Hematology SC Hematology GA 986CF UT WOS:000233426004393 ER PT J AU Chanan-Khan, AA Richardson, P Lonial, S Siegel, D Jagannath, S Mehta, J Doran, J Singhal, S AF Chanan-Khan, AA Richardson, P Lonial, S Siegel, D Jagannath, S Mehta, J Doran, J Singhal, S TI Safety and efficacy of bortezomib in multiple myeloma patients with renal failure requiring dialysis. SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 Roswell Pk Canc Inst, Buffalo, NY 14263 USA. Dana Farber Canc Inst, Boston, MA USA. Emory Univ, Atlanta, GA 30322 USA. Hackensack Univ Hosp, Hackensack, NJ USA. Northwestern Univ, Evanston, IL 60208 USA. NR 0 TC 5 Z9 5 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2005 VL 106 IS 11 MA 2550 BP 716A EP 717A PN 1 PG 2 WC Hematology SC Hematology GA 986CF UT WOS:000233426004397 ER PT J AU Richardson, P Chanan-Khan, A Schlossman, R Munshi, N Wen, P Briemberg, H Kuter, D Oaklander, A Lodial, S Hassoun, H Doss, D Lunde, L Hayes, S McKenney, M Hande, K Lai, L Freeman, A Dinand, K McAlister, C Warren, D Collins, D Esseltine, D Amato, A Anderson, K AF Richardson, P Chanan-Khan, A Schlossman, R Munshi, N Wen, P Briemberg, H Kuter, D Oaklander, A Lodial, S Hassoun, H Doss, D Lunde, L Hayes, S McKenney, M Hande, K Lai, L Freeman, A Dinand, K McAlister, C Warren, D Collins, D Esseltine, D Amato, A Anderson, K TI A Multicenter phase II trial of bortezomib in patients with previously untreated multiple myeloma: Efficacy with manageable toxicity in patients with unexpectedly high rates of baseline peripheral neuropathy. SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 Dana Farber Canc Inst, Boston, MA USA. Massachusetts Gen Hosp, Boston, MA 02114 USA. Emory Univ, Atlanta, GA 30322 USA. Mem Sloan Kettering Canc Ctr, New York, NY 10021 USA. NR 0 TC 11 Z9 12 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 2005 VL 106 IS 11 MA 2548 BP 716A EP 716A PN 1 PG 1 WC Hematology SC Hematology GA 986CF UT WOS:000233426004395 ER PT J AU Jagannath, S Siegel, D Richardson, P Mazumder, A Sydor, J Goddard, J Walker, J Patterson, J Normant, E Tong, J Palombella, V Anderson, K Adams, J Grayzel, D AF Jagannath, S Siegel, D Richardson, P Mazumder, A Sydor, J Goddard, J Walker, J Patterson, J Normant, E Tong, J Palombella, V Anderson, K Adams, J Grayzel, D TI Phase I clinical trial of IPI-504, a novel, water-soluble Hsp90 inhibitor, in patients with Relapsed/Refractory multiple myeloma (MM). SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 St Vincents Comprehens Canc Ctr, Ctr Myeloma Res, New York, NY USA. Hackensack Univ, Med Ctr, Hackensack, NJ USA. Dana Farber Canc Inst, Jerome Lipper Multiple Myeloma Ctr, Dept Med Oncol, Boston, MA 02115 USA. Infin Pharmaceut Inc, Cambridge, MA 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 2005 VL 106 IS 11 MA 2560 BP 719A EP 720A PN 1 PG 2 WC Hematology SC Hematology GA 986CF UT WOS:000233426004407 ER PT J AU Mateos, MV Blade, J Prosper, F Lahuerta, JJ Garcia-Sanz, R Cibeira, M Rusinol, L Escalante, F Ruiz, M Richardson, PG Miguel, JFS AF Mateos, MV Blade, J Prosper, F Lahuerta, JJ Garcia-Sanz, R Cibeira, M Rusinol, L Escalante, F Ruiz, M Richardson, PG Miguel, JFS TI Preliminary report from an exploratory Phase II trial with Plitidepsin (Aplidin (R)) in patients with refractory/relapsed multiple myeloma. SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 Hosp Univ Salamanca, Dept Hematol, Salamanca, Spain. Hosp Clin Barcelona, Dept Hematol, E-08036 Barcelona, Spain. Clin Univ Navarra, Dept Hematol, Navarra, Spain. Hosp 12 Octubre, Dept Hematol, E-28041 Madrid, Spain. PharMamar SAU, Clin R&D, Madrid, Spain. Dana Farber Canc Inst, Jerome Lipper Multiple Myeloma Ctr, Boston, MA USA. NR 0 TC 2 Z9 2 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 2005 VL 106 IS 11 MA 2569 BP 722A EP 722A PN 1 PG 1 WC Hematology SC Hematology GA 986CF UT WOS:000233426004416 ER PT J AU Hussein, MA Berenson, JR Niesvizky, R Munshi, NC Harrop, KL McDonald, M Drachman, JG AF Hussein, MA Berenson, JR Niesvizky, R Munshi, NC Harrop, KL McDonald, M Drachman, JG TI A phase I humanized Anti-CD40 monoclonal antibody (SGN-40) in patients with multiple myeloma. SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 Cleveland Clin Taussig Canc Ctr, Cleveland Clin Multiple Myeloma Res Program, Cleveland, OH USA. Inst Myeloma & Bone Canc Res, Los Angeles, CA USA. Cornell Univ, Weill Med Coll, New York, NY 10021 USA. Dana Farber Canc Inst, Boston, MA 02115 USA. Seattle Genet Inc, Bothell, WA USA. NR 0 TC 5 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 2005 VL 106 IS 11 MA 2572 BP 723A EP 723A PN 1 PG 1 WC Hematology SC Hematology GA 986CF UT WOS:000233426004419 ER PT J AU O'Neil, J Calvo, J McKenna, K Krishnamoorthy, V Aster, JC Bassing, CH Alt, FW Kelliher, M Look, AT AF O'Neil, J Calvo, J McKenna, K Krishnamoorthy, V Aster, JC Bassing, CH Alt, FW Kelliher, M Look, AT TI Activating Notch1 mutations in mouse models of T-ALL. SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 Dana Farber Canc Inst, Dept Pediat Oncol, Boston, MA 02115 USA. Univ Massachusetts, Sch Med, Dept Canc Biol, Worcester, MA 01605 USA. Brigham & Womens Hosp, Dept Pathol, Boston, MA 02115 USA. Childrens Hosp, Howard Hughes Med Inst, Boston, MA 02115 USA. Harvard Univ, Sch Med, Dept Genet, Boston, MA 02115 USA. Ctr Blood Res, Boston, MA 02115 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2005 VL 106 IS 11 MA 2609 BP 734A EP 734A PN 1 PG 1 WC Hematology SC Hematology GA 986CF UT WOS:000233426004456 ER PT J AU Owens, BM Yu, L Steidl, U Kutok, JL Clayton, LK Wagner, K Iwasaki, H Liu, CH Hackanson, B Akashi, K Plass, C Tenen, DG Rosenbauer, F AF Owens, BM Yu, L Steidl, U Kutok, JL Clayton, LK Wagner, K Iwasaki, H Liu, CH Hackanson, B Akashi, K Plass, C Tenen, DG Rosenbauer, F TI Identification of ID4 as a cooperating second hit for T cell lymphoma development in PU.1 URE Delta/Delta mice. SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 Harvard Univ, Inst Med, Boston, MA 02115 USA. Ohio State Univ, Div Hematol Oncol, Columbus, OH 43210 USA. Brigham & Womens Hosp, Dept Pathol, Boston, MA 02115 USA. Harvard Univ, Sch Med, Dana Farber Canc Inst, Immunobiol Lab, Boston, MA 02115 USA. Harvard Univ, Sch Med, Dana Farber Canc Inst, Dept Canc Immunol & AIDS, Boston, MA 02115 USA. RI Plass, Christoph/H-7192-2014 NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2005 VL 106 IS 11 MA 2613 BP 734A EP 735A PN 1 PG 2 WC Hematology SC Hematology GA 986CF UT WOS:000233426004460 ER PT J AU Pasqualucci, L Compagno, M Houldsworth, J Monti, S Grunn, A Shipp, MA Dalla-Favera, R AF Pasqualucci, L Compagno, M Houldsworth, J Monti, S Grunn, A Shipp, MA Dalla-Favera, R TI Inactivation of the PRDM1/BLIMP1 gene in non-GC-type diffuse large B-cell lymphoma. SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 Columbia Univ, Inst Canc Genet, New York, NY 10027 USA. Columbia Univ, Herbert Irving Comprehens Canc Ctr, New York, NY 10027 USA. Mem Sloan Kettering Canc Ctr, Cell Biol Program, New York, NY 10021 USA. Broad Inst, Cambridge, MA USA. Dana Farber Canc Inst, Boston, MA 02115 USA. NR 0 TC 0 Z9 0 U1 0 U2 2 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2005 VL 106 IS 11 MA 2614 BP 735A EP 735A PN 1 PG 1 WC Hematology SC Hematology GA 986CF UT WOS:000233426004461 ER PT J AU Yang, H Reheman, A Chen, PG Hynes, RO Freedman, J Wagner, DD Ni, HY AF Yang, H Reheman, A Chen, PG Hynes, RO Freedman, J Wagner, DD Ni, HY TI Fibrinogen and von Willebrand factor-independent platelet aggregation: The essential roles of beta 3 integrin, thrombin, and divalent Ca2+ cations. SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 Univ Toronto, Dept Lab Med & Pathobiol, Toronto, ON, Canada. St Michaels Hosp, Toronto, ON M5B 1W8, Canada. Canadian Blood Serv, Toronto, ON, Canada. Howard Hughes Med Inst, MIT, Dept Biol, Boston, MA 02115 USA. Ctr Canc Res, Boston, MA 02115 USA. Harvard Univ, Sch Med, Dept Pathol, Boston, MA 02115 USA. Harvard Univ, Sch Med, CBR Inst Biomed Res, 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 2005 VL 106 IS 11 MA 2651 BP 744A EP 744A PN 1 PG 1 WC Hematology SC Hematology GA 986CF UT WOS:000233426004498 ER PT J AU Dole, VS Bergmeier, W Eichenberger, SC Wagner, DD AF Dole, VS Bergmeier, W Eichenberger, SC Wagner, DD TI Downregulation of P-selectin from activated platelets involves both receptor internalization and shedding upon binding to PSGL-1. SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 CBR Inst Biomed Res Inc, CBRI, 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 2005 VL 106 IS 11 MA 2656 BP 745A EP 746A PN 1 PG 2 WC Hematology SC Hematology GA 986CF UT WOS:000233426004503 ER PT J AU Attar, EC De Angelo, DJ Sirulnik, A Wadleigh, M Ballen, KK Miller, KB Galinsky, I Neuberg, D Trehu, E Schenkein, D Stone, RM Amrein, PC AF Attar, EC De Angelo, DJ Sirulnik, A Wadleigh, M Ballen, KK Miller, KB Galinsky, I Neuberg, D Trehu, E Schenkein, D Stone, RM Amrein, PC TI Addition of bortezomib (Velcade) to AML induction chemotherapy is well tolerated and results in a high complete remission rate SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 Massachusetts Gen Hosp, Ctr Canc, Hematol Oncol Unit, Boston, MA 02114 USA. Dana Farber Canc Inst, Boston, MA 02115 USA. Beth Israel Deaconess Med Ctr, Hematol Malignancy Unit, Boston, MA 02215 USA. Millennium Pharmaceut Inc, Cambridge, MA 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 2005 VL 106 IS 11 MA 2782 BP 780A EP 780A PN 1 PG 1 WC Hematology SC Hematology GA 986CF UT WOS:000233426005102 ER PT J AU Rosenblatt, J Stone, R Lenahan, C Wu, Z Vasir, B DeAngelo, DJ Galinsky, I Miller, K Levine, JD Joyce, R Kufe, D Avigan, D AF Rosenblatt, J Stone, R Lenahan, C Wu, Z Vasir, B DeAngelo, DJ Galinsky, I Miller, K Levine, JD Joyce, R Kufe, D Avigan, D TI Leukemia derived dendritic cells (LDCs) are functionally deficient and inferior to DC/leukemia fusion cells as a tumor vaccine for AML SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 Beth Israel Deaconess Med Ctr, Boston, MA 02215 USA. Dana Farber Canc Inst, Boston, MA 02115 USA. NR 0 TC 0 Z9 0 U1 0 U2 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 2005 VL 106 IS 11 MA 2788 BP 782A EP 782A PN 1 PG 1 WC Hematology SC Hematology GA 986CF UT WOS:000233426005108 ER PT J AU Gabrilove, JL McConnell, MJ Berkofsky-Fessler, W Sirulnik, AL Sharma, S Silverman, LR Isola, L Mandeli, J Licht, J AF Gabrilove, JL McConnell, MJ Berkofsky-Fessler, W Sirulnik, AL Sharma, S Silverman, LR Isola, L Mandeli, J Licht, J TI A phase I-II pilot study of divalproex sodium alone and in combination with all-trans-retinoic acid (ATRA) in relapsed or refractory acute myeloid leukemia SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 Mt Sinai Sch Med, 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 2005 VL 106 IS 11 MA 2799 BP 785A EP 785A PN 1 PG 1 WC Hematology SC Hematology GA 986CF UT WOS:000233426005119 ER PT J AU LaCasce, A Niland, J Kho, ME TerVeer, A Friedberg, JW Rodriguez, MA Czuczman, MS Millenson, M Zelenetz, AD Nademanee, AP Weeks, JC AF LaCasce, A Niland, J Kho, ME TerVeer, A Friedberg, JW Rodriguez, MA Czuczman, MS Millenson, M Zelenetz, AD Nademanee, AP Weeks, JC TI Potential impact of pathologic review on therapy in non-Hodgkin's lymphoma (NHL): Analysis from the national comprehensive cancer network (NCCN) NHL outcomes project SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 Dana Farber Canc Inst, Boston, MA 02115 USA. Roswell Pk Canc Inst, Buffalo, NY 14263 USA. Wilmot Canc Ctr, Rochester, NY USA. Fox Chase Canc Ctr, Philadelphia, PA 19111 USA. City Hope Canc Ctr, Duarte, CA USA. MD Anderson Canc Ctr, Houston, TX USA. Mem Sloan Kettering Canc Ctr, New York, NY 10021 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2005 VL 106 IS 11 MA 2816 BP 789A EP 789A PN 1 PG 1 WC Hematology SC Hematology GA 986CF UT WOS:000233426005136 ER PT J AU Koptyra, M Houghtaling, S Grompe, M Skorski, T AF Koptyra, M Houghtaling, S Grompe, M Skorski, T TI Fanconi anemia D2 protein contributes to BCR/ABL-mediated transformation of hematopoietic cells SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 Temple Univ, Ctr Biotechnol, Philadelphia, PA 19122 USA. Oregon Hlth & Sci Univ, Portland, OR USA. Harvard Univ, Sch Med, Dana Farber Canc Inst, Boston, MA 02115 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2005 VL 106 IS 11 MA 2878 BP 806A EP 807A PN 1 PG 2 WC Hematology SC Hematology GA 986CF UT WOS:000233426005198 ER PT J AU Shaffer, JM Villard, J Means, T Dombkowski, D Dey, B McAffee, S Ballen, K Power, K Saidman, S Preffer, F Spitzer, TR Sykes, M AF Shaffer, JM Villard, J Means, T Dombkowski, D Dey, B McAffee, S Ballen, K Power, K Saidman, S Preffer, F Spitzer, TR Sykes, M TI Fludarabine treatment is associated with depletion of host CD4+CD25(high), FOXP3+, CTLA-4+cells and increased Incidences of full donor chimerism and GVHD in non-myeloablative haploidentical hematopoietic cell transplant recipients SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA 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 2005 VL 106 IS 11 MA 2898 BP 813A EP 813A PN 1 PG 1 WC Hematology SC Hematology GA 986CF UT WOS:000233426005218 ER PT J AU Sharma, S Lichtenstein, A AF Sharma, S Lichtenstein, A TI Premature termination codon mutations in chronic lymphocytic leukemia (CLL): Identification of potential tumor suppressors in CLL including E-cadherin SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 Univ Calif Los Angeles, W Los Angeles VA Med Ctr, Los Angeles, CA USA. NR 0 TC 0 Z9 0 U1 0 U2 2 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2005 VL 106 IS 11 MA 2935 BP 824A EP 824A PN 1 PG 1 WC Hematology SC Hematology GA 986CF UT WOS:000233426005255 ER PT J AU Okuya, M Kurosawa, H Matsunaga, T Eguchi, M Furukawa, Y Inukai, T Matsui, H Look, AT Inaba, T AF Okuya, M Kurosawa, H Matsunaga, T Eguchi, M Furukawa, Y Inukai, T Matsui, H Look, AT Inaba, T TI lPivotal role of survivin in leukemogenesis by E2A-HLF chimeric transcription factor. SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 Dokkyo Univ, Sch Med, Mibu, Tochigi 32102, Japan. Jichi Med Sch, Stem Cell Regulat, Minami Kawachi, Tochigi 32904, Japan. Ymanashi Univ, Tamaho, Yamanashi, Japan. Hiroshima Univ, Res Inst Radiat Biol & Med, Hiroshima, Japan. Dana Farber Canc Inst, Boston, MA USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2005 VL 106 IS 11 MA 2988 BP 837A EP 837A PN 1 PG 1 WC Hematology SC Hematology GA 986CF UT WOS:000233426005308 ER PT J AU Li, Z Klusmann, JH Godinho, FJ Lee, HW Reinhardt, D Orkin, SH AF Li, Z Klusmann, JH Godinho, FJ Lee, HW Reinhardt, D Orkin, SH TI A genome-wide retroviral insertional mutagenesis screen for genes cooperating with truncated, oncogenic GATA1s. SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 Childrens Hosp, Boston, MA 02115 USA. Harvard Univ, Sch Med, Boston, MA 02115 USA. Dana Farber Canc Inst, Boston, MA 02115 USA. Howard Hughes Med Inst, Boston, MA 02115 USA. Hannover Med Sch, D-3000 Hannover, Germany. RI 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 2005 VL 106 IS 11 MA 2990 BP 838A EP 838A PN 1 PG 1 WC Hematology SC Hematology GA 986CF UT WOS:000233426005310 ER PT J AU Haspel, RL Kao, GS Yeap, B Spitzer, TR Ritz, J Antin, JH Ballen, K AF Haspel, RL Kao, GS Yeap, B Spitzer, TR Ritz, J Antin, JH Ballen, K TI Pre-infusion characteristics of the predominant cord blood unit correlate with hematopoietic engraftment in the setting of non-myeloablative double cord blood transplant (DCBT). SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 Massachusetts Gen Hosp, Dept Pathol, Boston, MA 02114 USA. Massachusetts Gen Hosp, Dept Med, Boston, MA 02114 USA. Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02115 USA. Massachusetts Gen Hosp, MGH Biostat Ctr, 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 2005 VL 106 IS 11 MA 3027 BP 848A EP 848A PN 1 PG 1 WC Hematology SC Hematology GA 986CF UT WOS:000233426005347 ER PT J AU Parkman, R Cohen, G Carter, SL Weinberg, KI Masinsin, B Guinan, EC Kurtzberg, J Wagner, JE Kernan, NA AF Parkman, R Cohen, G Carter, SL Weinberg, KI Masinsin, B Guinan, EC Kurtzberg, J Wagner, JE Kernan, NA TI Antigen-specific T lymphocyte function following unrelated cord blood transplantation (UCBT). SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 Childrens Hosp Los Angeles, Div Immunol Res, Los Angeles, CA 90027 USA. Emmes Corp, Rockville, MD USA. Dana Farber Canc Inst, Hematopoiet Stem Cell Transplantat Program, Boston, MA USA. Duke Univ, Med Ctr, Pediat Bone Marrow & Stem Cell Transplant Program, Durham, NC USA. Univ Minnesota, Adult & Pediat Blood & Bone Marrow Transplant Pro, Minneapolis, MN USA. Mem Sloan Kettering Canc Ctr, Unrelated Donor Program, 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 2005 VL 106 IS 11 MA 3032 BP 849A EP 849A PN 1 PG 1 WC Hematology SC Hematology GA 986CF UT WOS:000233426005352 ER PT J AU Bellucci, R Gallagher, M Oertelt, S Zorn, E Alyea, EP Soiffer, R Wu, CJ Munshi, NC Gershwin, E Ritz, J AF Bellucci, R Gallagher, M Oertelt, S Zorn, E Alyea, EP Soiffer, R Wu, CJ Munshi, NC Gershwin, E Ritz, J TI Patients who respond to donor lymphocyte infusion (DLI) have an antibody response against PDC-E2, the immunodominant autoantigens of primary biliary cirrhosis (PBC), but with different specificity. SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 Harvard Univ, Sch Med, Dana Farber Canc Inst, Boston, MA 02115 USA. Univ Calif Davis, Davis, CA 95616 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 2005 VL 106 IS 11 MA 3105 BP 868A EP 868A PN 1 PG 1 WC Hematology SC Hematology GA 986CF UT WOS:000233426005425 ER PT J AU Krishnamurti, L Wu, C Baker, KS Wagner, JE AF Krishnamurti, L Wu, C Baker, KS Wagner, JE TI Matched sibling donor hematopoietic cell transplantation for sickle cell disease using a reduced intensity conditioning regimen can lead to stable long term engraftment. SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 Childrens Hosp Pittsburgh, Div Hematol Oncol, BMT, Pittsburgh, PA 15213 USA. Dana Farber Canc Inst, Boston, MA 02115 USA. Univ Minnesota, Minneapolis, MN USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2005 VL 106 IS 11 MA 3172 BP 886A EP 886A PN 1 PG 1 WC Hematology SC Hematology GA 986CF UT WOS:000233426005492 ER PT J AU Tholouli, E Di Vizio, D O'Connell, F Loda, M Twomey, D Golub, T Levenson, R Hoyland, J Yin, JL Byers, R AF Tholouli, E Di Vizio, D O'Connell, F Loda, M Twomey, D Golub, T Levenson, R Hoyland, J Yin, JL Byers, R TI Quantum dot based duplex in situ hybridisation for gene expression profiling SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 Manchester Royal Infirm, Univ Dept Haematol, Manchester, Lancs, England. Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02115 USA. MIT, Broad Inst, Canc Program, Cambridge, MA 02139 USA. Cambridge Res & Instrumentat, Woburn, MA USA. Univ Manchester, Div Lab & Regenerat Med, Manchester, Lancs, England. NR 0 TC 0 Z9 0 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 2005 VL 106 IS 11 MA 3265 BP 913A EP 913A PN 1 PG 1 WC Hematology SC Hematology GA 986CF UT WOS:000233426006049 ER PT J AU Soupir, CP Vergilio, JA Dal Cin, P Muzikansky, A Kantarjian, HM Jones, D Hasserjian, RR AF Soupir, CP Vergilio, JA Dal Cin, P Muzikansky, A Kantarjian, HM Jones, D Hasserjian, RR TI Philadelphia chromosome positive acute myeloid leukemia: An aggressive acute leukemia with clinicopathologic features distinct from chronic myeloid leukemia in blast crisis SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 Massachusetts Gen Hosp, Ctr Biostat, Boston, MA 02114 USA. Brigham & Womens Hosp, Boston, MA 02115 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 2005 VL 106 IS 11 MA 3290 BP 920A EP 920A PN 1 PG 1 WC Hematology SC Hematology GA 986CF UT WOS:000233426006074 ER PT J AU Lafuente, EM Constantine, EM Salanga, M Boussiotis, VA AF Lafuente, EM Constantine, EM Salanga, M Boussiotis, VA TI RIAM, a novel Rap-1 effector, is recruited at the immunological synapse and the lipid rafts and links TCR-mediated signals to the actin cytoskeleton SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 Massachusetts Gen Hosp, Bone Marrow Transplantat TBRC, Boston, MA 02114 USA. Childrens Hosp, 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 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 2005 VL 106 IS 11 MA 3299 BP 922A EP 923A PN 1 PG 2 WC Hematology SC Hematology GA 986CF UT WOS:000233426006083 ER PT J AU Li, LQ Fehr, T Boussiotis, VA AF Li, LQ Fehr, T Boussiotis, VA TI Rap1-GTP promotes the generation and effector function of cytotoxic CD8+T cells. SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA 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 2005 VL 106 IS 11 MA 3325 BP 929A EP 929A PN 1 PG 1 WC Hematology SC Hematology GA 986CF UT WOS:000233426006109 ER PT J AU Korfel, A Jahnke, K O'Neill, BP Blay, JY Abrey, L Martus, P Poortmans, PMP Shenkier, TN Batchelor, TT Neuwelt, EA Raizer, JJ Pels, H Herrlinger, U Thiel, E AF Korfel, A Jahnke, K O'Neill, BP Blay, JY Abrey, L Martus, P Poortmans, PMP Shenkier, TN Batchelor, TT Neuwelt, EA Raizer, JJ Pels, H Herrlinger, U Thiel, E TI International primary central nervous system lymphoma collaborative group (IPCG) study on low-grade primary central nervous system lymphoma in immunocompetent patients. SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 Charite Univ Med Berlin, Berlin, Germany. Mayo Clin, Ctr Canc, Neuro Oncol Program, Rochester, MN USA. Ctr Leon Berard, Unite Cytekines & Canc, F-69373 Lyon, France. Hop Edouard Herriot, Unite Cytekines & Canc, F-69373 Lyon, France. Mem Sloan Kettering Canc Ctr, New York, NY 10021 USA. Charite Univ Med Berlin, Berlin, Germany. Dr Bernard Verbeeten Inst, Tilburg, Netherlands. British Columbia Canc Agcy, Vancouver, BC V5Z 4E6, Canada. Harvard Univ, Massachusetts Gen Hosp, Sch Med, Boston, MA 02115 USA. Oregon Hlth & Sci Univ, Blood Brain Barrier & Neurooncol Program, Portland, OR 97201 USA. Northwestern Univ, Feinberg Sch Med, Davee Dept Neurol, Chicago, IL 60611 USA. Ruhr Univ Bochum, Knappschaftskrankenhaus Bochum Langendreer, D-4630 Bochum, Germany. Univ Tubingen, Ctr Neurol, Tubingen, Germany. RI Poortmans, P.M.P./L-4581-2015; Blay, Jean-Yves/N-3966-2016 OI 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 J9 BLOOD JI Blood PD NOV 16 PY 2005 VL 106 IS 11 MA 3343 BP 934A EP 934A PN 1 PG 1 WC Hematology SC Hematology GA 986CF UT WOS:000233426006127 ER PT J AU Rodig, SJ Abramson, JS Pinkus, GS Treon, SP Shipp, MA Kutok, JL AF Rodig, SJ Abramson, JS Pinkus, GS Treon, SP Shipp, MA Kutok, JL TI Evaluation of CD52 expression in hematopoietic neoplasms by standard immunohistochemistry: Implications for the expanded use of alemtuzumab (CAMPATH-1H) in the treatment of hematological malignancies. SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 Brigham & Womens Hosp, Dept Pathol, Boston, MA 02115 USA. Dana Farber Canc Inst, Dept Adult Oncol, Boston, MA 02115 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2005 VL 106 IS 11 MA 3346 BP 935A EP 935A PN 1 PG 1 WC Hematology SC Hematology GA 986CF UT WOS:000233426006130 ER PT J AU Burger, R Legouill, S Tai, YT Shringarpure, R Podar, K Catley, L Tassone, P Neri, P Hideshima, T Chauhan, D Caulder, E Vaddi, K Neilan, CL Gramatzki, M 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 Caulder, E Vaddi, K Neilan, CL Gramatzki, M Fridman, JS Anderson, KC TI The JAK inhibitor INCB20 induces antiproliferative and apoptotic effects in human myeloma cells in vitro and in vivo SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 Univ Kiel, Dept Med 2, Div Stem Cell Transplantat & Immunotherapy, D-24098 Kiel, Germany. Dana Farber Canc Inst, Dept Med Oncol, Jerome Lipper Multiple Myeloma Ctr, Boston, MA USA. Incyte Corp, Wilmington, DE USA. RI Gramatzki, Martin/A-9533-2010; 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 2005 VL 106 IS 11 MA 3357 BP 938A EP 938A PN 1 PG 1 WC Hematology SC Hematology GA 986CF UT WOS:000233426006141 ER PT J AU Schittenhelm, MM Shiraga, S Schroeder, A Corbin, AS Griffith, D Lee, FY Deininger, MW Druker, BJ Heinrich, MC AF Schittenhelm, MM Shiraga, S Schroeder, A Corbin, AS Griffith, D Lee, FY Deininger, MW Druker, BJ Heinrich, MC TI Dasatinib (BMS-354825), a multi-targeted kinase inhibitor, inhibits the kinase activity of wild-type, juxtamembrane and activation loop mutant kit isoforms associated with human malignancies SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 Univ Tubingen, Tubingen, Germany. Oregon Hlth & Sci Univ, Inst Canc, Portland, OR 97201 USA. Portland VA Med Ctr, Portland, OR USA. Bristol Myers Squibb Co, Princeton, NJ 08543 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 2005 VL 106 IS 11 MA 3358 BP 938A EP 939A PN 1 PG 2 WC Hematology SC Hematology GA 986CF UT WOS:000233426006142 ER PT J AU Chauhan, D Chao, TH Catley, L Nicholson, B Velanker, M Hideshima, T Berkers, C Ovaa, H Neuteboom, S Palladino, M Anderson, KC AF Chauhan, D Chao, TH Catley, L Nicholson, B Velanker, M Hideshima, T Berkers, C Ovaa, H Neuteboom, S Palladino, M Anderson, KC TI In vitro and in vivo proteasome activity profiles of bortezomib and a novel proteasome inhibitor NPI-0052 SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 Harvard Univ, Sch Med, Dana Farber Canc Inst, Boston, MA 02115 USA. Nereus Pharmaceut Inc, San Diego, CA USA. RI Catley, Laurence/E-5313-2013; Berkers, Celia/I-3848-2016 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 2005 VL 106 IS 11 MA 3363 BP 940A EP 940A PN 1 PG 1 WC Hematology SC Hematology GA 986CF UT WOS:000233426006147 ER PT J AU Crawford, LJA Ovaa, H Walker, B Chauhan, D Anderson, KC Morris, TCM Irvine, AE AF Crawford, LJA Ovaa, H Walker, B Chauhan, D Anderson, KC Morris, TCM Irvine, AE TI Evaluation of the specificity and cytotoxicity of three proteasome inhibitors SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 Queens Univ Belfast, Belfast, Antrim, North Ireland. Harvard Univ, Sch Med, Boston, MA 02115 USA. Netherlands Canc Inst, Div Cellular Biochem, NL-1066 CX Amsterdam, Netherlands. Dana Farber Canc Inst, Boston, MA 02115 USA. Belfast City Hosp, Belfast BT9 7AD, Antrim, North Ireland. RI IRVINE, ALEXANDRA/B-3497-2009 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 2005 VL 106 IS 11 MA 3366 BP 941A EP 941A PN 1 PG 1 WC Hematology SC Hematology GA 986CF UT WOS:000233426006150 ER PT J AU Chauhan, D Catley, L Velankar, M Letai, A Hideshima, T Podar, K Yasui, H Mitsiades, N Mitsiades, C Tai, YT Raje, N Munshi, N Palladino, MA Anderson, KC AF Chauhan, D Catley, L Velankar, M Letai, A Hideshima, T Podar, K Yasui, H Mitsiades, N Mitsiades, C Tai, YT Raje, N Munshi, N Palladino, MA Anderson, KC TI Requirement of caspase-8 versus caspase-9 during apoptosis in multiple myeloma cells induced by Bortezomib - Or a novel proteasome inhibitor NPI-0052 SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 Harvard Univ, Sch Med, Dana Farber Canc Inst, Boston, MA 02115 USA. Nereus Pharmaceut Inc, San Diego, CA 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 2005 VL 106 IS 11 MA 3378 BP 944A EP 944A PN 1 PG 1 WC Hematology SC Hematology GA 986CF UT WOS:000233426006162 ER PT J AU Raje, N Kumar, S Hideshima, T Ishitsuka, K Yasui, H Tai, YT Shiraishi, N Kizeltepe, T Chhetri, S Vallet, S Schlossman, RL Richardson, PG Munshi, NC Anderson, KC AF Raje, N Kumar, S Hideshima, T Ishitsuka, K Yasui, H Tai, YT Shiraishi, N Kizeltepe, T Chhetri, S Vallet, S Schlossman, RL Richardson, PG Munshi, NC Anderson, KC TI The role of B cell-activating factor (BAFF) in the biology of multiple myeloma (MM) SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 Dana Farber Canc Inst, Boston, MA 02115 USA. Massachusetts Gen Hosp, Boston, MA 02114 USA. Mayo Clin, Div Hematol, Rochester, MN USA. RI Kumar, Shaji/A-9853-2008 OI Kumar, Shaji/0000-0001-5392-9284 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 2005 VL 106 IS 11 MA 3380 BP 944A EP 945A PN 1 PG 2 WC Hematology SC Hematology GA 986CF UT WOS:000233426006164 ER PT J AU Tai, YT Li, XF Coffey, R Breitkreutz, I Catley, L Schlossman, RL Richardson, PG Munshi, NC Treon, SP Anderson, KC AF Tai, YT Li, XF Coffey, R Breitkreutz, I Catley, L Schlossman, RL Richardson, PG Munshi, NC Treon, SP Anderson, KC TI CD27-mediated apoptosis is dependent on siva-induced caspase activation in human multiple myeloma SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 Dana Farber Canc Inst, Boston, MA 02115 USA. RI Catley, Laurence/E-5313-2013 NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2005 VL 106 IS 11 MA 3398 BP 949A EP 949A PN 1 PG 1 WC Hematology SC Hematology GA 986CF UT WOS:000233426006182 ER PT J AU Frost, P Hoang, B Shi, YJ Yan, HJ Lichtenstein, A AF Frost, P Hoang, B Shi, YJ Yan, HJ Lichtenstein, A TI Anti-angiongenic effects of mTOR-inhibitors is regulated by AKT activity in multiple myeloma cells SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 W Los Angeles VA Med Ctr, Dept Hematol Oncol, Los Angeles, 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 2005 VL 106 IS 11 MA 3406 BP 951A EP 951A PN 1 PG 1 WC Hematology SC Hematology GA 986CF UT WOS:000233426006190 ER PT J AU Lipton, A Coleman, RE Major, P Brown, JE Lee, KA Smith, M Saad, F Chen, YM Hei, YJ Cook, R AF Lipton, A Coleman, RE Major, P Brown, JE Lee, KA Smith, M Saad, F Chen, YM Hei, YJ Cook, R TI Baseline N-telopeptide levels correlate with risk of skeletal morbidity in patients with multiple myeloma during zoledronic acid therapy. SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 Penn State Univ, Milton S Hershey Med Ctr, Dept Med, Hershey, PA 17033 USA. Weston Pk Hosp, Dept Oncol, Ctr Canc Res, Yorkshire Canc Res Acad Unit Clin Oncol, Sheffield, S Yorkshire, England. McMaster Univ, Juravinski Canc Ctr, Dept Oncol, Hamilton, ON, Canada. Univ Waterloo, Waterloo, ON N2L 3G1, Canada. Massachusetts Gen Hosp, Dept Oncol, Boston, MA 02114 USA. CHU Montreal, Hop Notre Dame de Bon Secours, Dept Oncol, Montreal, PQ, Canada. Novartis Pharmaceut Corp, Novartis Oncol, E Hanover, NJ USA. NR 0 TC 0 Z9 0 U1 0 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 2005 VL 106 IS 11 MA 3456 BP 964A EP 965A PN 1 PG 2 WC Hematology SC Hematology GA 986CF UT WOS:000233426006240 ER PT J AU Blotta, S Bellucci, R Tassone, P Prabhala, R Neri, P Shammas, M Batchu, RR Bae, JE Li, C Venuta, S Ritz, J Anderson, KC Munshi, NC AF Blotta, S Bellucci, R Tassone, P Prabhala, R Neri, P Shammas, M Batchu, RR Bae, JE Li, C Venuta, S Ritz, J Anderson, KC Munshi, NC TI Identification of target antigens recognized in MGUS for immunotherapeutic approaches. SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 Dana Farber Canc Inst, Jerome Lipper Multiple Myeloma Ctr, Boston, MA 02115 USA. Harvard Univ, Sch Med, Va Boston Healthcare Syst, Boston, MA 02115 USA. Univ Magna Graecia, Catanzaro, Italy. Ctr Canc, Catanzaro, Italy. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2005 VL 106 IS 11 MA 3463 BP 966A EP 966A PN 1 PG 1 WC Hematology SC Hematology GA 986CF UT WOS:000233426006247 ER PT J AU Prabhala, RH Neri, P Tassone, P Bae, JE Shammas, MA Daley, JF Song, WH Bertheau, R Chauhan, D Bachu, RB Thatte, H Anderson, K Munshi, NC AF Prabhala, RH Neri, P Tassone, P Bae, JE Shammas, MA Daley, JF Song, WH Bertheau, R Chauhan, D Bachu, RB Thatte, H Anderson, K Munshi, NC TI Dysfunctional T regulatory cells in myeloma: Molecular mechanisms of dysregulation. SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 Harvard Univ, Sch Med, Dana Farber Canc Inst, Boston, MA 02115 USA. VA Boston Healthcare Syst, W Roxbury, MA USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2005 VL 106 IS 11 MA 3462 BP 966A EP 966A PN 1 PG 1 WC Hematology SC Hematology GA 986CF UT WOS:000233426006246 ER PT J AU Bae, J Mitsiades, C Prabhala Prabhala, R Yu-Tzu, T Martinson, J Hartson, S Hideshima, T Catley, L Li, XF Babu Batchu, R Bertheau, R Masood, S Samala, S Miller, J Anderson, K Munshi, N AF Bae, J Mitsiades, C Prabhala Prabhala, R Yu-Tzu, T Martinson, J Hartson, S Hideshima, T Catley, L Li, XF Babu Batchu, R Bertheau, R Masood, S Samala, S Miller, J Anderson, K Munshi, N TI Hsp90 is critical for the regulation of human T lymphocytes and NK cell phenotype and function. SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 Harvard Univ, Sch Med, Dana Farber Canc Inst, Boston, MA 02115 USA. Rush Univ, Med Ctr, Chicago, IL 60612 USA. Oklahoma State Univ, Stillwater, OK 74078 USA. Univ Minnesota, Ctr Canc, Minneapolis, MN 55455 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 2005 VL 106 IS 11 MA 3464 BP 967A EP 967A PN 1 PG 1 WC Hematology SC Hematology GA 986CF UT WOS:000233426006248 ER PT J AU Bae, J Martinson, J Tai, YT Neri, P Tassone, P Li, XF Coffey, R Xia, ZN Prabhala, R Anderson, K Munshi, N AF Bae, J Martinson, J Tai, YT Neri, P Tassone, P Li, XF Coffey, R Xia, ZN Prabhala, R Anderson, K Munshi, N TI Development of novel CD138 antigen-specific peptide capable of eliciting myeloma-specific cytotoxic T lymphocytes response. SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 Harvard Univ, Sch Med, Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02115 USA. Rush Univ, Med Ctr, Dept Immunol, Chicago, IL 60612 USA. Harvard Univ, Sch Med, Dept Med, Boston, MA 02115 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2005 VL 106 IS 11 MA 3465 BP 967A EP 967A PN 1 PG 1 WC Hematology SC Hematology GA 986CF UT WOS:000233426006249 ER PT J AU Lonial, S Richardson, P Sonneveld, P Schuster, M Irwin, D Stadtmauer, E Facon, T Harousseau, J Ben-Yehuda, D Goldschmidt, H Reece, D San Miguel, J Blade, J Boccadoro, M Cavenagh, J Dalton, W Boral, A Schenkein, D Anderson, K AF Lonial, S Richardson, P Sonneveld, P Schuster, M Irwin, D Stadtmauer, E Facon, T Harousseau, J Ben-Yehuda, D Goldschmidt, H Reece, D San Miguel, J Blade, J Boccadoro, M Cavenagh, J Dalton, W Boral, A Schenkein, D Anderson, K TI Hematologic profiles in the phase 3 APEX trial. SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 Emory Univ, Atlanta, GA 30322 USA. Dana Farber Canc Inst, Boston, MA USA. Univ Rotterdam Hosp, Rotterdam, Netherlands. NY Presbyterian Hosp, New York, NY USA. Alta Bates Canc Ctr, Berkeley, CA USA. Univ Penn, Ctr Canc, Philadelphia, PA 19104 USA. Hosp Claude Huriez, Lille, France. Hadassah Univ Hosp, Jerusalem, Israel. Univ Heidelberg, D-6900 Heidelberg, Germany. Hosp Univ Salamanca, Salamanca, Spain. Univ Barcelona, E-08007 Barcelona, Spain. Univ Turin, I-10124 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 17 Z9 17 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2005 VL 106 IS 11 MA 3474 BP 970A EP 970A PN 1 PG 1 WC Hematology SC Hematology GA 986CF UT WOS:000233426006258 ER PT J AU Kumar, S Greipp, PR Haug, J Kline, M Blood, E Chng, WJ Lust, JA Bergsagel, L Gertz, MA Fonseca, R Rajkumar, SV AF Kumar, S Greipp, PR Haug, J Kline, M Blood, E Chng, WJ Lust, JA Bergsagel, L Gertz, MA Fonseca, R Rajkumar, SV TI Comparison of myeloma cell gene expression profiles pre and post thalidomide-dexamethasone therapy provides insight into potential mechanisms. SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 Mayo Clin, Rochester, MN USA. Mayo Clin, Scottsdale, AZ USA. Dana Farber Canc Inst, ECOG, Ctr Stat, Boston, MA 02115 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 2005 VL 106 IS 11 MA 3480 BP 971A EP 972A PN 1 PG 2 WC Hematology SC Hematology GA 986CF UT WOS:000233426006264 ER PT J AU Anagnostopoulos, A Treon, SP Zervas, K Branagan, A Gika, D Zomas, A Kyrtsonis, MC Vassou, A Anagnostopoulos, N Pangalis, G Dimopoulos, MA AF Anagnostopoulos, A Treon, SP Zervas, K Branagan, A Gika, D Zomas, A Kyrtsonis, MC Vassou, A Anagnostopoulos, N Pangalis, G Dimopoulos, MA TI Predictive factors for response and progression after treatment with rituximab in previously untreated patients with Waldenstrom's macroglobulinemia (WM). SO BLOOD LA English DT Meeting Abstract CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol C1 Greek Myeloma Study Grp, Dept Clin Therapeut, Athens, Greece. 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 2005 VL 106 IS 11 MA 3485 BP 973A EP 973A PN 1 PG 1 WC Hematology SC Hematology GA 986CF UT WOS:000233426006269 ER EF