FN Thomson Reuters Web of Science™ VR 1.0 PT J AU Wexler, DJ Grant, RW Wittenberg, E Bosch, JL Cagliero, E Delahanty, L Blais, MA Meigs, JB AF Wexler, DJ Grant, RW Wittenberg, E Bosch, JL Cagliero, E Delahanty, L Blais, MA Meigs, JB TI Correlates of health-related quality of life in type 2 diabetes SO DIABETOLOGIA LA English DT Article DE adult diabetes; chronic disease; health-related quality of life ID HUI3 UTILITY SCORES; INDEX MARK 3; POPULATION HEALTH; CONSTRUCT-VALIDITY; DEPRESSION; COMMUNITY; SYMPTOMS; MELLITUS AB Aims/hypothesis: We assessed the impact of medical comorbidities, depression, and treatment intensity on quality of life in a large primary care cohort of patients with type 2 diabetes. Methods: We used the Health Utilities Index-III, an instrument that measures health-related quality of life based on community preferences in units of health utility (scaled from 0=death to 1.0=perfect health), in 909 primary care patients with type 2 diabetes. Demographic and clinical correlates of health-related quality of life were assessed. Results: The median health utility score for this population was 0.70 (interquartile range 0.39-0.88). In univariate analyses, older age, female sex, low socioeconomic status, cardiovascular disease, microvascular complications, congestive heart failure, peripheral vascular disease, chronic lung disease, depression, insulin use and number of medications correlated with decreased quality of life, while obesity, hypertension and hypercholesterolaemia did not. In multiple regression analyses, microvascular complications, heart failure and depression were most strongly related to decreased health-related quality of life, independently of duration of diabetes; in these models, diabetes patients with depression had a utility of 0.59, while patients without symptomatic comorbidities did not have a significantly reduced quality of life. Treatment intensity remained a significant negative correlate of quality of life in multivariable models. Conclusions/interpretation: Patients with type 2 diabetes have a substantially decreased quality of life in association with symptomatic complications. The data suggest that treatment of depression and prevention of complications have the greatest potential to improve health-related quality of life in type 2 diabetes. C1 Massachusetts Gen Hosp, Diabet Unit, Dept Med, Boston, MA 02114 USA. Massachusetts Gen Hosp, Div Gen Med, Dept Med, Boston, MA USA. Harvard Univ, Sch Med, Boston, MA USA. Massachusetts Gen Hosp, Inst Technol Assessment, Boston, MA 02114 USA. Erasmus MC Univ Med Ctr, Dept Epidemiol & Biostat, Rotterdam, Netherlands. Erasmus MC Univ Med Ctr, Dept Radiol, Rotterdam, Netherlands. Massachusetts Gen Hosp, Dept Psychiat, Boston, MA 02114 USA. RP Wexler, DJ (reprint author), Massachusetts Gen Hosp, Diabet Unit, Dept Med, Boston, MA 02114 USA. EM dwexler@partners.org OI Grant, Richard/0000-0002-6164-8025 FU NIDDK NIH HHS [DK067452] NR 35 TC 108 Z9 113 U1 3 U2 18 PU SPRINGER PI NEW YORK PA 233 SPRING STREET, NEW YORK, NY 10013 USA SN 0012-186X J9 DIABETOLOGIA JI Diabetologia PD JUL PY 2006 VL 49 IS 7 BP 1489 EP 1497 DI 10.1007/s00125-006-0249-9 PG 9 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA 049OO UT WOS:000238026100005 PM 16752167 ER PT J AU Pihlajamaki, J Salmenniemi, U Vanttinen, M Ruotsalainen, E Kuusisto, J Vauhkonen, I Kainulainen, S Ng, MCY Cox, NJ Bell, GI Laakso, M AF Pihlajamaki, J Salmenniemi, U Vanttinen, M Ruotsalainen, E Kuusisto, J Vauhkonen, I Kainulainen, S Ng, MCY Cox, NJ Bell, GI Laakso, M TI Common polymorphisms of calpain-10 are associated with abdominal obesity in subjects at high risk of type 2 diabetes SO DIABETOLOGIA LA English DT Article DE calpain-10; insulin resistance; insulin secretion; type 2 diabetes; visceral obesity ID HUMAN FAT-CELLS; INSULIN-RESISTANCE; PRO12ALA POLYMORPHISM; GLUCOSE-TOLERANCE; PPAR-GAMMA-2 GENE; ADIPOSE-TISSUE; WEIGHT CHANGE; CAPN10 GENE; VARIANTS; MELLITUS AB Aims/hypothesis: The mechanisms by which the calpain-10 gene (CAPN10) affects the risk of type 2 diabetes are unclear. Therefore, we investigated the effects of four polymorphisms in CAPN10 (single nucleotide polymorphism [SNP]-43, SNP-44, Insertion/Deletion [Indel]-19 and SNP-63) on insulin secretion, insulin action and abdominal fat distribution in offspring of patients with type 2 diabetes. Subjects and methods: Insulin secretion was determined by an IVGTT, insulin action by the hyperinsulinaemic-euglycaemic clamp and abdominal fat distribution by computed tomography in 158 non-diabetic offspring (age 34.9 +/- 6.3 years [mean +/- SD], BMI 26.2 +/- 4.9 kg/m(2)) of type 2 diabetic patients. Results: SNP-43 (p=0.009 over the three genotypes, adjusted for age, sex, BMI and family relationship) and haplotypes carrying the A allele of SNP-43 were associated with intra-abdominal fat area. The A allele of SNP-43 was associated with intra-abdominal fat area in men (p=0.014) but not in women. SNP-44, InDel-19 and SNP-63 were not associated with intra-abdominal fat area or insulin action. Furthermore, we demonstrated in a separate sample of middle-aged men (n=234) who had a history of type 2 diabetes in first-degree relatives that the A allele of SNP-43 was associated with a large waist circumference, and high insulin levels in an OGTT. Conclusions/intrepretation: SNP-43 of CAPN10 may contribute to the risk of diabetes by regulating abdominal obesity in subjects with high risk of type 2 diabetes. C1 Joslin Diabet Ctr, Boston, MA USA. Harvard Univ, Sch Med, Boston, MA USA. Univ Kuopio, Dept Med, FIN-70211 Kuopio, Finland. Univ Kuopio, Dept Clin Radiol, Kuopio, Finland. Univ Chicago, Dept Med, Chicago, IL USA. Univ Chicago, Dept Human Genet, Chicago, IL USA. RP Pihlajamaki, J (reprint author), Joslin Diabet Ctr, Boston, MA USA. EM Jussi.Pihlajamaki@joslin.harvard.edu FU NIDDK NIH HHS [DK-47486, DK-20595] NR 37 TC 12 Z9 13 U1 0 U2 1 PU SPRINGER PI NEW YORK PA 233 SPRING STREET, NEW YORK, NY 10013 USA SN 0012-186X J9 DIABETOLOGIA JI Diabetologia PD JUL PY 2006 VL 49 IS 7 BP 1560 EP 1566 DI 10.1007/s00125-006-0270-z PG 7 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA 049OO UT WOS:000238026100014 PM 16752174 ER PT J AU McHorney, CA Martin-Harris, B Robbins, J Rosenbek, J AF McHorney, Colleen A. Martin-Harris, Bonnie Robbins, JoAnne Rosenbek, John TI Clinical validity of the SWAL-QOL and SWAL-CARE outcome tools with respect to bolus flow measures SO DYSPHAGIA LA English DT Article DE deglutition disorders; quality of life; swallowing; patient satisfaction; deglutition ID QUALITY-OF-LIFE; OROPHARYNGEAL DYSPHAGIA; RHEUMATOID-ARTHRITIS; PROGNOSTIC VALUE; HEALTH; ADULTS; SCALE; FATIGUE; DISEASE; RELIABILITY AB The aim of this study was to quantify the association between a dysphagia-specific quality of life (SWAL-QOL) and quality of care (SWAL-CARE) questionnaire and four measures of bolus flow. Three hundred eighty-six people with oropharyngeal dysphagia completed a videofluoroscopic examination of their swallowing structure and physiology. They also completed the SWAL-QOL and SWAL-CARE surveys. Measures of bolus flow patterns for each swallow were analyzed from videofluoroscopic recordings and correlated with the SWAL-QOL and SWAL-CARE scale scores. The SWAL-QOL and SWAL-CARE scales were modestly related to the four measures of the bolus flow. The SWAL-QOL and SWAL-CARE were most related to measures of oral transit duration and total swallow duration. The SWAL-QOL and SWAL-CARE scales were least related to pharyngeal transit duration. Results were stronger for semisolid trials than for liquid trials. Results were generally weak for the Penetration Aspiration Scale. For all of the significant relationships, the greater the bolus flow severity, the worse the quality of life. The observed modest correlations suggest that patient-centered quality-of-life measures and clinician-driven bolus flow measures provide distinct yet complementary information about oropharyngeal dysphagia. Both sets of measures should be used in dysphagia effectiveness and outcomes research. C1 Merck & Co Inc, West Point, PA 19486 USA. Med Univ S Carolina, Dept Otolaryngol Head & Neck Surg, MUSC Evelyn Trammell Inst Voice & Swalowing, Charleston, SC 29425 USA. Med Univ S Carolina, Coll Hlth Profess, Charleston, SC 29425 USA. Univ Wisconsin, Sch Med, Madison, WI USA. William S Middleton Mem Vet Adm Med Ctr, Madison, WI 53705 USA. Univ Florida, Dept Communicat Disorders, Gainesville, FL USA. Univ Florida, Sch Med, Dept Neurol, Gainesville, FL USA. RP McHorney, CA (reprint author), Merck & Co Inc, WP39-166,770 Sumneytown Pike, West Point, PA 19486 USA. EM colleen_mchorney@merck.com FU NIA NIH HHS [R01 AG022067] NR 44 TC 33 Z9 38 U1 1 U2 5 PU SPRINGER PI NEW YORK PA 233 SPRING STREET, NEW YORK, NY 10013 USA SN 0179-051X J9 DYSPHAGIA JI Dysphagia PD JUL PY 2006 VL 21 IS 3 BP 141 EP 148 DI 10.1007/s00455-005-0026-9 PG 8 WC Otorhinolaryngology SC Otorhinolaryngology GA 081HL UT WOS:000240307800001 PM 16715210 ER PT J AU Huang, DS Khoe, M Ilic, D Bryer-Ash, M AF Huang, DS Khoe, M Ilic, D Bryer-Ash, M TI Reduced expression of focal adhesion kinase disrupts insulin action in skeletal muscle cells SO ENDOCRINOLOGY LA English DT Article ID PHOSPHATIDYLINOSITOL 3-KINASE ACTIVITY; RECEPTOR SUBSTRATE-1 PHOSPHORYLATION; TOKUSHIMA FATTY RAT; GLUCOSE-TRANSPORT; PLASMA-MEMBRANE; GLYCOGEN-SYNTHESIS; TYROSINE PHOSPHATASE; DNA-SYNTHESIS; IN-VIVO; STIMULATION AB Integrins mediate interactions between cells and extracellular matrix proteins that modulate growth factor signaling. Focal adhesion kinase (FAK) is a key multifunctional integrin pathway protein. We recently reported that disruption of FAK impairs insulin-mediated glycogen synthesis in hepatocytes. To test the hypothesis that FAK regulates skeletal muscle insulin action, we reduced FAK expression in L6 myotubes using FAK antisense. In untransfected myotubes, insulin stimulated both FAK tyrosine phosphorylation and kinase activity. Cells treated with antisense FAK showed 78 and 53% reductions in FAK mRNA and FAK protein, respectively, whereas insulin receptor substrate 1/2 and paxillin abundance were unaffected. Insulin-stimulated U-14C-glucose incorporation into glycogen was abolished by FAK antisense, and 2-deoxy-glucose uptake and glucose transporter 4 (GLUT4) translocation were both markedly attenuated. Antisense FAK did not alter GLUT1 or GLUT3 protein abundance. Immunofluorescence staining showed decreased FAK Tyr(397) phosphorylation and reduced actin stress fibers. Thus, in skeletal myotubes, FAK regulates the insulin-mediated cytoskeletal rearrangement essential for normal glucose transport and glycogen synthesis. Integrin signaling may play an important regulatory role in muscle insulin action. C1 Univ Calif Los Angeles, David Geffen Sch Med, Div Endocrinol Diabet & Hypertens, Los Angeles, CA 90095 USA. Univ Calif Los Angeles, Gonda Goldschmied Diabet Ctr, W Los Angeles Vet Adm Med Ctr, Los Angeles, CA 90095 USA. Univ Calif San Francisco, Dept Stomatol & Anat, San Francisco, CA 94143 USA. RP Bryer-Ash, M (reprint author), Univ Calif Los Angeles, David Geffen Sch Med, Div Endocrinol Diabet & Hypertens, 900 Vet Ave,Warren Hall Room 24-130, Los Angeles, CA 90095 USA. EM mbryerash@mednet.ucla.edu NR 51 TC 25 Z9 25 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 JUL PY 2006 VL 147 IS 7 BP 3333 EP 3343 DI 10.1210/en.2005-0382 PG 11 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA 053NS UT WOS:000238312400022 PM 16574795 ER PT J AU Sidis, Y Mukherjee, A Keutmann, H Delbaere, A Sadatsuki, M Schneyer, A AF Sidis, Y Mukherjee, A Keutmann, H Delbaere, A Sadatsuki, M Schneyer, A TI Biological activity of follistatin isoforms and follistatin-like-3 is dependent on differential cell surface binding and specificity for activin, myostatin, and bone morphogenetic proteins SO ENDOCRINOLOGY LA English DT Article ID FOLLICLE-STIMULATING-HORMONE; MESSENGER-RIBONUCLEIC-ACID; PITUITARY FOLLISTATIN; HEPARAN-SULFATE; GENE-EXPRESSION; TRANSGENIC MICE; INHIBIN; OVEREXPRESSION; LOCALIZATION; AUTOCRINE AB Follistatin (FST) and FST-like-3 (FSTL3) are activin-binding and neutralization proteins that also bind myostatin. Three FST isoforms have been described that differ in tissue distribution and cell-surface binding activity, suggesting that the FST isoforms and FSTL3 may have some nonoverlapping biological actions. We produced recombinant FST isoforms and FSTL3 and compared their biochemical and biological properties. Activin-binding affinities and kinetics were comparable between the isoforms and FSTL3, whereas cell-surface binding differed markedly (FST288 > FST303 > FST315 > FSTL3). Inhibition of endogenous activin bioactivity, whether the FST isoforms were administered endogenously or exogenously, correlated closely with surface binding activity, whereas neutralization of exogenous activin when FST and FSTL3 were also exogenous was consistent with their equivalent activin-binding affinities. This difference in activin inhibition was also evident in an in vitro bioassay because FST288 suppressed, whereas FST315 enhanced, activin-dependent TT cell proliferation. Moreover, when FSTL3, which does not associate with cell membranes, was expressed as a membrane-anchored protein, its endogenous activin inhibitory activity was dramatically increased. In competitive binding assays, myostatin was more potent than bone morphogenetic proteins (BMPs) 6 and 7, and BMPs 2 and 4 were inactive in binding to FST isoforms, whereas none of the BMPs tested competed with activin for binding to FSTL3. Neutralization of exogenous BMP or myostatin bioactivity correlated with the relative abilities of the isoforms to bind cell-surface proteoglycans. These results indicate that the differential biological actions among the FST isoforms and FSTL3 are primarily dependent on their relative cell-surface binding ability and ligand specificity. C1 Massachusetts Gen Hosp, Reprod Endocrine Unit, Boston, MA 02114 USA. RP Schneyer, A (reprint author), Massachusetts Gen Hosp, Reprod Endocrine Unit, BHX-5, Boston, MA 02114 USA. EM Schneyer.alan@mgh.harvard.edu FU NICHD NIH HHS [R01HD39777]; NIDDK NIH HHS [R01DK55838, R01DK053828] NR 52 TC 104 Z9 108 U1 0 U2 3 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 JUL PY 2006 VL 147 IS 7 BP 3586 EP 3597 DI 10.1210/en.2006-0089 PG 12 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA 053NS UT WOS:000238312400049 PM 16627583 ER PT J AU Wiese, C Grosser, T Kovalenko, O Collins, D Kratz, W Rydberg, B Schild, D AF Wiese, C. Grosser, T. Kovalenko, O. Collins, D. Kratz, W. Rydberg, B. Schild, D. TI RAD51AP1/PIR51 is required for DNA repair and for the maintenance of genomic stability after DNA damage. SO ENVIRONMENTAL AND MOLECULAR MUTAGENESIS LA English DT Meeting Abstract CT 37th Annual Meeting of the Environmental-Mutagen-Society CY SEP 16-20, 2006 CL Vancouver, CANADA SP Environm Mutagen Soc ID PROTEIN C1 Lawrence Berkeley Natl Lab, Berkeley, CA USA. Dana Farber Canc Inst, Boston, MA 02115 USA. NR 2 TC 0 Z9 0 U1 0 U2 3 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 0893-6692 J9 ENVIRON MOL MUTAGEN JI Environ. Mol. Mutagen. PD JUL PY 2006 VL 47 IS 6 BP 422 EP 422 PG 1 WC Environmental Sciences; Genetics & Heredity; Toxicology SC Environmental Sciences & Ecology; Genetics & Heredity; Toxicology GA 072BP UT WOS:000239647900094 ER PT J AU Hart, JE Laden, F Schenker, MB Garshick, E AF Hart, Jaime E. Laden, Francine Schenker, Marc B. Garshick, Eric TI Chronic obstructive pulmonary disease mortality in diesel-exposed railroad workers SO ENVIRONMENTAL HEALTH PERSPECTIVES LA English DT Article DE chronic obstructive pulmonary disease; COPD; nonmalignant respiratory disease; occupational exposure; vehicle emissions ID PARTICULATE AIR-POLLUTION; CHRONIC RESPIRATORY SYMPTOMS; EXHAUST EXPOSURE; LUNG-CANCER; OCCUPATIONAL EXPOSURES; DEATH CERTIFICATE; COPD; PARTICLES; EPIDEMIOLOGY; ASSOCIATION AB Diesel exhaust is a mixture of combustion gases and ultrafine particles coated with organic compounds. There is concern whether exposure can result in or worsen obstructive airway diseases, but there is only limited information to assess this risk U.S. railroad workers have been exposed to diesel exhaust since diesel locomotives were introduced after World War 11, and by 1959, 95% of the locomotives were diesel. We conducted a case-control study of railroad worker deaths between 1981 and 1982 using U.S. Railroad Retirement Board job records and next-of-kin smoking, residential, and vitamin use histories. There were 536 cases with chronic obstructive pulmonary disease (COPD) and 1,525 controls with causes of death not related to diesel exhaust or fine particle exposure. After adjustment for age, race, smoking, U.S. Census region of death, vitamin use, and total years off work, engineers and conductors with diesel-exhaust exposure from operating trains had an increased risk of COPD mortality. The odds of COPD mortality increased with years of work in these jobs, and those who had worked ! 16 years as an engineer or conductor after 1959 had an odds ratio of 1.61 (95% confidence interval, 1.12-2.30). These results suggest that diesel-exhaust exposure contributed to COPD mortality in these workers. Further study is needed to assess whether this risk is observed after exposure to exhaust from later-generation diesel engines with modern emission controls. C1 Brigham & Womens Hosp, Channing Lab, Boston, MA 02115 USA. Harvard Univ, Sch Med, Boston, MA 02115 USA. Harvard Univ, Sch Publ Hlth, Exposure Epidemiol & Risk Program, Dept Environm Hlth, Boston, MA 02115 USA. Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA. Univ Calif Davis, Dept Publ Hlth Sci, Davis, CA 95616 USA. VA Boston Healthcare Syst, Pulm & Crit Care Med Sect, Boston, MA USA. RP Hart, JE (reprint author), Channing Labs, 181 Longwood Ave, Boston, MA 02115 USA. EM Jaime.hart@channing.harvard.edu FU NCI NIH HHS [CA79725, R01 CA079725, R01 CA079725-01A1]; PHS HHS [CCR115818] NR 57 TC 29 Z9 29 U1 2 U2 6 PU US DEPT HEALTH HUMAN SCIENCES PUBLIC HEALTH SCIENCE PI RES TRIANGLE PK PA NATL INST HEALTH, NATL INST ENVIRONMENTAL HEALTH SCIENCES, PO BOX 12233, RES TRIANGLE PK, NC 27709-2233 USA SN 0091-6765 J9 ENVIRON HEALTH PERSP JI Environ. Health Perspect. PD JUL PY 2006 VL 114 IS 7 BP 1013 EP 1017 DI 10.1289/ehp.8743 PG 5 WC Environmental Sciences; Public, Environmental & Occupational Health; Toxicology SC Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology GA 063QR UT WOS:000239035100030 PM 16835052 ER PT J AU Schecter, A Birnbaum, L Ryan, JJ Constable, JD AF Schecter, A Birnbaum, L Ryan, JJ Constable, JD TI Dioxins: An overview SO ENVIRONMENTAL RESEARCH LA English DT Review DE dioxins; poisoning; Yushchenko; agent orange; TCDD ID 2,3,7,8-TETRACHLORODIBENZO-P-DIOXIN TCDD INTOXICATION; POLYCHLORINATED DIBENZOFURANS PCDFS; OPERATION RANCH HAND; AIR-FORCE VETERANS; AGENT-ORANGE; VIETNAM VETERANS; ENVIRONMENTAL CONTAMINANT; AROMATIC-HYDROCARBONS; OCCUPATIONAL EXPOSURE; CHLORINATED DIOXIN AB This review article summarizes what is known about human health following exposure to dioxins. It is meant primarily for health professionals but was also written with the general public in mind. The need for Such an article became apparent to the authors following media inquiries at the time the then Ukraine presidential candidate Victor Yushchenko was deliberately poisoned with the most toxic dioxin, tetrachlorodibenzodioxin or TCDD. (c) 2006 Elsevier Inc. All rights reserved. C1 Univ Texas, Hlth Sci Ctr, Sch Publ Hlth, Dallas, TX 75390 USA. US EPA, Off Res & Dev, Expt Toxicol Div, Natl Hlth & Environm Effects Res Lab, Res Triangle Pk, NC 27711 USA. Hlth Canada, Ottawa, ON K1A 0L2, Canada. Harvard Univ, Massachusetts Gen Hosp, Sch Med, Boston, MA 02115 USA. RP Schecter, A (reprint author), Univ Texas, Hlth Sci Ctr, Sch Publ Hlth, Dallas Campus, Dallas, TX 75390 USA. EM arnold.schecter@utsouthwestern.edu NR 108 TC 243 Z9 259 U1 12 U2 61 PU ACADEMIC PRESS INC ELSEVIER SCIENCE PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA SN 0013-9351 J9 ENVIRON RES JI Environ. Res. PD JUL PY 2006 VL 101 IS 3 BP 419 EP 428 DI 10.1016/j.envres.2005.12.003 PG 10 WC Environmental Sciences; Public, Environmental & Occupational Health SC Environmental Sciences & Ecology; Public, Environmental & Occupational Health GA 056LI UT WOS:000238524000018 PM 16445906 ER PT J AU Davis, ME Smith, TJ Laden, F Hart, JE Ryan, LM Garshick, E AF Davis, ME Smith, TJ Laden, F Hart, JE Ryan, LM Garshick, E TI Modeling particle exposure in US trucking terminals SO ENVIRONMENTAL SCIENCE & TECHNOLOGY LA English DT Article ID DIESEL-EXHAUST; ULTRAFINE PARTICLES; ELEMENTAL CARBON; SUBMICROMETER PARTICLES; SAMPLING ARTIFACTS; RISK ASSESSMENT; MAJOR HIGHWAY; LUNG-CANCER; URBAN AREAS; EMISSIONS AB Multi-tiered sampling approaches are common in environmental and occupational exposure assessment, where exposures for a given individual are often modeled based on simultaneous measurements taken at multiple indoor and outdoor sites. The monitoring data from such studies is hierarchical by design, imposing a complex covariance structure that must be accounted for in order to obtain unbiased estimates of exposure. Statistical methods such as structural equation modeling (SEM) represent a useful alternative to simple linear regression in these cases, providing simultaneous and unbiased predictions of each level of exposure based on a set of covariates specific to the exposure setting. We test the SEM approach using data from a large exposure assessment of diesel and combustion particles in the U. S. trucking industry. The exposure assessment includes data from 36 different trucking terminals across the United States sampled between 2001 and 2005, measuring PM2.5 and its elemental carbon (EC), organic carbon (OC) components, by personal monitoring, and sampling at two indoor work locations and an outdoor "background" location. Using the SEM method, we predict the following: (1) personal exposures as a function of work-related exposure and smoking status; (2) work-related exposure as a function of terminal characteristics, indoor ventilation, job location, and background exposure conditions; and ( 3) background exposure conditions as a function of weather, nearby source pollution, and other regional differences across terminal sites. The primary advantage of SEMs in this setting is the ability to simultaneously predict exposures at each of the sampling locations, while accounting for the complex covariance structure among the measurements and descriptive variables. The statistically significant results and high R-2 values observed from the trucking industry application supports the broader use of this approach in exposure assessment modeling. C1 Harvard Univ, Sch Publ Hlth, Dept Environm Hlth, Boston, MA 02215 USA. Univ Massachusetts, Environm Earth & Ocean Sci Dept, Boston, MA 02125 USA. Brigham & Womens Hosp, Channing Lab, Boston, MA 02115 USA. Harvard Univ, Sch Med, Boston, MA 02115 USA. Harvard Univ, Sch Publ Hlth, Dept Biostat, Boston, MA 02115 USA. VA Boston Healthcare Syst, Pulm & Crit Care Med Sect, Boston, MA 02132 USA. RP Davis, ME (reprint author), Harvard Univ, Sch Publ Hlth, Dept Environm Hlth, 401 Pk Dr, Boston, MA 02215 USA. EM medavis@hsph.harvard.edu RI Ryan, Louise/A-4562-2009 OI Ryan, Louise/0000-0001-5957-2490 FU NCI NIH HHS [R01 CA090792, R01 CA90792] NR 30 TC 29 Z9 29 U1 0 U2 12 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA SN 0013-936X J9 ENVIRON SCI TECHNOL JI Environ. Sci. Technol. PD JUL 1 PY 2006 VL 40 IS 13 BP 4226 EP 4232 DI 10.1021/es052477m PG 7 WC Engineering, Environmental; Environmental Sciences SC Engineering; Environmental Sciences & Ecology GA 058DQ UT WOS:000238645400034 PM 16856739 ER PT J AU Handforth, A DeSalles, AAF Krahl, SE AF Handforth, Adrian DeSalles, Antonio A. F. Krahl, Scott E. TI Deep brain stimulation of the subthalamic nucleus as adjunct treatment for refractory epilepsy SO EPILEPSIA LA English DT Article DE epilepsy; deep brain stimulation; subthalamus; STN; DBS ID SUBSTANTIA-NIGRA; ENTOPEDUNCULAR NUCLEUS; SEIZURES; ACID; SITE; RATS AB Purpose: We studied the efficacy and safety of bilateral subthalamic deep brain stimulation (DBS) for refractory partial-onset epilepsy in two cases. Methods: This was an open treatment pilot study for subjects who had failed numerous medications and had seizure injuries. Seizure counts and adverse events were collected during a 3-4 month baseline, and for 26-32 months after DBS surgery, with AEDs held constant. Results: Case 1, age 45, with bitemporal seizures, had about half the seizure frequency but still fell with injuries. Case 2, age 46, with left frontal encephalomalacia, had a frequency reduction of about one-third, but a more meaningful reduction of seizure severity and injuries. Conclusions: Subthalamic DBS partly reduced partial-onset seizures, but the quality of life was more affected by seizure-related injuries. C1 VA Greater Los Angeles Healthcare Syst, Neurol Serv, Dept Neurol, Los Angeles, CA 90073 USA. VA Greater Los Angeles Healthcare Syst, Dept Neurosurg, Los Angeles, CA 90073 USA. VA Greater Los Angeles Healthcare Syst, Res Serv, Los Angeles, CA 90073 USA. VA Greater Los Angeles Healthcare Syst, Dev Serv, Los Angeles, CA 90073 USA. Univ Calif Los Angeles, Div Neurosurg, Los Angeles, CA 90024 USA. RP Handforth, A (reprint author), VA Greater Los Angeles Healthcare Syst, Neurol Serv, Dept Neurol, W127,11301 Wilshire Blvd, Los Angeles, CA 90073 USA. EM charles.handforth@med.va.gov NR 10 TC 61 Z9 66 U1 0 U2 3 PU BLACKWELL PUBLISHING PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DQ, OXON, ENGLAND SN 0013-9580 J9 EPILEPSIA JI Epilepsia PD JUL PY 2006 VL 47 IS 7 BP 1239 EP 1241 DI 10.1111/j.1528-1167.2006.00563.x PG 3 WC Clinical Neurology SC Neurosciences & Neurology GA 064WD UT WOS:000239119700019 PM 16886990 ER PT J AU Maree, AO Jneid, H Palacios, IF AF Maree, AO Jneid, H Palacios, IF TI Percutaneous closure of a post-infarction ventricular septal defect that recurred after surgical repair SO EUROPEAN HEART JOURNAL LA English DT Editorial Material C1 Massachusetts Gen Hosp, Div Cardiol, Boston, MA 02114 USA. RP Maree, AO (reprint author), Massachusetts Gen Hosp, Div Cardiol, GRB 853,55 Fruit St, Boston, MA 02114 USA. EM amaree@mgh.harvard.edu NR 0 TC 3 Z9 3 U1 0 U2 0 PU OXFORD UNIV PRESS PI OXFORD PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND SN 0195-668X J9 EUR HEART J JI Eur. Heart J. PD JUL PY 2006 VL 27 IS 13 BP 1626 EP 1626 DI 10.1093/eurheartj/ehi600 PG 1 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA 056PK UT WOS:000238537400023 PM 16230303 ER PT J AU Mitsiades, CS Mitsiades, NS Munshi, NC Richardson, PG Anderson, KC AF Mitsiades, Constantine S. Mitsiades, Nicholas S. Munshi, Nikhil C. Richardson, Paul G. Anderson, Kenneth C. TI The role of the bone microenvironment in the pathophysiology and therapeutic management of multiple myeloma: Interplay of growth factors, their receptors and stromal interactions SO EUROPEAN JOURNAL OF CANCER LA English DT Review DE multiple myeloma ID NF-KAPPA-B; COLONY-STIMULATING FACTOR; FACTOR-I RECEPTOR; THALIDOMIDE PLUS DEXAMETHASONE; FARNESYL TRANSFERASE INHIBITOR; HISTONE DEACETYLASE INHIBITION; OVERCOMES DRUG-RESISTANCE; TYROSINE KINASE INHIBITOR; NEWLY-DIAGNOSED MYELOMA; HUMAN-SKIN FIBROBLASTS AB The close relationship between the biological behaviour of malignant cells and the local microenvironment where they reside is a feature of diverse neoplasias. Multiple myeloma (MM) is considered a main disease model for the study of such interactions and the mechanisms that can lead to bone-related clinical complications, as well as the role of these interactions in attenuating the activity of conventional anti-MM therapeutics, such as dexamethasone and cytotoxic chemotherapeutics. This review focuses on recent progress in the study of interactions of MM cells with their local microenvironment. Major emphasis is placed on how bone marrow stromal cells (BMSCs) and other normal constituents of the bone marrow milieu promote, through cell adhesion- and cytokine-mediated mechanisms, the ability of MM cells to resist conventional anti-MM therapies. The review also addresses ongoing research into these mechanisms, which has already provided several new molecular targets and corresponding therapeutic strategies, such as the proteasome inhibitor bortezomib and thalidomide derivatives (e.g. lenalidomide), for the management of myeloma. (c) 2006 Elsevier Ltd. All rights reserved. C1 Harvard Univ, Sch Med, Jerome Lipper Multiple Myeloma Ctr, Dept Med Oncol,Dana Farber Canc Inst, Boston, MA 02115 USA. Harvard Univ, Sch Med, Dept Med, Boston, MA 02115 USA. RP Mitsiades, CS (reprint author), Harvard Univ, Sch Med, Jerome Lipper Multiple Myeloma Ctr, Dept Med Oncol,Dana Farber Canc Inst, 44 Binney St, Boston, MA 02115 USA. EM constantine_mitsiades@dfci.harvard.edu NR 114 TC 124 Z9 127 U1 4 U2 8 PU ELSEVIER SCI LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND SN 0959-8049 J9 EUR J CANCER JI Eur. J. Cancer PD JUL PY 2006 VL 42 IS 11 BP 1564 EP 1573 DI 10.1016/j.ejca.2005.12.025 PG 10 WC Oncology SC Oncology GA 078DG UT WOS:000240081100008 PM 16765041 ER PT J AU Gudavalli, MR Cambron, JA McGregor, M Jedlicka, J Keenum, M Ghanayem, AJ Patwardhan, AG AF Gudavalli, Maruti Ram Cambron, Jerrilyn A. McGregor, Marion Jedlicka, James Keenum, Michael Ghanayem, Alexander J. Patwardhan, Avinash G. TI A randomized clinical trial and subgroup analysis to compare flexion-distraction with active exercise for chronic low back pain SO EUROPEAN SPINE JOURNAL LA English DT Article DE low back pain; chiropractic; physical therapy; chronic pain; randomized clinical trial ID STABILIZING EXERCISE; SPINAL MANIPULATION; PREDICTION RULE; THERAPY AB Many clinical trials on chiropractic management of low back pain have neglected to include specific forms of care. This study compared two well-defined treatment protocols. The objective was to compare the outcome of flexion-distraction (FD) procedures performed by chiropractors with an active trunk exercise protocol (ATEP) performed by physical therapists. A randomized clinical trial study design was used. Subjects, 18 years of age and older, with a primary complaint of low back pain (> 3 months) were recruited. A 100 mm visual analogue scale (VAS) for perceived pain, the Roland Morris (RM) Questionnaire for low back function, and the SF-36 for overall health status served as primary outcome measures. Subjects were randomly allocated to receive either FD or ATEP. The FD intervention consisted of the application of flexion and traction applied to specific regions in the low back, with the aid of a specially designed manipulation table. The ATEP intervention included stabilizing and flexibility exercises, the use of modalities, and cardiovascular training. A total of 235 subjects met the inclusion/exclusion criteria and signed the informed consent. Of these, 123 were randomly allocated to FD and 112 to the ATEP. Study patients perceived significantly less pain and better function after intervention, regardless of which group they were allocated to (P < 0.01). Subjects randomly allocated to the flexion-distraction group had significantly greater relief from pain than those allocated to the exercise program (P=0.01). Subgroup analysis indicated that subjects categorized as chronic, with moderate to severe symptoms, improved most with the flexion-distraction protocol. Subjects categorized with recurrent pain and moderate to severe symptoms improved most with the exercise program. Patients with radiculopathy did significantly better with FD. There were no significant differences between groups on the Roland Morris and SF-36 outcome measures. Overall, flexion-distraction provided more pain relief than active exercise; however, these results varied based on stratification of patients with and without radiculopathy and with and without recurrent symptoms. The subgroup analysis provides a possible explanation for contrasting results among randomized clinical trials of chronic low back pain treatments and these results also provide guidance for future work in the treatment of chronic low back pain. C1 Palmer Coll Chiropract, Davenport, IA USA. Natl Univ Hlth Sci, Lombard, IL USA. Orthosport Phys Therapy, Forest Pk, IL USA. Loyola Univ, Stritch Sch Med, Maywood, IL 60153 USA. US Dept Vet Affairs, Vet Affairs Edward Hines Jr Hosp, Hines, IL 60141 USA. RP Gudavalli, MR (reprint author), Palmer Coll Chiropract, Davenport, IA USA. EM gudavalli_r@palmer.edu FU BHP HRSA HHS [R18 AH 10001] NR 34 TC 48 Z9 48 U1 0 U2 10 PU SPRINGER PI NEW YORK PA 233 SPRING STREET, NEW YORK, NY 10013 USA SN 0940-6719 J9 EUR SPINE J JI Eur. Spine J. PD JUL PY 2006 VL 15 IS 7 BP 1070 EP 1082 DI 10.1007/s00586-005-0021-8 PG 13 WC Clinical Neurology; Orthopedics SC Neurosciences & Neurology; Orthopedics GA 063SG UT WOS:000239039300005 PM 16341712 ER PT J AU Yang, J Li, TS AF Yang, Jun Li, Tiansen TI Focus on molecules: Rootletin SO EXPERIMENTAL EYE RESEARCH LA English DT Editorial Material DE retinal degeneration; ciliary rootlet; photoreceptors; cytoskeleton; cilia ID CILIARY ROOTLET C1 Harvard Univ, Sch Med, Massachusetts Eye & Ear Infirm, Berman Gund Lab Study Retinal Degenerat, Boston, MA 02114 USA. RP Li, TS (reprint author), Harvard Univ, Sch Med, Massachusetts Eye & Ear Infirm, Berman Gund Lab Study Retinal Degenerat, Boston, MA 02114 USA. EM tli@meei.harvard.edu NR 3 TC 3 Z9 4 U1 2 U2 2 PU ACADEMIC PRESS LTD ELSEVIER SCIENCE LTD PI LONDON PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND SN 0014-4835 J9 EXP EYE RES JI Exp. Eye Res. PD JUL PY 2006 VL 83 IS 1 BP 1 EP 2 DI 10.1016/j.exer.2005.10.013 PG 2 WC Ophthalmology SC Ophthalmology GA 054WD UT WOS:000238408400001 PM 16318850 ER PT J AU Filippopoulos, T Matsubara, A Danias, J Huang, W Dobberfuhl, A Ren, LZ Mittag, T Miller, JW Grosskreutz, CL AF Filippopoulos, Theodoros Matsubara, Akihisa Danias, John Huang, Wei Dobberfuhl, Adam Ren, Lizhen Mittag, Thomas Miller, Joan W. Grosskreutz, Cynthia L. TI Predictability and limitations of non-invasive murine tonometry: Comparison of two devices SO EXPERIMENTAL EYE RESEARCH LA English DT Article DE glaucoma; mouse; non-invasive; tonometry; intraocular pressure (IOP); model; DBA/2J ID MEASURING INTRAOCULAR-PRESSURE; I COLLAGEN MUTATION; APPLANATION TONOMETRY; OCULAR HYPERTENSION; MICE; GLAUCOMA; LATANOPROST; TONOPEN; RAT AB Our purpose was to evaluate the accuracy; reproducibility and predictive ability of two non-invasive tonometers developed for intraocular pressure (IOP) measurements in the mouse. The prototype impact-rebound tonometer (I-R) and a prototype optical interferometry tonometer (OIT) utilizing a fiberoptic pressure sensor, were compared. Enucleated eyes from C57/BL6 mice were used for the calibration. The anterior chamber was cannulated and the IOP was adjusted in increments of 5 cm of H2O (open stopcock method). A calibration curve was generated for each individual eye along with a master calibration curve for all eyes. Two operators measured the IOP. The instruments were then used in alternating order to measure the IOP in C57/BL6 and in DBA2/J animals. The same eyes were subsequently cannulated and the error of the non-invasive tonometers was determined. Both tonometers yielded almost equivalent ex vivo calibration curves with individual R-2 of 0.9878 and 0.9902 respectively. Both instruments were highly reproducible. In vivo the I-R tonometer underestimated while the OIT overestimated the IOP. This error was systematic and therefore predictable. The confidence intervals of this error were determined by comparing the IOP estimates provided by each tonometer with the measurements obtained invasively by cannulation in vivo. The 95% CI of the error were 2.36 mmHg for the I-R and 2.62 mmHg for the OIT respectively. Non-invasive tonometry in the mouse is feasible. Both non-invasive instruments provide accurate and reproducible measurements with the OIT requiring calibration curves for each individual. investigator. (c) 2006 Elsevier Ltd. All rights reserved. C1 Harvard Univ, Sch Med, Massachusetts Eye & Ear Infirm, Howe Lab,Glaucoma Serv, Boston, MA 02114 USA. Harvard Univ, Sch Med, Massachusetts Eye & Ear Infirm, Angiogenesis Lab,Retina Serv, Boston, MA 02114 USA. Mt Sinai Sch Med, Dept Ophthalmol, New York, NY USA. RP Filippopoulos, T (reprint author), Harvard Univ, Sch Med, Massachusetts Eye & Ear Infirm, Howe Lab,Glaucoma Serv, 243 Charles St, Boston, MA 02114 USA. EM theodoros_filippopoulos@brown.edu; akihisa_matsubara@meei.harvard.edu; john.danias@mssm.edu; wei_huang@meei.harvard.edu; adobberfuhl@neaq.org; thomas.mittag@mssm.edu; cynthia_grosskreutz@meei.harvard.edu FU NEI NIH HHS [EY13399, EY 01867, EY 13467, R01 EY015224, R03 EY13732]; PHS HHS [K08 00390] NR 28 TC 27 Z9 28 U1 0 U2 1 PU ACADEMIC PRESS LTD ELSEVIER SCIENCE LTD PI LONDON PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND SN 0014-4835 J9 EXP EYE RES JI Exp. Eye Res. PD JUL PY 2006 VL 83 IS 1 BP 194 EP 201 DI 10.1016/j.exer.2005.12.005 PG 8 WC Ophthalmology SC Ophthalmology GA 054WD UT WOS:000238408400021 PM 16564045 ER PT J AU Wanahita, A Davis, B Hamill, RJ Goldsmith, EA Rodgers, JR Cook, RG Lamphear, JG Musher, DM AF Wanahita, A Davis, B Hamill, RJ Goldsmith, EA Rodgers, JR Cook, RG Lamphear, JG Musher, DM TI Clostridium difficile lacks detectable superantigen activity SO FEMS IMMUNOLOGY AND MEDICAL MICROBIOLOGY LA English DT Article DE Clostridium difficile; superantigen; leukocytosis ID PERFRINGENS ENTEROTOXIN; TOXIN-A; LEUKOCYTOSIS; INFECTION; DIARRHEA; ACTIVATION; CELLS AB Clostridium difficile colitis causes striking leukocytosis. We examined the possibility that toxins A or B, or other nontoxin products of C. difficile, act as superantigens, thereby stimulating leukocytosis. Our results failed to show major histocompatibility complex class II-dependent T lymphocyte proliferation, the hallmark of superantigen activity. Elevated white blood cell counts in C. difficile colitis are probably due to increased generation of cytokines such as interleukin-6 (IL-6) or IL-8. C1 Vet Affairs Med Ctr, Infect Dis Sect, Houston, TX 77030 USA. Michael E DeBakey Vet Affairs Med Ctr, Houston, TX USA. Baylor Coll Med, Dept Med, Houston, TX 77030 USA. Baylor Coll Med, Dept Mol Virol & Microbiol, Houston, TX 77030 USA. Baylor Coll Med, Dept Immunol, Houston, TX 77030 USA. RP Musher, DM (reprint author), Vet Affairs Med Ctr, Infect Dis Sect, Houston, TX 77030 USA. EM musher@med.va.gov FU NIAID NIH HHS [R01 AI30036, T32-AI07495] NR 18 TC 0 Z9 1 U1 1 U2 3 PU BLACKWELL PUBLISHING PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DQ, OXON, ENGLAND SN 0928-8244 J9 FEMS IMMUNOL MED MIC JI FEMS Immunol. Med. Microbiol. PD JUL PY 2006 VL 47 IS 2 BP 275 EP 277 DI 10.1111/j.1574-695X.2006.00089.x PG 3 WC Immunology; Infectious Diseases; Microbiology SC Immunology; Infectious Diseases; Microbiology GA 059VY UT WOS:000238761500014 PM 16831215 ER PT J AU Asmis, R Qiao, M Rossi, RR Cholewa, J Xu, L Asmis, LM AF Asmis, R Qiao, M Rossi, RR Cholewa, J Xu, L Asmis, LM TI Adriamycin promotes macrophage dysfunction in mice SO FREE RADICAL BIOLOGY AND MEDICINE LA English DT Article DE adriamycin; macrophage; thiol oxidation; cell death; wound healing; protein-S-glutathionylation ID NF-KAPPA-B; TRANSCRIPTION FACTOR; CARDIOLIPIN REQUIREMENT; OXIDATIVE STRESS; DB/DB MICE; IN-VITRO; CARDIOTOXICITY; NUCLEAR; REDOX; MOUSE AB Impaired wound healing contributes to the morbidity and mortality associated with adriamycin chemotherapy. Macrophages are essential for tissue repair and loss of macrophage function leads to impaired wound healing. We recently showed that adriamycin is a potent inducer of thiol oxidation and cell injury in cultured macrophages (FASEB J. 19:1866-1868; 2005). Here we tested the hypothesis that adriamycin also promotes oxidative stress and macrophage dysfunction in vivo. We treated FVB mice twice a week either with low doses of adriamycin (4 mg/kg) or with the same volume of saline by tail vein injection for a total of 8 injections. Wound healing was significantly delayed in adriamycin-treated mice. The number of resident peritoneal macrophages was decreased by 30% and macrophage recruitment in response to thiogycolate stimulation was decreased by 46% in mice treated with adriamycin. LPS-induced TNF alpha and IL-1 beta secretion from macrophages of adriamycin-treated mice was decreased by 28.7 and 29.5%, respectively, compared to macrophages isolated from saline-injected mice. Peritoneal macrophages isolated from adriamycin-treated mice also showed increased formation of reactive oxygen species and enhanced protein-S-glutathionylation. In summary, our results show that low cumulative doses of adriamycin are sufficient both to promote sustained thiol oxidative stress and macrophage dysfunction in vivo and to delay tissue repair, suggesting that macrophage dysfunction contributes to impaired wound healing associated with adriamycin chemotherapy. (c) 2006 Elsevier Inc. All fights reserved. C1 Univ Texas, Hlth Sci Ctr, Div Nephrol, San Antonio, TX 78229 USA. S Texas Vet Hlth Care Syst, San Antonio, TX 78229 USA. Univ Rochester, Med Ctr, Rochester, NY 14642 USA. Univ Kentucky, Grad Ctr Nutr Sci, Lexington, KY USA. Univ Zurich Hosp, Div Hematol, CH-8091 Zurich, Switzerland. RP Asmis, R (reprint author), Univ Texas, Hlth Sci Ctr, Div Nephrol, 7703 Floyd Curl Dr,MSC 7882, San Antonio, TX 78229 USA. EM asmis@uthscsa.edu FU NHLBI NIH HHS [R01 HL-70963] NR 41 TC 15 Z9 15 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0891-5849 J9 FREE RADICAL BIO MED JI Free Radic. Biol. Med. PD JUL 1 PY 2006 VL 41 IS 1 BP 165 EP 174 DI 10.1016/j.freeradbiomed.2006.03.027 PG 10 WC Biochemistry & Molecular Biology; Endocrinology & Metabolism SC Biochemistry & Molecular Biology; Endocrinology & Metabolism GA 058LV UT WOS:000238667400018 PM 16781464 ER PT J AU Akiba, Y Ghayouri, S Takeuchi, T Mizumori, M Guth, PH Engel, E Swenson, ER Kaunitz, JD AF Akiba, Yasutada Ghayouri, Sara Takeuchi, Tetsu Mizumori, Misa Guth, Paul H. Engel, Eli Swenson, Erik R. Kaunitz, Jonathan D. TI Carbonic anhydrases and mucosal vanilloid receptors help mediate the hyperemic response to luminal CO2 in rat duodenum SO GASTROENTEROLOGY LA English DT Article ID AVIAN INTRAPULMONARY CHEMORECEPTORS; STIMULATED HCO3-SECRETION; GASTRIC-ACID-SECRETION; BLOOD-FLOW; GASTROINTESTINAL-TRACT; INTRACELLULAR PH; BICARBONATE SECRETION; AFFERENT NEURONS; ALKALINE SECRETION; EPITHELIAL-CELLS AB Background & Aims: The duodenal mucosa is exposed to PCO2 > 200 mm Hg due to the luminal mixture of gastric acid with secreted bicarbonate, which augments mucosal protective mechanisms. We examined the hyperemic response to elevated luminal PCO2 in the duodenum of anesthetized rats luminally exposed to high CO2 saline to help elucidate luminal acid-sensing mechanisms. Methods: Blood flow was measured by laser Doppler, and intracellular pH of epithelial cells by measured by ratio microimaging. The permeant carbonic anhydrase (CA) inhibitor methazolamide, relatively impermeant CA inhibitor benzolamide, vanilloid receptor antagonist capsazepine, or sodium-hydrogen exchanger 1 (NHE-1) inhibitor dimethyl amiloride were perfused with or without the high CO2 solution. Results: The high CO2 solution increased duodenal blood flow, which was abolished by pretreatment with methazolamide or capsazepine or by dimethyl amiloride coperfusion. Sensory denervation with capsaicin also abolished the CO2 effects. Benzolamide dose-dependently inhibited CO2-induced hyperemia and at 100 nmol/L inhibited CO2-induced intracellular acidification. The membrane-bound CA isoforms IV, IX, XII, and XIV and cytosolic CA II and the vanilloid receptor 1 (TRPV1) were expressed in duodenum and stomach. Dorsal root ganglion and no-dose ganglion expressed all isoforms except for CA IX. Conclusions: The duodenal hyperemic response to luminal CO2 is dependent on cytosolic and membrane-bound CA isoforms, NHE-1, and TRPV1. CO2-induced intracellular acidification was inhibited by selective extracellular CA inhibition, suggesting that CO2 diffusion across the epithelial apical membrane is mediated by extracellular CA. NHE-1 activation preceding TRPV1 stimulation suggests that luminal CO2 is sensed as H+ in the subepithelium. C1 W Los Angeles VA Med Ctr, Los Angeles, CA 90073 USA. RP Kaunitz, JD (reprint author), W Los Angeles VA Med Ctr, Bldg 114,Suite 217,11301 Wilshire Blvd, Los Angeles, CA 90073 USA. EM jake@ucla.edu FU NIDDK NIH HHS [R01 DK54221, P30 DK0413] NR 76 TC 36 Z9 43 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 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD JUL PY 2006 VL 131 IS 1 BP 142 EP 152 DI 10.1053/j.gastro.2006.04.018 PG 11 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA 062YQ UT WOS:000238983300023 PM 16831598 ER PT J AU Hajjar, RJ Samulski, RJ AF Hajjar, RJ Samulski, RJ TI A silver bullet to treat heart failure SO GENE THERAPY LA English DT Editorial Material ID GENE-TRANSFER; MUSCULAR-DYSTROPHY; CARDIOMYOPATHY C1 Harvard Univ, Massachusetts Gen Hosp, Sch Med, Charlestown, MA 02129 USA. Gene Therapy Ctr, Chapel Hill, NC 27599 USA. RP Hajjar, RJ (reprint author), Harvard Univ, Massachusetts Gen Hosp, Sch Med, 149 13th St,CNY-4,Room 4215, Charlestown, MA 02129 USA. EM rhajjar@partners.org; rjs@med.unc.edu NR 9 TC 9 Z9 9 U1 0 U2 0 PU NATURE PUBLISHING GROUP PI LONDON PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND SN 0969-7128 J9 GENE THER JI Gene Ther. PD JUL PY 2006 VL 13 IS 13 BP 997 EP 997 DI 10.1038/sj.gt.3302747 PG 1 WC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Genetics & Heredity; Medicine, Research & Experimental SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Genetics & Heredity; Research & Experimental Medicine GA 054ZT UT WOS:000238418900001 PM 17262904 ER PT J AU Yuasa, MS Masutani, C Hirano, A Cohn, MA Yamaizumi, M Nakatani, Y Hanaoka, F AF Yuasa, MS Masutani, C Hirano, A Cohn, MA Yamaizumi, M Nakatani, Y Hanaoka, F TI A human DNA polymerase eta complex containing Rad18, Rad6 and Rev1; proteomic analysis and targeting of the complex to the chromatin-bound fraction of cells undergoing replication fork arrest SO GENES TO CELLS LA English DT Article ID PIGMENTOSUM VARIANT CELLS; XERODERMA-PIGMENTOSUM; TRANSLESION SYNTHESIS; Y-FAMILY; MOUSE HOMOLOGS; UV-LIGHT; POL-ETA; REPAIR; MUTATIONS; FIDELITY AB DNA polymerase eta (Pol eta) is responsible for efficient translesion synthesis (TLS) past cis-syn cyclobutane thymine dimers (TT dimers), the major DNA lesions induced by UV irradiation. Loss of human Pol eta leads to xeroderma pigmentosum variant syndrome, clearly indicating that Pol eta plays a vital role in preventing skin cancer caused by exposure to sunlight. To further examine Pol eta functions and the mechanisms that regulate this important protein, Pol eta complexes were purified from HeLa cells over-expressing epitope-tagged Pol eta, and polypeptides associated with Pol eta, including Rad18, Rad6 and Rev1, were identified by a combination of mass spectrometry and Western blot analysis. The chromatin-bound fractions of cells subjected to UV irradiation, S phase synchronization, or S phase arrest were specifically enriched in such complexes. These results suggest that arrested replication forks strengthen interactions among Pol eta, Rad18/Rad6 and Rev1, consistent with the requirement for effective TLS by Pol eta at sites of DNA lesions. C1 Osaka Univ, Grad Sch Frontier Biosci, Suita, Osaka 5650871, Japan. Japan Sci & Technol Agcy, SORST, Suita, Osaka 5650871, Japan. Osaka Univ, Grad Sch Med, Suita, Osaka 5650871, Japan. Dana Farber Canc Inst, Boston, MA 02115 USA. Harvard Univ, Sch Med, Boston, MA 02115 USA. Kumamoto Univ, Inst Mol Embryol & Genet, Kumamoto 8620976, Japan. RIKEN, Discovery Res Inst, Celluler Physiol Lab, Wako, Saitama 3510198, Japan. RP Hanaoka, F (reprint author), Osaka Univ, Grad Sch Frontier Biosci, 1-3 Yamada Oka, Suita, Osaka 5650871, Japan. EM fhanaoka@fbs.osaka-u.ac.jp RI Masutani, Chikahide/I-6160-2014; OI Cohn, Martin/0000-0002-2988-3009 NR 50 TC 38 Z9 38 U1 1 U2 2 PU BLACKWELL PUBLISHING PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DQ, OXON, ENGLAND SN 1356-9597 J9 GENES CELLS JI Genes Cells PD JUL PY 2006 VL 11 IS 7 BP 731 EP 744 DI 10.1111/j.1365-2443.2006.00974.x PG 14 WC Cell Biology; Genetics & Heredity SC Cell Biology; Genetics & Heredity GA 055PN UT WOS:000238462800003 PM 16824193 ER PT J AU Swinburne, IA Meyer, CA Liu, XS Silver, PA Brodsky, AS AF Swinburne, Ian A. Meyer, Clifford A. Liu, X. Shirley Silver, Pamela A. Brodsky, Alexander S. TI Genomic localization of RNA binding proteins reveals links between pre-mRNA processing and transcription SO GENOME RESEARCH LA English DT Article ID POLYMERASE-II; SPLICING FACTORS; IN-VIVO; NUCLEAR EXPORT; EXON INCLUSION; ELONGATION; ALPHA; DNA; RECRUITMENT; YEAST AB Pre-mRNA processing often occurs in coordination with transcription thereby coupling these two key regulatory events. As such, many proteins involved in mRNA processing associate with the transcriptional machinery and are in proximity to DNA. This proximity allows for the mapping of the genomic associations of RNA binding proteins by chromatin immunoprecipitation (ChIP) as a way of determining their sites of action on the encoded mRNA. Here, we used ChIP combined with high-density microarrays to localize on the human genome three functionally distinct RNA binding proteins: the splicing factor polypyrimidine tract binding protein (PTBP1/hnRNP I), the mRNA export factor THO complex subunit 4 (ALY/THOC4), and the 3' end cleavage stimulation factor 64 kDa (CSTF2). We observed interactions at promoters, internal exons, and 3' ends of active genes. PTBP1 had biases toward promoters and often coincided with RNA polymerase II (RNA Pol II). The 3' processing factor, CSTF2, had biases toward 3' ends but was also observed at promoters. The mRNA processing and export factor, ALY, mapped to some exons but predominantly localized to introns and did not coincide with RNA Pol II. Because the RNA binding proteins did not consistently coincide with RNA Pol II, the data support a processing mechanism driven by reorganization of transcription complexes as opposed to a scanning mechanism. In sum, we present the mapping in mammalian cells of RNA binding proteins across a portion of the genome that provides insight into the transcriptional assembly of RNA-protein complexes. C1 Harvard Univ, Sch Med, Dept Syst Biol, Boston, MA 02115 USA. Harvard Univ, Sch Publ Hlth, Boston, MA 02115 USA. Dana Farber Canc Inst, Dept Biostat, Boston, MA 02115 USA. Dana Farber Canc Inst, Dept Computat Sci, Boston, MA 02115 USA. Dana Farber Canc Inst, Dept Canc Biol, Boston, MA 02115 USA. RP Brodsky, AS (reprint author), Brown Univ, Dept Mol Biol Cell Biol & Biochem, Ctr Genom & Proteom, Providence, RI 02903 USA. EM Pamela_Silver@hms.harvard.edu; Alexander_Brodsky@brown.edu FU NHGRI NIH HHS [R01 HG004069-01, R01 HG004069]; NIDDK NIH HHS [T90 DK070078, T90 DK070078-01] NR 63 TC 33 Z9 33 U1 1 U2 5 PU COLD SPRING HARBOR LAB PRESS, PUBLICATIONS DEPT PI WOODBURY PA 500 SUNNYSIDE BLVD, WOODBURY, NY 11797-2924 USA SN 1088-9051 J9 GENOME RES JI Genome Res. PD JUL PY 2006 VL 16 IS 7 BP 912 EP 921 DI 10.1101/gr.5211806 PG 10 WC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Genetics & Heredity SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Genetics & Heredity GA 059DB UT WOS:000238712400011 PM 16769980 ER PT J AU Kitada, M Rowitch, DH AF Kitada, Masaaki Rowitch, David H. TI Transcription factor co-expression patterns indicate heterogeneity of oligodendroglial subpopulations in adult spinal cord SO GLIA LA English DT Article DE CNS development; oligodendrocyte; transcription factor; cell fate; neural stem cell ID PROGENITOR CELLS; FACTOR OLIG2; PRECURSOR CELLS; SONIC HEDGEHOG; BHLH PROTEINS; WHITE-MATTER; EXPRESSION; DIFFERENTIATION; NKX2.2; CNS AB Oligodendrocytes and their precursors serve critical roles in the maintenance of neurological function. Although activity of the transcription factors (TFs) Olig1, Olig2, Sox10, and Nkx2.2 is required during early oligodendrocyte development, their later expression in adult central nervous system is rather poorly characterized. Here we have analyzed co-expression patterns of these transcriptional proteins in the mouse cervical spinal cord. Our findings indicate that TF co-expression patterns describe heterogeneity in adult oligodendroglial populations (1) in distinct sub-regions of grey and white matter and (2) with respect to level of maturation from proliferating precursors to myelinating oligodendrocytes. Our findings suggest that TF co-expression patterns identify and might regulate distinct functional classes of grey and white matter oligodendroglia. (c) 2006 Wiley-Liss, Inc. C1 Dana Farber Canc Inst, Dept Pediat Oncol, Boston, MA 02115 USA. Childrens Hosp, Div Hematol, Boston, MA 02115 USA. Childrens Hosp, Div Neonatol, Boston, MA 02115 USA. RP Rowitch, DH (reprint author), Dana Farber Canc Inst, Dept Pediat Oncol, Rm 640D,44 Binney St, Boston, MA 02115 USA. EM david_rowitch@dfci.harvard.edu RI Messier, Claude/A-2322-2008 OI Messier, Claude/0000-0002-4791-1763 FU NINDS NIH HHS [R01NS40511] NR 36 TC 81 Z9 85 U1 3 U2 4 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 0894-1491 J9 GLIA JI Glia PD JUL PY 2006 VL 54 IS 1 BP 35 EP 46 DI 10.1002/glia.20354 PG 12 WC Neurosciences SC Neurosciences & Neurology GA 050JZ UT WOS:000238084900004 PM 16673374 ER PT J AU Sarkar, S Woolf, CJ Hobson, AR Thompson, DG Aziz, Q AF Sarkar, S Woolf, CJ Hobson, AR Thompson, DG Aziz, Q TI Perceptual wind-up in the human oesophagus is enhanced by central sensitisation SO GUT LA English DT Article ID POSTINJURY PAIN HYPERSENSITIVITY; D-ASPARTATE RECEPTOR; TEMPORAL SUMMATION; VISCERAL PAIN; ELECTRICAL-STIMULATION; SECONDARY HYPERALGESIA; CENTRAL MECHANISMS; SPINAL-CORD; 2ND PAIN; CAPSAICIN AB Background: Oesophageal acid infusion induces enhanced pain hypersensitivity in non-acid exposed upper oesophagus (secondary hyperalgesia) in patients with non-cardiac chest pain, thus suggesting central sensitisation contributes to visceral pain hypersensitivity in functional gut disorders (FGD). Perceptual wind-up (increased pain perception to constant intensity sensory stimuli at frequencies >= 0.3 Hz) is used as a proxy for central sensitisation to investigate pain syndromes where pain hypersensitivity is important (for example, fibromyalgia). Aims: Wind-up in central sensitisation induced human visceral pain hypersensitivity has not been explored. We hypothesised that if wind-up is a proxy for central sensitisation induced human visceral pain hypersensitivity, then oesophageal wind-up should be enhanced by secondary hyperalgesia. Methods: In eight healthy volunteers (seven males; mean age 32 years), perception at pain threshold to a train of 20 electrical stimuli applied to the hand and upper oesophagus (UO) at either 0.1 Hz (control) or 2 Hz was determined before and one hour after a 30 minute lower oesophageal acid infusion. Results: Wind-up occurred only with the 2 Hz train in the UO and hand (both p = 0.01). Following acid infusion, pain threshold decreased (17 (4)%; p = 0.01) in the UO, suggesting the presence of secondary hyperalgesia. Wind-up to the 2 Hz train increased in the UO (wind-up ratio 1.4 (0.1) to 1.6 (0.1); p = 0.03) but not in the hand (wind-up ratio 1.3 (0.1) and 1.3 (0.1); p = 0.3) Conclusion: Enhanced wind-up after secondary oesophageal hyperalgesia suggests that visceral pain hypersensitivity induced by central sensitisation results from increased central neuronal excitability. Wind-up may offer new opportunities to investigate the contribution of central neuronal changes to symptoms in FGD. C1 Hope Hosp, Dept GI Sci, Salford M6 8HD, Lancs, England. Univ Manchester, Manchester, Lancs, England. Massachusetts Gen Hosp, Dept Anesthesia & Crit Care, Boston, MA 02114 USA. Harvard Univ, Sch Med, Boston, MA 02115 USA. RP Sarkar, S (reprint author), Hope Hosp, Dept GI Sci, Clin Sci Bldg, Salford M6 8HD, Lancs, England. EM sanchoy@aol.com FU Medical Research Council [G0300195] NR 52 TC 24 Z9 24 U1 0 U2 1 PU B M J PUBLISHING GROUP PI LONDON PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND SN 0017-5749 J9 GUT JI Gut PD JUL PY 2006 VL 55 IS 7 BP 920 EP 925 DI 10.1136/gut.2005.073643 PG 6 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA 051UR UT WOS:000238187600007 PM 16492716 ER PT J AU Ogino, S Cantor, M Kawasaki, T Brahmandam, M Kirkner, GJ Weisenberger, DJ Campan, M Laird, PW Loda, M Fuchs, CS AF Ogino, S Cantor, M Kawasaki, T Brahmandam, M Kirkner, GJ Weisenberger, DJ Campan, M Laird, PW Loda, M Fuchs, CS TI CpG island methylator phenotype (CIMP) of colorectal cancer is best characterised by quantitative DNA methylation analysis and prospective cohort studies SO GUT LA English DT Article ID TIME PCR ASSAY; COLON-CANCER; MICROSATELLITE INSTABILITY; PROMOTER HYPERMETHYLATION; SERRATED ADENOMA; MUTATION; TUMORS; PATTERNS; FIELD; GENE AB Background: The concept of CpG island methylator phenotype ( CIMP) is not universally accepted. Even if specific clinicopathological features have been associated with CIMP, investigators often failed to demonstrate a bimodal distribution of the number of methylated markers, which would suggest CIMP as a distinct subtype of colorectal cancer. Previous studies primarily used methylation specific polymerase chain reaction which might detect biologically insignificant low levels of methylation. Aim: To demonstrate a distinct genetic profile of CIMP colorectal cancer using quantitative DNA methylation analysis that can distinguish high from low levels of DNA methylation. Materials and methods: We developed quantitative real time polymerase chain reaction (MethyLight) assays and measured DNA methylation (percentage of methylated reference) of five carefully selected loci (promoters of CACNA1G, CDKN2A (p16), CRABP1, MLH1, and NEUROG1) in 460 colorectal cancers from large prospective cohorts. Results: There was a clear bimodal distribution of 80 microsatellite instability-high (MSI-H) tumours according to the number of methylated promoters, with no tumours showing 3/5 methylated loci. Thus we defined CIMP as having >= 4/5 methylated loci, and 17% (78) of the 460 tumours were classified as CIMP. CIMP was significantly associated with female sex, MSI, BRAF mutations, and wild-type KRAS. Both CIMP MSI-H tumours and CIMP microsatellite stable (MSS) tumours showed much higher frequencies of BRAF mutations (63% and 54%) than non-CIMP counterparts (non-CIMP MSI-H (0%, p < 10(-5)) and non-CIMP MSS tumours (6.6%, p < 10(-4)), respectively). Conclusion: CIMP is best characterised by quantitative DNA methylation analysis. CIMP is a distinct epigenotype of colorectal cancer and may be less frequent than previously reported. C1 Harvard Univ, Sch Med, Brigham & Womens Hosp, Dept Pathol, Boston, MA 02115 USA. Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02115 USA. Harvard Univ, Sch Med, Boston, MA 02115 USA. Brigham & Womens Hosp, Dept Med, Boston, MA 02115 USA. Univ So Calif, Dept Surg, Keck Sch Med, Kenneth Norris Jr Comprehens Canc Ctr, Los Angeles, CA USA. Univ So Calif, Dept Biochem & Mol Biol, Keck Sch Med, Kenneth Norris Jr Comprehens Canc Ctr, Los Angeles, CA USA. RP Ogino, S (reprint author), Harvard Univ, Sch Med, Brigham & Womens Hosp, Dept Pathol, 75 Francis St, Boston, MA 02115 USA. EM shuji_ogino@dfci.harvard.edu RI Laird, Peter/G-8683-2012 FU NCI NIH HHS [P01 CA87969-03, P01 CA055075, P01 CA087969, P01 CA55075-13, R01 CA075090] NR 47 TC 216 Z9 221 U1 0 U2 7 PU B M J PUBLISHING GROUP PI LONDON PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND SN 0017-5749 J9 GUT JI Gut PD JUL PY 2006 VL 55 IS 7 BP 1000 EP 1006 DI 10.1136/gut.2005.082933 PG 7 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA 051UR UT WOS:000238187600022 PM 16407376 ER PT J AU Jagannath, S Richardson, PG Barlogie, B Berenson, JR Singhal, S Irwin, D Srkalovic, G Schenkein, DP Esseltine, DL Anderson, KC AF Jagannath, Sundar Richardson, Paul G. Barlogie, Bart Berenson, James R. Singhal, Seema Irwin, David Srkalovic, Gordan Schenkein, David P. Esseltine, Dixie L. Anderson, Kenneth C. CA SUMMIT CREST Incestigators TI Bortezomib in combination with dexamethasone for the treatment of patients with relapsed and/or refractory multiple myeloma with less than optimal response to bortezomib alone SO HAEMATOLOGICA-THE HEMATOLOGY JOURNAL LA English DT Article; Proceedings Paper CT 9th Annual Congress of the European-Hematology-Association CY JUN 10-13, 2004 CL Geneva, SWITZERLAND SP European Hematol Assoc DE multiple myeloma; bortezomib; dexamethasone; phase 2 ID HIGH-DOSE DEXAMETHASONE; NF-KAPPA-B; CHEMOTHERAPEUTIC-AGENTS; THALIDOMIDE; CELLS; THERAPY; INTERLEUKIN-6; SENSITIVITY; PREVENTION; CISPLATIN AB Background and Objectives. The efficacy and safety of added dexamethasone were assessed in patients with relapsed and/or refractory multiple myeloma who had a suboptimal response to bortezomib alone. Design and Methods. In two previously reported, open-label, multicenter phase 2 studies, bortezomib 1.0 or 1.3 mg/m(2) was administered intravenously twice weekly for 2 weeks of a 3-week cycle for up to 8 cycles to patients who had failed either >= 2 lines of therapy (SUMMIT, n=202) or first-line therapy (CREST, n=54). Patients with progressive disease after the first two cycles or stable disease after four cycles of bortezomib were eligible for addition of oral dexamethasone 20 mg on the day of and after each bortezomib dose. Responses were assessed by an Independent Review Committee using European Group for Blood and Marrow Transplantation criteria. Results. Addition of dexamethasone to bortezomib was associated with improved responses in 13 of 74 evaluable patients (18%) in SUMMIT and 9 of 27 (33%) in CREST; eight of these 22 patients had been previously refractory to dexamethasone. There were 2 complete, 8 partial, and 12 minimal responses. Dexamethasone did not appear to alter the type or number of adverse events. Treatment-emergent adverse events reported in >= 20% of patients receiving combination therapy were fatigue (25%), thrombocytopenia (24%), insomnia (21%), and nausea (20%). Interpretation and Conclusions. Addition of dexamethasone to bortezomilb in patients with relapsed and/or refractory myeloma who had suboptimal responses to bortezomib C1 St Vincent Comprehens Canc Ctr, New York, NY USA. Dana Farber Canc Inst, Boston, MA 02115 USA. Univ Arkansas Med Sci, Little Rock, AR 72205 USA. Cedars Sinai Med Ctr, Los Angeles, CA 90048 USA. NE Mem Hosp, Chicago, IL USA. Alta Bates Canc Ctr, Berkeley, CA USA. Sparrow Reg Canc Ctr, Lansing, MI USA. Millennium Pharmaceut Inc, Cambridge, MA USA. RP Jagannath, S (reprint author), St Vincent Comprehens Canc Ctr, 325 W 15th St, New York, NY USA. EM sjagannath@aptiumoncology.com NR 27 TC 115 Z9 124 U1 0 U2 0 PU FERRATA STORTI FOUNDATION PI PAVIA PA STRADA NUOVA 134, 27100 PAVIA, ITALY SN 0390-6078 J9 HAEMATOL-HEMATOL J JI Haematol-Hematol. J. PD JUL PY 2006 VL 91 IS 7 BP 929 EP 934 PG 6 WC Hematology SC Hematology GA 060RP UT WOS:000238819600009 PM 16818280 ER PT J AU Farwell, DG Kezirian, EJ Heydt, JL Yueh, B Futran, ND AF Farwell, DG Kezirian, EJ Heydt, JL Yueh, B Futran, ND TI Efficacy of small reconstruction plates in vascularized bone graft mandibular reconstruction SO HEAD AND NECK-JOURNAL FOR THE SCIENCES AND SPECIALTIES OF THE HEAD AND NECK LA English DT Article; Proceedings Paper CT 6th International Conference on Head and Neck Cancer CY AUG 07-11, 2004 CL Washington, DC SP Amer Head & Neck Soc DE reconstruction; mandible; locking; plate; complication ID HYPERBARIC-OXYGEN THERAPY; FREE-FLAP; OROMANDIBULAR RECONSTRUCTION; OSTEORADIONECROSIS; FIXATION; COMPLICATIONS; SURGERY; SYSTEM; THORP; NECK AB Background: Utilization of vascularized bone grafts rigidly fixated with titanium reconstruction plates is the method of choice for reconstruction of segmental mandibular defects. We hypothesized that the use of the newer 2.0-mm locking reconstruction plate (LRP) is not associated with higher rates of complications when compared with larger, previously used plating systems. Methods: A retrospective case series of 184 patients undergoing 185 vascularized bone graft reconstruction procedures of the mandible was conducted. Results. There were 37 plate complications. There was no significant difference in complication rates for the 2 most used plate types (14.5% with the 2.0-mm LRP and 22.2% with the 2.4-mm LRP). Conclusions: Use of the smaller 2.0-mm LRP was not associated with an increase in the complications of plate fracture, exposure, infection, or nonunion, Because of its lower profile and ease of application, the 2.0-mm LRP is our plate of choice for mandibular reconstruction. (c) 2006 Wiley Periodicals, Inc. C1 Univ Calif Davis, Dept Otolaryngol Head & Neck Surg, Sacramento, CA 95817 USA. Univ Calif San Francisco, Dept Otolaryngol Head & Neck Surg, San Francisco, CA 94143 USA. Univ Washington, Dept Otolaryngol Head & Neck Surg, Seattle, WA 98195 USA. VA Puget Sound Healthcare Syst, Surg & Perioperat Care Serv, Seattle, WA USA. RP Farwell, DG (reprint author), Univ Calif Davis, Dept Otolaryngol Head & Neck Surg, 2521 Stockton Blvd,Suite 7200, Sacramento, CA 95817 USA. OI Yueh, Bevan/0000-0003-1380-1053 NR 24 TC 8 Z9 8 U1 0 U2 0 PU JOHN WILEY & SONS INC PI HOBOKEN PA 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 1043-3074 J9 HEAD NECK-J SCI SPEC JI Head Neck-J. Sci. Spec. Head Neck PD JUL PY 2006 VL 28 IS 7 BP 573 EP 579 DI 10.1002/hed.20455 PG 7 WC Otorhinolaryngology; Surgery SC Otorhinolaryngology; Surgery GA 058UM UT WOS:000238690100001 PM 16755584 ER PT J AU Rivolta, C Mcgee, TL Frio, TR Jensen, RV Berson, EL Dryja, TP AF Rivolta, Carlo McGee, Terri L. Frio, Thomas Rio Jensen, Roderick V. Berson, Eliot L. Dryja, Thaddeus P. TI Variation in retinitis pigmentosa-11 (PRPF31 or RP11) gene expression between symptomatic and asymptomatic patients with dominant RP11 mutations SO HUMAN MUTATION LA English DT Article DE retinitis pigmentosa; RP11; PRPF3 1; RHO; penetrance ID NONSENSE-MEDIATED DECAY; SPLICING-FACTOR GENES; MESSENGER-RNA; ERYTHROPOIETIC PROTOPORPHYRIA; INCOMPLETE PENETRANCE; CHINESE FAMILY; RHODOPSIN GENE; RP9 FORM; SPECTRIN; PROTEIN AB Dominant mutations in the mRNA splicing factor gene PRPF31 (RP11) cause retinitis pigmentosa with reduced penetrance. We studied the expression of RP11 in lymphoblast cell lines from 10 patients, including three who were clinically asymptomatic, with six distinct RP11 mutations. Five of the six mutations were characterized and all five created premature nonsense codons or eliminated the normal initiation codon. Semiquantitative RT-PCR indicated that an average of only 17% of the RP11 mRNA was derived from the mutant allele, likely because the mutant mRNA transcripts were degraded by nonsense,mediated decay. Gene expression levels were measured by Affymetrix and CodeLink microarrays and, for RP11 transcripts, also by real-time PCR. Combined wild-type-plus-mutant RP11 mRNA expression from symptomatic patients was 52 to 77% of that in controls (p <= 0.0005). Clinically asymptomatic carriers had levels of RP11 mRNA similar to controls and 29-42% higher than in clinically affected patients (0.0001 < p < 0.05, varying according to measurement technique). Expression levels of seven housekeeping genes (4-15 exons each) and 11 single-exon histone genes showed no substantial differences between affected patients with RP11 mutations and controls. Our results indicate that penetrance of dominant RP11 mutations correlates with the expression level of the remaining wild-type RP11 allele. Because RP11 mutations are apparently null alleles and because nonpenetrance correlates with high wild-type allele expression, the phenotypic effect of RP11 mutations is likely due to haploinsufficiency. The similar mRNA expression levels from genes with and without introns suggest that there is no generalized RNA splicing abnormality in RP 11 patients. Hum Mutat 2 7 (7), 644-653, 2006. Published 2006 Wiley-Liss, Inc.(dagger). C1 Harvard Univ, Sch Med, Massachusetts Eye & Ear Infirm, Ocular Mol Genet Inst, Boston, MA 02114 USA. Harvard Univ, Sch Med, Massachusetts Eye & Ear Infirm, Berman Gund Lab Study Retinal Degenerat, Boston, MA USA. Harvard Univ, Brigham & Womens Hosp, Sch Med, Dept Neurol, Boston, MA USA. Univ Massachusetts, Dept Phys, Boston, MA USA. Univ Lausanne, Dept Med Genet, Lausanne, Switzerland. RP Dryja, TP (reprint author), Harvard Univ, Sch Med, Massachusetts Eye & Ear Infirm, Ocular Mol Genet Inst, 243 Charles St, Boston, MA 02114 USA. EM thaddeus.dryja@meei.harvard.edu OI Rivolta, Carlo/0000-0002-0733-9950 FU NEI NIH HHS [EY00169, EY08683, EY14104] NR 33 TC 47 Z9 47 U1 0 U2 3 PU WILEY-BLACKWELL PI MALDEN PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA SN 1059-7794 J9 HUM MUTAT JI Hum. Mutat. PD JUL PY 2006 VL 27 IS 7 BP 644 EP 653 DI 10.1002/humu.20325 PG 10 WC Genetics & Heredity SC Genetics & Heredity GA 056TR UT WOS:000238548500006 PM 16708387 ER PT J AU Rabban, JT Koerner, FC Lerwill, MF AF Rabban, Joseph T. Koerner, Frederick C. Lerwill, Melinda F. TI Solid papillary ductal carcinoma in situ versus usual ductal hyperplasia in the breast: a potentially difficult distinction resolved by cytokeratin 5/6 SO HUMAN PATHOLOGY LA English DT Article; Proceedings Paper CT Meeting of the United-States-and-Canadian-Academy-of-Pathology CY FEB 28, 2005 CL San Antonio, TX SP US Canadian Acad Pathol DE solid papillary ductal carcinoma in situ; usual ductal hyperplasia; cytokeratin 5/6; breast ID MALIGNANT INTRADUCTAL PROLIFERATIONS; SMOOTH MUSCLE ACTIN; DIFFERENTIAL-DIAGNOSIS; EPITHELIAL PROLIFERATIONS; LUMINAL KERATINS; COLLAGEN-IV; BENIGN; CELLS; ANTIBODIES; LESIONS AB The solid papillary variant of ductal carcinoma in situ is an uncommon entity, which usually presents in the seventh or eighth decade and may be associated with invasive mucinous carcinoma. Solid papillary ductal carcinoma in situ (SP-DCIS) shares many morphological features with usual ductal hyperplasia (UDH) involving a papilloma: papillary architecture, solid growth, cellular streaming, and low-grade nuclear features. These similarities can make the distinction between these 2 entities challenging. Recent studies have demonstrated that immunohistochemical staining for cytokeratin 5/6 can distinguish UDH from conventional forms of ductal carcinoma in situ. Most of the epithelial cells of UDH express cytokeratin 5/6, but the tumor cells of ductal carcinoma in situ do not. We tested the hypothesis that the results of staining for cytokeratin 5/6 can distinguish UDH from the solid papillary variant of ductal carcinoma in situ. Immunohistochemical staining of 14 cases of SP-DCIS and 9 cases of UDH (4 involving papillomas) was performed using cytokeratin 5/6 antibody clone D5/16 B4. Strong cytoplasmic or membrane staining was considered positive. The hyperplastic cells in all cases of UDH showed strong staining for cytokeratin 5/6. The percentage of positive cells ranged from 50% to 80%. None of the SP-DCIS tumor cells stained for cytokeratin 5/6; however, many cases did show staining of occasional entrapped, benign epithelial, and myoepithelial cells. We conclude that the absence of strong cytokeratin 5/6 expression by SP-DCIS distinguishes it from its morphological mimic, UDH. Pathologists must guard against misinterpreting SP-DCIS as UDH in those cases in which the carcinoma cells engulf cytokeratin 5/6-expressing residual, native epithelial cells. (c) 2006 Elsevier Inc. All rights reserved. C1 Univ Calif San Francisco, Dept Pathol, San Francisco, CA 94143 USA. Massachusetts Gen Hosp, Dept Pathol, Boston, MA 02114 USA. RP Rabban, JT (reprint author), Univ Calif San Francisco, Dept Pathol, Box 0102, San Francisco, CA 94143 USA. EM joseph.rabban@ucsf.edu NR 23 TC 27 Z9 29 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 0046-8177 J9 HUM PATHOL JI Hum. Pathol. PD JUL PY 2006 VL 37 IS 7 BP 787 EP 793 DI 10.1016/j.humpath.2006.02.016 PG 7 WC Pathology SC Pathology GA 060RM UT WOS:000238819300003 PM 16784976 ER PT J AU Koralov, SB Novobrantseva, TI Konigsmann, J Ehlich, A Rajewsky, K AF Koralov, Sergei B. Novobrantseva, Tatiana I. Koenigsmann, Jessica Ehlich, Andreas Rajewsky, Klaus TI Antibody repertoires generated by V-H replacement and direct V-H to J(H) joining SO IMMUNITY LA English DT Article ID VARIABLE REGION GENE; STRAND BREAK REPAIR; HUMAN-B-LYMPHOCYTES; HEAVY-CHAIN LOCUS; V(D)J RECOMBINATION; SEQUENCE HOMOLOGIES; RECEPTOR REVISION; SOMATIC MUTATION; MAMMALIAN-CELLS; IMMUNE-RESPONSE AB The immunoglobulin heavy chain repertoire is generated by somatic rearrangement of variable (V-H), diversity (D-H), and joining (J(H)) elements. It can be further diversified by V-H replacement, where nonrearranged V-H genes invade preexisting V(H)D(H)J(H) joints. To study the impact and mechanism of V-H replacement, we generated mice in which antibody production depends on the replacement of a nonproductive V(H)D(H)J(H) rearrangement inserted into its physiological position in the immunoglobulin heavy chain locus. In these mice a highly diverse heavy chain repertoire resulted from V-H replacement and a second process of noncanonical V(D)J recombination, direct V-H to J(H) joining. V-H replacement rarely generated detectable sequence duplications but often proceeded through recombination between the conserved homologous sequences at the 3' end of V-H. Thus, V-H replacement is an efficient mechanism of antibody diversification, and its impact on the overall antibody repertoire could be greater than anticipated because it frequently leaves no molecular footprint. C1 Harvard Univ, Sch Med, CBR Inst Biomed Res, Boston, MA 02115 USA. Univ Cologne, Inst Genet, D-50931 Cologne, Germany. RP Rajewsky, K (reprint author), Harvard Univ, Sch Med, CBR Inst Biomed Res, 200 Longwood Ave, Boston, MA 02115 USA. EM rajewsky@cbr.med.harvard.edu FU NIAID NIH HHS [AI052343, AI054636] NR 50 TC 42 Z9 42 U1 0 U2 1 PU CELL PRESS PI CAMBRIDGE PA 1100 MASSACHUSETTS AVE, CAMBRIDGE, MA 02138 USA SN 1074-7613 J9 IMMUNITY JI Immunity PD JUL PY 2006 VL 25 IS 1 BP 43 EP 53 DI 10.1016/j.immuni.2006.04.016 PG 11 WC Immunology SC Immunology GA 072ZX UT WOS:000239713000009 PM 16860756 ER PT J AU Patterson, HCK Kraus, M Kim, YM Ploegh, H Rajewsky, K AF Patterson, Heide Christine K. Kraus, Manfred Kim, You-Me Ploegh, Hidde Rajewsky, Klaus TI The B cell receptor promotes B cell activation and proliferation through a non-ITAM tyrosine in the Ig alpha cytoplasmic domain SO IMMUNITY LA English DT Article ID ANTIGEN RECEPTOR; LINKER PROTEIN; MOTIF ITAM; KAPPA-B; BLNK; LYMPHOCYTES; MICE; SLP-65; SYK; PHOSPHORYLATION AB In addition to the tyrosines of the Ig alpha and beta immunoreceptor tyrosine-based activation motifs (ITAMs), the evolutionarily conserved Ig alpha non-ITAM tyrosine 204 becomes phosphorylated upon antigen recognition by the B cell receptor (BCR). Here we demonstrate that splenic B cells from mice with a targeted mutation of Ig alpha Y204 exhibited an isolated defect in T cell-independent B cell activation, proliferation, and antibody response upon BCR engagement, yet normal BCR capping, antigen internalization, antigen presentation, and T cell-dependent antibody production. Mutant B cells, present in normal numbers, exhibited unimpaired BCR-induced spleen tyrosine kinase (Syk) phosphorylation but reduced B cell linker protein (BLNK) phosphorylation, calcium flux, and nuclear factor kappa B (NF kappa B), c-jun N-terminal kinase (JNK), and extracellular signal-regulated kinase (ERK) activation. These results suggest that Ig alpha non-ITAM tyrosine 204 promotes a distinct cellular response, namely T-independent B cell proliferation and differentiation via phosphorylation of the adaptor BLNK. C1 CBR Inst Biomed Res, Boston, MA 02115 USA. Whitehead Inst Biomed Res, Cambridge, MA 02142 USA. RP Rajewsky, K (reprint author), CBR Inst Biomed Res, Boston, MA 02115 USA. EM rajewsky@cbr.med.harvard.edu RI Kim, You-Me/I-5553-2013 OI Kim, You-Me/0000-0001-8780-704X FU NIAID NIH HHS [R37 AI054636] NR 43 TC 36 Z9 38 U1 0 U2 4 PU CELL PRESS PI CAMBRIDGE PA 1100 MASSACHUSETTS AVE, CAMBRIDGE, MA 02138 USA SN 1074-7613 J9 IMMUNITY JI Immunity PD JUL PY 2006 VL 25 IS 1 BP 55 EP 65 DI 10.1016/j.immuni.2006.04.014 PG 11 WC Immunology SC Immunology GA 072ZX UT WOS:000239713000010 PM 16860757 ER PT J AU Ciofani, M Knowles, GC Wiest, DL von Boehmer, H Zuniga-Pflucker, JC AF Ciofani, Maria Knowles, Gisele C. Wiest, David L. von Boehmer, Harald Zuniga-Pflucker, Juan Carlos TI Stage-specific and differential notch dependency at the alpha beta and gamma delta T lineage bifurcation SO IMMUNITY LA English DT Article ID CELL-DEVELOPMENT; PRE-TCR; THYMOCYTE DIFFERENTIATION; THYMIC DEVELOPMENT; BETA/GAMMA-DELTA; FATE; EXPRESSION; MICE; SELECTION; REARRANGEMENT AB Signals transduced by Notch receptors are indispensable for T cell specification and differentiation of up T lineage cells. However, the role of Notch signals during alpha beta versus gamma delta T lineage decision remains controversial. Here, we addressed this question by employing a clonal analysis of CD4(-)CD8(-) (DN) progenitor potential to position the divergence of alpha beta and gamma delta T cell lineages to the late DN2 to DN3 developmental stages. Accordingly, alpha beta and gamma delta precursor frequencies within these T cell progenitor subsets were determined, both in the presence and absence of Notch signaling through Delta-like 1. Notch signals were found to be critical for the DN to CD4(+)CD8(+) (DP) transition, irrespective of the identity (pT alpha beta or gamma delta) of the inducing T cell receptor complex, whereas gamma delta T cells developed from gamma delta TCR-expressing T cell progenitors in the absence of further Notch ligand interaction. Collectively, our findings demonstrate a differential, stage-specific requirement for Notch receptor-ligand interactions in the differentiation of up and gamma delta T cells from T cell progenitors. C1 Univ Toronto, Sunnybrook Res Inst, Dept Immunol, Toronto, ON M4N 3M5, Canada. Fox Chase Canc Ctr, Div Basic Sci, Immunobiol Working Grp, Philadelphia, PA 19111 USA. Harvard Univ, Sch Med, Dana Farber Canc Inst, Boston, MA 02115 USA. RP Zuniga-Pflucker, JC (reprint author), Univ Toronto, Sunnybrook Res Inst, Dept Immunol, 2075 Bayview Ave, Toronto, ON M4N 3M5, Canada. EM jczp@sri.utoronto.ca RI Zuniga-Pflucker, Juan/H-1295-2012; OI Wiest, David/0000-0002-0792-3188 NR 50 TC 127 Z9 128 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 JUL PY 2006 VL 25 IS 1 BP 105 EP 116 DI 10.1016/j.immuni.2006.05.010 PG 12 WC Immunology SC Immunology GA 072ZX UT WOS:000239713000014 PM 16814577 ER PT J AU Mempel, TR Pittet, MJ Khazaie, K Weninger, W Weissleder, R von Boehmer, H von Andrian, UH AF Mempel, Thorsten R. Pittet, Mikael J. Khazaie, Khashayarsha Weninger, Wolfgang Weissleder, Ralph von Boehmer, Harald von Andrian, Ulrich H. TI Regulatory T cells reversibly suppress cytotoxic T cell function independent of effector differentiation SO IMMUNITY LA English DT Article ID IMMUNOLOGICAL SELF-TOLERANCE; LYTIC GRANULE EXOCYTOSIS; ANTIGEN-PRESENTING CELLS; DENDRITIC CELLS; LYMPH-NODES; IN-VIVO; TOLL-LIKE; TUMOR; CD8; BETA AB Mechanisms of dominant tolerance have evolved within the mammalian immune system to prevent inappropriate immune responses. CD4(+)CD25(+) regulatory T (T-reg) cells have emerged as central constituents of this suppressive activity. By using multiphoton intravital microscopy in lymph nodes (LNs) of anesthetized mice, we have analyzed how cytotoxic T lymphocytes (CTLs) interact with antigen-presenting target cells in the presence or absence of activated T-reg cells. Nonregulated CTLs killed their targets at a 6.6-fold faster rate than regulated CTLs. In spite of this compromised effector activity, regulated CTLs exhibited no defect in proliferation, induction of cytotoxic effector molecules and secretory granules, in situ motility, or ability to form antigen-dependent conjugates with target cells. Only granule exocytosis by CTLs was markedly impaired in the presence of T-reg cells. This selective form of regulation did not require prolonged contact between CTLs and T-reg cells but depended on CTL responsiveness to transforming growth factor-beta. CTLs quickly regained full killing capacity in LNs upon selective removal of T-reg cells. Thus, T-reg cells reversibly suppress CTL-mediated immunity by allowing acquisition of full effector potential but withholding the license to kill. C1 Massachusetts Gen Hosp, Ctr Mol Imaging Res, Charlestown, MA 02129 USA. Harvard Univ, Sch Med, Boston, MA 02129 USA. Harvard Univ, Sch Med, Dana Farber Canc Inst, 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. RP Pittet, MJ (reprint author), Massachusetts Gen Hosp, Ctr Mol Imaging Res, Bldg 149,13th St, Charlestown, MA 02129 USA. EM mpittet@hms.harvard.edu RI von Andrian, Ulrich/A-5775-2008; OI Weninger, Wolfgang/0000-0003-3133-8699 FU NCI NIH HHS [P50-CA-86355, R01-CA104547, R01-CA96978, R24-CA92782]; NHLBI NIH HHS [T32-HL-066987-04, P01-HL56949, R01-HL54936]; NIAID NIH HHS [R01-AI-061663, R37 AI53102] NR 50 TC 286 Z9 296 U1 2 U2 14 PU CELL PRESS PI CAMBRIDGE PA 1100 MASSACHUSETTS AVE, CAMBRIDGE, MA 02138 USA SN 1074-7613 J9 IMMUNITY JI Immunity PD JUL PY 2006 VL 25 IS 1 BP 129 EP 141 DI 10.1016/j.immuni.2006.04.015 PG 13 WC Immunology SC Immunology GA 072ZX UT WOS:000239713000016 PM 16860762 ER PT J AU Nath, N Prasad, R Giri, S Singh, AK Singh, I AF Nath, N Prasad, R Giri, S Singh, AK Singh, I TI T-bet is essential for the progression of experimental autoimmune encephalomyelitis SO IMMUNOLOGY LA English DT Article DE EAE; T-bet; T-cells; IL-10; autoimmunity ID EXPERIMENTAL ALLERGIC ENCEPHALOMYELITIS; CENTRAL-NERVOUS-SYSTEM; CELL-DIFFERENTIATION; MULTIPLE-SCLEROSIS; BALB/C MICE; GAMMA; IL-4-DEFICIENT; CHEMOKINES; INDUCTION; IL-10 AB Experimental autoimmune encephalomyelitis (EAE) is mediated by myelin-specific CD4(+) T helper 1 (Th1) cells, while recovery from the disease is associated with the presence of Th2 cells. Here we used animals with targeted deletion of the T-bet gene to determine its role in the progression of EAE. T-bet regulates the production of interferon-gamma (IFN-gamma) in CD4(+) and natural killer cells, and CD4(+) T cells from T-bet-deficient mice were unable to differentiate into a Th1 phenotype. Moreover BALB/c mice deficient in T-bet were resistant to the induction of EAE disease, with minimal inflammatory infiltrates in the central nervous system. These mice were resistant to EAE induction even when PLP(180-199) peptide specific effector T cells from BALB/c wild type were transferred to BALB/c T-bet-deficient mice. This resistance to EAE is may be caused by the production of the anti-inflammatory cytokine interleukin-10 (IL-10) from the spleen cells upon ex vivo stimulation with PLP(180-199) peptide and in vivo presence in the central nervous system. There was no difference in the recall responses in spleen cells from T-bet-deficient and wild type mice; however, less secretion of IFN-gamma was observed from primed splenocytes. The expression of IFN-gamma was less in the central nervous system of T-bet-deficient mice whereas IL-10 was significantly higher in T-bet-deficient as compared to wild type mice. These data indicate that T-bet genes play a critical role in maintaining the encephalitogenic nature of CD4(+) T cells in autoimmune responses during EAE disease progression. C1 Med Univ S Carolina, Childrens Res Inst, Dept Pediat, Charleston, SC 29425 USA. Ralph H Johnson VA Med Ctr, Dept Pathol & Lab Med, Charleston, SC USA. RP Singh, I (reprint author), Med Univ S Carolina, Childrens Res Inst, Dept Pediat, 173 Ashley Ave,505 Childrens Res Inst, Charleston, SC 29425 USA. EM singhi@musc.edu FU NINDS NIH HHS [NS-34741, NS-37766, NS-40144, NS-40810, NS-22576] NR 32 TC 39 Z9 40 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 JUL PY 2006 VL 118 IS 3 BP 384 EP 391 DI 10.1111/j.1365-2567.2006.02385.x PG 8 WC Immunology SC Immunology GA 054RR UT WOS:000238396800011 PM 16827899 ER PT J AU Wozniak, KL Vyas, JM Levitz, SM AF Wozniak, KL Vyas, JM Levitz, SM TI In vivo role of dendritic cells in a murine model of pulmonary cryptococcosis SO INFECTION AND IMMUNITY LA English DT Article ID RAT ALVEOLAR MACROPHAGES; ANTIGEN-PRESENTING CELLS; NECROSIS-FACTOR-ALPHA; CD8+ T-CELLS; HUMAN NEUTROPHILS; MYCOBACTERIUM-TUBERCULOSIS; CAPSULAR POLYSACCHARIDE; INFLAMMATORY RESPONSE; LYMPH-NODES; NEOFORMANS INFECTION AB Dendritic cells (DC) have been shown to phagocytose and kill Cryptococcus neoformans in vitro and are believed to be important for inducing protective immunity against this organism. Exposure to C. neoformans occurs mainly by inhalation, and in this study we examined the in vivo interactions of C. neoformans with DC in the lung. Fluorescently labeled live C. neoformans and heat-killed C. neoformans were administered intra-nasally to C57BL/6 mice. At specific times postinoculation, mice were sacrificed, and lungs were removed. Single-cell suspensions of lung cells were prepared, stained, and analyzed by microscopy and flow cytometry. Within 2 It postinoculation, fluorescently labeled C. neoformans had been internalized by DC, macrophages, and neutrophils in the mouse lung. Additionally, lung DC from mice infected for 7 days showed increased expression of the maturation markers CD80, CD86, and major histocompatibility complex class II. Finally, ex vivo incubation of lung DC from infected mice with Cryptococcus-specific T cells resulted in increased, interleukin-2 production compared to the production by DC from naive mice, suggesting that there was antigen-specific T-cell activation. This study demonstrated that DC in the lung are capable of phagocytosing Cryptococcus in vivo and presenting antigen to C. neoformans-specific T cells ex vivo, suggesting that these cells have roles in innate and adaptive pulmonary defenses against cryptococcosis. C1 Boston Univ, Med Ctr, Infect Dis Sect, Evans Mem Dept Med, Boston, MA 02218 USA. Massachusetts Gen Hosp, Dept Med, Div Infect Dis, Boston, MA 02114 USA. RP Levitz, SM (reprint author), Boston Univ, Med Ctr, Infect Dis Sect, Evans Mem Dept Med, 650 Albany St, Boston, MA 02218 USA. EM slevitz@bu.edu RI Vyas, Jatin/Q-1627-2016 OI Vyas, Jatin/0000-0002-9985-9565 FU NIAID NIH HHS [R01 AI25780, 5K08 AI57999, K08 AI057999, R01 AI025780, R01 AI025780-20, R01 AI025780-21, R01 AI025780-22, R01 AI037532, R01 AI066087, R01 AI066087-01, R01 AI066087-02, R01 AI37532, T32 AI052070] NR 82 TC 45 Z9 48 U1 0 U2 1 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA SN 0019-9567 J9 INFECT IMMUN JI Infect. Immun. PD JUL PY 2006 VL 74 IS 7 BP 3817 EP 3824 DI 10.1128/IAI.00317-06 PG 8 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA 057JJ UT WOS:000238591800012 PM 16790753 ER PT J AU Goncalves, RB Leshem, O Bernards, K Webb, JR Stashenko, PP Campos-Neto, A AF Goncalves, RB Leshem, O Bernards, K Webb, JR Stashenko, PP Campos-Neto, A TI T-cell-expression cloning of Porphyromonas gingivalis genes coding for T helper-biased immune responses during infection SO INFECTION AND IMMUNITY LA English DT Article ID ALVEOLAR BONE LOSS; ANTIOXIDANT DEFENSE-MECHANISMS; GRAM-NEGATIVE BACTERIA; PERIODONTAL-DISEASE; BACTEROIDES-GINGIVALIS; PROGRESSIVE PERIODONTITIS; ANTIBODY-RESPONSE; LEISHMANIA-MAJOR; ORAL INFECTION; ANTIGENS AB Exposure of the mouse oral cavity to Porphyromonas gingivalis results in the development of gingivitis and periapical bone loss, which apparently are associated with a Th1 response to bacterial antigens. We have used this infection model in conjunction with direct T-cell expression cloning to identify bacterial antigens that induce a preferential or biased T helper response during the infectious process. A P. gingivalis-specific CD4 T-cell line derived from mice at 3 weeks postchallenge was used to directly screen a P. gingivalis genomic expression library. This screen resulted in the identification of five genes coding for previously identified proteins and three other putative protein antigens. One of the identified proteins, P. gingivalis thiol peroxidase, was studied in detail because this molecule belongs to a protein family that is apparently involved in microbial pathogenesis. Infection of mice with P. gingivalis, either via the subcutaneous route or after exposure of the animal's oral cavity to viable bacteria, resulted in the induction of a strong thiol peroxidase-specific immune response characterized by the production of high titers of specific serum immunoglobulin G2a antibody and the production of gamma interferon by antigen-stimulated lymphoid cells, a typical Th1-biased response. Thus, the use of a proven T-cell expression cloning approach and a mouse model of periodontal disease resulted in the identification and characterization of P. gingivalis proteins that might be involved in pathogenesis. C1 Forsyth Inst, Boston, MA 02115 USA. Univ Estadual Campinas, Piracicaba Sch Dent, Piracicaba, SP, Brazil. Infect Dis Res Inst, Seattle, WA USA. British Columbia Canc Agcy, Deeley Res Ctr, Victoria, BC, Canada. Boston Univ, Henry M Goldman Sch Dent Med, Boston, MA 02215 USA. RP Stashenko, PP (reprint author), Forsyth Inst, 140 Fenway, Boston, MA 02115 USA. EM pstashenko@forsyth.org; acampos@forsyth.org FU NCRR NIH HHS [C06RR11244]; NIDCR NIH HHS [R01 DE009018, R01-DE-09018] NR 47 TC 10 Z9 12 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 JUL PY 2006 VL 74 IS 7 BP 3958 EP 3966 DI 10.1128/IAI.02029-05 PG 9 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA 057JJ UT WOS:000238591800028 PM 16790769 ER PT J AU Dyer, GSM Vrahas, MS AF Dyer, George S. M. Vrahas, Mark S. TI Review of the pathophysiology and acute management of haemorrhage in pelvic fracture SO INJURY-INTERNATIONAL JOURNAL OF THE CARE OF THE INJURED LA English DT Review DE pelvic; fracture; haemorrhage; management; external fixator; angiography; embolisation ID ANGIOGRAPHIC EMBOLIZATION; RESUSCITATION; RING; CLASSIFICATION; REQUIREMENTS; OXYGENATION; DISRUPTION; INJURIES; PATTERN; TRAUMA AB Mortality following pelvic fractures has declined dramatically as better methods of controlling haemorrhage, such as angioembolisation to control arterial bleeding, have been introduced. But about 10% of patients still die, despite these advances. To save these patients, the key questions in managing pelvic fractures are: which patients are at highest risk for a life-threatening bleed, in these patients, what is the exact anatomical source of the bleeding and what is the best way to stop it? There is wide consensus that bleeding is most likely to occur with unstable fractures. However, it remains difficult to predict which fractures will actually cause excessive bleeding. Current treatment protocols rely on angiographic embolisation and external fixation, either alone or in combination. Direct pelvic packing is gaining in popularity, but, ultimately, the ideal treatment method remains unclear. The purpose of this review is to examine our current understanding of the pathophysiology and management of bleeding pelvic fractures. (C) 2005 Elsevier Ltd. All rights reserved. C1 Massachusetts Gen Hosp, Dept Orthopaed Surg, Boston, MA 02114 USA. Harvard Combined Orthopaed Residency, Boston, MA USA. Brigham & Womens Hosp, Boston, MA 02115 USA. RP Dyer, GSM (reprint author), Massachusetts Gen Hosp, Dept Orthopaed Surg, 55 Fruit St, Boston, MA 02114 USA. EM gdyer@partners.org NR 31 TC 47 Z9 52 U1 0 U2 0 PU ELSEVIER SCI LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND SN 0020-1383 J9 INJURY JI Injury-Int. J. Care Inj. PD JUL PY 2006 VL 37 IS 7 BP 602 EP 613 DI 10.1016/j.injury.2005.09.007 PG 12 WC Critical Care Medicine; Emergency Medicine; Orthopedics; Surgery SC General & Internal Medicine; Emergency Medicine; Orthopedics; Surgery GA 062BV UT WOS:000238920300004 PM 16309680 ER PT J AU Dec, GW AF Dec, GW TI Recognizing the apical ballooning syndrome in the intensive care unit SO INTENSIVE CARE MEDICINE LA English DT Editorial Material ID MYOCARDIAL DYSFUNCTION; STRESS; STATES; FEATURES; DISEASE C1 Massachusetts Gen Hosp, Div Cardiol, Boston, MA 02114 USA. RP Dec, GW (reprint author), Massachusetts Gen Hosp, Div Cardiol, 55 Fruit St,Mailstop 817, Boston, MA 02114 USA. EM gdec@partners.org NR 13 TC 1 Z9 1 U1 0 U2 0 PU SPRINGER PI NEW YORK PA 233 SPRING STREET, NEW YORK, NY 10013 USA SN 0342-4642 J9 INTENS CARE MED JI Intensive Care Med. PD JUL PY 2006 VL 32 IS 7 BP 962 EP 964 DI 10.1007/s00134-006-0201-y PG 3 WC Critical Care Medicine SC General & Internal Medicine GA 056CJ UT WOS:000238498400003 PM 16791657 ER PT J AU Lichterfeld, M Williams, KL Mui, SK Shah, SS Mothe, BR Sette, A Kim, A Johnston, MN Burgett, N Frahm, N Cohen, D Brander, C Rosenberg, ES Walker, BD Altfeld, M Yu, XG AF Lichterfeld, M Williams, KL Mui, SK Shah, SS Mothe, BR Sette, A Kim, A Johnston, MN Burgett, N Frahm, N Cohen, D Brander, C Rosenberg, ES Walker, BD Altfeld, M Yu, XG TI T cell receptor cross-recognition of an HIV-1CD8+T cell epitope presented by closely related alleles from the HLA-A3 superfamily SO INTERNATIONAL IMMUNOLOGY LA English DT Article DE cross-presentation; cross-recognition; cytotoxic T cells; HIV-1; HLA-A3 superfamily ID CLASS-I MOLECULES; LYMPHOCYTE EPITOPES; PEPTIDE-BINDING; VIRUS TYPE-1; MHC; CTL; SPECIFICITY; RESPONSES; ALPHA; CYTOTOXICITY AB HLA-A3 and -A11 share similar peptide-binding motifs, however, it is unclear if promiscuous epitope presentation by HLA-A3 or HLA-A11 is associated with promiscuous TCR recognition. Here, we show that despite widespread cross-presentation of identical HIV-1 peptides in HIV-1-infected individuals expressing HLA-A3 or HLA-A11, peptides presented by HLA-A3 or HLA-A11 commonly exhibited clear immune distinctiveness with exclusive TCR recognition. Yet, using HLA-A3 and HLA-A11 tetramers for testing T cell cross-recognition of the HIV-1 Nef QK10 epitope, we observed in two study persons that specific CD8+ T cell populations were able to cross-recognize this peptide in the context of both HLA-A3 and HLA-A11. This cross-recognition was mediated by single cross-reactive TCRs, as shown by TCR sequencing in conjunction with TCR V beta chain immunostaining. In each cross-reactive cell population, multiple TCR beta chain variants were detected in the presence of only one TCR alpha chain variant. Thus, despite distinct TCR recognition of HLA-A3 or HLA-A11 presented HIV-1 peptides in the vast majority of cases, specific TCRs can cross-recognize their antigen in the context of both HLA-A3 and HLA-A11. C1 Massachusetts Gen Hosp, Partners AIDS Res Ctr, Boston, MA 02114 USA. Harvard Univ, Sch Med, Div Aids, Boston, MA 02114 USA. Calif State Univ San Marcos, Dept Biol Sci, San Marcos, CA USA. La Jolla Inst Allergy & Immunol, San Diego, CA USA. Fenway Community Hlth, Boston, MA USA. Howard Hughes Med Inst, Chevy Chase, MD USA. RP Yu, XG (reprint author), Massachusetts Gen Hosp, Partners AIDS Res Ctr, Boston, MA 02114 USA. EM xyu@partners.org OI Brander, Christian/0000-0002-0548-5778 FU NIAID NIH HHS [N01-AI-30024] NR 36 TC 15 Z9 17 U1 0 U2 0 PU OXFORD UNIV PRESS PI OXFORD PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND SN 0953-8178 J9 INT IMMUNOL JI Int. Immunol. PD JUL PY 2006 VL 18 IS 7 BP 1179 EP 1188 DI 10.1093/intimm/dxl052 PG 10 WC Immunology SC Immunology GA 056PP UT WOS:000238537900017 PM 16772368 ER PT J AU Young, MRI AF Young, MRI TI Cytokine-containing gelfoam implants at a postsurgical tumor excision site to stimulate local immune reactivity SO INTERNATIONAL JOURNAL OF CANCER LA English DT Article DE CD34(+) cells; chemoattraction; dendritic cells; differentiation; GM-CSF; immunotherapy; tumor; VEGF ID ENDOTHELIAL GROWTH-FACTOR; CD34(+) PROGENITOR CELLS; IMMATURE MYELOID CELLS; DENDRITIC CELLS; PROSTATE-CANCER; NECK-CANCER; CLINICAL-RESPONSES; PERIPHERAL-BLOOD; PHASE-II; T-CELLS AB We previously demonstrated increased numbers of CD34(+) progenitor cells in the peripheral blood of tumor bearers. Also demonstrated was the feasibility of chemoattracting these cells by sponge implants containing VEGF. The present study used a murine Lewis lung carcinoma (LLC) model to test if CD34(+) cells that are chemoattracted to a tumor excision site can be differentiated in situ into dendritic cells and whether this leads to increased local immune reactivity. After surgically excising established LLC tumors, mice received at the excision site gelatin sponge implants containing VEGF to chemoattract CD34(+) cells, and/or GM-CSF plus SCF to induce CD34(+) cell differentiation into dendritic cells. In some studies, lysates of GFP-transfected LLC cells (LLCGFP) were also included in the implants as a source of tumor antigen. After 2 weeks, implants and local lymph nodes were removed and analyzed. Implants containing VEGF, GM-CSF/SCF or VEGF/GM:CSF/SCF had a higher proportion of CD34(+) cells compared to control implants. However, the number of dendritic cells,vas higher in implants containing GM-CSF/SCF or VEGF/GM-CSF/SCF than those containing either VEGF or diluent. Regional lymph node from mice containing GM-CSF/SCF or VEGF/GM-CSF/SCF implants showed increased dendritic cell levels. However, when lysates from LLCGFP were added to the implants, the highest proportion of dendritic cells associated with GFP was in lymph nodes of mice containing GM-CSF/SCF implants. Lymph node cells from mice with GM-CSF/SCF or VEGF/GM-CSF/SCF had a higher level of proliferation and IFN-gamma secretion in response to in vitro LLC lysate challenge, with the greatest response being from lymph node cells of mice with GM-CSF/SCF implants. These results suggest the feasibility of using GM-CSF/SCF-containing implants to increase dendritic cell levels, uptake of tumor antigens, trafficking to lymph nodes and stimulation of immune reactivity at tumor excision sites with residual tumor. (c) 2006 Wiley-Liss, Inc. C1 Ralph H Johnson VA Med Ctr, Res Serv 151, Dept Res Serv, Charleston, SC 29401 USA. Med Univ S Carolina, Dept Med, Charleston, SC 29425 USA. Med Univ S Carolina, Dept Otolaryngol, Charleston, SC 29425 USA. RP Young, MRI (reprint author), Ralph H Johnson VA Med Ctr, Res Serv 151, Dept Res Serv, 109 Bee St, Charleston, SC 29401 USA. EM rita.young@med.va.gov FU NCI NIH HHS [CA-97813, CA-85266] NR 34 TC 0 Z9 1 U1 0 U2 0 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 0020-7136 J9 INT J CANCER JI Int. J. Cancer PD JUL 1 PY 2006 VL 119 IS 1 BP 133 EP 138 DI 10.1002/ijc.21806 PG 6 WC Oncology SC Oncology GA 041CH UT WOS:000237430200018 PM 16450395 ER PT J AU Herzog, DB Franko, DL Dorer, DJ Keel, PK Jackson, S Manzo, MP AF Herzog, DB Franko, DL Dorer, DJ Keel, PK Jackson, S Manzo, MP TI Drug abuse in women with eating disorders SO INTERNATIONAL JOURNAL OF EATING DISORDERS LA English DT Article DE drug abuse; women; eating disorders ID BULIMIA-NERVOSA; ALCOHOL-USE; SUBSTANCE USE; COMORBIDITY; RELATIVES; ANOREXIA AB Objective: Drug abuse in women with eating disorders has received relatively little attention. The frequency of drug use disorder (DUD) by specific drug type was examined in the current longitudinal study. Method: In a prospective study, women diagnosed with either anorexia nervosa (AN; n = 136) or bulimia nervosa (BN; n = 110), were interviewed and assessed for research diagnostic criteria (RDC) DUD every 6-12 months over 8.6 years. Results: Forty-two (17%) women in the current longitudinal study had a lifetime history of DUD, with 19 prospective onsets over the course of the study (9 AN and 10 BN). The most commonly abused illicit drugs were amphetamines, cocaine, and marijuana, and rates of DUD did not differ between intake diagnoses of AN and BN. Conclusion: Drug abuse in women with eating disorders is an area of clinical concern and should be monitored routinely throughout the treatment process. (c) 2006 by Wiley Periodicals, Inc. C1 Massachusetts Gen Hosp, Dept Psychiat, Boston, MA 02114 USA. Northeastern Univ, Dept Counseling & appl Educ Psychol, Boston, MA 02115 USA. Massachusetts Gen Hosp, Dept Biostat, Boston, MA 02114 USA. Univ Iowa, Dept Psychol, Iowa City, IA 52242 USA. RP Herzog, DB (reprint author), Massachusetts Gen Hosp, Dept Psychiat, 32 Fruit St,YAW 6900, Boston, MA 02114 USA. EM dherzog@partners.org FU NIDA NIH HHS [1 R03 DA015414-01A1] NR 23 TC 35 Z9 37 U1 4 U2 6 PU JOHN WILEY & SONS INC PI HOBOKEN PA 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 0276-3478 J9 INT J EAT DISORDER JI Int. J. Eating Disord. PD JUL PY 2006 VL 39 IS 5 BP 364 EP 368 DI 10.1002/eat.20257 PG 5 WC Psychology, Clinical; Nutrition & Dietetics; Psychiatry; Psychology SC Psychology; Nutrition & Dietetics; Psychiatry GA 053ZB UT WOS:000238343800002 PM 16565976 ER PT J AU Frisch, MJ Herzog, DB Franko, DL AF Frisch, MJ Herzog, DB Franko, DL TI Residential treatment for eating disorders SO INTERNATIONAL JOURNAL OF EATING DISORDERS LA English DT Article DE residential treatment; eating disorders; program effectiveness ID ANOREXIA-NERVOSA; HOSPITALIZATION AB Objective: The current study describes residential treatment for eating disorders in the United States. Method: A national study involving 22 residential eating disorder treatment programs was conducted using a survey to determine treatment program descriptions and trends. Data from 19 respondents, representing 86% of all residential treatment programs in the United States, were examined. Results: Residential treatment options for individuals with anorexia nervosa and bulimia nervosa are becoming increasingly more common. A wide variety of techniques and methods are employed in the treatment of individuals with eating disorders in residential treatment programs. The average length of stay in treatment was 83 days, with an average cost per day of $956 U.S. dollars. Conclusion: The residential treatment of individuals with eating disorders is a growing, variable, and largely unregulated enterprise. Future research is needed to focus on quantifying treatment program effectiveness in the residential treatment of individuals with eating disorders. (c) 2006 by Wiley Periodicals, Inc. C1 Univ Minnesota, Dept Psychiat, Minneapolis, MN 55454 USA. Massachusetts Gen Hosp, Dept Psychiat, Boston, MA 02114 USA. Northeastern Univ, Dept Counseling & Appl Educ Psychol, Boston, MA 02115 USA. RP Frisch, MJ (reprint author), Univ Minnesota, Dept Psychiat, Riverside Profess Bldg,606 24th Ave S,Suite 602, Minneapolis, MN 55454 USA. EM tris0039@umn.edu NR 10 TC 18 Z9 18 U1 0 U2 5 PU JOHN WILEY & SONS INC PI HOBOKEN PA 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 0276-3478 J9 INT J EAT DISORDER JI Int. J. Eating Disord. PD JUL PY 2006 VL 39 IS 5 BP 434 EP 442 DI 10.1002/eat.20255 PG 9 WC Psychology, Clinical; Nutrition & Dietetics; Psychiatry; Psychology SC Psychology; Nutrition & Dietetics; Psychiatry GA 053ZB UT WOS:000238343800011 PM 16528698 ER PT J AU Lam, MM Corless, CL Goldblum, JR Heinrich, MC Downs-Kelly, E Rubin, BP AF Lam, Maggie M. Corless, Christopher L. Goldblum, John R. Heinrich, Michael C. Downs-Kelly, Erinn Rubin, Brian P. TI Extragastrointestinal stromal tumors presenting as vulvovaginal/rectovaginal septal masses: A diagnostic pitfall SO INTERNATIONAL JOURNAL OF GYNECOLOGICAL PATHOLOGY LA English DT Article DE gastrointestinal stromal tumor; GIST; vulvovaginal septum ID SOFT-TISSUE; AGGRESSIVE ANGIOMYXOMA; C-KIT; MUTATIONS; EFFICACY; NEOPLASM; SAFETY; VAGINA; KINASE; VULVA AB Gastrointestinal stromal tumors (GIST) are the most common mesenchymal tumors of the gastrointestinal (GI) tract. Most GISTs arise in the stomach and small bowel, whereas a small number occur elsewhere in the GI tract. Rare cases are identified outside the GI tract and are collectively known as extragastrointestinal stromal tumors (EGISTs). Because of their malignant potential and recent advances in the management of GISTs with imatinib mesylate (Gleevec, Glivec), it is imperative that these tumors are diagnosed correctly. In this study, we reviewed the clinical and pathologic characteristics of 3 cases of EGIST presenting as vulvovaginal/rectovaginal septal masses that were originally misdiagnosed, presumably due to their unusual anatomic locations. The original diagnoses were leiomyoma in one case and leiomyosarcoma in 2 cases. The lesions were localized to the rectovaginal septum (1) or vagina (2) and ranged from 4 to 8 cm in diameter. All 3 lesions had a spindle cell morphology that mimicked a smooth muscle tumor. Mitotic figures numbered from 12/50 to 16/50 high power fields (HPFs; median 15). Immunohistochemistry revealed that all 3 cases were strongly positive for KIT (CD 117) and CD34 and negative for smooth muscle actin, desmin, pan-cytokeratin, and estrogen receptor. KIT sequence analysis revealed oncogenic mutations in all 3 cases. The first tumor recurred at 2 years and the second tumor recurred at 10 years; the third case is too recent for meaningful follow-up. EGISTs that present as gynecologic masses are rare but may be more common than is currently recognized. Misdiagnosis may lead to inappropriate therapy because conventional chemotherapy and radiotherapy are not effective in the treatment of GISTs, whereas imatimb mesylate (Gleevec, Glivec) has a proven role in managing these tumors. Thus, it is imperative to consider EGISTs in the differential diagnosis of mesenchymal neoplasms in the vulvovaginal/rectovaginal septum. C1 Univ Washington, Med Ctr, Dept Pathol Anat, Seattle, WA 98195 USA. Oregon Hlth Sci Univ, Dept Pathol, Portland, OR 97201 USA. Oregon Hlth Sci Univ, Div Hematol Oncol, Inst Canc, Portland, OR 97201 USA. Cleveland Clin Fdn, Dept Anat Pathol, Cleveland, OH 44195 USA. Portland VA Med Ctr, Portland, OR USA. RP Rubin, BP (reprint author), Univ Washington, Med Ctr, Dept Pathol Anat, 1959 NE Pacific St,Box 356100, Seattle, WA 98195 USA. EM bprubin@u.washington.edu NR 22 TC 43 Z9 45 U1 0 U2 2 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0277-1691 J9 INT J GYNECOL PATHOL JI Int. J. Gynecol. Pathol. PD JUL PY 2006 VL 25 IS 3 BP 288 EP 292 DI 10.1097/01.pgp.0000215291.22867.18 PG 5 WC Obstetrics & Gynecology; Pathology SC Obstetrics & Gynecology; Pathology GA 061JV UT WOS:000238869100014 PM 16810068 ER PT J AU Adler, L Durell, T Wilens, T Paczkowski, M Schuh, K AF Adler, L. Durell, T. Wilens, T. Paczkowski, M. Schuh, K. TI Atomoxetine treatment for ADHD: Younger adults compared with older adults SO INTERNATIONAL JOURNAL OF NEUROPSYCHOPHARMACOLOGY LA English DT Meeting Abstract CT 25th CINP Congress CY JUL 09-13, 2006 CL Chicago, IL SP CINP C1 NYU, Sch Med, New York, NY USA. Lilly Res Labs, Indianapolis, IN USA. Massachusetts Gen Hosp, Boston, MA 02114 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU CAMBRIDGE UNIV PRESS PI NEW YORK PA 32 AVENUE OF THE AMERICAS, NEW YORK, NY 10013-2473 USA SN 1461-1457 J9 INT J NEUROPSYCHOPH JI Int. J. Neuropsychopharmacol. PD JUL PY 2006 VL 9 SU 1 BP S135 EP S136 PG 2 WC Clinical Neurology; Neurosciences; Pharmacology & Pharmacy; Psychiatry SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry GA 070BO UT WOS:000239495500528 ER PT J AU Adler, L Wilens, T Gao, H Detke, HC Levine, LR AF Adler, L. Wilens, T. Gao, H. Detke, H. C. Levine, L. R. TI Do adults and adolescents with ADHD respond differently to atomoxetine? SO INTERNATIONAL JOURNAL OF NEUROPSYCHOPHARMACOLOGY LA English DT Meeting Abstract CT 25th Congress of the Collegium-Internationale-Neuro-Psychopharmacologicum (CINP)/29th Annual Meeting of the Canadian-College-of-Neuropsychopharmacology CY JUL 09-13, 2006 CL Chicago, IL SP Collegium Int Neuro Psychopharmacol, Canadian Coll Neuro Psychopharmacol C1 NYU, Sch Med, New York, NY USA. Massachusetts Gen Hosp, Boston, MA 02114 USA. Lilly Res Labs, Indianapolis, IN USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU CAMBRIDGE UNIV PRESS PI NEW YORK PA 32 AVENUE OF THE AMERICAS, NEW YORK, NY 10013-2473 USA SN 1461-1457 J9 INT J NEUROPSYCHOPH JI Int. J. Neuropsychopharmacol. PD JUL PY 2006 VL 9 SU 1 BP S134 EP S134 PG 1 WC Clinical Neurology; Neurosciences; Pharmacology & Pharmacy; Psychiatry SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry GA 070BO UT WOS:000239495500523 ER PT J AU Adler, LA Spencer, T Wang, J Pestreich, L Muniz, R AF Adler, L. A. Spencer, T. Wang, J. Pestreich, L. Muniz, R. TI Efficacy and safety of once-daily extended-release dexmethylphenidate 30 and 40 mg in adults with ADHD: A double-blind, fixed-dose, placebo-controlled, randomized study SO INTERNATIONAL JOURNAL OF NEUROPSYCHOPHARMACOLOGY LA English DT Meeting Abstract CT 25th CINP Congress CY JUL 09-13, 2006 CL Chicago, IL SP CINP C1 NYU, Sch Med, New York, NY USA. Massachusetts Gen Hosp, Boston, MA 02114 USA. Nova Pharmaceut Corp, E Hanover, NJ USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU CAMBRIDGE UNIV PRESS PI NEW YORK PA 32 AVENUE OF THE AMERICAS, NEW YORK, NY 10013-2473 USA SN 1461-1457 J9 INT J NEUROPSYCHOPH JI Int. J. Neuropsychopharmacol. PD JUL PY 2006 VL 9 SU 1 BP S229 EP S229 PG 1 WC Clinical Neurology; Neurosciences; Pharmacology & Pharmacy; Psychiatry SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry GA 070BO UT WOS:000239495501292 ER PT J AU Adler, LA Spencer, TJ Williams, DW Moore, RJ Michelson, D AF Adler, L. A. Spencer, T. J. Williams, D. W. Moore, R. J. Michelson, D. TI Long-term, open-label safety and efficacy of atomoxetine in adults with attention-deficit/hyperactivity disorder: Final report of a 4-year study SO INTERNATIONAL JOURNAL OF NEUROPSYCHOPHARMACOLOGY LA English DT Meeting Abstract CT 25th Congress of the Collegium-Internationale-Neuro-Psychopharmacologicum (CINP)/29th Annual Meeting of the Canadian-College-of-Neuropsychopharmacology CY JUL 09-13, 2006 CL Chicago, IL SP Collegium Int Neuro Psychopharmacol, Canadian Coll Neuro Psychopharmacol C1 NYU, New York, NY USA. Massachusetts Gen Hosp, Boston, MA 02114 USA. Lilly Res Labs, Indianapolis, IN USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU CAMBRIDGE UNIV PRESS PI NEW YORK PA 32 AVENUE OF THE AMERICAS, NEW YORK, NY 10013-2473 USA SN 1461-1457 J9 INT J NEUROPSYCHOPH JI Int. J. Neuropsychopharmacol. PD JUL PY 2006 VL 9 SU 1 BP S134 EP S135 PG 2 WC Clinical Neurology; Neurosciences; Pharmacology & Pharmacy; Psychiatry SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry GA 070BO UT WOS:000239495500524 ER PT J AU Endicott, J Pollack, M Russell, J Raskin, J Detke, M Erickson, J Pritchet, Y Ball, S Swindle, R AF Endicott, J. Pollack, M. Russell, J. Raskin, J. Detke, M. Erickson, J. Pritchet, Y. Ball, S. Swindle, R. TI Duloxetine treatment for functional improvement in generalized anxiety disorder: Three independent studies SO INTERNATIONAL JOURNAL OF NEUROPSYCHOPHARMACOLOGY LA English DT Meeting Abstract CT 25th CINP Congress CY JUL 09-13, 2006 CL Chicago, IL SP CINP C1 Columbia Univ, Sch Med, New York, NY 10027 USA. Harvard Univ, Sch Med, Massachusetts Gen Hosp, Cambridge, MA 02138 USA. Eli Lilly & Co, Indianapolis, IN 46285 USA. Harvard Univ, Sch Med, McLean Hosp, Cambridge, MA 02138 USA. Indiana Univ, Sch Med, Bloomington, IN 47405 USA. Medfocus, Indianapolis, IN USA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU CAMBRIDGE UNIV PRESS PI NEW YORK PA 32 AVENUE OF THE AMERICAS, NEW YORK, NY 10013-2473 USA SN 1461-1457 J9 INT J NEUROPSYCHOPH JI Int. J. Neuropsychopharmacol. PD JUL PY 2006 VL 9 SU 1 BP S116 EP S116 PG 1 WC Clinical Neurology; Neurosciences; Pharmacology & Pharmacy; Psychiatry SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry GA 070BO UT WOS:000239495500457 ER PT J AU Gharabawi, G Canuso, C Pandina, G Bossie, C Kujawa, M Kosik-Gonzalez, C Turkoz, I Papakostas, GI AF Gharabawi, G. Canuso, C. Pandina, G. Bossie, C. Kujawa, M. Kosik-Gonzalez, C. Turkoz, I. Papakostas, G. I. TI A double-blind placebo-controlled study of adjunctive risperidone for treatment-resistant major depressive disorder SO INTERNATIONAL JOURNAL OF NEUROPSYCHOPHARMACOLOGY LA English DT Meeting Abstract CT 25th CINP Congress CY JUL 09-13, 2006 CL Chicago, IL SP CINP C1 Massachusetts Gen Hosp, Depress Clin & Res Program, Boston, MA 02114 USA. RI Papakostas, George/I-6905-2013 OI Papakostas, George/0000-0002-2465-5103 NR 0 TC 4 Z9 4 U1 0 U2 0 PU CAMBRIDGE UNIV PRESS PI NEW YORK PA 32 AVENUE OF THE AMERICAS, NEW YORK, NY 10013-2473 USA SN 1461-1457 J9 INT J NEUROPSYCHOPH JI Int. J. Neuropsychopharmacol. PD JUL PY 2006 VL 9 SU 1 BP S236 EP S236 PG 1 WC Clinical Neurology; Neurosciences; Pharmacology & Pharmacy; Psychiatry SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry GA 070BO UT WOS:000239495501317 ER PT J AU Greenberg, B Malone, D Rauch, S Rezai, A Friehs, G Rasmussen, S AF Greenberg, B. Malone, D. Rauch, S. Rezai, A. Friehs, G. Rasmussen, S. TI Deep brain stimulation for OCD SO INTERNATIONAL JOURNAL OF NEUROPSYCHOPHARMACOLOGY LA English DT Meeting Abstract CT 25th CINP Congress CY JUL 09-13, 2006 CL Chicago, IL SP CINP C1 Brown Univ, Sch Med, Dept Psychiat, Providence, RI 02912 USA. Brown Univ, Sch Med, Dept Neurosurg, Providence, RI 02912 USA. Butler Hosp, Providence, RI 02906 USA. Cleveland Clin, Dept Psychiat, Cleveland, OH 44106 USA. Cleveland Clin, Dept Neurosurg, Cleveland, OH 44106 USA. Harvard Univ, Sch Med, Dept Psychiat, Cambridge, MA 02138 USA. Massachusetts Gen Hosp, Boston, MA 02114 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU CAMBRIDGE UNIV PRESS PI NEW YORK PA 32 AVENUE OF THE AMERICAS, NEW YORK, NY 10013-2473 USA SN 1461-1457 J9 INT J NEUROPSYCHOPH JI Int. J. Neuropsychopharmacol. PD JUL PY 2006 VL 9 SU 1 BP S30 EP S30 PG 1 WC Clinical Neurology; Neurosciences; Pharmacology & Pharmacy; Psychiatry SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry GA 070BO UT WOS:000239495500114 ER PT J AU Hammerness, P AF Hammerness, P. TI Stimulant therapy in adult ADHD SO INTERNATIONAL JOURNAL OF NEUROPSYCHOPHARMACOLOGY LA English DT Meeting Abstract CT 25th CINP Congress CY JUL 09-13, 2006 CL Chicago, IL SP CINP C1 Massachusetts Gen Hosp, Dept Pediat Psychopharmacol, Boston, MA 02114 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU CAMBRIDGE UNIV PRESS PI NEW YORK PA 32 AVENUE OF THE AMERICAS, NEW YORK, NY 10013-2473 USA SN 1461-1457 J9 INT J NEUROPSYCHOPH JI Int. J. Neuropsychopharmacol. PD JUL PY 2006 VL 9 SU 1 BP S51 EP S51 PG 1 WC Clinical Neurology; Neurosciences; Pharmacology & Pharmacy; Psychiatry SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry GA 070BO UT WOS:000239495500205 ER PT J AU Joshi, G Wozniak, J Geller, D Petty, C Vivas, F Biederman, J AF Joshi, G. Wozniak, J. Geller, D. Petty, C. Vivas, F. Biederman, J. TI Examining the clinical characteristics by comorbidity status to explore the relationship between comorbid bipolar disorder and obsessive-compulsive disorder in children and adolescents SO INTERNATIONAL JOURNAL OF NEUROPSYCHOPHARMACOLOGY LA English DT Meeting Abstract CT 25th CINP Congress CY JUL 09-13, 2006 CL Chicago, IL SP CINP C1 Massachusetts Gen Hosp, Boston, MA 02114 USA. NR 4 TC 0 Z9 0 U1 0 U2 1 PU CAMBRIDGE UNIV PRESS PI NEW YORK PA 32 AVENUE OF THE AMERICAS, NEW YORK, NY 10013-2473 USA SN 1461-1457 J9 INT J NEUROPSYCHOPH JI Int. J. Neuropsychopharmacol. PD JUL PY 2006 VL 9 SU 1 BP S180 EP S181 PG 2 WC Clinical Neurology; Neurosciences; Pharmacology & Pharmacy; Psychiatry SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry GA 070BO UT WOS:000239495501121 ER PT J AU Marder, SR Crandall, D Pultz, J Carson, WH Gutierrez-Esteinou, R Tran, QV Marcus, RN AF Marder, S. R. Crandall, D. Pultz, J. Carson, W. H. Gutierrez-Esteinou, R. Tran, Q. -V. Marcus, R. N. TI The effectiveness of the novel atypical antipsychotic aripiprazole according to levels of agitation at baseline in patients with acute schizophrenia SO INTERNATIONAL JOURNAL OF NEUROPSYCHOPHARMACOLOGY LA English DT Meeting Abstract CT 25th CINP Congress CY JUL 09-13, 2006 CL Chicago, IL SP CINP C1 W Los Angeles VA Med Ctr, Los Angeles, CA USA. Bristol Myers Squibb Co, New York, NY 10154 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU CAMBRIDGE UNIV PRESS PI NEW YORK PA 32 AVENUE OF THE AMERICAS, NEW YORK, NY 10013-2473 USA SN 1461-1457 J9 INT J NEUROPSYCHOPH JI Int. J. Neuropsychopharmacol. PD JUL PY 2006 VL 9 SU 1 BP S277 EP S277 PG 1 WC Clinical Neurology; Neurosciences; Pharmacology & Pharmacy; Psychiatry SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry GA 070BO UT WOS:000239495501470 ER PT J AU Monkul, ES Matsuo, K Nicoletti, MA Brambilla, R Sassi, RB Hatch, JP Mallinger, AG Keshavan, MS Soares, JC AF Monkul, E. S. Matsuo, K. Nicoletti, M. A. Brambilla, R. Sassi, R. B. Hatch, J. P. Mallinger, A. G. Keshavan, M. S. Soares, J. C. TI Dorsolateral prefrontal gray matter increases in healthy individuals after lithium treatment: A voxel-based morphometry study SO INTERNATIONAL JOURNAL OF NEUROPSYCHOPHARMACOLOGY LA English DT Meeting Abstract CT 25th Congress of the Collegium-Internationale-Neuro-Psychopharmacologicum (CINP)/29th Annual Meeting of the Canadian-College-of-Neuropsychopharmacology CY JUL 09-13, 2006 CL Chicago, IL SP Collegium Int Neuro Psychopharmacol, Canadian Coll Neuro Psychopharmacol C1 Univ Texas, Hlth Sci Ctr San Antonio, Dept Psychiat, Div Mood & Anxiety Disorders,MOOD CNS Program, San Antonio, TX 78285 USA. S Texas Vet Hlth Care Syst, Audie L Murphy Div, San Antonio, TX USA. Dokuz Eylul Univ, Sch Med, Dept Psychiat, Izmir, Turkey. Univ Udine, Sect Psychiat, Dept Pathol & Expt & Clin Med, I-33100 Udine, Italy. Sci Inst IRCCS E, Medea, Italy. Univ Sao Paulo, Sch Med, Dept Psychiat, BR-05508 Sao Paulo, Brazil. Univ Pittsburgh, Sch Med, Dept Psychiat, Western Psychiat Inst & Clin, Pittsburgh, PA 15260 USA. Univ Pittsburgh, Sch Med, Dept Pharmacol, Pittsburgh, PA 15260 USA. Univ Texas, Hlth Sci Ctr San Antonio, Dept Radiol, San Antonio, TX 78285 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU CAMBRIDGE UNIV PRESS PI NEW YORK PA 32 AVENUE OF THE AMERICAS, NEW YORK, NY 10013-2473 USA SN 1461-1457 J9 INT J NEUROPSYCHOPH JI Int. J. Neuropsychopharmacol. PD JUL PY 2006 VL 9 SU 1 BP S180 EP S180 PG 1 WC Clinical Neurology; Neurosciences; Pharmacology & Pharmacy; Psychiatry SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry GA 070BO UT WOS:000239495501120 ER PT J AU Monuteaux, M AF Monuteaux, M. TI Long-term follow up of boys and girls with ADHD: Results from a 10-year study SO INTERNATIONAL JOURNAL OF NEUROPSYCHOPHARMACOLOGY LA English DT Meeting Abstract CT 25th CINP Congress CY JUL 09-13, 2006 CL Chicago, IL SP CINP C1 Massachusetts Gen Hosp, Dept Pediat Psychopharmacol, Boston, MA 02114 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU CAMBRIDGE UNIV PRESS PI NEW YORK PA 32 AVENUE OF THE AMERICAS, NEW YORK, NY 10013-2473 USA SN 1461-1457 J9 INT J NEUROPSYCHOPH JI Int. J. Neuropsychopharmacol. PD JUL PY 2006 VL 9 SU 1 BP S51 EP S51 PG 1 WC Clinical Neurology; Neurosciences; Pharmacology & Pharmacy; Psychiatry SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry GA 070BO UT WOS:000239495500207 ER PT J AU Pitman, RK AF Pitman, R. K. TI Neuroimaging studies of post-traumatic stress disorder SO INTERNATIONAL JOURNAL OF NEUROPSYCHOPHARMACOLOGY LA English DT Meeting Abstract CT 25th CINP Congress CY JUL 09-13, 2006 CL Chicago, IL SP CINP C1 Massachusetts Gen Hosp, Dept Psychiat, Boston, MA 02114 USA. Harvard Univ, Sch Med, Cambridge, MA 02138 USA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU CAMBRIDGE UNIV PRESS PI NEW YORK PA 32 AVENUE OF THE AMERICAS, NEW YORK, NY 10013-2473 USA SN 1461-1457 J9 INT J NEUROPSYCHOPH JI Int. J. Neuropsychopharmacol. PD JUL PY 2006 VL 9 SU 1 BP S69 EP S69 PG 1 WC Clinical Neurology; Neurosciences; Pharmacology & Pharmacy; Psychiatry SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry GA 070BO UT WOS:000239495500278 ER PT J AU Pollack, M Stein, D Mangano, R Entsuah, R AF Pollack, M. Stein, D. Mangano, R. Entsuah, R. TI Employing pooled analysis of venlafaxine XR in the short-term treatment of panic disorder to predict clinical outcomes SO INTERNATIONAL JOURNAL OF NEUROPSYCHOPHARMACOLOGY LA English DT Meeting Abstract CT 25th CINP Congress CY JUL 09-13, 2006 CL Chicago, IL SP CINP C1 Massachusetts Gen Hosp, Boston, MA 02114 USA. Univ Cape Town, ZA-7925 Cape Town, South Africa. NR 0 TC 0 Z9 0 U1 0 U2 1 PU CAMBRIDGE UNIV PRESS PI NEW YORK PA 32 AVENUE OF THE AMERICAS, NEW YORK, NY 10013-2473 USA SN 1461-1457 J9 INT J NEUROPSYCHOPH JI Int. J. Neuropsychopharmacol. PD JUL PY 2006 VL 9 SU 1 BP S116 EP S117 PG 2 WC Clinical Neurology; Neurosciences; Pharmacology & Pharmacy; Psychiatry SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry GA 070BO UT WOS:000239495500459 ER PT J AU Pollack, MH AF Pollack, M. H. TI Review of currently available treatment options: Major depression and comorbid conditions SO INTERNATIONAL JOURNAL OF NEUROPSYCHOPHARMACOLOGY LA English DT Meeting Abstract CT 25th CINP Congress CY JUL 09-13, 2006 CL Chicago, IL SP CINP C1 Harvard Univ, Sch Med, Dept Psychiat, Cambridge, MA 02138 USA. Massachusetts Gen Hosp, Ctr Anxiety & Traumat Stress Disorders, Boston, MA 02114 USA. NR 0 TC 0 Z9 0 U1 1 U2 1 PU CAMBRIDGE UNIV PRESS PI NEW YORK PA 32 AVENUE OF THE AMERICAS, NEW YORK, NY 10013-2473 USA SN 1461-1457 J9 INT J NEUROPSYCHOPH JI Int. J. Neuropsychopharmacol. PD JUL PY 2006 VL 9 SU 1 BP S93 EP S93 PG 1 WC Clinical Neurology; Neurosciences; Pharmacology & Pharmacy; Psychiatry SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry GA 070BO UT WOS:000239495500374 ER PT J AU Pompili, M Baldessarini, RJ Tondo, L De Pisa, E Girardi, P Ferracuti, S Tatarelli, R AF Pompili, M. Baldessarini, R. J. Tondo, L. De Pisa, E. Girardi, P. Ferracuti, S. Tatarelli, R. TI Suicidal ideation and intravenous antidepressant therapy in acutely depressed bipolar and unipolar patients. SO INTERNATIONAL JOURNAL OF NEUROPSYCHOPHARMACOLOGY LA English DT Meeting Abstract CT 25th CINP Congress CY JUL 09-13, 2006 CL Chicago, IL SP CINP C1 Univ Roma La Sapienza, St Andreas Hosp, Dept Psychiat, Rome, Italy. Harvard Univ, Sch Med, Dept Psychiat, Boston, MA 02115 USA. Massachusetts Gen Hosp, Int Consortium Bipolar Disorder Res, McLean Div, Boston, MA 02115 USA. Univ Cagliari, Dept Psychol, Ctr Lucio Bini Mood Disorders Res Ctr, Cagliari, Italy. NR 0 TC 0 Z9 0 U1 0 U2 1 PU CAMBRIDGE UNIV PRESS PI NEW YORK PA 32 AVENUE OF THE AMERICAS, NEW YORK, NY 10013-2473 USA SN 1461-1457 J9 INT J NEUROPSYCHOPH JI Int. J. Neuropsychopharmacol. PD JUL PY 2006 VL 9 SU 1 BP S112 EP S113 PG 2 WC Clinical Neurology; Neurosciences; Pharmacology & Pharmacy; Psychiatry SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry GA 070BO UT WOS:000239495500444 ER PT J AU Rauch, SL AF Rauch, S. L. TI Neuroimaging findings and neurocircuitry models of OCD: An update SO INTERNATIONAL JOURNAL OF NEUROPSYCHOPHARMACOLOGY LA English DT Meeting Abstract CT 25th CINP Congress CY JUL 09-13, 2006 CL Chicago, IL SP CINP C1 Massachusetts Gen Hosp, Dept Psychiat, Boston, MA 02114 USA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU CAMBRIDGE UNIV PRESS PI NEW YORK PA 32 AVENUE OF THE AMERICAS, NEW YORK, NY 10013-2473 USA SN 1461-1457 J9 INT J NEUROPSYCHOPH JI Int. J. Neuropsychopharmacol. PD JUL PY 2006 VL 9 SU 1 BP S29 EP S29 PG 1 WC Clinical Neurology; Neurosciences; Pharmacology & Pharmacy; Psychiatry SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry GA 070BO UT WOS:000239495500111 ER PT J AU Rauch, SL AF Rauch, S. L. TI Translational studies of extinction and circuitry models of anxiety disorders SO INTERNATIONAL JOURNAL OF NEUROPSYCHOPHARMACOLOGY LA English DT Meeting Abstract CT 25th CINP Congress CY JUL 09-13, 2006 CL Chicago, IL SP CINP C1 Massachusetts Gen Hosp, Dept Psychiat, Boston, MA 02114 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU CAMBRIDGE UNIV PRESS PI NEW YORK PA 32 AVENUE OF THE AMERICAS, NEW YORK, NY 10013-2473 USA SN 1461-1457 J9 INT J NEUROPSYCHOPH JI Int. J. Neuropsychopharmacol. PD JUL PY 2006 VL 9 SU 1 BP S10 EP S10 PG 1 WC Clinical Neurology; Neurosciences; Pharmacology & Pharmacy; Psychiatry SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry GA 070BO UT WOS:000239495500034 ER PT J AU Sachs, G Crandall, D Rollin, L Forbes, A Gutierrez-Esteinou, R Pikalov, A Sanchez, R AF Sachs, G. Crandall, D. Rollin, L. Forbes, A. Gutierrez-Esteinou, R. Pikalov, A. Sanchez, R. TI The effect of high or low levels of agitation at baseline on the antimanic response to aripiprazole in patients with bipolar I disorder SO INTERNATIONAL JOURNAL OF NEUROPSYCHOPHARMACOLOGY LA English DT Meeting Abstract CT 25th CINP Congress CY JUL 09-13, 2006 CL Chicago, IL SP CINP C1 Massachusetts Gen Hosp, Boston, MA 02114 USA. Bristol Myers Squibb Co, New York, NY 10154 USA. Otsuka Amer Pharmaceut Inc, Rockville, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU CAMBRIDGE UNIV PRESS PI NEW YORK PA 32 AVENUE OF THE AMERICAS, NEW YORK, NY 10013-2473 USA SN 1461-1457 J9 INT J NEUROPSYCHOPH JI Int. J. Neuropsychopharmacol. PD JUL PY 2006 VL 9 SU 1 BP S109 EP S109 PG 1 WC Clinical Neurology; Neurosciences; Pharmacology & Pharmacy; Psychiatry SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry GA 070BO UT WOS:000239495500430 ER PT J AU Seidman, LJ Thermenos, HW Milanovic, SM Goldstein, JM Buka, SL Poldrack, RA Koch, JK Faraone, SV Tsuang, MT AF Seidman, L. J. Thermenos, H. W. Milanovic, S. M. Goldstein, J. M. Buka, S. L. Poldrack, R. A. Koch, J. K. Faraone, S. V. Tsuang, M. T. TI Altered brain activation in adults at genetic risk for bipolar psychosis: A functional magnetic resonance imaging study of working memory SO INTERNATIONAL JOURNAL OF NEUROPSYCHOPHARMACOLOGY LA English DT Meeting Abstract CT 25th CINP Congress CY JUL 09-13, 2006 CL Chicago, IL SP CINP C1 Harvard Univ, Sch Med, Dept Psychiat, Beth Israel Deaconess Med Ctr, Cambridge, MA 02138 USA. Massachusetts Gen Hosp, Boston, MA 02114 USA. RI Buka, Stephen/H-7335-2014 OI Buka, Stephen/0000-0002-8578-9308 NR 0 TC 0 Z9 0 U1 1 U2 2 PU CAMBRIDGE UNIV PRESS PI NEW YORK PA 32 AVENUE OF THE AMERICAS, NEW YORK, NY 10013-2473 USA SN 1461-1457 J9 INT J NEUROPSYCHOPH JI Int. J. Neuropsychopharmacol. PD JUL PY 2006 VL 9 SU 1 BP S23 EP S24 PG 2 WC Clinical Neurology; Neurosciences; Pharmacology & Pharmacy; Psychiatry SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry GA 070BO UT WOS:000239495500090 ER PT J AU Tohen, M Kryzhanovskaya, L Carlson, G DelBello, M Wozniak, J Kowatch, R Wagner, K Findling, R Lin, D Robertson-Plouch, C Xu, W Huang, X Dittman, R Biederman, J AF Tohen, M. Kryzhanovskaya, L. Carlson, G. DelBello, M. Wozniak, J. Kowatch, R. Wagner, K. Findling, R. Lin, D. Robertson-Plouch, C. Xu, W. Huang, X. Dittman, R. Biederman, J. TI Analyses of treatment efficacy in subtypes of adolescent patients with bipolar disorder treated with olanzapine for acute mania; A 3-week randomized double-blind placebo-controlled study. SO INTERNATIONAL JOURNAL OF NEUROPSYCHOPHARMACOLOGY LA English DT Meeting Abstract CT 25th CINP Congress CY JUL 09-13, 2006 CL Chicago, IL SP CINP C1 Lilly Res Labs, Indianapolis, IN 02178 USA. Harvard Univ, Sch Med, McLean Hosp, Belmont, MA 11794 USA. SUNY Stony Brook, Sch Med, Stony Brook, NY USA. Univ Cincinnati, Coll Med, Cincinnati, OH 02115 USA. Harvard Univ, Sch Med, Massachusetts Gen Hosp, Boston, MA 77555 USA. Univ Texas, Med Branch, Galveston, TX 44106 USA. Case Western Reserve Univ, Cleveland, OH USA. Lilly Deutschland Med Dept, Bad Homburg, Germany. Univ Hamburg, Hamburg, Germany. NR 0 TC 0 Z9 0 U1 0 U2 0 PU CAMBRIDGE UNIV PRESS PI NEW YORK PA 32 AVENUE OF THE AMERICAS, NEW YORK, NY 10013-2473 USA SN 1461-1457 J9 INT J NEUROPSYCHOPH JI Int. J. Neuropsychopharmacol. PD JUL PY 2006 VL 9 SU 1 BP S191 EP S191 PG 1 WC Clinical Neurology; Neurosciences; Pharmacology & Pharmacy; Psychiatry SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry GA 070BO UT WOS:000239495501157 ER PT J AU Weisberg, R Fava, M Hartford, J Erickson, J D'Souza, D Russell, J AF Weisberg, R. Fava, M. Hartford, J. Erickson, J. D'Souza, D. Russell, J. TI Efficacy of duloxetine in the treatment of generalized anxiety disorder in patients with clinically significant painful physical symptoms SO INTERNATIONAL JOURNAL OF NEUROPSYCHOPHARMACOLOGY LA English DT Meeting Abstract CT 25th CINP Congress CY JUL 09-13, 2006 CL Chicago, IL SP CINP C1 Brown Univ, Providence, RI 02912 USA. Massachusetts Gen Hosp, Boston, MA 02114 USA. Harvard Univ, Sch Med, Boston, MA 02114 USA. Hartford Res Grp, Florence, KY USA. Lilly Res Labs, Indianapolis, IN USA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU CAMBRIDGE UNIV PRESS PI NEW YORK PA 32 AVENUE OF THE AMERICAS, NEW YORK, NY 10013-2473 USA SN 1461-1457 J9 INT J NEUROPSYCHOPH JI Int. J. Neuropsychopharmacol. PD JUL PY 2006 VL 9 SU 1 BP S118 EP S118 PG 1 WC Clinical Neurology; Neurosciences; Pharmacology & Pharmacy; Psychiatry SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry GA 070BO UT WOS:000239495500464 ER PT J AU Worthington, JJ AF Worthington, J. J., III TI Advances in the treatment of PTSD SO INTERNATIONAL JOURNAL OF NEUROPSYCHOPHARMACOLOGY LA English DT Meeting Abstract CT 25th CINP Congress CY JUL 09-13, 2006 CL Chicago, IL SP CINP C1 Massachusetts Gen Hosp, Boston, MA 02114 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU CAMBRIDGE UNIV PRESS PI NEW YORK PA 32 AVENUE OF THE AMERICAS, NEW YORK, NY 10013-2473 USA SN 1461-1457 J9 INT J NEUROPSYCHOPH JI Int. J. Neuropsychopharmacol. PD JUL PY 2006 VL 9 SU 1 BP S69 EP S70 PG 2 WC Clinical Neurology; Neurosciences; Pharmacology & Pharmacy; Psychiatry SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry GA 070BO UT WOS:000239495500279 ER PT J AU Counter, SA Buchanan, LH Ortega, F AF Counter, S. Allen Buchanan, Leo H. Ortega, Fernando TI Neurocognitive screening of mercury-exposed children of Andean gold miners SO INTERNATIONAL JOURNAL OF OCCUPATIONAL AND ENVIRONMENTAL HEALTH LA English DT Article DE methylmercury; elemental mercury; neurotoxicity; cognitive; Raven's Coloured Progressive Matrices; pediatric; environmental ID PRENATAL EXPOSURE; BLOOD MERCURY; URINE; HAIR; METHYLMERCURY; RESPONSES; LEAD; AGE AB Performance on Raven's Coloured Progressive Matrices (RCPM) test of visual-spatial reasoning was used to evaluate the effects of mercury (Hg) exposure on 73 Andean children aged 5 to 11 years (mean: 8.4) living in the Nambija and Portovelo gold mining areas of Ecuador, where Hg is widely used in amalgamation. Mean levels of Hg found in blood (H9(B)), urine (Hg-U), and hair (Hg-H) samples were 5.1 mu g/L (SD: 2.4; range: 1-10 mu g/L), 13.3 mu g/L (SD: 25.9; range: 1-166 mu g/L), and 8.5 mu g/g (SD: 22.8; range: 1-135 mu g/g), respectively. Of the children in the Nambija area 67-84.9% had abnormal RCPM standard scores (i.e., <= 25%tile), depending on the test norm used in the data analysis. Higher standard scores for Peruvian (t = 4.77; p = < 0.0001) and Puerto Rican (t = 4.51; p = < 0.0001) norms than for U.S. norms suggested a linguistic influence. No difference was found between Peruvian and Puerto Rican norms (t = 0.832; p = < 0.408), which showed a significant positive correlation (r = 0.915, p = < 0.0001). Children with abnormal Hg-B and Hg-H levels had significantly lower scores on the RCPM subtest B than did children with nontoxic Hg levels (t = -2.16; p = < 0.034). These results suggest that a substantial number of Hg-exposed children in the Nambija study area have neurocognitive deficits in visual-spatial reasoning. C1 Harvard Univ, Sch Med, Biol Labs, Dept Neurol, Cambridge, MA 02138 USA. Massachusetts Gen Hosp, Dept Neurol, Boston, MA 02114 USA. Univ Massachusetts, Sch Med, Dept Pediat, Shriver Ctr, Waltham, MA USA. Harvard Univ, Hlth Serv, Dept Audiol, Cambridge, MA 02138 USA. Univ San Francisco Quito, Dept Med, Quito, Ecuador. RP Counter, SA (reprint author), Harvard Univ, Sch Med, Biol Labs, Dept Neurol, 16 Divin Ave, Cambridge, MA 02138 USA. EM allen_Counter@harvard.edu NR 31 TC 17 Z9 17 U1 0 U2 3 PU ABEL PUBLICATION SERVICES PI BURLINGTON PA 1611 AQUINAS COURT, BURLINGTON, NC 27215 USA SN 1077-3525 J9 INT J OCCUP ENV HEAL JI Int. J. Occup. Environ. Health PD JUL-SEP PY 2006 VL 12 IS 3 BP 209 EP 214 PG 6 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA 077QD UT WOS:000240043900003 PM 16967826 ER PT J AU Allen, AM Czerminska, M Janne, PA Sugarbaker, DJ Bueno, R Harris, JR Court, L Baldini, EH AF Allen, AM Czerminska, M Janne, PA Sugarbaker, DJ Bueno, R Harris, JR Court, L Baldini, EH TI Fatal pneumonitis associated with intensity-modulated radiation therapy for mesothelioma SO INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS LA English DT Article DE mesothelioma; intensity-modulated radiation therapy; pneumonitis; mean lung dose ID MALIGNANT PLEURAL MESOTHELIOMA; CELL LUNG-CANCER; DOSE-VOLUME HISTOGRAM; STUDY-GROUP TRIAL; EXTRAPLEURAL PNEUMONECTOMY; PHASE-I; PULMONARY COMPLICATIONS; HEMITHORACIC RADIATION; TRIMODALITY THERAPY; DOSIMETRIC FACTORS AB Purpose: To describe the initial experience at Dana-Farber Cancer Institute/Brigham and Women's Hospital with intensity-modulated radiation therapy (IMRT) as adjuvant therapy after extrapleural pneumonectomy (EPP) and adjuvant chemotherapy. Methods and Materials: The medical records of patients treated with IMRT after EPP and adjuvant chemotherapy were retrospectively reviewed. IMRT was given to a dose of 54 Gy to the clinical target volume in 1.8 Gy daily fractions. Treatment was delivered with a dynamic multileaf collimator using a sliding window technique. Eleven of 13 patients received heated intraoperative cisplatin chemotherapy (225 mg/m(2)). Two patients received neoadjuvant intravenous cisplatin/pemetrexed, and 10 patients received adjuvant cisplatin/pemetrexed chemotherapy after EPP but before radiation therapy. All patients received at least 2 cycles of intravenous chemotherapy. The contralateral lung was limited to a V20 (volume of lung receiving 20 Gy or more) of 20% and a mean lung dose (MLD) of 15 Gy. All patients underwent fluorodeoxyglucose positron emission tomography (FDG-PET) for staging, and any FDG-avid areas in the hemithorax were given a simultaneous boost of radiotherapy to 60 Gy. Statistical comparisons were done using two-sided t test. Results: Thirteen patients were treated with IMRT from December 2004 to September 2005. Six patients developed fatal pneumonitis after treatment. The median time from completion of IMRT to the onset of radiation pneumonitis was 30 days (range 5-57 days). Thirty percent of patients (4 of 13) developed acute Grade 3 nausea and vomiting. One patient developed acute Grade 3 thrombocytopenia. The median V20, MLD, and V5 (volume of lung receiving 5 Gy or more) for the patients who developed pneumonitis was 17.6 % (range, 15.3-22.3 %), 15.2 Gy (range, 13.3-17 Gy), and 98.6% (range, 81-100%), respectively, as compared with 10.9% (range, 5.5-24.7%) (p = 0.08), 12.9 Gy (range, 8.7-16.9 Gy) (p = 0.07), and 90% (range, 66-98.3%) (p = 0.20), respectively, for the patients who did not develop pneumonitis. Conclusions: Intensity-modulated RT treatment for mesothelioma after EPP and adjuvant chemotherapy resulted in a high rate of fatal pneumonitis when standard dose parameters were used. We therefore recommend caution in the utilization of this technique. Our data suggest that with IMRT, metrics such as V5 and MLD should be considered in addition to V20 to determine tolerance levels in future patients. (c) 2006 Elsevier Inc. C1 Dana Farber Canc Inst, Dept Radiat Oncol, Boston, MA 02115 USA. Brigham & Womens Hosp, Boston, MA 02115 USA. Brigham & Womens Hosp, Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02115 USA. Brigham & Womens Hosp, Dept Med, Boston, MA 02115 USA. Brigham & Womens Hosp, Div Thorac Surg, Boston, MA 02115 USA. Harvard Univ, Sch Med, Boston, MA 02115 USA. RP Allen, AM (reprint author), Dana Farber Canc Inst, Dept Radiat Oncol, Dana L2,44 Binney St, Boston, MA 02115 USA. EM aallen@lroc.harvard.edu NR 30 TC 169 Z9 182 U1 2 U2 10 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 JUL 1 PY 2006 VL 65 IS 3 BP 640 EP 645 DI 10.1016/j.ijrobp.2006.03.012 PG 6 WC Oncology; Radiology, Nuclear Medicine & Medical Imaging SC Oncology; Radiology, Nuclear Medicine & Medical Imaging GA 052ON UT WOS:000238243100002 PM 16751058 ER PT J AU Ho, AY Atencio, DP Peters, S Stock, RG Formenti, SC Cesaretti, JA Green, S Haffty, B Drumea, K Leitzin, L Kuten, A Azria, D Ozsahin, M Overgaard, J Andreassen, CN Trop, CS Park, J Rosenstein, BS AF Ho, AY Atencio, DP Peters, S Stock, RG Formenti, SC Cesaretti, JA Green, S Haffty, B Drumea, K Leitzin, L Kuten, A Azria, D Ozsahin, M Overgaard, J Andreassen, CN Trop, CS Park, J Rosenstein, BS TI Genetic predictors of adverse radiotherapy effects: The gene-pare project SO INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS LA English DT Review DE genetic predictors; adverse radiotherapy effects; breast cancer; prostate cancer ID BREAST-CANCER PATIENTS; PERFORMANCE LIQUID-CHROMATOGRAPHY; SINGLE-NUCLEOTIDE POLYMORPHISMS; ATAXIA-TELANGIECTASIA GENE; NORMAL-TISSUE RADIOSENSITIVITY; ATM SEQUENCE VARIANTS; DNA-REPAIR GENE; RADIATION SENSITIVITY; IN-VITRO; MUTATION DETECTION AB Purpose: The development of adverse effects resulting from the radiotherapy of cancer limits the use of this treatment modality. The validation of a test capable of predicting which patients would be most likely to develop adverse responses to radiation treatment, based on the possession of specific genetic variants, would therefore be of value. The purpose of the Genetic Predictors of Adverse Radiotherapy Effects (Gene-PARE) project is to help achieve this goal. Methods and Materials: A continuously expanding biorepository has been created consisting of frozen lymphocytes and DNA isolated from patients treated with radiotherapy. In conjunction with this biorepository, a database is maintained with detailed clinical information pertaining to diagnosis, treatment, and outcome. The DNA samples are screened using denaturing high performance liquid chromatography (DHPLC) and the Surveyor nuclease assay for variants in ATM, TGFB1, XRCC1, XRCC3, SOD2, and hHR21. It is anticipated that additional genes that control the biologic response to radiation will be screened in future work. Results: Evidence has been obtained that possession of variants in genes, the products of which play a role in radiation response, is predictive for the development of adverse effects after radiotherapy. Conclusions: It is anticipated that the Gene-PARE project will yield information that will allow radiation oncologists to use genetic data to optimize treatment on an individual basis. (c) 2006 Elsevier Inc. C1 Mt Sinai Sch Med, Dept Radiat Oncol, New York, NY 10029 USA. Mt Sinai Sch Med, Dept Community & Prevent Med, New York, NY 10029 USA. Mt Sinai Sch Med, Dept Dermatol, New York, NY 10029 USA. NYU, Sch Med, Dept Radiat Oncol, New York, NY USA. Yale Univ, Sch Med, Dept Therapeut Radiol, New Haven, CT 06510 USA. Rambam Med Ctr, Dept Oncol, Haifa, Israel. CRLC Val Aurelle, Dept Radiat Oncol, Montpellier, France. CHUV, Dept Radiat Oncol, Lausanne, Switzerland. Aarhus Univ Hosp, Dept Expt Clin Oncol, DK-8000 Aarhus, Denmark. Bronx Vet Adm Med Ctr, Dept Urol, Bronx, NY USA. Bronx Vet Adm Med Ctr, Dept Radiat Oncol, Bronx, NY USA. RP Rosenstein, BS (reprint author), Mt Sinai Sch Med, Dept Radiat Oncol, Box 1236,1 Gustave Levy Pl, New York, NY 10029 USA. EM bariy.rosenstein@mssm.edu RI Rosenstein, Barry/A-7420-2009 NR 128 TC 78 Z9 81 U1 0 U2 6 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 JUL 1 PY 2006 VL 65 IS 3 BP 646 EP 655 DI 10.1016/j.ijrobp.2006.03.006 PG 10 WC Oncology; Radiology, Nuclear Medicine & Medical Imaging SC Oncology; Radiology, Nuclear Medicine & Medical Imaging GA 052ON UT WOS:000238243100003 PM 16751059 ER PT J AU D'Amico, AV Kantoff, P Loffredo, M Renshaw, AA Loffredo, B Chen, MH AF D'Amico, AV Kantoff, P Loffredo, M Renshaw, AA Loffredo, B Chen, MH TI Predictors of mortality after prostate-specific antigen failure SO INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS LA English DT Article DE prostate cancer; prostate-specific antigen; mortality ID RANDOMIZED CONTROLLED-TRIAL; PREOPERATIVE PSA VELOCITY; CANCER-SPECIFIC MORTALITY; RADICAL PROSTATECTOMY; RADIATION-THERAPY; MITOXANTRONE; PREDNISONE; DOCETAXEL; SURVIVAL; RISK AB Purpose: We identified factors associated with the length of survival after prostate-specific antigen (PSA) failure. Methods and Materials: The study cohort comprised 81 of 206 men enrolled on a randomized trial evaluating external-beam radiation therapy (RT) with or without androgen suppression therapy (AST) and who experienced PSA failure. Salvage AST was administered at a PSA level of similar to 10 ng/mL as per protocol. Cox regression was used to determine factors associated with length of survival after PSA failure. Results: A PSA DT (doubling time) < 6 months (p = 0.04) and age at the time of PSA failure (p = 0.009) were significantly associated with length of survival. By 5 years, 35% and 65% of all-cause mortality was from prostate cancer in men whose age at PSA failure was 75 or higher vs. < 75, respectively. Across all ages, 0%, 4%, as compared with 63% of men, were estimated to die of prostate cancer within 5 years after PSA failure if their PSA DT was > 12, 6-12, or < 6 months, respectively. Conclusions: Advanced age and a PSA DT < 6 months at the time of PSA failure are associated with a significantly shorter survival. (c) 2006 Elsevier Inc. C1 Brigham & Womens Hosp, Dept Radiat Oncol, Boston, MA 02215 USA. Brigham & Womens Hosp, Dept Med Oncol, Boston, MA 02215 USA. Brigham & Womens Hosp, Dept Pathol, Boston, MA 02215 USA. Dana Farber Canc Inst, Boston, MA 02115 USA. Univ Connecticut, Dept Stat, Storrs, CT 06269 USA. RP D'Amico, AV (reprint author), Brigham & Womens Hosp, Dept Radiat Oncol, 75 Francis St,L-2 Level, Boston, MA 02215 USA. EM adamico@lroc.harvard.edu NR 21 TC 27 Z9 27 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 JUL 1 PY 2006 VL 65 IS 3 BP 656 EP 660 DI 10.1016/j.ijrobp.2006.01.053 PG 5 WC Oncology; Radiology, Nuclear Medicine & Medical Imaging SC Oncology; Radiology, Nuclear Medicine & Medical Imaging GA 052ON UT WOS:000238243100004 PM 16682147 ER PT J AU Bortfeld, T Paganetti, H AF Bortfeld, T Paganetti, H TI The biologic relevance of daily dose variations in adaptive treatment planning SO INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS LA English DT Article DE adaptive radiotherapy; IMRT; linear-quadratic model; interplay effect; dose variation ID FRACTION ORGAN MOTION; RADIATION-THERAPY; RADIOTHERAPY; DELIVERY; OPTIMIZATION; ERRORS; MODEL AB Purpose: To explore the biologic relevance of deviations from the intended uniform fractionation scheme. Methods and Materials: We study the effect of the variance of the dose per fraction on the normalized total dose (NTD), which incorporates the linear-quadratic model of radiation effects. In regions of steep dose gradients, we determine the shift between NTD isodose lines and physical isodose lines. We also look at ways to compensate for dose-variation effects through dose adjustments, without changing the number of fractions. Results: Simple equations quantify effects of dose variation on the NTD. If the standard deviation of the dose is 10% of the daily dose fraction, the effects on the NTD for a given point in the irradiated area are always less than 1 %, independent of the biologic parameters. In adaptive dose-correction schemes, the dose correction should be applied uniformly over the remaining fractions, to minimize the variance. Incomplete repair leads to a coupling of doses delivered on different days, which complicates the issue. Repopulation appears to be insignificant in the context of this study (constant overall treatment time). Conclusions: A variation of the dose between fractions always leads to a larger biologic effect than does the same total dose delivered with standard uniform fractionation. The increase in NTD is negligible if the standard deviation of the dose is less than 10% of the dose per fraction. (c) 2006 Elsevier Inc. C1 Harvard Univ, Dept Radiat Oncol, Massachusetts Gen Hosp, Sch Med, Boston, MA 02114 USA. RP Bortfeld, T (reprint author), Harvard Univ, Dept Radiat Oncol, Massachusetts Gen Hosp, Sch Med, 30 Fruit St, Boston, MA 02114 USA. EM tbortfeld@partners.org; hpaganetti@partners.org FU NCI NIH HHS [P01 CA21239] NR 22 TC 16 Z9 16 U1 0 U2 4 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0360-3016 J9 INT J RADIAT ONCOL JI Int. J. Radiat. Oncol. Biol. Phys. PD JUL 1 PY 2006 VL 65 IS 3 BP 899 EP 906 DI 10.1016/j.ijrobp.2006.02.036 PG 8 WC Oncology; Radiology, Nuclear Medicine & Medical Imaging SC Oncology; Radiology, Nuclear Medicine & Medical Imaging GA 052ON UT WOS:000238243100037 PM 16751072 ER PT J AU Baird, JD Arroyo, LG Vengust, M McGurrin, MKJ Rodriguez-Palacios, A Kenney, DG Aravagiri, M Maylin, GA AF Baird, JD Arroyo, LG Vengust, M McGurrin, MKJ Rodriguez-Palacios, A Kenney, DG Aravagiri, M Maylin, GA TI Adverse extrapyramidal effects in four horse given fluphenazine decanoate SO JAVMA-JOURNAL OF THE AMERICAN VETERINARY MEDICAL ASSOCIATION LA English DT Article ID NEUROLEPTIC MALIGNANT SYNDROME; ANTIPSYCHOTIC-DRUGS; PLASMA; MANAGEMENT; PRIAPISM AB Case Description-4 racehorses were examined because of markedly abnormal behavior following administration of fluphenazine decanoate. Clinical Findings-Clinical signs included restlessness, agitation, profuse sweating, hypermetria, aimless circling, intense pawing and striking with the thoracic limbs, and rhythmic swinging of the head and neck alternating with episodes of severe stupor. Fluphenazine was detected in serum or plasma from all 4 horses. The dose of fluphenazine decanoate administered to 3 of the 4 horses was within the range (25 to 50 mg) routinely administered to adult humans. Treatment and Outcome-In 2 horses, there was no response to IV administration of diphenhydramine hydrochloride, but the abnormal behavior in these 2 horses appeared to resolve following administration of benztropine mesylate, and both horses returned to racing. The other 2 horses responded to diphenhydramine administration. One returned to racing. The other was euthanized because of severe neurologic signs, respiratory failure, and acute renal failure. Clinical Relevance-Findings indicate that adverse extrapyramical effects may occur in horses given fluphenazine decanoate. These effects appear to be unpredictable and may be severe and life threatening. Use of fluphenazine decanoate as an anxiolytic in performance horses is not permitted in many racing and horse show jurisdictions, and analytic procedures are now available to detect the presence of fluphenazine in serum or plasma. C1 Univ Guelph, Ontario Vet Coll, Dept Clin Studies, Guelph, ON N1G 2W1, Canada. Vet Adm Greater Los Angeles Healthcare Syst, Los Angeles, CA 91311 USA. Cornell Univ, Coll Vet Med, Dept Populat Med & Diagnost Sci, Equine Drug Testing & Res Program, Ithaca, NY 14850 USA. RP Baird, JD (reprint author), Univ Guelph, Ontario Vet Coll, Dept Clin Studies, Guelph, ON N1G 2W1, Canada. RI Rodriguez-Palacios, Alex/C-2191-2011; OI Rodriguez-Palacios, Alexander/0000-0003-0713-5605 NR 37 TC 12 Z9 12 U1 0 U2 3 PU AMER VETERINARY MEDICAL ASSOC PI SCHAUMBURG PA 1931 N MEACHAM RD SUITE 100, SCHAUMBURG, IL 60173-4360 USA SN 0003-1488 J9 JAVMA-J AM VET MED A JI JAVMA-J. Am. Vet. Med. Assoc. PD JUL 1 PY 2006 VL 229 IS 1 BP 104 EP 110 DI 10.2460/javma.229.1.104 PG 7 WC Veterinary Sciences SC Veterinary Sciences GA 058TN UT WOS:000238687600036 PM 16817724 ER PT J AU Pumbwe, L Ueda, O Yoshimura, F Chang, A Smith, RL Wexler, HM AF Pumbwe, Lilian Ueda, Ohmi Yoshimura, Fuminobu Chang, Abraham Smith, Rachel L. Wexler, Hannah M. TI Bacteroides fragilis BmeABC efflux systems additively confer intrinsic antimicrobial resistance SO JOURNAL OF ANTIMICROBIAL CHEMOTHERAPY LA English DT Article DE membrane proteins; co-expression; susceptibility ID MULTIPLE ANTIBIOTIC-RESISTANCE; PSEUDOMONAS-AERUGINOSA PAO1; EXTENSIVE DNA INVERSIONS; MEXC-MEXD-OPRJ; ANAEROBIC-BACTERIA; ESCHERICHIA-COLI; DRUG-RESISTANCE; MULTIDRUG-RESISTANCE; CAMPYLOBACTER-JEJUNI; SPIRAL GRADIENT AB Objectives: To determine the prevalence of expression and function(s) of Bacteroides fragilis RND family efflux transport systems (bmeABC1-16). Methods: The mRNA transcripts of bmeB efflux pump genes were detected in a wild-type strain ADB77 by RT-PCR and expression in different strains was quantified by comparative quantitative real-time RT-PCR. In order to determine independent or additive functions, BmeB 1, 3, 12 and 15 (the first efflux pumps identified) were deleted as singles, doubles, triples or quadruples by the double cross-over technique with pAD13242 and antimicrobial susceptibility was assayed by the spiral gradient endpoint technique. Results: All efflux pumps except bmeB9 were expressed in the wild-type parental strain. Susceptibility to beta-lactams, fluoroquinolones, ethidium bromide, SDS and triclosan was increased in ADB77 Delta bmeB3 (up to 3-fold) and ADB77 Delta bmeB1 Iota bmeB3 Delta bmeB12 (up to 5-fold). Expression of bmeB9 was increased and that of bmeB11 repressed in the latter deletant. A quadruple deletant (ADB77 Delta bmeB1 Delta bmeB3 Delta b-bmeB12 Delta bmeB15) had similar changes as well as a 2-fold increase in expression of bmeB16 and norfloxacin resistance. Expression of bmeB3 was increased in two triple deletants ADB77 Delta bmeB1 Delta bbmeB12 Delta bmeB15-type I (2-fold) and ADB77 Delta bmeB1 Delta bmeB12 Delta bmeB15-type II (5.8-fold). Antimicrobial MICs were also increased in the latter deletant; ampicillin (2.6-fold), cefoperazone (3.4-fold), cefoxitin (1.8-fold), tetracycline (36.4-fold), SDS (1.7-fold) and triclosan (2-fold). Conclusions: These data demonstrate that constitutive bmeB expression is prevalent in B. fragilis. At least seven BmeB efflux pumps are functional in transporting antimicrobials and have overlapping substrate profiles, and at least four confer intrinsic resistance. C1 Greater Los Angeles Vet Adm Healthcare Syst, Los Angeles, CA USA. Univ Calif Los Angeles, Dept Med, Los Angeles, CA 90024 USA. Matsumoto Dent Univ, Dept Oral Microbiol, Shiojiri, Japan. Aichi Gakuin Univ, Sch Dent, Dept Microbiol, Nagoya, Aichi 464, Japan. RP Wexler, HM (reprint author), Greater Los Angeles Vet Adm Healthcare Syst, Los Angeles, CA USA. EM hwexler@ucla.edu NR 40 TC 28 Z9 30 U1 0 U2 5 PU OXFORD UNIV PRESS PI OXFORD PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND SN 0305-7453 EI 1460-2091 J9 J ANTIMICROB CHEMOTH JI J. Antimicrob. Chemother. PD JUL PY 2006 VL 58 IS 1 BP 37 EP 46 DI 10.1093/jac/dkl202 PG 10 WC Infectious Diseases; Microbiology; Pharmacology & Pharmacy SC Infectious Diseases; Microbiology; Pharmacology & Pharmacy GA 071UF UT WOS:000239628700007 PM 16757501 ER PT J AU Jain, S van Ulsen, P Schmidt, MA Fernandez, R Tommassen, J Goldberg, MB AF Jain, S van Ulsen, P Schmidt, MA Fernandez, R Tommassen, J Goldberg, MB TI Polar localization of the autotransporter family of large bacterial virulence proteins SO JOURNAL OF BACTERIOLOGY LA English DT Article ID OUTER-MEMBRANE PROTEIN; COLI STRAIN-2787 O126-H27; SHIGELLA-FLEXNERI 2A; ACTIN-BASED MOTILITY; ESCHERICHIA-COLI; BORDETELLA-PERTUSSIS; DIFFUSE ADHERENCE; AIDA-I; MOLECULAR CHARACTERIZATION; UNIPOLAR LOCALIZATION AB Autotrans porters are an extensive family of large secreted virulence-associated proteins of gram-negative bacteria. Secretion of such large proteins poses unique challenges to bacteria. We demonstrate that autotransporters from a wide variety of rod-shaped pathogens, including IcsA and SepA of Shigella flexneri, AIDA-I of diffusely adherent Escherichia coli, and BrkA of Bordetella pertussis, are localized to the bacterial pole. The restriction of autotransporters to the pole is dependent on the presence of a complete lipopolysaccharide (LPS), consistent with known effects of LPS composition on membrane fluidity. Newly synthesized and secreted BrkA is polar even in the presence of truncated LPS, and all autotransporters examined are polar in the cytoplasm prior to secretion. Together, these findings are consistent with autotransporter secretion occurring at the poles of rod-shaped gram-negative organisms. Moreover, NalP, an autotransporter of spherically shaped Neisseria meningitidis contains the molecular information to localize to the pole of Escherichia coli. In N. meningitidis, NalP is secreted at distinct sites around the cell. These data are consistent with a model in which the secretion of large autotransporters occurs via specific conserved pathways located at the poles of rod-shaped bacteria, with profound implications for the underlying physiology of the bacterial cell and the nature of bacterial pathogen-host interactions. C1 Harvard Univ, Sch Med, Massachusetts Gen Hosp, Dept Med,Div Infect Dis, Cambridge, MA 02139 USA. Univ Utrecht, Inst Biomembranes, Dept Mol Microbiol, Utrecht, Netherlands. Zentrum Mol Biol Entzundung, Inst Infektiol, Munster, Germany. Univ British Columbia, Life Sci Ctr, Dept Microbiol & Immunol, Vancouver, BC V6T 1Z3, Canada. RP Goldberg, MB (reprint author), Harvard Univ, Sch Med, Massachusetts Gen Hosp, Dept Med,Div Infect Dis, 65 Landsdowne St, Cambridge, MA 02139 USA. EM mgoldberg1@partners.org RI Tommassen, Jan/I-1690-2016 OI Tommassen, Jan/0000-0001-7633-4945 FU NIAID NIH HHS [AI061073, AI35817, R01 AI035817, R21 AI061073] NR 52 TC 50 Z9 51 U1 0 U2 7 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA SN 0021-9193 J9 J BACTERIOL JI J. Bacteriol. PD JUL PY 2006 VL 188 IS 13 BP 4841 EP 4850 DI 10.1128/JB.00326-06 PG 10 WC Microbiology SC Microbiology GA 058KT UT WOS:000238664600029 PM 16788193 ER PT J AU Moffitt, T Chen, YC Prahl, SA AF Moffitt, Theodore Chen, Yin-Chu Prahl, Scott A. TI Preparation and characterization of polyurethane optical phantoms SO JOURNAL OF BIOMEDICAL OPTICS LA English DT Article DE tissue; reflectance; transmission; photostable ID NEAR-INFRARED SPECTROSCOPY; DOMAIN PHOTON MIGRATION; DIFFUSE-REFLECTANCE; NONINVASIVE DETERMINATION; COLLECTION EFFICIENCY; REPRODUCIBLE PHANTOM; TISSUE; SCATTERING; DESIGN; MEDIA AB We describe a method for the preparation of a polyurethane phantom to simulate the optical properties of biologic tissues at two wavelengths in the visible and near-infrared spectral range. We characterize the addition of added molecular absorbers with relatively narrow absorption bands [full width at half maximum (FWHM) 32 and 76 nm for Epolight 6084 and 4148, respectively] for independent absorption at 690 nm for absorption up to 5 cm(-1), and 830 nm for absorptions up to 3 cm(-1). Absorption by both dyes is linear with concentration in these respective regions and is consistent in polyurethane both before and after curing. The dyes are stable over long durations with no more than 4% change. The absorption of visible light by polyurethane decreases with time and is stable by one year with a drop of 0.03 +/- 0.003 cm(-1) from 500 to 830 nm. The scattering properties are selected by the addition of TiO2 particles to the polyurethane, which we functionally describe for the 690- and 830-nm wavelengths as related to the weight per volume. We demonstrate that the variation in absorption and scattering properties for large batch fabrication (12 samples) is +/- 3%. The optical properties of the phantoms have not significantly changed in a period of exceeding one year, which makes them suitable for use as a reference standard. (c) 2006 Society of Photo-Optical Instrumentation Engineers. C1 Oregon Med Laser Ctr, Portland, OR 97225 USA. Massachusetts Gen Hosp, Wellman Ctr Photomed Dermatol, Boston, MA 02114 USA. RP Prahl, SA (reprint author), Oregon Med Laser Ctr, 9205 SW Barnes Rd, Portland, OR 97225 USA. EM prahl@bme.ogi.edu NR 27 TC 52 Z9 52 U1 2 U2 9 PU SPIE-INT SOCIETY OPTICAL ENGINEERING PI BELLINGHAM PA 1000 20TH ST, PO BOX 10, BELLINGHAM, WA 98225 USA SN 1083-3668 J9 J BIOMED OPT JI J. Biomed. Opt. PD JUL-AUG PY 2006 VL 11 IS 4 AR 041103 DI 10.1117/1.2240972 PG 10 WC Biochemical Research Methods; Optics; Radiology, Nuclear Medicine & Medical Imaging SC Biochemistry & Molecular Biology; Optics; Radiology, Nuclear Medicine & Medical Imaging GA 093IM UT WOS:000241162000008 PM 16965131 ER PT J AU Popescu, G Badizadegan, K Dasari, RR Feld, MS AF Popescu, Gabriel Badizadegan, Kamran Dasari, Ramachandra R. Feld, Michael S. TI Observation of dynamic subdomains in red blood cells SO JOURNAL OF BIOMEDICAL OPTICS LA English DT Article DE microscopy; phase retrieval; Fourier phase microscopy ID PHASE MICROSCOPY; MEMBRANE FLUCTUATIONS; ERYTHROCYTES; SHAPE; UNDULATIONS AB We quantify the nanoscale structure and low-frequency dynamics associated with live red blood cells. The membrane displacements are measured using quantitative phase images provided by Fourier phase microscopy, with an average path-length stability of 0.75 nm over 45 min. The results reveal the existence of dynamic, independent subdomains across the cells that fluctuate at various dominant frequencies. (c) 2006 Society of Photo-Optical Instrumentation Engineers. C1 MIT, George R Harrison Spect Lab, Cambridge, MA 02139 USA. Harvard Univ, Sch Med, Boston, MA 02114 USA. Massachusetts Gen Hosp, Dept Pathol, Boston, MA 02114 USA. RP Popescu, G (reprint author), MIT, George R Harrison Spect Lab, 77 Massachusetts Ave, Cambridge, MA 02139 USA. EM gpopescu@mit.edu FU NCRR NIH HHS [P41 RR 02594] NR 18 TC 38 Z9 38 U1 2 U2 5 PU SPIE-INT SOCIETY OPTICAL ENGINEERING PI BELLINGHAM PA 1000 20TH ST, PO BOX 10, BELLINGHAM, WA 98225 USA SN 1083-3668 J9 J BIOMED OPT JI J. Biomed. Opt. PD JUL-AUG PY 2006 VL 11 IS 4 AR 040503 DI 10.1117/1.2221867 PG 3 WC Biochemical Research Methods; Optics; Radiology, Nuclear Medicine & Medical Imaging SC Biochemistry & Molecular Biology; Optics; Radiology, Nuclear Medicine & Medical Imaging GA 093IM UT WOS:000241162000003 PM 16965126 ER PT J AU Selb, J Joseph, DK Boas, DA AF Selb, Juliette Joseph, Danny K. Boas, David A. TI Time-gated optical system for depth-resolved functional brain imaging SO JOURNAL OF BIOMEDICAL OPTICS LA English DT Article DE diffuse optical tomography; time domain system; optical properties characterization; depth-resolved imaging; functional brain imaging ID NEAR-INFRARED SPECTROSCOPY; CEREBRAL HEMODYNAMICS; SCATTERING MEDIA; REFLECTANCE; TOMOGRAPHY; ACTIVATION; STIMULATION; OXYGENATION; ACCURACY; PHOTONS AB We present a time-domain optical system for functional imaging of the adult head. We first describe the instrument, which is based on a Ti: Sapphire pulsed laser (wavelength 750 - 850 nm) and an intensified CCD camera enabling parallel detection of multiple fibers. We characterize the system in terms of sensitivity and signal-to-noise ratio, instrument response function, cross-talk, stability, and reproducibility. We then describe two applications of the instrument: the characterization of baseline optical properties of homogeneous scattering media, and functional brain imaging. For the second application, we developed a two-part probe consisting in two squares of 4 x 4 sources and 3 x 3 detectors. The laser source is time-multiplexed to define 4 states of 8 sources that can be turned on during the same camera frame while minimizing cross-talk. On the detection side, we use for each detector 7 fibers of different lengths creating an optical delay, and enabling simultaneous detection in 7 windows (by steps of 500 ps) for each detector. This multiple window detection allows depth sensitivity. The imaging probe was tested on dynamic phantoms and a preliminary result on an adult performing a motor task shows discrimination between superficial and cortical responses to the stimulus on both hemispheres. (c) 2006 Society of Photo-Optical Instrumentation Engineers. C1 Massachusetts Gen Hosp, Photon Migrat Imaging Lab, Athinoula A Martinos Ctr, Charlestown, MA 02129 USA. RP Selb, J (reprint author), Massachusetts Gen Hosp, Photon Migrat Imaging Lab, Athinoula A Martinos Ctr, Bldg 149,13th St, Charlestown, MA 02129 USA. EM juliette@nmr.mgh.harvard.edu FU NCRR NIH HHS [P41-RR14075]; NIBIB NIH HHS [R01-EB002482]; NICHD NIH HHS [R01 HD042908, R01 HD042908-03, R01-HD42908] NR 39 TC 56 Z9 56 U1 0 U2 4 PU SPIE-INT SOCIETY OPTICAL ENGINEERING PI BELLINGHAM PA 1000 20TH ST, PO BOX 10, BELLINGHAM, WA 98225 USA SN 1083-3668 J9 J BIOMED OPT JI J. Biomed. Opt. PD JUL-AUG PY 2006 VL 11 IS 4 AR 044008 DI 10.1117/1.2337320 PG 13 WC Biochemical Research Methods; Optics; Radiology, Nuclear Medicine & Medical Imaging SC Biochemistry & Molecular Biology; Optics; Radiology, Nuclear Medicine & Medical Imaging GA 093IM UT WOS:000241162000042 PM 16965165 ER PT J AU Sun, TT Paul, IA Ho, IK AF Sun, Ting-Ting Paul, Ian A. Ho, Ing K. TI Motor functions but not learning and memory are impaired upon repeated exposure to sub-lethal doses of methyl parathion SO JOURNAL OF BIOMEDICAL SCIENCE LA English DT Article DE learning and memory; methyl parathion; motor functions; repeated treatment ID CHRONIC CHOLINESTERASE INHIBITION; RATS; DIISOPROPYLFLUOROPHOSPHATE; RECEPTORS; TOLERANCE; CHLORPYRIFOS; DOPAMINE; PESTICIDES; DISULFOTON; MECHANISMS AB Our previous work showed that repeated exposure to methyl parathion (MP) caused a prolonged inhibition of acetylcholinesterase (AChE) activity (similar to 80%) and down-regulation of M-1 and M-2 muscarinic receptors (up to 38%) in rats at brain regions, including frontal cortex, striatum, hippocampus and thalamus. In the present neurobehavioral study, we found this repeated MP treatment had suppressant effects on rat's locomotor activity. However, we observed no evidence of long-term effects of MP on associative learning and memory. Our data demonstrated that repeated exposure to MP caused some functional deficits in CNS, but motor activity and associative learning/memory process might differ in the sensitivity to its toxic effect. The motor dysfunctions in MP-treated rats may be mediated via reciprocal balance between cholinergic and dopaminergic systems at striatum following cholinergic over-stimulation. Our findings also suggest that the CNS deficits induced by repeated exposure to MP or other organophosphate (OP) pesticides cannot be attributed entirely to the inhibition of AChE. To accurately assess the neuro-toxic risk by occupational exposure to sub-lethal doses of MP, novel biomarkers besides in vivo anticholinesterase potency are needed. C1 Univ Mississippi, Med Ctr, Dept Pharmacol & Toxicol, Jackson, MS 39216 USA. Harvard Univ, Sch Med, Massachusetts Gen Hosp, MassGen Inst Neurodegenerat Dis, Charlestown, MA 02129 USA. RP Ho, IK (reprint author), Univ Mississippi, Med Ctr, Dept Pharmacol & Toxicol, Jackson, MS 39216 USA. EM iho@pharmacology.umsmed.edu RI Ho, Ing-Kang /E-3941-2010 NR 28 TC 4 Z9 9 U1 0 U2 2 PU SPRINGER PI DORDRECHT PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS SN 1021-7770 J9 J BIOMED SCI JI J. Biomed. Sci. PD JUL PY 2006 VL 13 IS 4 BP 515 EP 523 DI 10.1007/s11373-006-9075-9 PG 9 WC Cell Biology; Medicine, Research & Experimental SC Cell Biology; Research & Experimental Medicine GA 060WT UT WOS:000238833300008 PM 16645783 ER PT J AU Lozano-Calderon, SA Doornberg, J Ring, D AF Lozano-Calderon, SA Doornberg, J Ring, D TI Fractures of the dorsal articular margin of the distal part of the radius with dorsal radiocarpal subluxation SO JOURNAL OF BONE AND JOINT SURGERY-AMERICAN VOLUME LA English DT Article ID BARTONS FRACTURES; DISLOCATIONS; CLASSIFICATION; END AB Background: Fractures of the volar articular margin of the distal part of the radius with volar radiocarpal subluxation (Barton fractures) are well recognized, and substantial data are available to guide their treatment. In contrast, fractures of the dorsal articular margin of the distal part of the radius with dorsal radiocarpal subluxation (sometimes referred to as dorsal or reverse Barton fractures) are rarely mentioned, and there are very little data to guide their treatment. Methods: Twenty patients with a fracture of the dorsal articular margin of the distal part of the radius with dorsal radiocarpal subluxation were evaluated. A spectrum of volar injuries was observed: two patients had torn volar ligaments; ten had a displaced, rotated volar marginal lip fracture; six had impaction of the volar aspect of the articular surface; and two had no appreciable volar injury. Fourteen of the twenty patients also had impacted central articular fragments. Eighteen patients underwent surgical reconstruction of the articular surface and application of dorsal buttress plates with use of a variety of surgical approaches. At the time of follow-up, the outcome was assessed radiographically and with use of the modified Mayo wrist score and the Disabilities of the Arm, Shoulder and Hand (DASH) questionnaire. Results: At an average of thirty months postoperatively, nineteen fractures had healed without substantial loss of alignment and one patient had recurrent dorsal subluxation after plate removal. The final average amount of wrist and forearm motion was 59 degrees of flexion, 56 degrees of extension, 87 degrees of pronation, and 85 degrees of supination. The average grip strength was 85% of that of the contralateral, uninjured hand. The final functional result according to the system of Gartland and Werley was rated as excellent or good for eighteen patients and as fair for two. The average modified Mayo wrist score was 75 points, and the average DASH score was 15 points. Conclusions: Fractures of the dorsal articular margin of the distal part of the radius with dorsal radiocarpal subluxation are accompanied by a spectrum of volar injuries, including ligament injuries, avulsion fractures, and impaction of the articular surface. Despite the relative complexity of these injuries, satisfactory wrist function can be achieved with operative treatment in most patients. C1 Massachusetts Gen Hosp, Dept Orthopaed Surg, Hand & Upper Extrem Serv, Yawkey Ctr, Boston, MA 02114 USA. RP Lozano-Calderon, SA (reprint author), Massachusetts Gen Hosp, Dept Orthopaed Surg, Hand & Upper Extrem Serv, Yawkey Ctr, Suite 2100,55 Fruit St, Boston, MA 02114 USA. EM dring@partners.org NR 32 TC 13 Z9 15 U1 0 U2 0 PU JOURNAL BONE JOINT SURGERY INC PI NEEDHAM PA 20 PICKERING ST, NEEDHAM, MA 02192 USA SN 0021-9355 J9 J BONE JOINT SURG AM JI J. Bone Joint Surg.-Am. Vol. PD JUL PY 2006 VL 88A IS 7 BP 1486 EP 1493 DI 10.2106/JBJS.E.00930 PG 8 WC Orthopedics; Surgery SC Orthopedics; Surgery GA 058YZ UT WOS:000238701800009 PM 16818974 ER PT J AU Hampton, BJ Harris, WH AF Hampton, BJ Harris, WH TI Primary cementless acetabular components in hips with severe developmental dysplasia or total dislocation - A concise follow-up, at an average of sixteen years, of a previous report SO JOURNAL OF BONE AND JOINT SURGERY-AMERICAN VOLUME LA English DT Article ID SURVIVORSHIP ANALYSIS; CONGENITAL DYSPLASIA; FEMORAL-HEAD; BONE-GRAFT; ARTHROPLASTY; REPLACEMENT; CLASSIFICATION; PLACEMENT AB We previously reported the seven-year results of the use of a hemispherical, porous-coated acetabular component in twenty consecutive primary total hip arthroplasties in a highly selected group, namely, patients with severe developmental dysplasia or total dislocation of the hip. The present report describes the outcomes of those hips nine years later, at an average follow-up of sixteen years (range, 11.5 to nineteen years). Since the time of our prior report, two shells were revised; one revision was done because of aseptic loosening and the other, because of polyethylene liner dissociation without tine fracture. The remaining shells were well fixed. No pelvic osteolysis was evident on plain radiographs. The average polyethylene liner wear rate was 0.09 mm/yr. With failure defined as aseptic loosening of the shell, the average sixteen-year survival for the shell was 92%. We believe that this cup had excellent fixation at a long duration of follow-up of sixteen years in this highly selected set of patients with difficult hip problems. C1 Walter Reed Army Med Ctr, Dept Orthoped & Rehabil, Washington, DC 20307 USA. Massachusetts Gen Hosp, Harris Orthopaed Biomech & Biomat Lab, Boston, MA 02114 USA. RP Hampton, BJ (reprint author), Walter Reed Army Med Ctr, Dept Orthoped & Rehabil, 6900 Georgia Ave NW, Washington, DC 20307 USA. EM wharris.obbl@partners.org NR 23 TC 9 Z9 11 U1 2 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 JUL PY 2006 VL 88A IS 7 BP 1549 EP 1552 DI 10.2106/JBJS.E.00624 PG 4 WC Orthopedics; Surgery SC Orthopedics; Surgery GA 058YZ UT WOS:000238701800016 PM 16818981 ER PT J AU Bliziotes, M Sibonga, JD Turner, RT Orwoll, E AF Bliziotes, M Sibonga, JD Turner, RT Orwoll, E TI Periosteal remodeling at the femoral neck in nonhuman primates SO JOURNAL OF BONE AND MINERAL RESEARCH LA English DT Article; Proceedings Paper CT 24th Annual Meeting of the American-Society-for-Bone-and-Mineral-Research CY SEP 20-24, 2002 CL SAN ANTONIO, TX SP Amer Soc Bone & Mineral Res DE primate; osteoblasts; modeling and remodeling; bone histomorphometry; bone mineralization; periosteum ID INTRACAPSULAR HIP FRACTURE; BONE HISTOMORPHOMETRY; CORTICAL BONE; PROXIMAL FEMUR; OSTEOPOROSIS; SIZE; WOMEN; FRAGILITY; POROSITY; DENSITY AB Introduction: Bone size is an important determinant of bone strength, and cellular events at the periosteal surface could alter bone dimensions. We characterized periosteal cellular activity with dynamic histomorphometric studies of nonhuman primate femoral neck and shaft. Materials and Methods: Femur specimens from 16 intact adult male and female nonhuman primates (Rhesus [Macaca mulatta, n = 9] and Japanese Macaque [Macaca fuscata, n = 7]) were analyzed. Animals were double-labeled with tetracycline, and necropsy was performed 2-7 days after the last dose. We characterized periosteal resorptive activity in an additional group of five intact and four castrate female animals. Multiple group comparisons in intact animals were performed by one-way ANOVA followed by a Fisher PLSD posthoc test. In gonadectomized animals, Fisher's exact test was used for dichotomous and Mann-Whitney U-test for continuous variables. Results: Bone turnover in the periosteum of the femoral neck in intact animals was more rapid than at the femoral shaft but slower than in femoral neck cancellous bone. Similarly, in these intact animals, the eroded surface of cortical bone at the femoral neck periosteal surface was significantly greater than in the cancellous bone compartment (p < 0.0001) or on the femoral shaft (p < 0.0001). Gonadectomized female animals showed an increase in osteoclast number on the periosteal surface compared with intact controls (p < 0.01). Conclusions: We documented intramembranous periosteal bone turnover in the femoral neck by histomorphometric analyses. The tissue level bone formation rate was sufficient to add substantively to femoral neck size over time. Periosteal osteoclastic activity was not the result of the emergence of intracortical tunneling at the bone surface. Sex steroid deficiency produced an increase in osteoclast numbers at the periosteal surface. This is the first systematic documentation of periosteal turnover at the femoral neck. C1 Oregon Hlth & Sci Univ, Portland, OR 97201 USA. Portland VA Med Ctr, Portland, OR 97201 USA. Univ Space Res Assoc, Johnson Space Ctr, Div Space Life Sci, Houston, TX USA. Mayo Clin, Rochester, MN USA. Oregon State Univ, Dept Nutr & Exercise Sci, Corvallis, OR 97331 USA. RP Bliziotes, M (reprint author), Oregon Hlth & Sci Univ, Portland, OR 97201 USA. EM bliziote@ohsu.edu OI Orwoll, Eric/0000-0002-8520-7355 FU NIAMS NIH HHS [AR48833] NR 32 TC 20 Z9 20 U1 0 U2 1 PU AMER SOC BONE & MINERAL RES PI WASHINGTON PA 2025 M ST, N W, STE 800, WASHINGTON, DC 20036-3309 USA SN 0884-0431 J9 J BONE MINER RES JI J. Bone Miner. Res. PD JUL PY 2006 VL 21 IS 7 BP 1060 EP 1067 DI 10.1359/JBMR.060414 PG 8 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA 057MW UT WOS:000238600900014 PM 16813526 ER PT J AU Klein, MB Silver, G Gamelli, RL Gibran, NS Herndon, DN Hunt, JL Tompkins, RG AF Klein, Matthew B. Silver, Geoff Gamelli, Richard L. Gibran, Nicole S. Herndon, David N. Hunt, John L. Tompkins, Ronald G. CA Inflammation Host Response Injur TI Inflammation and the host response to injury: An overview of the multicenter study of the genomic and proteomic response to burn injury SO JOURNAL OF BURN CARE & RESEARCH LA English DT Article AB Inflammation and the Host Response to Injury is a prospective, multicenter, federally funded collaborative study of the genomic and proteomic basis for injury response. This study has brought together clinical specialists in burn injury with experts in genomics, proteomics, and bioinformatics to answer questions related to immunoinflammatory responses to injury. The purpose of this report is to describe the structure, organization, goals, and current progress of this Glue Grant project. C1 Univ Washington, Burn Ctr, Harborview Med Ctr, Seattle, WA 98195 USA. Loyola Univ, Med Ctr, Maywood, IL 60153 USA. SW Texas State Univ, Parkland Mem Hosp, Dallas, TX USA. Univ Texas, Med Branch, Galveston, TX 77555 USA. Shriners Hosp Children, Galveston, TX 77550 USA. Massachusetts Gen Hosp, Boston, MA 02114 USA. Shriners Hosp Children, Boston, MA USA. RP Klein, MB (reprint author), Univ Washington, Burn Ctr, Harborview Med Ctr, Seattle, WA 98195 USA. OI xiao, wenzhong/0000-0003-4944-6380; Baker, Henry/0000-0002-8273-5320 FU NIGMS NIH HHS [U54 GM062119] NR 1 TC 26 Z9 27 U1 0 U2 2 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 1559-047X J9 J BURN CARE RES JI J. Burn Care Res. PD JUL-AUG PY 2006 VL 27 IS 4 BP 448 EP 451 DI 10.1097/01.BCR.0000227477.33877.E6 PG 4 WC Emergency Medicine; Dermatology; Surgery SC Emergency Medicine; Dermatology; Surgery GA 066YV UT WOS:000239267600004 PM 16819346 ER PT J AU Schneider, JC Harris, NL El Shami, A Sheridan, RL Schulz, JT Bilodeau, ML Ryan, CM AF Schneider, Jeffrey C. Harris, Natalie L. El Shami, Amir Sheridan, Robert L. Schulz, John T., II Bilodeau, Mary-Liz Ryan, Colleen M. TI A descriptive review of neuropathic-like pain after burn injury SO JOURNAL OF BURN CARE & RESEARCH LA English DT Review ID POSTTRAUMATIC-STRESS-DISORDER; MANAGEMENT; PREVALENCE; VARIABLES; SEVERITY; TRIALS AB This study reviews the natural history of neuropathic-like pain after burn injury. We undertook a retrospective chart review during a 24-month period of patients treated at an outpatient burn center. The medical records of patients with neuropathic-like pain complaints, including the sensation of pins and needles, burning, stabbing, shooting, or "electric" sensations, were included for analysis. Medical and demographic data were collected. We identified 72 patients for inclusion in the study. The age was 44 +/- 2 years (mean +/- SEM), and TBSA burned was 18 +/- 3%. The first complaint of neuropathic-like symptoms was at 4.3 +/- 0.5 months after injury. Documentation of improvement in the symptoms occurred at 7.0 +/- 0.8 months. Symptoms persisted for 13.1 +/- 2.2 months after the injury. Patients were followed for 14.5 +/- 2.2 months. Documented initial pain severity score was 7 +/- 1 of 10. Typical exacerbating factors included temperature change, dependent position, light touch, and weight-bearing activities. Common alleviating factors included rest, massage, compression garment use, and elevation. Treatment regimens often included gabapentin (38%) and steroid injections (21%). Hypertrophic scarring (43%), pruritis (40%), and psychiatric diagnoses (36%) were common associated problems. There is a patterned natural history for neuropathic-like pain after burn injury. This clinical entity involves significant pain complaints and persists, on average, for greater than I year after injury, which underscores the importance of long-term outpatient care after burn injury. Furthermore, an understanding of the natural history will assist clinicians in prognosticating and caring for burn survivors with pain after wound closure. C1 Harvard Univ, Sch Med, Massachusetts Gen Hosp, Sumner Redstone Burn Ctr,Surg Serv, Boston, MA 02114 USA. Harvard Univ, Sch Med, Massachusetts Gen Hosp, Spaulding Rehab Hosp,Dept Phys Med & Rehabil, Boston, MA 02114 USA. Rosalind Franklin Univ Med & Sci, Chicago Med Sch, Chicago, IL USA. Shriners Burns Hosp, Boston, MA USA. Bridgeport Hosp, Sect Trauma Burns & Surg Crit Care, Yale New Haven Hlth Syst, Bridgeport, CT USA. RP Ryan, CM (reprint author), Harvard Univ, Sch Med, Massachusetts Gen Hosp, Sumner Redstone Burn Ctr,Surg Serv, Bigelow 1302,Fruit St, Boston, MA 02114 USA. NR 44 TC 41 Z9 42 U1 1 U2 7 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 1559-047X J9 J BURN CARE RES JI J. Burn Care Res. PD JUL-AUG PY 2006 VL 27 IS 4 BP 524 EP 528 DI 10.1097/01.BCR.0000226019.76946.5D PG 5 WC Emergency Medicine; Dermatology; Surgery SC Emergency Medicine; Dermatology; Surgery GA 066YV UT WOS:000239267600017 PM 16819359 ER PT J AU Kumbhani, DJ Sharma, GVRK Khuri, SF Kirdar, JA AF Kumbhani, DJ Sharma, GVRK Khuri, SF Kirdar, JA TI Fascicular conduction disturbances after coronary artery bypass surgery: A review with a meta-analysis of their long-term significance SO JOURNAL OF CARDIAC SURGERY LA English DT Review ID BUNDLE-BRANCH BLOCK; POSTOPERATIVE CONDUCTION; BLOOD CARDIOPLEGIA; CRYSTALLOID CARDIOPLEGIA; POTASSIUM CONCENTRATION; ATRIOVENTRICULAR-BLOCK; MYOCARDIAL-INFARCTION; CARDIAC-SURGERY; GRAFT-SURGERY; DEFECTS AB Fascicular conduction abnormalities are frequently reported following adult cardiac surgery, but their pathogenesis and long-term outcomes remain unclear. In this article, we review the epidemiological features, pathogenesis, diagnosis, and management, and the short-term and long-term significance of fascicular conduction abnormalities following coronary artery bypass graft (CABG) surgery, based on data from 30 studies. Conduction disturbances have an incidence of 3.4% to 55.8% after CABG surgery, the most common being right bundle branch block (RBBB). RBBB is usually transient and benign. Although a slew of factors have been implicated in the pathogenesis of fascicular conduction disturbances, the two most important factors are myocardial ischemia and type of cardioplegia. While a 12-lead electrocardiogram is the gold standard for diagnosis, additional tests such as myocardial enzymes or echocardiography may have additional diagnostic and prognostic value. Short-term prognosis after RBBB is good, but its impact on long-term survival is unclear. We conducted a meta-analysis, the first of its kind in this area, using long-term survival data from five studies. There was no difference in long-term survival between patients who developed conduction disturbances after CABG surgery, and those who did not, indicating a benign influence of conduction disturbances on long-term survival, and the lack of the necessity for monitoring or pacing. While the older literature reported an adverse impact of fascicular conduction disturbances on long-term survival, the more recent studies report a substantially reduced mortality after CABG surgery, despite a higher incidence of conduction disturbances, pointing to the effect of improved surgical techniques. C1 Harvard Univ, Sch Med, VA Boston Healthcare Syst, Dept Surg, W Roxbury, MA 02132 USA. Harvard Univ, Sch Med, VA Boston Healthcare Syst, Dept Cardiol, W Roxbury, MA 02132 USA. Brigham & Womens Hosp, Boston, MA 02115 USA. RP Kirdar, JA (reprint author), Harvard Univ, Sch Med, VA Boston Healthcare Syst, Dept Surg, 1400 VFW Pkwy, W Roxbury, MA 02132 USA. EM jkirdar@hms.harvard.edu NR 45 TC 4 Z9 4 U1 0 U2 0 PU BLACKWELL PUBLISHING PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DQ, OXON, ENGLAND SN 0886-0440 J9 J CARDIAC SURG JI J. Card. Surg. PD JUL-AUG PY 2006 VL 21 IS 4 BP 428 EP 434 DI 10.1111/j.1540-8191.2006.00264.x PG 7 WC Cardiac & Cardiovascular Systems; Surgery SC Cardiovascular System & Cardiology; Surgery GA 058HF UT WOS:000238655400024 PM 16846431 ER PT J AU Mansour, M Refaat, M Heist, EK Mela, T Cury, R Holmvang, G Ruskin, JN AF Mansour, M Refaat, M Heist, EK Mela, T Cury, R Holmvang, G Ruskin, JN TI Three-dimensional anatomy of the left atrium by magnetic resonance angiography: Implications for catheter ablation for atrial fibrillation SO JOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY LA English DT Article DE atrial fibrillation; pulmonary veins; left atrial appendage; catheter ablation ID COMPUTED-TOMOGRAPHY; PULMONARY VEINS; OSTIAL ABLATION AB Background: Pulmonary vein isolation (PVI) has become one of the primary treatments for symptomatic drug-refractory atrial fibrillation (AF). During this procedure, delivery of ablation lesions to certain regions of the left atrium can be technically challenging. Among the most challenging regions are the ridges separating the left pulmonary veins (LPV) from the left atrial appendage (LAA), and the right middle pulmonary vein (RMPV) from the right superior (RSPV) and right inferior (RIPV) pulmonary veins. A detailed anatomical characterization of these regions has not been previously reported. Methods: Magnetic resonance angiography (MRA) was performed in patients prior to undergoing PVI. Fifty consecutive patients with a RMPV identified by MRA were included in this study. Ridges associated with the left pulmonary veins were examined in an additional 30 patients who did not have a RMPV. Endoluminal views were reconstructed from the gadolinium-enhanced, breath-hold three-dimensional MRA data sets. Measurements were performed using electronic calipers. Results: The width of the ridge separating the LPV from the LAA was found to be 3.7 +/- 1.1 mm at its narrowest point. The segment of this ridge with a width of 5 mm or less was 16.6 +/- 6.4 mm long. The width of the ridges separating the RMPV from the RSPV and the RIPV was found to be 3.0 +/- 1.5 mm and 3.1 +/- 1.8 mm, respectively. There were no significant differences between LPV ridges for patients with versus without a RMPV. Conclusion: The width of the ridges of atrial tissue separating LPV from the LAA and the RMPV from its neighboring veins may explain the technical challenge in obtaining stable catheter positions in these areas. A detailed assessment of the anatomy of these regions may improve the safety and efficacy of catheter ablation at these sites. C1 Harvard Univ, Cardiac Arrhythmia Unit, Massachusetts Gen Hosp, Sch Med,Div Cardiol, Boston, MA 02114 USA. Harvard Univ, Cardiac Arrhythmia Unit, Massachusetts Gen Hosp, Sch Med,Dept Radiol, Boston, MA 02114 USA. Harvard Univ, Cardiac Arrhythmia Unit, Massachusetts Gen Hosp, Sch Med,Dept Internal Med, Boston, MA 02114 USA. RP Mansour, M (reprint author), Harvard Univ, Cardiac Arrhythmia Unit, Massachusetts Gen Hosp, Sch Med,Div Cardiol, Gray 109,55 Fruit St, Boston, MA 02114 USA. EM mmansour@partners.org NR 13 TC 41 Z9 41 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 JUL PY 2006 VL 17 IS 7 BP 719 EP 723 DI 10.1111/j.1540-8167.2006.00491.x PG 5 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA 054RI UT WOS:000238395900006 PM 16836666 ER PT J AU Kovacs, EM Makar, RS Gertler, FB AF Kovacs, EM Makar, RS Gertler, FB TI Tuba stimulates intracellular N-WASP-dependent actin assembly SO JOURNAL OF CELL SCIENCE LA English DT Article DE N-WASP; Tuba; invasion; cytoskeleton ID ALDRICH-SYNDROME PROTEIN; PHOSPHATIDYLINOSITOL 4-PHOSPHATE 5-KINASE; ARP2/3 COMPLEX; GROWTH-FACTOR; N-WASP-ARP2/3 COMPLEX; FILOPODIUM FORMATION; FIBROBLAST MOTILITY; ENA/VASP PROTEINS; RUFFLE FORMATION; BINDING-PROTEIN AB Tuba is a multidomain scaffolding protein that links cytoskeletal dynamics and membrane trafficking pathways. The N-terminus of Tuba binds dynamin1, and the C-terminus contains domains that can interact with signaling pathways and cytoskeletal regulatory elements. We investigated Tuba localization, distribution and function in B16 melanoma cells. Tuba overexpression stimulated dorsal ruffles that occurred independently of dynamin function. Tuba expression induced actin-driven motility of small puncta that required the C-terminal SH3, GEF and BAR domains. Additionally, Tuba was recruited to lipid vesicles generated by overexpression of phosphatidylinositol-4-phosphate 5-kinase type I alpha (PIP5K alpha), localizing prominently to the head of the comets and at lower levels along the actin tail. We propose that Tuba facilitates dorsal ruffling of melanoma cells through direct interaction with actin-regulatory proteins and the recruitment of signaling molecules to lipid microdomains for the coordinated assembly of a cytoskeletal network. Knockdown of Tuba by RNA interference (RNAi) attenuated PIP5K alpha-generated comet formation and the invasive behavior of B16 cells, implying that Tuba function is required for certain aspects of these processes. These results suggest first that Tuba-stimulated dorsal ruffling might represent a novel mechanism for the coordination of N-WASP-dependent cytoskeletal rearrangements and second that Tuba function is implicated in motility processes. C1 MIT, Dept Biol, Cambridge, MA 02139 USA. Massachusetts Gen Hosp, Dept Pathol, Boston, MA 02140 USA. RP Gertler, FB (reprint author), MIT, Dept Biol, 77 Massachusetts Ave, Cambridge, MA 02139 USA. EM fgertler@mit.edu FU NCI NIH HHS [T32-CA09216E-25]; NIGMS NIH HHS [GM58801] NR 59 TC 48 Z9 49 U1 0 U2 1 PU COMPANY OF BIOLOGISTS LTD PI CAMBRIDGE PA BIDDER BUILDING CAMBRIDGE COMMERCIAL PARK COWLEY RD, CAMBRIDGE CB4 4DL, CAMBS, ENGLAND SN 0021-9533 J9 J CELL SCI JI J. Cell Sci. PD JUL 1 PY 2006 VL 119 IS 13 BP 2715 EP 2726 DI 10.1242/jcs.03005 PG 12 WC Cell Biology SC Cell Biology GA 054YD UT WOS:000238413600009 PM 16757518 ER PT J AU Vallarta-Ast, N Krueger, D Binkley, N AF Vallarta-Ast, Nellie Krueger, Diane Binkley, Neil TI Addition of right lateral decubitus positioning improves vertebral visualization with VFA in selected patients SO JOURNAL OF CLINICAL DENSITOMETRY LA English DT Article DE VFA; DXA; vertebral fracture ID X-RAY ABSORPTIOMETRY; FRACTURE ASSESSMENT; DENSITOMETRY; DEFORMITY AB Densitometric vertebral fracture assessment (VFA) allows detection of clinically unappreciated vertebral fracture. However, vertebral visualization using VFA can be suboptimal. In such individuals, alternative spine positioning may enhance visualization. Consistent with this, we observed that reversal of positioning (right lateral decubitus rather than standard left lateral decubitus, subsequently referred to as "reverse" positioning) improved visualization in patients with suboptimal vertebral visualization. This report describes 33 such individuals (i.e., 30 men and 3 women); their mean age and their lowest T-score (L1-L4 spine, proximal femur or 0.3 radius) was 69.9 yr and 2.2. respectively. All images were acquired using a GE Healthcare Lunar Prodigy densitometer (GE Healthcare, Madison, WI). Reverse VIA increased the number of visualized vertebrae in 82% of these patients (27 of 33; p < 0.0001). Specifically, only 62% of vertebrae from T4-L5 were visualized using the standard left lateral position. Addition of either full or partial reverse VFA increased (p < 0.0001) the number of visualized vertebrae to 83% (384 of 462). In this cohort, reverse positioning allowed detection of 4 additional vertebral fractures, including two in patients without previously identified fractures. We conclude that in selected patients with suboptimal vertebral visualization on VFA, addition of reverse positioning improves visualization and may enhance vertebral fracture detection. C1 Univ Wisconsin, Osteoporosis Res Program, Madison, WI 53705 USA. Univ Wisconsin, Osteoporosis Clin Ctr, Madison, WI USA. William S Middleton Mem Vet Adm Med Ctr, Madison, WI 53705 USA. RP Vallarta-Ast, N (reprint author), Univ Wisconsin, Osteoporosis Res Program, 2870 Univ Ave,Suite 100, Madison, WI 53705 USA. EM vallarta-ast@med.va.gov NR 13 TC 6 Z9 6 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 1094-6950 J9 J CLIN DENSITOM JI J. Clin. Densitom. PD JUL-SEP PY 2006 VL 9 IS 3 BP 375 EP 379 DI 10.1016/j.jocd.2006.05.009 PG 5 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA 081MH UT WOS:000240321200019 PM 16931359 ER PT J AU Bonnick, S Saag, KG Kiel, DP McClung, M Hochberg, M Burnett, SAM Sebba, A Kagan, R Chen, E Thompson, DE de Papp, AE AF Bonnick, Sydney Saag, Kenneth G. Kiel, Douglas P. McClung, Michael Hochberg, Marc Burnett, Sherri-Ann M. Sebba, Anthony Kagan, Risa Chen, Erluo Thompson, Desmond E. de Papp, Anne E. CA FACT investigators TI Comparison of weekly treatment of postmenopausal osteoporosis with alendronate versus risedronate over two years SO JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM LA English DT Article ID BONE-MINERAL DENSITY; FRACTURE INTERVENTION TRIAL; VERTEBRAL FRACTURES; RANDOMIZED-TRIAL; NONVERTEBRAL FRACTURES; ANTIRESORPTIVE AGENTS; RISK; WOMEN; REDUCTION; TURNOVER AB Objective: A 1-yr extension of the Fosamax Actonel Comparison Trial was completed to compare changes in bone mineral density (BMD), bone turnover, and upper gastrointestinal tolerability over 2 yr of treatment. Design: This was a randomized, double-blind extension conducted at 72 U. S. sites. Patients and Methods: Of the 1053 women who completed yr 1, 833 postmenopausal women with low BMD entered the extension, continuing their same treatment allocation [once-weekly (OW) alendronate 70 mg or OW risedronate 35 mg]. Changes in BMD at the hip trochanter, total hip, femoral neck, and lumbar spine and in markers of bone turnover were compared at 24 months. Tolerability was assessed by adverse experience reporting. Results: Alendronate produced greater increases from baseline in BMD at 24 months than did risedronate at the trochanter (alendronate, 4.6%; risedronate, 2.5%, P < 0.001) as well as at all other BMD sites. Significantly more alendronate than risedronate patients had measured BMD increases of 0% or more and 3% or more at all BMD sites (P < 0.001), and fewer alendronate patients had measured decreases of 3% or more at all BMD sites. Significantly greater reductions in all biochemical markers of bone turnover occurred with alendronate, compared with risedronate. No differences were seen in occurrence or discontinuations due to upper gastrointestinal adverse experiences. Conclusions: Patients receiving 70 mg OW alendronate had greater gains in BMD, were more likely to maintain or gain BMD, and had greater reductions in bone turnover markers than patients receiving 35 mg OW risedronate after 24 months, with no differences in upper gastrointestinal tolerability. C1 Clin Res Ctr N Texas, Denton, TX 76210 USA. Univ Alabama, Div Clin Immunol & Rheumatol, Birmingham, AL 35294 USA. Beth Israel Deaconess Med Ctr, Boston, MA 02215 USA. Harvard Univ, Sch Med, Boston, MA 02215 USA. Oregon Osteoporosis Ctr, Portland, OR 97213 USA. Univ Maryland, Sch Med, Baltimore, MD 21201 USA. Massachusetts Gen Hosp, Endocrine Unit, Boston, MA 02114 USA. Arthritis Associates, Palm Harbor, FL 34684 USA. Fdn Osteoporosis Res & Educ, Oakland, CA 94612 USA. Merck & Co Inc, West Point, PA 19486 USA. RP Bonnick, S (reprint author), Clin Res Ctr N Texas, 2921 Country Club Rd,Suite 101, Denton, TX 76210 USA. EM sbonnick@msn.com OI Burnett-Bowie, Sherri-Ann/0000-0002-0064-096X; McClung, Michael/0000-0002-7827-0778; Kiel, Douglas/0000-0001-8474-0310 NR 24 TC 80 Z9 83 U1 0 U2 4 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 JUL PY 2006 VL 91 IS 7 BP 2631 EP 2637 DI 10.1210/jc.2005-2602 PG 7 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA 060ZI UT WOS:000238840600029 PM 16636120 ER PT J AU Menzaghi, C Coco, A Salvemini, L Thompson, R De Cosmo, S Doria, A Trischitta, V AF Menzaghi, Claudia Coco, Angelo Salvemini, Lucia Thompson, Ryan De Cosmo, Salvatore Doria, Alessandro Trischitta, Vincenzo TI Heritability of serum resistin and its genetic correlation with insulin resistance-related features in nondiabetic Caucasians SO JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM LA English DT Article ID TYPE-2; PHENOTYPES; VARIANTS; GENOTYPE; MARKERS; OBESITY; LOCUS; RISK AB Context: Serum levels of resistin are believed to modulate insulin resistance in humans. Objective: The aim of this study was to investigate whether serum resistin levels are genetically controlled and whether this control is shared with other insulin resistance traits. Design and Methods: The study cohort included 264 nondiabetic probands, Caucasian from Italy, and their 473 adult family members. Phenotypic characterization included anthropometric variables, blood pressure, fasting glucose and insulin, lipid profile, and resistin levels. Genotypes were determined at position g. -420C -> G (rs1862513), IVS2+181G -> A (rs3745367), and GAT(n) polymorphisms of the resistin (RETN) gene. Results: In the 264 unrelated probands, resistin levels were significantly (P < 0.01) correlated with adiposity, blood pressure, C-reactive protein, and the metabolic syndrome score. In a variance component analysis of the 264 probands and their 473 relatives, about 70% of the observed variation of serum resistin levels was heritable (P < 0.0001). A small, but significant (P = 0.004) proportion of this variance was explained by the G -> A variation at position IVS2 + 181 of the RETN gene. Significant genetic correlations (P < 0.05) were observed between resistin and body mass index (rho(g) = 0.30), waist circumference (rho(g) = 0.32), the insulin resistance index HOMA(IR) (rho(g) = 0.28), and the metabolic syndrome score (rho(g) = 0.35). Conclusions: These data indicate that serum resistin is highly heritable and has some common genetic background with traits related to insulin resistance, reinforcing the hypothesis that this adipokine may play a pathogenic role in insulin resistance-related abnormalities, including type 2 diabetes and cardiovascular disease. C1 IRCCS Casa Sollievo Sofferenza, Res Unit Diabetol & Endocrinol, I-71013 San Giovanni Rotondo, Italy. Harvard Univ, Sch Med, Joslin Diabet Ctr, Boston, MA 02115 USA. Harvard Univ, Sch Med, Dept Med, Boston, MA 02115 USA. Univ Roma La Sapienza, Dept Clin Sci, I-00161 Rome, Italy. RP Menzaghi, C (reprint author), IRCCS Casa Sollievo Sofferenza, Res Unit Diabetol & Endocrinol, I-71013 San Giovanni Rotondo, Italy. EM menzaghi@operapadrepio.it; vincenzo.trischitta@uniroma1.it RI De Cosmo, Salvatore/J-7420-2016; Trischitta, Vincenzo/K-1487-2016; Salvemini, Lucia/K-2121-2016; OI De Cosmo, Salvatore/0000-0001-8787-8286; Trischitta, Vincenzo/0000-0003-1174-127X; Salvemini, Lucia/0000-0001-8776-9477; Menzaghi, Claudia/0000-0002-7438-8955 FU NHLBI NIH HHS [HL73168]; NIDDK NIH HHS [DK36836] NR 20 TC 77 Z9 78 U1 2 U2 5 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 JUL PY 2006 VL 91 IS 7 BP 2792 EP 2795 DI 10.1210/jc.2005-2715 PG 4 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA 060ZI UT WOS:000238840600054 PM 16670163 ER PT J AU Sands, BE Sandborn, WJ Wolf, DC Katz, S Safdi, M Schwartz, DA Hanauer, SB AF Sands, Bruce E. Sandborn, William J. Wolf, Douglas C. Katz, Seymour Safdi, Michael Schwartz, David A. Hanauer, Stephen B. TI Pilot feasibility studies of leukocytapheresis with the adacolumn apheresis system in patients with active ulcerative colitis or Crohn disease SO JOURNAL OF CLINICAL GASTROENTEROLOGY LA English DT Article DE ulcerative colitis; Crohn disease; inflammatory bowel disease; leukocytapheresis; granulocytes ID INFLAMMATORY-BOWEL-DISEASE; MONOCYTE ADSORPTION APHERESIS; ACTIVITY INDEX; THERAPY; GRANULOCYTE; ADJUNCT; SAFETY AB Goals: Two uncontrolled, multicenter feasibility studies evaluated safety and pilot efficacy of selective granulocyte and monocyte adsorption apheresis (GMA) with the Adacolumn Apheresis System for treatment of moderate-to-severe ulcerative colitis (UC) and Crohn disease (CD) patients refractory/intolerant to conventional pharmacologic therapy. Background: Patients with UC and CD, characterized by elevations in peripheral blood granulocytes, monocytes/macrophages, and proinflammatory mediators, may benefit from reductions in activated granulocytes and monocytes by selective apheresis. Methods: Patients underwent weekly Adacolumn sessions for 5 weeks. Pilot efficacy assessments used disease activity index (DAI) for UC (0-12) or CD activity index (CDAI; 0-600) for CD. Results: Eleven of 15 UC patients completed all 5 treatments. Mean DAI scores fell from 8.4 +/- 1.3 (baseline) to 5.2 +/- 2.9 (week 7). Five patients had DAI reductions of >= 3 points at week 7. Fourteen of 15 CD patients completed all 5 treatments. Mean CDAI scores fell from 308.0 +/- 76.5 (baseline) to 200.6 +/- 117.4 (week 7). Nine CD patients responded (CDAI reductions >= 70 points) at week 7. Remission (CDAI score <= 150 at week 7) was observed in 6 patients. There were no device-related serious adverse effects. Conclusions: Treatment with Adacolumn may be feasible and effective in patients with moderate-to-severe refractory inflammatory bowel disease. Larger sham-controlled studies are ongoing. C1 Massachusetts Gen Hosp, MGH Crohns & Colitis Ctr, Boston, MA 02114 USA. Massachusetts Gen Hosp, Gastrointestinal Unit, Boston, MA 02114 USA. Mayo Clin, Div Gastroenterol & Hepatol, Rochester, MN USA. Atlanta GI Associates, Atlanta, GA USA. Long Isl Clin Res Associates, Great Neck, NY USA. Consultants Clin Res, Cincinnati, OH USA. Vanderbilt Univ, Med Ctr, Div Gastroenterol, Nashville, TN USA. Univ Chicago, Med Ctr, Sect Gastroenterol Nutr & Hepatol, Chicago, IL 60637 USA. RP Sands, BE (reprint author), Massachusetts Gen Hosp, MGH Crohns & Colitis Ctr, 165 cambridge St,9th Floor, Boston, MA 02114 USA. EM bsands@partners.org OI Schwartz, David/0000-0002-7026-7099 NR 21 TC 21 Z9 21 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0192-0790 J9 J CLIN GASTROENTEROL JI J. Clin. Gastroenterol. PD JUL PY 2006 VL 40 IS 6 BP 482 EP 489 DI 10.1097/00004836-200607000-00005 PG 8 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA 065CJ UT WOS:000239136700005 PM 16825929 ER PT J AU Shoelson, SE Lee, J Goldfine, AB AF Shoelson, Steven E. Lee, Jongsoon Goldfine, Allison B. TI Inflammation and insulin resistance SO JOURNAL OF CLINICAL INVESTIGATION LA English DT Review ID TUMOR-NECROSIS-FACTOR; FACTOR-ALPHA BLOCKADE; INNATE IMMUNE-SYSTEM; C-REACTIVE PROTEIN; BLOOD-CELL COUNT; KAPPA-B-ALPHA; DIABETES-MELLITUS; ADIPOSE-TISSUE; RECEPTOR SUBSTRATE-1; VISCERAL FAT AB Over a hundred years ago, high doses of salicylates were shown to lower glucose levels in diabetic patients. This should have been an important clue to link inflammation to the pathogenesis of type 2 diabetes (T2D), but the antihyperglycemic and andinflammatory effects of salicylates were not connected to the pathogenesis of insulin resistance until recently. Together with the discovery of an important role for tissue macrophages, these new findings are helping to reshape thinking about how obesity increases the risk for developing T2D and the metabolic syndrome. The evolving concept of insulin resistance and T2D as having immunological components and an improving picture of how inflammation modulates metabolism provide new opportunities for using andinflammatory strategies to correct the metabolic consequences of excess adiposity. C1 Harvard Univ, Sch Med, Joslin Diabet Ctr, Boston, MA 02215 USA. Harvard Univ, Sch Med, Dept Med, Boston, MA 02215 USA. RP Shoelson, SE (reprint author), Harvard Univ, Sch Med, Joslin Diabet Ctr, 1 Joslin Pl, Boston, MA 02215 USA. EM steven.shoelson@joslin.harvard.edu NR 95 TC 1689 Z9 1762 U1 38 U2 289 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 JUL PY 2006 VL 116 IS 7 BP 1793 EP 1801 DI 10.1172/JCI29069 PG 9 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA 062DN UT WOS:000238924900008 PM 16823477 ER PT J AU MacRae, CA Birchmeier, W Thierfelder, L AF MacRae, Calurn A. Birchmeier, Walter Thierfelder, Ludwig TI Arrhythmogenic right ventricular cardiomyopathy: moving toward mechanism SO JOURNAL OF CLINICAL INVESTIGATION LA English DT Editorial Material ID NAXOS-DISEASE; WOOLLY HAIR; RECESSIVE MUTATION; DESMOPLAKIN; DELETION; PLAKOPHILIN-2; PLAKOGLOBIN; CARDIOGENESIS; KERATODERMA; INHIBITION AB Mutations in genes encoding desmosomal proteins have been identified as the major cause of arrhythmogenic right ventricular dysplasia/cardiomyopathy (ARVC), in which the right ventricle is "replaced" by fibro-fatty tissue, resulting in lethal arrhythmias. In this issue of the JCI, Garcia-Gras et al. demonstrate that cardiac-specific loss of the desmosomal protein desmoplakin is sufficient to cause nuclear translocation of plakoglobin, upregulation of adipogenic genes in vitro, and a shift from a cardiomyocyte to an adipocyte cell fate in vivo (see the related article beginning on page 2012). This evidence for potential Wnt/beta-catenin signaling defects sets the scene for a comprehensive exploration of the contributions of this pathway to the pathophysiology of ARVC, not only through perturbation of cardiac patterning and development, but also through effects on myocardial differentiation and physiology. C1 Massachusetts Gen Hosp, Cardiovasc Res Ctr, Boston, MA 02129 USA. Harvard Univ, Sch Med, Boston, MA 02115 USA. Max Delbruck Ctr Mol Med, Berlin, Germany. HELIOS Clin, Charite, Franz Volhard Clin, Berlin, Germany. RP MacRae, CA (reprint author), Massachusetts Gen Hosp, Cardiovasc Res Ctr, CNY149-4218,149 13th St, Boston, MA 02129 USA. EM macrae@cvrc.mgh.harvard.edu; lthier@mdc-berlin.de NR 24 TC 27 Z9 28 U1 0 U2 0 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 JUL PY 2006 VL 116 IS 7 BP 1825 EP 1828 DI 10.1172/JCI29174 PG 4 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA 062DN UT WOS:000238924900012 PM 16823481 ER PT J AU Chien, KR AF Chien, Kenneth R. TI Lost and found: cardiac stem cell therapy revisited SO JOURNAL OF CLINICAL INVESTIGATION LA English DT Editorial Material ID RANDOMIZED CONTROLLED-TRIAL; ACUTE MYOCARDIAL-INFARCTION; BONE-MARROW-CELLS; HEART; REGENERATION; REPAIR; TRANSPLANTATION; ASTAMI; AMI AB Several clinical trials of bone marrow stem cell therapy for myocardial infarction are ongoing, but the mechanistic basis for any potential therapeutic effect is currently unclear. A growing body of evidence suggests that the potential improvement in cardiac function is largely independent of cardiac muscle regeneration. A study by Fazel et al. in this issue of the JCI provides evidence that bone marrow-derived c-kit(+) cells can lead to an improvement in cardiac function in mutant hypomorphic c-kit mice that is independent of transdifferentiation into either cardiac muscle or endothelial cells, but rather is associated with the release of angiogenic cytokines and associated neovascularization in the infarct border zone (see the related article beginning on page 1865). These findings suggest the potential therapeutic effect of specific paracrine pathways for angiogenesis in improving cardiac function in the injured heart. C1 Harvard Univ, Cardiovasc Res Ctr, Richard B Simches Res Ctr,Harvard Stem Cell Inst, Massachusetts Gen Hosp,Sch Med,Dept Cell Biol, Boston, MA 02114 USA. RP Chien, KR (reprint author), Harvard Univ, Cardiovasc Res Ctr, Richard B Simches Res Ctr,Harvard Stem Cell Inst, Massachusetts Gen Hosp,Sch Med,Dept Cell Biol, CPZN 3208,185 Cambridge St, Boston, MA 02114 USA. EM kchien@partners.org NR 18 TC 39 Z9 46 U1 0 U2 1 PU AMER SOC CLINICAL INVESTIGATION INC PI ANN ARBOR PA 35 RESEARCH DR, STE 300, ANN ARBOR, MI 48103 USA SN 0021-9738 J9 J CLIN INVEST JI J. Clin. Invest. PD JUL PY 2006 VL 116 IS 7 BP 1838 EP 1840 DI 10.1172/JCI29050 PG 3 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA 062DN UT WOS:000238924900016 PM 16823485 ER PT J AU Yang, D Zhang, Y Nguyen, HG Koupenova, M Chauhan, AK Makitalo, M Jones, MR Hilaire, CS Seldin, DC Toselli, P Larnperti, E Schreiber, BM Gavras, H Wagner, DD Ravid, K AF Yang, Dan Zhang, Ying Nguyen, Hao G. Koupenova, Milka Chauhan, Anil K. Makitalo, Maria Jones, Matthew R. Hilaire, Cynthia St. Seldin, David C. Toselli, Paul Larnperti, Edward Schreiber, Barbara M. Gavras, Haralambos Wagner, Denisa D. Ravid, Katya TI The A(2B) adenosine receptor protects against inflammation and excessive vascular adhesion SO JOURNAL OF CLINICAL INVESTIGATION LA English DT Article ID SMOOTH-MUSCLE-CELLS; HUMAN ENDOTHELIAL-CELLS; NF-KAPPA-B; A(2A) RECEPTORS; MICE LACKING; TRANSCRIPTIONAL REGULATION; DEFICIENT MICE/; TRANSGENIC MICE; NERVOUS-SYSTEM; BLOOD-PRESSURE AB Adenosine has been described as playing a role in the control of inflammation, but it has not been certain which of its receptors mediate this effect. Here, we generated an A(2B) adenosine receptor-knockout/reporter gene-knock-in (A(2B)AR-knockout/reporter gene-knock-in) mouse model and showed receptor gene expression in the vasculature and macrophages, the ablation of which causes low-grade inflammation compared with age-, sex-, and strain-matched control mice. Augmentation of proinflammatory cytokines, such as TNF-alpha, and a consequent downregulation of I kappa B-alpha are the underlying mechanisms for an observed upregulation of adhesion molecules in the vasculature of these A(2B)AR-null mice. Intriguingly, leukocyte adhesion to the vasculature is significantly increased in the A(2B)AR-knockout mice. Exposure to an endotoxin results in augmented proinflammatory cytokine levels in A(2B)AR-null mice compared with control mice. Bone marrow transplantations indicated that bone marrow (and to a lesser extent vascular) A(2B)ARs regulate these processes. Hence, we identify the A(2B)AR as a new critical regulator of inflammation and vascular adhesion primarily via signals from hematopoietic cells to the vasculature, focusing attention on the receptor as a therapeutic target. C1 Boston Univ, Sch Med, Dept Biochem, Boston, MA 02118 USA. Boston Univ, Sch Med, Whitaker Cardiovasc Inst, Boston, MA 02118 USA. Harvard Univ, Sch Med, CBR, Inst Biomed Res, Boston, MA USA. Harvard Univ, Sch Med, Dept Pathol, Boston, MA 02115 USA. Boston Univ, Sch Med, Dept Med, Boston, MA 02118 USA. RP Ravid, K (reprint author), Boston Univ, Sch Med, Dept Biochem, K225, Boston, MA 02118 USA. EM ravid@biochem.bumc.bu.edu RI St. Hilaire, Cynthia/I-4713-2014; OI Ravid, Katya/0000-0002-9918-3024; St. Hilaire, Cynthia/0000-0003-1871-6915; Schreiber, Barbara/0000-0001-8560-4249 FU NHLBI NIH HHS [HL13262, P01 HL013262, R37 HL041002]; PHS HHS [41002] NR 61 TC 208 Z9 212 U1 2 U2 8 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 JUL PY 2006 VL 116 IS 7 BP 1913 EP 1923 DI 10.1172/JCI27933 PG 11 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA 062DN UT WOS:000238924900024 PM 16823489 ER PT J AU Halvas, EK Aldrovandi, GM Balfe, P Beck, IA Boltz, VF Coffin, JM Frenkel, LM Hazelwood, JD Johnson, VA Kearney, M Kovacs, A Kuritzkes, DR Metzner, KJ Nissley, DV Nowicki, M Palmer, S Ziermann, R Zhao, RY Jennings, CL Bremer, J Brambilla, D Mellors, JW AF Halvas, Elias K. Aldrovandi, Grace M. Balfe, Peter Beck, Ingrid A. Boltz, Valerie F. Coffin, John M. Frenkel, Lisa M. Hazelwood, J. Darren Johnson, Victoria A. Kearney, Mary Kovacs, Andrea Kuritzkes, Daniel R. Metzner, Karin J. Nissley, Dwight V. Nowicki, Marek Palmer, Sarah Ziermann, Rainer Zhao, Richard Y. Jennings, Cheryl L. Bremer, James Brambilla, Don Mellors, John W. TI Blinded, multicenter comparison of methods to detect a drug-resistant mutant of human immunodeficiency virus type 1 at low frequency SO JOURNAL OF CLINICAL MICROBIOLOGY LA English DT Article ID REVERSE-TRANSCRIPTASE; IN-VIVO; MUTATIONS; THERAPY; POPULATIONS; INTERRUPTION; INHIBITORS; GENOTYPE; MULTIPLE; PROTEASE AB We determined the abilities of 10 technologies to detect and quantify a common drug-resistant mutant of human immunodeficiency virus type 1 (lysine to asparagine at codon 103 of the reverse transcriptase) using a blinded test panel containing mutant-wild-type mixtures ranging from 0.01% to 100% mutant. Two technologies, allele-specific reverse transcriptase PCR and a Ty1HRT yeast system, could quantify the mutant down to 0.1 to 0.4%. These technologies should help define the impact of low-frequency drug-resistant mutants on response to antiretroviral therapy. C1 Univ Pittsburgh, Dept Med, Div Infect Dis, Pittsburgh, PA 15261 USA. Childrens Hosp Los Angeles, Keck Sch Med, Los Angeles, CA 90027 USA. Columbia Univ, New York, NY USA. Univ Washington, Seattle, WA 98195 USA. NCI, HIV Drug Resistance Program, Frederick, MD 21701 USA. Birmingham VA Med Ctr, Birmingham, AL USA. Univ Alabama, Birmingham, AL USA. Univ So Calif, Los Angeles, CA USA. Brigham & Womens Hosp, Sect Retroviral Therapeut, Boston, MA 02115 USA. Harvard Univ, Sch Med, Div AIDS, Boston, MA USA. Univ Erlangen Nurnberg, Erlangen, Germany. NCI, Basic Res Program, SAIC Frederick, Frederick, MD 21701 USA. Bayer Healthcare Diagnost, Berkeley, CA USA. Univ Maryland, Sch Med, Baltimore, MD 21201 USA. Rush Med Coll, Chicago, IL 60612 USA. New England Res Inst, Watertown, MA 02172 USA. RP Mellors, JW (reprint author), Univ Pittsburgh, Dept Med, Div Infect Dis, S818 Scaife Hall,3550 Terrace St, Pittsburgh, PA 15261 USA. EM Mellors@msx.dept-med.pitt.edu RI Metzner, Karin/G-5319-2011 OI Metzner, Karin/0000-0003-4862-1503 FU NCI NIH HHS [N01CO12400, N01-CO-12400]; NIAID NIH HHS [AI-60354, N01-AI-85354, N01AI85354, P30 AI027767, P30 AI060354, P30AI27767, U01 AI038858, U01AI38858, UM1 AI106716]; NICHD NIH HHS [HD 40777, R01 HD040777] NR 20 TC 84 Z9 88 U1 0 U2 2 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA SN 0095-1137 J9 J CLIN MICROBIOL JI J. Clin. Microbiol. PD JUL PY 2006 VL 44 IS 7 BP 2612 EP 2614 DI 10.1128/JCM.00449-06 PG 3 WC Microbiology SC Microbiology GA 065JY UT WOS:000239157400053 PM 16825395 ER PT J AU Joffe, S Miller, FG AF Joffe, Steven Miller, Franklin G. TI Rethinking risk-benefit assessment for phase I cancer trials SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Editorial Material ID CLINICAL-TRIALS; ETHICAL CONSIDERATIONS; ANTICANCER AGENTS; ONCOLOGY TRIALS; CHILDREN; DESIGN; THERAPY; CONDUCT; CONSENT; DRUG C1 Dana Farber Canc Inst, Dept Pediat Oncol, Boston, MA 02115 USA. Childrens Hosp, Dept Med, Boston, MA 02115 USA. NIH, Dept Clin Bioeth, Bethesda, MD 20892 USA. RP Joffe, S (reprint author), Dana Farber Canc Inst, Dept Pediat Oncol, Boston, MA 02115 USA. OI Joffe, Steven/0000-0002-0667-7384 FU NCI NIH HHS [CA096872] NR 42 TC 42 Z9 43 U1 1 U2 2 PU AMER SOC CLINICAL ONCOLOGY PI ALEXANDRIA PA 330 JOHN CARLYLE ST, STE 300, ALEXANDRIA, VA 22314 USA SN 0732-183X J9 J CLIN ONCOL JI J. Clin. Oncol. PD JUL 1 PY 2006 VL 24 IS 19 BP 2987 EP 2990 DI 10.1200/JCO.2005.04.9296 PG 4 WC Oncology SC Oncology GA 063AC UT WOS:000238987200005 PM 16809725 ER PT J AU Richardson, PG Briemberg, H Jagannath, S Wen, PY Barlogie, B Berenson, J Singhal, S Siegel, DS Irwin, D Schuster, M Srkalovic, G Alexanian, R Rajkumar, SV Limentani, S Alsina, M Orlowski, RZ Najarian, K Esseltine, D Anderson, KC Amato, AA AF Richardson, Paul G. Briemberg, Hannah Jagannath, Sundar Wen, Patrick Y. Barlogie, Bart Berenson, James Singhal, Seema Siegel, David S. Irwin, David Schuster, Michael Srkalovic, Gordan Alexanian, Raymond Rajkumar, S. Vincent Limentani, Steven Alsina, Melissa Orlowski, Robert Z. Najarian, Kevin Esseltine, Dixie Anderson, Kenneth C. Amato, Anthony A. TI Frequency, characteristics, and reversibility of peripheral neuropathy during treatment of advanced multiple myeloma with bortezomib SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Article ID PHASE-I TRIAL; DIABETIC POLYNEUROPATHY; REFRACTORY MYELOMA; DEXAMETHASONE; THERAPY; QUESTIONNAIRE; CHEMOTHERAPY; MALIGNANCIES; COMBINATION; THALIDOMIDE AB Purpose To determine the frequency, characteristics, and reversibility of peripheral neuropathy from bortezomib treatment of advanced multiple myeloma. Patients and Methods Peripheral neuropathy was assessed in two phase 11 studies in 256 patients with relapsed and/or refractory myeloma treated with bortezomib 1.0 or 1.3 mg/m(2) intravenous bolus on days 1, 4, 8, and 11, every 21 days, for up to eight cycles. Peripheral neuropathy was evaluated at baseline, during the study, and after the study by patient-reported symptoms using the Functional Assessment of Cancer Therapy Scale/Gynecologic Oncology Group-Neurotoxicity (FACT/GOG-Ntx) questionnaire and neurologic examination. During the study, peripheral neuropathy was also evaluated by investigator assessment. A subset of patients underwent nerve conduction studies (n = 13). Results Before treatment, 194 (81%) of 239 patients had peripheral neuropathy by FACT/GOG-Ntx questionnaire, and 203 (83%) of 244 patients had peripheral neuropathy by neurologic examination. Treatment-emergent neuropathy was reported in 35% of patients, including 37% (84 of 228 patients) receiving bortezomib 1.3 mg/m(2) and 21% (six of 28 patients) receiving bortezomib 1.0 mg/m(2). Grade 1 or 2, 3, and 4 neuropathy occurred in 22%, 13%, and 0.4% of patients, respectively. The incidence of grade 2 >= 3 neuropathy was higher among patients with baseline neuropathy by FACT/GOG-Ntx questionnaire compared with patients without baseline neuropathy (14% v 4%, respectively). In all 256 patients, neuropathy led to dose reduction in 12% and discontinuation in 5%. Of 35 patients with neuropathy grade 3 and/or requiring discontinuation, resolution to baseline or improvement occurred in 71%. Conclusion Bortezomib-associated peripheral neuropathy seemed reversible in the majority of patients after dose reduction or discontinuation. Although severe neuropathy was more frequent in the presence of baseline neuropathy, the overall occurrence was independent of baseline neuropathy or type of prior therapy. C1 Dana Farber Canc Inst, Boston, MA 02115 USA. Brigham & Womens Hosp, Boston, MA 02115 USA. Millennium Pharmaceut Inc, Cambridge, MA USA. St Vincents Canc Ctr, New York, NY USA. York Presbyterian Hosp, New York, NY USA. Univ Arkansas, Little Rock, AR 72204 USA. Inst Myeloma & Bone Canc Res, W Hollywood, CA USA. Alta Bates Canc Ctr, Berkeley, CA USA. Robert H Lurie Canc Ctr, Chicago, IL USA. Hackensack Univ, Med Ctr, Hackensack, NJ USA. New Sparrow Reg Canc Ctr, Lansing, MI USA. Univ Texas, MD Anderson Canc Ctr, Houston, TX 77030 USA. Mayo Clin & Mayo Fdn, Rochester, MN 55905 USA. Carolinas Hematol Oncol Assoc, Charlotte, NC USA. H Lee Moffit Canc Ctr & Res Inst, Tampa, FL USA. Univ N Carolina, Chapel Hill, NC USA. RP Richardson, PG (reprint author), Dana Farber Canc Inst, 44 Binney St,Dama 1B02, Boston, MA 02115 USA. EM paul_richardson@dfci.harvard.edu OI Rajkumar, S. Vincent/0000-0002-5862-1833 NR 20 TC 334 Z9 349 U1 3 U2 10 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 JUL 1 PY 2006 VL 24 IS 19 BP 3113 EP 3120 DI 10.1200/JCO.2005.04.7779 PG 8 WC Oncology SC Oncology GA 063AC UT WOS:000238987200024 PM 16754936 ER PT J AU Habermann, TM Weller, EA Morrison, VA Gascoyne, RD Cassileth, PA Cohn, JB Dakhil, SR Woda, B Fisher, RI Peterson, BA Horning, SJ AF Habermann, Thomas M. Weller, Edie A. Morrison, Vicki A. Gascoyne, Randy D. Cassileth, Peter A. Cohn, Jeffrey B. Dakhil, Shaker R. Woda, Bruce Fisher, Richard I. Peterson, Bruce A. Horning, Sandra J. TI Rituximab-CHOP versus CHOP alone or with maintenance rituximab in older patients with diffuse large B-cell lymphoma SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Article ID NON-HODGKINS-LYMPHOMA; ANTI-CD20 MONOCLONAL-ANTIBODY; 2-STAGE RANDOMIZATION DESIGNS; STANDARD REGIMEN CHOP; DETUDE-DES-LYMPHOMES; ELDERLY-PATIENTS; CLINICAL-TRIALS; AGGRESSIVE LYMPHOMA; TREATMENT POLICIES; INITIAL TREATMENT AB Purpose To address early and late treatment failures in older patients with diffuse large B-cell lymphoma (DLBCL), we designed a two-stage randomized trial of cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) versus rituximab plus CHOP (R-CHOP), with a second random assignment to maintenance rituximab (MR) or observation in responding patients. Patients and Methods Untreated DLBCL patients who were 60 years or older were randomly assigned to R-CHOP (n = 318) or CHOP (n = 314); 415 responders were randomly assigned to MR (n = 207) or observation (n 208). The primary end point was failure-free survival (FFS). All P values were two sided. Results Three-year FFS rate was 53% for R-CHOP patients and 46% for CHOP patients (P=.04) at a median follow-up time of 3.5 years. Two-year FFS rate from second random assignment was 76% for MR compared with 61% for observation (P=.009). No significant differences in survival were seen according to induction or maintenance therapy. FFS was prolonged with MR after CHOP (P=.0004) but not after R-CHOP (P=.81) with 2-year FFS rates from second random assignment of 77%, 79%, 74%, and 45% for R-CHOP, R-CHOP + MR, CHOP + MR, and CHOP, respectively. In a secondary analysis excluding MR patients, R-CHOP alone reduced the risks of treatment failure (P=.003) and death (P=.05) compared with CHOP alone. Conclusion Rituximab administered as induction or maintenance with CHOP chemotherapy significantly prolonged FFS in older DLBCL patients. After R-CHOP, no benefit was provided by MR. These results, which are consistent with an additive effect of rituximab, suggest that future studies could focus on maintenance strategies with novel agents as well as new induction therapies. C1 Mayo Clin & Mayo Fdn, Div Hematol, Rochester, MN 55905 USA. Univ Minnesota, Vet Adm Med Ctr, Minneapolis, MN USA. Dana Farber Canc Inst, Ctr Stat, Boston, MA 02115 USA. Univ Massachusetts, Sch Med, Worcester, MA USA. Univ Miami, Miami, FL 33152 USA. Albert Einstein Canc Ctr, Philadelphia, PA USA. Wichita Community Clin Oncol Program, Wichita, KS USA. Univ Rochester, Rochester, NY USA. Stanford Univ, Stanford, CA 94305 USA. British Columbia Canc Agcy, Vancouver, BC V5Z 4E6, Canada. RP Habermann, TM (reprint author), Mayo Clin & Mayo Fdn, Div Hematol, 200 1st St SW, Rochester, MN 55905 USA. EM habermann.thomas@mayo.edu FU NCI NIH HHS [CA23318, CA11083, CA13650, CA16450, CA21115, CA32291, CA35431, CA66636] NR 33 TC 719 Z9 758 U1 2 U2 23 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 JUL 1 PY 2006 VL 24 IS 19 BP 3121 EP 3127 DI 10.1200/JCO.2005.05.1003 PG 7 WC Oncology SC Oncology GA 063AC UT WOS:000238987200025 PM 16754935 ER PT J AU Barredo, JC Devidas, M Lauer, SJ Billett, A Marymont, M Pullen, J Camitta, B Winick, N Carroll, W Ritchey, AK AF Barredo, Julio C. Devidas, Meenakshi Lauer, Stephen J. Billett, Amy Marymont, MaryAnne Pullen, Jeanette Camitta, Bruce Winick, Naomi Carroll, William Ritchey, A. Kim TI Isolated CNS relapse of acute lymphoblastic leukemia treated with intensive systemic chemotherapy and delayed CNS radiation: A pediatric oncology group study SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Article; Proceedings Paper CT 39th Annual Meeting of the American-Society-of-Clinical-Oncology CY MAY 31-JUN 03, 2003 CL CHICAGO, IL SP Amer Soc Clin Oncol ID ISOLATED EXTRAMEDULLARY RELAPSE; BONE-MARROW-TRANSPLANTATION; ACUTE LYMPHOCYTIC-LEUKEMIA; CHILDHOOD-CANCER; FOLLOW-UP; CHILDREN; TRIAL; RISK; IRRADIATION; SURVIVORS AB Prognosis and outcome of children with isolated CNS relapse of acute lymphoblastic leukemia (ALL) has depended on duration of first complete remission (CR1). This study intensified systemic therapy by delaying CNS radiation for 12 months and tailored CNS radiation by CR1 duration. Patients and Methods Seventy-six children with first isolated CNS relapse of ALL were treated with systemic chemotherapy that effectively penetrates into the CSF and intrathecal chemotherapy for 12 months. Patients with CR1 of less than 18 months received craniospinal radiation (24 Gy cranial/15 Gy spinal), whereas those with CRI of 18 months or more received cranial radiation only (18 Gy), followed by maintenance chemotherapy. Additionally, asymptomatic patients were enrolled in a thiotepa up-front therapeutic window. Results Seventy-four (97.4%) of 76 eligible patients achieved a second remission. Overall 4-year event-free survival (EFS) for the 71 precursor B-cell patients was 70.1% 5.8%. CRI duration and National Cancer Institute (NCI; National Institutes of Health, Bethesda, MID) risk group at initial diagnosis predicted outcome. Patients with CR1 of less than 18 months and 18 months or more had a 4-year EFS of 51.6% 11.3% and 77.7% +/- 6.4% (P=.027), respectively. NCI high-versus standard-risk 4-year EFS was 51.4% +/- 10.8% and 80.2% +/- 6.3% (P =.0018), respectively. A significant difference in EFS between standard risk/CR1 of at least 18 months and both high risk/CR1 of less than 18 months and high risk/CR1 of at least 18 months groups was detected (P=.0068 and .0314, respectively). Response rate to thiotepa was 78%. Most relapses involved the bone marrow, and three second malignancies were reported. Conclusion Twelve months of intensive systemic chemotherapy with reduced dose cranial radiation (18 Gy) is highly effective for children with isolated CNS relapse and CRI of 18 months or more. Novel strategies are needed for patients with CRI of less than 18 months. C1 Med Univ S Carolina, Dept Pediat, Charleston, SC 29425 USA. Univ Florida, Childrens Oncol Grp, Stat & Data Ctr, Gainesville, FL 32611 USA. Emory Univ, Sch Med, Dept Pediat, Atlanta, GA 30322 USA. Dana Farber Canc Inst, Dept Pediat, Boston, MA 02115 USA. Northwestern Univ, Chicago, IL 60611 USA. Univ Mississippi, Dept Pediat, Jackson, MS 39216 USA. Med Coll Wisconsin, Midw Childrens Canc Ctr, Milwaukee, WI 53226 USA. Univ Texas, SW Med Ctr, Dept Pediat, Dallas, TX 75230 USA. NYU, Med Ctr, Dept Pediat, New York, NY 10016 USA. Childrens Hosp Pittsburgh, Div Pediat Hematol Oncol, Pittsburgh, PA 15213 USA. RP Barredo, JC (reprint author), Med Univ S Carolina, Childrens Hosp, 135 Rutledge Ave, Charleston, SC 29425 USA. EM barredjc@musc.edu NR 36 TC 41 Z9 43 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 JUL 1 PY 2006 VL 24 IS 19 BP 3142 EP 3149 DI 10.1200/JCO.2005.03.3373 PG 8 WC Oncology SC Oncology GA 063AC UT WOS:000238987200028 PM 16809737 ER PT J AU Dougherty, DD Loh, R Jenike, MA Keuthen, NJ AF Dougherty, Darin D. Loh, Rebecca Jenike, Michael A. Keuthen, Nancy J. TI Single modality versus dual modality treatment for trichotillomania: Sertraline, behavioral therapy, or both? SO JOURNAL OF CLINICAL PSYCHIATRY LA English DT Article ID MGH HAIRPULLING SCALE; HABIT-REVERSAL; CONTROLLED-TRIAL; DOUBLE-BLIND; CLOMIPRAMINE; DEPRESSION; FLUOXETINE; INVENTORY AB Background. Trichotillomania is a psychiatric condition characterized by chronic hair pulling. Both cognitive behavioral therapy (CBT) and the selective serotonin reuptake inhibitors (SSRIs) have shown promise in the treatment of trichotillomania, with comparison studies favoring CBT over pharmacotherapy. However, no randomized, controlled studies to date have compared the efficacy of individual SSRI or CBT treatment to the combination of both treatment modalities. Method: In this study, which ran from February 2000 through April 2003, subjects who met DSM-IV criteria for trichotillomania were randomly assigned to treatment with sertraline or placebo in a double-blind study design. Following 12 weeks of active pharmacotherapy, subjects not demonstrating significant trichotillomania symptom improvement had habit reversal training (HRT) added to their treatment regimen. Primary outcome measures were the Hair Pulling Scale and the Clinical Global Impressions scale. R esults: Thirteen subjects completing the 22-week study received single modality treatment of either sertraline or HRT, and 11 received both modalities of treatment. Trichotillomania symptoms in both groups improved, although the dual modality treatment group demonstrated larger gains and were much more likely to reach responder status at final evaluation. Conclusion: These results suggest that the combination of sertraline and HRT may be more efficacious in the treatment of trichotillomania than either approach alone. C1 Massachusetts Gen Hosp, Dept Psychiat, Charlestown, MA 02129 USA. RP Dougherty, DD (reprint author), Massachusetts Gen Hosp, Dept Psychiat, CNY2612,,Bldg 149,13th St, Charlestown, MA 02129 USA. EM ddougherty@partners.org RI Citations, TLC SAB/C-4006-2011 NR 33 TC 39 Z9 39 U1 0 U2 3 PU PHYSICIANS POSTGRADUATE PRESS PI MEMPHIS PA P O BOX 240008, MEMPHIS, TN 38124 USA SN 0160-6689 J9 J CLIN PSYCHIAT JI J. Clin. Psychiatry PD JUL PY 2006 VL 67 IS 7 BP 1086 EP 1092 PG 8 WC Psychology, Clinical; Psychiatry SC Psychology; Psychiatry GA 070TU UT WOS:000239548300011 PM 16889452 ER PT J AU Davila, J Kamholz, BW Rayburn, NR Anderson, P AF Davila, J Kamholz, BW Rayburn, NR Anderson, P TI Perspectives on nontraditional research careers in clinical psychology SO JOURNAL OF CLINICAL PSYCHOLOGY LA English DT Article; Proceedings Paper CT 38th Annual Meeting of the Association-for-the-Advancement-of-Behavior-Therapy CY NOV, 2004 CL New Orleans, LA SP Assoc Advancement Behav Therapy DE nontraditional research positions; careers AB Building on a panel presentation titled "Career opportunities for behavioral scientists: Non-academic research settings," given at the November 2004 meeting of the Association for Advancement of Behavior Therapy, this article presents the experiences of three clinical psychologists who have careers in nontraditional research settings. These authors focus on three issues: (a) What nontraditional career did they pursue and why? (b) What, if anything, in their training prepared them for that career? (c) What advice would they give to students and young professionals who are considering pursuing a similar type of nontraditional career option? An introduction and concluding remarks that highlight recent trends in the academic job market and themes across each authors' experience are provided by the chair of the panel. (c) 2006 Wiley Periodicals, Inc. C1 SUNY Stony Brook, Dept Psychol, Stony Brook, NY 11794 USA. VA Boston Healthcare Syst, Boston, MA USA. Boston Univ, Boston, MA 02215 USA. RAND Corp, Los Angeles, CA USA. Georgia State Univ, Atlanta, GA USA. RP Davila, J (reprint author), SUNY Stony Brook, Dept Psychol, Stony Brook, NY 11794 USA. EM joanne.davila@stonybrook.edu; barbara.kamholz2@va.gov; rayburn@rand.org; psypxa@langate.gsu.edu FU NIDA NIH HHS [DA016138]; NIMH NIH HHS [R42MH060506-02A1, R01MH063904-1A2] NR 7 TC 2 Z9 2 U1 1 U2 2 PU JOHN WILEY & SONS INC PI HOBOKEN PA 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 0021-9762 J9 J CLIN PSYCHOL JI J. Clin. Psychol. PD JUL PY 2006 VL 62 IS 7 BP 907 EP 921 DI 10.1002/jclp.20275 PG 15 WC Psychology, Clinical SC Psychology GA 056EI UT WOS:000238503700009 PM 16688688 ER PT J AU Kuntzen, T Lauer, G Timm, J Berical, A zur Wiesch, JS Kim, A Ximenez, LL Chung, RT Walker, BD Allen, TM AF Kuntzen, T. Lauer, G. Timm, J. Berical, A. zur Wiesch, J. Schulze Kim, A. Ximenez, L. Lewis Chung, R. T. Walker, B. D. Allen, T. M. TI Forces driving viral sequence evolution in acute hepatitis C infection SO JOURNAL OF CLINICAL VIROLOGY LA English DT Meeting Abstract CT 12th International Symposium on Viral Hepatitis and Liver Disease CY JUL 01-05, 2006 CL Paris, FRANCE SP Pan-Amer Soc Clin Virol, European Soc Clin Virol C1 Harvard Univ, Sch Med, Massachusetts Gen Hosp, Partners AIDS Res Ctr, Charlestown, MA USA. Fiocruz MS, Inst Oswaldo Cruz, Dept Virol, BR-21045900 Rio De Janeiro, Brazil. Harvard Univ, Sch Med, Massachusetts Gen Hosp, Gastrointestinal Unit, Boston, MA USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 1386-6532 J9 J CLIN VIROL JI J. Clin. Virol. PD JUL PY 2006 VL 36 SU 2 BP S111 EP S111 DI 10.1016/S1386-6532(06)80343-4 PG 1 WC Virology SC Virology GA 064CR UT WOS:000239067300334 ER PT J AU Lewis-Ximenez, LL Espirito-Santo, MP Oliveira, JM Lauer, G Walker, B Yoshida, CFT Lampe, E AF Lewis-Ximenez, L. L. Espirito-Santo, M. P. Oliveira, J. M. Lauer, G. Walker, B. Yoshida, C. F. T. Lampe, E. TI Three cases of acute hepatitis C virus infection following dry sex SO JOURNAL OF CLINICAL VIROLOGY LA English DT Meeting Abstract CT 12th International Symposium on Viral Hepatitis and Liver Disease CY JUL 01-05, 2006 CL Paris, FRANCE SP Pan-Amer Soc Clin Virol, European Soc Clin Virol C1 Fdn Oswaldo Cruz, Dept Virol, Rio De Janeiro, Brazil. Massachusetts Gen Hosp, Res Ctr, Boston, MA 02114 USA. Massachusetts Gen Hosp, Div Infect Dis, Boston, MA 02114 USA. Howard Hughes Med Inst, Boston, MA 02115 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 1386-6532 J9 J CLIN VIROL JI J. Clin. Virol. PD JUL PY 2006 VL 36 SU 2 BP S154 EP S154 DI 10.1016/S1386-6532(06)80476-2 PG 1 WC Virology SC Virology GA 064CR UT WOS:000239067300466 ER PT J AU Longworth, S zur Wiesch, JS Kim, AY Kuntzen, T Timm, J Jones, A Chung, RT Allen, TM Walker, BD Lauer, GM AF Longworth, S. zur Wiesch, J. Schulze Kim, A. Y. Kuntzen, T. Timm, J. Jones, A. Chung, R. T. Allen, T. M. Walker, B. D. Lauer, G. M. TI Differential responsiveness of CD4 and CD8 T-cells during acute HCV re-infection SO JOURNAL OF CLINICAL VIROLOGY LA English DT Meeting Abstract CT 12th International Symposium on Viral Hepatitis and Liver Disease CY JUL 01-05, 2006 CL Paris, FRANCE SP Pan-Amer Soc Clin Virol, European Soc Clin Virol C1 Massachusetts Gen Hosp, Partners AIDS Res Ctr, Charlestown, MA USA. Massachusetts Gen Hosp, Howard Hughes Med Inst, Charlestown, MA USA. Harvard Univ, Sch Med, Charlestown, MA USA. Massachusetts Gen Hosp, GI Unit, Boston, MA 02114 USA. Harvard Univ, Sch Med, Boston, MA USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 1386-6532 J9 J CLIN VIROL JI J. Clin. Virol. PD JUL PY 2006 VL 36 SU 2 BP S56 EP S57 DI 10.1016/S1386-6532(06)80172-1 PG 2 WC Virology SC Virology GA 064CR UT WOS:000239067300163 ER PT J AU Nolan, B Kuntzen, T Jones, A Lewis-Ximenez, L Walker, BD Allen, TM Lauer, GM AF Nolan, B. Kuntzen, T. Jones, A. Lewis-Ximenez, L. Walker, B. D. Allen, T. M. Lauer, G. M. TI Dominant and subdominant T-cell responses and viral evolution in subjects with acute symptomatic HCV infection SO JOURNAL OF CLINICAL VIROLOGY LA English DT Meeting Abstract CT 12th International Symposium on Viral Hepatitis and Liver Disease CY JUL 01-05, 2006 CL Paris, FRANCE SP Pan-Amer Soc Clin Virol, European Soc Clin Virol C1 Massachusetts Gen Hosp, Partners AIDS Res Ctr, Charlestown, MA USA. Massachusetts Gen Hosp, Howard Hughes Med Inst, Charlestown, MA USA. Harvard Univ, Sch Med, Charlestown, MA USA. Inst Oswaldo Cruz, BR-20001 Rio De Janeiro, Brazil. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 1386-6532 J9 J CLIN VIROL JI J. Clin. Virol. PD JUL PY 2006 VL 36 SU 2 BP S122 EP S122 DI 10.1016/S1386-6532(06)80379-3 PG 1 WC Virology SC Virology GA 064CR UT WOS:000239067300370 ER PT J AU Oishi, N Masutomi, K Khurts, S Zhang, S Nakamoto, Y Kaneko, S Murakami, S AF Oishi, N. Masutomi, K. Khurts, S. Zhang, S. Nakamoto, Y. Kaneko, S. Murakami, S. TI Hepatitis B virus x protein overcomes oncogene-induced senescense with active H-Ras-V12 in human immortal cells SO JOURNAL OF CLINICAL VIROLOGY LA English DT Meeting Abstract CT 12th International Symposium on Viral Hepatitis and Liver Disease CY JUL 01-05, 2006 CL Paris, FRANCE SP Pan-Amer Soc Clin Virol, European Soc Clin Virol C1 Kanazawa Univ, Grad Sch Med, Dept Gastroenterol, Kanazawa, Ishikawa 920, Japan. Dana Farber Canc Inst, Dept Med Oncol & Biostat Sci, Boston, MA 02115 USA. Kanazawa Univ, Canc Res Inst, Dept Mol Oncol, Kanazawa, Ishikawa 920, Japan. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 1386-6532 J9 J CLIN VIROL JI J. Clin. Virol. PD JUL PY 2006 VL 36 SU 2 BP S68 EP S68 DI 10.1016/S1386-6532(06)80206-4 PG 1 WC Virology SC Virology GA 064CR UT WOS:000239067300197 ER PT J AU Timm, J Li, B Bhattacharya, T Daniels, MG Reyor, LL Allgaier, R Kuntzen, T Fischer, W Duncan, J zur Wiesch, JS Kim, A Frahm, N Branderl, C Chung, RT Lauer, GM Korber, BT Walker, BD Allen, TM AF Timm, J. Li, B. Bhattacharya, T. Daniels, M. G. Reyor, L. L. Allgaier, R. Kuntzen, T. Fischer, W. Duncan, J. zur Wiesch, J. Schulze Kim, A. Frahm, N. Brander, C. Chung, R. T. Lauer, G. M. Korber, B. T. Walker, B. D. Allen, T. M. TI HLA-associated sequence polymorphisms in HCV reveal the reproducibility of immune responses and constraints on viral evolution SO JOURNAL OF CLINICAL VIROLOGY LA English DT Meeting Abstract CT 12th International Symposium on Viral Hepatitis and Liver Disease CY JUL 01-05, 2006 CL Paris, FRANCE SP Pan-Amer Soc Clin Virol, European Soc Clin Virol C1 Massachusetts Gen Hosp, Gastrointestinal Unit, Charlestown, MA USA. Los Alamos Natl Lab, Los Alamos, NM USA. RI Bhattacharya, Tanmoy/J-8956-2013 OI Bhattacharya, Tanmoy/0000-0002-1060-652X NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 1386-6532 J9 J CLIN VIROL JI J. Clin. Virol. PD JUL PY 2006 VL 36 SU 2 BP S119 EP S120 DI 10.1016/S1386-6532(06)80371-9 PG 2 WC Virology SC Virology GA 064CR UT WOS:000239067300362 ER PT J AU Holalkere, NS Sahani, DV Blake, MA Halpern, EF Hahn, PF Mueller, PR AF Holalkere, Nagarai-Setty Sahani, Dushyant V. Blake, Michael A. Halpern, Elkan F. Hahn, Peter F. Mueller, Peter R. TI Characterization of small liver lesions: Added role of MR after MDCT SO JOURNAL OF COMPUTER ASSISTED TOMOGRAPHY LA English DT Article DE small liver lesion; MDCT; MRI ID SMALL HEPATIC-LESIONS; CONTRAST-ENHANCED CT; GADOLINIUM ENHANCEMENT; BREAST-CANCER; PREVALENCE; ROUTINE AB Objective: The purpose of this study is to evaluate the added role of magnetic resonance imaging (MR) in characterizing subcentimeter focal liver lesion(s) detected on multidetector row helical computed tomography (MDCT). Materials and Methods: A retrospective analysis was performed in 59 noncirrhotic patients with focal subcentimeter liver lesion(s) detected on a 4- or 16-slice MDCT. All patients had a gadolinium enhanced liver MR on 1.5-T systems within 6 weeks after MDCT. Imaging diagnosis was graded on an ordinal scale of 0-5 (0, normal; 1, definitely benign; and 5, definitely malignant). The final diagnosis was established either by histopathology or follow-up imaging for a period of at least 6 months. Receiver operating characteristic analysis was performed to compare the performances of MDCT and MR in characterization of subcentimeter liver lesions. Results: A total of 178 lesions were detected on MDCT in 59 patients. Of these lesions, 129 (72.5%) lesions were benign and the remaining 49 were malignant. The sensitivity, specificity, positive predictive value, and negative predictive value in differentiation of benign from malignant lesions on MDCT were 81.2%, 77.3%, 60.5%, 90.6% and on MR were 83.3%, 97.5%, 92.1%, and 94.4%, respectively. Comparative receiver operating characteristic analysis showed an area under curve for MDCT = 0.76 and MR = 0.95 (P < 0.001). Conclusions: Liver MR has significantly higher accuracy for characterization of subcentimeter focal liver lesions discovered on MDCT. C1 Massachusetts Gen Hosp, Boston, MA 02114 USA. RP Sahani, DV (reprint author), Massachusetts Gen Hosp, White 270,55 Fruit St, Boston, MA 02114 USA. EM dsahani@partners.org NR 14 TC 35 Z9 39 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0363-8715 J9 J COMPUT ASSIST TOMO JI J. Comput. Assist. Tomogr. PD JUL-AUG PY 2006 VL 30 IS 4 BP 591 EP 596 DI 10.1097/00004728-200607000-00007 PG 6 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA 067WO UT WOS:000239333500007 PM 16845289 ER PT J AU Forbes, F Peyrard, N Fraley, C Georgian-Smith, D Goldhaber, DM Raftery, AE AF Forbes, Florence Peyrard, Nathalie Fraley, Chris Georgian-Smith, Dianne Goldhaber, David M. Raftery, Adrian E. TI Model-based region-of-interest selection in dynamic breast MRI SO JOURNAL OF COMPUTER ASSISTED TOMOGRAPHY LA English DT Article DE image segmentation; region of interest selection; magnetic resonance imaging; MR mammography; dynamic contrast-enhanced breast MRI; time-signal intensity curves; model-based clustering; Bayesian morphology ID CONTRAST-ENHANCED MRI; NEURAL-NETWORKS; IMAGES; MAMMOGRAPHY; LESIONS; CANCER; SEGMENTATION; TUMORS; MORPHOLOGY; ALGORITHM AB Magnetic resonance imaging (MRI) is emerging as a, powerful tool for the diagnosis of breast abnormalities. Dynamic analysis of the temporal pattern of contrast uptake has been applied in differential diagnosis of benign and malignant lesions to improve. specificity. Selecting a region of interest (ROI) is an almost universal step in the process of examining the contrast uptake characteristics of a breast lesion. We propose an ROI selection method that combines model-based clustering of the pixels with Bayesian morphology, a new statistical image segmentation method. We then investigate tools for subsequent analysis of signal intensity time course data in the selected region. Results on a database of 19 patients indicate that the method provides informative segmentations and good detection rates. C1 Univ Washington, Dept Stat, Seattle, WA 98195 USA. Zirst, Inria Rhone Alpes, Equipe MISTIS, F-38334 Montbonnot St Martin, St Ismier, France. INRA, Biometr & Artificial Intelligence Dept, F-84914 Avignon 9, France. Harvard Univ, Sch Med, Massachusetts Gen Hosp, Dept Radiol, Boston, MA USA. Int MRI Accreditat Resources, San Francisco, CA USA. RP Fraley, C (reprint author), Univ Washington, Dept Stat, Seattle, WA 98195 USA. EM fraley@stat.washington.edu FU NIBIB NIH HHS [8 R01 EB002137-02] NR 47 TC 10 Z9 10 U1 1 U2 4 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0363-8715 EI 1532-3145 J9 J COMPUT ASSIST TOMO JI J. Comput. Assist. Tomogr. PD JUL-AUG PY 2006 VL 30 IS 4 BP 675 EP 687 DI 10.1097/00004728-200607000-00020 PG 13 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA 067WO UT WOS:000239333500020 PM 16845302 ER PT J AU Pike, L Petravicz, J Wang, S AF Pike, Lisa Petravicz, Jeremy Wang, Samuel TI Bioluminescence imaging after HSV amplicon vector delivery into brain SO JOURNAL OF GENE MEDICINE LA English DT Article DE HSV; amplicon; bioluminescence; rapamycin; regulation; vector ID GENE-EXPRESSION; IN-VIVO; REGULATED EXPRESSION; SYSTEM; THERAPY; APOPTOSIS; ELEMENT; CELLS; MICE; DNA AB Background Firefly luciferase (Fluc) has routinely been used to quantitate and analyze gene expression in vitro by measuring the photons emitted after the addition of ATP and luciferin to a test sample. It is now possible to replace luminometer-based analysis of luciferase activity and measure luciferase activity delivered by viral vectors directly in live animals over time using digital imaging techniques. Methods An HSV amplicon vector expressing Fluc cDNA from an inducible promoter was delivered to cells in culture and into the mouse brain. In culture, expression of Fluc was measured after induction in a dose-dependent manner by a biochemical assay, and then confirmed by Western blot analysis and digital imaging. The vectors were then stereotactically injected into the mouse brain and Fluc expression measured non-invasively using bioluminescence imaging. Results Rapamycin-mediated induction of Fluc from an HSV amplicon vector in culture resulted in dose-dependent expression of Fluc when measured using a luminometer and by digital analysis. In mouse cortex, a single injection of an HSV amplicon vector (2 mu l, 1 x 10(8) transducing units (t.u.)/ml) expressing Fluc from a viral promoter (CMV) was sufficient to detect robust luciferase activity for at least I week. Similarly, an HSV amplicon vector expressing Fluc under an inducible promoter was also detectable in the mouse cortex after a single dose (2 mu l, 1 x 10(8) t.u./ml) for up to 5 days, with no detectable signal in the uninduced state. Conclusions This HSV amplicon vector-based system allows for fast, non-invasive, semi-quantitative analysis of gene expression in the brain. Copyright (c) 2006 John Wiley & Sons, Ltd. C1 Massachusetts Gen Hosp, Dept Neurol, Charlestown, MA 02129 USA. Harvard Univ, Sch Med, Neurosci Program, Charlestown, MA 02129 USA. RP Wang, S (reprint author), Massachusetts Gen Hosp E, Ctr Neurosci, 13th St,Bldg 149, Charlestown, MA 02129 USA. EM swang@helix.mgh.harvard.edu FU NCI NIH HHS [CA86355]; NINDS NIH HHS [NS24279] NR 24 TC 11 Z9 12 U1 0 U2 0 PU JOHN WILEY & SONS LTD PI CHICHESTER PA THE ATRIUM, SOUTHERN GATE, CHICHESTER PO19 8SQ, W SUSSEX, ENGLAND SN 1099-498X J9 J GENE MED JI J. Gene. Med. PD JUL PY 2006 VL 8 IS 7 BP 804 EP 813 DI 10.1002/jgm.909 PG 10 WC Biotechnology & Applied Microbiology; Genetics & Heredity; Medicine, Research & Experimental SC Biotechnology & Applied Microbiology; Genetics & Heredity; Research & Experimental Medicine GA 068KE UT WOS:000239371800002 PM 16602134 ER PT J AU Fowler, FJ Barry, MJ Walker-Corkery, B Caubet, JF Bates, DW Lee, JM Hauser, A McNaughton-Collins, M AF Fowler, FJ Barry, MJ Walker-Corkery, B Caubet, JF Bates, DW Lee, JM Hauser, A McNaughton-Collins, M TI The impact of a suspicious prostate biopsy on patients' psychological, socio-behavioral, and medical care outcomes SO JOURNAL OF GENERAL INTERNAL MEDICINE LA English DT Article DE prostate biopsy; prostate cancer; screening ID SERVICES-TASK-FORCE; QUALITY-OF-LIFE; BREAST-CANCER; UNITED-STATES; COLORECTAL-CANCER; SEXTANT BIOPSIES; PREFERENCES; HUSBANDS; YIELD; WIVES AB OBJECTIVE: To evaluate the psychological, socio-behavioral, and medical implications of apparently false-positive prostate cancer screening results. METHODS: One hundred and twenty-one men with a benign prostate biopsy performed in response to a suspicious screening test (biopsy group) and 164 men with a normal prostate-specific antigen (PSA) test result (normal PSA group) responded to a questionnaire 6 weeks, 6 and 12 months after their biopsy or PSA test. RESULTS: The mean (+/- SD) age of respondents was 61 +/- 9 years (range, 41 to 88 years). One year later, 26% (32/121) of men in the biopsy group reported having worried "a lot" or "some of the time" that they may develop prostate cancer, compared with 6% (10/164) in the normal PSA group (P < .001). Forty-six percent of the biopsy group reported thinking their wife or significant other was concerned about prostate cancer, versus 14% in the normal PSA group (P < .001). Medical record review showed that biopsied men were more likely than those in the normal PSA group to have had at least I follow-up PSA test over the year (73% vs 42%, P < .001), more likely to have had another biopsy (15% vs 1%, P < .001), and more likely to have visited a urologist (71% vs 13%, P <. 001). CONCLUSION. One year later, men who underwent prostate biopsy more often reported worrying about prostate cancer. In addition, there were related psychological, socio-behavioral, and medical care implications. These hidden tolls associated with screening should be considered in the discussion about the benefits and risks of prostate cancer screening. C1 Massachusetts Gen Hosp, Div Gen Med, Boston, MA 02114 USA. Univ Massachusetts, Survey Res Ctr, Boston, MA 02125 USA. Brigham & Womens Hosp, Div Gen Med, Boston, MA 02115 USA. Brigham & Womens Hosp, Div Urol, Boston, MA 02115 USA. Boston Med Ctr, Div Gen Med, Boston, MA USA. RP McNaughton-Collins, M (reprint author), Massachusetts Gen Hosp, Div Gen Med, 50 Stainford St,9th Floor, Boston, MA 02114 USA. EM mmcnaughton-collins@partners.org NR 25 TC 33 Z9 33 U1 0 U2 1 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 JUL PY 2006 VL 21 IS 7 BP 715 EP 721 DI 10.1111/j.1525-1497.2006.00464.x PG 7 WC Health Care Sciences & Services; Medicine, General & Internal SC Health Care Sciences & Services; General & Internal Medicine GA 053NX UT WOS:000238313000009 PM 16808772 ER PT J AU Coulter, ID Hardy, ML Morton, SC Hilton, LG Tu, WL Valentine, D Shekelle, PG AF Coulter, Ian D. Hardy, Mary L. Morton, Sally C. Hilton, Lara G. Tu, Wenli Valentine, Di Shekelle, Paul G. TI Antioxidants vitamin C and vitamin E for the prevention and treatment of cancer SO JOURNAL OF GENERAL INTERNAL MEDICINE LA English DT Article DE vitamin C; vitamin E; systematic review; cancer; antioxidant ID NUTRITION INTERVENTION TRIALS; SUPPLEMENTAL ALPHA-TOCOPHEROL; RANDOMIZED CONTROLLED-TRIAL; DISEASE-SPECIFIC MORTALITY; BETA-CAROTENE; MINERAL SUPPLEMENTATION; COLORECTAL ADENOMAS; CLINICAL-TRIALS; ASCORBIC-ACID; MALE SMOKERS AB OBJECTIVE: To evaluate the evidence of the supplements vitamin C and vitamin E for treatment and prevention of cancer. METHODS: Systematic review of trials and meta-analysis. DATA SOURCES AND MAIN RESULTS: Thirty-eight studies showed scant evidence that vitamin C or vitamin E beneficially affects survival. In the ATBC Cancer Prevention Study Group, no statistically significant effect of treatment was seen for any cancer individually, and our pooled relative risk (regardless of tumor type) for a-tocopherol alone was 0.91 (95% confidence interval [CI]: 0.74, 1.12). All cause mortality was not significant. In the Linxian General Population Trial, the relative risks for cancer death for vitamin C (combined with molybdenum) was 1.06 (95% CI: 0.92, 1.21) and for vitamin E (combined with beta-carotene and selenium) was 0.87 (95% CI: 0.76, 1.00). We identified only 3 studies that reported statistically significant beneficial results: vitamin C (in combination with BCG) was found to be beneficial in a single trial of bladder cancer and vitamin E (in combination with omega-3 fatty acid) increased survival in patients with advanced cancer. In the ATBC trial, in analyses of 6 individual cancers, the prevention of prostate cancer in subjects treated with alpha-tocopherol was statistically significant (RR = 0.64, 95% CI: 0.44, 0.94). CONCLUSIONS: The systematic review of the literature does not support the hypothesis that the use of supplements of vitamin C or vitamin E in the doses tested helps prevent and/or treat cancer in the populations tested. There were isolated findings of benefit, which require confirmation. C1 RAND Corp, So Calif Evidence Based Practice Ctr, Santa Monica, CA USA. Univ Calif Los Angeles, Sch Dent, Los Angeles, CA 90024 USA. Univ So Calif, Los Angeles, CA 90089 USA. Cedars Sinai Integrat Med Med Grp Inc, Los Angeles, CA USA. RAND Corp, Greater Los Angeles VA Healthcare Syst, Los Angeles, CA USA. Samuell Inst Informat Biol, Alexandria, VA USA. RP Coulter, ID (reprint author), 1776 Main St,POB 2138, Santa Monica, CA 90407 USA. EM coulter@rand.org FU PHS HHS [290-97-0001] NR 46 TC 61 Z9 65 U1 0 U2 15 PU SPRINGER PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA SN 0884-8734 J9 J GEN INTERN MED JI J. Gen. Intern. Med. PD JUL PY 2006 VL 21 IS 7 BP 735 EP 744 DI 10.1111/j.1525-1497.2006.0483.x PG 10 WC Health Care Sciences & Services; Medicine, General & Internal SC Health Care Sciences & Services; General & Internal Medicine GA 053NX UT WOS:000238313000012 PM 16808775 ER PT J AU Labarere, J Stone, RA Obrosky, DS Yealy, DM Meehan, TP Auble, TE Fine, JM Graff, LG Fine, MJ AF Labarere, J Stone, RA Obrosky, DS Yealy, DM Meehan, TP Auble, TE Fine, JM Graff, LG Fine, MJ TI Factors associated with the hospitalization of low-risk patients with community-acquired pneumonia in a cluster-randomized trial SO JOURNAL OF GENERAL INTERNAL MEDICINE LA English DT Article DE pneumonia; community-acquired infections; patient admission; risk factors; emergency service; hospital ID PREDICTION RULE; OUTCOMES; GUIDELINES; MANAGEMENT; COST; CARE AB BACKGROUND: Many low-risk patients with pneumonia are hospitalized despite recommendations to treat such patients in the outpatient setting. OBJECTIVE: To identify the factors associated with the hospitalization of low-risk patients with pneumonia. METHODS: We analyzed data collected by retrospective chart review for 1,889 low-risk patients (Pneumonia Severity Index [PSI] risk classes I to III without evidence of arterial oxygen desaturation) enrolled in a cluster-randomized trial conducted in 32 emergency departments. RESULTS: Overall, 845 (44.7%) of all low-risk patients were treated as inpatients. Factors independently associated with an increased odds of hospitalization included PSI risk classes II and III, the presence of medical or psychosocial contraindications to outpatient treatment, comorbid conditions that were not contained in the PSI (cognitive impairment, history of coronary artery disease, diabetes mellitus, or pulmonary disease), multilobar radiographic infiltrates, and home therapy with oxygen, corticosteroids, or antibiotics before presentation. While 32.8% of low-risk inpatients had a contraindication to outpatient treatment and 47.1% had one or more preexisting treatments, comorbid conditions, or radiographic abnormalities not contained in the PSI, 20.1% had no identifiable risk factors for hospitalization other than PSI risk class II or III. CONCLUSIONS: Hospital admission appears justified for one-third of low-risk inpatients based upon the presence of one or more contraindications to outpatient treatment. At least one-fifth of low-risk inpatients did not have a contraindication to outpatient treatment or an identifiable risk factor for hospitalization, suggesting that treatment of a larger proportion of such low-risk patients in the outpatient setting could be achieved without adversely affecting patient outcomes. C1 VA Pittsburgh Healthcare Syst, VA Ctr Hlth Equ Res & Promot, Pittsburgh, PA 15240 USA. UJF, Grenoble Univ Hosp, UMR CNRS 5525, ThEMAS TIMC IMAG, Grenoble, France. Univ Pittsburgh, Grad Sch Publ Hlth, Dept Biostat, Pittsburgh, PA 15260 USA. Univ Pittsburgh, Dept Emergency Med, Pittsburgh, PA 15260 USA. Yale Univ, Sch Med, Dept Med, New Haven, CT 06520 USA. Qualidigm, Middletown, CT USA. Norwalk Hosp, Pulm & Crit Care Med Sect, Norwalk, CT 06856 USA. Univ Connecticut, Sch Med, Dept Emergency Med, Farmington, CT USA. New Britain Gen Hosp, Dept Emergency Med, New Britain, CT USA. Univ Pittsburgh, Dept Med, Div Gen Internal Med, Pittsburgh, PA 15260 USA. RP Fine, MJ (reprint author), VA Pittsburgh Healthcare Syst, VA Ctr Hlth Equ Res & Promot, Univ Dr C,Bldg 28,1A102, Pittsburgh, PA 15240 USA. EM Michael.Fine@med.va.gov RI Labarere, Jose/N-1688-2014; OI Labarere, Jose/0000-0001-7621-6586 FU AHRQ HHS [R01 HS010049, R01 HS10049]; NIAID NIH HHS [5K24 AI01769, K24 AI001769] NR 25 TC 22 Z9 23 U1 1 U2 1 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 JUL PY 2006 VL 21 IS 7 BP 745 EP 752 DI 10.1111/j.1525-1497.2006.00510.x PG 8 WC Health Care Sciences & Services; Medicine, General & Internal SC Health Care Sciences & Services; General & Internal Medicine GA 053NX UT WOS:000238313000013 PM 16808776 ER PT J AU Andermahr, J Lozano-Calderon, S Trafton, T Crisco, JJ Ring, D AF Andermahr, Jonas Lozano-Calderon, Santiago Trafton, Ted Crisco, Joseph J. Ring, David TI The volar extension of the lunate facet of the distal radius: A quantitative anatomic study SO JOURNAL OF HAND SURGERY-AMERICAN VOLUME LA English DT Article DE distal radius fracture; volar lunate facet; anatomy ID FIXATION; WRIST AB Purpose: To describe quantitatively the protrusion of the volar part of the lunate facet of the distal radius articular surface anterior to the volar metaphyseal cortex, which is susceptible to fracture and can be difficult to control with plates and screws alone. Methods: Quantitative anatomic measurements of 48 3-dimensional computed tomography scans of the distal radius were analyzed to quantify the anatomy of the volar part of the lunate facet of the distal radius. The measurements were scaled to account for overall bone size. Male and female anatomies were compared. Results: The height and width of the volar extension of the lunate facet were 3 +/- 1 mm and 19 +/- 4 mm, respectively. The mean height of the lunate facet was 19 +/- 3 mm. An average of 16% of the lunate facet projects anterior to the flat volar surface of the distal radius. The thickness of the volar extension of the lunate facet averaged 5 +/- 1 mm. There were no statistically significant differences between men and women for any of the scaled measurements. Conclusions: The observation that the volar lunate facet projects approximately 3 mm (or 16% of the dorsal-volar height of the lunate facet) anterior to the flat volar surface of the distal radius and is approximately 5 mm thick helps explain its relative vulnerability to injury and the difficulty encountered when trying to secure it with a plate and screws. C1 Massachusetts Gen Hosp, Dept Orthopaed Surg, Hand & Upper Extrem Serv, Yawkey Ctr, Boston, MA 02114 USA. Univ Cologne, Clin Trauma Hand & Reconstruct Surg, Cologne, Germany. Rhode Isl Hosp, Brown Med Sch, Dept Orthopaed Surg, Providence, RI USA. RP Ring, D (reprint author), Massachusetts Gen Hosp, Dept Orthopaed Surg, Hand & Upper Extrem Serv, Yawkey Ctr, Ste 2100,55 Fruit St, Boston, MA 02114 USA. EM dring@partners.org FU NIAMS NIH HHS [AR44005] NR 7 TC 21 Z9 21 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 0363-5023 J9 J HAND SURG-AM JI J. Hand Surg.-Am. Vol. PD JUL-AUG PY 2006 VL 31A IS 6 BP 892 EP 895 DI 10.1016/j.jhsa.2006.03.01 PG 4 WC Orthopedics; Surgery SC Orthopedics; Surgery GA 065TZ UT WOS:000239184000003 PM 16843146 ER PT J AU Lewinsohn, DM Grotzke, JE Heinzel, AS Zhu, L Ovendale, PJ Johnson, M Alderson, MR AF Lewinsohn, DM Grotzke, JE Heinzel, AS Zhu, L Ovendale, PJ Johnson, M Alderson, MR TI Secreted proteins from mycobacterium tuberculosis gain access to the cytosolic MHC class-1 antigen-processing pathway SO JOURNAL OF IMMUNOLOGY LA English DT Article ID CD8(+) T-CELLS; CLASS-I PRESENTATION; ENHANCED PROTECTION; CROSS-PRESENTATION; DENDRITIC CELLS; CALMETTE-GUERIN; INFECTED-CELLS; LYMPHOCYTES; MACROPHAGES; PHAGOSOMES AB CD8(+) T cells play an important role in the host response to infection with Mycobacterium tuberculosis (Mtb). Mtb resides in an arrested phagosome that is phenotypically similar to an early endosome. The mechanisms by which Mtb-derived Ags gain access to the HLA-I-processing pathway are incompletely characterized. Studies with CD8(+) T cell lines have suggested that Mtb Ags gain access to the HLA-I pathway in an alternate vacuolar pathway that is both brefeldin A (BFA) and TAP independent. To define the requirements of entry of Ag into the HLA-I pathway, we have used human CD8(+) T cell clones specific for the secreted Mtb Ag CFP10. Human monocyte-derived dendritic cells were pulsed with CFP10 expressed in a recombinant adenovirus, surface adsorbed to microspheres, or in its native form by Mtb. When delivered by adenovirus, processing and presentation of CFP10 were blocked by both BFA and the proteasomal blocker lactacystin. In contrast, processing of CFP10 adsorbed to the surface of microspheres was not affected by either of these Ag-processing inhibitors. BFA, lactacystin, and TAP inhibition blocked the recognition of Mtb-infected dendritic cells, suggesting that processing was via a cytosolic pathway for this secreted protein Ag. We conclude that secreted proteins from Mtb can be processed in a BFA- and proteasome-dependent manner, consistent with egress of Ag into the cytosol and subsequent loading of proteasomally derived peptides. C1 Oregon Hlth Sci Univ, R&D 11, Portland VA Med Ctr, Div Pulm & Crit Care Med, Portland, OR 97239 USA. Oregon Hlth Sci Univ, Dept Mol Microbiol & Immunol, Portland, OR 97239 USA. Corixa, Seattle, WA 98104 USA. RP Lewinsohn, DM (reprint author), Oregon Hlth Sci Univ, R&D 11, Portland VA Med Ctr, Div Pulm & Crit Care Med, 3710 US Vet Rd, Portland, OR 97239 USA. EM lewinsod@OHSU.edu FU NIAID NIH HHS [1K08 AI 01644, R01 AI 48090] NR 36 TC 41 Z9 41 U1 0 U2 2 PU AMER ASSOC IMMUNOLOGISTS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA SN 0022-1767 J9 J IMMUNOL JI J. Immunol. PD JUL 1 PY 2006 VL 177 IS 1 BP 437 EP 442 PG 6 WC Immunology SC Immunology GA 055ST UT WOS:000238471400053 PM 16785540 ER PT J AU Walensky, RP Paltiel, AD Losina, E Mercincavage, LM Schackman, BR Sax, PE Weinstein, MC Freedberg, KA AF Walensky, Rochelle P. Paltiel, A. David Losina, Elena Mercincavage, Lauren M. Schackman, Bruce R. Sax, Paul E. Weinstein, Milton C. Freedberg, Kenneth A. TI The survival benefits of AIDS treatment in the United States SO JOURNAL OF INFECTIOUS DISEASES LA English DT Article; Proceedings Paper CT 12th Conference on Retroviruses and Opportunistic Infections CY FEB 22-25, 2005 CL Boston, MA ID HUMAN-IMMUNODEFICIENCY-VIRUS; ACTIVE ANTIRETROVIRAL THERAPY; BONE-MARROW TRANSPLANTATION; MYCOBACTERIUM-AVIUM COMPLEX; NON-HODGKINS-LYMPHOMA; HIV-INFECTED ADULTS; COST-EFFECTIVENESS; MYOCARDIAL-INFARCTION; OPPORTUNISTIC INFECTIONS; PEDIATRIC SPECTRUM AB Background. As widespread adoption of potent combination antiretroviral therapy ( ART) reaches its tenth year, our objective was to quantify the cumulative survival benefits of acquired immunodeficiency syndrome ( AIDS) care in the United States. Methods. We defined eras corresponding to advances in standards of human immunodeficiency virus ( HIV) disease care, including opportunistic infection prophylaxis, treatment with ART, and the prevention of mother-to-child transmission ( pMTCT) of HIV. Per-person survival benefits for each era were determined using a mathematical simulation model. Published estimates provided the number of adult patients with new diagnoses of AIDS who were receiving care in the United States from 1989 to 2003. Results. Compared with survival associated with untreated HIV disease, per-person survival increased 0.26 years with Pneumocystis jiroveci pneumonia prophylaxis alone. Four eras of increasingly effective ART in addition to prophylaxis resulted in per-person survival increases of 7.81, 11.05, 11.57, and 13.33 years, compared with the absence of treatment. Treatment for patients with AIDS in care in the United States since 1989 yielded a total survival benefit of 2.8 million years. pMTCT averted nearly 2900 infant infections, equivalent to 137,000 additional years of survival benefit. Conclusions. At least 3.0 million years of life have been saved in the United States as a direct result of care of patients with AIDS, highlighting the significant advances made in HIV disease treatment. C1 Massachusetts Gen Hosp, Div Gen Med, Dept Med, Boston, MA 02114 USA. Massachusetts Gen Hosp, Div Infect Dis, Dept Med, Boston, MA 02114 USA. Harvard Univ, Sch Med, Ctr AIDS Res, Boston, MA 02115 USA. Harvard Univ, Sch Publ Hlth, Dept Hlth Policy & Management, Boston, MA 02115 USA. Boston Univ, Sch Publ Hlth, Dept Biostat, Boston, MA 02215 USA. Boston Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02215 USA. Brigham & Womens Hosp, Div Infect Dis, Boston, MA 02115 USA. Yale Univ, Sch Med, Div Hlth Policy & Adm, New Haven, CT USA. Cornell Univ, Weill Med Coll, Dept Publ Hlth, New York, NY 10021 USA. RP Walensky, RP (reprint author), Massachusetts Gen Hosp, Div Gen Med, Dept Med, 50 Staniford St,9th Fl, Boston, MA 02114 USA. EM rwalensky@partners.org FU NIAID NIH HHS [K24 AI062476, K23 AI001794, K23AI01794, K24AI062476, K25 AI050436, K25AI50436, P30 AI060354, P30AI060354, R01 AI042006, R01AI42006]; NIDA NIH HHS [K01 DA017179, K01DA017179, R01 DA015612, R01DA015612]; NIMH NIH HHS [R01 MH065869, R01MH65869]; PHS HHS [S1396-20/21] NR 51 TC 318 Z9 331 U1 1 U2 13 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0022-1899 J9 J INFECT DIS JI J. Infect. Dis. PD JUL 1 PY 2006 VL 194 IS 1 BP 11 EP 19 DI 10.1086/505147 PG 9 WC Immunology; Infectious Diseases; Microbiology SC Immunology; Infectious Diseases; Microbiology GA 053WS UT WOS:000238337400004 PM 16741877 ER PT J AU Giri, S Khan, M Rattan, R Singh, I Singh, AK AF Giri, S. Khan, M. Rattan, R. Singh, I. Singh, A. K. TI Krabbe disease: psychosine-mediated activation of phospholipase A2 in oligodendrocyte cell death SO JOURNAL OF LIPID RESEARCH LA English DT Article DE twitcher; apopoptosis; sPLA2 inhibitor; LPC ID HUMAN T-LYMPHOCYTES; INDUCED THYMOCYTE APOPTOSIS; NF-KAPPA-B; ARACHIDONIC-ACID; TWITCHER MOUSE; FACTOR RECEPTOR; LATE-ONSET; OXIDATIVE STRESS; POTENTIAL ROLE; GLIAL-CELLS AB Globoid cell leukodystrophy (Krabbe disease) is an inherited neurological disorder caused by the pathogenomic accumulation of psychosine (galactosylsphingosine), a substrate for the deficient enzyme galactocerebroside beta-galactosidase. This study underscores the mechanism of action of psychosine in the regulation of oligodendrocyte cell death via the generation of lysophosphatidylcholine (LPC) and arachidonic acid (AA) by the activation of secretory phospholipase A2 (sPLA2). There was a significant increase in the level of LPC, indicating a phospholipase A2 (PLA2)dependent pathobiology, in the brains of Krabbe disease patients and those of twitcher mice, an animal model of Krabbe disease. In vitro studies of the treatment of primary oligodendrocytes and the oligodendrocyte MO3.13 cell line with psychosine also showed the generation of LPC and the release of AA in a dose- and time-dependent manner, indicating psychosine- induced activation of PLA2. Studies with various pharmacological inhibitors of cytosolic phospholipase A2 and sPLA2 and psychosine-mediated induction of sPLA2 enzymatic activity in media supernatant suggest that psychosine- induced release of AA and generation of LPC is mainly contributed by sPLA2. An inhibitor of sPLA2, 7,7-dimethyl eicosadienoic acid, completely attenuated the psychosine-mediated accumulation of LPC levels, release of AA, and generation of reactive oxygen species, and blocked oligodendroyte cell death, as evident from cell survival, DNA fragmentation, and caspase 3 activity assays. This study documents for the first time that psychosine-induced cell death is mediated via the sPLA2 signaling pathway and that inhibitors of sPLA2 may hold a therapeutic potential for protection against oligodendrocyte cell death and resulting demyelination in Krabbe disease. C1 Ralph Johnson Vet Affairs Med Ctr, Dept Pathol & Lab Med, Charleston, SC 29425 USA. Mayo Clin & Mayo Fdn, Dept Lab Med & Pathol, Div Expt Pathol, Rochester, MN 55905 USA. Med Univ S Carolina, Charles P Darby Childrens Res Inst, Dept Pediat, Charleston, SC 29425 USA. Med Univ S Carolina, Charles P Darby Childrens Res Inst, Dept Pathol & Lab Med, Charleston, SC 29425 USA. RP Singh, AK (reprint author), Ralph Johnson Vet Affairs Med Ctr, Dept Pathol & Lab Med, Charleston, SC 29425 USA. EM singhi@musc.edu FU NINDS NIH HHS [NS-22576, NS-34741, NS-37766, NS-40810] NR 80 TC 59 Z9 61 U1 0 U2 3 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA SN 0022-2275 J9 J LIPID RES JI J. Lipid Res. PD JUL PY 2006 VL 47 IS 7 BP 1478 EP 1492 DI 10.1194/jlr.M600084-JLR200 PG 15 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA 064SW UT WOS:000239110400016 PM 16645197 ER PT J AU Georgakoudi, I AF Georgakoudi, I TI The color of cancer SO JOURNAL OF LUMINESCENCE LA English DT Article; Proceedings Paper CT 15th International Conferene on Dynamical Processes in Excited States of Solids CY AUG 01-05, 2005 CL Fudan Univ, Shanghai, PEOPLES R CHINA SP Natl Nat Sci Fdn China, Sci & Technol Commiss Shanghai Municipal, Chinese Phys Soc, Shanhai Phys Soc, Chinese Luminescence Soc, Surface Phys Lab, Fudan Univ, Phys Dept & Synchrotron Radiat Res Ctr, Univ Sci & Technol China, Natl Synchrotron Radiat Lab, Natl Lab Infrared Phys, Shanghai Inst Tech Phys, Changchun Inst Opt, Key Lab HO Fudan Univ DE optical diagnostics; spectroscopy; fluorescence; reflectance; light scattering; cancer detection ID LIGHT-SCATTERING SPECTROSCOPY; IN-VIVO; REFLECTANCE; FLUORESCENCE AB Optical spectroscopic techniques examine different types of light-tissue interactions and provide biochemical and morphological information that can be used to characterize changes that take place as tissues become diseased. Tissue is a turbid medium with significant levels of scattering and absorption. To understand the origins of the spectroscopic signals emitted from tissue, it is necessary to use models that take into account the manner in which tissue components interact with light. Using such model-based methods, we extract quantitative information related to different tissue parameters that change with progression to cancer. Specifically, we combine information from simultaneously measured fluorescence and reflectance spectra using a model based on Monte Carlo simulations of light propagation in tissue to remove distortions introduced in the fluorescence spectra by tissue scattering and absorption. We can then extract in a quantitative way differences in the biochemical composition of healthy and pre-cancerous tissues. Tissue reflectance spectra are analyzed using a diffusion-theory-based model to describe changes in the corresponding scattering and absorption properties of normal and diseased sites. Information on the spectra of light singly backscattered from tissues is extracted and analyzed to detect changes in the size and refractive index of cell nuclei. The combined use of intrinsic fluorescence, diffuse reflectance and light scattering spectroscopy yields complementary information which can be used to detect pre-cancers. (c) 2006 Elsevier B.V. All rights reserved. C1 Tufts Univ, Dept Biomed Engn, Medford, MA 02155 USA. Harvard Univ, Massachusetts Gen Hosp, Sch Med, Wellman Labs Photomed, Boston, MA 02115 USA. RP Georgakoudi, I (reprint author), Tufts Univ, Dept Biomed Engn, 4 Colby St,Rm 153, Medford, MA 02155 USA. EM irene.georgakoudi@tufts.edu NR 12 TC 18 Z9 18 U1 0 U2 2 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0022-2313 J9 J LUMIN JI J. Lumines. PD JUL-OCT PY 2006 VL 119 BP 75 EP 83 DI 10.1016/j.jlumin.2005.12.015 PG 9 WC Optics SC Optics GA 034JR UT WOS:000236925800018 ER PT J AU Lorenz, C Benner, T Lopez, CJ Ay, H Zhu, MW Aronen, H Karonen, J Liu, YW Nuutinen, J Sorensen, AG AF Lorenz, Cory Benner, Thomas Lopez, Chloe Joan Ay, Hakan Zhu, Ming Wang Aronen, Hannu Karonen, Jari Liu, Yawu Nuutinen, Juho Sorensen, A. Gregory TI Effect of using local arterial input functions on cerebral blood flow estimation SO JOURNAL OF MAGNETIC RESONANCE IMAGING LA English DT Article DE magnetic resonance imaging; perfusion-weighted; stroke assessment; cerebral blood flow; magnetic resonance imaging; stroke AB Purpose: To investigate a previously developed method for perfusion-weighted MRI (PWI) cerebral blood flow (CBF) estimation that uses local arterial input functions (AIFs) in stroke patients, and determine its ability to correct delay and/or dispersion (D/D) errors. Materials and Methods: Analysis was performed on dynamic susceptibility contrast data from 36 stroke patients, and CBF maps were calculated with global- and local-AIF techniques using standard SVP based methods. The ratios of these maps were calculated and the mean ratios were calculated for voxels with both normal and abnormal time to peak or width. The locations of the voxels with high locally-defined to globally-defined CBF ratios were also mapped and the average underlying concentration-time curves for these voxels were calculated. Results: The ratio of CBF estimates based on local AIFs to global AIFs was on average increased for D/D voxels. The voxels in which this ratio was high were commonly concentrated in the ipsilateral hemisphere, and these voxels also displayed underlying concentration-time curves that showed delay or dispersion. Conversely, there were no such findings based on high globally-defined to locally-defined CBF ratios. Conclusion: The local-AIF technique results in an increase in the calculated-CBF values for tissues with D/D, consistent with a reduction in the errors associated with D/D. C1 Harvard Univ, MIT, Div Hlth Sci & Technol, Charlestown, MA USA. Massachusetts Gen Hosp, Athinoula A Martinos Ctr Biomed Imaging, Boston, MA 02114 USA. MIT, Dept Elect Engn & Comp Sci, Cambridge, MA 02139 USA. Massachusetts Gen Hosp, Stroke Serv, Boston, MA 02114 USA. Kuopio Univ Hosp, Kuopio, Finland. Helsinki Brain Res Ctr, Funct Brain Imaging Unit, Helsinki, Finland. RP Sorensen, AG (reprint author), 149 13th St,Room 2301, Charlestown, MA 02129 USA. EM sorensen@nmr.mgh.harvard.edu FU NCRR NIH HHS [P41RR14075]; NINDS NIH HHS [NS38477] NR 7 TC 21 Z9 22 U1 0 U2 3 PU JOHN WILEY & SONS INC PI HOBOKEN PA 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 1053-1807 J9 J MAGN RESON IMAGING JI J. Magn. Reson. Imaging PD JUL PY 2006 VL 24 IS 1 BP 57 EP 65 DI 10.1002/jmri.20625 PG 9 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA 061TG UT WOS:000238894900007 PM 16767708 ER PT J AU Takaya, N Cai, JM Ferguson, MS Yarnykh, VL Chu, BC Saam, T Polissar, NL Sherwood, J Cury, RC Anders, RJ Broschat, KO Hinton, D Furie, KL Hatsukami, TS Yuan, C AF Takaya, Norihide Cai, Jianming Ferguson, Marina S. Yarnykh, Vasily L. Chu, Baocheng Saam, Tobias Polissar, Nayak L. Sherwood, Jane Cury, Ricardo C. Anders, Robert J. Broschat, Kay O. Hinton, Denise Furie, Karen L. Hatsukami, Thomas S. Yuan, Chun TI Intra- and interreader reproducibility of magnetic resonance imaging for quantifying the lipid-rich necrotic core is improved with gadolinium contrast enhancement SO JOURNAL OF MAGNETIC RESONANCE IMAGING LA English DT Article DE necrotic core; MRI; contrast enhancement; reproducibility; carotid artery; atherosclerosis ID CAROTID ATHEROSCLEROTIC PLAQUES; CORONARY-ARTERY DISEASE; HIGH-RESOLUTION MRI; IN-VIVO MRI; FIBROUS-CAP; LOWERING THERAPY; INTRAVASCULAR ULTRASOUND; CONTROLLED-TRIAL; REGRESSION; PERFUSION AB Purpose: To test the hypothesis that intra- and interreader reproducibility for measuring the lipid-rich necrotic core (LR-NC) size is significantly improved with gadolinium (Gd) contrast-enhanced magnetic resonance imaging (CEMRI) compared to non-CEMRI. Materials and Methods: Thirty-seven individuals with > 50% carotid artery stenosis underwent carotid MRI at 1.5T (pre- and postcontrast T1-weighted (T1W), T2-weighted (T2W), proton density-weighted (PDW), and three-dimensional time-of-flight (TOF) sequences). Two independent readers measured the mean area of the LR-NC from the precontrast images only, followed by a second measurement using the additional postcontrast images. One reader repeated the measurements after an interval of five months. Intra- and interreader reproducibility was analyzed by means of the intraclass correlation coefficient (ICC), coefficient of variation (CV), and standard deviation (SD). Results: The CV decreased from 33.7% to 8.8% for intrareader measurements of the LR-NC, and from 33.5% to 17.6% for interreader measurements. The SD was significantly smaller with CEMRI than with non-CEMRI (P = 0.003 and P = 0.006, respectively). The ICC increased from 0.94 to 0.99 and from 0.85 to 0.93 for the intra- and interreader measurements, respectively. Conclusion: Reader reproducibility for in vivo MRI quantification of LR-NC size is significantly improved by the addition of Gd contrast in individuals with > 50% carotid stenosis. C1 Univ Washington, Dept Radiol, Seattle, WA 98195 USA. Juntendo Univ, Sch Med, Dept Cardiol, Tokyo 113, Japan. Mt Whisper Light Stat Consulting, Seattle, WA USA. Massachusetts Gen Hosp, Dept Cardiol, Boston, MA 02114 USA. Massachusetts Gen Hosp, Dept Radiol, Boston, MA 02114 USA. Massachusetts Gen Hosp, Dept Neurol, Boston, MA 02114 USA. Pfizer Pharmaceut Facil, Skokie, IL USA. VA Puget Sound Hlth Care Syst, Dept Surg, Seattle, WA USA. Univ Washington, Seattle, WA 98195 USA. RP Yuan, C (reprint author), Univ Washington, Dept Radiol, 1959 Pacific St NE,Box 357115, Seattle, WA 98195 USA. EM eyuan@u.washington.edu RI Yarnykh, Vasily/G-8757-2016; Yarnykh, Vasiliy/N-7635-2014 OI Yarnykh, Vasily/0000-0002-1583-8979; FU NHLBI NIH HHS [R01HL56874] NR 38 TC 50 Z9 51 U1 0 U2 1 PU JOHN WILEY & SONS INC PI HOBOKEN PA 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 1053-1807 J9 J MAGN RESON IMAGING JI J. Magn. Reson. Imaging PD JUL PY 2006 VL 24 IS 1 BP 203 EP 210 DI 10.1002/jmri.20599 PG 8 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA 061TG UT WOS:000238894900026 PM 16739123 ER PT J AU Chen, HY Stratton, HH Caraco, TB White, DJ AF Chen, Haiyan Stratton, Howard H. Caraco, Thomas B. White, Dennis J. TI Spatiotemporal Bayesian analysis of Lyme disease in New York State, 1990-2000 SO JOURNAL OF MEDICAL ENTOMOLOGY LA English DT Article DE crude rate; empirical Bayes; fully Bayesian; Lyme disease; spatiotemporal ID INCIDENCE RATES; EPIDEMIC AB Mapping ordinarily increases our understanding of nontrivial spatial and temporal heterogeneities in disease rates. However, the large Dumber of parameters required by the corresponding statistical models often complicates detailed analysis. This study investigates the feasibility of a fully Bayesian hierarchical regression approach to the problem and identifies how it outperforms two more popular methods: crude rate estimates (CRE) and empirical Bayes standardization (EBS). in particular, we apply a fully Bayesian approach to the spatiotemporal analysis of Lyme disease incidence in New York state for the period 1990-2000. These results are compared with those obtained by CRE and EBS in Chen et al. (2005). We show that the fully Bayesian regression model not only gives more reliable estimates of disease rates than the other two approaches but also allows for tractable models that can accommodate more numerous sources of variation and unknown parameters. C1 Dana Farber Canc Inst, Dept Biostat & Computat Biol, Boston, MA 02115 USA. SUNY Albany, Dept Biometry & Stat, Sch Publ Hlth, Rensselaer, NY 12144 USA. SUNY Albany, Dept Biol Sci, Albany, NY 12222 USA. SUNY Albany, Sch Publ Hlth, Dept Epidemiol, Rensselaer, NY 12144 USA. RP Chen, HY (reprint author), Dana Farber Canc Inst, Dept Biostat & Computat Biol, Boston, MA 02115 USA. FU ODCDC CDC HHS [U50/CCU206575] NR 32 TC 6 Z9 6 U1 1 U2 4 PU ENTOMOLOGICAL SOCIETY AMERICA PI LANHAM PA 10001 DEREKWOOD LANE, STE 100, LANHAM, MD 20706-4876 USA SN 0022-2585 J9 J MED ENTOMOL JI J. Med. Entomol. PD JUL PY 2006 VL 43 IS 4 BP 777 EP 784 DI 10.1603/0022-2585(2006)43[777:SBAOLD]2.0.CO;2 PG 8 WC Entomology; Veterinary Sciences SC Entomology; Veterinary Sciences GA 062ZU UT WOS:000238986400019 PM 16892639 ER PT J AU Cobb, NK Graham, AL AF Cobb, Nathan K. Graham, Amanda L. TI Characterizing Internet searchers of smoking cessation information SO JOURNAL OF MEDICAL INTERNET RESEARCH LA English DT Article DE smoking; cessation; Internet; search engine; query ID PUBLIC-HEALTH; PROGRAM; SMOKERS; TRIAL; WEB AB Background: The Internet is a viable channel to deliver evidence-based smoking cessation treatment that has the potential to make a large population impact on reducing smoking prevalence. There is high demand for smoking cessation information and support on the Internet. Approximately 7% (10.2 million) of adult American Internet users have searched for information on quitting smoking. Little is known about these individuals, their smoking status, what type of cessation services they are seeking on the Internet, or how frequently these searches for cessation information are conducted. Objective: The primary goal of this study was to characterize individuals who search for smoking cessation information on the Internet to determine appropriate triage and treatment strategies. The secondary goal was to estimate the incidence of searches for cessation information using publicly available search engine data. Methods: We recruited individuals who clicked on a link to a leading smoking cessation website (QuitNet) from within the results of a search engine query. Individuals were "intercepted" before seeing the QuitNet home page and were invited to participate in the study. Those accepting the invitation were routed to an online survey about demographics, smoking characteristics, preferences for specific cessation services, and Internet search patterns. To determine the generalizability of our sample, national datasets on search engine usage patterns, market share, and keyword rankings were examined. These datasets were then used to estimate the number of queries for smoking cessation information each year. Results: During the 10-day study period, 2265 individuals were recruited and 29% (N = 655) responded. Of these, 59% were female and overall tended to be younger than the previously characterized general Internet population. Most (76%) respondents were current smokers; 17% had quit within the last 7 days, and 7% had quit more than 7 days ago. Slightly more than half of active smokers (53%) indicated that they were planning to quit in the next 30 days. Smokers were more likely to seek information on how to quit and on medications; former smokers were more interested in how to cope with withdrawal. All participants rated withdrawal information and individually tailored information as being more useful, while displaying little interest in telephone counseling, expert support, or peer support. Publicly available data from large search engines suggest that 4 million Americans search for resources on smoking cessation each year. Conclusions: This study adds to the limited data available on individuals who search for smoking cessation information on the Internet, supports the prior estimates of the size of the population, and indicates that these individuals are in appropriate stages for both active cessation interventions and aggressive relapse prevention efforts. Continued development and evaluation of online interventions is warranted, and organizations seeking to promote cessation should carefully evaluate the Internet as a possible modality for treatment and as a gateway to other traditional programs. C1 Massachusetts Gen Hosp, Pulm & CC Unit, Boston, MA 02114 USA. Brown Univ, Sch Med, Dept Psychiat & Human Behav, Providence, RI 02912 USA. RP Cobb, NK (reprint author), Massachusetts Gen Hosp, Pulm & CC Unit, Bul 148,55 Fruit St, Boston, MA 02114 USA. EM nkcobb@partners.org OI Cobb, Nathan/0000-0003-4210-226X FU NCI NIH HHS [R01 CA104836-03, R01 CA104836] NR 19 TC 39 Z9 39 U1 0 U2 1 PU JOURNAL MEDICAL INTERNET RESEARCH PI TORONTO PA TORONTO GENERAL HOSPITAL, R FRASER ELLIOTT BLDG, 4TH FL, R 4S435, 190 ELIZABETH ST, TORONTO, ON M5G 2C4, CANADA SN 1438-8871 J9 J MED INTERNET RES JI J. Med. Internet Res. PD JUL-SEP PY 2006 VL 8 IS 3 DI 10.2196/jmir.8.3.e17 PG 10 WC Health Care Sciences & Services; Medical Informatics SC Health Care Sciences & Services; Medical Informatics GA 103NX UT WOS:000241895100006 PM 17032633 ER PT J AU Zhang, M Michael, LH Grosjean, SA Kelly, RA Carroll, MC Entman, ML AF Zhang, Ming Michael, Lloyd H. Grosjean, Sandrine A. Kelly, Ralph A. Carroll, Michael C. Entman, Mark L. TI The role of natural IgM in myocardial ischemia-reperfusion injury SO JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY LA English DT Article DE natural antibody; complement; myocardial ischemia-reperfusion injury; infarction; apoptosis; neutrophil ID COMPLEMENT RECEPTOR TYPE-1; ADULT CARDIAC MYOCYTE; ISCHEMIA/REPERFUSION INJURY; INDUCED APOPTOSIS; SKELETAL-MUSCLE; MURINE MODEL; INFLAMMATORY RESPONSE; BINDING LECTIN; MICE DEFICIENT; HUMAN SERUM AB Myocardial ischemia-reperfusion injury represents a combination of factors, namely the intrinsic cellular response to ischemia and the extrinsic acute inflammatory response. Recent studies in mesenteric and skeletal muscle reperfusion models identified natural IgM as a major initiator of pathology through the activation of the complement system and inflammatory cells. To determine whether a similar mechanism is involved in myocardial tissues, mice bearing an altered natural IgM repertoire (Cr2(-/-)) were examined in a murine model of coronary artery ischemia. Notably, these mice were significantly protected based on the reduced infarct size, limited apoptosis of cardiomyocytes, and decreased neutrophil infiltration. Protection was IgM-dependent as reconstitution of these mice with wild-type IgM restored myocardial reperfusion injury. These results support a model in which natural IgM initiates the acute inflammatory response in the myocardium following ischemia and reperfusion. (c) 2006 Elsevier Inc. All rights reserved. C1 Baylor Coll Med, Cardiovasc Sci Sect, Methodist Hosp, Houston, TX 77030 USA. Baylor Coll Med, DeBakey Heart Ctr, Houston, TX 77030 USA. Harvard Univ, Sch Med, Dept Pathol, Boston, MA 02115 USA. Harvard Univ, Sch Med, CBR Inst Biomed Res Inc, Boston, MA 02115 USA. Brigham & Womens Hosp, Div Cardiovasc, Boston, MA 02115 USA. Genzyme Corp, Framingham, MA 01701 USA. Harvard Univ, Sch Med, Dept Pediat, Boston, MA 02115 USA. RP Entman, ML (reprint author), Baylor Coll Med, Cardiovasc Sci Sect, Methodist Hosp, Houston, TX 77030 USA. EM mentman@bcm.med.edu FU NHLBI NIH HHS [HL-42550]; NIGMS NIH HHS [P50 GM52585] NR 51 TC 39 Z9 39 U1 1 U2 6 PU ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD PI LONDON PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND SN 0022-2828 EI 1095-8584 J9 J MOL CELL CARDIOL JI J. Mol. Cell. Cardiol. PD JUL PY 2006 VL 41 IS 1 BP 62 EP 67 DI 10.1016/j.yjmcc.2006.02.006 PG 6 WC Cardiac & Cardiovascular Systems; Cell Biology SC Cardiovascular System & Cardiology; Cell Biology GA 072RK UT WOS:000239690500011 PM 16781728 ER PT J AU Lo, EH AF Lo, E. H. TI The neurovascular unit: a model for functional and dysfunctional coupling in brain SO JOURNAL OF NEUROCHEMISTRY LA English DT Meeting Abstract CT 7th Biennial Meeting of the Asian-Pacific-Society-for-Neurochemistry CY JUL 02-05, 2006 CL Singapore, SINGAPORE SP Asia Pacific Soc Neurochem C1 Harvard Univ, Sch Med, Massachusetts Gen Hosp, Dept Neurol & Radiol, Cambridge, MA 02138 USA. Harvard Univ, Sch Med, Program Neurosci, Cambridge, MA 02138 USA. 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 0022-3042 J9 J NEUROCHEM JI J. Neurochem. PD JUL PY 2006 VL 98 SU 1 BP 84 EP 84 PG 1 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA 066QQ UT WOS:000239245600189 ER PT J AU Kondo, M Melcher, C Erfurth, ML Schmucker, D AF Kondo, Masahiro Melcher, Christoph Erfurth, Maria-Luise Schmucker, Dietmar TI Function and molecular diversity of the hypervariable receptor Dscam SO JOURNAL OF NEUROGENETICS LA English DT Meeting Abstract C1 Harvard Med Sch, Dana Farber Canc Inst, Dept Neurobiol, Boston, MA 02115 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU TAYLOR & FRANCIS LTD PI ABINGDON PA 4 PARK SQUARE, MILTON PARK, ABINGDON OX14 4RN, OXON, ENGLAND SN 0167-7063 J9 J NEUROGENET JI J. Neurogenet. PD JUL-DEC PY 2006 VL 20 IS 3-4 BP 148 EP 148 PG 1 WC Genetics & Heredity; Neurosciences SC Genetics & Heredity; Neurosciences & Neurology GA 123QD UT WOS:000243309500106 ER PT J AU Park, S Gianna-Poulin, C Black, FO Wood, S Merfeld, DM AF Park, Sukyung Gianna-Poulin, Claire Black, F. Owen Wood, Scott Merfeld, Daniel M. TI Roll rotation cues influence roll tilt perception assayed using a somatosensory technique SO JOURNAL OF NEUROPHYSIOLOGY LA English DT Article ID QUALITATIVELY DIFFERENT MECHANISMS; PERCEIVED BODY POSITION; GRAVITO-INERTIAL CUES; LINEAR ACCELERATION; ECCENTRIC ROTATION; SQUIRREL-MONKEY; VESTIBULOOCULAR REFLEX; VESTIBULAR PERCEPTION; OCULOGRAVIC ILLUSION; OCULAR TORSION AB We investigated how the nervous system processes ambiguous cues from the otolith organs by measuring roll tilt perception elicited by two motion paradigms. In one paradigm ( tilt), eight subjects were sinusoidally tilted in roll with the axis of rotation near ear level. Stimulus frequencies ranged from 0.005 to 0.7 Hz, and the peak amplitude of tilt was 20. During this paradigm, subjects experienced a sinusoidal variation of interaural gravitational force with a peak of 0.34 g. The second motion paradigm ( translation) was designed to yield the same sinusoidal variation in interaural force but did not include a roll canal cue. This was achieved by sinusoidally translating the subjects along their interaural axis. For the 0.7-Hz translation trial, the subjects were simply translated from side to side. A centrifuge was used for the 0.005- to 0.5-Hz translation trials; the subjects were rotated in yaw at 250 degrees/s for 5 min before initiating sinusoidal translations yielding an interaural otolith stimulus composed of both centrifugal and radial acceleration. Using a somatosensory task to measure roll tilt perception, we found substantial differences in tilt perception during the two motion paradigms. Because the primary difference between the two motion paradigms was the presence of roll canal cues during roll tilt trials, these perceptual differences suggest that canal cues influence tilt perception. Specifically, rotational cues provided by the semicircular canals help the CNS resolve ambiguous otolith cues during head tilt, yielding more accurate tilt perception. C1 Massachusetts Eye & Ear Infirm, Jenks Vestibular Physiol Lab, Boston, MA 02114 USA. Harvard Univ, Sch Med, Dept Otol & Laryngol, Boston, MA USA. Korea Adv Inst Sci & Technol, Dept Mech Engn, Taejon, South Korea. Legacy Clin Res & Technol, Portland, OR USA. RP Merfeld, DM (reprint author), Massachusetts Eye & Ear Infirm, Jenks Vestibular Physiol Lab, Room 421,MEEI,243 Charles St, Boston, MA 02114 USA. EM dan_merfeld@meei.harvard.edu RI Park, Sukyung/C-1628-2011 FU NIDCD NIH HHS [R01 DC004158, F32 DC000205, R01 DC000205, DC-00205, DC-004158] NR 39 TC 19 Z9 19 U1 0 U2 1 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA SN 0022-3077 J9 J NEUROPHYSIOL JI J. Neurophysiol. PD JUL PY 2006 VL 96 IS 1 BP 486 EP 491 DI 10.1152/jn.01163.2005 PG 6 WC Neurosciences; Physiology SC Neurosciences & Neurology; Physiology GA 052VQ UT WOS:000238262400044 PM 16571732 ER PT J AU Bandyopadhyay, S Hartley, DM Cahill, CM Lahiri, DK Chattopadhyay, N Rogers, JT AF Bandyopadhyay, Sanghamitra Hartley, Dean M. Cahill, Catherine M. Lahiri, Debomay K. Chattopadhyay, Naibedya Rogers, Jack T. TI Interleukin-1 alpha stimulates non-amyloidogenic pathway by alpha-secretase (ADAM-10 and ADAM-17) cleavage of APP in human astrocytic cells involving p38 MAP kinase SO JOURNAL OF NEUROSCIENCE RESEARCH LA English DT Article DE inflammation; Alzheimer's disease; MAP kinase; matrix metalloproteinase; RNA interference ID NECROSIS-FACTOR-ALPHA; NF-KAPPA-B; PRECURSOR PROTEIN; ALZHEIMERS-DISEASE; BETA-PEPTIDE; PHOSPHATIDYLINOSITOL 3-KINASE; MESSENGER-RNA; ACTIVATION; EXPRESSION; NEUROINFLAMMATION AB Interleukin-1 alpha (IL-1 alpha) stimulates a disintegrin and metalloproteinase, ADAM-17 synthesis, consistent with activation of the soluble fragment of Amyloid Precursor Protein, APP, (sAPP alpha) in human primary astrocytes. To characterize the mechanism by which IL-1 alpha promotes the non-amyloiclogenic pathway of APP metabolism, we used U373 MG astrocytoma cells. IL-alpha significantly increased levels of ADAM-10 and ADAM-17 mRNA in 16 hr. Upregulation of ADAM-17 mRNA by IL-1 alpha was more pronounced despite higher basal levels of ADAM-10 mRNA. This pattern was also observed at the protein level with the upregulation of a-secretase. RNA interference (RNAi) of ADAM-10 and ADAM-17 inhibited IL-1 alpha-stimulated sAPP alpha release and the effect was more pronounced with ADAM-17 RNAi. Concomitantly, the level of sAPP alpha was significantly increased by IL-1 alpha in 48 hr; however, IL-1 alpha stimulated cell-associated APP levels maximally at 6 h but the induction declined at 48 hr. IL-1 alpha treatment of cells for 48 h reduced both intracellular and secreted levels of amyloid-beta, A beta-40, and A beta-42 peptides. Multiple MAP kinases (MAPK), including MEK/ERK, p38 kinase, PI3 kinase (PI3K) but not JNK were involved in the regulation of IL-1 alpha-stimulated alpha-secretase activity and sAPP alpha release. p38 MAPK seems to be the most proximal of these MAPKs, as it was the earliest to be activated by IL-1 alpha and blocking this pathway attenuated activation of IL-1 alpha-induced MEK and PI3K pathways. Our data show a complex mechanism of sAPP alpha regulation by IL-1 alpha that involves ADAM-10, ADAM-17 and p38 MAPK upstream of MEK and PI3K. (c) 2006 Wiley-Liss, Inc. C1 Harvard Univ, Dept Psychiat & Genet, Neurochem Lab, Massachusetts Gen Hosp,Med Sch, Charlestown, MA 02129 USA. Harvard Univ, Aging Res Unit, Neurochem Lab, Massachusetts Gen Hosp,Med Sch, Charlestown, MA 02129 USA. Harvard Univ, Sch Med, Brigham & Womens Hosp, Dept Neurol, Boston, MA 02115 USA. Harvard Univ, Sch Med, Beth Israel Deaconess Med Ctr, Dept Surg, Boston, MA 02115 USA. Indiana Univ, Inst Psychiat Res, Indianapolis, IN 46204 USA. Harvard Univ, Sch Med, Brigham & Womens Hosp, Dept Med,Div Endocrinol Diabet & Hypertens, Boston, MA 02115 USA. RP Rogers, JT (reprint author), Harvard Univ, Dept Psychiat & Genet, Neurochem Lab, Massachusetts Gen Hosp,Med Sch, Charlestown, MA 02129 USA. EM jtrogers@rics.bwh.harvard.edu OI Bandyopadhyay, Sanghamitra /0000-0002-1490-3599; Chattopadhyay, Naibedya/0000-0003-2473-0246 FU NIA NIH HHS [R01 AG18884, R01 AG20181] NR 37 TC 42 Z9 43 U1 0 U2 2 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 0360-4012 J9 J NEUROSCI RES JI J. Neurosci. Res. PD JUL PY 2006 VL 84 IS 1 BP 106 EP 118 DI 10.1002/jnr.20864 PG 13 WC Neurosciences SC Neurosciences & Neurology GA 061UD UT WOS:000238897400010 PM 16724341 ER PT J AU Ran, QT Gu, MJ Van Remmen, H Strong, R Roberts, JL Richardson, A AF Ran, Qitao Gu, Mingjun Van Remmen, Holly Strong, Randy Roberts, James L. Richardson, Arlan TI Glutathione peroxidase 4 protects cortical neurons from oxidative injury and amyloid toxicity SO JOURNAL OF NEUROSCIENCE RESEARCH LA English DT Article DE Gpx4; oxidative stress; cortical neurons; beta-amyloid ID MEMBRANE LIPID-PEROXIDATION; BETA-PEPTIDE; A-BETA; NEURODEGENERATIVE DISORDERS; ALDEHYDIC PRODUCT; HYDROGEN-PEROXIDE; INDUCED APOPTOSIS; CYTOCHROME-C; CELL-DEATH; HYDROPEROXIDE AB Polyunsaturated fatty acids (PUFA) in membrane lipids are prone to attack by reactive oxygen species (ROS), and the resulting lipid peroxidation can cause injury and death of cells. Glutathione peroxidase 4 (Gpx4) is an antioxidant defense enzyme that can directly detoxify lipid hydroperoxides generated by ROS. Overexpression of Gpx4 has been shown to be protective against oxidative damage in several cell lines. We examined in this study the stress response of neurons with increased expression of Gpx4, because neurons are especially vulnerable to oxidative injury as a result of their high content of PUFA. Our results show that primary culture cortical neurons derived from Gpx4 transgenic mice, which had increased expression of Gpx4, had increased cell survival and reduced level of apoptosis after exposure to t-butyl hydroperoxide and hydrogen peroxide. We also studied the protective role of Gpx4 against P-amyloid toxicity, because P-amyloid-induced neural toxicity is believed to be mediated through lipid peroxidation. Primary culture cortical neurons from Gpx4 transgenic mice had significantly less cell toxicity than their wildtype counterparts after exposure to A beta(25-35) and A beta(1-40) peptides, and apoptosis induced by A beta(25-35) was attenuated in neurons from Gpx4 transgenic mice. Our data demonstrate that overexpression of Gpx4 protects neurons against oxidative injury and P-amyloid-induced cytotoxicity. (c) 2006 Wiley-Liss, Inc. C1 Univ Texas, Hlth Sci Ctr San Antonio, Dept Cellular & Struct Biol, San Antonio, TX 78229 USA. Univ Texas, Hlth Sci Ctr San Antonio, 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. Univ Texas, Hlth Sci Ctr San Antonio, Dept Pharmacol, San Antonio, TX 78229 USA. RP Ran, QT (reprint author), Univ Texas, Hlth Sci Ctr San Antonio, Dept Cellular & Struct Biol, 7703 Floyd Curl Dr, San Antonio, TX 78229 USA. EM ran@uthscsa.edu FU NIA NIH HHS [K01 AG22014] NR 45 TC 43 Z9 47 U1 2 U2 3 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 0360-4012 J9 J NEUROSCI RES JI J. Neurosci. Res. PD JUL PY 2006 VL 84 IS 1 BP 202 EP 208 DI 10.1002/jnr.20868 PG 7 WC Neurosciences SC Neurosciences & Neurology GA 061UD UT WOS:000238897400018 PM 16673405 ER PT J AU Yaffe, K Blackwell, T Whitmer, RA Krueger, K Barrett-Connor, E AF Yaffe, K. Blackwell, T. Whitmer, R. A. Krueger, K. Barrett-Connor, E. TI Glycosylated hemoglobin level and development of mild cognitive impairment or dementia in older women SO JOURNAL OF NUTRITION HEALTH & AGING LA English DT Article DE dementia; diabetes; mild cognitive impairment; glucose ID INSULIN-DEGRADING ENZYME; ALZHEIMERS-DISEASE; ELDERLY POPULATION; GLUCOSE-TOLERANCE; RISK-FACTORS; MEN; PERFORMANCE; DECLINE; HEALTH; ADULTS AB Background: Biological mechanisms linking diabetes and cognition continue to grow, yet the association remains controversial in elders. Whether glycosylated hemoglobin (HbA(1c)) level, a marker of glucose control, is predictive of the development of cognitive impairment or dementia is unknown. We determined the association between HbA(1c) level and risk of developing cognitive impairment in older women, mostly without diabetes. Methods: We studied 1983 postmenopausal women (mean age, 67.2 years) with osteoporosis who had HbA(1c) level measured at baseline. Development of mild cognitive impairment (MCI) or dementia over 4 years was determined as part of a dementia ancillary study. We analyzed risk of MCI or dementia for every 1% of HbA(1c) as well as risk associated with HbA(1c) >= 7%. Results: The mean level of HbA(1c) was 5.8% (range 3.0% to 12.1%) and 86 (4.3%) women developed MCI or dementia. For every 1% increase in HbA(1c), women had a greater age-adjusted likelihood of developing MCI (OR= 1.50; 95% Cl 1.14-1.97) and of developing MCI or dementia (OR=1.40; 95% Cl 1.08 - 1.83). For those with HbA(1c) level >= 7% (n=49), the age-adjusted risk for developing MCI was increased nearly 4-fold (OR= 3.70; 95% Cl 1.51-9.09) and was increased nearly 3-fold for developing MCI or dementia (OR=2.86; 95% Cl 1.17-6.98). When we excluded women with diagnosed diabetes (n=53), the association between HbA(1c) and MCI lessened somewhat but remained elevated (unadjusted OR=1.59; 95% Cl 1.01-2.50; age-adjusted OR=1.42; 95% Cl 0.89-2.28). Multivariate analyses adjusted for age, education, race, depression, alcohol use and treatment with raloxifene yielded similar results. Interpretation: We found an association between HbA(1c) level and risk of developing MCI or dementia in postmenopausal osteoporotic women primarily without diabetes. Our findings support the hypothesis that glucose dysregulation is a predictor for cognitive impairment. C1 Univ Calif San Francisco, Dept Psychiat, San Francisco, CA 94121 USA. Univ Calif San Francisco, Dept Neurol, San Francisco, CA 94121 USA. Univ Calif San Francisco, Dept Epidemiol, San Francisco, CA 94121 USA. San Francisco VA Med Ctr, San Francisco, CA USA. Calif Pacific Med Ctr, San Francisco, CA 94115 USA. Kaiser Permanente, Div Res, Oakland, CA 94612 USA. Eli Lilly & Co, Lilly Res Labs, Indianapolis, IN 46285 USA. Univ Calif San Diego, Dept Family & Prevent Med, San Diego, CA 92103 USA. RP Yaffe, K (reprint author), Univ Calif San Francisco, Dept Psychiat, Box 181,4150 Clement St, San Francisco, CA 94121 USA. EM Kristine.Yaffe@ucsf.edu NR 26 TC 11 Z9 11 U1 1 U2 4 PU SERDI EDITION PI PARIS PA 320 RUE SAINT-HONORE, PARIS, 75001, FRANCE SN 1279-7707 J9 J NUTR HEALTH AGING JI J. Nutr. Health Aging PD JUL-AUG PY 2006 VL 10 IS 4 BP 292 EP 295 PG 4 WC Geriatrics & Gerontology; Nutrition & Dietetics SC Geriatrics & Gerontology; Nutrition & Dietetics GA 080NX UT WOS:000240255700010 ER PT J AU Doornberg, JN Ring, D Jupiter, JB AF Doornberg, Job N. Ring, David Jupiter, Jesse B. TI Static progressive splinting for posttraumatic elbow stiffness SO JOURNAL OF ORTHOPAEDIC TRAUMA LA English DT Article DE elbow; trauma; posttraurnatic elbow stiffness; treatment; splinting ID OPERATIVE RELEASE; ARTHROSCOPIC TREATMENT; SURGICAL-TREATMENT; LATERAL APPROACH; CONTRACTURE; ARTHROPLASTY; TRAUMA; MOTION; JOINT; ARTHROLYSIS AB Objectives: To determine the value of static progressive splinting in helping patients with posttraumatic elbow stiffness regain functional motion and avoid operative treatment for stiffness. Design: Retrospective case series. Setting: Level I Trauma Center. Patients and Intervention: Over a 3-year period, 29 consecutive patients with elbow stiffness after trauma (flexion contracture greater than 30 degrees or flexion less than 130 degrees) were treated with static progressive elbow splinting when a standard exercise program was no longer achieving gains in motion. Three patients were treated after the injury alone; 14 were treated after operative treatment of the initial injury, and 12 after a secondary operative contracture release for posttraumatic stiffness. Splinting was initiated on an average of 55 days (range, 15 to 200 d) after injury or operative treatment. Main Outcome Measurements: Ulnohumeral range of motion before and after splint treatment. Results: The flexion are improved from 71 degrees (range, 0 to 100 degrees) before splinting to 112 degrees (range, 20 to 150 degrees) after splinting. After splinting, 3 patients had a flexion contracture greater than 30 degrees and 10 patients (34%) had fewer than 130 degrees of flexion. Only 3 patients-2 with heterotopic bone and I with an associated ulnar neuropathy-requested an operation to address elbow stiffness. Patients who were splinted after the initial injury (n = 17, average improvement(fl-ext) = 51 37 degrees) regained greater motion during splint wear than patients treated after elbow capsulectomy (n = 12, average improvement(fl-ext) = 22 +/- 24 degrees). Conclusions: Static progressive splinting can help gain additional motion when standard exercises seem stagnant or inadequate particularly after the original injury. Operative treatment of stiffness was avoided in most patients. C1 Harvard Univ, Dept Orthopaed Surg, Yawkey Ctr, Massachusetts Gen Hosp,Sch Med,Orthopaed Hand & U, Boston, MA 02114 USA. Univ Amsterdam, Acad Med Ctr, Orthotrauma Res Ctr Amsterdam, NL-1105 AZ Amsterdam, Netherlands. RP Ring, D (reprint author), Harvard Univ, Dept Orthopaed Surg, Yawkey Ctr, Massachusetts Gen Hosp,Sch Med,Orthopaed Hand & U, Suite 2100, Boston, MA 02114 USA. EM dring@partners.org NR 41 TC 26 Z9 31 U1 1 U2 5 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0890-5339 J9 J ORTHOP TRAUMA JI J. Orthop. Trauma PD JUL PY 2006 VL 20 IS 6 BP 400 EP 404 DI 10.1097/00005131-200607000-00006 PG 5 WC Orthopedics; Sport Sciences SC Orthopedics; Sport Sciences GA 064TD UT WOS:000239111100006 PM 16825965 ER PT J AU Borens, O Sen, MK Huang, RC Richmond, J Kloen, P Jupiter, JB Helfet, DL AF Borens, Olivier Sen, Milan K. Huang, Russel C. Richmond, Jeffrey Kloen, Peter Jupiter, Jesse B. Helfet, David L. TI Anterior tension band plating for anterior tibial stress fractures in high-performance female athletes - A report of 4 cases SO JOURNAL OF ORTHOPAEDIC TRAUMA LA English DT Article DE tibial shaft fracture; stress fracture; tension band plating; athlete ID LONG-BONE FRACTURES; SHOCK-WAVE THERAPY; DELAYED UNION; NONUNIONS AB Stress fracture of the anterior tibial cortex is an extremely challenging fracture to treat, especially in the high-performance female athlete who requires rapid return to competition. Previous reports have not addressed treating these fractures in the world-class athlete with anterior plating. We hypothesize that anterior plating is a biomechanically sound approach to treatment of these fractures, and will lead to an earlier return to full activity than either nonoperative treatment or intramedullary nailing. We present a retrospective series of 4 case reports of 4 world-class female athletes with stress fractures of the anterior tibial cortex treated by anterior plating between 2001 and 2004. Average follow-up was 15 months (range 12 to 48 mo). Anterior tension band plating resulted in fracture healing in all 4 cases and return to full activity at a mean of 10 weeks. All patients returned to preinjury competitive levels. There were no complications of infection, nonunion, or malunion. Anterior tension-band plating of an anterior tibial stress fracture leads to rapid fracture healing and return to competition for high-performance female athletes. This approach should be considered in those athletes who wish to avoid the more prolonged convalescence associated with nonoperative treatment, or the problems, especially of the knee, associated with intramedullary nailing. C1 Hosp Special Surg, New York, NY 10021 USA. Netherlands Acad Med Ctr, NL-1100 DD Amsterdam, Netherlands. Massachusetts Gen Hosp, Boston, MA 02114 USA. RP Helfet, DL (reprint author), Hosp Special Surg, 535 E 70th St, New York, NY 10021 USA. EM helfetd@hss.edu NR 28 TC 15 Z9 16 U1 0 U2 1 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0890-5339 J9 J ORTHOP TRAUMA JI J. Orthop. Trauma PD JUL PY 2006 VL 20 IS 6 BP 425 EP 430 DI 10.1097/00005131-200607000-00011 PG 6 WC Orthopedics; Sport Sciences SC Orthopedics; Sport Sciences GA 064TD UT WOS:000239111100011 PM 16825970 ER PT J AU Bhattacharyya, T Michelson, J AF Bhattacharyya, Timothy Michelson, James TI Ankle fracture - Opinion: Open reduction and internal fixation SO JOURNAL OF ORTHOPAEDIC TRAUMA LA English DT Editorial Material ID CLOSED TREATMENT; SUPINATION; MANAGEMENT; BEARING; MOTION; BRACE; CAST C1 Massachusetts Gen Hosp, Orthopaed Associates, Boston, MA 02114 USA. RP Bhattacharyya, T (reprint author), Massachusetts Gen Hosp, Orthopaed Associates, 55 Fruit St,YAW 3C, Boston, MA 02114 USA. NR 18 TC 1 Z9 2 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0890-5339 J9 J ORTHOP TRAUMA JI J. Orthop. Trauma PD JUL PY 2006 VL 20 IS 7 BP 512 EP 514 DI 10.1097/00005131-200608000-00011 PG 3 WC Orthopedics; Sport Sciences SC Orthopedics; Sport Sciences GA 073LI UT WOS:000239744000011 PM 16891945 ER PT J AU Rossi, S Ou, W Tang, D Bhattacharya, N Dei Tos, AP Fletcher, JA Loda, M AF Rossi, S. Ou, W. Tang, D. Bhattacharya, N. Dei Tos, A. P. Fletcher, J. A. Loda, M. TI Gastrointestinal stromal turnours overexpress fatty acid synthase SO JOURNAL OF PATHOLOGY LA English DT Article DE fatty acid synthase; gastrointestinal stromal tumour; tissue microarray; proliferation; siRNA ID C-KIT; CELL-PROLIFERATION; PROSTATE-CANCER; POLY(ADP-RIBOSE) POLYMERASE; ACQUIRED-RESISTANCE; PROGNOSTIC VALUE; TUMORS; EXPRESSION; IMATINIB; MUTATION AB Fatty acid synthase (FASN), a key enzyme for de novo lipogenesis, is overexpressed in many malignant tumours and is associated with aggressive biological behaviour. FASN expression and its possible relationship with more aggressive behaviour in gastrointestinal stromal tumours (GISTs) have not been addressed to date. Here, FASN expression was assessed by immunohistochemistry in 60 primary GISTs (28 low/intermediate risk and 32 high risk) and seven metastatic GISTs. Sixteen smooth muscle gastrointestinal tumours were used as controls. FASN was overexpressed in 36 of 60 GISTs (60%): in 12 of 28 (42%) low/intermediate-risk GISTs and in 24 of 32 (75%) high-risk GISTs (p < 0.05). Two primary and seven metastatic GISTs and five GIST cell lines (GIST882, GIST430, GIST522, GIST62, and GIST48), analysed by western blot, showed variable FASN expression. Most metastatic samples expressed high levels of FASN protein. Additionally, seven of 60 GISTs showed a proliferation rate higher than 10% by Ki67 and all of them expressed FASN (p < 0.04). Finally, proliferation and apoptosis were investigated after FASN silencing in, GIST882 cells, which displayed the highest FASN expression. siRNA-mediated FASN knock-down inhibited expression of the proliferation marker cyclin A, whereas no changes in p27 and cleaved PARP expression were seen. It is concluded that FASN is preferentially overexpressed in high-risk and metastatic GISTs, and that its overexpression likely contributes to cell proliferation. Copyright (c) 2006 Pathological Society of Great Britain and Ireland. C1 Reg Hosp Treviso, Dept Pathol, Treviso, Italy. Harvard Univ, Sch Med, Brigham & Womens Hosp, Dept Med Oncol,Dana Farber Canc Inst, Boston, MA 02115 USA. RP Dei Tos, AP (reprint author), Reg Hosp Treviso, Dept Pathol, Treviso, Italy. EM apdeitos@ulss.tv.it OI Rossi, Sabrina/0000-0001-9122-1308 FU NCI NIH HHS [P01-CA89021, P50CA90381] NR 45 TC 27 Z9 29 U1 2 U2 3 PU JOHN WILEY & SONS LTD PI CHICHESTER PA THE ATRIUM, SOUTHERN GATE, CHICHESTER PO19 8SQ, W SUSSEX, ENGLAND SN 0022-3417 J9 J PATHOL JI J. Pathol. PD JUL PY 2006 VL 209 IS 3 BP 369 EP 375 DI 10.1002/path.1983 PG 7 WC Oncology; Pathology SC Oncology; Pathology GA 061MJ UT WOS:000238876300011 PM 16583360 ER PT J AU Gupta, G Walton, DS AF Gupta, Gaurav Walton, David S. TI Infantile glaucoma associated with cranio-cerebello-cardiac syndrome SO JOURNAL OF PEDIATRIC OPHTHALMOLOGY & STRABISMUS LA English DT Editorial Material ID 3C SYNDROME AB We report the second case of infantile glaucoma associated with cranio-cerebello-cardiac (3C) syndrome. An infant with systemic features consistent with 3C syndrome presented with glaucoma and underwent a goniotomy for each eye. Patients with 3C syndrome should be evaluated for glaucoma. C1 Rhode Isl Hosp, Brown Med Sch, Providence, RI USA. Harvard Univ, Sch Med, Massachusetts Eye & Ear Infirm, Boston, MA USA. RP Gupta, G (reprint author), Dept Ophthalmol, 593 Eddy St,APC 7th Floor, Providence, RI 02903 USA. NR 3 TC 1 Z9 1 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0191-3913 J9 J PEDIAT OPHTH STRAB JI J. Pediatr. Ophthalmol. Strabismus. PD JUL-AUG PY 2006 VL 43 IS 4 BP 244 EP 245 PG 2 WC Ophthalmology; Pediatrics SC Ophthalmology; Pediatrics GA 067HW UT WOS:000239293500014 PM 16915906 ER PT J AU Wilens, TE Newcorn, JH Kratochvil, CJ Gao, H Thomason, CK Rogers, AK Feldman, PD Levine, LR AF Wilens, Timothy E. Newcorn, Jeffrey H. Kratochvil, Christopher J. Gao, Haitao Thomason, Christine K. Rogers, Ann K. Feldman, Peter D. Levine, Louise R. TI Long-term atomoxetine treatment in adolescents with attention-deficit/hyperactivity disorder SO JOURNAL OF PEDIATRICS LA English DT Article ID DEFICIT-HYPERACTIVITY DISORDER; HEALTH MULTIMODAL TREATMENT; DAILY OROS METHYLPHENIDATE; OPEN-LABEL; GROWTH DEFICITS; ADHD TREATMENT; DOUBLE-BLIND; CHILDREN; SAMPLE; RELIABILITY AB Objective: To determine the efficacy and safety of atomoxetine in adolescent subjects treated for attention-deficit/hyperactivity, disorder (ADHD) for up to 2 years. Study design: Data from 13 atomoxetine studies (6 double-blind, 7 open-label) were pooled for subjects age 12 to 18 with ADHD as defined by the American Psychiatric Association's Diagnostic and Statistical Manual of Mental Disorders IV. Results: Of the 601 atomoxetine-treated subjects in this meta-and-lysis, 537 (89.4%) completed 3 months of acute treatment. A total of 259 subjects (48.4%) are continuing atomoxetine treatment; 219 of these subjects have completed at least 2 years of treatment. The mean dose of atomoxetine at endpoint was 1.41 mg/kg/day. Mean ADHD Rating Scale IV, parent version, investigator-administered and -scored total scores showed significant improvement (P < .001) over the first 3 months. Symptoms remained improved up to 24 months without dosage escalation. During the 2-year treatment period, 99 (16.5%) subjects discontinued treatment due to lack of effectiveness, and 31 (5.2%) subjects discontinued treatment due to adverse events. No clinically significant abnormalities in height, weight, blood pressure, pulse, mean laboratory values, or electrocardiography parameters were found. Conclusions: Two-year data from this ongoing study indicate that atomoxetine maintains efficacy among adolescents with ADHD, with no evidence of drug tolerance and no new or unexpected safety concerns. C1 Massachusetts Gen Hosp, Dept Psychiat, Yawkey Ctr Outpatient Care, Boston, MA 02114 USA. Mt Sinai Med Ctr, Dept Psychiat, New York, NY 10029 USA. Univ Nebraska, Med Ctr, Dept Psychiat, Omaha, NE USA. Eli Lilly & Co, Lilly Res Labs, Indianapolis, IN 46285 USA. RP Wilens, TE (reprint author), Massachusetts Gen Hosp, Dept Psychiat, Yawkey Ctr Outpatient Care, 32 Fruit St, Boston, MA 02114 USA. EM twilens@partners.org OI Newcorn, Jeffrey /0000-0001-8993-9337 NR 41 TC 58 Z9 61 U1 1 U2 3 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 JUL PY 2006 VL 149 IS 1 BP 112 EP 119 DI 10.1016/j.jpeds.2006.01.052 PG 8 WC Pediatrics SC Pediatrics GA 068DI UT WOS:000239352000028 PM 16860138 ER PT J AU Ungar, D Joffe, S Kodish, E AF Ungar, David Joffe, Steven Kodish, Eric TI Children are not small adults: Documentation of assent for research involving children SO JOURNAL OF PEDIATRICS LA English DT Article; Proceedings Paper CT Conference on Current Controversies in Pediatric Research Ethics CY JUL 22-23, 2005 CL Seattle, WA SP Ctr Pediat Bioethics Childrens Hosp & Reg Med Ctr ID INFORMED CONSENT FORMS; CLINICAL ANESTHESIA; SURGERY RESEARCH; UNDERSTAND; TRIALS AB Obtaining assent is an important part of research involving children, both from an ethical and regulatory perspective. Current practice for documenting assent is derived largely from documentation of informed consent for adults as there is little guidance in federal regulations. We propose a new approach to documenting assent. C1 Penn State Childrens Hosp, Div Pediat Hematol Oncol, Hershey, PA 17033 USA. Dana Farber Canc Inst, Dept Pediat Oncol, Boston, MA 02115 USA. Cleveland Clin Fdn, Dept Bioeth, Lerner Coll Med Case, Cleveland, OH 44195 USA. RP Ungar, D (reprint author), Penn State Childrens Hosp, Div Pediat Hematol Oncol, MC085, Hershey, PA 17033 USA. EM dungar@psu.edu OI Joffe, Steven/0000-0002-0667-7384 NR 14 TC 27 Z9 29 U1 0 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 JUL PY 2006 VL 149 IS 1 SU S BP S31 EP S33 DI 10.1016/j.jpeds.2006.04.048 PG 3 WC Pediatrics SC Pediatrics GA 069HW UT WOS:000239438000007 PM 16829240 ER PT J AU Garrett, N Roumanas, ED Blackwell, KE Freymiller, E Abemayor, E Wong, WK Gerratt, B Berke, G Beumer, J Kapur, KK AF Garrett, Neal Roumanas, Eleni D. Blackwell, Keith E. Freymiller, Earl Abemayor, Elliot Wong, Weng Kee Gerratt, Bruce Berke, Gerald Beumer, John, III Kapur, Krishan K. TI Efficacy of conventional and implant-supported mandibular resection prostheses: Study overview and treatment outcomes SO JOURNAL OF PROSTHETIC DENTISTRY LA English DT Article; Proceedings Paper CT 6th Meeting of the International-Society-for-Maxillofacial-Rehabilitation CY JUN, 2004 CL Maastricht, NETHERLANDS SP Int Soc Maxillofacial Rehabilitat ID FOREARM FLAP RECONSTRUCTION; COOPERATIVE-DENTAL-IMPLANT; REMOVABLE PARTIAL DENTURES; POORLY FITTING DENTURES; BLADE-VENT IMPLANTS; MASTICATORY FUNCTION; OROMANDIBULAR RECONSTRUCTION; OSSEOINTEGRATED IMPLANTS; DIABETIC-PATIENTS; PRIMARY CLOSURE AB Statement of problem. While surgical restoration of mandibular resections has advanced dramatically with free-flap techniques, oral function and patient perceptions of function, as well as treatment outcomes, often indicate significant impairment. Purpose. This longitudinal prospective study was designed to determine whether conventional prostheses (CP) or implant-supported prostheses (IP) and current surgical reconstructive procedures restore patients' oral functions and quality of life to their status prior to segmental mandibulectomy with immediate fibula free-flap reconstruction. Study, design and implementation, characteristics of the study sample, treatment completion rates, and selected presurgical and postsurgical functional and perceptual outcomes are presented. Material and methods. Forty-six subjects were enrolled. Longitudinal evaluations of medical and dental histories, oromaxillofacial examinations, questionnaires, and sensory and functional tests were planned before and after surgery and after CP and IP treatment. Sample characteristics are described with descriptive statistics and comparisons of subject responses to questionnaire items at entry and postsurgical intervals were made with Fisher exact tests (alpha = .05). Results. Conventional prostheses were completed in 33 of 46 subjects, and 16 of 33 CP subjects were treated with IP. Reasons for noncompletion of IP were recurrent/metastatic disease (16), refusal of implant therapy (7), lost to follow-up (4), treatment with a reconstruction plate (1), excessive radiation at implant sites (1), and death (1). AD 16 recurrences/metastases occurred within 13 months of surgery. Only 3 of the 58 implants placed in 17 participants were considered failures. One failed due to lack of integration 31 weeks following placement, and 2 were buried due to unacceptable positioning for prosthetic restoration during denture fabrication. The remaining 55 implants were successful at final evaluation, ranging from 58 to 123 weeks following implant placement (mean duration = 78.9 +/- 16.0 weeks). Conclusions. While 72% (33/46) of the subjects enrolled were able and willing to complete treatment with CP, only 35% (16/46) completed IP treatment. Careful consideration must be given to selection of the type of prosthetic rehabilitation and the timing of implant placement if an IP is planned. C1 Univ Calif Los Angeles, Sch Dent, Jane & Jerry Weintraub Ctr Reconstruct Biotechnol, Div Adv Prosthodont Biomat & Hosp Dent, Los Angeles, CA 90095 USA. Univ Calif Los Angeles, David Geffen Sch Med, Div Head & Neck Surg, Los Angeles, CA 90024 USA. Univ Calif Los Angeles, Sch Publ Hlth, Dept Biostat, Los Angeles, CA 90024 USA. Vet Adm Greater Los Angeles Healthcare Syst, Dent Res Lab, Los Angeles, CA USA. Univ Calif Los Angeles, Sch Dent, Div Diagnost & Surg Sci, Los Angeles, CA 90024 USA. Univ Calif Los Angeles, Sch Dent, Sect Oral & Maxillofacial Surg, Los Angeles, CA 90024 USA. RP Garrett, N (reprint author), Univ Calif Los Angeles, Sch Dent, Jane & Jerry Weintraub Ctr Reconstruct Biotechnol, Div Adv Prosthodont Biomat & Hosp Dent, 10833 Le Conte Ave,B3-087 CHS, Los Angeles, CA 90095 USA. EM ngarrett@ucla.edu OI Gerratt, Bruce/0000-0001-7032-1051 FU NCRR NIH HHS [C06 RR 14529-01]; NIDCR NIH HHS [1R01 DE 11255] NR 59 TC 54 Z9 54 U1 0 U2 4 PU MOSBY, INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 USA SN 0022-3913 J9 J PROSTHET DENT JI J. Prosthet. Dent. PD JUL PY 2006 VL 96 IS 1 BP 13 EP 24 DI 10.1016/j.prosdent.2006.05.010 PG 12 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA 070CW UT WOS:000239498900003 PM 16872926 ER PT J AU Sachs, G Sanchez, R Marcus, R Stock, E McQuade, R Carson, W Abou-Gharbia, N Impellizzeri, C Kaplita, S Rollin, L Iwamoto, T AF Sachs, Gary Sanchez, Raymond Marcus, Ronald Stock, Elyse McQuade, Robert Carson, William Abou-Gharbia, Neveen Impellizzeri, Cheryl Kaplita, Stephen Rollin, Linda Iwamoto, Taro CA Aripiprazote Study Grp TI Aripiprazole in the treatment of acute manic or mixed episodes in patients with bipolar I disorder: a 3-week placebo-controlled study SO JOURNAL OF PSYCHOPHARMACOLOGY LA English DT Article DE aripiprazole; bipolar I disorder; efficacy; safety ID DOUBLE-BLIND; SCHIZOAFFECTIVE DISORDER; VS. HALOPERIDOL; PARTIAL AGONIST; RATING-SCALE; SCHIZOPHRENIA; EFFICACY; SAFETY; OLANZAPINE; DEPRESSION AB This study compares the efficacy, safety, and tolerability of a partial dopamine agonist, aripiprazole, with placebo in the treatment of patients with bipolar I disorder experiencing an acute manic or mixed episode. In total, 272 hospitalized patients were randomized to aripiprazole 30mg/day or placebo in this 3-week, double-blind, placebo-controlled trial. Dosing could be reduced to 15 mg/day for tolerability and, subsequently, increased to 30mg/day based on clinical response. Primary efficacy measure was mean change from baseline to endpoint in Young Mania Rating Scale (YMRS) total score; response was defined as >= 50% decrease from baseline YMRS score. Adpiprazole-treated patients demonstrated significantly greater improvement from baseline to endpoint in mean YMRS total scores compared with placebo-treated patients as early as Day 4 and sustained through Week 3. A significantly higher response rate was observed in aripiprazole-treated patients (53% vs. 32% at endpoint). Aripiprazote produced significantly greater improvements from baseline on other efficacy assessments compared with placebo, including Clinical Global Impression - Bipolar Version Severity and Improvement scores. The 30mg/day dose was maintained by 85% of aripiprazole-treated patients. Incidence of discontinuations due to adverse events was similar for aripiprazole (8.8%) and placebo (7.5%). Aripiprazote treatment resulted in no significant difference from placebo in change in mean body weight and was not associated with elevated serum prolactin or QT(c) prolongation. In conclusion, aripiprazole demonstrated superior efficacy to placebo in the treatment of patients with bipolar I disorder presenting with acute manic or mixed episodes, and exhibited a favourable safety and tolerability profile. C1 Massachusetts Gen Hosp, Dept Psychiat, Bipolar Res Program, Boston, MA 02114 USA. Bristol Myers Squibb Co, Wallingford, CT 06492 USA. Otsuka Amer Pharmaceut Inc, Princeton, NJ USA. Bristol Myers Squibb Co, Princeton, NJ 08543 USA. Otsuka Pharmaceut Co Ltd, Chiyoda Ku, Tokyo, Japan. RP Sachs, G (reprint author), Massachusetts Gen Hosp, Dept Psychiat, Bipolar Res Program, 50 Staniford St,Suite 580, Boston, MA 02114 USA. EM SachsG@aol.com NR 38 TC 161 Z9 165 U1 1 U2 3 PU SAGE PUBLICATIONS LTD PI LONDON PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND SN 0269-8811 J9 J PSYCHOPHARMACOL JI J. Psychopharmacol. PD JUL PY 2006 VL 20 IS 4 BP 536 EP 546 DI 10.1177/0269881106059693 PG 11 WC Clinical Neurology; Neurosciences; Pharmacology & Pharmacy; Psychiatry SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry GA 064WV UT WOS:000239122300008 PM 16401666 ER PT J AU Wilens, TE Biederman, J AF Wilens, Timothy E. Biederman, Joseph TI Alcohol, drugs, and attention-deficit/hyperactivity disorder: a model for the study of addictions in youth SO JOURNAL OF PSYCHOPHARMACOLOGY LA English DT Review DE alcohol abuse; ADHD; drugs ID DEFICIT-HYPERACTIVITY DISORDER; SUBSTANCE USE DISORDERS; RANDOMIZED CONTROLLED-TRIAL; FOLLOW-UP; MATERNAL SMOKING; CONDUCT DISORDER; PSYCHIATRIC COMORBIDITY; DEPENDENT DELINQUENTS; CIGARETTE-SMOKING; RESEARCH CRITERIA AB There has been increasing interest in the developmental origins of substance use disorders (SUDs) in children and adolescents. Because of its early onset, high prevalence and known risk for SUD, attention deficit hyperactivity disorder (ADHD) is a model developmental disorder to evaluate in context to SUDs. A selected review of the literature was undertaken examining ADHD as an antecedent disorder to subsequent SUD. AND and its co-occurring comorbid psychopathology increase the risk for cigarette smoking and SUD and is associated with greater SUD severity and chronicity. The treatment of ADHD appears to decrease the risk for cigarette smoking and SUD. ADHD is an important antecedent disorder in children and adolescents worthy of further targeted preventive efforts to diminish the risk for cigarette smoking and SUD. C1 Massachusetts Gen Hosp, Yawkey Ctr Outpatient Care, Clin Res Program Pediat Psychopharmacol, Boston, MA 02114 USA. Harvard Univ, Sch Med, Boston, MA 02115 USA. RP Wilens, TE (reprint author), Massachusetts Gen Hosp, Yawkey Ctr Outpatient Care, Clin Res Program Pediat Psychopharmacol, YAW CA, Boston, MA 02114 USA. EM twilens@partners.org FU NIDA NIH HHS [DA14419, DA016264] NR 103 TC 52 Z9 52 U1 3 U2 18 PU SAGE PUBLICATIONS LTD PI LONDON PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND SN 0269-8811 J9 J PSYCHOPHARMACOL JI J. Psychopharmacol. PD JUL PY 2006 VL 20 IS 4 BP 580 EP 588 DI 10.1177/0269881105058776 PG 9 WC Clinical Neurology; Neurosciences; Pharmacology & Pharmacy; Psychiatry SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry GA 064WV UT WOS:000239122300014 PM 16174669 ER PT J AU Liu, GJ Huang, WD Moir, RD Vanderburg, CR Lai, B Peng, ZC Tanzi, RE Rogers, JT Huang, XD AF Liu, GJ Huang, WD Moir, RD Vanderburg, CR Lai, B Peng, ZC Tanzi, RE Rogers, JT Huang, XD TI Metal exposure and Alzheimer's pathogenesis SO JOURNAL OF STRUCTURAL BIOLOGY LA English DT Review DE metal; Alzheimer's disease; amyloid precursor protein; A beta amyloidosis; laser capture microdissection; X-ray fluorescence microscopy ID AMYLOID PRECURSOR PROTEIN; LASER CAPTURE MICRODISSECTION; PRIMARY NEURONAL CULTURES; A-BETA PEPTIDE; TRANSGENIC MICE; HYDROGEN-PEROXIDE; OXIDATIVE STRESS; SENILE PLAQUES; BINDING-SITE; IN-VIVO AB With the growing aging population in Western countries, Alzheimer's disease (AD) has become a major public health concern. No preventive measure and effective treatment for this burdensome disease is currently available. Genetic, biochemical, and neuropathological data strongly suggest that A beta amyloidosis, which originates from the amyloidogenic processing of a metalloprotein-amyloid precursor protein (APP), is the key event in AD pathology. However, neurochemical factors that impact upon the age-dependent cerebral AD amyloidogenesis are not well recognized. Growing data indicate that cerebral dysregulation of biometals, environmental metal exposure, and oxidative stress contribute to AD pathology. Herein we provided further evidence that both metals (such as Cu) and H2O2 promote formation of neurotoxic A beta oligomers. Moreover, we first demonstrated that laser capture microdissection coupled with X-ray fluorescence microscopy can be applied to determine elemental profiles (S, Fe, Cu, and Zn) in A beta amyloid plaques. Clearly the fundamental biochemical mechanisms linking brain biometal metabolism, environmental metal exposure, and AD pathophysiology warrant further investigation. Nevertheless, the study of APP and A beta metallobiology may identify potential targets for therapeutic intervention and/or provide diagnostic methods for AD. (c) 2006 Elsevier Inc. All rights reserved. C1 Massachusetts Gen Hosp, MassGen Inst Neurodegenerat Dis, Genet & Aging Res Unit, Charlestown, MA 02129 USA. Harvard Univ, Sch Med, Charlestown, MA 02129 USA. Univ Sci & Technol China, Sch Earth & Space Sci, Div Environm Sci, Hefei 230026, Peoples R China. Massachusetts Gen Hosp, Dept Neurol, Charlestown, MA 02129 USA. Harvard Univ, Sch Med, Charlestown, MA 02129 USA. Massachusetts Gen Hosp, Adv Tissue Resource Ctr, Harvard Ctr Neurodegenerat & Repair, Charlestown, MA 02129 USA. Massachusetts Gen Hosp, Dept Psychiat, Neurochem Lab, Neurosci & Drug Discovery Unit, Charlestown, MA 02129 USA. Argonne Natl Lab, Adv Photon Source, Argonne, IL 60439 USA. RP Huang, XD (reprint author), Massachusetts Gen Hosp, MassGen Inst Neurodegenerat Dis, Genet & Aging Res Unit, Charlestown, MA 02129 USA. EM huangx@helix.mgh.harvard.edu RI Liu, Guijian/M-9597-2014 FU NIA NIH HHS [5 R01 AG20181]; NIMH NIH HHS [5 K01 MH002001] NR 67 TC 70 Z9 71 U1 2 U2 10 PU ACADEMIC PRESS INC ELSEVIER SCIENCE PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA SN 1047-8477 J9 J STRUCT BIOL JI J. Struct. Biol. PD JUL PY 2006 VL 155 IS 1 BP 45 EP 51 DI 10.1016/jjsb.2005.12.011 PG 7 WC Biochemistry & Molecular Biology; Biophysics; Cell Biology SC Biochemistry & Molecular Biology; Biophysics; Cell Biology GA 058AS UT WOS:000238637100007 PM 16503166 ER PT J AU DeLaney, TF AF DeLaney, TF TI Diagnosis of sarcoma by core biopsy SO JOURNAL OF SURGICAL ONCOLOGY LA English DT Editorial Material ID FINE-NEEDLE-ASPIRATION; SOFT-TISSUE MASSES; ACCURACY; LESIONS; TUMORS C1 Massachusetts Gen Hosp, Dept Radiat Oncol, Francis H Burr Proton Therapy Ctr, NE Proton Therapy Ctr, Boston, MA 02114 USA. RP DeLaney, TF (reprint author), Massachusetts Gen Hosp, Dept Radiat Oncol, Francis H Burr Proton Therapy Ctr, NE Proton Therapy Ctr, Boston, MA 02114 USA. EM tdelaney@partners.org NR 11 TC 2 Z9 2 U1 1 U2 1 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 0022-4790 J9 J SURG ONCOL JI J. Surg. Oncol. PD JUL 1 PY 2006 VL 94 IS 1 BP 1 EP 2 DI 10.1002/jso.20505 PG 2 WC Oncology; Surgery SC Oncology; Surgery GA 058ZU UT WOS:000238703900001 PM 16788935 ER PT J AU Raut, CP Pisters, PWT AF Raut, CP Pisters, PWT TI Retroperitoneal sarcomas: Combined-modality treatment approaches SO JOURNAL OF SURGICAL ONCOLOGY LA English DT Review DE retroperitoneal sarcoma; soft tissue sarcoma; external beam radiation; intraoperative radiation; chemoradiation ID SOFT-TISSUE SARCOMA; ELECTRON-BEAM RADIOTHERAPY; ADJUVANT RADIATION-THERAPY; OF-FLORIDA EXPERIENCE; PROGNOSTIC FACTORS; SINGLE INSTITUTION; MANAGEMENT; SURVIVAL; TRIAL; RESECTION AB Retroperitoneal sarcomas (RPS) are rare tumors, accounting for approximately 15% of soft tissue sarcomas. Surgical resection of localized tumors with gross and microscopically negative margins remains the standard of care. However, because RPS are frequently large and locally advanced, resections are often incomplete, resulting in local recurrence. Investigators are evaluating combined-modality therapies to improve local control and disease-specific survival. This review outlines current concepts and evolving treatment strategies in the diagnosis, staging, and management of RPS. C1 Univ Texas, MD Anderson Canc Ctr, Dept Surg Oncol, Houston, TX 77030 USA. Brigham & Womens Hosp, Dept Surg, Boston, MA 02115 USA. Dana Farber Canc Inst, Boston, MA 02115 USA. RP Pisters, PWT (reprint author), Univ Texas, MD Anderson Canc Ctr, Dept Surg Oncol, Unit 444,1515 Holcombe Blvd, Houston, TX 77030 USA. EM ppisters@mdanderson.org NR 30 TC 56 Z9 65 U1 0 U2 2 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 0022-4790 J9 J SURG ONCOL JI J. Surg. Oncol. PD JUL 1 PY 2006 VL 94 IS 1 BP 81 EP 87 DI 10.1002/jso.20543 PG 7 WC Oncology; Surgery SC Oncology; Surgery GA 058ZU UT WOS:000238703900015 PM 16788949 ER PT J AU Chen, DC Agopian, VG Avansino, JR Lee, JK Farley, SM Stelzner, M AF Chen, David C. Agopian, Vatche G. Avansino, Jeffrey R. Lee, Jane K. Farley, Steven M. Stelzner, Matthias TI Optical tissue window: A novel model for optimizing engraftment of intestinal stem cell organoids SO JOURNAL OF SURGICAL RESEARCH LA English DT Article; Proceedings Paper CT 39th Annual Meeting of the Association-for-Academic-Surgery CY FEB 07-11, 2005 CL San Diego, CA SP Assoc Acad Surg DE intestinal stem cell; transplantation; dorsal skin fold chamber; polyglycolic acid ID ENGINEERED SMALL-INTESTINE; SHORT-BOWEL SYNDROME; CHAMBER; MANAGEMENT; ANGIOGENESIS AB Background. Intestinal malabsorption disorders and short bowel syndrome lead to significant morbidity. We recently demonstrated that grafting of intestinal organoids can grow a bioengineered intestinal neomucosa and cure bile acid malabsorption in rats. Now we have developed a novel system that permits direct observation of intestinal organoids in vivo to optimize conditions for engraftment. Methods. Optical Windows were created in C57BL/6J mice by externalizing an omental pedicle into a dorsal skin flap chamber. Following creation of windows, 5000 intestinal organoids from green-fluorescent protein transgene (GFP)(+) donor mice were seeded directly either on omentum or on polyglycolic acid (PGA) disks that had been placed on omentum at 1 or 5 days. Engraftment of green fluorescent cells was evaluated on postseeding days 1, 3, 5, 7, 10, 12, and 21 using fluorescence microscopy. Results. An initial group had seeding onto omentum (n = 5) or biopolymer disks (n = 5) on postoperative day 1. After 7 days, there was mucosal cell engraftment onto omental tissue and biopolymers. GFP(+) organoids engrafted significantly better when seeded onto biopolymers compared to omentum (P < 0.05). In a second study with increased sample size (n = 24) up to day 12, all four groups demonstrated adherence and growth. However, GFP(+) organoids seeded onto delayed PGA biopolymer demonstrated significantly better engraftment (P < 0.05). Conclusions. This novel system allows continuous in vivo observation of engrafted cells that are seeded on externalized omentum. The use of PGA mesh biopolymer may improve engraftment of intestinal organoids. (c) 2006 Elsevier Inc. All rights reserved. C1 Univ Calif Los Angeles, Dept Surg, VA Greater Los Angeles Hlth Care Syst, Los Angeles, CA 90024 USA. Univ Washington, VA Puget Sound Hlth Care Syst, Dept Surg, Seattle, WA 98195 USA. RP Chen, DC (reprint author), Univ Calif Los Angeles, Dept Surg, VA Greater Los Angeles Hlth Care Syst, 10833 Le Conte Ave, Los Angeles, CA 90024 USA. EM dcchen@mednet.ucla.edu NR 24 TC 7 Z9 7 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 0022-4804 J9 J SURG RES JI J. Surg. Res. PD JUL PY 2006 VL 134 IS 1 BP 52 EP 60 DI 10.1016/j.jss.2006.03.029 PG 9 WC Surgery SC Surgery GA 062FE UT WOS:000238929200007 PM 16697415 ER PT J AU Songer, JE Rosowski, JJ AF Songer, Jocelyn E. Rosowski, John J. TI The effect of superior-canal opening on middle-ear input admittance and air-conducted stapes velocity in chinchilla SO JOURNAL OF THE ACOUSTICAL SOCIETY OF AMERICA LA English DT Article ID HEARING-LOSS; DEHISCENCE; DEPENDENCE; MECHANISMS; IMPEDANCE; VERTIGO AB The recent discovery of superior semicircular canal (SC) dehiscence syndrome as a clinical entity affecting both the auditory and vestibular systems has led to the investigation of the impact of a SC opening on the mechanics of hearing. It is hypothesized that the hole in the SC acts as a "third window" in the inner ear which shunts sound-induced stapes volume velocity away from the cochlea through the opening in the SC. To test the hypothesis and to understand the third window mechanisms the middle-ear input admittance and sound-induced stapes velocity were measured in chinchilla before and after surgically introducing a SC opening and after patching the opening. The extent to which patching returned the system to the presurgical state is used as a control criterion. In eight chinchilla ears a statistically significant, reversible increase in low-frequency middle-ear input admittance magnitude occurred as a result of opening the SC. In six ears a statistically significant feversible increase in stapes velocity was observed. Both of these changes are consistent with the hole creating a shunt pathway that increases the cochlear input admittance. (c) 2006 Acoustical Society of America. 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 02114 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 [T32 DC000038, R01 DC000194, R01 DC000194-23, T32 DC-00038] NR 30 TC 32 Z9 32 U1 0 U2 2 PU ACOUSTICAL SOC AMER AMER INST PHYSICS PI MELVILLE PA STE 1 NO 1, 2 HUNTINGTON QUADRANGLE, MELVILLE, NY 11747-4502 USA SN 0001-4966 J9 J ACOUST SOC AM JI J. Acoust. Soc. Am. PD JUL PY 2006 VL 120 IS 1 BP 258 EP 269 DI 10.1121/1.2204356 PG 12 WC Acoustics; Audiology & Speech-Language Pathology SC Acoustics; Audiology & Speech-Language Pathology GA 061TV UT WOS:000238896500024 PM 16875223 ER PT J AU Vaughan, N Storzbach, D Furukawa, I AF Vaughan, Nancy Storzbach, Daniel Furukawa, Izumi TI Sequencing versus nonsequencing working memory in understanding of rapid speech by older listeners SO JOURNAL OF THE AMERICAN ACADEMY OF AUDIOLOGY LA English DT Article DE aging; cognition; memory; speech recognition ID ORDERED POINTING TASK; ADULT AGE-DIFFERENCES; HEARING-AID FITTINGS; PROCESSING RESOURCES; COGNITIVE-ABILITIES; IMPAIRED CHILDREN; SERIAL ORDER; LANGUAGE; RECOGNITION; ATTENTION AB The goal of this study was to identify specific neurocognitive deficits that are associated with older listeners' difficulty understanding rapid speech. Older listeners performed speech recognition tests comprised of time-compressed sentences with and without context, and on a neurocognitive battery aimed specifically at testing working memory, processing speed, and attention. A principle component analysis identified three main cognitive components as follows: a sequencing working memory (WM-S) component, a nonsequencing working memory (WM-NS) component, and a processing speed (PS) component. Each of the cognitive component scores was divided into high, mid, and low categories. Sentence performance of the cognitive subgroups was compared within each component. The results showed that, with hearing loss and age accounted for, the cognitive score groups differed similarly on the sentence condition scores also at 50 and 60% time compression, particularly on the subgroups of the WM-S component. The results suggest that deficits in a separate working memory function identified as sequencing were associated with differences in ability to understand time-compressed speech in this study. C1 Portland VA Med Ctr, Natl Ctr Rehabilitat Auditory Res, Portland, OR 97239 USA. RP Vaughan, N (reprint author), Portland VA Med Ctr, Natl Ctr Rehabilitat Auditory Res, Portland, OR 97239 USA. EM nancy.vaughan@med.va.gov NR 54 TC 19 Z9 19 U1 1 U2 5 PU AMER ACADEMY OF AUDIOLOGY PI RESTON PA 11730 PLAZA DRIVE, STE 300, RESTON, VA 20190 USA SN 1050-0545 J9 J AM ACAD AUDIOL JI J. Am. Acad. Audiol. PD JUL-AUG PY 2006 VL 17 IS 7 BP 506 EP 518 DI 10.3766/jaaa.17.7.6 PG 13 WC Audiology & Speech-Language Pathology; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Otorhinolaryngology GA 091JO UT WOS:000241023600006 PM 16927515 ER PT J AU Francis, S Kozak, KZ Heilig, L Lundahl, K Bowland, T Hester, E Best, A Dellavalle, RP AF Francis, S Kozak, KZ Heilig, L Lundahl, K Bowland, T Hester, E Best, A Dellavalle, RP TI Dermatology Internet Yellow Page advertising SO JOURNAL OF THE AMERICAN ACADEMY OF DERMATOLOGY LA English DT Article; Proceedings Paper CT 63rd Annual Meeting of the American-Academy-of-Dermatology CY FEB 18-22, 2005 CL New Orleans, LA SP Amer Acad Dermatol ID PHYSICIANS AB Background: Patients may use Internet Yellow Pages to help select a physician. Objective. We sought to describe dermatology Internet Yellow Page advertising. Methods: Dermatology advertisements in Colorado, California, New York, and Texas at 3 Yellow Page World Wide Web sites were systematically examined. Results. Most advertisements (76%; 223/292) listed only one provider, 56 listed more than one provider, and 13 listed no practitioner names. Five advertisements listed provider names without any credentialing letters, 265 listed at least one doctor of medicine or osteopathy, and 9 listed only providers with other credentials (6 doctors of podiatric medicine and 3 registered nurses). Most advertisements (61%; 179/292) listed a doctor of medicine or osteopathy claiming board certification, 78% (139/179) in dermatology and 22% (40/179) in other medical specialties. Four (1%; 4/292) claims of board certification could not be verified (one each in dermatology, family practice, dermatologic/cosmetologic surgery, and laser surgery). Board certification could be verified for most doctors of medicine and osteopathy not advertising claims of board certification (68%; 41/60; 32 dermatology, 9 other specialties). A total of 50 advertisements (17%) contained unverifiable or no board certification information, and 47 (16%) listed a physician with verifiable board certification in a field other than dermatology. Limitations: All Internet Yellow Page World Wide Web sites and all US states were not examined. Conclusion: Nonphysicians, physicians board certified in medical specialties other than dermatology, and individuals without verifiable board certification in any medical specialty are advertising in dermatology Internet Yellow Pages. Many board-certified dermatologists are not advertising this certification. C1 Denver Vet Affairs Med Ctr, Dept Dermatol, Denver, CO 80220 USA. Univ Colorado, Dept Dermatol, Denver, CO 80202 USA. Hlth Sci Ctr, Aurora, CO USA. St Elizabeth Hosp, Utica, NY USA. Univ Denver, Sturm Coll Law, Denver, CO 80208 USA. RP Dellavalle, RP (reprint author), Denver Vet Affairs Med Ctr, Dept Dermatol, 1055 Clermont St,Mail Stop 165, Denver, CO 80220 USA. EM robert.dellavalle@uchsc.edu RI Dellavalle, Robert/L-2020-2013 OI Dellavalle, Robert/0000-0001-8132-088X FU NCI NIH HHS [K-07CA92550]; NIAMS NIH HHS [T32 AR07411] NR 12 TC 1 Z9 1 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 JUL PY 2006 VL 55 IS 1 BP 67 EP 70 DI 10.1016/j.jaad.2006.03.021 PG 4 WC Dermatology SC Dermatology GA 058BV UT WOS:000238640200008 PM 16781294 ER PT J AU Sanchez-Carpintero, I Martinez, MI Mihm, MC AF Sanchez-Carpintero, I Martinez, MI Mihm, MC TI Clinical and histopathologic observations of the action of imiquimod in an epithelioid hemangioendothelioma and Paget's mammary disease SO JOURNAL OF THE AMERICAN ACADEMY OF DERMATOLOGY LA English DT Article; Proceedings Paper CT 20th World Congress of Dermatology CY JUL 03-05, 2002 CL PARIS, FRANCE ID IMMUNE-RESPONSE MODIFIER; INFANTILE HEMANGIOMA; TOPICAL IMIQUIMOD; 5-PERCENT CREAM; CELLS; APOPTOSIS; EXPRESSION; AGONISTS AB An epithelioid hemangioendothelioma and Paget's disease of the breast were treated with topical imiquimod 5% cream with very impressive results. In both of the tumors complete disappearance of the lesions occurred. In this article, in addition to describing the treatment approach, the findings in biopsy specimens of the epithelioid hemangioendothelioma and the Paget's disease before, during, and after therapy will be described. The histologic findings show ample evidence that there is both a lymphocytic T helper 1-like and T helper 2-like response from imiquimod. Direct evidence of lymphocytotoxicity was found. Furthermore, mast cells appear to be involved in the development of regression in the vascular tumor. Although the study is very limited and reports only two cases, the results are striking. We considered it important to describe these findings because of their possible use in developing strategies for the application of imiquimod in the treatment of other tumors in human beings. C1 Univ Navarra Clin, Dept Dermatol, Pamplona 31080, Spain. Massachusetts Gen Hosp, Dept Pathol, Boston, MA 02114 USA. Harvard Univ, Cambridge, MA 02138 USA. Clin Amer, Dept Dermatol, San Juan, PR USA. RP Sanchez-Carpintero, I (reprint author), Univ Navarra Clin, Dept Dermatol, Pio 12,36, Pamplona 31080, Spain. EM isanchezc@unav.es NR 22 TC 7 Z9 8 U1 0 U2 0 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 JUL PY 2006 VL 55 IS 1 BP 75 EP 79 DI 10.1016/j.jaad.2006.01.056 PG 5 WC Dermatology SC Dermatology GA 058BV UT WOS:000238640200011 PM 16781296 ER PT J AU Guss, D Bhattacharyya, T AF Guss, Daniel Bhattacharyya, Timothy TI Perioperative management of the obese orthopaedic patient SO JOURNAL OF THE AMERICAN ACADEMY OF ORTHOPAEDIC SURGEONS LA English DT Review ID TOTAL KNEE ARTHROPLASTY; BODY-MASS INDEX; MORBIDLY OBESE; TOTAL HIP; RISK-FACTORS; VENOUS THROMBOEMBOLISM; DURATION PROPHYLAXIS; PULMONARY-EMBOLISM; SPINAL SURGERY; REPLACEMENT AB With nearly a third of American adults considered be obese, it is increasingly important that orthopaedic surgeons be familiar with management issues pertinent to these patients. Preoperative examination must assess cardiopulmonary status and other comorbid conditions, most notably diabetes. Intraoperative considerations include requirements for special equipment, patient positioning, intravenous line placement, central monitoring lines, and anesthesia specific to the physiologic changes in obese patients. Postoperatively, obese patients have higher rates of deep vein thrombosis and wound sepsis than do nonobese patients, and they may differ from other patients in supplemental oxygen requirements, medication dosing, and outcomes in intensive care units. Obese patients can successfully undergo virtually all orthopaedic procedures; however, the procedures are frequently more technically challenging, and obese patients appear to have higher rates of prosthetic failure, infection, hardware failure, and fracture malunion, although many of these complications can be minimized by appropriate countermeasures. C1 Brigham & Womens Hosp, Massachusetts Gen Hosp, Partners Orthopaed Trauma Serv, Boston, MA 02118 USA. Harvard Univ, Combined Orthopaed Residency Program, Boston, MA 02115 USA. RP Bhattacharyya, T (reprint author), Brigham & Womens Hosp, Massachusetts Gen Hosp, Partners Orthopaed Trauma Serv, Yawkey 3600,55 Fruit St, Boston, MA 02118 USA. NR 53 TC 44 Z9 45 U1 0 U2 1 PU AMER ACAD ORTHOPAEDIC SURGEONS PI ROSEMENT PA 6300 N RIVER ROAD, ROSEMENT, IL 60018-4262 USA SN 1067-151X J9 J AM ACAD ORTHOP SUR JI J. Am. Acad. Orthop. Surg. PD JUL PY 2006 VL 14 IS 7 BP 425 EP 432 PG 8 WC Orthopedics SC Orthopedics GA 065RX UT WOS:000239178100005 PM 16822890 ER PT J AU Hickman, D King-Herbert, A Murphy, SJ AF Hickman, Debra King-Herbert, Angela Murphy, Stephanie J. TI The Laboratory Animal Boards Study Group: A multifaceted tool for preparation for the American College of Laboratory Animal Medicine board examination SO JOURNAL OF THE AMERICAN ASSOCIATION FOR LABORATORY ANIMAL SCIENCE LA English DT Article AB Preparation for the specialty board examination for the American College of Laboratory Animal Medicine (ACLAM) is an intensive process that is facilitated by geographic regions where many people studying for the exam are located in close proximity. However, many people work at institutions that are distant from these 'study centers.' Approximately 10 y ago, the Laboratory Animal Boards Study Group (LABSG) online journal club was established to provide a forum for journal review for examination preparation. Over the years, the mission of this group has expanded to include practice examinations and practicals, questions from common resources, and summaries and questions from common laboratory animal science journals. These study aids are beneficial for those preparing for the ACLAM certification examination. They are also beneficial for those preparing for the technician and manager certification examinations offered by the American Association for Laboratory Animal Science (AALAS). This article is intended to be an introduction to the variety of study aids available through the LABSG online journal review club and the LABSG web page (www.labsg.org). It also provides details on the demographics of participants and an exploration of how this resource enhances examination preparation. C1 Portland VA Med Ctr, Portland, OR USA. Natl Inst Environm Hlth Sci, Res Triangle Pk, NC USA. Oregon Hlth Sci Univ, Dept Anesthesiol & Perioperat Med, Portland, OR 97201 USA. RP Hickman, D (reprint author), Portland VA Med Ctr, Portland, OR USA. EM Debra.Hickman@med.va.gov RI Hickman, Debra/D-3289-2009 NR 6 TC 2 Z9 2 U1 0 U2 0 PU AMER ASSOC LABORATORY ANIMAL SCIENCE PI MEMPHIS PA 9190 CRESTWYN HILLS DR, MEMPHIS, TN 38125 USA SN 1060-0558 J9 J AM ASSOC LAB ANIM JI J. Amer. Assoc. Lab. Anim. Sci. PD JUL PY 2006 VL 45 IS 4 BP 33 EP 39 PG 7 WC Veterinary Sciences; Zoology SC Veterinary Sciences; Zoology GA 068DL UT WOS:000239352300007 PM 16884177 ER PT J AU Black, JH Casey, PJ Albadawi, H Cambria, RP Watkins, MT AF Black, James H. Casey, Patrick J. Albadawi, Hassan Cambria, Richard P. Watkins, Michael T. TI Poly adenosine diphosphate-ribose polymerase inhibitor PJ34 abolishes systemic proinflammatory responses to thoracic aortic ischemia and reperfusion SO JOURNAL OF THE AMERICAN COLLEGE OF SURGEONS LA English DT Article; Proceedings Paper CT 58th Annual Meeting of the Society-for-Vascular-Surgery CY JUN 03-06, 2004 CL Anaheim, CA SP Soc Vasc Surg ID COLONY-STIMULATING FACTOR; POLY(ADP-RIBOSE) POLYMERASE; ANEURYSM REPAIR; INFLAMMATORY RESPONSE; POTENT INHIBITOR; NEUTROPHIL ACTIVATION; PULMONARY-FUNCTION; ORGAN DYSFUNCTION; VISCERAL ISCHEMIA; HEMORRHAGIC-SHOCK AB BACKGROUND: Systemic inflammatory responses contribute to mortality after thoracoabdominal aneurysm repair. Poly adenosine diphosphate (ADP) ribose polymerase (PARP) activity is known to modulate inflammation in animal models of injury. The effect of the PARP inhibitor PJ34 and genetic deletion of PARP-1(PARP -/-) on the systemic inflammatory response after thoracic aortic ischemia reperfusion (TAR) is not known. STUDY DESIGN: In one group, all mice were subject to TAR followed by 48 hours of reperfusion. Treated mice (PJ, n = 24) were given PJ34 IP; untreated mice (UN, n = 41) received normal saline intraperitoneally. The number of mice in each group was selected to have a similar number of survivors by 48 hours. In a second group, sham animals were subjected to mediastinotomy alone (sham, n = 10) without TAR, and were compared with mice with deletion of the PARP-1 isoform (PARP-1 -/-, n = 11) subjected to TAR. Tissue extracts were assayed for keratinocyte derived chemokine and granulocyte colony stimulating factor. Serum was assayed for interleukin-6. RESULTS: PJ34 treatment decreased mortality throughout the experimental protocol. There were no mortalities in the sham operated mice or PARP -/- mice subjected to TAR. PJ34 treatment decreased serum levels of interleukin-6 (p = 0.01) and hepatic levels of interleukin-6 mRNA when compared with untreated and PARP-/- mice (p < 0.01). Only liver and kidney cytokine levels were decreased by PJ34 treatment (p < 0.05). In PARP-/- mice subjected to TAR, tissue cytokine levels were not different from those in sham mice. CONCLUSIONS: PARP inhibition may represent a novel therapeutic approach to minimizing inflammatory sequelae after TAR. C1 Harvard Univ, Sch Med, Massachusetts Gen Hosp, Dept Surg,Div Vasc & Endovasc Surg, Boston, MA 02114 USA. VA Boston Healthcare Syst, Dept Surg, Boston, MA USA. RP Watkins, MT (reprint author), Harvard Univ, Sch Med, Massachusetts Gen Hosp, Dept Surg,Div Vasc & Endovasc Surg, 15 Parkman St,Ste 458, Boston, MA 02114 USA. NR 49 TC 16 Z9 17 U1 0 U2 1 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 JUL PY 2006 VL 203 IS 1 BP 44 EP 53 DI 10.1016/j.jamcollsurg.2006.04.004 PG 10 WC Surgery SC Surgery GA 059GG UT WOS:000238720700006 PM 16798486 ER PT J AU Saint, S Kaufman, SR Rogers, MAM Baker, PD Ossenkop, K Lipsky, BA AF Saint, Sanjay Kaufman, Samuel R. Rogers, Mary A. M. Baker, Paul D. Ossenkop, Kathleen Lipsky, Benjamin A. TI Condom versus indwelling urinary catheters: A randomized trial SO JOURNAL OF THE AMERICAN GERIATRICS SOCIETY LA English DT Article DE urinary catheter; urinary tract infection; bacteriuria; cognitive impairment ID NURSING-HOME PATIENTS; LONG-TERM-CARE; TRACT-INFECTIONS; SPECIMEN COLLECTION; PATIENT SAFETY; BACTERIURIA; MEN; PREVALENCE; INCONTINENCE; HOSPITALS AB OBJECTIVES: To compare condom and indwelling urinary catheters in terms of infection risk and patient satisfaction. DESIGN: A prospective, randomized, unblinded, controlled trial. SETTING: An academically affiliated Veterans Affairs Medical Center. PARTICIPANTS: Hospitalized men aged 40 and older who required a urinary collection device. MEASUREMENTS: The incidence of adverse outcomes (bacteriuria, symptomatic urinary tract infection (UTI), or death) and patient device-related satisfaction as determined according to a questionnaire. Dementia status was recorded to assess effect modification by the presence of dementia. RESULTS: Seventy-five subjects were randomized: 41 receiving an indwelling catheter and 34 a condom catheter. The incidence of an adverse outcome was 131/1,000 patient-days with an indwelling catheter and 70/1,000 patient-days with a condom catheter (P = .07). The median time to an adverse event was 7 days in the indwelling group and 11 days in the condom group. After adjusting for other risk factors, it was found that condom catheter use reduced adverse outcomes (P = .04). Patients without dementia who had an indwelling catheter were approximately five times as likely to develop bacteriuria or symptomatic UTI or to die (hazard ratio = 4.84, 95% confidence interval = 1.46-16.02) as those with a condom catheter (P = .01). Patients reported that condom catheters were more comfortable (P = .02) and less painful (P = .02) than indwelling catheters. CONCLUSION: The use of condom catheters is less likely to lead to bacteriuria, symptomatic UTI, or death than the use of indwelling catheters. This protection is especially apparent in men without dementia. C1 Ann Arbor Dept Vet Affairs Hlth Serv, Res & Dev Ctr Excellence, Ctr Practice Management & Outcomes Res, Ann Arbor, MI USA. Univ Michigan, Div Gen Med, Dept Internal Med, Ann Arbor, MI USA. Univ Michigan, Dept Vet Affairs, Patient Safety Enhancement Program, Ann Arbor, MI USA. Vet Affairs Puget Sound Hlth Care Syst, Seattle Div, Seattle, WA USA. Univ Washington, Sch Med, Dept Med, Seattle, WA 98195 USA. RP Saint, S (reprint author), Room 7E08,300 NIB,Campus Box 0429, Ann Arbor, MI 48109 USA. EM saint@umich.edu RI Lipsky, Benjamin/B-4645-2013; OI Lipsky, Benjamin A./0000-0001-9886-5114 NR 31 TC 64 Z9 65 U1 0 U2 2 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 JUL PY 2006 VL 54 IS 7 BP 1055 EP 1061 DI 10.1111/j.1532-5415.2006.00785.x PG 7 WC Geriatrics & Gerontology; Gerontology SC Geriatrics & Gerontology GA 062XB UT WOS:000238978900004 PM 16866675 ER PT J AU Shannon, GR Wilber, KH Allen, D AF Shannon, George R. Wilber, Kathleen H. Allen, Douglas TI Reductions in costly healthcare service utilization: Findings from the Care Advocate Program SO JOURNAL OF THE AMERICAN GERIATRICS SOCIETY LA English DT Article DE managed care; care management; home- and community-based services ID LONG-TERM-CARE; MANAGED CARE; OLDER-PEOPLE; INTERVENTION; EXPENDITURES; MORTALITY; OUTCOMES; SYSTEMS; ELDERS AB OBJECTIVES: To determine whether a telephone care-management intervention for high-risk Medicare health maintenance organization (HMO) health plan enrollees can reduce costly medical service utilization. DESIGN: Randomized, controlled trial measuring health-care services utilization over three 12-month periods (pre-, during, and postintervention). SETTING: Two social service organizations partnered with a Medicare HMO and four contracted medical groups in southern California. PARTICIPANTS: Eight hundred twenty-three patients aged 65 and older; eligibility was determined using an algorithm to target older adults with high use of insured healthcare services. INTERVENTION: After assessment, members in the intervention group were offered mutually agreed upon referrals to home- and community-based services (HCBS), medical groups, or Medicare HMO health plan and followed monthly for 1 year. MEASUREMENTS: Insured medical service utilization was measured across three 12-month periods. Acceptance and utilization of Care Advocate (CA) referrals were measured during the 12-month intervention period. RESULTS: CA intervention members were significantly more likely than controls to use primary care physician services (odds ratio (OR) 2.05, P < .001), and number of hospital admissions (OR 0.43, P < .01) and hospital days (OR = 0.39, P < .05) were significantly more stable for CA group members than for controls. CONCLUSION: Results suggest that a modest intervention linking older adults to HCBS may have important cost-saving implications for HMOs serving community-dwelling older adults with high healthcare service utilization. Future studies, using a national sample, should verify the role of telephone care management in reducing the use of costly medical services. C1 VA Greater Los Angeles Ctr Excellence, Sepulveda, CA 91343 USA. Univ So Calif, Ethel Percy Andrus Gerontol Ctr, Los Angeles, CA 90089 USA. Greater Newport Physicians IPA, Newport Beach, CA USA. RP Shannon, GR (reprint author), VA Greater Los Angeles Ctr Excellence, 16111 Plummer St 152,Bldg 25, Sepulveda, CA 91343 USA. EM gshannon@usc.edu NR 28 TC 16 Z9 16 U1 2 U2 3 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 JUL PY 2006 VL 54 IS 7 BP 1102 EP 1107 DI 10.1111/j.1532-5415.20066.00799.x PG 6 WC Geriatrics & Gerontology; Gerontology SC Geriatrics & Gerontology GA 062XB UT WOS:000238978900011 PM 16866682 ER PT J AU Mueller, PW Rogus, JJ Cleary, PA Zhao, Y Smiles, AM Steffes, MW Bucksa, J Gibson, TB Cordovado, SK Krolewski, AS Nierras, CR Warram, JH AF Mueller, PW Rogus, JJ Cleary, PA Zhao, Y Smiles, AM Steffes, MW Bucksa, J Gibson, TB Cordovado, SK Krolewski, AS Nierras, CR Warram, JH TI Genetics of Kidneys in Diabetes (GoKinD) study: A genetics collection available for identifying genetic susceptibility factors for diabetic nephropathy in type 1 diabetes SO JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY LA English DT Article ID TRANSMISSION DISEQUILIBRIUM TEST; SAMPLE-SIZE REQUIREMENTS; STAGE RENAL-DISEASE; IDDM; STRATIFICATION; POPULATION; COMPLICATION; ASSOCIATION; MELLITUS; HISTORY AB The Genetics of Kidneys in Diabetes (GoKinD) study is an initiative that aims to identify genes that are involved in diabetic nephropathy. A large number of individuals with type 1 diabetes were screened to identify two subsets, one with clear-cut kidney disease and another with normal renal status despite long-term diabetes. Those who met additional entry criteria and consented to participate were enrolled. When possible, both parents also were enrolled to form family trios. As of November 2005, GoKinD included 3075 participants who comprise 671 case singletons, 623 control singletons, 272 case trios, and 323 control trios. Interested investigators may request the DNA collection and corresponding clinical data for GoKinD participants using the instructions and application form that are available at http://www.gokind.org/access. Participating scientists will have access to three data sets, each with distinct advantages. The set of 1294 singletons has adequate power to detect a wide range of genetic effects, even those of modest size. The set of case trios, which has adequate power to detect effects of moderate size, is not susceptible to false-positive results because of population substructure. The set of control trios is critical for excluding certain false-positive results that can occur in case trios and may be particularly useful for testing gene-environment interactions. Integration of the evidence from these three components into a single, unified analysis presents a challenge. This overview of the GoKinD study examines in detail the power of each study component and discusses analytic challenges that investigators will face in using this resource. C1 Joslin Diabet Ctr, Sect Genet & Epidemiol, Div Res, Boston, MA 02215 USA. Ctr Dis Control & Prevent, Diabet & Mol Risk Assessment Lab, Atlanta, GA USA. George Washington Univ, Biostat Ctr, Washington, DC USA. Univ Minnesota, Minneapolis, MN 55455 USA. Aspen Syst Inc, Rockville, MD USA. Juvenile Diabet Res Fdn, New York, NY USA. RP Warram, JH (reprint author), Joslin Diabet Ctr, Sect Genet & Epidemiol, Div Res, 1 Joslin Pl, Boston, MA 02215 USA. EM james.warram@joslin.harvard.edu FU NIDDK NIH HHS [PL105-33]; None [PL107-360, PL106-554]; PHS HHS [106-554, 107-360, PL 105-33, PL105-33, PL106-554, PL107-360] NR 26 TC 77 Z9 79 U1 1 U2 1 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 1046-6673 J9 J AM SOC NEPHROL JI J. Am. Soc. Nephrol. PD JUL PY 2006 VL 17 IS 7 BP 1782 EP 1790 DI 10.1681/ASN.2005080822 PG 9 WC Urology & Nephrology SC Urology & Nephrology GA 059NG UT WOS:000238738900009 PM 16775037 ER PT J AU Ozcan, A Digonnet, MJF Kino, GS AF Ozcan, A Digonnet, MJF Kino, GS TI Minimum-phase-function-based processing in frequency-domain optical coherence tomography systems SO JOURNAL OF THE OPTICAL SOCIETY OF AMERICA A-OPTICS IMAGE SCIENCE AND VISION LA English DT Article ID FIBER BRAGG GRATINGS; SPECTRAL INTERFEROMETRY; SIGNAL RECONSTRUCTION; MAGNITUDE; TRANSFORM; ALGORITHM AB We present a simple processing technique that uses the concept of minimum-phase functions to improve frequency-domain optical coherence tomography systems. Our approach removes the autocorrelation noise and therefore increases both the accessible depth range and the recovery accuracy. To our knowledge, this is the first time that the concept of minimum-phase functions has been applied to improve optical coherence tomography. (C) 2006 Optical Society of America. C1 Stanford Univ, Edward L Ginzton Lab, Stanford, CA 94305 USA. RP Ozcan, A (reprint author), Harvard Univ, Sch Med, Massachusetts Gen Hosp, Boston, MA 02114 USA. EM aozcan@mgh.harvard.edu NR 25 TC 12 Z9 12 U1 0 U2 1 PU OPTICAL SOC AMER PI WASHINGTON PA 2010 MASSACHUSETTS AVE NW, WASHINGTON, DC 20036 USA SN 1084-7529 J9 J OPT SOC AM A JI J. Opt. Soc. Am. A-Opt. Image Sci. Vis. PD JUL PY 2006 VL 23 IS 7 BP 1669 EP 1677 DI 10.1364/JOSAA.23.001669 PG 9 WC Optics SC Optics GA 057WW UT WOS:000238626900015 PM 16783430 ER PT J AU Keith, RL Geraci, MW AF Keith, Robert L. Geraci, Mark W. TI Prostacyclin in lung cancer SO JOURNAL OF THORACIC ONCOLOGY LA English DT Editorial Material ID SMOOTH-MUSCLE CELLS; PROLIFERATOR-ACTIVATED RECEPTORS; PROSTAGLANDIN ENDOPEROXIDES; SYNTHASE; STIMULATION; EXPRESSION; GENE; MITOGEN; GROWTH C1 Denver VA Med Ctr, Dept Med, Div Pulm Sci & Crit Care Med, Denver, CO 80220 USA. Univ Colorado, Hlth Sci Ctr, Dept Med, Denver, CO 80262 USA. RP Keith, RL (reprint author), Denver VA Med Ctr, Dept Med, Div Pulm Sci & Crit Care Med, 1055 Clermont St,Box 111A, Denver, CO 80220 USA. NR 23 TC 6 Z9 6 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 1556-0864 J9 J THORAC ONCOL JI J. Thorac. Oncol. PD JUL PY 2006 VL 1 IS 6 BP 503 EP 505 DI 10.1097/01243894-200607000-00001 PG 3 WC Oncology; Respiratory System SC Oncology; Respiratory System GA 065WT UT WOS:000239191500001 PM 17409908 ER PT J AU Janne, PA Wozniak, AJ Belani, CP Keohan, ML Ross, HJ Polikoff, JA Mintzer, DM Ye, ZS Monberg, MJ Obasaju, CK AF Jaenne, Pasi A. Wozniak, Antoinette J. Belani, Chandra P. Keohan, Mary-Louise Ross, Helen J. Polikoff, Jonathan A. Mintzer, David M. Ye, Zhishen Monberg, Matthew J. Obasaju, Coleman K. CA pemetrexed expanded access program in TI Pemetrexed alone or in combination with cisplatin in previously treated malignant pleural mesothelioma: Outcomes from a phase IIIB expanded access program SO JOURNAL OF THORACIC 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 DE malignant pleural mesothelioma; pemetrexed; cisplatin; expanded access program; compassionate use ID CANCER COOPERATIVE GROUP; LEUKEMIA GROUP-B; MULTITARGETED ANTIFOLATE; TRIAL; DOXORUBICIN; LY231514; THERAPY; TRENDS; MTA AB Background: In a randomized phase III trial, pemetrexed plus cisplatin was associated with improved survival compared with cisplatin alone for patients with malignant pleural mesothelioma (MPM). However, there are limited data available on the efficacy of these and other chemotherapy regimens in patients who have received previous systemic chemotherapy. To gather additional efficacy and safety data of pemetrexed/cisplatin and pemetrexed alone in previously treated patients, we examined patients treated on the Eli Lilly and Company expanded access program (EAP). Patients and Methods: Patients with malignant mesothelioma were enrolled in this trial. Of 1056 patients receiving at least one dose of the study drug, 187 (17.7%) were previously treated patients with MPM. Patients were treated every 21 days with pemetrexed 500 mg/m(2) alone (n = 91) or in combination with cisplatin 75 mg/m(2) (n = 96) for a maximum of six cycles. All patients received folic acid and vitamin B12 supplementation and steroid prophylaxis. Serious adverse events (SAEs) were reported by investigators and compiled in a pharmaco-vigilance database for all patients enrolled in the EAR Results: Median age of the previously treated pleural mesothelioma subset was 66 years (range, 27-87 years). Based on 153 evaluable patients (a subset of the larger intent-to-treat population of 187), the overall response rate was 32.5% for pemetrexed and cisplatin and 5.5% for pemetrexed alone. The disease control rate (response rate + stable disease) was 68.7% for pemetrexed and cisplatin and 46.6% for pemetrexed alone. Median survival was 7.6 months for pemetrexed plus cisplatin (67% censored) and 4.1 months for pemetrexed alone (55% censored). The most commonly reported serious adverse events in the overall EAP irrespective of causality were dehydration (7.2%), nausea (5.2%), vomiting (4.9%), dyspnea (3.8%), and pulmonary embolism (2.4%). Conclusions: The data from this EAP study suggest that patients with previously treated MPM can benefit from treatment with pemetrexed alone or in combination with cisplatin. The treatment is associated with acceptable toxicity. 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. Wayne State Univ, Karmanos Inst, Detroit, MI USA. Univ Pittsburgh, Inst Canc, Pittsburgh, PA 15260 USA. Columbia Presbyterian Med Ctr, New York, NY 10032 USA. Oregon Hlth Sci Univ, Portland, OR 97201 USA. Kaiser Hosp, San Diego, CA USA. Penn Hosp, Philadelphia, PA 19107 USA. Eli Lilly & Co, Indianapolis, IN 46285 USA. RP Janne, PA (reprint author), Dana Farber Canc Inst, Dept Med Oncol, Lowe Ctr Thorac Oncol, 44 Binney St,Dana 1234, Boston, MA 02115 USA. EM Pasi_Janne@dfci.harvard.edu NR 34 TC 37 Z9 37 U1 0 U2 2 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 1556-0864 J9 J THORAC ONCOL JI J. Thorac. Oncol. PD JUL PY 2006 VL 1 IS 6 BP 506 EP 512 PG 7 WC Oncology; Respiratory System SC Oncology; Respiratory System GA 065WT UT WOS:000239191500002 PM 17409909 ER PT J AU Inaba, K Munera, F McKenney, M Rivas, L de Moya, M Bahouth, H Cohn, S AF Inaba, Kenji Munera, Felipe McKenney, Mark Rivas, Luis de Moya, Marc Bahouth, Hany Cohn, Stephen TI Prospective evaluation of screening multislice helical computed tomographic angiography in the initial evaluation of penetrating neck injuries SO JOURNAL OF TRAUMA-INJURY INFECTION AND CRITICAL CARE LA English DT Article; Proceedings Paper CT 35th Annnual Meeting of the Western-Trauma-Association CY FEB 27-MAR 05, 2005 CL Jackson Hole, WY SP Western Trauma Assoc DE penetrating injury; trauma; wounds and injuries; neck; radiography; diagnostic imaging; computed tomography ID OCCULT ARTERIAL INJURIES; PHYSICAL-EXAMINATION; EXTREMITY TRAUMA; VASCULAR INJURIES; GUNSHOT INJURIES; CT ANGIOGRAPHY; MANAGEMENT; ARTERIOGRAPHY; SCAN AB Background: The optimal management strategy for patients sustaining penetrating neck injury without an urgent indication for operative exploration remains controversial. The objective of this study was to prospectively assess multislice helical computed tomography angiography (MCTA) as a stand alone screening modality for the initial evaluation of hemodynamically stable patients with penetrating neck injuries. Our hypothesis was that MCTA is a sensitive diagnostic screening test that could noninvasively evaluate the vascular and aerodigestive structures of the neck. Methods: After Institutional Review Board approval, all penetrating neck injuries assessed during a 16-month period were prospectively evaluated at a Level I trauma center. Patients without an indication for urgent neck exploration underwent MCTA screening. MCTA accuracy was tested against an aggregate gold standard of final diagnosis encompassing all imaging, surgical procedures and clinical follow-up obtained. Results: In all, 106 injuries penetrated the platysma; 15 required urgent exploration and 91 underwent MCTA (34 gunshot wounds/57 stab wounds). Nineteen external wounds were in zone 1, 39 were in zone 2, 10 in zone 3, and 23 traversed multiple zones. MCTA was nondiagnostic in 2.2% secondary to artifact from retained missile fragments. Follow-up was achieved in 84.5% of patients for a mean of 33.3 days (range: 2-150). MCTA achieved 100% sensitivity and 93.5% specificity in detecting all vascular and aerodigestive injuries sustained. MCTA correctly identified two tracheal and two carotid artery injuries requiring operative or endovascular repair in asymptomatic patients. No injuries requiring intervention were missed by MCTA. Conclusions: In the initial evaluation of stable penetrating neck injuries, MCTA appears to be a sensitive and safe screening modality. Further investigation is warranted. C1 Univ So Calif, Med Ctr, Div Trauma & Surg Crit Care, LAC, Los Angeles, CA 90033 USA. Univ Miami, Div Emergency Radiol, Ryder Trauma Ctr, Miami, FL 33152 USA. Univ Miami, Div Trauma & Crit Care, Ryder Trauma Ctr, Miami, FL 33152 USA. Massachusetts Gen Hosp, Div Trauma Emergency Surg & Surg Crit Care, Boston, MA USA. Univ Texas, Hlth Sci Ctr, Dept Surg, San Antonio, TX 78284 USA. RP Inaba, K (reprint author), Univ So Calif, Med Ctr, Div Trauma & Surg Crit Care, LAC, 1200 N State St 10-750, Los Angeles, CA 90033 USA. EM kinaba@surgery.usc.edu NR 27 TC 46 Z9 48 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 JUL PY 2006 VL 61 IS 1 BP 144 EP 149 DI 10.1097/01.ta.0000222711.01410.bc PG 6 WC Critical Care Medicine; Surgery SC General & Internal Medicine; Surgery GA 065TV UT WOS:000239183600032 PM 16832262 ER PT J AU Grocela, JA Kanji, A Ternullo, J AF Grocela, JA Kanji, A Ternullo, J TI Prediction of Medicare drug formulary drugs for treatment of overactive bladder SO JOURNAL OF UROLOGY LA English DT Article DE bladder; urinary incontinence; Medicare; pharmaceutical preparations; health policy AB Purpose: With the establishment and signing into law the Medicare and Prescription Drug Improvement and Modernization Act of 2003, also known as Medicare Part D, medical costs are expected to soar. In fact, the program is expected to cost more than a trillion dollars through 2015. Establishment of the Medicare Part D drug formulary will allow cost containment but still absorb patient and physician preferences as well as a consideration of efficacy and safety data. Materials and Methods: Potential Medicare formulary choices were examined in the anticholinergic class, as commonly used by urologists, and small in number of available drugs. Formulary selection parties and issues were individually analyzed, including the government in respect to cost containment, patients in relation to efficacy and cost, physicians in relation to preferences and influence and drug companies in relation to lobbying power, country of base of operations and market shares. Costs to Medicare and patients were calculated using discount Internet sites for pricing and simulated using Medicare Part D benefits. Results: Generic oxybutynin is likely to be included because it is the least expensive to patients and Medicare, but it has the lowest efficacy. Detrol (R) LA is likely to be the long acting choice due to efficacy, cost and manufacture by a United States based company. Conclusions: A simulation of cost analysis of anticholinergics for treatment of overactive bladder would help urologists better understand the Medicare formulary selection process. C1 Harvard Univ, Sch Business, Massachusetts Gen Hosp, Dept Urol, Boston, MA 02114 USA. Harvard Univ, Sch Publ Hlth, Dept Telemed, Boston, MA 02114 USA. Harvard Univ, Sch Publ Hlth, Partners Healthcare Syst, Boston, MA 02114 USA. RP Grocela, JA (reprint author), Harvard Univ, Sch Business, Massachusetts Gen Hosp, Dept Urol, Bigelow 1102, Boston, MA 02114 USA. EM jgrocela@partners.org NR 5 TC 0 Z9 0 U1 1 U2 2 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0022-5347 J9 J UROLOGY JI J. Urol. PD JUL PY 2006 VL 176 IS 1 BP 252 EP 255 DI 10.1016/S0022-5347(06)00591-X PG 4 WC Urology & Nephrology SC Urology & Nephrology GA 053IE UT WOS:000238298000061 PM 16753413 ER PT J AU Li, X Li, Y Stremlau, M Yuan, W Song, B Perron, M Sodroski, J AF Li, X Li, Y Stremlau, M Yuan, W Song, B Perron, M Sodroski, J TI Functional replacement of the RING, B-Box 2, and coiled-coil domains of tripartite motif 5 alpha (TRIM5 alpha) by heterologous TRIM domains SO JOURNAL OF VIROLOGY LA English DT Article ID RESTRICTION FACTOR TRIM5-ALPHA; IMMUNODEFICIENCY-VIRUS TYPE-1; RETROVIRUS RESTRICTION; POSTENTRY RESTRICTION; B30.2(SPRY) DOMAIN; MONKEY TRIM5-ALPHA; SIMIAN CELLS; OLD-WORLD; PROTEIN; HIV-1 AB Tripartite motif 5 alpha (TRIM5 alpha) restricts some retroviruses, including human immunodeficiency virus type 1 (HIV-1), from infecting the cells of particular species. TRIM5a is a member of the TRIM family of proteins, which contain RING, B-box, coiled-coil (CC), and, in some cases, B30.2(SPRY) domains. Here we investigated the abilities of domains from TRIM proteins (TRIM6, TRIM34, and TRIM21) that do not restrict HIV-1 infection to substitute for the domains of rhesus monkey TRIM5 alpha (TRIM5 alpha(rh)). The RING, B-box 2, and CC domains of the paralogous TRIM6 and TRIM34 proteins functionally replaced the corresponding TRIM5 alpha(rh) domains, allowing HIV-1 restriction. By contrast, similar chimeras containing the components of TRIM21, a slightly more distant relative of TRIM5, did not restrict HIV-1 infection. The TRIM21 B-box 2 domain and its flanking linker regions contributed to the functional defectiveness of these chimeras. All of the chimeric proteins formed trimers. All of the chimeras that restricted HIV-1 infection bound the assembled HIV-1 capsid complexes. These results indicate that heterologous RING, B-box 2, and CC domains from related TRIM proteins can functionally substitute for TRIM5 alpha(rh) domains. C1 Harvard Univ, Sch Med, Dana Farber Canc Inst, Dept Canc Immunol & AIDS,Div AIDS, Boston, MA 02115 USA. Harvard Univ, Sch Publ Hlth, Dept Immunol & Infect Dis, Boston, MA 02115 USA. RP Sodroski, J (reprint author), Harvard Univ, Sch Med, Dana Farber Canc Inst, Dept Canc Immunol & AIDS,Div AIDS, 44 Binney St JFB 824, Boston, MA 02115 USA. EM joseph_sodroski@dfci.harvard.edu RI Li, Xing/D-3852-2009; Li, Yuan/B-4098-2013 FU NHLBI NIH HHS [HL 54785, P50 HL054785]; NIAID NIH HHS [P30 AI028691, AI 063987, R01 AI063987] NR 41 TC 41 Z9 43 U1 1 U2 6 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 JUL PY 2006 VL 80 IS 13 BP 6198 EP 6206 DI 10.1128/JVI.00283-06 PG 9 WC Virology SC Virology GA 054MJ UT WOS:000238380700001 PM 16775307 ER PT J AU Kasprowicz, V Isa, A Jeffery, K Broliden, K Tolfvenstam, T Klenerman, P Bowness, P AF Kasprowicz, V. Isa, A. Jeffery, K. Broliden, K. Tolfvenstam, T. Klenerman, P. Bowness, P. TI A highly restricted T-cell receptor dominates the CD8(+) T-cell response to parvovirus B19 infection in HLA-A*2402-positive individuals SO JOURNAL OF VIROLOGY LA English DT Article ID STRUCTURAL BASIS; CTL EPITOPES; IDENTIFICATION; RECOGNITION; LYMPHOCYTES; HIV-1; USAGE; TCR AB Six of seven HLA-A*2402-positive individuals with acute parvovirus B19 infections made vigorous CD8-positive cytotoxic T-cell (CTL) responses to the viral epitope FYTPLADQF. All responders showed highly focused T-cell receptor (TCR) usage, using almost exclusively BV5.1. The BV5.1 TCR dominated the acute response, was maintained over time, and was also used by a remotely infected individual. Nine CTL clones and two oligoclonal lines obtained from three unrelated individuals used BV5.1, BJ2.1, and a conserved TCR CDR3 of nine amino acids. This commonly recognized epitope is likely important in long-term protective immunity and should be included in vaccine design. C1 Weatherall Inst Mol Med, MRC Human Immunol Unit, Oxford, England. Karolinska Inst, Div Clin Virol, Stockholm, Sweden. John Radcliffe Hosp, Dept Virol, Oxford OX3 9DU, England. Univ Oxford, Nuffield Dept Med, Oxford, England. RP Kasprowicz, V (reprint author), Harvard Univ, Massachusetts Gen Hosp, Sch Med, Partners AIDS Res Ctr, 149 13th St,6th Floor, Charlestown, MA 02129 USA. EM vkasprowicz@partners.org OI Tolfvenstam, Thomas/0000-0003-3549-8083; bowness, paul/0000-0003-4597-0484 FU Medical Research Council [MC_U137884185] NR 13 TC 8 Z9 9 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 JUL PY 2006 VL 80 IS 13 BP 6697 EP 6701 DI 10.1128/JVI.02388-05 PG 5 WC Virology SC Virology GA 054MJ UT WOS:000238380700052 PM 16775358 ER PT J AU Blutt, SE Fenaux, M Warfield, KL Greenberg, HB Conner, ME AF Blutt, SE Fenaux, M Warfield, KL Greenberg, HB Conner, ME TI Active viremia in rotavirus-infected mice SO JOURNAL OF VIROLOGY LA English DT Article ID EXTRAINTESTINAL SPREAD; HISTOLOGIC DISTRIBUTION; HETEROLOGOUS ROTAVIRUS; RHESUS ROTAVIRUS; NEONATAL MOUSE; CHILDREN; MODEL; GASTROENTERITIS; ANTIGENEMIA; PROTECTION AB Rotavirus circulates extraintestinally in animals used as models for rotavirus infection and in children. Rotavirus infection in mice was used to define host or viral factors that affect rotavirus viremia. Antigenemia was observed with homologous and heterologous rotaviruses, and neither age nor mouse strain genetics altered the occurrence of rotavirus antigenemia or viremia. Rotavirus RNA and infectious virus were present in sera and associated with the plasma fraction of blood in all infected mice. These findings indicate that antigenemia/viremia occurs routinely in rotavirus infections and imply that infectious rotavirus has access to any extraintestinal cell within contact of blood. C1 Baylor Coll Med, Dept Mol Virol & Microbiol, Houston, TX 77030 USA. Stanford Univ, Sch Med, Dept Gastroenterol, Palo Alto, CA 94304 USA. Michael E Debakey Vet Affairs Med Ctr, Houston, TX 77030 USA. RP Conner, ME (reprint author), Baylor Coll Med, Dept Mol Virol & Microbiol, 1 Baylor Plaza, Houston, TX 77030 USA. EM mconner@bcm.tmc.edu FU NIAID NIH HHS [AI 21362, AI 24998, AI 10604, F32 AI010604, R01 AI021362, R01 AI024998, R21 AI024998, R37 AI021362, R56 AI021362]; NIDDK NIH HHS [DK 56338, P30 DK056338] NR 31 TC 31 Z9 34 U1 0 U2 0 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 JUL PY 2006 VL 80 IS 13 BP 6702 EP 6705 DI 10.1128/JVI.00329-06 PG 4 WC Virology SC Virology GA 054MJ UT WOS:000238380700053 PM 16775359 ER PT J AU Yuan, W Bazick, J Sodroski, J AF Yuan, W Bazick, J Sodroski, J TI Characterization of the multiple conformational states of free monomeric and trimeric human immunodeficiency virus envelope glycoproteins after fixation by cross-linker SO JOURNAL OF VIROLOGY LA English DT Article ID GP41 TRANSMEMBRANE GLYCOPROTEIN; GP120 GLYCOPROTEIN; ANTIBODY NEUTRALIZATION; OLIGOMERIC STRUCTURE; RECEPTOR-BINDING; HIV-1 ENTRY; DISTINCT CONFORMATIONS; MONOCLONAL-ANTIBODIES; VARIABLE REGIONS; EPITOPE EXPOSURE AB The human immunodeficiency virus type 1 (HIV-1) gp120 exterior and gp41 transmembrane envelope glycoproteins assemble into trimers on the virus surface that represent potential targets for antibodies. Potent neutralizing antibodies bind the monomeric gp120 glycoprotein with small changes in entropy, whereas unusually large decreases in entropy accompany gp120 binding by soluble CD4 and less potent neutralizing antibodies. The high degree of conformational flexibility in the free gp120 molecule implied by these observations has been suggested to contribute to masking the trimer from antibodies that recognize the gp120 receptor-binding regions. Here we use cross-linking and recognition by antibodies to investigate the conformational states of gp120 monomers and soluble and cell surface forms of the trimeric HIV-1 envelope glycoproteins. The fraction of monomeric and trimeric envelope glycoproteins able to be recognized after fixation was inversely related to the entropic changes associated with ligand binding. In addition, fixation apparently limited the access of antibodies to the V3 loop and gp41-interactive surface of gp120 only in the context of trimeric envelope glycoproteins. The results support a model in which the unliganded monomeric and trimeric HIV-1 envelope glycoproteins sample several different conformations. Depletion of particular fixed conformations by antibodies allowed characterization of the relationships among the conformational states. Potent neutralizing antibodies recognize the greatest number of conformations and therefore can bind the virion envelope glycoproteins more rapidly and completely than weakly neutralizing antibodies. Thus, the conformational flexibility of the HIV-1 envelope glycoproteins creates thermodynamic and kinetic barriers to neutralization by antibodies directed against the receptor-binding regions of gp120. C1 Harvard Univ, Sch Med, Dana Farber Canc Inst, Dept Canc Immunol & AIDS,Dept Pathol,Div AIDS, Boston, MA 02115 USA. Harvard Univ, Sch Publ Hlth, Dept Immunol & Infect Dis, Boston, MA 02115 USA. RP Sodroski, J (reprint author), Harvard Univ, Sch Med, Dana Farber Canc Inst, Dept Canc Immunol & AIDS,Dept Pathol,Div AIDS, 44 Binney St,JFB 824, Boston, MA 02115 USA. EM joseph_sodroski@dfci.harvard.edu FU NIAID NIH HHS [U19 AI067854, AI24755, AI39420, AI40895, AI42848, AI67854, P30 AI042848, R01 AI039420, R01 AI040895, R37 AI024755, U01 AI067854] NR 76 TC 54 Z9 55 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 JUL PY 2006 VL 80 IS 14 BP 6725 EP 6737 DI 10.1128/JVI.00118-06 PG 13 WC Virology SC Virology GA 059ZF UT WOS:000238770000001 PM 16809278 ER PT J AU Li, Y Li, X Stremlau, M Lee, M Sodroski, J AF Li, Y Li, X Stremlau, M Lee, M Sodroski, J TI Removal of arginine 332 allows human TRIM5 alpha to bind human immunodeficiency virus capsids and to restrict infection SO JOURNAL OF VIROLOGY LA English DT Article ID MURINE LEUKEMIA-VIRUS; POSTENTRY RESTRICTION; B30.2(SPRY) DOMAIN; CYCLOPHILIN-A; SIMIAN CELLS; HIV-1; SUSCEPTIBILITY; DETERMINANTS; REGIONS; TROPISM AB Human TRIM5 alpha (TRIM5 alpha(hu)) only modestly inhibits human immunodeficiency virus type 1 (HIV-1) and does not inhibit simian immunodeficiency virus (SIVmac). Alteration of arginine 332 in the TRIM5 alpha(hu) B30.2 domain to proline, the residue found in rhesus monkey TRIM5 alpha, has been shown to create a potent restricting factor for both HIV-1 and SIVmac. Here we demonstrate that the potentiation of HIV-1 inhibition results from the removal of a positively charged residue at position 332 of TRIM5 alpha(hu). The increase in restricting activity correlated with an increase in the ability of TRIMS',, mutants lacking arginine 332 to bind HIV-1 capsid complexes. A change in the cyclophilin A-binding loop of the HIV-1 capsid decreased TRIM5 alpha(hu). R332P binding and allowed escape from restriction. The ability of TRIM5 alpha(hu) to restrict SIVmac could be disrupted by the presence of any charged residue at position 332. Thus, charged residues in the v1 region of the TRIM5 alpha(hu) B30.2 domain can modulate capsid binding and restriction potency. Therapeutic strategies designed to neutralize arginine 332 of TRIM5 alpha(hu) might potentiate the innate resistance of human cells to HIV-1 infection. C1 Harvard Univ, Sch Med, Dana Farber Canc Inst, Dept Canc Immunol & AIDS, Boston, MA 02115 USA. Harvard Univ, Sch Med, Dept Pathol, Div AIDS, Boston, MA 02115 USA. Harvard Univ, Sch Med, Sch Publ Hlth, Dept Immunol & Infect Dis, Boston, MA 02115 USA. RP Sodroski, J (reprint author), Harvard Univ, Sch Med, Dana Farber Canc Inst, Dept Canc Immunol & AIDS, 44 Binney St,JFB 824, Boston, MA 02115 USA. EM joseph_sodroski@dfci.harvard.edu RI Li, Xing/D-3852-2009; Li, Yuan/B-4098-2013 FU NIAID NIH HHS [AI063987, AI60354, P30 AI060354, R01 AI063987] NR 29 TC 100 Z9 108 U1 0 U2 5 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 JUL PY 2006 VL 80 IS 14 BP 6738 EP 6744 DI 10.1128/JVI.00270-06 PG 7 WC Virology SC Virology GA 059ZF UT WOS:000238770000002 PM 16809279 ER PT J AU Bashirova, AA Bleiber, G Qi, Y Hutcheson, H Yamashita, T Johnson, RC Cheng, J Alter, G Goedert, JJ Buchbinder, S Hoots, K Vlahov, D May, M Maldarelli, F Jacobson, L O'Brien, SJ Telenti, A Carrington, M AF Bashirova, AA Bleiber, G Qi, Y Hutcheson, H Yamashita, T Johnson, RC Cheng, J Alter, G Goedert, JJ Buchbinder, S Hoots, K Vlahov, D May, M Maldarelli, F Jacobson, L O'Brien, SJ Telenti, A Carrington, M TI Consistent effects of TSG101 genetic variability on multiple outcomes of exposure to human immunodeficiency virus type 1 SO JOURNAL OF VIROLOGY LA English DT Article ID CELL-CYCLE ARREST; ESCRT-I; ENDOSOMAL TRAFFICKING; SORTING COMPLEX; LATE DOMAIN; PROTEIN; UBIQUITIN; INTERACTS; HOMOLOG; E2 AB Tumor susceptibility gene 101 (TSG101) encodes a host cellular protein that is appropriated by human immunodeficiency virus type 1 (HIV-1) in the budding process of viral particles from infected cells. Variation in the coding or noncoding regions of the gene could potentially affect the degree of TSG101-mediated release of viral particles. While the coding regions of the gene were found to lack nonsynonymous variants, two polymorphic sites in the TSGI01 5' area were identified that were associated with the rate of AIDS progression among Caucasians. These single-nucleotide polymorphisms (SNPs), located at positions -183 and +181 relative to the translation start, specify three haplotypes termed A, B, and C, which occur at frequencies of 67%, 21%, and 12%, respectively. Haplotype C is associated with relatively rapid AIDS progression, while haplotype B is associated with slower disease progression. Both effects were dominant over the intermediate haplotype A. The haplotypes also demonstrated parallel effects on the rate of CD4 T-cell depletion and viral load increase over time, as well as a possible influence on HIV-1 infection. The data raise the hypothesis that noncoding variation in TSG101 affects the efficiency of TSG101-mediated release of viral particles from infected cells, thereby altering levels of plasma viral load and subsequent disease progression. C1 NCI, SAIC Frederick Inc, Lab Genom Divers, Frederick, MD 21702 USA. Univ Lausanne Hosp, Inst Microbiol, Lausanne, Switzerland. Univ Lausanne Hosp, Div Infect Dis, Lausanne, Switzerland. Johns Hopkins Univ, Sch Hyg & Publ Hlth, Dept Epidemiol, Baltimore, MD USA. Massachusetts Gen Hosp, Partners AIDS Res Ctr, Charlestown, MA 02129 USA. NCI, Viral Epidemiol Branch, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA. Univ Calif San Francisco, San Francisco, CA 94143 USA. Univ Texas, Hlth Sci Ctr, Gulf States Hemophilia Ctr, Houston, TX USA. Univ Bristol, Dept Social Med, Bristol, Avon, England. NCI, HIV Drug Resistance Program, Bethesda, MD 20892 USA. RP Carrington, M (reprint author), NCI, SAIC Frederick Inc, Lab Genom Divers, Frederick, MD 21702 USA. EM carringt@mail.ncifcrf.gov RI May, Margaret/E-8099-2013; SHCS, all/G-4072-2011; SHCS, int. coll. A/G-4083-2011; Johnson, Randall/B-1517-2014 OI May, Margaret/0000-0002-9733-1003; Johnson, Randall/0000-0001-7754-0847 FU NCI NIH HHS [N01CO12400] NR 39 TC 17 Z9 18 U1 0 U2 0 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 JUL PY 2006 VL 80 IS 14 BP 6757 EP 6763 DI 10.1128/JVI.00094-06 PG 7 WC Virology SC Virology GA 059ZF UT WOS:000238770000004 PM 16809281 ER PT J AU Brockman, MA Verschoor, A Zhu, J Carroll, MC Knipe, DM AF Brockman, MA Verschoor, A Zhu, J Carroll, MC Knipe, DM TI Optimal long-term humoral responses to replication-defective herpes simplex virus require CD21/CD35 complement receptor expression on stromal cells SO JOURNAL OF VIROLOGY LA English DT Article ID FOLLICULAR DENDRITIC CELLS; LIVED PLASMA-CELLS; IMMUNE-RESPONSES; VIRAL-INFECTION; IMMUNIZATION; ANTIGEN; MUTANT; PROTECTION; INDUCTION; ANTIBODY AB Replication-defective herpes simplex virus (HSV) strains elicit durable immune responses and protect against virulent HSV challenge in mice, despite being unable to establish latent infection in neuronal cells. Mechanisms for generating long-lived immunity in the absence of viral persistence remain uncertain. In animals immunized with replication-defective HSV, durable serum immunoglobulin G (IgG) responses were elicited. Surprisingly, Western blot analyses revealed that the specificities of antiviral IgG changed over time, and antibody reactivity to some viral proteins was detected only very late. Thus, some of the durable IgG activity appeared to be contributed by either new or significantly enhanced antibody responses at late times. Following immunization, radiation bone marrow-chimeric mice lacking complement receptors CD21 and CD35 on stromal cells elicited only short-lived serum IgG and failed to mount recall responses to subsequent HSV exposure. Our results suggest that complement-mediated retention of viral antigens by stromal cells, such as follicular dendritic cells, is critical for optimal maintenance of antibody responses and B-cell memory following vaccination with replication-defective HSV. C1 Harvard Univ, Sch Med, Dept Microbiol & Mol Genet, Boston, MA 02115 USA. Harvard Univ, Sch Med, Dept Pediat & Pathol, Boston, MA 02115 USA. Harvard Univ, Sch Med, Program Virol, Boston, MA 02115 USA. CBR Inst Biomed Res, Boston, MA 02115 USA. RP Knipe, DM (reprint author), Harvard Univ, Sch Med, Dept Microbiol & Mol Genet, 200 Longwood Ave, Boston, MA 02115 USA. EM David_Knipe@hms.harvard.edu OI Brockman, Mark/0000-0001-6432-1426 FU NIAID NIH HHS [R56 AI057552, AI57552, P01 AI042257, P01 AI046006, P01-AI042257, P02-AI046006, R01 AI057552] NR 39 TC 20 Z9 21 U1 0 U2 0 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 JUL PY 2006 VL 80 IS 14 BP 7111 EP 7117 DI 10.1128/JVI.01421-05 PG 7 WC Virology SC Virology GA 059ZF UT WOS:000238770000039 PM 16809316 ER PT J AU Chang, VW AF Chang, V. W. TI Residential racial isolation and body mass index among U.S. adults SO JOURNAL OF WOMENS HEALTH LA English DT Meeting Abstract C1 VAMC, Ctr Hlth Equ Res & Promot, Philadelphia, PA USA. Univ Penn, Sch Med, Philadelphia, PA 19104 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 1540-9996 J9 J WOMENS HEALTH JI J. Womens Health PD JUL PY 2006 VL 15 IS 6 BP 677 EP 678 PG 2 WC Public, Environmental & Occupational Health; Medicine, General & Internal; Obstetrics & Gynecology; Women's Studies SC Public, Environmental & Occupational Health; General & Internal Medicine; Obstetrics & Gynecology; Women's Studies GA 079LG UT WOS:000240177200020 ER PT J AU Pippins, JR Brawarsky, P Jackson, RA Fuentes-Afflick, E Haas, JS AF Pippins, Jennifer R. Brawarsky, Phyllis Jackson, Rebecca A. Fuentes-Afflick, Elena Haas, Jennifer S. TI Association of breastfeeding with maternal depressive symptoms SO JOURNAL OF WOMENS HEALTH LA English DT Article ID EARLY TERMINATION; AFRICAN-AMERICAN; LOW-INCOME; CES-D; PREGNANT-WOMEN; UNITED-STATES; OLDER ADULTS; HEALTH; RISK; DURATION AB Purpose: To identify risk factors for lack of breastfeeding initiation and duration of < 1 month among a racially diverse cohort of women. In particular, our interest was to examine depressive symptoms during pregnancy as a potential risk factor for not initiating or continuing breastfeeding. Methods: Survey and medical record data from a cohort of pregnant women from the San Francisco Bay area who delivered a singleton infant (n = 1448) were analyzed to examine lack of breastfeeding initiation and duration of < 1 month. Results: In this study, 5.6% of women did not initiate breastfeeding, and 11.1% of women who initiated breastfeeding had a duration of breastfeeding of < 1 month. There were no racial or ethnic differences in initiation of breastfeeding after adjusting for demographic and clinical characteristics. At 1 month postpartum, African American women were more likely than white women to have a duration of breastfeeding lasting < 1 month. Depressive symptoms during or prior to pregnancy had no effect on initiation of breastfeeding even when symptoms were persistent. Women with persistent depressive symptoms ( symptoms at two time points, including one prior to delivery) were more likely to have breastfeeding duration of < 1 month ( odds ratio [OR] 1.77, 95% confidence interval [95% CI] 1.10- 2.86), whereas depressive symptoms at a single time point were not associated with breastfeeding duration of < 1 month. Conclusions: Addressing depressive symptoms experienced by women both during and after pregnancy may improve the duration of breastfeeding. C1 Brigham & Womens Hosp, Div Gen Med & Primary Care, Dept Med, Boston, MA 02120 USA. Childrens Hosp, Dept Med, Boston, MA 02115 USA. Brigham & Womens Hosp, Dept Med, Boston, MA 02115 USA. Massachusetts Gen Hosp, Dept Pediat, Boston, MA 02114 USA. Harvard Univ, Sch Med, Boston, MA 02115 USA. Univ Calif San Francisco, Dept Obstet Gynecol & Reprod Sci, San Francisco, CA 94143 USA. Univ Calif San Francisco, Dept Epidemiol & Biostat, San Francisco, CA 94143 USA. Univ Calif San Francisco, Dept Pediat, San Francisco, CA 94143 USA. RP Haas, JS (reprint author), Brigham & Womens Hosp, Div Gen Med & Primary Care, Dept Med, 1620 Tremont St, Boston, MA 02120 USA. EM jhaas@partners.org FU NICHD NIH HHS [R01 HD037389, R01 HD037389-03, R01 HD37389] NR 46 TC 27 Z9 27 U1 3 U2 9 PU MARY ANN LIEBERT INC PI NEW ROCHELLE PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA SN 1540-9996 J9 J WOMENS HEALTH JI J. Womens Health PD JUL PY 2006 VL 15 IS 6 BP 754 EP 762 DI 10.1089/jwh.2006.15.754 PG 9 WC Public, Environmental & Occupational Health; Medicine, General & Internal; Obstetrics & Gynecology; Women's Studies SC Public, Environmental & Occupational Health; General & Internal Medicine; Obstetrics & Gynecology; Women's Studies GA 079LG UT WOS:000240177200058 PM 16910907 ER PT J AU Fried, LF Shlipak, MG Stehman-Breen, C Mittalhenkle, A Seliger, S Samak, M Robbins, J Siscovick, D Harris, TB Newman, AB Cauley, JA AF Fried, Linda F. Shlipak, Michael G. Stehman-Breen, Catherine Mittalhenkle, Anuja Seliger, Stephen Samak, Mark Robbins, John Siscovick, David Harris, Tamara B. Newman, Anne B. Cauley, Jane A. TI Kidney function predicts the rate of bone loss in older individuals: The cardiovascular health study SO JOURNALS OF GERONTOLOGY SERIES A-BIOLOGICAL SCIENCES AND MEDICAL SCIENCES 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 SERUM CYSTATIN-C; GLOMERULAR-FILTRATION-RATE; MINERAL DENSITY; POSTMENOPAUSAL WOMEN; RENAL-INSUFFICIENCY; HIP FRACTURE; ELDERLY-MEN; OSTEOPOROSIS; RISK; ALENDRONATE AB Background. Results of cross-sectional analyses of the association of kidney function with bone mineral density (BMD) have been conflicting. We examined the association of cystatin-C, a new marker of kidney function that is unrelated to lean mass, with initial and follow-up BMD, in an ancillary study of the Cardiovascular Health Study, a population-based cohort of individuals >= 65 years old. Methods. Two years after measurement of cystatin-C and other covariates, the first BMD was measured in Pittsburgh, Pennsylvania and Davis, California, by using dual energy x-ray absorptiometry. Follow-up BMD was measured in Pittsburgh 4 years later. Associations of cystatin-C with initial BMD and the change in BMD (%/y) at the hip were examined with linear regression. Analyses were conducted separately for men and women. Results. In 1519 participants who had cystatin-C and initial BMD assessed, 614 had follow-up BMD. The percent annual change in BMD at the total hip by cystatin-C quartiles was -0.24, -0.13, -0.40, and -0.66%/y (first to fourth quartile) in women and -0.02, -0.30, -0.18, and -0.94%/y in men. After adjusting for potential confounders, cystatin-C was marginally associated with initial BMD in men but not women. Cystatin-C was associated with bone loss in men; after adjustment for weight loss, cystatin-C was not associated with bone loss in women. Conclusion. Kidney dysfunction, as assessed by cystatin-C, is associated with a more rapid loss of BMD at the hip, especially in men. Further studies are needed to confirm these findings and to determine whether this loss leads to an elevated risk of fracture. C1 VA Pittsburgh Healthcare Syst, Pittsburgh, PA 15240 USA. Univ Pittsburgh, Sch Med, Dept Med, Pittsburgh, PA 15260 USA. VA Med Ctr, San Francisco, CA USA. Univ Calif San Francisco, Dept Med, San Francisco, CA 94143 USA. Amgen Inc, Thousand Oaks, CA USA. Oregon Hlth Sci Univ, Dept Med, Portland, OR 97201 USA. Univ Maryland, Dept Med, College Pk, MD 20742 USA. Tufts Univ, New England Med Ctr, Dept Med, Boston, MA 02111 USA. Univ Calif Davis, Dept Med, Davis, CA 95616 USA. Univ Washington, Dept Med, Seattle, WA 98195 USA. NIA, NIH, Bethesda, MD 20892 USA. Univ Pittsburgh, Grad Sch Publ Hlth, Dept Epidemiol, Pittsburgh, PA 15260 USA. RP Fried, LF (reprint author), VA Pittsburgh Healthcare Syst, Univ Dr,Mailstop 111F-U, Pittsburgh, PA 15240 USA. EM linda.fried@med.va.gov RI Newman, Anne/C-6408-2013; Cauley, Jane/N-4836-2015 OI Newman, Anne/0000-0002-0106-1150; Cauley, Jane/0000-0003-0752-4408 FU NHLBI NIH HHS [N01-HC-35129, N01 HC-15103, N01-HC-85079, N01-HC-85086] NR 31 TC 27 Z9 27 U1 0 U2 1 PU GERONTOLOGICAL SOCIETY AMER PI WASHINGTON PA 1030 15TH ST NW, STE 250, WASHINGTON, DC 20005202-842 USA SN 1079-5006 J9 J GERONTOL A-BIOL JI J. Gerontol. Ser. A-Biol. Sci. Med. Sci. PD JUL PY 2006 VL 61 IS 7 BP 743 EP 748 PG 6 WC Geriatrics & Gerontology; Gerontology SC Geriatrics & Gerontology GA 071ZO UT WOS:000239642600017 PM 16870638 ER PT J AU Baumgarten, M Margolis, DJ Localio, AR Kagan, SH Lowe, RA Kinosian, B Holmes, JH Abbuhl, SB Kavesh, W Ruffin, A AF Baumgarten, Mona Margolis, David J. Localio, A. Russell Kagan, Sarah H. Lowe, Robert A. Kinosian, Bruce Holmes, John H. Abbuhl, Stephanie B. Kavesh, William Ruffin, Althea TI Pressure ulcers among elderly patients early in the hospital stay SO JOURNALS OF GERONTOLOGY SERIES A-BIOLOGICAL SCIENCES AND MEDICAL SCIENCES LA English DT Article ID NURSING-HOME RESIDENTS; RISK-FACTORS; PREDICTIVE-VALIDITY; NATIONAL-HEALTH; SORE PREVENTION; BRADEN SCALE; INCONTINENCE AB Background. Pressure ulcers among elderly hospital patients diminish quality of life and increase the cost of hospital care. Evidence suggests that pressure ulcers can arise after only a few hours of immobility. The goals of this study were to estimate the incidence of hospital-acquired pressure ulcers in the first 2 days of the hospital stay and to identify patient characteristics associated with higher incidence. Methods. A prospective cohort study was performed between 1998 and 2001. A total of 3233 patients 65 years old or older admitted through the Emergency Department to the inpatient Medical Service at two study hospitals were examined by a research nurse on the third day of hospitalization. Pressure ulcers were ascertained using standard criteria and were classified as either preexisting, possibly hospital-acquired, or definitely hospital-acquired. Results. There were 201 patients with one or more possibly or definitely hospital-acquired pressure ulcers for a cumulative incidence of 6.2% (95% confidence interval, 5.4%-7.1%). Most of the pressure ulcers were stage 2, and the majority were in the sacral area or on the heels. In multivariable analysis, pressure ulcer incidence was significantly associated with increasing age, male gender, dry skin, urinary and fecal incontinence, difficulty turning in bed, nursing home residence prior to admission, recent hospitalization, and poor nutritional status. Conclusions. A small but significant proportion of elderly emergently admitted hospital patients acquire pressure ulcers soon after their admission. New models of care may be required to ensure that preventive interventions are provided very early in the elderly person's hospital stay. C1 Univ Maryland, Sch Med, Baltimore, MD 21201 USA. Univ Penn, Sch Med, Philadelphia, PA 19104 USA. Univ Penn, Sch Nursing, Philadelphia, PA 19104 USA. Oregon Hlth Sci Univ, Portland, OR 97201 USA. Philadelphia VA Med Ctr, Philadelphia, PA USA. RP Baumgarten, M (reprint author), Univ Maryland, Sch Med, 660 W Redwood St,Suite 200, Baltimore, MD 21201 USA. EM mbaumgar@epi.umaryland.edu FU NIA NIH HHS [R01-AG-14127] NR 52 TC 63 Z9 65 U1 0 U2 6 PU GERONTOLOGICAL SOCIETY AMER PI WASHINGTON PA 1030 15TH ST NW, STE 250, WASHINGTON, DC 20005202-842 USA SN 1079-5006 J9 J GERONTOL A-BIOL JI J. Gerontol. Ser. A-Biol. Sci. Med. Sci. PD JUL PY 2006 VL 61 IS 7 BP 749 EP 754 PG 6 WC Geriatrics & Gerontology; Gerontology SC Geriatrics & Gerontology GA 071ZO UT WOS:000239642600018 PM 16870639 ER PT J AU Kellum, J Palevsky, PM AF Kellum, John Palevsky, Paul M. TI Renal support in acute kidney injury SO LANCET LA English DT Editorial Material ID CONTINUOUS VENOVENOUS HEMOFILTRATION; CRITICALLY-ILL PATIENTS; REPLACEMENT THERAPY; FAILURE; INTERMITTENT; DIALYSIS; TRIAL; HEMODIALYSIS; GUIDELINES C1 Univ Pittsburgh, Sch Med, Dept Crit Care Med, Pittsburgh, PA 15261 USA. Univ Pittsburgh, Sch Med, Dept Med, Pittsburgh, PA 15261 USA. VA Pittsburgh Healthcare Syst, Renal Sect, Pittsburgh, PA USA. RP Kellum, J (reprint author), Univ Pittsburgh, Sch Med, Dept Crit Care Med, Pittsburgh, PA 15261 USA. EM kellumja@ccm.upmc.edu NR 14 TC 13 Z9 13 U1 0 U2 0 PU LANCET LTD PI LONDON PA 84 THEOBALDS RD, LONDON WC1X 8RR, ENGLAND SN 0140-6736 J9 LANCET JI Lancet PD JUL-AUG PY 2006 VL 368 IS 9533 BP 344 EP 345 DI 10.1016/S0140-6736(06)69084-3 PG 2 WC Medicine, General & Internal SC General & Internal Medicine GA 069JJ UT WOS:000239441900006 PM 16876645 ER PT J AU Jiang, Z Chu, PGG Woda, BA Rock, KL Liu, Q Hsieh, CC Li, CZ Chen, WG Duan, HO McDougal, S Wu, CL AF Jiang, Zhong Chu, Peigou G. Woda, Bruce A. Rock, Kenneth L. Liu, Qin Hsieh, Chung-Cheng Li, Cuizhen Chen, Wengang Duan, Hai Ou McDougal, Scott Wu, Chin-Lee TI Analysis of RNA-binding protein IMP3 to predict metastasis and prognosis of renal-cell carcinoma: a retrospective study SO LANCET ONCOLOGY LA English DT Article ID MESSENGER-RNA; CANCER; EXPRESSION; SURVIVAL; THERAPY; DOMAIN; KOC AB Background Distant metastasis is the main cause of death from renal-cell carcinoma, and the metastatic potential of tumours is often unpredictable. We aimed to investigate whether IMP3, an oncofetal RNA-binding protein, can be used as a biomarker to predict metastasis and prognosis of renal-cell carcinoma. Methods We studied 501 primary and metastatic renal-cell tumours. 371 patients with localised primary tumours were further investigated by use of survival analysis. We assessed IMP3 expression in tumour tissues by immunohistochemistry, and IMP3 mRNA and protein expression in selected tissues by quantitative real-time PCR and western blot analysis. Findings Compared with non-metastatic renal-cell tumours, IMP3 expression was greatly increased not only in metastatic tumours but also in a subset of primary tumours; that were likely to subsequently develop metastases. Patients with primary localised tumours that did not express IMP3 had a longer metastasis-free survival and overall survival than did those with tumours expressing IMP3 (p < 0(.)0001). Patients with IMP3-positive localised tumours had a much lower 5-year metastasis-free survival than did those with IMP3-negative tumours (for stage I tumours, 44% vs 98%, hazard ratio 17(.)18 [95% CI 7.82-37(.)78]; stage II, 41% vs 94%, 10(.)14 [3(.)46-29(.)68]; stage III, 16% vs 62%, 4(.)04 [2(.)23-7(.)31]). IMP3 expression was also associated with reduced 5-year overall survival (stage I, 32% vs 89%, 6(.)44 [3(.)63-11(.)42]; stage II, 41% vs 88%, 6(.)93 [2(.)63-18(.)27]; stage III, 14% vs 58%, 3(.)46 [1(.)98-6(.)05]). Multivariable analysis of IMP3 status (positive vs negative) in primary tumours showed hazard ratios of 5(.)84 (95% CI 3(.)60-9(.)49) for metastasis-free survival and 4(.)01 (2(.)66-6(.)05) for overall survival (both p < 0(.)0001), which were much higher than hazard ratios associated with other independent risk factors. Interpretation IMP3 is an independent prognostic marker that can be used at initial diagnosis of renal-cell carcinoma to identify patients who have a high potential to develop metastasis and who might benefit from early systemic treatment. C1 Univ Massachusetts, Med Ctr, Dept Pathol, Worcester, MA USA. Univ Massachusetts, Med Ctr, Dept Cell Biol, Worcester, MA USA. City Hope Natl Med Ctr, Div Pathol, Los Angeles, CA USA. Massachusetts Gen Hosp, Dept Pathol, Boston, MA 02114 USA. Harvard Univ, Sch Med, Boston, MA USA. RP Jiang, Z (reprint author), Three Biotech, Dept Pathol, 1 Innovat Dr, Worcester, MA 01605 USA. EM jiangz@ummhc.org NR 21 TC 148 Z9 160 U1 0 U2 3 PU LANCET LTD PI LONDON PA 84 THEOBALDS RD, LONDON WC1X 8RR, ENGLAND SN 1470-2045 J9 LANCET ONCOL JI Lancet Oncol. PD JUL PY 2006 VL 7 IS 7 BP 556 EP 564 DI 10.1016/S1470-2045(06)70732-X PG 9 WC Oncology SC Oncology GA 060SP UT WOS:000238822200022 PM 16814207 ER PT J AU Pandolfino, T Laubach, HJ Gagnon, D Avram, M Manstein, D AF Pandolfino, Tomi Laubach, Hans J. Gagnon, Denise Avram, Mathew Manstein, Dieter TI Rapid and scarless wound healing after CO2 laser-assisted ablative fractional photothermolysis of non-facial skin SO LASERS IN SURGERY AND MEDICINE LA English DT Meeting Abstract CT 26th Annual Meeting of the American-Society-for-Laser-Medicine-and-Surgery CY APR 05-09, 2006 CL Boston, MA SP Amer Soc Laser Med & Surg C1 Harvard Univ, Sch Med, Massachusetts Gen Hosp, Wellman Ctr Photomed, Boston, MA USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 0196-8092 J9 LASER SURG MED JI Lasers Surg. Med. PD JUL PY 2006 VL 38 IS 6 BP 648 EP 648 PG 1 WC Dermatology; Surgery SC Dermatology; Surgery GA 072VL UT WOS:000239701000014 ER PT J AU van Vlierberghe, P Meijerink, JPP Lee, C Ferrando, AA T Look, A van Wering, ER Beverloo, HB Aster, JC Pieters, R AF van Vlierberghe, P. Meijerink, J. P. P. Lee, C. Ferrando, A. A. T Look, A. van Wering, E. R. Beverloo, H. B. Aster, J. C. Pieters, R. TI A new recurrent 9q34 duplication in pediatric T-cell acute lymphoblastic leukemia SO LEUKEMIA LA English DT Article DE array-CGH; 9q34 duplication; pediatric T-ALL ID COMPARATIVE GENOMIC HYBRIDIZATION; HIGH-RESOLUTION ANALYSIS; DNA COPY NUMBER; GENE; PROTEIN; TRANSLOCATION; MICROARRAYS; EXPRESSION; DISEASE; CANCER AB Over the last decade, genetic characterization of T-cell acute lymphoblastic leukemia (T-ALL) has led to the identification of a variety of chromosomal abnormalities. In this study, we used array-comparative genome hybridization (array-CGH) and identified a novel recurrent 9q34 amplification in 33% (12/ 36) of pediatric T-ALL samples, which is therefore one of the most frequent cytogenetic abnormalities observed in T-ALL thus far. The exact size of the amplified region differed among patients, but the critical region encloses similar to 4 Mb and includes NOTCH1. The 9q34 amplification may lead to elevated expression of various genes, and MRLP41, SSNA1 and PHPT1 were found significantly expressed at higher levels. Fluorescence in situ hybridization (FISH) analysis revealed that this 9q34 amplification was in fact a 9q34 duplication on one chromosome and could be identified in 17 -39 percent of leukemic cells at diagnosis. Although this leukemic subclone did not predict for poor outcome, leukemic cells carrying this duplication were still present at relapse, indicating that these cells survived chemotherapeutic treatment. Episomal NUP214-ABL1 amplification and activating mutations in NOTCH1, two other recently identified 9q34 abnormalities in T-ALL, were also detected in our patient cohort. We showed that both of these genetic abnormalities occur independently from this newly identified 9q34 duplication. C1 Sophia Childrens Univ Hosp, Erasmus MC, Dept Pediat Oncol Hematol, NL-3000 CB Rotterdam, Netherlands. Harvard Univ, Sch Med, Brigham & Womens Hosp, Dept Pathol, Boston, MA 02115 USA. Harvard Univ, Sch Med, Dept Pediat Oncol, Dana Farber Canc Inst, Boston, MA 02115 USA. Harvard Univ, Sch Med, Div Hematol Oncol, Childrens Hosp, Boston, MA 02115 USA. DCOG, The Hague, Netherlands. Erasmus MC, Dept Clin Genet, Rotterdam, Netherlands. RP Meijerink, JPP (reprint author), Sophia Childrens Univ Hosp, Erasmus MC, Dept Pediat Oncol Hematol, Room Sp 2456,Dr Molewaterpl 60,POB 2060, NL-3000 CB Rotterdam, Netherlands. EM j.meijerink@erasmusmc.nl RI Van Vlierberghe, Pieter/G-8894-2013; Ferrando, Adolfo /Q-7026-2016; Meijerink, Jules/D-4393-2017 OI Van Vlierberghe, Pieter/0000-0001-9063-7205; Meijerink, Jules/0000-0002-6860-798X NR 29 TC 35 Z9 36 U1 0 U2 4 PU NATURE PUBLISHING GROUP PI LONDON PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND SN 0887-6924 J9 LEUKEMIA JI Leukemia PD JUL PY 2006 VL 20 IS 7 BP 1245 EP 1253 DI 10.1038/sj.leu.2404247 PG 9 WC Oncology; Hematology SC Oncology; Hematology GA 064JM UT WOS:000239085100009 PM 16673019 ER PT J AU Cripe, LD Rader, K Tallman, MS Gordon, MS Paietta, E Bennett, J Neuberg, D Litzow, MR O'Brien, TE Rowe, JM AF Cripe, LD Rader, K Tallman, MS Gordon, MS Paietta, E Bennett, J Neuberg, D Litzow, MR O'Brien, TE Rowe, JM TI Phase II trial of subcutaneous recombinant human interleukin 11 with subcutaneous recombinant human granulocyte-macrophage colony stimulating factor in patients with acute myeloid leukemia (AML) receiving high-dose cytarabine during induction: ECOG 3997 SO LEUKEMIA RESEARCH LA English DT Article DE acute myeloid leukemia; thrombocytopenia; recombinant interleukin 11; high-dose cytarabine; induction chemotherapy ID ACUTE MYELOGENOUS LEUKEMIA; HUMAN MEGAKARYOCYTE GROWTH; PLACEBO-CONTROLLED TRIAL; ONCOLOGY-GROUP; DOUBLE-BLIND; CHEMOTHERAPY; THROMBOCYTOPENIA; DAUNORUBICIN; REMISSION; THERAPY AB Randomized trials of substituting high-dose cytarabine (HiDAC) for standard dose cytarabine (SDAC) during induction therapy for newly diagnosed AML have not demonstrated an improvement in the complete remission (CR) rate. Phase II trials of the scheduled administration of HiDAC after SDAC suggest an improved outcome. The hematological complications of intensification are considerable. GM-CSF after chemotherapy improved the survival of older patients in a randomized trial. Recombinant human interleukin 11, a thrombopoietic cytokine, reduced the incidence of chemotherapy-induced thrombocytopenia in patients with solid tumors. Therefore, 34 patients were treated, with newly diagnosed AML less than 56 years of age, with daunorubicin 45 mg/m(2) on days 1-3, cytarabine 100 mg/m(2) days 1-7 and cytarabine 2 g/m(2) for 12 h on days 8-10 (7 + 3 + 3). rhIL-11 (50 mu g/kg/day,) and GM-CSF (250 mu g/kg/day) were administered subcutaneously from day 11 until recovery. The complete remission rate was 59% (90% C.I. 43-73%). The median time to recovery of neutrophils to > 500 and platelets to >= 20,000 mu l(-1) was 27 days (95% C.I. 27-30 days) and 25 days (95% C.I. 24-29 days), respectively. The trial does not confirm the high CR rate observed in phase II trials, despite optimal supportive care. (c) 2005 Elsevier Ltd. All rights reserved. C1 Indiana Univ, Med Ctr, Indianapolis, IN USA. Dana Farber Canc Inst, Boston, MA 02115 USA. Northwestern Univ, Feinberg Sch Med, Chicago, IL 60611 USA. Arizona Canc Ctr, Phoenix, AZ USA. Our Lady Mercy Med Ctr, Bronx, NY USA. Univ Rochester, Ctr Canc, Rochester, NY USA. Mayo Clin, Rochester, MN USA. Case Western Reserve Univ, Cleveland, OH 44106 USA. Rambam Med Ctr, Haifa, Israel. RP Cripe, LD (reprint author), Indiana Univ, Med Ctr, Indianapolis, IN USA. EM lcripe@iupui.edu FU NCI NIH HHS [CA14548, CA23318, CA13650, CA66636, CA17145, CA21115, CA49883, CA11083] NR 18 TC 3 Z9 3 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND SN 0145-2126 J9 LEUKEMIA RES JI Leuk. Res. PD JUL PY 2006 VL 30 IS 7 BP 823 EP 827 DI 10.1016/j.leukres.2005.11.006 PG 5 WC Oncology; Hematology SC Oncology; Hematology GA 060FK UT WOS:000238787600009 PM 16413056 ER PT J AU Wiggins, GC Triantafyllou, C Potthast, A Reykowski, A Nittka, M Wald, LL AF Wiggins, G. C. Triantafyllou, C. Potthast, A. Reykowski, A. Nittka, M. Wald, L. L. TI 32-Channel 3 tesla receive-only phased-array head coil with soccer-ball element geometry SO MAGNETIC RESONANCE IN MEDICINE LA English DT Article DE phased array; 32-channel; RF coil design; SNR; g-factor ID TO-NOISE RATIO; SURFACE COILS; SENSITIVITY; SENSE; SPECTROSCOPY; PERFORMANCE; DESIGN; MRI AB A 32-channel 3T receive-only phased-array head coil was developed for human brain imaging. The helmet-shaped array was designed to closely fit the head with individual overlapping circular elements arranged in patterns of hexagonal and pentagonal symmetry similar to that of a soccer ball. The signal-to-noise ratio (SNR) and noise amplification (g-factor) in accelerated imaging applications were quantitatively evaluated in phantom and human images and compared with commercially available head coils. The 32-channel coil showed SNR gains of up to 3.5-fold in the cortex and 1.4-fold in the corpus callosum compared to a (larger) commercial eight-channel head coil. The experimentally measured g-factor performance of the helmet array showed significant improvement compared to the eight-channel array (peak g-factor 59% and 26% of the eight-channel values for four- and fivefold acceleration). The performance of the arrays is demonstrated in high-resolution and highly accelerated brain images. C1 Massachusetts Gen Hosp, AA Martinos Ctr Biomed Imaging, Dept Radiol, Boston, MA 02129 USA. Siemens Med Solut, Erlangen, Germany. Invivo Corp, Gainesville, FL USA. RP Wiggins, GC (reprint author), AA Martinos Ctr Biomed Imaging, Bldg 149,13th St,Mailcode 149-2301, Boston, MA 02129 USA. EM gwiggins@nmr.mgh.harvard.edu RI Triantafyllou, Christina/E-7724-2011; Wald, Lawrence/D-4151-2009 FU NCRR NIH HHS [5P41RR014075-05] NR 18 TC 193 Z9 194 U1 2 U2 14 PU JOHN WILEY & SONS INC PI HOBOKEN PA 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 0740-3194 J9 MAGN RESON MED JI Magn. Reson. Med. PD JUL PY 2006 VL 56 IS 1 BP 216 EP 223 DI 10.1002/mrm.20925 PG 8 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA 060TD UT WOS:000238823600024 PM 16767762 ER PT J AU Steinman, MA Ranji, SR Shojania, KG Gonzales, R AF Steinman, Michael A. Ranji, Sumant R. Shojania, Kaveh G. Gonzales, Ralph TI Improving antibiotic selection - A systematic review and quantitative analysis of quality improvement strategies SO MEDICAL CARE LA English DT Article DE quality improvement; antibiotic use; meta analysis ID RANDOMIZED CONTROLLED-TRIAL; RESPIRATORY-TRACT INFECTIONS; GENERAL-PRACTICE; PRIMARY-CARE; EDUCATIONAL INTERVENTION; PRESCRIBER FEEDBACK; DRUG-TREATMENT; OTITIS-MEDIA; HEALTH-CARE; PRESCRIPTION AB Objective: We sought to assess which interventions are most effective at improving the prescribing of recommended antibiotics for acute outpatient infections. Design and Methods: We undertook a systematic review with quantitative analysis of the Cochrane Registry Effective Practice and Organization of Care (EPOC) database, supplemented by MEDLINE and hand-searches. Inclusion criteria included clinical trials with contemporaneous or strict historical controls that reported data on antibiotic selection in acute outpatient infections. The effect size of studies with different intervention types were compared using nonparametric statistics. To maximize comparability between studies, quantitative analysis was restricted to studies that reported absolute changes in the amount of or percent compliance with recommended antibiotic prescribing. Results: Twenty-six studies reporting 33 trials met inclusion criteria. Most interventions used clinician education alone or in combination with audit and feedback. Among the 22 comparisons amenable to quantitative analysis, recommended antibiotic prescribing improved by a median of 10.6% (interquartile range [IQR] 3.4-18.2%). Trials evaluating clinician education alone reported larger effects than interventions combining clinician education with audit and feedback (median effect size 13.9% [IQR 8.6-21.6%] vs. 3.4% [IQR 1.8-9.7%], P = 0.03). This result was confounded by trial sample size, as trials having a smaller number of participating clinicians reported larger effects and were more likely to use clinician education alone. Active forms of education, sustained interventions, and other features traditionally associated with successful quality improvement interventions were not associated with effect size and showed no evidence of confounding the association between clinician education-only strategies and outcome. Conclusions: Multidimensional interventions using audit and feedback to improve antibiotic selection were less effective than interventions using clinician education alone. Although confounding may partially account for this finding, our results suggest that enhancing the intensity of a focused intervention may be preferable to a less intense, multidimensional approach. C1 Univ Calif San Francisco, Dept Med, San Francisco, CA 94121 USA. Univ Calif San Francisco, Div Gen Internal Med, San Francisco, CA 94121 USA. San Francisco VA Med Ctr, Div Geriatr, San Francisco, CA USA. Univ Ottawa, Ottawa, ON K1N 6N5, Canada. Ottawa Hlth Res Inst, Clin Epidemiol Program, Ottawa, ON, Canada. RP Steinman, MA (reprint author), Univ Calif San Francisco, Dept Med, 4150 Clement St,Box 181G, San Francisco, CA 94121 USA. EM mike.steinman@ucsf.edu NR 50 TC 37 Z9 39 U1 1 U2 1 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0025-7079 J9 MED CARE JI Med. Care PD JUL PY 2006 VL 44 IS 7 BP 617 EP 628 DI 10.1097/01.mlr.0000215846.25591.22 PG 12 WC Health Care Sciences & Services; Health Policy & Services; Public, Environmental & Occupational Health SC Health Care Sciences & Services; Public, Environmental & Occupational Health GA 060MM UT WOS:000238806300003 PM 16799356 ER PT J AU Egede, LE AF Egede, Leonard E. TI Disease-focused or integrated treatment: Diabetes and depression SO MEDICAL CLINICS OF NORTH AMERICA LA English DT Article ID INTERNATIONAL PRIMARY-CARE; PLACEBO-CONTROLLED TRIAL; MAJOR DEPRESSION; MEDICATION ADHERENCE; COMORBID DEPRESSION; GLYCEMIC CONTROL; ANTIDEPRESSANT TREATMENT; RANDOMIZED-TRIAL; CHRONIC ILLNESS; OLDER PATIENTS AB Diabetes and depression are chronic debilitating conditions that are associated with significant morbidity, mortality, and health care costs. Most patients who have diabetes are treated in primary care settings; however, multiple studies have shown that recognition and treatment of depression is less than optimal in this setting. This article reviews the literature on the adverse health outcomes of the coexistence of diabetes and depression, the challenges of treating coexisting diabetes and depression in a fragmented health care system, and the need for integrated care as a strategy to improve the quality of care for patients with complex medical illnesses (eg, patients who have coexisting diabetes and depression). C1 Med Univ S Carolina, Ctr Hlth Dispar Res, Charleston, SC 29425 USA. Ralph H Johnson VAMC, Charleston VA Targeted Res Enhancement Program, Charleston, SC USA. RP Egede, LE (reprint author), Med Univ S Carolina, Ctr Hlth Dispar Res, 135 Rutledge Ave,Room 280H,POB 250593, Charleston, SC 29425 USA. EM egedel@musc.edu FU AHRQ HHS [5K08HS11418] NR 88 TC 10 Z9 10 U1 3 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 0025-7125 J9 MED CLIN N AM JI Med. Clin. N. Am. PD JUL PY 2006 VL 90 IS 4 BP 627 EP + DI 10.1016/j.mcna.2006.04.001 PG 21 WC Medicine, General & Internal SC General & Internal Medicine GA 071QB UT WOS:000239615600008 PM 16843766 ER PT J AU Swan, JS Lawrence, WF Roy, J AF Swan, J. Shannon Lawrence, William F. Roy, Jessica TI Process utility in breast biopsy SO MEDICAL DECISION MAKING LA English DT Article DE health utilities; health status measures; quality-adjusted life years; utility assessment; cost-effectiveness ID COST-EFFECTIVENESS; TIME-TRADEOFF; STANDARD-GAMBLE; HEALTH STATE; DISEASE; ANGIOGRAPHY; PREFERENCES; QUALITY; VALUES; STROKE AB Purpose. To determine whether the waiting trade-off (WTO) is feasible for differentiating short-term biopsy preferences in an acute situation where anxiety is the symptomatic disease state. Methods, 75 women with past experience of either breast core-needle biopsy (CNB), more invasive excisional surgical biopsy (EXB), or both, had telephone WTO assessments. Patients' baseline and test-related anxiety were valued by time trade-off (TTO) used to scale the WTO. Rating scales (RS) were obtained for convergent validity assessment with WTO and TTO. Results. Data were obtained in 38 women who hod both CNB and EXB ("paired") and 20 who had CNB only and 16 who had EXB only ("unpaired"). Patients rated only the procedure(s) they experienced. Median paired and mean unpaired WTO scores indicated patients were willing to wait significantly longer to avoid EXB (P = 0.0003, P = 0.0002, respectively). The waiting time difference between EXB and CNB was 2.1 weeks greater in unpaired data than paired data. RS scores comparing the procedures were significantly different only for paired data (P < 0.05). Median TTO preferences for baseline (1.00) and test anxiety (0.93) obtained in 74 patients were significantly different (P < 0.0001) and consistent with RS. Correlation was noted between WTO and RS (-0.307 to -0.453, P = 0.0205 to 0,0001). The median EXB quality-adjusted life years toll (similar to 1.5 quality-adjusted life days) calculated from pooled WTO data (paired and unpaired) from 54 patients is near a threshold in a published model. Conclusion. The WTO is feasible for discriminating preferences for short-term health states in an acute medical scenario where it might have been expected to be impracticable. C1 Indiana Univ, Dept Radiol, Educ & Res Inst, Indianapolis, IN 46204 USA. Agcy Hlth Res & Qual, Ctr Outcomes & Effectiveness, Rockville, MD USA. RP Swan, JS (reprint author), Harvard Univ, Sch Med, Massachusetts Gen Hosp, Inst Technol Assessment, 101 Merrimac St,10th Floor, Boston, MA 02114 USA. EM shannon@mgh-ita.org NR 26 TC 22 Z9 22 U1 1 U2 3 PU SAGE PUBLICATIONS INC PI THOUSAND OAKS PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA SN 0272-989X J9 MED DECIS MAKING JI Med. Decis. Mak. PD JUL-AUG PY 2006 VL 26 IS 4 BP 347 EP 359 DI 10.1177/0272989X06290490 PG 13 WC Health Care Sciences & Services; Medical Informatics SC Health Care Sciences & Services; Medical Informatics GA 066PV UT WOS:000239243500008 PM 16855124 ER PT J AU Rider, EA Keefer, CH AF Rider, EA Keefer, CH TI Communication skills competencies: definitions and a teaching toolbox SO MEDICAL EDUCATION LA English DT Article DE communication; clinical competence, standards; teaching, methods; curriculum; physician-patient relations ID PHYSICIAN-PATIENT COMMUNICATION; STRUCTURED CLINICAL EXAMINATION; CARE; REFLECTION; EMPATHY AB BACKGROUND Doctors' interpersonal and communication skills correlate with improved health care outcomes. International medical organisations require competency in communication skills. The Accreditation Council for Graduate Medical Education (ACGME) developed a toolbox for assessing this competency and 5 others, yet none initially for teaching these skills. PURPOSE AND METHODS The original focus in the development of the ACGME competencies was evaluation. This paper represents a significant step toward defining methods for teaching communication skills competencies. A total of 16 medical education leaders from medical schools worldwide, participating in the 2003 Harvard Macy Institute Program for Physician Educators, worked together to: (1) further define the ACGME competency in interpersonal and communication skills; (2) delineate teaching strategies for each level of medical education; and (3) create a teaching toolbox to integrate communication skills competencies into medical curricula. Four subgroups defined subcompetencies, identified teaching strategies for undergraduate, graduate and postgraduate medical training and brought their work to the larger group. The expanded communication competencies and teaching strategies were determined by a consensus of the larger group, presented to 80 Harvard Macy Scholars and Faculty for further discussion, then finalised by consensus. CONCLUSION The teaching toolbox expands the ACGME core communication competencies, adds 20 subcompetencies and connects these competencies to teaching strategies at each level of medical training. It represents the collaboration and consensus of a diverse international group of medical education leaders in a variety of medical specialities and institutions, all involved in teaching communication skills. The toolbox is applicable globally across different settings and specialities, and is sensitive to different definitions of health care. C1 Harvard Univ, Sch Med, Commun Skills Teaching Program, Boston, MA USA. Massachusetts Gen Hosp, Stoeckle Ctr Primary Care Innovat, Programs Commun Skills, Boston, MA 02114 USA. Childrens Hosp, Program Enhance Relat & Commun Skills, Boston, MA 02115 USA. Brigham & Womens Hosp, Boston, MA 02115 USA. Childrens Hosp, Brazelton Inst, Boston, MA 02115 USA. Childrens Hosp, Touchpoints Ctr, Boston, MA 02115 USA. RP Rider, EA (reprint author), Harvard Sch Med Pediat, 1153 Ctr St,Suite 31, Boston, MA 02130 USA. EM elizabeth_rider@hms.harvard.edu NR 37 TC 57 Z9 60 U1 5 U2 24 PU BLACKWELL PUBLISHING PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DQ, OXON, ENGLAND SN 0308-0110 J9 MED EDUC JI Med. Educ. PD JUL PY 2006 VL 40 IS 7 BP 624 EP 629 DI 10.1111/j.1365-2929.2006.02500.x PG 6 WC Education, Scientific Disciplines; Health Care Sciences & Services SC Education & Educational Research; Health Care Sciences & Services GA 055YN UT WOS:000238487400004 PM 16836534 ER PT J AU Lu, HM AF Lu, Hsiao-Ming TI On measuring depth-dose distribution of range-modulated proton therapy fields SO MEDICAL PHYSICS LA English DT Article DE depth-dose scanning; proton therapy AB Depth-dose profile measurements are frequently performed for the characterization of spread-out Bragg peak treatment fields in proton therapy. The measured distribution often contains a significant amount of noise with a persistent pattern. As a result, substantial smoothing has to be applied which can alter a measurement. We explored the origin of the observed noise by closely examining the sampling process in the scanning algorithm. We will show that the time characteristics of the signal in the range-modulated proton therapy beams differ significantly from those in the photon beams, and as a result the measurement error is very sensitive to the sampling duration. The observed noise results mainly from inappropriate choices for this value, rather than from the dose distribution itself. Increasing the value arbitrarily may actually increase the noise magnitude. We will demonstrate that with an optimal value for the sampling duration and its accurate control, the noise magnitude can be reduced significantly, without increasing the measurement time. (C) 2006 American Association of Physicists in Medicine. C1 Harvard Univ, Massachusetts Gen Hosp, Sch Med, Francis H Burr Proton Therapy Ctr, Boston, MA 02114 USA. RP Lu, HM (reprint author), Harvard Univ, Massachusetts Gen Hosp, Sch Med, Francis H Burr Proton Therapy Ctr, Boston, MA 02114 USA. EM hmlu@partners.org FU NCI NIH HHS [5 P01 CA21239-24] NR 7 TC 3 Z9 3 U1 0 U2 0 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 JUL PY 2006 VL 33 IS 7 BP 2362 EP 2368 DI 10.1118/1.2207214 PG 7 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA 065QH UT WOS:000239173900006 PM 16898438 ER PT J AU Wu, T Moore, RH Kopans, DB AF Wu, Tao Moore, Richard H. Kopans, Daniel B. TI Voting strategy for artifact reduction in digital breast tomosynthesis SO MEDICAL PHYSICS LA English DT Article DE digital breast tomosynthesis; 3D reconstruction; artifact reduction ID OF-PLANE STRUCTURES; FILTERED BACKPROJECTION; RECONSTRUCTION; REMOVAL; MAMMOGRAPHY AB Artifacts are observed in digital breast tomosynthesis (DBT) reconstructions due to the small number of projections and the narrow angular range that are typically employed in tomosynthesis imaging. In this work, we investigate the reconstruction artifacts that are caused by high-attenuation features in breast and develop several artifact reduction methods based on a "voting strategy." The voting strategy identifies the projection(s) that would introduce artifacts to a voxel and rejects the projection(s) when reconstructing the voxel. Four approaches to the voting strategy were compared, including projection segmentation, maximum contribution deduction, one-step classification, and iterative classification. The projection segmentation method, based on segmentation of high-attenuation features from the projections, effectively reduces artifacts caused by metal and large calcifications that can be reliably detected and segmented from projections. The other three methods are based on the observation that contributions from artifact-inducing projections have higher value than those from normal projections. These methods attempt to identify the projection(s) that would cause artifacts by comparing contributions from different projections. Among the three methods, the iterative classification method provides the best artifact reduction; however, it can generate many false positive classifications that degrade the image quality. The maximum contribution deduction method and one-step classification method both reduce artifacts well from small calcifications, although the performance of artifact reduction is slightly better with the one-step classification. The combination of one-step classification and projection segmentation removes artifacts from both large and small calcifications. (C) 2006 American Association of Physicists in Medicine. C1 Massachusetts Gen Hosp, Boston, MA 02114 USA. RP Wu, T (reprint author), Holog Inc, 35 Crosby Dr, Bedford, MA 01730 USA. EM twu@hologic.com NR 18 TC 42 Z9 42 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 JUL PY 2006 VL 33 IS 7 BP 2461 EP 2471 DI 10.1118/1.2207127 PG 11 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA 065QH UT WOS:000239173900017 PM 16898449 ER PT J AU Wecht, JM Marsico, R Weir, JP Spungen, AM Bauman, WA De Meersman, RE AF Wecht, Jill M. Marsico, Robert Weir, Joseph P. Spungen, Ann M. Bauman, William A. De Meersman, Ronald E. TI Autonomic recovery from peak arm exercise in fit and unfit individuals with paraplegia SO MEDICINE AND SCIENCE IN SPORTS AND EXERCISE LA English DT Article DE vagal cardiac control; spinal cord injury; endurance training; postexercise sympathetic response ID HEART-RATE-VARIABILITY; CARDIOVASCULAR CONTROL; CARDIAC-OUTPUT; DIFFUSING-CAPACITY; SPECTRUM ANALYSIS; MORTALITY; SEDENTARY; ACETYLENE; STANDARDS; FITNESS AB Introduction: Altered autonomic cardiovascular control in persons with paraplegia may reflect peripheral sympathetic denervation caused by the injury or deconditioning due to skeletal muscle paralysis. Parameters of autonomic cardiovascular control may be improved in fit persons with paraplegia similar to effects reported in the noninjured population. Purpose: To determine differences in resting and recovery HR and cardiac autonomic control in fit and unfit individuals with paraplegia. Methods: Eighteen healthy males with paraplegia below T-6 were studied; nine participated in aerobic exercise conditioning (fit: >= 30 min-d(-1), 3 d-wk(-1), >= 6 months), and nine were sedentary (unfit). Analysis of heart rate variability (HRV) was used to determine spectral power (In transformed) in the high-(lnHF) and low-frequency (lnLF) bandwidths, and the LF/HF ratio was calculated. Data were collected at baseline (BL) and at 2, 10, 30, 60, and 90 min of recovery from peak arm cycle ergometry. Results: The relative intensity achieved on the peak exercise test was comparable between the groups (i.e., 88% peak predicted HR). However, peak watts (P < 0.001) and oxygen consumption (P < 0.01) were higher in the fit compared with the unfit group (56 and 51%, respectively). Recovery lnHF was increased (P < 0,05), and recovery lnLF (P < 0.01) and LF/HF (P < 0.05) were reduced in the fit compared with the unfit group. Mean recovery autonomic activity was not different from BL in the fit group. In the unfit group, mean recovery lnHF was reduced, and mean recovery lnLF and LF/HF remained elevated above BL. Conclusion: These data suggest that fit individuals with paraplegia have improved cardiac autonomic control during the postexercise recovery period compared with their unfit counterparts. C1 James J Peters Med Ctr, Spinal Cord Damage Res Ctr, Bronx, NY 10468 USA. VA RR&D Serv Ctr Excellence, Bronx, NY 10468 USA. CUNY Mt Sinai Sch Med, Dept Med, New York, NY 10029 USA. CUNY Mt Sinai Sch Med, Dept Rehabil Med, New York, NY 10029 USA. Des Moines Univ, Osteopath Med Ctr, Des Moines, IA USA. Columbia Univ Coll Phys & Surg, New York, NY 10032 USA. Columbia Univ Teachers Coll, New York, NY 10032 USA. RP Wecht, JM (reprint author), James J Peters Med Ctr, Spinal Cord Damage Res Ctr, 130 W Kingsbridge Rd, Bronx, NY 10468 USA. EM jm.wecht@med.va.gov NR 29 TC 9 Z9 9 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0195-9131 J9 MED SCI SPORT EXER JI Med. Sci. Sports Exerc. PD JUL PY 2006 VL 38 IS 7 BP 1223 EP 1228 DI 10.1249/01.mss.0000227306.34149.ba PG 6 WC Sport Sciences SC Sport Sciences GA 062UU UT WOS:000238971100005 PM 16826018 ER PT J AU Thurston, RC Joffe, H Soares, CN Harlow, BL AF Thurston, Rebecca C. Joffe, Hadine Soares, Claudio N. Harlow, Bernard L. TI Physical activity and risk of vasomotor symptoms in women with and without a history of depression: results from the Harvard Study of Moods and Cycles SO MENOPAUSE-THE JOURNAL OF THE NORTH AMERICAN MENOPAUSE SOCIETY LA English DT Article DE hot flashes; hot flushes; menopause; physical activity; exercise; vasomotor symptoms ID HORMONE REPLACEMENT THERAPY; RANDOMIZED CONTROLLED-TRIAL; POSTMENOPAUSAL WOMEN; HOT FLASHES; PERIMENOPAUSAL WOMEN; MAJOR DEPRESSION; LIFE-STYLE; MENOPAUSAL SYMPTOMS; EXERCISE; HEALTH AB Objective: To examine whether physical activity was associated with decreased risk of vasomotor symptoms in a prospective study of women transitioning through menopause. Design: Hypotheses were evaluated in the Harvard Study of Moods and Cycles, a longitudinal study of women with and without a history of major depression (N = 523). Ordinal logistic regression models were utilized to assess the odds of vasomotor symptoms (none, mild, moderate/severe; Greene Climacteric Scale) associated with physical activity (quartiles of metabolic equivalent-hours per week) at study enrollment and over a 3- to 5-year follow-up period. Results: No significant associations between physical activity and vasomotor symptoms were observed for the sample as a whole. However, exploratory analyses stratified by depression history revealed that among the 157 women with a lifetime history of major depression, high (odds ratio [OR] = 0.28, 95% CI: 0.09-0.83) or moderately high (OR = 0.33, 95% CI: 0.11-0.99) physical activity proximal to the vasomotor assessment, as well as consistently high (OR = 0.27, 95% CI: 0.10-0.75) or increasing (OR = 0.33, 95% CI: 0.12-0.92) physical activity over the duration of the 3- to 5-year follow-up period was associated with decreased vasomotor symptoms relative to sedentary behavior. No significant associations were observed for women without a history of depression. Conclusions: Physical activity may be associated with decreased risk of vasomotor symptoms among women with a history of major depression. C1 Univ Pittsburgh, Sch Med, Dept Psychiat, Pittsburgh, PA 15213 USA. Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Psychiat, Boston, MA USA. McMaster Univ, Dept Psychiat & Behav Neurosci, Hamilton, ON, Canada. Harvard Univ, Brigham & Womens Hosp, Sch Med, Obstet & Gynecol Epidemiol Ctr, Boston, MA 02115 USA. RP Thurston, RC (reprint author), Univ Pittsburgh, Sch Med, Dept Psychiat, 3811 Ohara St, Pittsburgh, PA 15213 USA. EM thurstonrc@upmc.edu FU NIMH NIH HHS [5K23MH066978, R01-MH-50013] NR 47 TC 35 Z9 35 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 1072-3714 J9 MENOPAUSE JI Menopause-J. N. Am. Menopause Soc. PD JUL-AUG PY 2006 VL 13 IS 4 BP 553 EP 560 DI 10.1097/01.gme.0000227332.43243.00 PG 8 WC Obstetrics & Gynecology SC Obstetrics & Gynecology GA 067PM UT WOS:000239315100005 PM 16837876 ER PT J AU Murphey, RD Zon, LI AF Murphey, R. D. Zon, L. I. TI Small molecule screening in the zebrafish SO METHODS LA English DT Article DE zebrafish; embryos; chemical genetics; small molecule; drug screen ID DIFFERENT DEVELOPMENTAL-STAGES; EXPOSURE ROUTES; MODEL; EXPRESSION; CHEMISTRY; NEOPLASIA; EMBRYOS AB The zebrafish is an ideal organism for small molecule studies. The ability to use the whole organism allows complex in vivo phenotypes to be assayed and combines animal testing with screening. Embryos are easily treatable by waterborne exposure. The small size and abundance of embryos make zebrafish suitable for screening in a high-throughput manner in 96- or 48-well plates. Zebrafish embryos have successfully been used in chemical genetic screens to elucidate biological pathways and find chemical suppressors. Small molecules discovered by screening zebrafish disease models may also be useful as lead compounds for drug development as there appears to be a high level of conservation of drug activity between mammals and zebrafish. Here we provide the technical aspects of treating embryos with small molecules and performing chemical screens with zebrafish. (c) 2006 Elsevier Inc. All rights reserved. C1 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. RP Zon, LI (reprint author), Childrens Hosp, Dana Farber Canc Inst, Howard Hughes Med Inst, Stem Cell Program, 1 Blackfan Circle, Boston, MA 02115 USA. EM zon@enders.tch.harvard.edu FU NICHD NIH HHS [1R01 HD044930]; NIDDK NIH HHS [1 R01 DK55381] NR 23 TC 72 Z9 76 U1 1 U2 13 PU ACADEMIC PRESS INC ELSEVIER SCIENCE PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA SN 1046-2023 J9 METHODS JI Methods PD JUL PY 2006 VL 39 IS 3 BP 255 EP 261 DI 10.1016/j.ymeth.2005.09.019 PG 7 WC Biochemical Research Methods; Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA 084AN UT WOS:000240504000011 PM 16877005 ER PT J AU Dickie, R Bachoo, RM Rupnick, MA Dallabrida, SM DeLoid, GM Lai, J DePinho, RA Rogers, RA AF Dickie, R. Bachoo, R. M. Rupnick, M. A. Dallabrida, S. M. DeLoid, G. M. Lai, J. DePinho, R. A. Rogers, R. A. TI Three-dimensional visualization of microvessel architecture of whole-mount tissue by confocal microscopy SO MICROVASCULAR RESEARCH LA English DT Article DE 3C; clearing; confocal microscopy; lectin; Mercox; morphology; tumor; whole mount ID LASER-SCANNING MICROSCOPY; ENDOTHELIAL-CELLS; BLOOD-VESSELS; EXPRESSION; LECTIN; DIFFERENTIATION; ANGIOGENESIS; FLUORESCENCE; XENOPUS; MUSCLE AB The three-dimensional architecture of the nascent microvascular network is a critical determinant of vascular perfusion in the setting of regenerative growth, vasculopathies and cancer. Current methods for microvessel visualization are limited by insufficient penetration and instability of endothelial immunolabels, inadequate vascular perfusion by the high-viscosity polymers used for vascular casting, and destruction of tissue stroma during the processing required for scanning electron microscopy. The aim of this study was to develop whole-mount tissue processing methods for 3D in situ visualization of the microvasculature that were also compatible with supplementary labeling for other structures of interest in the tissue microenvironment. Here, we present techniques that allow imaging of the microvasculature by confocal microscopy, to depths of up to 1500 mu m below the specimen surface. Our approach includes labeling luminal surfaces of endothelial cells by i.v. injection of fluorescently conjugated lectin and filling the microvasculature with carbon or fluorescent nanoparticles/Mercox, followed by optical clearing of thick tissue sections to reduce light scatter and permit 3D visualization of microvessel morphology deep into the sample. Notably, tissue stroma is preserved, allowing simultaneous labeling of other structures by immunohistochemistry or nuclear dyes. Results are presented for various murine tissues including fat, muscle, heart and brain under conditions of normal health, as well as in the setting of a glioma model growing in the subcutaneous space or orthotopically in the brain parenchyma. (c) 2006 Elsevier Inc. All rights reserved. C1 Harvard Univ, Sch Publ Hlth, Dept Environm Hlth, Biomed Imaging Lab, Boston, MA 02115 USA. Univ Texas, SW Med Ctr, Dept Neurol & Med, Dallas, TX 75235 USA. Childrens Hosp, Dept Surg Res, Vasc Biol Program, Boston, MA 02215 USA. Brigham & Womens Hosp, Div Cardiovasc, Boston, MA 02115 USA. Harvard Univ, Sch Med, Dept Med, Boston, MA 02115 USA. Harvard Univ, Sch Med, Dept Genet, Boston, MA 02115 USA. Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02115 USA. Dana Farber Canc Inst, Ctr Appl Canc Sci, Boston, MA 02115 USA. RP Dickie, R (reprint author), Harvard Univ, Sch Publ Hlth, Dept Environm Hlth, Biomed Imaging Lab, 665 Huntington Ave,Bldg 1,Room G24, Boston, MA 02115 USA. EM rdickie@hsph.harvard.edu FU NCI NIH HHS [P01 CA 45548, P01 CA095616, P01 CA45548, U01 CA84313]; NHLBI NIH HHS [HL 65960]; NIEHS NIH HHS [ES00002] NR 30 TC 47 Z9 53 U1 2 U2 8 PU ACADEMIC PRESS INC ELSEVIER SCIENCE PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA SN 0026-2862 J9 MICROVASC RES JI Microvasc. Res. PD JUL-SEP PY 2006 VL 72 IS 1-2 BP 20 EP 26 DI 10.1016/j.mvr.2006.05.003 PG 7 WC Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 079YV UT WOS:000240214700004 PM 16806289 ER PT J AU Eisen, SA Karlinsky, J Jackson, LW Blanchard, M Kang, HK Murphy, FM Alpern, R Reda, DJ Toomey, R Battistone, MJ Parks, BJ Klimas, N Pak, HS Hunter, J Lyons, MJ Henderson, WG AF Eisen, Seth A. Karlinsky, Joel Jackson, Leila W. Blanchard, Melvin Kang, Han K. Murphy, Frances M. Alpern, Renee Reda, Domenic J. Toomey, Rosemary Battistone, Michael J. Parks, Becky J. Klimas, Nancy Pak, Hon S. Hunter, Joyce Lyons, Michael J. Henderson, William G. CA Gulf War Study Participating TI Spouses of Persian Gulf War I Veterans: Medical evaluation of a US cohort SO MILITARY MEDICINE LA English DT Article ID CHRONIC-FATIGUE-SYNDROME; POSTTRAUMATIC-STRESS-DISORDER; VIETNAM VETERANS; HEALTH; ILLNESSES; PARTNERS; CRITERIA AB Ten years after the 1991 Persian Gulf War (GW I), a comprehensive evaluation of a national cohort of deployed veterans (DV) demonstrated a higher prevalence of several medical conditions, in comparison to a similarly identified cohort of non-deployed veterans (NDV). The present study determined the prevalence of medical conditions among nonveteran spouses of these GW I DV and NDV. A cohort of 490 spouses of GW I DV and 537 spouses of GW I NDV underwent comprehensive face-to-face examinations. No significant differences in health were detected except that spouses of DV were less likely to have one or more of a group of six common skin conditions. We conclude that, 10 years after GW I, the general physical health of spouses of GW I DV is similar to that of spouses of NDV. C1 St Louis Vet Affairs Med Ctr, Med Serv, St Louis, MO 63106 USA. St Louis Vet Affairs Med Ctr, Res Serv, St Louis, MO 63106 USA. Washington Univ, Sch Med, Dept Internal Med, Div Gen Med Sci, St Louis, MO 63110 USA. Boston Healthcare Syst, Vet Affairs Med Ctr, Boston, MA 02130 USA. Boston Univ, Sch Med, Dept Med, Boston, MA 02118 USA. Dept Vet Affairs, Environm Epidemiol Serv, Washington, DC 20420 USA. Vet Hlth Adm, Dept Vet Affairs, Washington, DC 20420 USA. US Dept Vet Affairs, Vet Affairs Edward Hines Jr Hosp, Cooperat Studies Program Coordinating Ctr, Hines, IL 60141 USA. Brockton Vet Affairs Med Ctr, Res Serv, Brockton, MA 02301 USA. Brockton Vet Affairs Med Ctr, Psychiat Serv, Brockton, MA 02301 USA. Harvard Univ, Sch Med, Massachusetts Mental Hlth Ctr, Dept Psychiat, Boston, MA 02215 USA. Harvard Univ, Inst Psychiat Epidemiol & Genet, Boston, MA 02130 USA. Vet Affairs Salt Lake City Hlth Care Syst, Salt Lake City, UT 84148 USA. Univ Utah, Hlth Sci Ctr, Dept Med, Salt Lake City, UT 84132 USA. St Louis Vet Affairs Med Ctr, Neurol Serv, St Louis, MO 63106 USA. Washington Univ, Sch Med, Dept Neurol, St Louis, MO 63110 USA. Vet Affairs Med Ctr, Miami, FL 33125 USA. Univ Miami, Sch Med, Dept Med, Miami, FL 33136 USA. Brooke Army Med Ctr, Dept Dermatol, Ft Sam Houston, TX 78234 USA. W Palm Beach Vet Affairs Med Ctr, W Palm Beach, FL 33410 USA. Boston Univ, Dept Psychol, Boston, MA 02215 USA. Harvard Univ, Sch Med, Brockton W Roxbury Vet Affairs Med Ctr, Dept Psychiat, Brockton, MA 02301 USA. RP Eisen, SA (reprint author), St Louis Vet Affairs Med Ctr, Med Serv, 151JC,915 N Grand Ave, St Louis, MO 63106 USA. RI Lyons, Michael/B-6119-2011; OI Lyons, Michael/0000-0001-6516-9219 NR 22 TC 2 Z9 2 U1 0 U2 1 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 JUL PY 2006 VL 171 IS 7 BP 613 EP 618 PG 6 WC Medicine, General & Internal SC General & Internal Medicine GA 061IG UT WOS:000238864300010 PM 16895127 ER PT J AU Zeber, JE Copeland, LA Grazier, KL AF Zeber, John E. Copeland, Laurel A. Grazier, Kyle L. TI Serious mental illness, aging, and utilization patterns among Veterans SO MILITARY MEDICINE LA English DT Article; Proceedings Paper CT Annual Research Meeting of the Department-of-Veterans-Affairs CY FEB 12-14, 2003 CL Washington, DC SP Dept Veterans Affairs ID HEALTH-CARE UTILIZATION; QUALITY-OF-LIFE; OLDER-ADULTS; EMERGENCY-DEPARTMENT; SOCIOECONOMIC-STATUS; MEDICAL-SERVICES; MAINTENANCE ORGANIZATION; MAJOR DEPRESSION; BIPOLAR DISORDER; TREATMENT COSTS AB As veterans age, chronic physical and psychiatric conditions increasingly challenge the Veterans Health Administration. We examine influences of age and diagnosis on health care utilization, within the context of the 1995 deinstitutionalization policy of the Veterans Health Administration. Veterans were hospitalized repeatedly over 5 years with diagnoses of schizophrenia, bipolar disorder, depression, or alcohol dependence (N = 7,719). Inpatient days decreased 14% from baseline while outpatient (OP) visits increased 63%, consistent with deinstitutionalization. In adjusted models, OP utilization greatly increased with age, but psychiatric visits-notably alcohol treatment-dropped sharply. Emergency visits rose after 1997, particularly for ethnic minorities. Individuals ages 35-49 and 50-64 years were the greatest consumers of OP care; these large, aging cohorts will continue to require additional services, taxing a burdened system. Utilization patterns evolve across the life course, requiring foresight to address changing demographic demands. Careful attention to mental health utilization patterns may help policy makers and providers understand psychiatric needs in older patients. C1 S Texas Vet Hlth Care Syst HSR&D, Dept Vet Affairs, Vet Evidence Based Res Disseminat Implementat Res, San Antonio, TX 78229 USA. Univ Michigan, Sch Publ Hlth, Dept Hlth Policy & Management, Ann Arbor, MI 48109 USA. RP Zeber, JE (reprint author), S Texas Vet Hlth Care Syst HSR&D, Dept Vet Affairs, Vet Evidence Based Res Disseminat Implementat Res, San Antonio, TX 78229 USA. OI Copeland, Laurel/0000-0002-9478-0209 NR 74 TC 6 Z9 6 U1 3 U2 5 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 JUL PY 2006 VL 171 IS 7 BP 619 EP 626 PG 8 WC Medicine, General & Internal SC General & Internal Medicine GA 061IG UT WOS:000238864300011 PM 16895128 ER PT J AU Juszczynski, P Kutok, JL Li, C Mitra, J Aguiar, RCT Shipp, MA AF Juszczynski, Przemyslaw Kutok, Jeffery L. Li, Cheng Mitra, Joydeep Aguiar, Ricardo C. T. Shipp, Margaret A. TI BAL1 and BBAP are regulated by a gamma interferon-responsive bidirectional promoter and are overexpressed in diffuse large B-cell lymphomas with a prominent inflammatory infiltrate SO MOLECULAR AND CELLULAR BIOLOGY LA English DT Article ID TRANSCRIPTION FACTOR-BINDING; ACTIVATED KILLER-CELLS; RING-FINGER DOMAIN; IFN-GAMMA; GENOMIC SEQUENCES; GENE-EXPRESSION; NUCLEAR IMPORT; TUMOR-CELLS; PROTEIN; MECHANISM AB BAL1 is a transcription modulator that is overexpressed in chemoresistant, diffuse large B-cell lymphomas (DLBCLs). BAL1 complexes with a recently described DELTEX family member termed BBAP. Herein, we characterized BAL1 and BBAP expression in primary DLBCL subtypes defined by their comprehensive transcriptional profiles. BAL1 and BBAP were most abundant in lymphomas with a brisk host inflammatory response, designated host response (HR) tumors. Although these DLBCLs include significant numbers of tumor-infiltrating lymphocytes and interdigitating dendritic cells, BAL1 and BBAP were expressed primarily by malignant B cells, prompting speculation that the genes might be induced by host-derived inflammatory mediators such as gamma interferon (IFN-gamma). In fact, IFN-gamma induced BAL1 and BBAP expression in DLBCL cell lines; doxycycline-induced BAL1 also increased the expression of multiple IFN-stimulated genes, directly implicating BAL1 in an IFN signaling pathway. We show that BAL1 and BBAP are located on chromosome 3q21 in a head-to-head orientation and are regulated by a IFN-gamma-responsive bidirectional promoter. BBAP regulates the subcellular localization of BAL1 by a dynamic shuttling mechanism, highlighting the functional requirement for coordinated BBAP and BAL1 expression. IFN-gamma-induced BAL1/BBAP expression contributes to the molecular signature of HR DLBCLs and highlights the interplay between the inflammatory infiltrate and malignant B cells in these tumors. C1 Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02115 USA. Brigham & Womens Hosp, Dept Pathol, Boston, MA 02115 USA. Harvard Univ, Sch Publ Hlth, Dept Biostat, Boston, MA 02115 USA. RP Shipp, MA (reprint author), Dana Farber Canc Inst, Dept Med Oncol, 44 Binney St, Boston, MA 02115 USA. EM Margaret_Shipp@dfci.harvard.edu NR 39 TC 52 Z9 55 U1 0 U2 1 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 JUL PY 2006 VL 26 IS 14 BP 5348 EP 5359 DI 10.1128/MCB.02351-05 PG 12 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA 062AZ UT WOS:000238918000013 PM 16809771 ER PT J AU Ishiguro, K Green, T Rapley, J Wachtel, H Giallouhakis, C Landty, A Cao, Z Lu, N Takafumi, A Goto, H Daly, MJ Xavier, RJ AF Ishiguro, Kazuhiro Green, Todd Rapley, Joseph Wachtel, Heather Giallouhakis, Cosmas Landty, Aimee Cao, Zhifang Lu, Naifang Takafumi, Ando Goto, Hidemi Daly, Mark J. Xavier, Ramnik J. TI Ca2+/calmodulin-dependent protein kinase II is a modulator of CARMA1-mediated NF-kappa B activation SO MOLECULAR AND CELLULAR BIOLOGY LA English DT Article ID T-CELL; MALT LYMPHOMA; DIFFERENTIAL REQUIREMENT; IMMUNOLOGICAL SYNAPSE; UBIQUITIN LIGASE; CARMA1; BCL10; PHOSPHORYLATION; TCR; REGULATOR AB CARMAI is a central regulator of NF-kappa B activation in lymphocytes. CARMA1 and BcI10 functionally interact and control NF-kappa B signaling downstream of the T-cell receptor (TCR). Computational analysis of expression neighborhoods of CARMA1-Bcl10MALT 1 for enrichment in kinases identified calmodulin-dependent protein kinase II (CaMKII) as an important component of this pathway. Here e report that Ca2+/CaMKHII redistributed to the immune synapse following T-cell activation and that CaMKHII is critical for NF-kappa B activation induced by TCR stimulation. Furthermore. CaMKII enhances GARMA1-induced NF-kappa B activation. Moreover, we have shown that CaMKII phosphorylates CARMA1 on Ser109 and that the phosphorylation facilitates the interaction between CARMAI and Bcl10. These results provide a novel function for CaMKII in TCR signaling and CARMAI-induced NF-kappa B activation. C1 Massachusetts Gen Hosp, Ctr Computat & Integrat Biol, Boston, MA 02114 USA. Massachusetts Gen Hosp, Dept Med, Boston, MA 02114 USA. Nagoya Univ, Grad Sch Med, Dept Therapeut Med, Nagoya, Aichi 4668550, Japan. Massachusetts Gen Hosp, Ctr Human Genet Res, Boston, MA 02114 USA. Massachusetts Gen Hosp, Massachusetts Inst Technol, Boston, MA 02114 USA. Massachusetts Gen Hosp, Broad Inst Harvard, Boston, MA 02114 USA. Massachusetts Gen Hosp, Dept Mol Biol, Boston, MA 02114 USA. RP Xavier, RJ (reprint author), Massachusetts Gen Hosp, Ctr Computat & Integrat Biol, Boston, MA 02114 USA. EM Xavier@molbio.mgh.harvard.edu OI Ishiguro, Kazuhiro/0000-0003-1776-2805 FU NIDDK NIH HHS [DK43351, P30 DK043351, P30 DK040561, P30 DK040561-11] NR 52 TC 53 Z9 55 U1 1 U2 1 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 JUL PY 2006 VL 26 IS 14 BP 5497 EP 5508 DI 10.1128/MCB.02469-05 PG 12 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA 062AZ UT WOS:000238918000024 PM 16809782 ER PT J AU Zacharakis, G Shih, H Ripoll, J Weissleder, R Ntziachristos, V AF Zacharakis, Giannis Shih, Helen Ripoll, Jorge Weissleder, Ralph Ntziachristos, Vasilis TI Normalized transillumination of fluorescent proteins in small animals SO MOLECULAR IMAGING LA English DT Article DE transillumination imaging; fluorescence-mediated molecular imaging; gene expression.; whole-animal imaging ID OPTICAL MAMMOGRAPHY; IN-VIVO; TOMOGRAPHY; BODY; CELLS; LIGHT AB We investigated the capacity of normalized transillumination methods in imaging fluorescent proteins in visible light, in phantoms and in live mice. We demonstrate significant imaging improvements over epi-illumination imaging, as commonly applied today. Of particular importance is the significant betterment in contrast achieved, due to minimization of the influence of autofluorescence and the enhancement of depth sensitivity compared to epi-illumination imaging. Although normalized transillumination does not match the accuracy and quantification capacity of tomographic imaging, it nevertheless attains key advantages over other planar optical imaging methods while preserving implementation simplicity. Due to the balance achieved between simplicity and accuracy, normalized transillumination approaches could serve as an important alternative molecular imaging method. C1 Harvard Univ, Sch Med, Massachusetts Gen Hosp, Ctr Mol Imaging Res, Charlestown, MA 02129 USA. Fdn Res & Technol Hellas, GR-71110 Iraklion, Greece. RP Zacharakis, G (reprint author), POB 1527, GR-71110 Iraklion, Crete, Greece. EM zahari@iesl.forth.gr; vasilis@helix.mgh.harvard.edu RI Zacharakis, Giannis/A-2544-2014; Ripoll, Jorge/J-8134-2012 OI Zacharakis, Giannis/0000-0002-6438-0773; Ripoll, Jorge/0000-0001-8856-7738 NR 20 TC 22 Z9 23 U1 0 U2 3 PU B C DECKER INC PI HAMILTON PA 50 KING STREET EAST, 2ND FLOOR, PO BOX 620, L C D 1, HAMILTON, ONTARIO L8N 3K7, CANADA SN 1535-3508 J9 MOL IMAGING JI Mol. Imaging PD JUL PY 2006 VL 5 IS 3 BP 153 EP 159 DI 10.2310/7290.2006.00018 PG 7 WC Biochemical Research Methods; Radiology, Nuclear Medicine & Medical Imaging SC Biochemistry & Molecular Biology; Radiology, Nuclear Medicine & Medical Imaging GA 085JO UT WOS:000240600600003 PM 16954030 ER PT J AU Kelly, KA Nahrendorf, M Yu, AM Reynolds, F Weissleder, R AF Kelly, Kimberly A. Nahrendorf, Matthias Yu, Amy M. Reynolds, Fred Weissleder, Ralph TI In vivo phage display selection yields atherosclerotic plaque targeted peptides for imaging SO MOLECULAR IMAGING AND BIOLOGY LA English DT Article DE phage display; atherosclerosis; VCAM-1 ID TAT PEPTIDE; NANOPARTICLES; LIBRARY; EXPRESSION; LESIONS AB Purpose: Atherosclerosis is a leading cause of morbidity and mortality in the Western world, yet specific imaging agents to detect and map inflammatory plaques are still lacking. Procedures: We used in vivo phage display to interrogate early atherosclerotic lesions present in ApoE-/- mice with the goal of identifying plaque-associated endothelial cell internalized affinity ligands. Results: We identified 30 phage families with some of these families exhibiting homology to known atherosclerotic proteins, namely, leukemia inhibitory factor, transferrin, and VLA-4. VLA-4 homologous peptides [termed vascular cellular adhesion molecule-1 (VCAM-1) internalizing pepticle-28 (VINP28)] bound to and were internalized by VCAM-1-expressing cells and were inhibited by soluble VCAM-1. In addition, a VINP28 modified multimodal nanoparticle showed high affinity for endothelial cells expressing VCAM-1 but low affinity for macrophages or smooth muscle cells. Conclusion: The identified peptides represent a set of probes to interrogate the cell surface repertoire and potentially allow early detection of atherosclerosis. C1 Harvard Univ, Sch Med, Massachusetts Gen Hosp, Ctr Mol Imaging Res, Charlestown, MA 02129 USA. RP Weissleder, R (reprint author), Harvard Univ, Sch Med, Massachusetts Gen Hosp, Ctr Mol Imaging Res, 149,13th St,Rm 5404, Charlestown, MA 02129 USA. EM weissleder@helix.mgh.harvard.edu NR 29 TC 72 Z9 74 U1 1 U2 13 PU SPRINGER PI NEW YORK PA 233 SPRING STREET, NEW YORK, NY 10013 USA SN 1536-1632 J9 MOL IMAGING BIOL JI Mol. Imaging. Biol. PD JUL-AUG PY 2006 VL 8 IS 4 BP 201 EP 207 DI 10.1007/s11307-006-0043-6 PG 7 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA 064XU UT WOS:000239124800001 PM 16791746 ER PT J AU Chen, HL Zhang, SMM Schwarzschild, MA Hernan, MA Ascherio, A AF Chen, Honglei Zhang, Shumin M. Schwarzschild, Michael A. Hernan, Miguel A. Ascherio, Alberto TI Survival of Parkinson's disease patients in a large prospective cohort of male health professionals SO MOVEMENT DISORDERS LA English DT Article DE Parkinson's disease; morality; survival; smoking; disease duration ID CIGARETTE-SMOKING; OLMSTED COUNTY; FOLLOW-UP; MORTALITY; PROGRESSION; RISK; NICOTINE; ONSET; DEATH; TIME AB Parkinson's disease (PD) patients have higher mortality than individuals without PD. However, most of the previous studies were based on prevalent cases and few examined the potential effects of duration and smoking on the survival of PD patients. We compared the survival experience of 288 men with incident PD diagnosed between 1986 and 2000 with that of 51,012 men free of PD in the Health Professionals Follow-up Study. As of January 2002, 92 deaths occurred among PD cases and 8,485 among men without PD. After controlling for age, men with PD had 60% higher mortality than those without PD (95% Cl: 1.3-2.0). PD mortality was strongly related to disease duration: compared with men without PD, the age-adjusted relative risk for PD patients was 1.1 during the first 5 years from diagnosis, 2.3 from 5 to 10 years, and 3.5 after 10 years (P < 0.0001 for trend). As expected, cigarette smoking was strongly and positively associated with total mortality among men free of PD (comparing >30 pack-years vs. never smokers, relative risk, 2.0; P < 0.0001 for trend), but this association was not observed among PD patients (RR: 1.0; P = 0.95 for trend). This study confirms that PD patients have a higher mortality than individuals without PD and that the excess mortality increases with disease duration. However, smoking seems to impose little additional risk among PD patients in this large cohort of health professionals. (C) 2006 Movement Disorder Society. C1 NIEHS, Epidemiol Branch, Res Triangle Pk, NC 27709 USA. Harvard Univ, Sch Publ Hlth, Dept Nutr, Boston, MA 02115 USA. Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA. Brigham & Womens Hosp, Dept Med, Div Prevent Med, Boston, MA 02115 USA. Harvard Univ, Sch Med, Boston, MA USA. Massachusetts Gen Hosp, Dept Neurol, Boston, MA 02114 USA. Brigham & Womens Hosp, Dept Med, Channing Lab, Boston, MA USA. RP Chen, HL (reprint author), NIEHS, Epidemiol Branch, Mail Drop A3-05,Bldg Rall 101 Room A362,111 WT Al, Res Triangle Pk, NC 27709 USA. EM Chenh2@niehs.nih.gov OI Chen, Honglei/0000-0003-3446-7779 FU Intramural NIH HHS; NCI NIH HHS [CA55075]; NINDS NIH HHS [NS048468, NS35624] NR 29 TC 42 Z9 43 U1 1 U2 2 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 0885-3185 J9 MOVEMENT DISORD JI Mov. Disord. PD JUL PY 2006 VL 21 IS 7 BP 1002 EP 1007 DI 10.1002/mds.20881 PG 6 WC Clinical Neurology SC Neurosciences & Neurology GA 067EW UT WOS:000239285600019 PM 16602107 ER PT J AU Fogel, B Wu, M Kremen, S Murthy, K Jackson, G Vanek, Z AF Fogel, Brent Wu, Mark Kremen, Sarah Murthy, Kolar Jackson, George Vanek, Zeba TI Creutzfeldt-Jakob disease presenting with alien limb sign SO MOVEMENT DISORDERS LA English DT Article DE Creutzfeldt-Jakob; magnetic resonance imaging; alien limb; video; corticobasal degeneration ID MIMICKING CORTICOBASAL DEGENERATION; HAND SYNDROME AB Creutzfeldt-Jakob disease is a fatal spongiform encephalopathy, which typically presents with a rapidly progressing dementia and additional neurological findings that can be quite variable and diverse. Here we report the unusual case of a patient who presented with left alien limb sign without overt cognitive impairment and was ultimately diagnosed with pathologically confirmed Creutzfeldt-Jakob disease. (C) 2006 Movement Disorder Society. C1 Univ Calif Los Angeles, Dept Neurol, Med Ctr, Los Angeles, CA 90095 USA. Vet Adm Greater Los Angeles Healthcare Ctr, Dept Neurol, Los Angeles, CA USA. RP Fogel, B (reprint author), Univ Calif Los Angeles, Dept Neurol, Med Ctr, 710 Westwood Plaza, Los Angeles, CA 90095 USA. EM bfogel@ucla.edu NR 13 TC 7 Z9 7 U1 0 U2 1 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 0885-3185 J9 MOVEMENT DISORD JI Mov. Disord. PD JUL PY 2006 VL 21 IS 7 BP 1040 EP 1042 DI 10.1002/mds.20858 PG 3 WC Clinical Neurology SC Neurosciences & Neurology GA 067EW UT WOS:000239285600027 PM 16552737 ER PT J AU Frontera, WR Choi, H Krishnan, G Krivickas, LS Sabharwal, S Teng, YD AF Frontera, WR Choi, H Krishnan, G Krivickas, LS Sabharwal, S Teng, YD TI Single muscle fiber size and contractility after spinal cord injury in rats SO MUSCLE & NERVE LA English DT Article DE chemically skinned single muscle fibers; contusion; myosin heavy chain isoform; specific force; spinal cord injury ID ATROPHY RESPONSES; PROTEIN DEFICITS; INACTIVITY; MARKERS; FORCE AB Spinal cord injury (SCI) results in muscle weakness but the degree of impairment at the level of single fibers is not known. The purpose of this study was to examine the effects of T9-level SCI on single muscle fibers from the tibialis anterior of rats. Significant decreases in cross-sectional area (CSA), maximal force (Po), and specific force (SF = Po/CSA) were noted at 2 weeks. Atrophy and force-generating capacity were reversed at 4 weeks, but SF remained impaired. Maximum shortening velocity (Vo) did not change after injury. SCI thus appears to affect various contractile properties of single muscle fibers differently. Normal cage activity may partially restore function but new interventions are needed to restore muscle fiber quality. C1 Harvard Univ, Sch Med, Dept Phys Med & Rehabil, Boston, MA 02114 USA. Spaulding Rehabil Hosp, Boston, MA 02114 USA. Harvard Univ, Sch Med, Dept Neurosurg, Boston, MA 02114 USA. Brigham & Womens Hosp, Childrens Hosp, Boston, MA 02115 USA. VA Boston Healthcare Syst, Spinal Cord Injury Res, W Roxbury, MA USA. RP Frontera, WR (reprint author), Harvard Univ, Sch Med, Dept Phys Med & Rehabil, 125 Nashua St, Boston, MA 02114 USA. EM frontera.walter@mgh.harvard.edu FU NIA NIH HHS [R01 AG018844-04]; NINDS NIH HHS [1-R01 NS40822] NR 17 TC 7 Z9 7 U1 0 U2 2 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 JUL PY 2006 VL 34 IS 1 BP 101 EP 104 DI 10.1002/mus.20530 PG 4 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA 058TR UT WOS:000238688000012 PM 16518854 ER PT J AU Kuo, WP Liu, F Trimarchi, J Punzo, C Lombardi, M Sarang, J Whipple, ME Maysuria, M Serikawa, K Lee, SY McCrann, D Kang, J Shearstone, JR Burke, J Park, DJ Wang, XW Rector, TL Ricciardi-Castagnoli, P Perrin, S Choi, SD Bumgarner, R Kim, JH Short, GF Freeman, MW Seed, B Jensen, R Church, GM Hovig, E Cepko, CL Park, P Ohno-Machado, L Jenssen, TK AF Kuo, Winston Patrick Liu, Fang Trimarchi, Jeff Punzo, Claudio Lombardi, Michael Sarang, Jasjit Whipple, Mark E. Maysuria, Malini Serikawa, Kyle Young Lee, Sun McCrann, Donald Kang, Jason Shearstone, Jeffrey R. Burke, Jocelyn Park, Daniel J. Wang, Xiaowei Rector, Trent L. Ricciardi-Castagnoli, Paola Perrin, Steven Choi, Sangdun Bumgarner, Roger Kim, Ju Han Short, Glenn F., III Freeman, Mason W. Seed, Brian Jensen, Roderick Church, George M. Hovig, Eivind Cepko, Connie L. Park, Peter Ohno-Machado, Lucila Jenssen, Tor-Kristian TI A sequence-oriented comparison of gene expression measurements across different hybridization-based technologies SO NATURE BIOTECHNOLOGY LA English DT Article ID OLIGONUCLEOTIDE ARRAY DATA; DNA MICROARRAY DATA; PLATFORM CONSISTENCY; ART.; CDNA; AFFYMETRIX; PROBES; LONG; CONCORDANCE; PERFORMANCE AB Over the last decade, gene expression microarrays have had a profound impact on biomedical research. The diversity of platforms and analytical methods available to researchers have made the comparison of data from multiple platforms challenging. In this study, we describe a framework for comparisons across platforms and laboratories. We have attempted to include nearly all the available commercial and 'in-house' platforms. Using probe sequences matched at the exon level improved consistency of measurements across the different microarray platforms compared to annotation-based matches. Generally, consistency was good for highly expressed genes, and variable for genes with lower expression values as confirmed by quantitative real-time (QRT)-PCR. Concordance of measurements was higher between laboratories on the same platform than across platforms. We demonstrate that, after stringent preprocessing, commercial arrays were more consistent than in- house arrays, and by most measures, one-dye platforms were more consistent than two-dye platforms. C1 Harvard Univ, Sch Dent Med, Dept Dev Biol, Boston, MA 02115 USA. Harvard Univ, Sch Med, Howard Hughes Med Inst, Dept Genet, Boston, MA 02115 USA. Brigham & Womens Hosp, Decis Syst Grp, Boston, MA USA. Norwegian Radium Hosp, Dept Tumor Biol, Inst Canc Res, Oslo, Norway. Univ Massachusetts, Dept Phys, Boston, MA 02125 USA. Univ Washington, Dept Otolaryngol Head & Neck Surg, Seattle, WA 98195 USA. Univ Washington, Dept Microbiol, Seattle, WA 98195 USA. CALTECH, Div Biol, Pasadena, CA 91125 USA. Boston Univ, Sch Med, Dept Biochem, Boston, MA 02215 USA. Macrogen Inc, Seoul, South Korea. Biogen Idec, Res Mol Discovery, Cambridge, MA USA. Massachusetts Gen Hosp, Dept Biol Mol, Boston, MA 02114 USA. Univ Milan, Dept Biotechnol & Biosci, I-20122 Milan, Italy. Ajou Univ, Dept Mol Sci & Technol, Suwon 441749, South Korea. Seoul Natl Univ, Coll Med, Seoul 151, South Korea. Harvard Univ, Sch Med, Childrens Hosp, Informat Program, Boston, MA 02115 USA. PubGene AS, Oslo, Norway. RP Kuo, WP (reprint author), Harvard Univ, Sch Dent Med, Dept Dev Biol, 188 Longwood Ave, Boston, MA 02115 USA. EM wkuo@genetics.med.harvard.edu RI Castagnoli, Paola/E-8288-2010; Kim, Ju Han/E-5983-2012; Bumgarner, Roger/K-3531-2015; Hovig, Eivind/H-2474-2011; OI Bumgarner, Roger/0000-0002-8168-6985; Hovig, Eivind/0000-0002-9103-1077; Shearstone, Jeffrey/0000-0002-6875-1826; Ohno-Machado, Lucila/0000-0002-8005-7327; Trimarchi, Jeffrey/0000-0001-7923-1538; Lee, Sun-Young/0000-0003-4146-6686 FU NEI NIH HHS [EY014466]; NHLBI NIH HHS [HL72358, HL072370, HL66678]; NIEHS NIH HHS [ES011387] NR 50 TC 118 Z9 124 U1 1 U2 10 PU NATURE PUBLISHING GROUP PI NEW YORK PA 75 VARICK STREET, 9TH FLOOR, NEW YORK, NY 10013-1917 USA SN 1087-0156 J9 NAT BIOTECHNOL JI Nat. Biotechnol. PD JUL PY 2006 VL 24 IS 7 BP 832 EP 840 DI 10.1038/nbt1217 PG 9 WC Biotechnology & Applied Microbiology SC Biotechnology & Applied Microbiology GA 063NJ UT WOS:000239025100034 PM 16823376 ER PT J AU Liu, Y Gray, NS AF Liu, Y Gray, NS TI Rational design of inhibitors that bind to inactive kinase conformations SO NATURE CHEMICAL BIOLOGY LA English DT Article ID P38 MAP KINASE; CYCLIN-DEPENDENT KINASE; TYROSINE KINASE; STRUCTURAL BASIS; POTENT; RECEPTOR; STI-571; SELECTIVITY; MECHANISM; DISCOVERY AB The majority of kinase inhibitors that have been developed so far-known as type I inhibitors-target the ATP binding site of the kinase in its active conformation, in which the activation loop is phosphorylated. Recently, crystal structures of inhibitors such as imatinib (STI571), BIRB796 and sorafenib (BAY43-9006)-known as type II inhibitors - have revealed a new binding mode that exploits an additional binding site immediately adjacent to the region occupied by ATP. This pocket is made accessible by an activation-loop rearrangement that is characteristic of kinases in an inactive conformation. Here, we present a structural analysis of binding modes of known human type II inhibitors and demonstrate that they conform to a pharmacophore model that is currently being used to design a new generation of kinase inhibitors. C1 Novartis Res Fdn, Dept Biol Chem, Genom Inst, San Diego, CA 92121 USA. Harvard Univ, Sch Med, Dana Farber Canc Inst, Boston, MA 02115 USA. RP Liu, Y (reprint author), Novartis Res Fdn, Dept Biol Chem, Genom Inst, 10675 John Jay Hopkins Dr, San Diego, CA 92121 USA. EM yliu@gnf.org; nathanael_gray@dfci.harvard.edu NR 36 TC 572 Z9 576 U1 9 U2 67 PU NATURE PUBLISHING GROUP PI NEW YORK PA 75 VARICK STREET, 9TH FLOOR, NEW YORK, NY 10013-1917 USA SN 1552-4450 J9 NAT CHEM BIOL JI Nat. Chem. Biol. PD JUL PY 2006 VL 2 IS 7 BP 358 EP 364 DI 10.1038/nchembio799 PG 7 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA 054KV UT WOS:000238376400008 PM 16783341 ER PT J AU Grinspoon, S AF Grinspoon, Steven TI Physiologic effects of GHRH in patients with HIV lipodystrophy: a model of acquired visceral adiposity SO NATURE CLINICAL PRACTICE ENDOCRINOLOGY & METABOLISM LA English DT Editorial Material ID HORMONE C1 Massachusetts Gen Hosp, Boston, MA 02114 USA. Harvard Univ, Sch Med, Boston, MA USA. RP Grinspoon, S (reprint author), Massachusetts Gen Hosp, Boston, MA 02114 USA. NR 2 TC 1 Z9 1 U1 0 U2 0 PU NATURE PUBLISHING GROUP PI NEW YORK PA 75 VARICK STREET, 9TH FLOOR, NEW YORK, NY 10013-1917 USA SN 1745-8366 J9 NAT CLIN PRACT ENDOC JI Nat. Clin. Pract. Endocrinol. Metab. PD JUL PY 2006 VL 2 IS 7 BP 355 EP 355 DI 10.1038/ncpendmet0225 PG 1 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA 064JN UT WOS:000239085200001 PM 16932313 ER PT J AU Lindhorst, S Cudkowicz, M AF Lindhorst, S Cudkowicz, M TI Is pentoxifylline safe and effective in patients with amyotrophic lateral sclerosis? SO NATURE CLINICAL PRACTICE NEUROLOGY LA English DT Editorial Material DE amyotrophic lateral sclerosis; pentoxifylline; phosphodiesterase (PDE4B); revised Amyotrophic Lateral Sclerosis Functional Rating Scale; riluzole C1 Massachusetts Gen Hosp, Neurol Clin Trials Unit, Boston, MA 02114 USA. Harvard Univ, Sch Med, Boston, MA USA. RP Cudkowicz, M (reprint author), Harvard Univ, Massachusetts Gen Hosp, Sch Med, Neurol Clin Trials Unit, Bldg 149,13th St CNY,Room 2274, Charlestown, MA 02129 USA. EM mcudkowicz@partners.org NR 5 TC 1 Z9 1 U1 0 U2 0 PU NATURE PUBLISHING GROUP PI NEW YORK PA 75 VARICK STREET, 9TH FLOOR, NEW YORK, NY 10013-1917 USA SN 1745-834X J9 NAT CLIN PRACT NEURO JI Nat. Clin. Pract. Neurol. PD JUL PY 2006 VL 2 IS 7 BP 364 EP 365 DI 10.1038/ncpneuro0238 PG 2 WC Clinical Neurology SC Neurosciences & Neurology GA 057IN UT WOS:000238589600008 PM 16932586 ER PT J AU Talcott, JA AF Talcott, James A. TI Are prostate cancer outcomes affected by a delay between diagnosis and radical prostatectomy? SO NATURE CLINICAL PRACTICE UROLOGY LA English DT Editorial Material DE biochemical recurrence; delay; prostate cancer; radical prostatectomy C1 Massachusetts Gen Hosp, Ctr Outcomes Res, Ctr Canc, Boston, MA 02114 USA. Harvard Univ, Sch Med, Boston, MA USA. RP Talcott, JA (reprint author), Massachusetts Gen Hosp, Ctr Outcomes Res, Ctr Canc, HO1-107,55 Fruit St, Boston, MA 02114 USA. EM jtalcott@partners.org NR 2 TC 0 Z9 0 U1 0 U2 0 PU NATURE PUBLISHING GROUP PI NEW YORK PA 75 VARICK STREET, 9TH FLOOR, NEW YORK, NY 10013-1917 USA SN 1743-4270 J9 NAT CLIN PRACT UROL JI Nat. Clin. Pract. Urol. PD JUL PY 2006 VL 3 IS 7 BP 356 EP 357 DI 10.1038/ncpuro0511 PG 2 WC Urology & Nephrology SC Urology & Nephrology GA 064JP UT WOS:000239085400003 PM 16835619 ER PT J AU Hyatt, G Melamed, R Park, R Seguritan, R Laplace, C Poirot, L Zucchelli, S Obst, R Matos, M Venanzi, E Goldrath, A Nguyen, L Luckey, J Yamagata, T Herman, A Jacobs, J Mathis, D Benoist, C AF Hyatt, Gordon Melamed, Rachel Park, Richard Seguritan, Reuben Laplace, Catherine Poirot, Laurent Zucchelli, Silvia Obst, Reinhard Matos, Michael Venanzi, Emily Goldrath, Ananda Nguyen, Linh Luckey, John Yamagata, Tetsuya Herman, Ann Jacobs, Jonathan Mathis, Diane Benoist, Christophe TI Gene expression microarrays: glimpses of the immunological genome SO NATURE IMMUNOLOGY LA English DT Editorial Material ID IMMUNE-SYSTEM; T-CELLS; REGULATORY NETWORKS; SIGNATURES; DISCOVERY; MODULES; PROGRESSION; LYMPHOCYTES; PLASTICITY; PATTERNS AB Successful microarray experimentation can generate enormous amounts of data, potentially very rich but also very unwieldy. Bold outlooks and new methods for data analysis and presentation should yield additional insight into the complexities of the immune system. C1 Brigham & Womens Hosp, Dept Med, Joslin Diabet Ctr, Sect Immunol & Immunogenet, Boston, MA 02215 USA. Harvard Univ, Sch Med, Boston, MA 02215 USA. RP Hyatt, G (reprint author), Brigham & Womens Hosp, Dept Med, Joslin Diabet Ctr, Sect Immunol & Immunogenet, Boston, MA 02215 USA. EM cbdm@joslin.harvard.edu OI Jacobs, Jonathan/0000-0003-4698-0254; Melamed, Rachel/0000-0003-3089-9806 FU NIAID NIH HHS [AI52343, AI51530]; NIAMS NIH HHS [AR046580]; NIDDK NIH HHS [DK60027, DK59658] NR 51 TC 48 Z9 49 U1 0 U2 2 PU NATURE PUBLISHING GROUP PI NEW YORK PA 75 VARICK STREET, 9TH FLOOR, NEW YORK, NY 10013-1917 USA SN 1529-2908 J9 NAT IMMUNOL JI Nat. Immunol. PD JUL PY 2006 VL 7 IS 7 BP 686 EP 691 DI 10.1038/ni0706-686 PG 6 WC Immunology SC Immunology GA 054LH UT WOS:000238377700003 PM 16785882 ER PT J AU Hirai, H Zhang, P Dayaram, T Hetherington, CJ Mizuno, S Imanishi, J Akashi, K Tenen, DG AF Hirai, H Zhang, P Dayaram, T Hetherington, CJ Mizuno, S Imanishi, J Akashi, K Tenen, DG TI C/EBP beta is required for 'emergency' granulopoiesis SO NATURE IMMUNOLOGY LA English DT Article ID COLONY-STIMULATING FACTOR; BINDING PROTEIN-ALPHA; RECEPTOR-DEFICIENT MICE; TRANSCRIPTION FACTOR; GRANULOCYTIC DIFFERENTIATION; HEPATOCYTE PROLIFERATION; MYELOID-LEUKEMIA; KNOCKOUT MICE; PLASMID DNA; MULTI-CSF AB During 'emergency' situations such as infections, host defense requires rapid mobilization of bone marrow granulocyte progenitors. 'Steady-state' granulopoiesis is absolutely dependent on the C/EBP alpha transcription factor, but the transcriptional mechanisms underlying emergency granulopoiesis remain unclear. Here we show that large numbers of granulocytes were generated from C/EBP alpha-deficient progenitors after cytokine stimulation in vivo. Cytokine treatment or fungal infection induced upregulation of C/EBP beta but not C/EBP alpha or C/EBP epsilon transcripts in granulocyte progenitors, and C/EBP beta-deficient progenitors showed decreased emergency-induced granulopoiesis in vitro and in vivo. C/EBPb inhibited proliferation less severely than did C/EBP alpha. These data suggest a critical function for C/EBP beta in emergency granulopoiesis, which demands both differentiation and proliferation of granulocyte precursors. C1 Harvard Univ, Inst Med, Boston, MA 02115 USA. Harvard Univ, Stem Cell Inst, Boston, MA 02115 USA. Kyoto Prefectural Univ Med, Dept Microbiol, Kyoto 602, Japan. Harvard Univ, Sch Med, Dana Farber Canc Inst, Dept Canc Immunol & AIDS, Boston, MA 02115 USA. Kyushu Univ Hosp, Ctr Cellular & Mol Med, Fukuoka 8120034, Japan. RP Tenen, DG (reprint author), Harvard Univ, Inst Med, Boston, MA 02115 USA. EM dtenen@bidmc.harvard.edu OI Tenen, Daniel/0000-0002-6423-3888 FU NHLBI NIH HHS [HL56745] NR 60 TC 170 Z9 172 U1 2 U2 7 PU NATURE PUBLISHING GROUP PI NEW YORK PA 75 VARICK STREET, 9TH FLOOR, NEW YORK, NY 10013-1917 USA SN 1529-2908 J9 NAT IMMUNOL JI Nat. Immunol. PD JUL PY 2006 VL 7 IS 7 BP 732 EP 739 DI 10.1038/ni1354 PG 8 WC Immunology SC Immunology GA 054LH UT WOS:000238377700018 PM 16751774 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 Transcription factor IRF4 controls plasma cell differentiation and class-switch recombination SO NATURE IMMUNOLOGY LA English DT Article ID CENTER B-CELLS; GERMINAL-CENTER FORMATION; REGULATORY FACTOR FAMILY; GENE-EXPRESSION; TERMINAL DIFFERENTIATION; SOMATIC HYPERMUTATION; PRIMARY IMMUNIZATION; AFFINITY MATURATION; BLIMP-1 EXPRESSION; HODGKIN LYMPHOMA AB B cells producing high-affinity antibodies are destined to differentiate into memory B cells and plasma cells, but the mechanisms leading to those differentiation pathways are mostly unknown. Here we report that the transcription factor IRF4 is required for the generation of plasma cells. Transgenic mice with conditional deletion of Irf4 in germinal center B cells lacked post-germinal center plasma cells and were unable to differentiate memory B cells into plasma cells. Plasma cell differentiation required IRF4 as well as the transcriptional repressor Blimp-1, which both acted 'upstream' of the transcription factor XBP-1. In addition, IRF4-deficient B cells had impaired expression of activation-induced deaminase and lacked class-switch recombination, suggesting an independent function for IRF4 in this process. These results identify IRF4 as a crucial transcriptional 'switch' in the generation of functionally competent plasma cells. C1 Columbia Univ, Inst Canc Genet, Dept Pathol, New York, NY 10032 USA. Columbia Univ, Herbert Irving Comprehens Canc Ctr, New York, NY 10032 USA. Harvard Univ, Sch Med, CBR Inst Biomed Res, Boston, MA 02115 USA. RP Dalla-Favera, R (reprint author), Columbia Univ, Inst Canc Genet, Dept Pathol, New York, NY 10032 USA. EM rd10@columbia.edu RI Ludwig, Thomas/Q-6484-2016; OI Ludwig, Thomas/0000-0003-3461-2585; Cattoretti, Giorgio/0000-0003-3799-3221 FU NCI NIH HHS [CA37295, CA098285, CA92625] NR 53 TC 330 Z9 332 U1 0 U2 13 PU NATURE PUBLISHING GROUP PI NEW YORK PA 75 VARICK STREET, 9TH FLOOR, NEW YORK, NY 10013-1917 USA SN 1529-2908 J9 NAT IMMUNOL JI Nat. Immunol. PD JUL PY 2006 VL 7 IS 7 BP 773 EP 782 DI 10.1038/ni1357 PG 10 WC Immunology SC Immunology GA 054LH UT WOS:000238377700023 PM 16767092 ER PT J AU Hyman, BT Growdon, JH AF Hyman, Bradley T. Growdon, John H. TI Can the immune system fight Alzheimer disease? SO NATURE MEDICINE LA English DT Editorial Material ID BETA IMMUNIZATION AN1792; PATHOLOGY; PEPTIDE; MOUSE AB Mobilizing the immune system may be a promising strategy to fight Alzheimer disease. A clinical trial has shed light on the therapeutic potential - and the pitfalls - of A beta immunization. C1 Massachusetts Gen Hosp, Dept Neurol, Boston, MA 02114 USA. RP Hyman, BT (reprint author), Massachusetts Gen Hosp, Dept Neurol, Boston, MA 02114 USA. EM bhyman@partners.org NR 7 TC 4 Z9 6 U1 1 U2 1 PU NATURE PUBLISHING GROUP PI NEW YORK PA 75 VARICK STREET, 9TH FLOOR, NEW YORK, NY 10013-1917 USA SN 1078-8956 J9 NAT MED JI Nat. Med. PD JUL PY 2006 VL 12 IS 7 BP 755 EP 756 DI 10.1038/nm0706-755 PG 2 WC Biochemistry & Molecular Biology; Cell Biology; Medicine, Research & Experimental SC Biochemistry & Molecular Biology; Cell Biology; Research & Experimental Medicine GA 061HS UT WOS:000238862800034 PM 16829929 ER PT J AU Thomas, RK Nickerson, E Simons, JF Janne, PA Tengs, T Yuza, Y Garraway, LA LaFramboise, T Lee, JC Shah, K O'Neill, K Sasaki, H Lindeman, N Wong, KK Borras, AM Gutmann, EJ Dragnev, KH DeBiasi, R Chen, TH Glatt, KA Greulich, H Desany, B Lubeski, CK Brockman, W Alvarez, P Hutchison, SK Leamon, JH Ronan, MT Turenchalk, GS Egholm, M Sellers, WR Rothberg, JM Meyerson, M AF Thomas, Roman K. Nickerson, Elizabeth Simons, Jan F. Janne, Pasi A. Tengs, Torstein Yuza, Yuki Garraway, Levi A. LaFramboise, Thomas Lee, Jeffrey C. Shah, Kinjal O'Neill, Keith Sasaki, Hidefumi Lindeman, Neal Wong, Kwok-Kin Borras, Ana M. Gutmann, Edward J. Dragnev, Konstantin H. DeBiasi, Ralph Chen, Tzu-Hsiu Glatt, Karen A. Greulich, Heidi Desany, Brian Lubeski, Christine K. Brockman, William Alvarez, Pablo Hutchison, Stephen K. Leamon, J. H. Ronan, Michael T. Turenchalk, Gregory S. Egholm, Michael Sellers, William R. Rothberg, Jonathan M. Meyerson, Matthew TI Sensitive mutation detection in heterogeneous cancer specimens by massively parallel picoliter reactor sequencing SO NATURE MEDICINE LA English DT Article ID CELL LUNG-CANCER; ACTIVATING MUTATIONS; ACQUIRED-RESISTANCE; KINASE INHIBITOR; EGF RECEPTOR; GEFITINIB; ERLOTINIB; THERAPY; DOMAIN AB The sensitivity of conventional DNA sequencing in tumor biopsies is limited by stromal contamination and by genetic heterogeneity within the cancer. Here, we show that microreactor-based pyrosequencing can detect rare cancer-associated sequence variations by independent and parallel sampling of multiple representatives of a given DNA fragment. This technology can thereby facilitate accurate molecular diagnosis of heterogeneous cancer specimens and enable patient selection for targeted cancer therapies. C1 Harvard Univ, Sch Med, Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02115 USA. MIT, Broad Inst, Cambridge, MA 02142 USA. Harvard Univ, Cambridge Ctr 7, Cambridge, MA 02142 USA. Dana Farber Canc Inst, Melanoma Program Med Oncol, Boston, MA 02115 USA. Nagoya City Univ, Sch Med, Dept Surg 2, Mizuho Ku, Nagoya, Aichi 4678601, Japan. Brigham & Womens Hosp, Dept Pathol, Boston, MA 02115 USA. Dana Farber Canc Inst, Translat Res Lab, Boston, MA 02115 USA. Dartmouth Hitchcock Med Ctr, Dept Pathol, Norris Cotton Canc Ctr, Lebanon, NH 03756 USA. Dartmouth Hitchcock Med Ctr, Dept Med, Norris Cotton Canc Ctr, Lebanon, NH 03756 USA. Harvard Univ, Sch Med, Dept Pathol, Boston, MA 02115 USA. Dana Farber Canc Inst, Ctr Canc Genome Discovery, Boston, MA 02115 USA. RP Meyerson, M (reprint author), Harvard Univ, Sch Med, Dana Farber Canc Inst, Dept Med Oncol, 44 Binney St, Boston, MA 02115 USA. EM matthew_meyerson@dfci.harvard.edu RI Meyerson, Matthew/E-7123-2012; Mendez, Pedro /J-8955-2016; OI Mendez, Pedro /0000-0001-6713-7907; wong, kwok kin/0000-0001-6323-235X FU NCI NIH HHS [T32 CA009172, R01CA098185] NR 19 TC 236 Z9 247 U1 1 U2 21 PU NATURE PUBLISHING GROUP PI NEW YORK PA 75 VARICK STREET, 9TH FLOOR, NEW YORK, NY 10013-1917 USA SN 1078-8956 J9 NAT MED JI Nat. Med. PD JUL PY 2006 VL 12 IS 7 BP 852 EP 855 DI 10.1038/nm1437 PG 4 WC Biochemistry & Molecular Biology; Cell Biology; Medicine, Research & Experimental SC Biochemistry & Molecular Biology; Cell Biology; Research & Experimental Medicine GA 061HS UT WOS:000238862800075 PM 16799556 ER PT J AU Fukumura, D Kashiwagi, S Jain, RK AF Fukumura, Dai Kashiwagi, Satoshi Jain, Rakesh K. TI The role of nitric oxide in tumour progression SO NATURE REVIEWS CANCER LA English DT Review ID ENDOTHELIAL GROWTH-FACTOR; NECROSIS-FACTOR-ALPHA; INDUCIBLE FACTOR-1 ACTIVATION; VASCULAR SMOOTH-MUSCLE; MURAL CELL RECRUITMENT; II GENE DISRUPTION; IN-VIVO; CARCINOMA-CELLS; MELANOMA-CELLS; SYNTHASE GENE AB Nitric oxide (NO) and nitric oxide synthases are ubiquitous in malignant tumours and are known to exert both pro- and anti-tumour effects. We summarize our current understanding of the role of NO in tumour progression, especially in relation to angiogenesis and vascular functions. We also discuss potential strategies for cancer treatment that modulate NO production and/or its downstream signalling pathways. C1 Massachusetts Gen Hosp, Dept Radiat Oncol, Edwin L Steele Lab, Boston, MA 02114 USA. Harvard Univ, Sch Med, Boston, MA 02114 USA. RP Fukumura, D (reprint author), Massachusetts Gen Hosp, Dept Radiat Oncol, Edwin L Steele Lab, Boston, MA 02114 USA. EM dai@steele.mgh.harvard.edu NR 168 TC 517 Z9 537 U1 3 U2 49 PU NATURE PUBLISHING GROUP PI LONDON PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND SN 1474-175X J9 NAT REV CANCER JI Nat. Rev. Cancer PD JUL PY 2006 VL 6 IS 7 BP 521 EP 534 DI 10.1038/nrc1910 PG 14 WC Oncology SC Oncology GA 065ZY UT WOS:000239200200014 PM 16794635 ER PT J AU Castano, AP Mroz, P Hamblin, MR AF Castano, Ana P. Mroz, Pawel Hamblin, Michael R. TI Photodynamic therapy and anti-tumour immunity SO NATURE REVIEWS CANCER LA English DT Review ID TOLL-LIKE RECEPTORS; NF-KAPPA-B; TETRA HYDROXYPHENYL CHLORIN; DENDRITIC CELL PRECURSORS; HEAT-SHOCK PROTEINS; MOUSE-TUMOR MODEL; IN-VIVO; T-CELLS; GENE-EXPRESSION; MEDIATED PHOTOSENSITIZATION AB Photodynamic therapy (PDT) uses non-toxic photosensitizers and harmless visible light in combination with oxygen to produce cytotoxic reactive oxygen species that kill malignant cells by apoptosis and/or necrosis, shut down the tumour microvasculature and stimulate the host immune system. In contrast to surgery, radiotherapy and chemotherapy that are mostly immunosuppressive, PDT causes acute inflammation, expression of heat-shock proteins, invasion and infiltration of the tumour by leukocytes, and might increase the presentation of tumour-derived antigens to T cells. C1 Massachusetts Gen Hosp, Wellman Ctr Photomed, Boston, MA 02114 USA. Harvard Univ, Sch Med, Dept Dermatol, Boston, MA 02115 USA. Harvard Mit Div Hlth Sci & Technol, Cambridge, MA USA. RP Hamblin, MR (reprint author), Massachusetts Gen Hosp, Wellman Ctr Photomed, Boston, MA 02114 USA. EM Hamblin@helix.mgh.harvard.edu OI Hamblin, Michael/0000-0001-6431-4605 FU NCI NIH HHS [R01 CA083882, R01 CA083882-03] NR 136 TC 730 Z9 756 U1 66 U2 286 PU NATURE PUBLISHING GROUP PI LONDON PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND SN 1474-175X J9 NAT REV CANCER JI Nat. Rev. Cancer PD JUL PY 2006 VL 6 IS 7 BP 535 EP 545 DI 10.1038/nrc1894 PG 11 WC Oncology SC Oncology GA 065ZY UT WOS:000239200200015 PM 16794636 ER PT J AU Taubman, MA Nash, DA AF Taubman, MA Nash, DA TI The scientific and public-health imperative for a vaccine against dental caries SO NATURE REVIEWS IMMUNOLOGY LA English DT Review ID SURFACE PROTEIN ANTIGEN; GLUCAN-BINDING-PROTEIN; STREPTOCOCCUS-MUTANS ANTIGEN; LOCAL PASSIVE-IMMUNIZATION; MONKEYS MACACA-FASCICULARIS; SECRETORY IMMUNOGLOBULIN-A; ACTIVE-SITE PEPTIDE; SALIVARY IMMUNOGLOBULIN; MONOCLONAL-ANTIBODIES; ORAL IMMUNIZATION AB Dental caries is caused by one of the most ubiquitous bacterial infections of humans. In many countries such as Brazil and China, this disease is reaching epidemic proportions, and it is clear that a more effective public-health measure to combat dental caries is needed, because disadvantaged children are the most severely affected. One of the main groups of oral microorganisms, the mutans streptococci, has been associated with the aetiology of dental caries, and preclinical studies of immunological interventions have shown the feasibility of interfering with this disease. Moreover, clinical trials have indicated that a mucosal immune response to a crucial antigen(s) of mutans streptococci can influence the pathogenesis of dental caries. Evidence that this antigen(s) is appropriate for use in a vaccine against dental caries, as well as evidence for an appropriate target population of individuals and a logical time of administration, has now emerged. C1 Forsyth Inst, Dept Immunol, Boston, MA 02115 USA. Univ Kentucky, Coll Dent, Dept Pediat Dent, Lexington, KY 40536 USA. RP Taubman, MA (reprint author), Forsyth Inst, Dept Immunol, 140 Fenway, Boston, MA 02115 USA. EM mtaubman@forsyth.org NR 104 TC 55 Z9 59 U1 0 U2 16 PU NATURE PUBLISHING GROUP PI LONDON PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND SN 1474-1733 J9 NAT REV IMMUNOL JI Nat. Rev. Immunol. PD JUL PY 2006 VL 6 IS 7 BP 555 EP 563 DI 10.1038/nri1857 PG 10 WC Immunology SC Immunology GA 056NG UT WOS:000238529900014 PM 16729013 ER PT J AU Govindarajan, A Kelleher, RJ Tonegawa, S AF Govindarajan, Arvind Kelleher, Raymond J. Tonegawa, Susumu TI Opinion - A clustered plasticity model of long-term memory engrams SO NATURE REVIEWS NEUROSCIENCE LA English DT Review ID CA1 PYRAMIDAL NEURONS; LOCAL PROTEIN-SYNTHESIS; HIPPOCAMPAL AREA CA1; FREELY MOVING RATS; LATE-PHASE LTP; SYNAPTIC PLASTICITY; DENDRITIC SPINES; DENTATE GYRUS; IN-VITRO; SIGNALING PATHWAY AB Long-term memory and its putative synaptic correlates the late phases of both long-term potentiation and long-term depression require enhanced protein synthesis. On the basis of recent data on translation-dependent synaptic plasticity and on the supralinear effect of activation of nearby synapses on action potential generation, we propose a model for the formation of long-term memory engrams at the single neuron level. In this model, which we call clustered plasticity, local translational enhancement, along with synaptic tagging and capture, facilitates the formation of long-term memory engrams through bidirectional synaptic weight changes among synapses within a dendritic branch. C1 MIT, Howard Hughes Med Inst, Picower Inst Learning & Memory, RIKEN Neurosci Res Ctr,Dept Biol, Cambridge, MA 02139 USA. MIT, Dept Brain & Cognit Sci, Cambridge, MA 02139 USA. Massachusetts Gen Hosp, Richard B Simches Res Ctr, Ctr Human Genet Res, Boston, MA 02114 USA. Massachusetts Gen Hosp, Richard B Simches Res Ctr, Dept Neurol, Boston, MA 02114 USA. RP Tonegawa, S (reprint author), MIT, Howard Hughes Med Inst, Picower Inst Learning & Memory, RIKEN Neurosci Res Ctr,Dept Biol, 77 Massachusetts Ave, Cambridge, MA 02139 USA. EM tonegawa@mit.edu NR 108 TC 156 Z9 161 U1 2 U2 13 PU NATURE PUBLISHING GROUP PI LONDON PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND SN 1471-0048 J9 NAT REV NEUROSCI JI Nat. Rev. Neurosci. PD JUL PY 2006 VL 7 IS 7 BP 575 EP 583 DI 10.1038/nrn1937 PG 9 WC Neurosciences SC Neurosciences & Neurology GA 055US UT WOS:000238476600017 PM 16791146 ER PT J AU Noronha, V Berliner, N Ballen, KK Lacy, J Kracher, J Baehring, J Henson, JW AF Noronha, Vanita Berliner, Nancy Ballen, Karen K. Lacy, Jill Kracher, Jean Baehring, Joachim Henson, John W. TI Treatment-related myelodysplasia/AML in a patient with a history of breast cancer and an oligodendroglioma treated with temozolomide: Case study and review of the literature SO NEURO-ONCOLOGY LA English DT Article DE brain neoplasm; glioblastoma; myelodysplastic syndrome; recurrent glioma; secondary leukemia; secondary myelodysplastic syndrome; temozolomide; treatment complication ID THERAPY-RELATED MYELODYSPLASIA; LEUKEMIA FOLLOWING TREATMENT; MALIGNANT GLIOMA; TRANSPLANTATION AB The emergence of temozolomide as an effective alkylating agent with little acute toxicity or cumulative myelosuppression has led to protracted courses of chemotherapy for many patients with gliomas. Secondary, or treatment-related, myelodysplasia (t-MDS) and acute myelogenous leukemia (t-AML) are life-threatening complications of alkylating chemotherapy and have been reported in patients with primary brain tumors. We describe a case of temozolomide-related t-MDS/AML and discuss the clinical features of this condition. Administration of an alkylating agent in patient populations with long median survivals must be undertaken with an understanding of the potential for this treatment complication. C1 Massachusetts Gen Hosp, Pappas Ctr Neurooncol, Boston, MA 02114 USA. Yale Univ, Sch Med, Dept Med, Div Med Oncol, New Haven, CT 06510 USA. Yale Univ, Sch Med, Yale Brain Tumor Ctr, Dept Neurol, New Haven, CT 06510 USA. Yale Univ, Sch Med, Yale Brain Tumor Ctr, Dept Neurosurg, New Haven, CT 06510 USA. Massachusetts Gen Hosp, Dept Med, Div Hematol, Boston, MA 02114 USA. Harvard Univ, Sch Med, Boston, MA 02115 USA. RP Henson, JW (reprint author), Massachusetts Gen Hosp, Pappas Ctr Neurooncol, Yawkey 9 E,Fruit St, Boston, MA 02114 USA. EM henson@helix.mgh.harvard.edu NR 14 TC 42 Z9 45 U1 0 U2 0 PU DUKE UNIV PRESS PI DURHAM PA 905 W MAIN ST, STE 18-B, DURHAM, NC 27701 USA SN 1522-8517 J9 NEURO-ONCOLOGY JI Neuro-Oncology PD JUL PY 2006 VL 8 IS 3 BP 280 EP 283 DI 10.1215/15228517-2006-003 PG 4 WC Oncology; Clinical Neurology SC Oncology; Neurosciences & Neurology GA 065QY UT WOS:000239175600008 PM 16728498 ER PT J AU Guidetti, P Bates, GP Graham, RK Hayden, MR Leavitt, BR MacDonald, ME Slow, EJ Wheeler, VC Woodman, B Schwarcz, R AF Guidetti, P Bates, GP Graham, RK Hayden, MR Leavitt, BR MacDonald, ME Slow, EJ Wheeler, VC Woodman, B Schwarcz, R TI Elevated brain 3-hydroxykynurenine and quinolinate levels in Huntington disease mice SO NEUROBIOLOGY OF DISEASE LA English DT Article DE excitotoxicity; free radicals; kynurenine monooxygenase; kynurenine pathway; microglia; neurodegeneration; NMDA ID YAC128 MOUSE MODEL; KYNURENINE PATHWAY METABOLISM; ASPARTATE RECEPTOR ACTIVATION; RAT STRIATUM; INTRASTRIATAL INJECTIONS; AXONAL-TRANSPORT; HUMAN ASTROCYTES; CELL-DEATH; IN-VIVO; ACID AB The brain levels of the endogenous excitotoxin quinolinic acid (QUIN) and its bioprecursor, the free radical generator 3-hydroxykynurenine (3-HK), are elevated in early stage Huntington disease (HD). We now examined the status of these metabolites in three mouse models of HD. In R6/2 mice, 3-HK levels were significantly and selectively elevated in the striatum, cortex and cerebellum starting at 4 weeks of age. In contrast, both 3-HK and QUIN levels were increased in the striatum and cortex of the full-length HD models, beginning at 8 months (YAC128) and 15 months (Hdh(Q92) and Hdh(Q111)), respectively. No changes were seen in 13-month-old shortstop mice, which show no signs of motor or cognitive dysfunction or selective neuropathology. These results demonstrate both important parallels and intriguing differences in the progressive neurochemical changes in these HD mouse models and support the hypothesis that QUIN may play a role in the striatal and cortical neurodegeneration of HD. (c) 2006 Elsevier Inc. All rights reserved. C1 Univ Maryland, Sch Med, Maryland Psychiat Res Ctr, Baltimore, MD 21228 USA. Univ London Kings Coll, Guys Hosp, Dept Med & Mol Genet, London SE1 9RT, England. Univ British Columbia, Dept Med Genet, Ctr Mol Med & Therapeut, Vancouver, BC V52 4H4, Canada. Massachusetts Gen Hosp, Mol Neurogenet Unit, Charlestown, MA 02129 USA. Massachusetts Gen Hosp, Ctr Human Genet Res, Charlestown, MA 02129 USA. RP Schwarcz, R (reprint author), Univ Maryland, Sch Med, Maryland Psychiat Res Ctr, Baltimore, MD 21228 USA. EM rschwarc@mprc.umaryland.edu RI Hayden, Michael/D-8581-2011; Leavitt, Blair/G-1934-2012; Bates, Gillian/E-1146-2012 OI Hayden, Michael/0000-0001-5159-1419; Bates, Gillian/0000-0002-4041-6305 FU NINDS NIH HHS [NS16367, NS32765]; Wellcome Trust [66270] NR 67 TC 80 Z9 82 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 0969-9961 J9 NEUROBIOL DIS JI Neurobiol. Dis. PD JUL PY 2006 VL 23 IS 1 BP 190 EP 197 DI 10.1016/j.nbd.2006.02.011 PG 8 WC Neurosciences SC Neurosciences & Neurology GA 057YY UT WOS:000238632300018 PM 16697652 ER PT J AU de Vasconcelos, AP Riban, V Wasterlain, C Nehlig, A AF de Vasconcelos, AP Riban, V Wasterlain, C Nehlig, A TI Role of endothelial nitric oxide synthase in cerebral blood flow changes during kainate seizures: A genetic approach using knockout mice SO NEUROBIOLOGY OF DISEASE LA English DT Article DE endothelial nitric oxide synthase; knockout mice; kainate seizures; intrahippocampal injection; cerebral blood flow ID TEMPORAL-LOBE EPILEPSY; HIPPOCAMPAL SCLEROSIS; LIMBIC SEIZURES; L-ARGININE; RAT; STIMULATION; HYPEREMIA; AUTOREGULATION; INHIBITION; LACKING AB The role of endothelial nitric oxide (NO) in the cerebrovascular response to partial seizures was investigated in mice deleted for the endothelial NO synthase gene (eNOS-/-) and in their paired wild-type (WT) congeners. Local cerebral blood flow (LCBF, quantitative [C-14] iodoantipyrine method) was measured 3-6 h after unilateral kainate (KA) injection in the dorsal hippocampus; controls received saline. In WT mice, KA seizures induced a 22 to 50% LCBF increase restricted to the ipsilateral hippocampus, while significant LCBF decreases (15-33%) were noticed in 22% of the contralateral areas, i.e., the parietal cortex, amygdala and three basal ganglia areas, compared to satine-injected WT mice. In eNOS-/- mice, no LCBF increases were recorded within the epileptic focus and generalized contralateral LCBF decreases (22-46%) were noticed in 2/3 of the brain areas, compared to saline-injected eNOS-/- mice. Thus, endothelial NO is the mediator of the cerebrovascular response within the epileptic focus and participates in the maintenance of LCBF in distant areas. (c) 2006 Elsevier Inc. All rights reserved. C1 INSERM, Fac Med, U 398, F-67085 Strasbourg, France. Univ Calif Los Angeles, Sch Med, Vet Affairs Greater Los Angeles Healthcare Syst, Dept Neurol, Los Angeles, CA 90095 USA. Univ Calif Los Angeles, Sch Med, Vet Affairs Greater Los Angeles Healthcare Syst, Brain Res Inst, Los Angeles, CA 90095 USA. RP de Vasconcelos, AP (reprint author), INSERM, Fac Med, U 398, 11 Rue Humann, F-67085 Strasbourg, France. EM Pereira@neurochem.u-strasbg.fr NR 61 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 0969-9961 J9 NEUROBIOL DIS JI Neurobiol. Dis. PD JUL PY 2006 VL 23 IS 1 BP 219 EP 227 DI 10.1016/j.nbd.2006.03.002 PG 9 WC Neurosciences SC Neurosciences & Neurology GA 057YY UT WOS:000238632300021 ER PT J AU Yenari, MA Han, HS AF Yenari, MA Han, HS TI Influence of hypothermia on post-ischemic inflammation: Role of nuclear factor kappa B (NF kappa B) SO NEUROCHEMISTRY INTERNATIONAL LA English DT Article; Proceedings Paper CT 36th Annual Meeting of the American-Society-for-Neurochemistry CY JUN 25-29, 2005 CL Madison, WI SP Amer Soc Neurochem DE hypothermia; NF kappa B target genes; TNF-alpha ID FOCAL CEREBRAL-ISCHEMIA; NITRIC-OXIDE SYNTHASE; NECROSIS-FACTOR-ALPHA; GLOBAL BRAIN ISCHEMIA; MILD HYPOTHERMIA; ARTERY OCCLUSION; EXPERIMENTAL STROKE; MICROGLIAL ACTIVATION; MODERATE HYPOTHERMIA; RAT-BRAIN AB Mild hypothermia is one of the most robust neuroprotectant studied in the laboratory to date. The reasons for this protective effect are likely multifactorial, but work from our laboratory and others have shown that this protection is associated with remarkable suppression of the inflammatory response that accompanies brain ischemia. Consistently, laboratories have shown that small decreases in brain temperature to 30-34 degrees C result in reduced inflammatory cell infiltrate, less microglial activation, and reduction of a variety of inflammatory mediators such as nitric oxide, inflammatory cytokines and superoxide. Nuclear factor-kappa B (NF kappa B) is a transcription factor that is activated after cerebral ischemia. NF kappa B activation leads to the expression of many inflammatory genes involved in the pathogenesis of stroke. Our laboratory has shown that hypothermia decreases NF kappa B translocation and binding activity, by affecting NF kappa B regulatory proteins. Mild hypothermia appears to suppress phosphorylation of NF kappa B's inhibitory protein (I kappa B-alpha) by decreasing expression and activity of I kappa B kinase-gamma (IKK). As a consequence, hypothermia suppressed gene expression of two NF kappa B target genes, inducible nitric oxide synthase and TNF-alpha. These data suggest that the protective effect of hypothermia on cerebral injury is, in part, related to NF kappa B inhibition due to decreased activity of IKK. (c) 2006 Elsevier Ltd. All rights reserved. C1 Univ Calif San Francisco, Dept Neurol, San Francisco, CA 94121 USA. San Francisco Vet Affairs Med Ctr, San Francisco, CA 94121 USA. Kyungpook Natl Univ, Sch Med, Dept Physiol, Taegu, South Korea. RP Yenari, MA (reprint author), Univ Calif San Francisco, Dept Neurol, 4150 Clement St, San Francisco, CA 94121 USA. EM yenari@alum.mit.edu FU NINDS NIH HHS [R01 NS 40516] NR 84 TC 62 Z9 72 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND SN 0197-0186 J9 NEUROCHEM INT JI Neurochem. Int. PD JUL PY 2006 VL 49 IS 2 BP 164 EP 169 DI 10.1016/j.neuint.2006.03.016 PG 6 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA 059XB UT WOS:000238764400008 PM 16750872 ER PT J AU Desikan, RS Segonne, F Fischl, B Quinn, BT Dickerson, BC Blacker, D Buckner, RL Dale, AM Maguire, RP Hyman, BT Albert, MS Killiany, RJ AF Desikan, Rahul S. Segonne, Florent Fischl, Bruce Quinn, Brian T. Dickerson, Bradford C. Blacker, Deborah Buckner, Randy L. Dale, Anders M. Maguire, R. Paul Hyman, Bradley T. Albert, Marilyn S. Killiany, Ronald J. TI An automated labeling system for subdividing the human cerebral cortex on MRI scans into gyral based regions of interest SO NEUROIMAGE LA English DT Article ID MAGNETIC-RESONANCE IMAGES; ALZHEIMERS-DISEASE; CORTICAL SURFACE; HUMAN BRAIN; PREFRONTAL CORTEX; COORDINATE SYSTEM; TEMPORAL-LOBE; VOLUME; ATLAS; DEMENTIA AB In this study, we have assessed the validity and reliability of an automated labeling system that we have developed for subdividing the human cerebral cortex on magnetic resonance images into gyral based regions of interest (ROIs). Using a dataset of 40 MRI scans we manually identified 34 cortical ROIs in each (if the individual hemispheres. This information was then encoded in the form of an atlas that was utilized to automatically label ROIs. To examine the validity, as well as the intra- and inter-rater reliability of the automated system, we used both intraclass correlation coefficients (ICC), and a new method known as mean distance maps, to assess the degree of mismatch between the manual and the automated sets of ROIs. When compared with the manual ROIs, the automated ROIs were highly accurate, with an average ICC of 0.835 across all of the ROIs, and a mean distance error of less than 1 mm. Intra- and inter-rater comparisons yielded little to no difference between the sets of ROIs. These findings suggest that the automated method we have developed for subdividing the human cerebral cortex into standard gyral-based neuroanatomical regions is both anatomically valid and reliable. This method may be useful for both morphometric and functional studies of the cerebral cortex as well as for clinical investigations aimed at tracking the evolution of disease-induced changes over time, including clinical trials in which MRI-based measures are used to examine response to treatment. (c) 2006 Elsevier Inc. All rights reserved. C1 Boston Univ, Sch Med, Dept Anat & Neurobiol, Boston, MA 02118 USA. Massachusetts Gen Hosp, Dept Radiol, Athinoula & Martinos Ctr Biomed Imaging, Dept Radiol, Charlestown, MA 02118 USA. MIT, CSAIL, Cambridge, MA 02139 USA. Massachusetts Gen Hosp, Dept Psychiat, Charlestown, MA 02129 USA. Harvard Univ, Dept Psychol, Cambridge, MA 02138 USA. Howard Hughes Med Inst, Coconut Grove, FL 33133 USA. Univ Calif San Diego, Sch Med, Dept Neurosci, San Diego, CA 92093 USA. Univ Calif San Diego, Sch Med, Dept Radiol, San Diego, CA 92093 USA. Univ Calif San Diego, Sch Med, Dept Cognit Sci, San Diego, CA 92093 USA. Massachusetts Gen Hosp, Dept Neurol, Charlestown, MA 02129 USA. Johns Hopkins Univ, Sch Med, Dept Neurol, Baltimore, MD 21287 USA. Pfizer Inc, Global Res & Dev, Groton, CT 06340 USA. RP Killiany, RJ (reprint author), Boston Univ, Sch Med, Dept Anat & Neurobiol, 715 Albany St,W701, Boston, MA 02118 USA. EM killiany@bu.edu RI Dale, Anders/A-5180-2010; OI Maguire, Ralph/0000-0003-3937-6622 FU NCRR NIH HHS [P41-RR14075, R01 RR 06594-01A1, U24 RR021382]; NIA NIH HHS [P01-AG04953]; NIBIB NIH HHS [R01 EB001550] NR 63 TC 2038 Z9 2054 U1 7 U2 71 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 JUL 1 PY 2006 VL 31 IS 3 BP 968 EP 980 DI 10.1016/j.neuroimage.2006.01.021 PG 13 WC Neurosciences; Neuroimaging; Radiology, Nuclear Medicine & Medical Imaging SC Neurosciences & Neurology; Radiology, Nuclear Medicine & Medical Imaging GA 054EB UT WOS:000238358500003 PM 16530430 ER PT J AU Walhovd, KB Fjell, AM Dale, AM Fischl, B Quinn, BT Makris, N Salat, D Reinvang, I AF Walhovd, KB Fjell, AM Dale, AM Fischl, B Quinn, BT Makris, N Salat, D Reinvang, I TI Regional cortical thickness matters in recall after months more than minutes SO NEUROIMAGE LA English DT Article ID HIPPOCAMPAL-FORMATION SIZE; HUMAN CEREBRAL-CORTEX; MEMORY PERFORMANCE; BRAIN VOLUME; HEALTHY-INDIVIDUALS; COORDINATE SYSTEM; WHITE-MATTER; OLDER-ADULTS; INTELLIGENCE; MRI AB The aim of this study was to determine the role of regional cortical thickness in recall of verbal material over an extended time period. MRI scans of healthy adults of varying ages were obtained. Two scans were averaged per person to achieve high spatial resolution, and a semi-automated method for continuous measurement of thickness across the entire cortical mantle was employed. Verbal memory tests assessing recall after 5 min, 30 min, and a mean interval of 83 days were administered. A general linear model (GLM) of the effects of thickness at each vertex on the different memory indices was computed, controlling for gender, age, IQ, and intracranial volume. These analyses were repeated with hippocampal volume as an additional variable to be controlled for, to assess to which extent effects of cortical thickness were independent of hippocampal size. Minute effects of cortical thickness were observed with regard to shorter time intervals (5 and 30 min). However, even when controlling for the effects of hippocampal volume, higher recall across months was associated with thicker cortex of distinct areas including parts of the gyros rectus, the middle frontal gyros, the paricto-occipital sulcus and the lingual gyrus of both hemispheres. In addition, hemisphere-specific associations were found in parts of the right temporal and parietal lobe as well as parts of the left precuneus. This supports a unique and critical role of the thickness of distinct cortical areas in recall after months, more than after minutes. (c) 2006 Elsevier Inc. All rights reserved. C1 Univ Oslo, Dept Psychol, N-0317 Oslo, Norway. Ullevaal Univ Hosp, Dept Neuropsychol, Oslo, Norway. Univ Calif San Diego, Dept Radiol, La Jolla, CA 92093 USA. Univ Calif San Diego, Dept Neurosci, La Jolla, CA 92093 USA. Harvard Univ, Massachusetts Gen Hosp, MGH NMR Ctr, Cambridge, MA 02138 USA. Norwegian Univ Sci & Technol, MR Ctr, Trondheim, Norway. MIT, Comp Sci & Artificial Intelligence Lab, Cambridge, MA 02139 USA. Harvard Univ, MGH, Ctr Morphometr Anal, Cambridge, MA 02138 USA. Univ Hosp, Rikshosp, Dept Psychosomat Med, Oslo, Norway. RP Walhovd, KB (reprint author), Univ Oslo, Dept Psychol, POB 1094 Blindern, N-0317 Oslo, Norway. EM k.b.walhovd@psykologi.uio.no RI Dale, Anders/A-5180-2010 FU NCRR NIH HHS [P41-RR14075, R01-RR13609, R01-RR16594]; NINDS NIH HHS [R01-NS39581] NR 58 TC 44 Z9 44 U1 1 U2 1 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 JUL 1 PY 2006 VL 31 IS 3 BP 1343 EP 1351 DI 10.1016/j.neuroimage.2006.01.011 PG 9 WC Neurosciences; Neuroimaging; Radiology, Nuclear Medicine & Medical Imaging SC Neurosciences & Neurology; Radiology, Nuclear Medicine & Medical Imaging GA 054EB UT WOS:000238358500036 PM 16540346 ER PT J AU Brown, RH AF Brown, R. H. TI Review of genetic approaches to understanding ALS, and implications for therapy SO NEUROMUSCULAR DISORDERS LA English DT Meeting Abstract CT 11th International Congress on Neuromuscular Diseases CY JUL 02-07, 2006 CL Istanbul, TURKEY C1 Harvard Univ, Sch Med, Massachusetts Gen Hosp, Day Neuromuscular Res Lab, Boston, MA USA. NR 0 TC 0 Z9 0 U1 1 U2 1 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND SN 0960-8966 J9 NEUROMUSCULAR DISORD JI Neuromusc. Disord. PD JUL PY 2006 VL 16 SU 1 BP S53 EP S53 PG 1 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA 066KX UT WOS:000239229400017 ER PT J AU Kuperberg, GR Kreher, DA Goff, D McGuire, PK David, AS AF Kuperberg, Gina R. Kreher, Donna A. Goff, Donald McGuire, Philip K. David, Anthony S. TI Building up linguistic context in schizophrenia: Evidence from self-paced reading SO NEUROPSYCHOLOGY LA English DT Article DE schizophrenia; language; semantics; syntax; context ID THOUGHT-DISORDER; COMMUNICATION DISORDERS; LANGUAGE ANALYSIS; BRAIN POTENTIALS; SENTENCES; SENSITIVITY; ERP; ABNORMALITIES; COMPREHENSION; INFORMATION AB An impairment in the build-up and use of context has been proposed as a core feature of schizophrenia. The current study tested the hypothesis that schizophrenia patients show impairments in building up context within sentences because of abnormalities in combining semantic with syntactic information. Schizophrenia patients and healthy controls read and made acceptability judgments about sentences containing verbs that were semantically associated with individual preceding words but that violated either the meaning (animacy/semantic constraints) or the syntactic structure (morphosymactic constraints) of their preceding contexts. To override these semantic associations and determine that such. sentences are unacceptable, participants must integrate semantic with syntactic information. These sentences were compared with congruous and pragmatically/semantically violated sentences that imposed fewer semantic-syntactic integration demands. At sentence-final words and decisions, patients showed smaller reaction time differences than controls to animacy/semantically violated or morphosyntactically violated sentences relative to pragmatically/semantically violated or nonviolated sentences. The relative insensitivity to these violations in patients with schizophrenia may arise from impairments in combining semantic and syntactic information to build up sentence context. C1 Tufts Univ, Dept Psychol, Medford, MA 02155 USA. Massachusetts Gen Hosp, Dept Psychiat, Boston, MA 02114 USA. Inst Psychiat, Dept Med Psychol, London, England. RP Kuperberg, GR (reprint author), CNY-2,Bldg 149,MGH E,13th St, Charlestown, MA 02129 USA. EM kuperber@nmr.mgh.harvard.edu RI David, Anthony/C-1315-2011 OI David, Anthony/0000-0003-0967-774X FU NIMH NIH HHS [R01 MH 071635]; Wellcome Trust NR 59 TC 21 Z9 22 U1 0 U2 2 PU AMER PSYCHOLOGICAL ASSOC/EDUCATIONAL PUBLISHING FOUNDATION PI WASHINGTON PA 750 FIRST ST NE, WASHINGTON, DC 20002-4242 USA SN 0894-4105 J9 NEUROPSYCHOLOGY JI Neuropsychology PD JUL PY 2006 VL 20 IS 4 BP 442 EP 452 DI 10.1037/0894-4105.20.4.442 PG 11 WC Psychology, Clinical; Neurosciences; Psychology SC Psychology; Neurosciences & Neurology GA 066SQ UT WOS:000239250800006 PM 16846262 ER PT J AU Nemeroff, CB Mayberg, HS Krahl, SE McNamara, J Frazer, A Henry, TR George, MS Charney, DS Brannan, SK AF Nemeroff, CB Mayberg, HS Krahl, SE McNamara, J Frazer, A Henry, TR George, MS Charney, DS Brannan, SK TI VNS therapy in treatment-resistant depression: Clinical evidence and putative neurobiological mechanisms SO NEUROPSYCHOPHARMACOLOGY LA English DT Article DE vagus nerve stimulation; treatment-resistant depression; mechanism of action; vagus nerve; neuroimaging; research ID VAGUS NERVE-STIMULATION; TRANSCRANIAL MAGNETIC STIMULATION; MEDICALLY INTRACTABLE SEIZURES; RANDOMIZED CONTROLLED-TRIAL; ELECTROCONVULSIVE-THERAPY; BLOOD-FLOW; PARTIAL EPILEPSY; BRAIN-STIMULATION; MAJOR DEPRESSION; LONG-TERM AB Currently available therapeutic interventions for treatment-resistant depression, including switch, combination, and augmentation strategies, are less than ideal. Observations of mood elevation during vagus nerve stimulation (VNS) therapy for pharmacoresistant epilepsy suggested a role for VNS therapy in refractory major depression and prompted clinical investigation of this neurostimulation modality. The VNS Therapy System (TM) has been available for treatment of pharmacoresistant epilepsy since 1997 and was approved by the US Food and Drug Administration for treatment-resistant depression in July, 2005. The physiology of the vagus nerve, mechanics of the VNS Therapy System (TM), and efficacy and safety in pharmacoresistant epilepsy are reviewed. Promising results of VNS therapy for treatment-resistant depression have been forthcoming from both acute and long-term studies, evidenced in part by progressive improvements in depression rating scale scores during the 1st year of treatment with maintenance of response thereafter. VNS therapy is well tolerated in patients with either pharmacoresistant epilepsy or treatment-resistant depression. As in epilepsy, the mechanisms of VNS therapy of treatment-resistant depression are incompletely understood. However, evidence from neuroimaging and other studies suggests that VNS therapy acts via innervation of the nucleus tractus solitarius, with secondary projections to limbic and cortical structures that are involved in mood regulation, including brainstem regions that contain serotonergic (raphe nucleus) and noradrenergic (locus ceruleus) perikarya that project to the forebrain. Mechanisms that mediate the beneficial effects of VNS therapy for treatment-resistant depression remain obscure. Suggestions for future research directions are described. C1 Emory Univ, Sch Med, Dept Psychiat & Behav Sci, Atlanta, GA 30322 USA. Mt Sinai Sch Med, New York, NY USA. Duke Univ, Med Ctr, Durham, NC USA. Univ Texas, Hlth Sci Ctr San Antonio, San Antonio, TX 78285 USA. Med Univ S Carolina, Charleston, SC 29425 USA. VA Greater Los Angeles Healthcare Syst, Los Angeles, CA USA. Cyberonics Inc, Houston, TX USA. RP Nemeroff, CB (reprint author), Emory Univ, Sch Med, Dept Psychiat & Behav Sci, 101 Woodruff Circle,Suite 4000, Atlanta, GA 30322 USA. EM cnemero@emory.edu OI Henry, Thomas/0000-0002-5708-903X NR 78 TC 158 Z9 161 U1 3 U2 13 PU NATURE PUBLISHING GROUP PI LONDON PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND SN 0893-133X J9 NEUROPSYCHOPHARMACOL JI Neuropsychopharmacology PD JUL PY 2006 VL 31 IS 7 BP 1345 EP 1355 DI 10.1038/sj.npp.1301082 PG 11 WC Neurosciences; Pharmacology & Pharmacy; Psychiatry SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry GA 054ZR UT WOS:000238418700001 PM 16641939 ER PT J AU Truong, MT Clair, EGS Donahue, BR Rush, SC Miller, DC Formenti, SC Knopp, EA Han, K Golfinos, JG AF Truong, Minh T. Clair, Eric G. St. Donahue, Bernadine R. Rush, Stephen C. Miller, Douglas C. Formenti, Silvia C. Knopp, Edmond A. Han, Kerry Golfinos, John G. TI Results of surgical resection for progression of brain metastases previously treated by gamma knife radiosurgery SO NEUROSURGERY LA English DT Article; Proceedings Paper CT 86th Annual Meeting of the American-Radium-Society CY MAY 01-05, 2004 CL Napa, CA SP Amer Radium Soc DE brain metastases; dynamic contrast-enhanced perfusion magnetic resonance imaging; magnetic resonance spectroscopy; radiosurgery; salvage therapy; treatment outcome ID PROTON MR SPECTROSCOPY; THERAPY-ONCOLOGY-GROUP; STEREOTACTIC RADIOSURGERY; RADIATION-THERAPY; RANDOMIZED-TRIAL; SINGLE; RADIOTHERAPY; PERFUSION; MANAGEMENT; CARCINOMA AB OBJECTIVE: To determine treatment outcome after surgical resection for progressive brain metastases after gamma knife radiosurgery (GKR) and to explore the role of dynamic contrast agent-enhanced perfusion magnetic resonance imaging (MRI) and proton spectroscopic MRI studies (MRS/P) in predicting pathological findings. METHODS: Between 1997 and 2002, 32 patients underwent surgical resection for suspected progression of brain metastases from a cohort of 245 patients with brain metastases treated with GKR. Postradiosurgery MRI surveillance was performed at 6 and 12 weeks, and then every 12 weeks after GKR. In some cases, additional MRI scanning with spectroscopy or perfusion (MRS/P) was used to aid differentiation of radiation change from tumor progression. The decision to perform neurosurgical-resection was based on MRI or clinical evidence of lesion progression among patients with a Karnofsky performance score of 60 or more and absent or stable systemic disease. RESULTS: Thirteen percent (32 out of 245) of patients and 6% (38 out of 611) of lesions required surgical resection after GKR. The median time from GKR to surgical resection was 8.6 months (range, 1.7-27.1 mo). The 6-, 12-, and 24-month actuarial survival from time of GKR was 97, 78, and 47% for the resected patients and 65, 40, and 19% for the nonresected patients (P < 0.0001). The two-year survival rate of patients requiring two resections after GKR was 100% compared with 39% for patients undergoing one resection (P = 0.02). The median survival of resected patients was 27.2 months (range, 7.0-72.5 mo) from the diagnosis of brain metastases, 19.9 months (range, 5.0-60.7 mo) from GKR, and 8.9 months (range, 0.2-53.1 mo) from surgical resection. Tumor was found in 90% of resected specimens and necrosis alone in 10%. MRS/P studies were performed in 15 resected patients. Overall, MRS/P predicted tumor in 11 lesions, confirmed pathologically in nine lesions, and necrosis alone was found in two. The MRS/P predicted necrosis alone in three, whereas pathology revealed viable tumor in two and necrosis in one lesion. CONCLUSION: Surgical intervention of progressive brain metastases after GKR in selected patients' leads to a meaningful improvement in survival rates. Further studies are necessary to determine the role of MRS/P in the postradiosurgery surveillance of brain metastases. C1 Boston Univ, Sch Med, Dept Radiat Oncol, Dept Radiat Oncol,Massachusetts Gen Hosp, Boston, MA 02215 USA. NYU, Dept Neurosurg, Sch Med, New York, NY USA. NYU, Dept Radiat Oncol, Sch Med, Maimonides Med Ctr, New York, NY USA. Long Isl Radiat Therapy, Manhasset, NY USA. NYU, Sch Med, Div Neuropathol, Dept Pathol, New York, NY USA. NYU, Sch Med, Div Neuropathol, Dept Radiol, New York, NY USA. RP Truong, MT (reprint author), Boston Univ, Med Ctr, Dept Radiat Oncol, 88 E Newton St,EB-11, Boston, MA 02118 USA. EM mttruong@partners.org OI Han, Kerry/0000-0001-7997-2037 NR 33 TC 31 Z9 32 U1 0 U2 4 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0148-396X J9 NEUROSURGERY JI Neurosurgery PD JUL PY 2006 VL 59 IS 1 BP 86 EP 95 DI 10.1227/01.NEU.0000219858.80351.38 PG 10 WC Clinical Neurology; Surgery SC Neurosciences & Neurology; Surgery GA 061PV UT WOS:000238885600021 PM 16823304 ER PT J AU Ji, XW Li, W Song, J Wei, LP Liu, XS AF Ji, Xuwo Li, Wei Song, Jun Wei, Liping Liu, X. Shirley TI CEAS: cis-regulatory element annotation system SO NUCLEIC ACIDS RESEARCH LA English DT Article ID BINDING-SITES; PROFILES; GENOME AB The recent availability of high-density human genome tiling arrays enables biologists to conduct ChIP-chip experiments to locate the in vivo-binding sites of transcription factors in the human genome and explore the regulatory mechanisms. Once genomic regions enriched by transcription factor ChIP-chip are located, genome-scale downstream analyses are crucial but difficult for biologists without strong bioinformatics support. We designed and implemented the first web server to streamline the ChIP-chip downstream analyses. Given genome-scale ChIP regions, the cis-regulatory element annotation system (CEAS) retrieves repeat-masked genomic sequences, calculates GC content, plots evolutionary conservation, maps nearby genes and identifies enriched transcription factor-binding motifs. Biologists can utilize CEAS to retrieve useful information for ChIP-chip validation, assemble important knowledge to include in their publication and generate novel hypotheses (e.g. transcription factor cooperative partner) for further study. CEAS helps the adoption of ChIP-chip in mammalian systems and provides insights towards a more comprehensive understanding of transcriptional regulatory mechanisms. The URL of the server is http://ceas.cbi.pku. edu.cn. C1 Peking Univ, Ctr Bioinformat, Natl Lab Prot Engn & Plant Genet Engn, Coll Life Sci, Beijing 100871, Peoples R China. Harvard Univ, Sch Publ Hlth, Dana Farber Canc Inst, Dept Biostat & Computat Biol, Boston, MA 02115 USA. RP Wei, LP (reprint author), Peking Univ, Ctr Bioinformat, Natl Lab Prot Engn & Plant Genet Engn, Coll Life Sci, Beijing 100871, Peoples R China. EM weilp@mail.cbi.pku.edu.cn; xsliu@jimmy.harvard.edu RI Li, Wei/A-8544-2009 FU NHGRI NIH HHS [R01 HG004069-02, R01 HG004069, R01 HG004069-01] NR 17 TC 115 Z9 117 U1 0 U2 3 PU OXFORD UNIV PRESS PI OXFORD PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND SN 0305-1048 J9 NUCLEIC ACIDS RES JI Nucleic Acids Res. PD JUL 1 PY 2006 VL 34 SI SI BP W551 EP W554 DI 10.1093/nar/gkl322 PG 4 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA 156LR UT WOS:000245650200110 PM 16845068 ER PT J AU Kaneki, M Hosoi, T Ouchi, Y Orimo, H AF Kaneki, Masao Hosoi, Takayuki Ouchi, Yasuyoshi Orimo, Hajime TI Pleiotropic actions of vitamin K: protector of bone health and beyond?. SO NUTRITION LA English DT Review DE menaquinone; phylloquinone; subclinical vitamin K deficiency; undercarboxylated osteocalcin; osteoporosis; hepatocellular carcinoma; atherosclerosis ID SERUM UNDERCARBOXYLATED OSTEOCALCIN; MATRIX GLA PROTEIN; GAMMA-CARBOXY PROTHROMBIN; MINERAL DENSITY; HEPATOCELLULAR-CARCINOMA; HIP-FRACTURE; POSTMENOPAUSAL WOMEN; ELDERLY-WOMEN; CIRCULATING LEVELS; ARTERIAL CALCIFICATION AB Vitamin K is a nutrient that was originally identified as an essential factor for blood coagulation. Recently, vitamin K has emerged as a potential protector against osteoporosis, atherosclerosis, and hepatocarcinoma. Accumulated evidence indicates that subclinical non-hemostatic vitamin K deficiency in extrahepatic tissues, particularly in bone and possibly in vasculature, exists widely in the otherwise healthy adult population. Vitamins K1 and K2 have been shown to exert protective effects against osteoporosis, although it is important that the beneficial effects will be further confirmed by large-scale, randomized, clinical trials. Increasing evidence implicates a role for vitamin K in calcification of arteries and atherogenesis. Moreover, the therapeutic potential of vitamin K2 as an antihepatoma drug has recently been highlighted. Most of the new biological functions of vitamin K in bone, vasculature, and hepatoma cells are considered attributable to promotion of gamma-carboxylation of glutamic acid residues in vitamin K-dependent proteins, which is shared by vitamins K1 and K2. In contrast, vitamin K2-specific, gamma-carboxylation-unrelated functions have also been demonstrated. Thus, biological differences between vitamins K1 and K2 and potential involvement of gamma-carboxylation-independent actions in the new roles of vitamin K remain open issues. Molecular bases of coagulation-unrelated pleiotropic actions of vitamin K and its implications in human health deserve further investigations. (C) 2006 Elsevier Inc. All rights reserved. C1 Harvard Univ, Sch Med, Massachusetts Gen Hosp, Dept Anesthesia & Crit Care, Charlestown, MA 02129 USA. Shriners Hosp Children, Boston, MA USA. Natl Ctr Geriatr & Gerontol, Dept Adv Med, Aichi, Japan. Univ Tokyo, Grad Sch Med, Dept Geriatr Med, Tokyo, Japan. Univ Hlth Sci, Yamanashi, Japan. RP Kaneki, M (reprint author), Harvard Univ, Sch Med, Massachusetts Gen Hosp, Dept Anesthesia & Crit Care, Charlestown, MA 02129 USA. EM mkaneki@partners.org NR 78 TC 28 Z9 29 U1 3 U2 9 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0899-9007 J9 NUTRITION JI Nutrition PD JUL-AUG PY 2006 VL 22 IS 7-8 BP 845 EP 852 DI 10.1016/j.nut.2006.05.003 PG 8 WC Nutrition & Dietetics SC Nutrition & Dietetics GA 064OM UT WOS:000239099000018 PM 16815498 ER PT J AU Peltola, P Pihlajamaki, J Koutnikova, H Ruotsalainen, E Salmenniemi, U Vauhkonen, I Kainulainen, S Gylling, H Miettinen, TA Auwerx, J Laakso, M AF Peltola, Paula Pihlajamaki, Jussi Koutnikova, Hana Ruotsalainen, Eija Salmenniemi, Urpu Vauhkonen, Ilkka Kainulainen, Sakari Gylling, Helena Miettinen, Tatu A. Auwerx, Johan Laakso, Markku TI Visceral obesity is associated with high levels of serum squalene SO OBESITY LA English DT Article DE squalene synthase; insulin resistance; type 2 diabetes; intra-abdominal obesity; cholesterol synthesis ID DEPENDENT DIABETES-MELLITUS; RECEPTOR-GAMMA EXPRESSION; LIVER-X RECEPTORS; CHOLESTEROL ABSORPTION; ADIPOCYTE DIFFERENTIATION; INSULIN-RESISTANCE; GLUCOSE-TOLERANCE; ADIPOSE-TISSUE; SYNTHASE GENE; FATTY-ACID AB Objective: To investigate the impact of visceral obesity on cholesterol metabolism in normoglycemic offspring of patients with type 2 diabetes. Research Methods and Procedures: The proportion of intra-abdominal fat (IAF) was measured by abdominal computer tomography, and serum cholesterol synthesis and absorption markers were determined by gas-liquid chromatography in 109 normoglycemic offspring of patients with type 2 diabetes. Insulin action was measured with the hyperinsulinemic euglycemic clamp. The gene encoding squalene synthase (farnesyl-diphosphate farnesyltransferase 1) was screened with the single-strand conformation polymorphism analysis and direct sequencing. Results: Cholesterol synthesis markers correlated positively with IAF (r = 0.213 to 0.309, p <= 0.027) and negatively with the rates of insulin-stimulated whole-body glucose uptake (r = -0.372 to -0.248, p <= 0.010). However, serum squalene, the first measured precursor of cholesterol synthesis, showed a positive correlation with IAF (r = 0.309, p = 0.001) without any association with subcutaneous fat or insulin sensitivity. Variation in the farnesyl-diphosphate farnesyltransferase I gene did not explain elevated serum squalene levels in viscerally obese subjects. From the cholesterol absorption markers, cholestanol was associated negatively with IAF and positively with whole-body glucose uptake (p < 0.05). Discussion: High serum squalene levels are associated with visceral obesity but not with subcutaneous obesity. Whether this finding is causally connected to visceral obesity remains to be established. C1 Univ Kuopio, Dept Med, SF-70210 Kuopio, Finland. Univ Kuopio, Dept Radiol, SF-70210 Kuopio, Finland. Univ Kuopio, Dept Clin Nutr, SF-70210 Kuopio, Finland. Inst Genet & Biol Mol & Cellulaire, Illkirch Graffenstaden, France. Univ Helsinki, Dept Med, Div Internal Med, Helsinki, Finland. RP Pihlajamaki, J (reprint author), Joslin Diabet Ctr, 1 Joslin Pl,Room 625, Boston, MA 02215 USA. EM JUSSI.PIHLAJAMAKI@UKU.FI NR 35 TC 18 Z9 18 U1 0 U2 3 PU NORTH AMER ASSOC STUDY OBESITY PI SILVER SPRING PA 8630 FENTON ST, SUITE 918, SILVER SPRING, MD 20910 USA SN 1071-7323 J9 OBESITY JI Obesity PD JUL PY 2006 VL 14 IS 7 BP 1155 EP 1163 DI 10.1038/oby.2006.132 PG 9 WC Endocrinology & Metabolism; Nutrition & Dietetics SC Endocrinology & Metabolism; Nutrition & Dietetics GA 077KP UT WOS:000240028500007 PM 16899796 ER PT J AU Delinsky, SS Latner, JD Wilson, GT AF Selwyn Delinsky, Sherrie Latner, Janet D. Wilson, G. Terence TI Binge eating and weight loss in a self-help behavior modification program SO OBESITY LA English DT Article DE disordered eating; continuing care; weight management; self-help; binge eating ID DISORDER EXAMINATION QUESTIONNAIRE; PSYCHIATRIC COMORBIDITY; OBESITY; WOMEN; LIFE; PSYCHOPATHOLOGY; INDIVIDUALS; MULTICENTER; MAINTENANCE; INTERVIEW AB Objective: To examine the occurrence of binge eating and its impact on weight loss outcomes among obese participants in the Trevose Behavior Modification Program, a lay-administered, lay-directed self-help weight loss program offering continuing care. Research Methods and Procedures: Participants completed questionnaires, and weight loss data were recorded prospectively. Results: Although objective bulimic episodes were reported by 41% of the sample, objective bulimic episodes were not associated with worse weight loss outcomes. Mean weight loss after 12 months was 18.2 kg (18.8% of initial body weight) for the treatment completers and 10.3 kg (10.5% of initial body weight) for the full sample (using intent-to-treat analyses, with baseline scores carried forward). Discussion: Substantial long-term weight loss, resulting from a continuing care treatment program, occurred in individuals both with and without frequent binge eating. C1 Massachusetts Gen Hosp, Dept Psychiat, Boston, MA 02114 USA. Harvard Univ, Sch Med, McLean Hosp, Boston, MA USA. Univ Hawaii Manoa, Dept Psychol, Manoa, HI USA. Rutgers State Univ, Dept Psychol, New Brunswick, NJ 08903 USA. RP Delinsky, SS (reprint author), Massachusetts Gen Hosp, Dept Psychiat, 15 Parkman St,WAC 812, Boston, MA 02114 USA. EM sdelinsky@partners.org NR 46 TC 24 Z9 24 U1 4 U2 5 PU NORTH AMER ASSOC STUDY OBESITY PI SILVER SPRING PA 8630 FENTON ST, SUITE 918, SILVER SPRING, MD 20910 USA SN 1071-7323 J9 OBESITY JI Obesity PD JUL PY 2006 VL 14 IS 7 BP 1244 EP 1249 DI 10.1038/oby.2006.141 PG 6 WC Endocrinology & Metabolism; Nutrition & Dietetics SC Endocrinology & Metabolism; Nutrition & Dietetics GA 077KP UT WOS:000240028500016 PM 16899805 ER PT J AU Rigotti, NA Park, ER Regan, S Chang, YC Perry, K Loudin, B Quinn, V AF Rigotti, Nancy A. Park, Elyse R. Regan, Susan Chang, Yuchiao Perry, Kristin Loudin, Beverly Quinn, Virginia TI Efficacy of telephone Counseling for pregnant smokers - A randomized controlled trial SO OBSTETRICS AND GYNECOLOGY LA English DT Article ID SMOKING-CESSATION; WOMEN; INTERVENTIONS; RELAPSE; SUPPORT; QUIT AB OBJECTIVE: Reducing tobacco use in pregnancy is a public health priority. Brief smoking counseling during prenatal care is effective but generates modest cessation rates. Telephone counseling is an effective smoking cessation method that could offer pregnant women convenient access to more intensive smoking cessation counseling. METHODS: The efficacy of proactive pregnancy-tailored telephone counseling for smoking cessation was compared with a "best- practice" brief-counseling control in a randomized controlled trial of 442 pregnant smokers referred by prenatal providers and a managed care plan. Trained counselors using cognitive-behavioral and motivational interviewing methods called intervention subjects throughout pregnancy and for 2 months postpartum (mean = 5 calls, mean total contact = 68 minutes). Controls received one 5-minute counseling call. RESULTS: Cotinine-valiclated 7-day tobacco abstinence rates in intervention and control groups were 10.0% and 7.5% at end of pregnancy (odds ratio [OR] 1.37, 95% confidence interval [CI] 0.69-2.70; number needed to treat = 40) and 6.7% versus 7.1% at 3 months postpartum (OR 0.93, 95% CI 0.44-1.99). The intervention increased end-of-pregnancy cessation rates among 201 light smokers (< 10 cigarettes/day at study enrollment) (intervention 19.1% versus control 8.4%; OR 2.58, 95% CI 1.1-6.1; number needed to treat = 9.3) and among 193 smokers who attempted to quit in pregnancy before enrollment (intervention 18.1% versus control 6.8%; OR 3.02, CI 1.15-7.94; number needed to treat = 8.8); 63% of the sample (n = 267) was in one of these subgroups. CONCLUSION: Proactive pregnancy-tailored telephone counseling did not outperform a brief "best practice" intervention among pregnant smokers. The intervention had efficacy in light smokers and in women who had attempted cessation earlier in pregnancy. Future studies should confirm whether telephone counseling benefits these groups of pregnant smokers. C1 Massachusetts Gen Hosp, Tobacco Res & Treatment Ctr, Inst Hlth Policy, Gen Med Div,Dept Med, Boston, MA 02114 USA. Massachusetts Gen Hosp, Dept Psychiat, Boston, MA 02114 USA. Harvard Univ, Sch Med, Boston, MA USA. Tufts Univ, Waltham, MA USA. Kaiser Permanente, Pasadena, CA USA. RP Rigotti, NA (reprint author), Massachusetts Gen Hosp, Tobacco Res & Treatment Ctr, Inst Hlth Policy, Gen Med Div,Dept Med, 50 Staniford St,9th Floor, Boston, MA 02114 USA. EM nrigotti@partners.org FU NHLBI NIH HHS [K24-HL04440] NR 35 TC 50 Z9 50 U1 1 U2 10 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0029-7844 J9 OBSTET GYNECOL JI Obstet. Gynecol. PD JUL PY 2006 VL 108 IS 1 BP 83 EP 92 DI 10.1097/01.AOG.0000218100.05601.f8 PG 10 WC Obstetrics & Gynecology SC Obstetrics & Gynecology GA 171XF UT WOS:000246768000014 PM 16816060 ER PT J AU Ryan, PD Goss, PE AF Ryan, Paula D. Goss, Paul E. TI Adjuvant hormonal therapy in peri- and postmenopausal breast cancer SO ONCOLOGIST LA English DT Article DE breast cancer; aromatase inhibitors; adjuvant; hormonal; postmenopause; perimenopause; review ID BONE-MINERAL DENSITY; AROMATASE INHIBITOR LETROZOLE; TAMOXIFEN-STIMULATED GROWTH; CARDIOVASCULAR RISK-FACTORS; TERM ESTROGEN DEPRIVATION; QUALITY-OF-LIFE; RANDOMIZED-TRIAL; PROGESTERONE-RECEPTOR; INTERGROUP EXEMESTANE; ADAPTIVE HYPERSENSITIVITY AB Tamoxifen has been the mainstay of endocrine treatment for early-stage breast cancer in both premenopausal and postmenopausal women for many years. Since 2001, the results of several large, randomized, clinical trials have provided evidence that aromatase inhibitor (AI) therapy, either upfront or in sequence after tamoxifen, improves disease-free survival and, in certain patients, overall survival for postmenopausal patients with hormone receptor-positive breast cancer. Thus far, with relatively short-term follow-up, AIs have been generally safe and well tolerated among the population of patients treated in these adjuvant trials. However, important side effects such as musculoskeletal and bone-related problems, including the risk for osteoporosis and fractures, remain of concern and warrant continued monitoring and follow-up. Several questions regarding the appropriate AI to use and the timing of AI therapy remain unresolved, and ongoing studies will help address these issues. Caution is warranted in the use of AIs in perimenopausal women, including those that develop chemotherapy-induced amenorrhea, and clinical evidence supports the role for AI use in postmenopausal women only. Areas of active investigation include the mechanisms of resistance to endocrine therapy with tamoxifen and AIs and clinical strategies to overcome this resistance. C1 [Ryan, Paula D.] Massachusetts Gen Hosp, Boston, MA 02114 USA. Massachusetts Gen Hosp, Boston, MA 02114 USA. RP Ryan, PD (reprint author), Massachusetts Gen Hosp, Cox 640,100 Blossom St, Boston, MA 02114 USA. EM pdryan@partners.org NR 89 TC 19 Z9 19 U1 0 U2 0 PU ALPHAMED PRESS PI DURHAM PA 318 BLACKWELL ST, STE 260, DURHAM, NC 27701-2884 USA SN 1083-7159 EI 1549-490X J9 ONCOLOGIST JI Oncologist PD JUL-AUG PY 2006 VL 11 IS 7 BP 718 EP 731 DI 10.1634/theoncologist.11-7-718 PG 14 WC Oncology SC Oncology GA 070OQ UT WOS:000239532800002 PM 16880231 ER PT J AU Zhu, AX AF Zhu, Andrew X. TI Systemic therapy of advanced hepatocellular carcinoma: How hopeful should we be? SO ONCOLOGIST LA English DT Review DE hepatocellular carcinoma; molecularly targeted agents; systemic therapy ID PHASE-II TRIAL; RANDOMIZED CONTROLLED-TRIAL; EPIDERMAL-GROWTH-FACTOR; COMBINATION CHEMOTHERAPY; FACTOR RECEPTOR; FACTOR-ALPHA; RETINOIC ACID; PROGNOSTIC-SIGNIFICANCE; ESTROGEN-RECEPTORS; UNITED-STATES AB Worldwide, hepatocellular carcinoma (HCC) is the fifth most common cancer and the third most common cause of cancer-related death. In the U.S., 18,510 new cancers of the liver and intrahepatic bile duct are expected in 2006, with an estimated 16,200 deaths. The incidence rates for HCC in the U.S. continued to rise steadily through 1998 and doubled during the period 1975-1995. Unresectable or metastatic HCC carries a poor prognosis, and systemic therapy with cytotoxic agents provides marginal benefit. A majority of HCC patients (>80%) presents with advanced or unresectable disease. Even for those with resected disease, the recurrence rate can be as high as 50% at 2 years. Because of the poor track record of systemic therapy in HCC, there has been a sense of nihilism for this disease in the oncology community for decades. However, with the arrival of newly developed molecularly targeted agents and the success of some of these agents in other traditionally challenging cancers, like renal cell carcinoma, there has recently been renewed interest in developing systemic therapy for HCC. This review attempts to concisely summarize the historical perspective and the current status of systemic therapy development in HCC. C1 Harvard Univ, Massachusetts Gen Hosp, Sch Med, Ctr Canc, Boston, MA USA. RP Zhu, AX (reprint author), Massachusetts Gen Hosp, Tucker Gosnell Ctr Gastrointestinal Canc, 100 Blossom St,Cox 640, Boston, MA 02114 USA. EM azhu@partners.org NR 114 TC 152 Z9 159 U1 0 U2 5 PU ALPHAMED PRESS PI DURHAM PA 318 BLACKWELL ST, STE 260, DURHAM, NC 27701-2884 USA SN 1083-7159 J9 ONCOLOGIST JI Oncologist PD JUL-AUG PY 2006 VL 11 IS 7 BP 790 EP 800 DI 10.1634/theoncologist.11-7-790 PG 11 WC Oncology SC Oncology GA 070OQ UT WOS:000239532800009 PM 16880238 ER PT J AU Higgins, H Berger, DL AF Higgins, Heather Berger, David L. TI RFA for liver tumors: Does it really work? SO ONCOLOGIST LA English DT Article DE radiofrequency ablation; liver tumors; hepatocellular carcinoma; liver metastases ID PERCUTANEOUS RADIOFREQUENCY ABLATION; SMALL HEPATOCELLULAR-CARCINOMA; HEPATIC COLORECTAL METASTASES; THERMAL ABLATION; CIRRHOTIC-PATIENTS; MULTIVARIATE-ANALYSIS; LOCAL RECURRENCE; TISSUE ABLATION; RESECTION; TRANSPLANTATION AB The use of radiofrequency ablation (RFA) is increasing in the treatment of both primary and metastatic hepatic tumors. However, the role of RFA has yet to be clearly defined in patients who are still considered amenable to surgical intervention. Future prospective studies are needed to define whether RFA can be used as an alternative to surgery in certain patient populations. In the interim, radiofrequency ablation technology will continue to advance and serve as both a palliative and potentially curative intervention for individuals with hepatic tumors. C1 Massachusetts Gen Hosp, Dept Surg, Boston, MA 02114 USA. RP Berger, DL (reprint author), Massachusetts Gen Hosp, Dept Gen Surg, Wang Ambulatory Care Ctr 465, 15 Parkman St, Boston, MA 02114 USA. EM dberger@partners.org NR 58 TC 22 Z9 25 U1 0 U2 0 PU ALPHAMED PRESS PI DURHAM PA 318 BLACKWELL ST, STE 260, DURHAM, NC 27701-2884 USA SN 1083-7159 J9 ONCOLOGIST JI Oncologist PD JUL-AUG PY 2006 VL 11 IS 7 BP 801 EP 808 DI 10.1634/theoncologist.11-7-801 PG 8 WC Oncology SC Oncology GA 070OQ UT WOS:000239532800010 PM 16880239 ER PT J AU Jacobsen, E AF Jacobsen, Eric TI Anaplastic large-cell lymphoma, T-/null-cell type SO ONCOLOGIST LA English DT Article DE anaplastic large cell lymphoma; lymphomatoid papulosis; cutaneous lymphoma; ALK ID NON-HODGKINS-LYMPHOMA; CD30-POSITIVE LYMPHOPROLIFERATIVE DISORDERS; HISTONE DEACETYLASE INHIBITOR; ANTI-CD30 ANTIBODY 5F11; ALK-POSITIVE LYMPHOMA; EPSTEIN-BARR-VIRUS; KINASE ALK; NPM-ALK; PROGNOSTIC-SIGNIFICANCE; MONOCLONAL-ANTIBODY AB Anaplastic large-cell lymphoma, T-/null-cell type (ALCL), is a rare disease that has only been well characterized for two decades. Despite this, the biology of ALCL is better understood than that of many other more common variants of lymphoma. This review focuses on the pathophysiology, clinical presentation, and therapy of ALCL, including stem cell transplantation. In particular, the text emphasizes how novel prognostic features and the evolving understanding of the biology of this disease will influence treatment selection and drug development. C1 Harvard Univ, Sch Med, Dana Farber Canc Inst, Lymphoma Program, Boston, MA 02115 USA. RP Jacobsen, E (reprint author), Harvard Univ, Sch Med, Dana Farber Canc Inst, Lymphoma Program, Dana 1B30,44 Binney St, Boston, MA 02115 USA. EM Eric_Jacobsen@dfci.harvard.edu NR 95 TC 32 Z9 37 U1 1 U2 1 PU ALPHAMED PRESS PI DURHAM PA 318 BLACKWELL ST, STE 260, DURHAM, NC 27701-2884 USA SN 1083-7159 J9 ONCOLOGIST JI Oncologist PD JUL-AUG PY 2006 VL 11 IS 7 BP 831 EP 840 DI 10.1634/theoncologist.11-7-831 PG 10 WC Oncology SC Oncology GA 070OQ UT WOS:000239532800013 PM 16880242 ER PT J AU Oh, WK Kantoff, PW AF Oh, William K. Kantoff, Philip W. TI The role of cytotoxic chemotherapy in prostate cancer - A critical reevaluation 20 years later - The Eisenberger/Sinibaldi article reviewed SO ONCOLOGY-NEW YORK LA English DT Editorial Material C1 Dana Farber Canc Inst, Lank Ctr Genitourinary Oncol, Boston, MA 02115 USA. Harvard Univ, Sch Med, Cambridge, MA 02138 USA. Harvard Univ, Sch Med, Boston, MA 02115 USA. RP Oh, WK (reprint author), Dana Farber Canc Inst, Lank Ctr Genitourinary Oncol, Boston, MA 02115 USA. RI Oh, William/B-9163-2012 OI Oh, William/0000-0001-5113-8147 NR 8 TC 0 Z9 0 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 JUL PY 2006 VL 20 IS 8 BP 867 EP 868 PG 2 WC Oncology SC Oncology GA V44BG UT WOS:000202977600006 ER PT J AU Houldin, AD Lewis, FM AF Houldin, Arlene D. Lewis, Frances Marcus TI Salvaging their normal lives: A qualitative study of patients with recently diagnosed advanced colorectal cancer SO ONCOLOGY NURSING FORUM LA English DT Article ID OF-LIFE; COLON-CANCER; HEALTH; SURVIVORS; ADJUSTMENT; SURGERY; DISEASE; COUPLES AB Purpose/Objectives: To describe the experiences of patients living with newly diagnosed stage III or IV colorectal cancer. Research Approach: Qualitative; inductive coding methods were used to identity open codes that were analyzed, compared, and grouped into categories. Setting: An urban ambulatory cancer center in the northeastern United States. Participants: 14 patients newly diagnosed with stage III or stage IV colorectal cancer. Methodologic Approach: Semistructured interviews were recorded on audiotape. Interviewers asked participants to describe their experiences with the diagnosis and treatment of colorectal cancer. Content analysis with inductive coding was used to code the transcribed interview data. Categories were reviewed and organized into larger groupings, from which the core category was derived. Main Research Variables: Experiences of living with a diagnosis of colorectal cancer, impact on daily living, quality of life, coping strategies used, level of preparedness, and impact on children. Findings: The coded interview data yielded six domains: feeling life is disrupted, experiencing physicians, feeling unprepared for everything, rethinking parenting, Wondering "why me?," and dealing with it. The core category that explained study participants' experiences with recently diagnosed colorectal cancer was "salvaging their normal lives." Conclusions: The dominant experience of the study participants focused on four aspects of their illness experience: (a) framing it in ways that enabled them to recreate a semblance of normalcy or of their preillness state, (b) trying to tell children about the illness in stabilizing ways, (c) generating or maintaining a positive outlook no matter what, and (d) concretely managing the distress of the illness and its symptoms. Interpretation: Targeted assessment is important in the six dimensions of the study domains. Clinicians who work with patients with cancer should offer support as patients search for meanings to explain this potentially devastating life event. Teaching active coping strategies as patients with advanced cancer struggle to come to terms with the demands of the disease while attempting to live their lives as fully and as normally as possible is important. C1 Univ Penn, Sch Nursing, Philadelphia, PA 19104 USA. Univ Penn, Adult Nurse Practitioner Oncol Adv Practice Nursi, Philadelphia, PA 19104 USA. Philadelphia Vet Affairs Med Ctr, Palliat Care Serv, Philadelphia, PA 19104 USA. Univ Washington, Sch Nursing, Seattle, WA 98195 USA. RP Houldin, AD (reprint author), Univ Penn, Sch Nursing, Philadelphia, PA 19104 USA. EM houldin@nursing.upenn.edu NR 39 TC 16 Z9 16 U1 1 U2 4 PU ONCOLOGY NURSING SOCIETY PI PITTSBURGH PA 125 ENTERPRISE DR, PITTSBURGH, PA 15275 USA SN 0190-535X J9 ONCOL NURS FORUM JI Oncol. Nurs. Forum PD JUL PY 2006 VL 33 IS 4 BP 719 EP 725 DI 10.1188/06.ONF.719-725 PG 7 WC Oncology; Nursing SC Oncology; Nursing GA 061PC UT WOS:000238883600015 PM 16858452 ER PT J AU Hatton, MP Kelley, JM Rubin, PAD AF Hatton, Mark P. Kelley, John M. Rubin, Peter A. D. TI Symmetry in healing after bilateral eyelid surgery SO OPHTHALMIC PLASTIC AND RECONSTRUCTIVE SURGERY LA English DT Article; Proceedings Paper CT Annual meeting of the American-Society-of-Ophthalmic-Plastic-and-Reconstructive-Surgery CY OCT 22-23, 2004 CL New Orleans, LA SP Amer Soc Ophthalm Plast Reconstructive Surg ID FIBRIN GLUE; FACE LIFTS; ARNICA; TRIAL AB Purpose: To determine whether surgery performed bilaterally (ptosis repair, blepharoplasty, or both) results in symmetric healing. Methods: Case series of 19 consecutive patients undergoing bilateral ptosis repair, blepharoplasty, or both. Patients were provided with questionnaires to determine their perception of the degree of symmetry in healing at four time points after bilateral surgery. Digital imaging analysis was used to measure the amount of bruising present on each side in a separate cohort of 10 patients undergoing bilateral eyelid surgery. Results: Asymmetry in bruising, swelling, and discomfort was reported by the majority of patients at each time point after surgery. For each measure (bruising, swelling, and discomfort), the percentage of patients reporting asymmetry peaked at day 3. Objective measurement 7 days after surgery showed that 50% of patients had more bruising on the right and 50% had more bruising on the left. The difference in the average area of bruising was not statistically significant between sides. Eight of 10 patients had less than a 10% difference in area of bruising between sides. Conclusions: Patients frequently perceive asymmetry in healing after bilateral eyelid surgery, but objective measurements show that asymmetry in bruising is typically small. C1 Massachusetts Eye & Ear Infirm, Eye Plast Orbital & Cosmet Surg, Boston, MA 02114 USA. Harvard Univ, Massachusetts Gen Hosp, Sch Med, Boston, MA USA. Endicott Coll, Beverly, MA USA. RP Rubin, PAD (reprint author), Massachusetts Eye & Ear Infirm, Eye Plast Orbital & Cosmet Surg, 243 Charles St, Boston, MA 02114 USA. EM eye_plastics@meei.harvard.edu FU NCCIH NIH HHS [1-R21-AT002564-01A1] NR 13 TC 3 Z9 3 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0740-9303 J9 OPHTHAL PLAST RECONS JI Ophthalmic Plast. Reconstr. Surg. PD JUL-AUG PY 2006 VL 22 IS 4 BP 266 EP 268 DI 10.1097/01.iop.0000225747.29778.3b PG 3 WC Ophthalmology; Surgery SC Ophthalmology; Surgery GA 065QX UT WOS:000239175500006 PM 16855497 ER PT J AU Koo, L Hatton, MP Rubin, PAD AF Koo, Lily Hatton, Mark P. Rubin, Peter A. D. TI When is enophthalmos "significant"'? SO OPHTHALMIC PLASTIC AND RECONSTRUCTIVE SURGERY LA English DT Article; Proceedings Paper CT Annual Meeting of the Association-for-Research-in-Vision-and-Ophthalmology CY APR 24-29, 2004 CL Ft Lauderdale, FL SP Assoc Res Vis & Ophthalmol ID BLOW-OUT FRACTURES; ORBITAL FLOOR FRACTURES; REPAIR; BLINDNESS; SURGERY AB Purpose: It is currently unknown how many measurable millimeters of enophthalmos may be noticeable to an observer. Identifying the amount of enophthalmos present may help to guide patients and clinicians in regard to surgical management of enophthalmos. Methods: The Massachusetts Eye and Ear Infirmary Oculoplastics imaging database was used to select 12 photographs of patients with unilateral enophthalmos whose measurements ranged between I mm and 8 mm for the study group and 12 photographs of patients who did not have enophthalmos as the control group. Observers were asked to review each of the photographs from both groups and to comment on whether the appearance was normal or abnormal. Results: There was no statistical difference found when observers reviewed photographs from the control group and patients whose measurements ranged between 1 mm and 2 mm (87%, 83% respondents identifying patients as normal, respectively). Twenty-eight percent of observers found patients with 3 mm and 4 mm of enophthalmos as having a normal appearance (P < 0.001). Ninety-seven percent of observers commented that patients with measurements of 5 mm and 8 mm had an abnormal appearance (P < 0.001). Conclusions: Patients with 2 mm and less of measurable enophthalmos had a normal appearance as frequently as those without enophthalmos. Nearly all patients with measurements of 5 mm and greater had abnormal appearances. The point at which enophthalmos becomes detectable lies between 3 mm and 4 rum. C1 Massachusetts Eye & Ear Infirm, Ophthalm Plast Orbital & Aesthet Surg, Boston, MA 02114 USA. RP Rubin, PAD (reprint author), Massachusetts Eye & Ear Infirm, Ophthalm Plast Orbital & Aesthet Surg, 243 Charles St, Boston, MA 02114 USA. EM eye_plastics@meei.harvard.edu NR 20 TC 15 Z9 16 U1 0 U2 1 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0740-9303 J9 OPHTHAL PLAST RECONS JI Ophthalmic Plast. Reconstr. Surg. PD JUL-AUG PY 2006 VL 22 IS 4 BP 274 EP 277 DI 10.1097/01.iop.0000226865.22184.6a PG 4 WC Ophthalmology; Surgery SC Ophthalmology; Surgery GA 065QX UT WOS:000239175500008 PM 16855499 ER PT J AU Singh, RP Tullis, S Hatton, M Rubin, PAD AF Singh, Rishi P. Tullis, Sara Hatton, Mark Rubin, Peter A. D. TI Orbital metastasis from ovarian carcinoma in a patient with BRCA2 mutation SO OPHTHALMIC PLASTIC AND RECONSTRUCTIVE SURGERY LA English DT Article ID EYE; SURVIVAL; BREAST AB A 45-year-old woman with BRCA-2 mutation-positive ovarian carcinoma had pain, swelling, and proptosis of her left eye. CT demonstrated a mass in the left orbit. Fine-needle aspiration and lateral orbitotomy were used to obtain tissue for diagnosis. Pathology confirmed poorly differentiated tumor cells consistent with ovarian carcinoma. Cytopathologic testing confirmed receptor and hormonal markers within the orbital specimen that were identical to specimens removed 4 years prior. C1 Massachusetts Eye & Ear Infirm, Eye Plast Orbit & Cosmet Surg, Boston, MA 02114 USA. RP Rubin, PAD (reprint author), Massachusetts Eye & Ear Infirm, Eye Plast Orbit & Cosmet Surg, 243 Charles St, Boston, MA 02114 USA. EM eye_plastics@meei.harvard.edu NR 9 TC 1 Z9 1 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0740-9303 J9 OPHTHAL PLAST RECONS JI Ophthalmic Plast. Reconstr. Surg. PD JUL-AUG PY 2006 VL 22 IS 4 BP 298 EP 299 DI 10.1097/01.iop.0000222355.09670.d7 PG 2 WC Ophthalmology; Surgery SC Ophthalmology; Surgery GA 065QX UT WOS:000239175500014 PM 16855505 ER PT J AU Pasquale, LR Kang, JH Manson, JE Willett, WC Rosner, BA Hankinson, SE AF Pasquale, LR Kang, JH Manson, JE Willett, WC Rosner, BA Hankinson, SE TI Prospective study of type 2 diabetes mellitus and risk of primary open-angle glaucoma in women SO OPHTHALMOLOGY LA English DT Article ID ELEVATED INTRAOCULAR-PRESSURE; VISUAL-FIELD DEFECTS; BEAVER DAM EYE; LIFE-STYLE; POPULATION; RETINOPATHY; PHOTOCOAGULATION; CLASSIFICATION; HYPERTENSION; PREVALENCE AB Purpose: To study the relation between type 2 diabetes mellitus (T2DM) and incident primary open-angle glaucoma (POAG) in women. Design: Prospective cohort analysis. Participants: Seventy-six thousand three hundred eighteen women enrolled in the Nurses' Health Study (NHS). Methods: Women enrolled in the NHS from 1980 to 2000 were observed. Eligible participants were at least 40 years old, did not have POAG at baseline, and reported receiving eye examinations during follow-up. Potential confounders were assessed on biennial questionnaires, and a diagnosis of T2DM was confirmed on a validated supplemental questionnaire. During follow-up, 429 self-reported POAG cases confirmed by medical chart review were identified. Main Outcome Measures: Multivariable rate ratios (RRs) of POAG and associated 95% confidence intervals (CIs) obtained from proportional hazards models. Results: After controlling for age, race, hypertension, body mass index, physical activity, alcohol intake, smoking, and family history of glaucoma, T2DM was positively associated with POAG (RR = 1.82 [95% CI = 1.23-2.70]). Nonetheless, the association did not strengthen with longer duration of diabetes: RR = 2.24 (95% CI = 1.31-3.84) for duration < 5 years versus RR = 1.54 (95% CI = 0.90-2.62) for duration >= 5 years). In secondary analyses, to evaluate the potential for detection bias we controlled for additional factors such as the number of eye examinations, but T2DM remained positively associated with POAG. Conclusion: Type 2 diabetes mellitus is associated with an increased risk of POAG in women. C1 Harvard Univ, Massachusetts Eye & Ear Infirm, Sch Med, Glaucoma Serv, Boston, MA 02114 USA. Harvard Univ, Sch Med, Brigham & Womens Hosp, Channing Lab,Dept Med, Boston, MA 02115 USA. Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA. Harvard Univ, Sch Publ Hlth, Brigham & Womens Hosp, Div Prevent Med, Boston, MA 02115 USA. Harvard Univ, Sch Publ Hlth, Dept Nutr, Boston, MA 02115 USA. Harvard Univ, Sch Publ Hlth, Dept Biostat, Boston, MA 02115 USA. RP Pasquale, LR (reprint author), Harvard Univ, Massachusetts Eye & Ear Infirm, Sch Med, Glaucoma Serv, 243 Charles St, Boston, MA 02114 USA. EM Louis_Pasquale@meei.harvard.edu FU NCI NIH HHS [CA 87969]; NEI NIH HHS [EY015473, EY09611] NR 48 TC 81 Z9 87 U1 1 U2 4 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 JUL PY 2006 VL 113 IS 7 BP 1081 EP 1086 DI 10.1016/j.ophthu.2006.01.066 PG 6 WC Ophthalmology SC Ophthalmology GA 059IV UT WOS:000238727400004 PM 16757028 ER PT J AU Kloek, CE Bilyk, JR Pribitkin, EA Rubin, PAD AF Kloek, CE Bilyk, JR Pribitkin, EA Rubin, PAD TI Orbital decompression as an alternative management strategy for patients with benign tumors located at the orbital apex SO OPHTHALMOLOGY LA English DT Article; Proceedings Paper CT Annual Meeting of the Association-for-Research-in-Vision-and-Ophthalmology CY APR 30-MAY 05, 2005 CL Ft Lauderdale, FL SP Assoc Res Vis & Ophthalmol ID OPTIC-NERVE DECOMPRESSION; SOLITARY FIBROUS TUMOR; ENDOSCOPIC APPROACH; NEUROPATHY; LESIONS; SINUS; SHEATH; HEMANGIOPERICYTOMA; ORBITOPATHY; ORBITOTOMY AB Purpose: Tumors located in the intraconal portion of the orbital apex, especially those inferior to the optic nerve, can be difficult to access surgically, carrying a significant risk of ocular morbidity. The purpose of this study was to investigate outcomes in 5 patients with benign-appearing but symptomatic tumors located in the intraconal portion of the orbital apex in which orbital decompression was performed as an alternative management strategy to resection. Design: Retrospective interventional case series. Participants: Five patients were diagnosed with a compressive optic neuropathy secondary to a benign-appearing tumor at the orbital apex. Intervention: Each patient underwent surgical decompression of the affected orbit. None of the patients had the tumor biopsied or resected. Main Outcome Measures: Best-corrected visual acuity (VA), pupillary responses, visual fields (VFs), color vision, and orbital imaging. Results: Each of the patients demonstrated improvement in visual function, as measured by VA, VFs, and, in some cases, color vision. One patient required a second orbital decompression for recurrent optic neuropathy 4 years after the initial decompression. Complications included ptosis and enophthalmos in 2 patients and diplopia in the extreme right gaze in 1 patient. Conclusions: Orbital decompression is a therapeutic option for patients with compressive optic neuropathies from benign orbital, apex tumors, offering potential improvement in optic nerve function while sparing morbidity from attempts at surgical resection. C1 Massachusetts Eye & Ear Infirm, Boston, MA 02114 USA. Wills Eye Hosp & Res Inst, Oculoplast & Orbital Surg Serv, Philadelphia, PA USA. Thomas Jefferson Univ, Dept Otolaryngol Head & Neck Surg, Philadelphia, PA 19107 USA. RP Rubin, PAD (reprint author), Massachusetts Eye & Ear Infirm, 243 Charles St, Boston, MA 02114 USA. EM Eye_plastics@meei.harvard.edu NR 36 TC 12 Z9 13 U1 0 U2 1 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 JUL PY 2006 VL 113 IS 7 BP 1214 EP 1219 DI 10.1016/j.ophtha.2006.01.064 PG 6 WC Ophthalmology SC Ophthalmology GA 059IV UT WOS:000238727400025 PM 16815404 ER PT J AU Hart, ES Albright, MB Rebello, GN Grottkau, BE AF Hart, Erin S. Albright, Maurice B. Rebello, Gleeson N. Grottkau, Brian E. TI Broken bones - Common pediatric fractures - Part I SO ORTHOPAEDIC NURSING LA English DT Article ID CHILD-ABUSE AB Musculoskeletal injuries are one of the most frequently encountered problems in pediatric practice, with fractures accounting for a surprisingly large percentage of these injuries. A fracture occurs when bone is subjected to more energy than it can absorb. Pediatric healthcare providers must have a good understanding of normal bone growth and development and must recognize common mechanisms of injury and fracture patterns seen in children. Nearly 20% of children who present with an injury have a fracture, and it is estimated that 42% of boys and 27% of girls will sustain a fracture during childhood (Wilkins, 1996). The immature skeleton has several unique properties that directly affect the management of fractures in children. C1 Massachusetts Gen Hosp, Yawkey Ctr Outpatient Care, Boston, MA 02114 USA. RP Hart, ES (reprint author), Massachusetts Gen Hosp, Yawkey Ctr Outpatient Care, Boston, MA 02114 USA. NR 18 TC 4 Z9 4 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0744-6020 J9 ORTHOP NURS JI Orthop. Nurs. PD JUL-AUG PY 2006 VL 25 IS 4 BP 251 EP 256 PG 6 WC Nursing; Orthopedics SC Nursing; Orthopedics GA 073AD UT WOS:000239713600004 PM 16900069 ER PT J AU Rosenthal, DI AF Rosenthal, Daniel I. TI Radiofrequency treatment SO ORTHOPEDIC CLINICS OF NORTH AMERICA LA English DT Article ID OSTEOID OSTEOMA; THERMAL ABLATION; BLOOD-FLOW; CATHETER ABLATION; HEPATIC-TUMORS; SPINAL TUMORS; BONE; COAGULATION; METASTASIS; OCCLUSION AB This article discusses radiofrequency energy as a treatment of musculoskeletal tumors focusing on osteoid osteomas. The technique has also been applied to a number of different primary musculoskeletal tumors and is increasingly being used as a palliative method in the management of painful skeletal metastases. Radiofrequency treatment of musculoskeletal tumors can be of great clinical value. When the low-power, highly limited methods are applied to small tumors such as osteoid osteomas, the technique is effective and exceptionally safe. Creation of larger thermal lesions, however, can be accompanied by significant risks, and the risk-to-benefit ratio should be carefully considered before undertaking such a treatment. C1 Massachusetts Gen Hosp, Dept Radiol, Boston, MA 02114 USA. Harvard Univ, Sch Med, Dept Radiol, Cambridge, MA 02138 USA. RP Rosenthal, DI (reprint author), Massachusetts Gen Hosp, Dept Radiol, 175 Cambridge St,Ste 200, Boston, MA 02114 USA. EM rosenthal.daniel@mgh.harvard.edu NR 40 TC 21 Z9 22 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 0030-5898 J9 ORTHOP CLIN N AM JI Orthop. Clin. North Am. PD JUL PY 2006 VL 37 IS 3 BP 475 EP + DI 10.1016/j.ocl.2006.05.004 PG 11 WC Orthopedics SC Orthopedics GA 075RR UT WOS:000239903400014 PM 16846772 ER PT J AU Stoler, JM Oaklander, AL AF Stoler, JM Oaklander, AL TI Patients with Ehlers Danlos syndrome and CRPS: A possible association? SO PAIN LA English DT Article DE connective tissue; pain; inherited disorder of collagen; genetics; reflex sympathetic dystrophy ID REFLEX SYMPATHETIC DYSTROPHY; NEUROPATHY; PAIN; HAPLOINSUFFICIENCY; COLLAGEN AB Rare patients are left with chronic pain, vasodysregulation, and other symptoms that define complex regional pain syndrome (CRPS), after limb traumas. The predisposing factors are unknown. Genetic factors undoubtedly contribute, but have not yet been identified. We report four CRPS patients also diagnosed with the classical or hypermobility forms of Ehlers Danlos syndrome (EDS), inherited disorders of connective tissue. These patients had been diagnosed using standard diagnostic criteria for CRPS and for EDS. All had sustained joint injury; in three this had been surgically treated. The association of these two diagnoses leads us to hypothesize that EDS might contribute to the development of CRPS in one or more of the following ways: via stretch injury to nerves traversing hypermobile joints, increased fragility of nerve connective tissue, or nerve trauma from more frequent surgery. We review the clinical presentation of the different Ehlers Danlos syndromes and provide clinical criteria that can be used to screen CRPS patients for EDS for clinical or research purposes. (c) 2006 International Association for the Study of Pain. Published by Elsevier B.V. All rights reserved. C1 Harvard Univ, Sch Med, Massachusetts Gen Hosp, Dept Pediat,Genet & Teratol Unit, Boston, MA 02115 USA. Harvard Univ, Sch Med, Massachusetts Gen Hosp, Nerve Injry Unit,Dept Anesthesia & Crit Care, Boston, MA 02115 USA. Harvard Univ, Sch Med, Massachusetts Gen Hosp, Nerve Injury Unit,Dept Neurol, Boston, MA 02115 USA. Harvard Univ, Sch Med, Massachusetts Gen Hosp, Dept Neuropathol,Nerve Injury Unit, Boston, MA 02115 USA. RP Stoler, JM (reprint author), Harvard Univ, Sch Med, Massachusetts Gen Hosp, Dept Pediat,Genet & Teratol Unit, Boston, MA 02115 USA. EM jstoler@partners.org FU NINDS NIH HHS [R01NS42866] NR 25 TC 16 Z9 16 U1 0 U2 1 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0304-3959 J9 PAIN JI Pain PD JUL PY 2006 VL 123 IS 1-2 BP 204 EP 209 DI 10.1016/j.pain.2006.02.022 PG 6 WC Anesthesiology; Clinical Neurology; Neurosciences SC Anesthesiology; Neurosciences & Neurology GA 059PX UT WOS:000238745800025 PM 16600507 ER PT J AU Gallagher, RM Polomano, R AF Gallagher, Rollin M. Polomano, Rosemary TI Early, continuous, and restorative pain management in injured soldiers: The challenge ahead SO PAIN MEDICINE LA English DT Editorial Material ID NEUROPATHIC PAIN; MECHANISMS; DIAGNOSIS; MORPHINE; FREEDOM; RAT C1 Univ Penn, Philadelphia VA Med Ctr, Philadelphia, PA 19104 USA. Univ Penn, Sch Nursing, Philadelphia, PA 19104 USA. RP Gallagher, RM (reprint author), Univ Penn, Philadelphia VA Med Ctr, Philadelphia, PA 19104 USA. NR 14 TC 6 Z9 6 U1 0 U2 0 PU BLACKWELL PUBLISHING PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DQ, OXON, ENGLAND SN 1526-2375 J9 PAIN MED JI Pain Med. PD JUL-AUG PY 2006 VL 7 IS 4 BP 284 EP 286 DI 10.1111/j.1526-4637.2006.00188.x PG 3 WC Medicine, General & Internal SC General & Internal Medicine GA 065LS UT WOS:000239162000001 PM 16898936 ER PT J AU Marcus, KJ AF Marcus, KJ TI Intracranial germinomas: Can we improve upon our success? Commentary SO PEDIATRIC BLOOD & CANCER LA English DT Editorial Material ID GERM-CELL TUMORS; RADIATION-THERAPY; RADIOTHERAPY; CHEMOTHERAPY C1 Brigham & Womens Dana Farber Canc Care Childrens, Dept Radiat Oncol, Boston, MA USA. Harvard Univ, Sch Med, Boston, MA 02115 USA. RP Marcus, KJ (reprint author), Childrens Hosp, Div Radiat Oncol, 300 Longwood Ave, Boston, MA 02115 USA. EM Kmarcus@LROC.Harvard.edu NR 8 TC 1 Z9 1 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 JUL PY 2006 VL 47 IS 1 BP 2 EP 3 DI 10.1002/pbc.20528 PG 2 WC Oncology; Hematology; Pediatrics SC Oncology; Hematology; Pediatrics GA 045XI UT WOS:000237775600002 PM 16047367 ER PT J AU Ochala, J Dorer, DJ Frontera, WR Krivickas, LS AF Ochala, Julien Dorer, David J. Frontera, Walter R. Krivickas, Lisa S. TI Single skeletal muscle fiber behavior after a quick stretch in young and older men: a possible explanation of the relative preservation of eccentric force in old age SO PFLUGERS ARCHIV-EUROPEAN JOURNAL OF PHYSIOLOGY LA English DT Article DE aging; skinned single muscle fiber; mechanics; stretch response ID MYOSIN HEAVY-CHAIN; CONTRACTILE PROPERTIES; FLIGHT-MUSCLE; ACTIVATION; ISOFORMS; TOMOGRAPHY; MECHANISM; STIFFNESS; STRENGTH; VELOCITY AB The origins of the smaller age-related decrease in eccentric force compared to isometric and concentric conditions in vivo remain unclear. Could this originate from contractile elements of muscle cells? The main intent of the current investigation was to assess the force behavior of muscle cells with aging, during lengthening. Chemically skinned single muscle fibers (n=235) from m. vastus lateralis of six young (mean age 31.6 years) and six older men (mean age 66.1 years) were maximally activated with pCa 4.5 at 15 degrees C. Maximal isometric force and cross-sectional area were measured allowing the calculation of the tension (T-0). A quick stretch (2 nm per half-sarcomere length) was applied and caused an immediate increase in tension followed by a decrease and a secondary delayed and transient rise in tension (phase 3); finally, the tension recovered a steady state value (phase 4). The tension enhancements during phase 3 (Delta T (3)) and phase 4 (Delta T (4)) were evaluated. The myosin heavy-chain isoform composition of each single fiber was determined by sodium dodecyl sulfate-polyacrylamide gel electrophoresis. Delta T (3) and Delta T (4) were preserved in older men for both type I and IIa fibers despite a reduction in T-0. Therefore, the age-related preservation of the tension increments after a quick stretch in single muscle fibers could explain in part the smaller decrease in force during eccentric contractions compared to isometric and concentric conditions in vivo with aging usually observed. C1 Univ Uppsala Hosp, Dept Neurosci, S-75185 Uppsala, Sweden. Spaulding Rehabil Hosp, Dept Phys Med & Rehabil, Muscle Cell Physiol Lab, Boston, MA USA. Harvard Univ, Sch Med, Boston, MA 02115 USA. Massachusetts Gen Hosp, Ctr Biostat, Boston, MA 02114 USA. Univ Bourgogne, Equipe INSERM, ERM 207, Fac Sci Sport, Dijon, France. RP Ochala, J (reprint author), Univ Uppsala Hosp, Dept Neurosci, Entrance 85,Room 6511, S-75185 Uppsala, Sweden. EM julien.ochala@neurofys.uu.se OI Ochala, Julien/0000-0002-6358-2920 FU NIA NIH HHS [AG18844-01] NR 35 TC 26 Z9 27 U1 0 U2 2 PU SPRINGER PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA SN 0031-6768 EI 1432-2013 J9 PFLUG ARCH EUR J PHY JI Pflugers Arch. PD JUL PY 2006 VL 452 IS 4 BP 464 EP 470 DI 10.1007/s00424-006-0065-6 PG 7 WC Physiology SC Physiology GA 056KV UT WOS:000238522600011 PM 16622703 ER PT J AU Risner, ME Saunders, AM Altman, JFB Ormandy, GC Craft, S Foley, IM Zvartau-Hind, ME Hosford, DA Roses, AD AF Risner, M. E. Saunders, A. M. Altman, J. F. B. Ormandy, G. C. Craft, S. Foley, I. M. Zvartau-Hind, M. E. Hosford, D. A. Roses, A. D. CA Rosiglitazone Alzheimer's Dis Stud TI Efficacy of rosiglitazone in a genetically defined population with mild-to-moderate Alzheimer's disease SO PHARMACOGENOMICS JOURNAL LA English DT Article DE rosiglitazone; Alzheimer's disease; apolipoprotein E; clinical trial; pharmacogenetics; ADAS-Cog ID ACTIVATED RECEPTOR-GAMMA; APOLIPOPROTEIN-E; TRANSGENIC MICE; TYPE-4 ALLELE; DEMENTIA; ASSOCIATION; THIAZOLIDINEDIONE; RISK; METABOLISM; EPSILON-4 AB Mild-to-moderate AD patients were randomized to placebo or rosiglitazone (RSG) 2, 4 or 8 mg. Primary end points at Week 24 were mean change from baseline in AD Assessment Scale-Cognitive (ADAS-Cog) and Clinician's Interview-Based Impression of Change Plus Caregiver Input global scores in the intention-to-treat population (N=511), and results were also stratified by apolipoprotein E (APOE) genotype (n=323). No statistically significant differences on primary end points were detected between placebo and any RSG dose. There was a significant interaction between APOE epsilon(4) allele status and ADAS-Cog (P=0.014). Exploratory analyses demonstrated significant improvement in ADAS-Cog in APOE epsilon(4)-negative patients on 8mg RSG (P=0.024; not corrected for multiplicity). APOE epsilon 4-positive patients did not show improvement and showed a decline at the lowest RSG dose (P=0.012; not corrected for multiplicity). Exploratory analyses suggested that APOE epsilon 4 non-carriers exhibited cognitive and functional improvement in response to RSG, whereas APOE epsilon 4 allele carriers showed no improvement and some decline was noted. These preliminary findings require confirmation in appropriate clinical studies. C1 GlaxoSmithKline Inc, Res & Dev, World Wide Dept, Res Triangle Pk, NC 27709 USA. GlaxoSmithKline Inc, Res & Dev, Genet Res, Res Triangle Pk, NC 27709 USA. GlaxoSmithKline Inc, Res & Dev, World Wide Dev, Harlow, Essex, England. GlaxoSmithKline Inc, Res & Dev, World Wide Dev, Greenford, Middx, England. Univ Washington, Sch Med, Dept Psychiat & Behav Sci, VA Puget Sound,Geriatr Res Educ & Clin Ctr, Seattle, WA USA. RP Risner, ME (reprint author), GlaxoSmithKline Inc, Res & Dev, World Wide Dept, 5 Moore Dr,MAI-C4497, Res Triangle Pk, NC 27709 USA. EM Marc.E.Risner@gsk.com NR 42 TC 384 Z9 410 U1 5 U2 14 PU NATURE PUBLISHING GROUP PI LONDON PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND SN 1470-269X J9 PHARMACOGENOMICS J JI Pharmacogenomics J. PD JUL-AUG PY 2006 VL 6 IS 4 BP 246 EP 254 DI 10.1038/sj.tpj.6500369 PG 9 WC Genetics & Heredity; Pharmacology & Pharmacy SC Genetics & Heredity; Pharmacology & Pharmacy GA 067NH UT WOS:000239309400004 PM 16446752 ER PT J AU Mesa, JM Zaporojan, V Weinand, C Johnson, TS Bonassar, L Randolph, MA Yaremchuk, MJ Butler, PE AF Mesa, John M. Zaporojan, Victor Weinand, Christian Johnson, Timothy S. Bonassar, Lawrence Randolph, Mark A. Yaremchuk, Michael J. Butler, Peter E. TI Tissue engineering cartilage with aged articular chondrocytes in vivo SO PLASTIC AND RECONSTRUCTIVE SURGERY LA English DT Article; Proceedings Paper CT 4th Annual Meeting of the Tissue-Engineering-Society-International CY 2003 CL Orlando, FL SP Tissue Engn Soc Int ID GROWTH PLATE CHONDROCYTES; FIBRIN GLUE; INVITRO CULTURE; POLYMER; SENESCENCE; DEPENDENCE; REPAIR; VITRO AB Background: Tissue engineering has the potential to repair cartilage structures in middle-aged and elderly patients using their own "aged" cartilage tissue as a source of reparative chondrocytes. However, most studies on tissue-engineered cartilage I have used chondrocytes from postfetal or very young donors. The authors hypothesized that articular chondrocytes isolated from old animals could produce neo-cartilage in vivo as well as articular chondrocytes from young donors. Methods: Articular chondrocytes from 8-year-old sheep (old donors) and 3- to 6-month-old sheep (young donors) were isolated. Cells were mixed in fibrin gel polymer at 40 X 10(6) cells/ml until polymerization. Cell-polymer constructs were implanted into the subcutaneous tissue of nude mice and harvested at 7 and 12 weeks. Results: Samples and native articular cartilage controls were examined histologically and assessed biochemically for total DNA, glycosaminoglycan, and hydroxyproline content Histological analysis showed that samples made with chondrocytes from old donors accumutated basophilic extracellular matrix and sulfated glycosaminoglycans around the cells in a manner similar to that seen in samples made with chondrocytes from young donors at 7 and 12 weeks. Biochemical analysis revealed that DNA, glycosaminoglycan, and hydroxyproline content increased in chondrocytes from old donors over time in a pattern similar to that seen with chondrocytes from young donors. Conclusions: This study demonstrates that chondrocytes from old donors can be rejuvenated and can produce neocartilage just as chondrocytes from young donors do when encapsulated in fibrin gel polymer in vivo. This study suggests that middle-aged and elderly patients could benefit from cartilage tissue-engineering repair using their own "aged" articular cartilage as a source of reparative chondrocytes. C1 Harvard Univ, Massachusetts Gen Hosp, Sch Med, Div Plast Surg,Plast Surg Res Lab, Boston, MA 02114 USA. Univ Massachusetts, Sch Med, Ctr Tissue Engn, Worcester, MA USA. Cornell Univ, Sibley Sch Mech & Aerosp Engn, Ithaca, NY 14853 USA. Royal Free Hosp, Dept Plast & Reconstruct Surg, London NW3 2QG, England. RP Randolph, MA (reprint author), Harvard Univ, Massachusetts Gen Hosp, Sch Med, Div Plast Surg,Plast Surg Res Lab, WACC 453,15 Parkman St, Boston, MA 02114 USA. EM marandolph@partners.org RI Bonassar, Lawrence/C-2103-2016; OI Bonassar, Lawrence/0000-0003-1094-6433; Butler, Peter/0000-0001-7419-1493 NR 31 TC 24 Z9 26 U1 1 U2 1 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0032-1052 J9 PLAST RECONSTR SURG JI Plast. Reconstr. Surg. PD JUL PY 2006 VL 118 IS 1 BP 41 EP 49 DI 10.1097/01.prs.0000231929.37736.28 PG 9 WC Surgery SC Surgery GA 063VT UT WOS:000239048700007 PM 16816672 ER PT J AU Hu, PJ Xu, JL Ruvkun, G AF Hu, Patrick J. Xu, Jinling Ruvkun, Gary TI Two membrane-associated tyrosine phosphatase homologs potentiate C-elegans AKT-1/PKB signaling SO PLOS GENETICS LA English DT Review ID FORKHEAD TRANSCRIPTION FACTOR; CONTROLLING DAUER FORMATION; TUMOR-SUPPRESSOR PTEN; INSULIN-LIKE PEPTIDES; AGE-1 PI3 KINASE; CAENORHABDITIS-ELEGANS; LIFE-SPAN; LARVAL DEVELOPMENT; REPRODUCTIVE DEVELOPMENT; REGULATES LONGEVITY AB Akt/protein kinase B (PKB) functions in conserved signaling cascades that regulate growth and metabolism. In humans, Akt/PKB is dysregulated in diabetes and cancer; in Caenorhabditis elegans, Akt/PKB functions in an insulin-like signaling pathway to regulate larval development. To identify molecules that modulate C. elegans Akt/PKB signaling, we performed a genetic screen for enhancers of the akt-1 mutant phenotype (eak). We report the analysis of three eak genes. eak-6 and eak-5/sdf-9 encode protein tyrosine phosphatase homologs; eak-4 encodes a novel protein with an N-myristoylation signal. All three genes are expressed primarily in the two endocrine XXX cells, and their predicted gene products localize to the plasma membrane. Genetic evidence indicates that these proteins function in parallel to AKT-1 to inhibit the FoxO transcription factor DAF-16. These results define two membrane-associated protein tyrosine phosphatase homologs that may potentiate C. elegans Akt/PKB signaling by cell autonomous and cell nonautonomous mechanisms. Similar molecules may modulate Akt/PKB signaling in human endocrine tissues. C1 Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Mol Biol,Dept Genet, Cambridge, MA 02138 USA. Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Genet,Div Hematol Oncol, Cambridge, MA 02138 USA. RP Ruvkun, G (reprint author), Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Mol Biol,Dept Genet, Cambridge, MA 02138 USA. EM ruvkun@molbio.mgh.harvard.edu OI Hu, Patrick/0000-0002-5611-8062 FU NIDDK NIH HHS [K08 DK062884, K08-DK62884] NR 101 TC 28 Z9 43 U1 0 U2 3 PU PUBLIC LIBRARY SCIENCE PI SAN FRANCISCO PA 185 BERRY ST, STE 1300, SAN FRANCISCO, CA 94107 USA SN 1553-7390 J9 PLOS GENET JI PLoS Genet. PD JUL PY 2006 VL 2 IS 7 BP 930 EP 943 AR e99 DI 10.1371/journal.pgen.0020099 PG 14 WC Genetics & Heredity SC Genetics & Heredity GA 070BH UT WOS:000239494800003 PM 16839187 ER PT J AU Dykxhoorn, DM Lieberman, J AF Dykxhoorn, Derek M. Lieberman, Judy TI Silencing viral infection SO PLOS MEDICINE LA English DT Article ID SMALL INTERFERING RNA; FAS PROTECTS MICE; IN-VIVO; MODIFIED SIRNAS; T-CELLS; INHIBITION; EXPRESSION; HEPATITIS; MICRORNA; DELIVERY C1 Harvard Univ, Sch Med, CBR Inst Biomed Res, Boston, MA 02115 USA. Harvard Univ, Sch Med, Dept Pediat, Boston, MA 02115 USA. RP Lieberman, J (reprint author), Harvard Univ, Sch Med, CBR Inst Biomed Res, Boston, MA 02115 USA. EM lieberman@cbr.med.harvard.edu RI Lieberman, Judy/A-2717-2015; Dykxhoorn, Derek/D-1357-2015 FU NIAID NIH HHS [AI056900, U19 AI056900] NR 22 TC 33 Z9 38 U1 0 U2 0 PU PUBLIC LIBRARY SCIENCE PI SAN FRANCISCO PA 185 BERRY ST, STE 1300, SAN FRANCISCO, CA 94107 USA SN 1549-1277 J9 PLOS MED JI PLos Med. PD JUL PY 2006 VL 3 IS 7 BP 1000 EP 1004 AR e242 DI 10.1371/journal.pmed.0030242 PG 5 WC Medicine, General & Internal SC General & Internal Medicine GA 070AS UT WOS:000239493300018 PM 16848617 ER PT J AU Pikman, Y Lee, BH Mercher, T McDowell, E Ebert, BL Gozo, M Cuker, A Wernig, G Moore, S Galinsky, I DeAngelo, DJ Clark, JJ Lee, SJ Golub, TR Wadleigh, M Gilliland, DG Levine, RL AF Pikman, Yana Lee, Benjamin H. Mercher, Thomas McDowell, Elizabeth Ebert, Benjamin L. Gozo, Maricel Cuker, Adam Wernig, Gerlinde Moore, Sandra Galinsky, Ilene DeAngelo, Daniel J. Clark, Jennifer J. Lee, Stephanie J. Golub, Todd R. Wadleigh, Martha Gilliland, D. Gary Levine, Ross L. TI MPLW515L is anovel somatic activating mutation in myelofibrosis with myeloid metaplasia SO PLOS MEDICINE LA English DT Article ID MARROW TRANSPLANT MODEL; TYROSINE KINASE JAK2; POLYCYTHEMIA-VERA; MYELOPROLIFERATIVE DISORDERS; ESSENTIAL THROMBOCYTHEMIA; ERYTHROPOIETIN RECEPTOR; DISEASE; MICE; EXPRESSION; HEMATOPOIESIS AB Background: The JAK2V617F allele has recently been identified in patients with polycythemia vera (PV), essential thrombocytosis (ET), and myelofibrosis with myeloid metaplasia (MF). Subsequent analysis has shown that constitutive activation of the JAK-STAT signal transduction pathway is an important pathogenetic event in these patients, and that enzymatic inhibition of JAK2V617F may be of therapeutic benefit in this context. However, a significant proportion of patients with ET or MF are JAK2V617F-negative. We hypothesized that activation of the JAK-STAT pathway might also occur as a consequence of activating mutations in certain hematopoietic-specific cytokine receptors, including the erythropoietin receptor (EPOR), the thrombopoietin receptor (MPL), or the granulocyte-colony stimulating factor receptor (GCSFR). Methods and Findings: DNA sequence analysis of the exons encoding the transmembrane and juxtamembrane domains of EPOR, MPL, and GCSFR, and comparison with germline DNA derived from buccal swabs, identified a somatic activating mutation in the transmembrane domain of MPL (W515L) in 9% (4/45) of JAKV617F-negative MF. Expression of MPLW515L in 32D, UT7, or Ba/F3 cells conferred cytokine-independent growth and thrombopoietin hypersensitivity, and resulted in constitutive phosphorylation of JAK2, STAT3, STAT5, AKT, and ERK. Furthermore, a small molecule JAK kinase inhibitor inhibited MPLW515L-mediated proliferation and JAK-STAT signaling in vitro. In a murine bone marrow transplant assay, expression of MPLW515L, but not wild-type MPL, resulted in a fully penetrant myeloproliferative disorder characterized by marked thrombocytosis (Plt count 1.9-4.0 x 10(12)/L), marked splenomegaly due to extramedullary hematopoiesis, and increased reticulin fibrosis. Conclusions: Activation of JAK-STAT signaling via MPLW515L is an important pathogenetic event in patients with JAK2V617F-negative MF. The bone marrow transplant model of MPLW515L-mediated myeloproliferative disorders (MPD) exhibits certain features of human MF, including extramedullary hematopoiesis, splenomegaly, and megakaryocytic proliferation. Further analysis of positive and negative regulators of the JAK-STAT pathway is warranted in JAK2V617F-negative MPD. C1 Harvard Univ, Brigham & Womens Hosp, Sch Med, Boston, MA 02115 USA. Harvard Univ, Sch Med, Dana Farber Canc Inst, Boston, MA 02115 USA. Harvard Univ, Broad Inst, Cambridge, England. MIT, Cambridge, England. Howard Hughes Med Inst, Boston, MA 02115 USA. RP Levine, RL (reprint author), Harvard Univ, Brigham & Womens Hosp, Sch Med, Boston, MA 02115 USA. EM ross_levine@dfci.harvard.edu RI Mercher, Thomas/J-2446-2014; OI Mercher, Thomas/0000-0003-1552-087X; Pikman, Yana/0000-0002-5336-0216 FU NCI NIH HHS [CA66996, P01 CA066996, T32 CA009172]; NIDDK NIH HHS [DK50654, P01 DK050654] NR 36 TC 628 Z9 657 U1 4 U2 15 PU PUBLIC LIBRARY SCIENCE PI SAN FRANCISCO PA 185 BERRY ST, STE 1300, SAN FRANCISCO, CA 94107 USA SN 1549-1277 J9 PLOS MED JI PLos Med. PD JUL PY 2006 VL 3 IS 7 BP 1140 EP 1151 AR E270 DI 10.1371/journal.pmed.0030270 PG 12 WC Medicine, General & Internal SC General & Internal Medicine GA 070AS UT WOS:000239493300031 PM 16834459 ER PT J AU Tiamfook-Morgan, TO Harrison, TH Thomas, SH AF Tiamfook-Morgan, Tami O. Harrison, Tim H. Thomas, Stephen H. TI What happens to SpO(2) during air medical crew intubations? SO PREHOSPITAL EMERGENCY CARE LA English DT Article; Proceedings Paper CT Field Triage 2005 - A Meeting of Experts CY MAY 17-18, 2005 CL Atlanta, GA SP Natl Ctr Injury Preven & Control, Ctrs Disease Control & Preven, Div Injury Response DE prehospital; EMS; air transport; SpO(2) monitoring ID TRAUMATIC BRAIN-INJURY; RAPID-SEQUENCE INTUBATION; SEVERE HEAD-INJURY; ENDOTRACHEAL INTUBATION; HYPOXIA; HYPOTENSION; IMPACT; MODERATE; HYPOXEMIA; OUTCOMES AB Objectives. Studies finding adverse outcomes associated with emergency medical services intubation (ETI) have prompted recommendations for prehospital services to improve tracking of oxygenation during airway management. Our goals were to 1) implement a documentation requirement for helicopter EMS ( HEMS) crews, entailing tracking and notation of the lowest SpO(2) value (peri-ETI SpO(2) nadir) occurring during HEMS crew ETI, and 2) assess the findings associated with the peri-ETI SpO(2) documentation parameter. Methods. This was a prospective study conducted at an urban HEMS program with flight nurse/flight paramedic staffing and protocol-driven care. There were 200 consecutive cases undergoing HEMS ETI between April 2004 and July 2005. Univariate logistic regression with odds ratio (OR) was used to assess for association between ETI-related hypoxemia ( decrease in SpO(2) value to< 90% during ETI) and patient/ intubator characteristics. Results. HEMS crew ETI was successful in 189 (95.4%) of the 200 patients. The lowest peri-ETI SpO(2) value was specifically documented in 170 patients (85%) in the study group. In univariate analysis, successful crew ETI was correlated with avoidance of crew-recorded SpO(2) value decreasing to < 90% ( OR, 0.23; 95% confidence interval, 0.07 - 0.83). Similarly, requirement for multiple attempts at ETI was correlated with higher likelihood that crews recorded peri-ETI SpO(2) value decreasing to < 90% ( OR, 7.8; 95% confidence interval, 3.2 - 18.8). However, in nearly two thirds of cases in which multiple attempts were executed, the peri-ETI SpO(2) value remained > 90%. Of the seven patients in whom rescue laryngeal mask airways were placed, the peri-ETI SpO(2) value remained > 90% in three (42.9%). Conclusion. Documentation of crew-recorded peri-ETI SpO(2) nadir is a useful and practical prehospital data point. C1 Harvard Affiliated Emergency Med Residency, Boston, MA USA. Boston MedFlight, Boston, MA USA. Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Emergency Serv, Boston, MA USA. RP Tiamfook-Morgan, TO (reprint author), Brigham & Womens Hosp, Dept Emergency Med, Neville House,Suite 226, Boston, MA 02115 USA. EM ttiamfook@partners.org NR 27 TC 7 Z9 7 U1 0 U2 0 PU TAYLOR & FRANCIS INC PI PHILADELPHIA PA 325 CHESTNUT ST, SUITE 800, PHILADELPHIA, PA 19106 USA SN 1090-3127 J9 PREHOSP EMERG CARE JI Prehosp. Emerg. Care PD JUL-SEP PY 2006 VL 10 IS 3 BP 363 EP 368 DI 10.1080/10903120600725835 PG 6 WC Emergency Medicine; Public, Environmental & Occupational Health SC Emergency Medicine; Public, Environmental & Occupational Health GA 110RQ UT WOS:000242396800020 PM 16801281 ER PT J AU Lambert, MT Copeland, LA Sampson, N Duffy, SA AF Lambert, MT Copeland, LA Sampson, N Duffy, SA TI New-onset type-2 diabetes associated with atypical antipsychotic medications SO PROGRESS IN NEURO-PSYCHOPHARMACOLOGY & BIOLOGICAL PSYCHIATRY LA English DT Review DE atypical antipsychotic agents; body mass index; type-2 diabetes mellitus ID SCHIZOPHRENIA; RISPERIDONE; OLANZAPINE; MELLITUS; DATABASE; GLUCOSE; RISK AB Purpose: This study compared the one-year incidence of new-onset type-2 diabetes mellitus (DM) and changes in weight in patients with a variety of psychiatric diagnoses prescribed olanzapine, risperidone, or quetiapine, compared to a reference group receiving haloperidol and no other antipsychotic medication. Research design and methods: Data was abstracted from charts of subjects newly initiated and then maintained for one year on olanzapine (n = 112), risperidone (n = 100), quetiapine (n = 100), and haloperidol (it = 100). Baseline and one-year DM status, height, and weight were collected, as well as concurrent psychotropic medications, medical and psychiatric comorbidities. Findings: Using a multivariate model, logistic regression identified a significant association between olanzapine (but not other atypical agents) and the development of diabetes compared to haloperidol over the one-year period (odds ratio 8.4, 95% CI 1.8-38.7). Baseline obesity was independently associated with new-onset DM, but only marginally greater weight gain was found among olanzapine users. Conclusions: The middle-aged American veterans in this study cohort were highly vulnerable to the diabetogenic effects of olanzapine, but a close correlation with weight change was not found. Patients administered olanzapine should receive careful laboratory monitoring for elevated plasma, glucose in addition to weight measurement. Published by Elsevier Inc. C1 Univ Texas, SW Med Ctr, Dept Psychiat, Dallas, TX 75235 USA. S Texas Vet Hlth Care Syst, San Antonio, TX USA. VA Ann Arbor Hlth Serv Res & Dev, Ann Arbor, MI USA. Univ Michigan, Dept Otolaryngol, Ann Arbor, MI 48109 USA. Univ Michigan, Dept Psychiat, Ann Arbor, MI 48109 USA. RP Lambert, MT (reprint author), Univ Texas, SW Med Ctr, Ft Worth Outpatient Mental Hlth Clin, Ft Worth VA Mental Hlth Clin,Dept Psychiat, 6000 Western Pl,Suite 300, Ft Worth, TX 76107 USA. EM Michael.Lambert2@med.va.gov OI Copeland, Laurel/0000-0002-9478-0209 NR 22 TC 33 Z9 33 U1 0 U2 2 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND SN 0278-5846 J9 PROG NEURO-PSYCHOPH JI Prog. Neuro-Psychopharmacol. Biol. Psychiatry PD JUL PY 2006 VL 30 IS 5 BP 919 EP 923 DI 10.1016/j.pnpbp.2006.02.007 PG 5 WC Clinical Neurology; Neurosciences; Pharmacology & Pharmacy; Psychiatry SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry GA 055NU UT WOS:000238458200017 PM 16581171 ER PT J AU Porter, MP Stanford, JL Lange, PH AF Porter, MP Stanford, JL Lange, PH TI The distribution of serum prostate-specific antigen levels among American men: Implications for prostate cancer prevalence and screening SO PROSTATE LA English DT Article DE prostate-specific antigen; prostate cancer; screening; prevalence ID REFERENCE RANGES; CLINICAL-EVIDENCE; BLOOD-PRESSURE; UNITED-STATES; TRENDS; ADOLESCENTS; POPULATION; INSTITUTE; CHILDREN; ADULTS AB BACKGROUND. The purpose of this study was to describe the distribution of serum prostate-specific antigen (PSA) among American men and to estimate the number of prevalent cases of biopsy detectable prostate cancer among men with normal serum PSA. METHODS. We analyzed data of the National Health and Nutrition Examination Survey 2001-2002 (NHANES 2001-2002) data and combined these results with published data from the Prostate Cancer Prevention Trial (PCPT). RESULTS. Most men in the US have a serum PSA <= 4.0 ng/ml, and mean and median serum PSA values rise steadily with age. There are an estimated 1,607,585 (95% CI 1,370,848 - 1,844,322) prevalent cases of biopsy detectable prostate cancer in men aged 62-85 years with a serum PSA <= 4 ng/ml. Among men aged 62-75 years, there are an estimated 1,252,143 (95% CI 1,054,677-1,449,609) prevalent cases, including an estimated 195,499 (95% CI 140,234-250,764) high-grade tumors. CONCLUSION. A large number of prevalent cases of biopsy detectable prostate cancer exist in American men with a normal PSA. C1 VA Puget Sound Hlth Care Syst, Urol Sect, Seattle, WA 98108 USA. Univ Washington, Sch Med, Dept Urol, Seattle, WA 98195 USA. Fred Hutchinson Canc Res Ctr, Program Epidemiol, Div Publ Hlth Sci, Seattle, WA 98104 USA. RP Porter, MP (reprint author), VA Puget Sound Hlth Care Syst, Urol Sect, S-112-GU,1660 S Columbian Way, Seattle, WA 98108 USA. EM mporter@u.washington.edu NR 32 TC 13 Z9 13 U1 1 U2 1 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 0270-4137 J9 PROSTATE JI Prostate PD JUL 1 PY 2006 VL 66 IS 10 BP 1044 EP 1051 DI 10.1002/pros.20417 PG 8 WC Endocrinology & Metabolism; Urology & Nephrology SC Endocrinology & Metabolism; Urology & Nephrology GA 053SH UT WOS:000238324900004 PM 16598738 ER PT J AU Bauer, MS McBride, L Williford, WO Glick, H Kinosian, B Altshuler, L Beresford, T Kilbourne, AM Sajatovic, M AF Bauer, MS McBride, L Williford, WO Glick, H Kinosian, B Altshuler, L Beresford, T Kilbourne, AM Sajatovic, M CA Cooperative Studies Program 430 St TI Collaborative care for bipolar disorder: Part I. Intervention and implementation in a randomized effectiveness trial SO PSYCHIATRIC SERVICES LA English DT Article; Proceedings Paper CT 18th Mental Health Services Research Conference CY JUL 18-19, 2005 CL Washington, DC SP NIMH ID ASSERTIVE COMMUNITY TREATMENT; TREATMENT ENHANCEMENT PROGRAM; CLINICAL-PRACTICE GUIDELINES; IMPROVING PRIMARY-CARE; COGNITIVE THERAPY; CHRONIC ILLNESS; HEALTH-CARE; STEP-BD; RELAPSE PREVENTION; SELF-MANAGEMENT AB Outcome for bipolar disorder remains suboptimal despite the availability of efficacious treatments. To improve treatment effectiveness in clinical practice, a Veterans Affairs study team created a care model conceptually similar to the lithium clinics of the 1970s but augmented by principles of more recent collaborative care models for chronic medical illnesses. This intervention consists of improving patients' self-management skills through psychoeducation; supporting providers' decision making through simplified practice guidelines; and enhancing access to care, continuity of care, and information flow through the use of a nurse care coordinator. In this article, which is part I of a two-part report, the authors summarize the conceptual background and development of the intervention, describe the design of a three-year, 11-site randomized effectiveness trial, and report data describing its successful implementation. Trial design emphasized aspects of effectiveness to support generalizability of the findings and eventual dissemination of the intervention. Part II (see companion article, this issue) reports clinical, functional, and overall cost outcomes of the trial. C1 VAMC, Providence, RI 02908 USA. Brown Univ, Dept Psychiat, Providence, RI 02912 USA. VA Cooperat Studies Program, Perry Point, MD USA. Univ Maryland, Dept Biostat, College Pk, MD 20742 USA. Univ Penn, Sect Gen Med, Philadelphia, PA 19104 USA. Philadelphia VAMC, Philadelphia, PA USA. W Los Angeles VAMC, Los Angeles, CA USA. Univ Calif Los Angeles, Dept Psychiat, Los Angeles, CA 90024 USA. Denver VAMC, Denver, CO USA. Univ Colorado, Dept Psychiat, Sch Med, Denver, CO 80202 USA. Pittsburgh VAMC, Pittsburgh, PA USA. Case Western Reserve Univ, Dept Psychiat, Cleveland, OH 44106 USA. RP Bauer, MS (reprint author), VAMC, 116R,830 Chalkstone Ave, Providence, RI 02908 USA. EM mark.bauer@med.va.gov RI Sajatovic, Martha/I-8001-2014 NR 86 TC 91 Z9 92 U1 1 U2 15 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 JUL PY 2006 VL 57 IS 7 BP 927 EP 936 DI 10.1176/appi.ps.57.7.927 PG 10 WC Health Policy & Services; Public, Environmental & Occupational Health; Psychiatry SC Health Care Sciences & Services; Public, Environmental & Occupational Health; Psychiatry GA 059AX UT WOS:000238706800003 PM 16816276 ER PT J AU Bauer, MS McBride, L Williford, WO Glick, H Kinosian, B Altshuler, L Beresford, T Kilbourne, AM Sajatovic, M AF Bauer, MS McBride, L Williford, WO Glick, H Kinosian, B Altshuler, L Beresford, T Kilbourne, AM Sajatovic, M CA Cooperative Studies Program 430 St TI Collaborative care for bipolar disorder: Part II. Impact on clinical outcome, function, and costs SO PSYCHIATRIC SERVICES LA English DT Article; Proceedings Paper CT 18th Mental Health Services Research Conference CY JUL 18-19, 2005 CL Washington, DC SP NIMH ID ASSERTIVE COMMUNITY TREATMENT; RANDOMIZED CONTROLLED-TRIAL; LITHIUM MAINTENANCE TREATMENT; CONTROLLED 18-MONTH TRIAL; LONG-TERM EFFECTIVENESS; COGNITIVE THERAPY; DISEASE-MANAGEMENT; RELAPSE-PREVENTION; QUALITY IMPROVEMENT; DEPRESSED-PATIENTS AB Objective: The study addressed whether a collaborative model for chronic care, described in part I ( this issue), improves outcome for bipolar disorder. Methods: The intervention was designed to improve outcome by enhancing patient self-management skills with group psychoeducation; providing clinician decision support with simplified practice guidelines; and improving access to care, continuity of care, and information flow via nurse care coordinators. In an effectiveness design veterans with bipolar disorder at 11 Veterans Affairs hospitals were randomly assigned to three years of care in the intervention or continued usual care. Blinded clinical and functional measures were obtained every eight weeks. Intention-to-treat analysis (N=306) with mixed-effects models addressed the hypothesis that improvements would accrue over three years, consistent with social learning theory. Results: The intervention significantly reduced weeks in affective episode, primarily mania. Broad-based improvements were demonstrated in social role function, mental quality of life, and treatment satisfaction. Reductions in mean manic and depressive symptoms were not significant. The intervention was cost-neutral while achieving a net reduction of 6.2 weeks in affective episode. Conclusions: Collaborative chronic care models can improve some long-term clinical outcomes for bipolar disorder. Functional and quality-of-life benefits also were demonstrated, with most benefits accruing in years 2 and 3. C1 VAMC, Providence, RI 02908 USA. Brown Univ, Providence, RI 02912 USA. VA Cooperat Studies Program, Perry Point, MD USA. Univ Maryland, College Pk, MD 20742 USA. Univ Penn, Sect Gen Med, Philadelphia, PA 19104 USA. Philadelphia VAMC, Philadelphia, PA USA. W Los Angeles VAMC, Los Angeles, CA USA. Univ Calif Los Angeles, Los Angeles, CA 90024 USA. Denver VAMC, Denver, CO USA. Univ Colorado, Sch Med, Boulder, CO 80309 USA. Pittsburgh VAMC, Pittsburgh, PA USA. Case Western Reserve Univ, Cleveland, OH 44106 USA. RP Bauer, MS (reprint author), VAMC, 116R,830 Chalkstone Ave, Providence, RI 02908 USA. EM mark.bauer@med.va.gov RI Sajatovic, Martha/I-8001-2014 NR 71 TC 143 Z9 144 U1 3 U2 20 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 JUL PY 2006 VL 57 IS 7 BP 937 EP 945 DI 10.1176/appi.ps.57.7.937 PG 9 WC Health Policy & Services; Public, Environmental & Occupational Health; Psychiatry SC Health Care Sciences & Services; Public, Environmental & Occupational Health; Psychiatry GA 059AX UT WOS:000238706800004 PM 16816277 ER PT J AU Krahn, DD Bartels, SJ Coakley, E Oslin, DW Chen, HT McIntyre, J Chung, H Maxwell, J Ware, J Levkoff, SE AF Krahn, DD Bartels, SJ Coakley, E Oslin, DW Chen, HT McIntyre, J Chung, H Maxwell, J Ware, J Levkoff, SE TI PRISM-E: Comparison of integrated care and enhanced specialty referral models in depression outcomes SO PSYCHIATRIC SERVICES LA English DT Article ID RANDOMIZED CONTROLLED-TRIAL; LATE-LIFE DEPRESSION; COLLABORATIVE CARE; HEALTH-SERVICES; MENTAL-ILLNESS; UNITED-STATES; OLDER-ADULTS; DISABILITY; GUIDELINES; MANAGEMENT AB Objective: This study, entitled Primary Care Research in Substance Abuse and Mental Health for the Elderly, examined six-month outcomes for older primary care patients with depression who received different models of treatment. Methods: Clinical outcomes were compared for patients who were randomly assigned to integrated care or enhanced specialty referral. Integrated care consisted of mental health services co-located in primary care in collaboration with primary care physicians. Enhanced specialty referral consisted of referral to physically separate, clearly identified mental health or substance abuse clinics. Results: A total of 1,531 patients were included; their mean age was 73.9 years. Remission rates and symptom reduction for all depressive disorders were similar for the two models at the three- and six-month follow-ups. For the subgroup with major depression, the enhanced specialty referral model was associated with a greater reduction in depression severity than integrated care, but rates of remission and change in function did not differ across models of care for major depression. Conclusions: Six-month outcomes were comparable for the two models. For the subgroup with major depression, reduction in symptom severity was superior for those randomly assigned to the enhanced specialty referral group. C1 William S Middleton Mem Vet Adm Med Ctr, Dept Psychiat, Madison, WI USA. Univ Wisconsin, Dept Psychiat, Sch Med & Publ Hlth, Madison, WI 53705 USA. Dartmouth Coll, Dept Psychiat, Lebanon, NH 03756 USA. John Snow Inc, Hlth Serv Div, Boston, MA USA. Univ Penn, Dept Geriatr & Addict Psychiat, Philadelphia, PA 19104 USA. Brigham & Womens Hosp, Dept Psychiat, Boston, MA 02115 USA. Unity Hlth Syst, Dept Psychiat & Behav Hlth, Rochester, NY USA. Charles B Wang Community Hlth Ctr, Dept Res & Strateg Management, New York, NY USA. Harvard Univ, Sch Publ Hlth, Boston, MA 02115 USA. RP Krahn, DD (reprint author), William S Middleton Mem Vet Adm Med Ctr, Dept Psychiat, Madison, WI USA. EM krahn@med.va.gov NR 30 TC 56 Z9 57 U1 2 U2 3 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 JUL PY 2006 VL 57 IS 7 BP 946 EP 953 DI 10.1176/appi.ps.57.7.946 PG 8 WC Health Policy & Services; Public, Environmental & Occupational Health; Psychiatry SC Health Care Sciences & Services; Public, Environmental & Occupational Health; Psychiatry GA 059AX UT WOS:000238706800005 PM 16816278 ER PT J AU Oslin, DW Grantham, S Coakley, E Maxwell, J Miles, K Ware, J Blow, FC Krahn, DD Bartels, SJ Zubritsky, C AF Oslin, DW Grantham, S Coakley, E Maxwell, J Miles, K Ware, J Blow, FC Krahn, DD Bartels, SJ Zubritsky, C CA PRISM-E grp TI PRISM-E: Comparison of integrated care and enhanced specialty referral in managing at-risk alcohol use SO PSYCHIATRIC SERVICES LA English DT Article ID RANDOMIZED-TRIAL; INTERVENTIONS; PATTERNS AB Objective: This study was part of the Primary Care Research in Substance Abuse and Mental Health for the Elderly study (PRISM-E) and determined the relative effectiveness of two different models of care for reducing at-risk alcohol use among primary care patients aged 65 and older. Methods: This multisite study was a randomized clinical trial comparing integrated care with enhanced specialty referral for older primary care patients screened and identified to have at-risk drinking. Results: Before the study, the 560 participants consumed a mean of 17.9 drinks per week and had a mean of 21.1 binge episodes in the prior three months. At six months, both treatment groups reported lower levels of average weekly drinking (p <.001) and binge drinking (p <.001), despite low levels of treatment engagement. However, the declines did not differ significantly between treatment groups. Conclusions: These results suggest that older persons with at-risk drinking can substantially modify their drinking over time. Although no evidence suggested that the model of care was important in achieving this result, the magnitude of reduction in alcohol use was comparable with other intervention studies. C1 Univ Penn, Dept Psychiat, Philadelphia, PA USA. Philadelphia VAMC, Dept Psychiat, Philadelphia, PA USA. JSI Res & Training Inst, Boston, MA USA. New Hampshire Dartmouth Psychiat Res Ctr, Dept Psychiat, Concord, NH USA. Harvard Univ, Sch Publ Hlth, Dept Psychiat, Boston, MA 02115 USA. Univ Michigan, Dept Psychiat, Ann Arbor, MI 48109 USA. William S Middleton Mem Vet Adm Med Ctr, Dept Psychiat, Madison, WI USA. Dartmouth Coll, Dept Psychiat, Lebanon, NH 03756 USA. RP Oslin, DW (reprint author), Univ Penn, Dept Psychiat, 3535 Market St,Room 3002, Philadelphia, PA USA. EM oslin@mail.med.upenn.edu FU NIMH NIH HHS [K08 MH001599-05, K08 MH001599] NR 13 TC 32 Z9 32 U1 2 U2 2 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 JUL PY 2006 VL 57 IS 7 BP 954 EP 958 DI 10.1176/appi.ps.57.7.954 PG 5 WC Health Policy & Services; Public, Environmental & Occupational Health; Psychiatry SC Health Care Sciences & Services; Public, Environmental & Occupational Health; Psychiatry GA 059AX UT WOS:000238706800006 PM 16816279 ER PT J AU Miklowitz, DJ Otto, MW Wisniewski, SR Araga, M Frank, E Reilly-Harrington, NA Lembke, A Sachs, GS AF Miklowitz, DJ Otto, MW Wisniewski, SR Araga, M Frank, E Reilly-Harrington, NA Lembke, A Sachs, GS TI Psychotherapy, symptom outcomes, and role functioning over one year among patients with bipolar disorder SO PSYCHIATRIC SERVICES LA English DT Article ID COGNITIVE THERAPY; I DISORDER; DEPRESSION; TRIAL; PSYCHOEDUCATION; EFFICACY; RELAPSE; SCALE; MANIA AB Objective: Randomized trials indicate that psychosocial interventions are effective adjuncts to pharmacotherapy in bipolar disorder (1,2). A one-year naturalistic-prospective design was used to examine the association between psychotherapy use and the symptomatic and functional outcomes of patients with bipolar disorder. Methods: Patients with bipolar disorder in a depressed phase (N=248) were drawn from the first 1,000 enrollees (November 1999 to April 2002) in the Systematic Treatment Enhancement Program (STEP-BD), a study of patients with bipolar disorder receiving best-practice pharmacotherapy. Patients were seen in clinics and interviewed every three months over one year regarding use of psychotherapy services, symptoms, and role functioning. Mixed-effects regression models were used to examine whether the amount of psychotherapy the patients received during each three-month interval was associated with symptomatic or psychosocial functioning during the same or a subsequent three- month interval. Results: During the study year, 60 percent of the patients had at least one psychotherapy session. Among patients who began an interval with severe depressive symptoms or low functioning, having more frequent sessions of psychotherapy was associated with less severe mood symptoms and better functioning in the same or a subsequent study interval. In contrast, among patients who began an interval with less severe depressive symptoms or higher functioning, fewer psychotherapy sessions were associated with less severe depressive symptoms and greater functioning in the same or a subsequent interval. Conclusions: Intensive psychotherapy may be most applicable to severely ill patients with bipolar disorder, whereas briefer treatments may be adequate for less severely ill patients. C1 Univ Colorado, Dept Psychol, Boulder, CO 80309 USA. Boston Univ, Dept Psychol, Boston, MA 02215 USA. Univ Pittsburgh, Grad Sch Publ Hlth, Pittsburgh, PA 15260 USA. Univ Pittsburgh, Dept Psychiat, Pittsburgh, PA 15260 USA. Massachusetts Gen Hosp, Dept Psychiat, Boston, MA 02114 USA. Stanford Univ, Dept Psychiat, Palo Alto, CA 94304 USA. RP Miklowitz, DJ (reprint author), Univ Colorado, Dept Psychol, Muenzinger Bldg, Boulder, CO 80309 USA. EM miklow@psych.colorado.edu RI Page, Andrew/G-5438-2012; OI Page, Andrew/0000-0003-3133-2844; Wisniewski, Stephen/0000-0002-3877-9860 FU NIMH NIH HHS [N01-MH80001] NR 31 TC 13 Z9 13 U1 1 U2 13 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 JUL PY 2006 VL 57 IS 7 BP 959 EP 965 DI 10.1176/appi.ps.57.7.959 PG 7 WC Health Policy & Services; Public, Environmental & Occupational Health; Psychiatry SC Health Care Sciences & Services; Public, Environmental & Occupational Health; Psychiatry GA 059AX UT WOS:000238706800007 PM 16816280 ER PT J AU Moy, B Park, ER Feibelmann, S Chiang, S Weissman, JS AF Moy, Beverly Park, Elyse R. Feibelmann, Sandra Chiang, Sylvia Weissman, Joel S. TI Barriers to repeat mammography: Cultural perspectives of African-American, Asian, and Hispanic women SO PSYCHO-ONCOLOGY LA English DT Article DE mammography; cancer; race; barriers; breast; oncology ID BREAST-CARCINOMA SURVIVAL; SCREENING MAMMOGRAPHY; RACIAL-DIFFERENCES; CANCER; POPULATION; BEHAVIOR; PROGRAM; WHITE; BLACK; RACE AB Women of minority races and ethnicities have lower mammography return rates compared to Caucasians. To better understand barriers to mammography, we conducted six focus groups with 49 women of minority races and ethnicities (19 Asian, 16 African-American, and 14 Hispanic) recruited from outpatient medical clinics in Boston. Eligible women had at least one prior mammogram and no personal history of cancer. Discussions were recorded and transcribed, and thematic content analyses were performed. African-Americans and Hispanics felt that lack of insurance was not a barrier to mammography as they were aware of free programs. Some African-Americans avoided mammograms because they were fatalistic and believed that a breast cancer diagnosis would inevitably lead to death. African-Americans agreed that social issues, such as drug and domestic abuse, made obtaining preventive health care less important. Asian participants agreed that mammogram return rates were poor because appointments took time away from work. Asian and Hispanic women identified discourteous behavior by hospital staff as a barrier. Cultural barriers to repeat mammography appear to vary among different racial groups. Interventions to improve screening among minority populations may be more successful if they address group-specific concerns. Copyright (c) 2005 John Wiley & Sons, Ltd. C1 Harvard Univ, Massachusetts Gen Hosp, Sch Med, Gillette Ctr Womens Canc,Dept Med, Boston, MA 02114 USA. Massachusetts Gen Hosp, Inst Hlth Policy, Boston, MA 02114 USA. Harvard Univ, Dept Hlth Care Policy, Sch Med, Boston, MA 02114 USA. Massachusetts Gen Hosp, Interpreter Serv, Boston, MA 02114 USA. RP Moy, B (reprint author), Harvard Univ, Massachusetts Gen Hosp, Sch Med, Gillette Ctr Womens Canc,Dept Med, 55 Fruit St,Yawkey Bldg,Suite 9A, Boston, MA 02114 USA. EM bmoy@partners.org NR 31 TC 37 Z9 37 U1 0 U2 10 PU JOHN WILEY & SONS LTD PI CHICHESTER PA THE ATRIUM, SOUTHERN GATE, CHICHESTER PO19 8SQ, W SUSSEX, ENGLAND SN 1057-9249 J9 PSYCHO-ONCOL JI Psycho-Oncol. PD JUL PY 2006 VL 15 IS 7 BP 623 EP 634 DI 10.1002/pon.994 PG 12 WC Oncology; Psychology; Psychology, Multidisciplinary; Social Sciences, Biomedical SC Oncology; Psychology; Biomedical Social Sciences GA 067UW UT WOS:000239329100007 PM 16304623 ER PT J AU de Moor, JS de Moor, CA Basen-Engquist, K Kudelka, A Bevers, MW Cohen, L AF de Moor, Janet S. de Moor, Carl A. Basen-Engquist, Karen Kudelka, Andrzei Bevers, Michael W. Cohen, Lorenzo TI Optimism, distress, health-related quality of life, and change in cancer antigen 125 among patients with ovarian cancer undergoing chemotherapy SO PSYCHOSOMATIC MEDICINE LA English DT Article DE optimism; anxiety; depression; perceived stress; health-related quality of life; CA 125 ID GENERALIZED OUTCOME EXPECTANCIES; ENDOTHELIAL GROWTH-FACTOR; ARTERY BYPASS-SURGERY; DISPOSITIONAL OPTIMISM; PSYCHOLOGICAL DISTRESS; BREAST-CANCER; PROGNOSTIC-FACTORS; SOCIAL SUPPORT; PREDICTORS; WOMEN AB Objective: This study investigated whether situational and dispositional optimism were protective against dimensions of distress and aspects of health-related quality of life (HQoL) in patients with ovarian cancer undergoing chemotherapy. This study also evaluated whether optimism predicted a decrease in cancer antigen (CA) 125 levels during treatment. Methods: Ninety women with epithelial ovarian cancer were assessed at the start and end of chemotherapy. Optimism, distress, and HQoL were measured by self-report; CA 125 levels were gathered from patients' medical charts. Results: Both measures of optimism were inversely associated with baseline anxiety, perceived stress, and depression. In addition, situational optimism was positively associated with baseline social and physical well-being, and dispositional optimism was positively associated with baseline social and functional well-being. However, neither measure of optimism predicted domains of distress or HQoL at the follow-up assessment after controlling for baseline levels. Dispositional optimism predicted CA 125 at the end of treatment after controlling for baseline levels. However, neither situational nor dispositional optimism predicted CA 125 falling to normal levels (<= 35 U/mL). Conclusion: Consistent with prior research, optimism was inversely associated with distress and positively associated with HQoL in patients with ovarian cancer undergoing chemotherapy. Higher levels of dispositional optimism at the start of chemotherapy were associated with a greater decline in patients' CA 125 during treatment. C1 Dana Farber Canc Inst, Ctr Community Based Res, Boston, MA 02115 USA. Harvard Univ, Sch Publ Hlth, Boston, MA 02115 USA. Childrens Hosp, Boston, MA 02115 USA. Harvard Univ, Sch Med, Boston, MA 02115 USA. Univ Texas, MD Anderson Canc Ctr, Houston, TX 77030 USA. Pfizer Oncol, New York, NY USA. RP de Moor, JS (reprint author), Dana Farber Canc Inst, Ctr Community Based Res, 44 Binney St,Smith 342, Boston, MA 02115 USA. EM janet_demoor@dfci.harvard.edu FU PHS HHS [R25 57730] NR 50 TC 35 Z9 36 U1 2 U2 18 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0033-3174 J9 PSYCHOSOM MED JI Psychosom. Med. PD JUL-AUG PY 2006 VL 68 IS 4 BP 555 EP 562 DI 10.1097/01.psy.0000222379.71389.91 PG 8 WC Psychiatry; Psychology; Psychology, Multidisciplinary SC Psychiatry; Psychology GA 067VL UT WOS:000239330600007 PM 16868264 ER PT J AU Denninger, JW Papakostas, GI Mahal, Y Merens, W Alpert, JE Nierenberg, AA Yeung, A Fava, M AF Denninger, JW Papakostas, GI Mahal, Y Merens, W Alpert, JE Nierenberg, AA Yeung, A Fava, M TI Somatic symptoms in outpatients with major depressive disorder treated with fluoxetine SO PSYCHOSOMATICS LA English DT Article ID CHRONIC-FATIGUE-SYNDROME; PLACEBO-CONTROLLED TRIAL; DOUBLE-BLIND; PRIMARY-CARE; PHYSICAL SYMPTOMS; FIBROMYALGIA; COMPLAINTS; EFFICACY; MOCLOBEMIDE; DULOXETINE AB Among patients with major depressive disorder (MDD), physical and somatic symptoms are associated with a high degree of disability and healthcare utilization. However little is known regarding the treatment of these symptoms with standard pharmacotherapy. To measure somatic symptoms of depression, the authors administered The Symptom Questionnaire (Kellner) before and after 8 weeks of open-label treatment with fluoxetine, 20 mg/day, in 170 MDD outpatients (mean age: 40.4 years). Somatic symptom scores decreased significantly after fluoxetine treatment. The degree of reduction in somatic symptoms was significantly and positively correlated with the degree of improvement in depressive symptoms as measured by the 17-item Hamilton Rating Scale for Depression (Ham-D). Somatic symptom scores at baseline did not predict the degree of reduction in Ham-D scores during treatment. However, fluoxetine-remitters had significantly lower somatic symptom scores at end-point than responders who did not remit. Taken together these findings suggest that developing treatment strategies that successfully target somatic symptoms of depression may further improve the ability to treat depression to remission. C1 Massachusetts Gen Hosp, Depress Clin & Res Program, Dept Psychiat, Boston, MA 02114 USA. Harvard Univ, Sch Med, Boston, MA USA. RP Denninger, JW (reprint author), Massachusetts Gen Hosp, Depress Clin & Res Program, Dept Psychiat, 50 Staniford St,Suite 401, Boston, MA 02114 USA. EM jdenninger@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 [R01-MH-48-483-05] NR 36 TC 12 Z9 12 U1 2 U2 2 PU AMER PSYCHIATRIC PUBLISHING, INC PI ARLINGTON PA 1000 WILSON BOULEVARD, STE 1825, ARLINGTON, VA 22209-3901 USA SN 0033-3182 J9 PSYCHOSOMATICS JI Psychosomatics PD JUL-AUG PY 2006 VL 47 IS 4 BP 348 EP 352 DI 10.1176/appi.psy.47.4.348 PG 5 WC Psychiatry; Psychology SC Psychiatry; Psychology GA 059YK UT WOS:000238767900012 PM 16844895 ER PT J AU McCloskey, LA Lichter, E Williams, C Gerber, M Wittenberg, E Ganz, M AF McCloskey, LA Lichter, E Williams, C Gerber, M Wittenberg, E Ganz, M TI Assessing intimate partner violence in health care settings leads to women's receipt of interventions and improved health SO PUBLIC HEALTH REPORTS LA English DT Article ID DOMESTIC VIOLENCE; PROTECTION ORDERS; SCALES AB Objective. This study investigated whether disclosure of violence to health care providers and the receipt of interventions relate to women's exit from an abusive relationship and to their improved health. Methods. A volunteer sample of 132 women outpatients who described intimate partner violence during the preceding year were recruited from multiple hospital departments and community agencies in suburban and urban metropolitan Boston. Through in-person interviews, women provided information on demographics, past year exposure to violence, past year receipt of interventions, and whether they disclosed partner violence to their health care provider. They also described their past month health status with the 12-Item Short-Form Health Survey and further questions. Results. Of the 132 women, 44% had exited the abusive relationship. Among those who were no longer with their partner, 55% received a domestic violence intervention (e.g. advocacy, shelter, restraining order), compared with 37% of those who remained with their partner. Talking to their health care provider about the abuse increased women's likelihood of using an intervention (odds ratio [OR]=3.9). Those who received interventions were more likely to subsequently exit (OR=2.6) and women no longer with the abuser reported better physical health based on SF-12 summary scores (p=0.05) than women who stayed. Conclusions. Health care providers may make positive contributions to women's access to intimate partner violence services. Intimate partner violence interventions relate to women's reduced exposure to violence and better health. C1 Univ Penn, Sch Social Policy & Practice, Philadelphia, PA 19104 USA. Univ So Maine, Portland, ME 04103 USA. Dept Publ Hlth State Maine, Augusta, ME USA. Harvard Univ, Sch Publ Hlth, Boston, MA 02115 USA. Harvard Univ, Sch Med, Cambridge Hlth Alliance, Cambridge, MA 02138 USA. Harvard Univ, Massachusetts Gen Hosp, Sch Med, Boston, MA 02115 USA. RP McCloskey, LA (reprint author), Univ Penn, Sch Social Policy & Practice, 3701 Locust Walk, Philadelphia, PA 19104 USA. EM lmcclosk@sp2.upenn.edu NR 28 TC 35 Z9 35 U1 1 U2 7 PU ASSOC SCHOOLS PUBLIC HEALTH PI WASHINGTON PA 1101 15TH ST NW, STE 910, WASHINGTON, DC 20005 USA SN 0033-3549 J9 PUBLIC HEALTH REP JI Public Health Rep. PD JUL-AUG PY 2006 VL 121 IS 4 BP 435 EP 444 PG 10 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA 053TA UT WOS:000238326800013 PM 16827445 ER PT J AU Hoffmann, U Pena, AJ Cury, RC Abbara, S Ferencik, M Moselewski, F Siebert, U Brady, TJ Nagurney, JT AF Hoffmann, Udo Pena, Antonio J. Cury, Ricardo C. Abbara, Suhny Ferencik, Maros Moselewski, Fabian Siebert, Uwe Brady, Thomas J. Nagurney, John T. TI Cardiac CT in emergency department patients with acute chest pain SO RADIOGRAPHICS LA English DT Article ID ACUTE MYOCARDIAL-INFARCTION; SPIRAL COMPUTED-TOMOGRAPHY; CORONARY-ARTERY-DISEASE; MULTIDETECTOR ROW CT; PRACTICE GUIDELINES COMMITTEE; LEFT-VENTRICULAR FUNCTION; ELECTRON-BEAM TOMOGRAPHY; STABLE ANGINA-PECTORIS; ASSOCIATION TASK-FORCE; INTRAVASCULAR ULTRASOUND AB Current strategies for the triage of patients who have chest pain but normal initial cardiac enzyme levels and nondiagnostic electrocardiograms do not permit efficient risk stratification. The potentially fatal consequences and high malpractice costs of missed acute coronary syndromes lead every year to the unnecessary hospital admission of about 2.8 million patients who present with acute chest pain in emergency departments in the United States. Most of these patients are at very low risk for an acute coronary syndrome. However, the standard clinical work-up does not provide information about the presence and extent of coronary artery disease. In most patients (80%-94%) with an acute coronary syndrome, a significant coronary artery stenosis can be detected with selective coronary angiography. High levels of diagnostic accuracy also have been established for the detection of significant coronary artery stenosis with the use of 16- and 64-section multidetector computed tomography (CT) in patients with stable angina. Preliminary data indicate that multidetector CT also can help quantify and characterize coronary atherosclerotic plaque and that the CT findings are in good agreement with those at intravascular ultrasonography. Although multidetector CT provides accurate information about the presence of coronary artery disease, large blinded observational studies are warranted to identify CT characteristics with high accuracy for diagnosis of acute coronary syndromes. Such information would enable the conduct of randomized controlled trials to determine whether the detection of coronary stenosis and plaque with multidetector CT improves triage and reduces the costs or increases the cost-effectiveness of management of acute chest pain. (C) RSNA, 2006. C1 Massachusetts Gen Hosp, Dept Radiol, Boston, MA 02114 USA. Massachusetts Gen Hosp, Dept Emergency Med, Boston, MA 02114 USA. Harvard Univ, Sch Publ Hlth, Boston, MA 02115 USA. RP Hoffmann, U (reprint author), Massachusetts Gen Hosp, Dept Radiol, 165 Charles River Plaza,Suite 400, Boston, MA 02114 USA. EM uhoffman@partners.org NR 64 TC 28 Z9 32 U1 1 U2 2 PU RADIOLOGICAL SOC NORTH AMERICA PI OAK BROOK PA 820 JORIE BLVD, OAK BROOK, IL 60523 USA SN 0271-5333 J9 RADIOGRAPHICS JI Radiographics PD JUL-AUG PY 2006 VL 26 IS 4 BP 963 EP 978 DI 10.1148/rg.264055709 PG 16 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA 067LY UT WOS:000239305400002 PM 16844926 ER PT J AU Chen, L Chantra, PK Larsen, LH Barton, P Rohitopakarn, M Zhu, EQ Bassett, LW AF Chen, Lina Chantra, Prem K. Larsen, Linda H. Barton, Premsri Rohitopakarn, Montanan Zhu, Elise Q. Bassett, Lawrence W. TI Imaging characteristics of malignant lesions of the male breast SO RADIOGRAPHICS LA English DT Article; Proceedings Paper CT 90th Scientific Assembly and Annual Meeting of the Radiological-Society-of-North-America CY NOV 28-DEC 03, 2004 CL Chicago, IL SP Radiol Soc N Amer ID 1ST MANIFESTATION; CANCER; CARCINOMA; MANAGEMENT; FEATURES; DISEASE; GYNECOMASTIA; MAMMOGRAPHY AB Most men referred for breast imaging have palpable lumps, breast enlargement, or tenderness. Most of the evaluated lesions are benign. Male breast cancer accounts for less than 1% of total male breast lesions. Differentiation between benign and malignant masses is critical because it alleviates patient anxiety and allows unnecessary procedures to be avoided. Clinically suspicious lesions referred for imaging should first be evaluated with mammography. In patients with questionable findings at mammography and for lesions that are difficult to image with mammography, ultrasonography (US) is often useful for further characterization. A discrete mass at mammography or US is suspicious for malignancy. The relationship of the mass to the nipple should be carefully assessed; an eccentric location is highly suspicious for cancer. Secondary signs occur earlier in male patients because of smaller breast size. Such signs include nipple retraction, skin ulceration or thickening, increased breast trabeculation, and axillary adenopathy. US of the axillary region is helpful for staging. At pathologic analysis, cystic lesions commonly demonstrate malignant findings; therefore, all cysts and complex masses should be worked up as potentially malignant lesions. Benign conditions that may mimic male breast cancer include gynecomastia, lipoma, epidermal inclusion cyst, pseudoangiomatous stromal hyperplasia, and intraductal papilloma. (C) RSNA, 2006. C1 Univ Calif Los Angeles, Dept Radiol, Los Angeles, CA 90095 USA. W Los Angeles Vet Adm Healthcare Syst, Dept Radiol, Los Angeles, CA USA. Univ So Calif, Med Ctr, Dept Radiol, Los Angeles, CA USA. Univ Washington, Med Ctr, Dept Radiol, Seattle, WA 98195 USA. RP Chen, L (reprint author), Univ Calif Los Angeles, Dept Radiol, 200 UCLA Med Plaza,Room 165-47, Los Angeles, CA 90095 USA. EM lchen_mail@yahoo.com NR 23 TC 44 Z9 47 U1 0 U2 1 PU RADIOLOGICAL SOC NORTH AMERICA PI OAK BROOK PA 820 JORIE BLVD, OAK BROOK, IL 60523 USA SN 0271-5333 J9 RADIOGRAPHICS JI Radiographics PD JUL-AUG PY 2006 VL 26 IS 4 BP 993 EP 1006 DI 10.1148/rg.264055116 PG 14 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA 067LY UT WOS:000239305400005 PM 16844928 ER PT J AU Cury, RC Cattani, CAM Gabure, LAG Racy, DJ de Gois, JM Siebert, U Lima, SS Brady, TJ AF Cury, RC Cattani, CAM Gabure, LAG Racy, DJ de Gois, JM Siebert, U Lima, SS Brady, TJ TI Diagnostic performance of stress perfusion and delayed-enhancement MR imaging in patients with coronary artery disease SO RADIOLOGY LA English DT Article ID MAGNETIC-RESONANCE; MYOCARDIAL-PERFUSION; NONINVASIVE DETECTION; CONTRAST ENHANCEMENT; RESERVE; INJURY; FEASIBILITY; ANGIOGRAPHY; TOMOGRAPHY; INFARCTION AB Purpose: To prospectively determine the accuracy of a combined magnetic resonance (MR) imaging approach (stress first-pass perfusion imaging followed by delayed-enhancement imaging) for depicting clinically significant coronary artery stenosis (>= 70% stenosis) in patients suspected of having or known to have coronary artery disease (CAD), with coronary angiography serving as the reference standard. Materials and Methods: The committee on human research approved the study protocol, and all participants gave written informed consent. This study was HIPAA compliant. Forty-seven patients (38 men and nine women; mean age, 63 years +/- 5.3 [standard deviation]) scheduled for coronary angiography were prospectively enrolled: 33 were suspected of having CAD (group A) and 14 had experienced a previous myocardial infarction and were suspected of having new lesions (group B). The MR imaging protocol included cine function, gadolinium-enhanced stress and rest first-pass perfusion MR imaging, and delayed-enhancement MR imaging. Myocardial ischemia was defined as a segment with perfusion deficit at stress first-pass perfusion MR imaging and no hyperenhancement at delayed-enhancement imaging. Myocardial infarction was defined as an area with hyperenhancement at delayed-enhancement imaging. Results: One patient was excluded from analysis because of poor-quality MR images. Coronary angiography depicted significant stenosis in 30 of 46 patients (65%). In a per-vessel analysis (n = 138), stress first-pass perfusion MR imaging and delayed-enhancement imaging yielded sensitivity of 0.87, specificity of 0.89, and accuracy of 0.88, when compared with coronary angiography. The diagnostic accuracy of stress first-pass perfusion MR imaging and delayed-enhancement imaging was slightly better than that of stress and rest first-pass perfusion MR imaging in the entire population (0.88 vs 0.85), in group A (0.86 vs 0.82), and in group B (0.93 vs 0.90). Conclusion: Stress first-pass perfusion MR imaging followed by delayed-enhancement imaging is an accurate method to depict significant coronary stenosis in patients suspected of having or known to have CAD. C1 Beneficencia Portuguesa Hosp, Dept Radiol, Sao Paulo, Brazil. Beneficencia Portuguesa Hosp, Dept Cardiol, Sao Paulo, Brazil. Harvard Univ, Massachusetts Gen Hosp, Sch Med, Cardiac MRI Unit, Boston, MA 02115 USA. Harvard Univ, Massachusetts Gen Hosp, Sch Med, MGH Inst Technol Assessment, Boston, MA 02115 USA. RP Cury, RC (reprint author), Beneficencia Portuguesa Hosp, Dept Radiol, Sao Paulo, Brazil. EM rcury@partners.org NR 21 TC 73 Z9 78 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 JUL PY 2006 VL 240 IS 1 BP 39 EP 45 DI 10.1148/radiol.2401051161 PG 7 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA 055WH UT WOS:000238481000006 PM 16793971 ER PT J AU Hines-Peralta, A Sukhatme, V Regan, M Signoretti, S Liu, ZJ Goldberg, SN AF Hines-Peralta, A Sukhatme, V Regan, M Signoretti, S Liu, ZJ Goldberg, SN TI Improved tumor destruction with arsenic trioxide and radiofrequency ablation in three animal models SO RADIOLOGY LA English DT Article ID HEPATOCELLULAR-CARCINOMA; NECROSIS; OPPORTUNITIES; CHALLENGES; PERFUSION; CANCER; LIVER AB Purpose: To assess the extent of tumor blood flow reduction that is achievable with arsenic trioxide (As2O3) and the effect of As2O3 on radiofrequency (RF)-induced coagulation. Materials and Methods: All animal protocols and experiments were approved by an institutional animal care and use committee before the start of the study. Experiments were conducted in three tumor models: intrarenal VX2 sarcoma in 27 rabbits, RCC 786-0 human renal cell carcinoma in 24 nude mice, and R3230 mammary adenocarcinoma in 40 rats. One dose (0-7.5 mg per kilogram of body weight) of As2O3 was administered (intraperitoneally in rodents, intravenously in rabbits) 1, 6, or 24 hours before standardized RF ablation, which was performed by using a 1-cm active tip, with mean temperatures of 70 degrees C +/- 2 ( standard deviation) for 5 minutes in rodents and 90 degrees C +/- 2 for 6 minutes in rabbits. Laser Doppler flowmetry was used to quantify changes in blood flow, which were compared with diameters of induced tumor coagulation. Comparisons between groups were performed by using Student t tests or analysis of variance. The strengths of correlations between As2O3, tumor blood flow, and RF-induced coagulation were assessed by using linear and higher-order regression models and reported as R-2 computations. Results: Administration of As2O3 significantly (P < .05) reduced blood flow and increased tumor destruction in all tumor models. In VX2 sarcoma tumors, 1 mg/kg As2O3 reduced mean tumor blood flow to 46% +/- 13 of the normal value. The mean resultant coagulation (1.1 cm +/- 0.1) was significantly greater than that achieved with RF ablation alone (0.6 cm +/- 0.1, P < .01). In RCC 786-0 and R3230 tumors, 5 mg/kg As2O3 reduced mean tumor blood flow to 57% +/- 6 and 46% +/- 6 of normal, respectively, increasing mean ablation extent to 0.8 cm +/- 0.1 for both models, compared with those achieved with the control treatment (0.6 cm +/- 0.1 and 0.5 cm +/- 0.1, respectively; P < .05 for both comparisons). Dose studies revealed correlations between drug dose, tumor blood flow, and RF-induced coagulation in all three tumor models (R-2 = 0.60-0.79). Maximal RF synergy was observed 1 hour after As2O3 administration. Conclusion: As2O3 administration represents a transient noninvasive method of reducing tumor blood flow during RF ablation, enabling larger zones of tumor destruction in multiple tumor models. C1 Beth Israel Deaconess Med Ctr, Lab Minimally Invas Tumor Therapy, Dept Radiol, Boston, MA 02215 USA. Beth Israel Deaconess Med Ctr, Dept Med, Div Renal, Boston, MA 02215 USA. Dana Farber Canc Inst, Dept Biostat & Computat Biol, Boston, MA 02115 USA. Dana Farber Harvard Canc Ctr, Renal Canc Program, Boston, MA 02115 USA. Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02115 USA. Harvard Univ, Sch Med, Boston, MA 02115 USA. RP Goldberg, SN (reprint author), Beth Israel Deaconess Med Ctr, Lab Minimally Invas Tumor Therapy, Dept Radiol, 1 Deaconess Rd,WCC 308B, Boston, MA 02215 USA. EM sgoldber@caregroup.harvard.edu FU NCI NIH HHS [1 P50 CA10194-01] NR 28 TC 32 Z9 35 U1 0 U2 1 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 JUL PY 2006 VL 240 IS 1 BP 82 EP 89 DI 10.1148/radiol.2401050788 PG 8 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA 055WH UT WOS:000238481000011 PM 16720872 ER PT J AU Rastogi, N Sahani, DV Blake, MA Ko, DC Mueller, PR AF Rastogi, N Sahani, DV Blake, MA Ko, DC Mueller, PR TI Evaluation of living renal donors: Accuracy of three-dimensional 16-section CT SO RADIOLOGY LA English DT Article ID MULTIDETECTOR ROW CT; LAPAROSCOPIC NEPHRECTOMY; CLINICAL-APPLICATIONS/; MULTISECTION CT; KIDNEY DONORS; ANGIOGRAPHY; ANATOMY; VEIN AB Purpose: To retrospectively assess the sensitivity and specificity of three-dimensional (3D) 16-section computed tomography (CT) in the evaluation of vessels, pelvicalyceal system, and ureters in living renal donors, with surgical findings as the reference standard. Materials and Methods: This was a HIPAA-compliant study. Institutional review board approval was obtained for the review of subjects' medical records and data analysis, with waiver of informed consent. Forty-six renal donors (18 men, 28 women; mean age, 42 years) were examined with 16-section CT. Two blinded reviewers independently studied renal vascular and urographic anatomy of each donor CT scans by fist using 3D images alone, then transverse images alone, and finally transverse and 3D data set. Image quality, degree of diagnostic confidence, and time used for review were recorded. Sensitivity and specificity were calculated. Results: For 3D images, transverse images, and transverse in conjunction with 3D data sets, the respective sensitivity and specificity of CT in evaluation of accessory arteries by reviewer 1 were 100% and 100%, 89% and 100%, and 100% and 100%, and those by reviewer 2 were 89% and 97%, 89% and 100%, and 89% and 100%; the respective sensitivity and specificity in evaluation of venous anomalies by reviewer 1 were 100% and 98%, 100% and 98%, and 100% and 98%, and those by reviewer 2 were 100% and 98%, 100% and 95%, and 100% and 98%. For focused comprehensive assessment of renal donors with 3D scans alone, a reviewer on average (average of reviewers 1 and 2) used 2.4 minutes per scan, demonstrated full confidence in 93%, and rated the quality as excellent in 76%. Conclusion: For focused assessment of renal vascular and urographic anatomy, review of 3D data set alone provides high sensitivity and specificity with regard to findings seen at surgery. C1 Massachusetts Gen Hosp, Dept Radiol, Boston, MA 02114 USA. Massachusetts Gen Hosp, Dept Transplant Surg, Boston, MA 02114 USA. RP Sahani, DV (reprint author), Massachusetts Gen Hosp, Dept Radiol, 55 Fruit St,White 270, Boston, MA 02114 USA. EM dsahani@partners.org NR 26 TC 27 Z9 31 U1 0 U2 1 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 JUL PY 2006 VL 240 IS 1 BP 136 EP 144 DI 10.1148/radiol.2401050780 PG 9 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA 055WH UT WOS:000238481000017 PM 16720871 ER PT J AU Das, M Sauer, F Schoepf, UJ Khamene, A Vogt, SK Schaller, S Kikinis, R van Sonnenberg, E Silverman, SG AF Das, Marco Sauer, Frank Schoepf, U. Joseph Khamene, Ali Vogt, Sebastian K. Schaller, Stefan Kikinis, Ron van Sonnenberg, Eric Silverman, Stuart G. TI Augmented reality visualization for CT-guided interventions: System description, feasibility, and initial evaluation in an abdominal phantom SO RADIOLOGY LA English DT Article; Proceedings Paper CT 88th Scientific Assembly and Annual Meeting of the Radiological-Society-of-North-America CY DEC 01-06, 2002 CL CHICAGO, IL SP Radiol Soc N Amer ID FLUOROSCOPY; EXPOSURE; THERAPY AB The purpose of this study was to evaluate the feasibility and performance of an augmented reality (AR) visualization prototype for virtual computed tomography (CT)guided interventional procedures in a multimodality abdominal phantom. With the aid of AR guidance, three radiologists performed 30 attempts at targeting simulated liver lesions of different sizes ( range, 5 - 15 mm) with a biopsy needle. The position of the needle tip relative to the lesion was verified by using ultrasonography and CT. With AR guidance, lesions were successfully targeted with the first needle pass in all cases. On the basis of these results, AR visualization for CT-guided intervention appears feasible and allows intuitive and accurate lesion targeting in a phantom. C1 Harvard Univ, Sch Med, Brigham & Womens Hosp, Dept Radiol, Boston, MA 02115 USA. Harvard Univ, Sch Med, Brigham & Womens Hosp, Surg Planning Lab, Boston, MA 02115 USA. Univ Witten Herdecke, Inst Diagnost & Intervent Radiol, Muelheim Radiol Inst, Mulheim, Germany. Rhein Westfal TH Aachen, Dept Diagnost Radiol, D-5100 Aachen, Germany. Siemens Corp Res, Princeton, NJ USA. Med Univ S Carolina, Dept Radiol, Charleston, SC 29425 USA. Siemens Med Solut, CT Div, Forchheim, Germany. Harvard Univ, Sch Med, Dana Farber Canc Inst, Dept Radiol, Boston, MA 02115 USA. RP Schoepf, UJ (reprint author), Harvard Univ, Sch Med, Brigham & Womens Hosp, Dept Radiol, Boston, MA 02115 USA. EM schoepf@musc.edu NR 17 TC 23 Z9 24 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 JUL PY 2006 VL 240 IS 1 BP 230 EP 235 DI 10.1148/radiol.2401040018 PG 6 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA 055WH UT WOS:000238481000028 PM 16720866 ER PT J AU Liu, SS Warren, DT Wu, CL Ballantyne, JC Ginsberg, B Rathmell, JP Rosenquist, RW Viscusi, ER AF Liu, Spencer S. Warren, Daniel T. Wu, Christopher L. Ballantyne, Jane C. Ginsberg, Brian Rathmell, James P. Rosenquist, Richard W. Viscusi, Eugene R. TI A lovely idea: Forming an ASRA acute postoperative pain (AcutePOP) database SO REGIONAL ANESTHESIA AND PAIN MEDICINE LA English DT Editorial Material ID SURGERY C1 Virginia Mason Med Ctr, Dept Anesthesiol, Seattle, WA 98101 USA. Univ Washington, Seattle, WA 98195 USA. Johns Hopkins Univ, Dept Anesthesiol & Crit Care Med, Baltimore, MD 21205 USA. Massachusetts Gen Hosp, Dept Anesthesia, Boston, MA 02114 USA. Duke Univ, Dept Anesthesiol, Durham, NC USA. Univ Vermont, Coll Med, Dept Anesthesiol, Burlington, VT USA. Univ Iowa, Dept Anesthesia, Iowa City, IA USA. Thomas Jefferson Univ, Dept Anesthesiol, Philadelphia, PA 19107 USA. RP Liu, SS (reprint author), Virginia Mason Med Ctr, Dept Anesthesiol, Seattle, WA 98101 USA. NR 9 TC 11 Z9 12 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 1098-7339 J9 REGION ANESTH PAIN M JI Region. Anesth. Pain Med. PD JUL-AUG PY 2006 VL 31 IS 4 BP 291 EP 293 DI 10.1016/j.rapm.2006.05.006 PG 3 WC Anesthesiology SC Anesthesiology GA 069TG UT WOS:000239470500002 PM 16857547 ER PT J AU Seidman, LJ Giuliano, AJ Smith, CW Stone, WS Glatt, SJ Meyer, E Faraone, SV Tsuang, MT Cornblatt, B AF Seidman, Larry J. Giuliano, Anthony J. Smith, Christopher W. Stone, William S. Glatt, Stephen J. Meyer, Eric Faraone, Stephen V. Tsuang, Ming T. Cornblatt, Barbara TI Neuropsychological functioning in adolescents and young adults at genetic risk for schizophrenia and affective psychoses: Results from the Harvard and Hillside Adolescent High Risk studies SO SCHIZOPHRENIA BULLETIN LA English DT Review DE schizophrenia; affective psychoses; genetics; neurocognition; intelligence ID UNAFFECTED 1ST-DEGREE RELATIVES; CONTINUOUS PERFORMANCE-TEST; EDINBURGH HIGH-RISK; BIPOLAR DISORDER; SUSTAINED ATTENTION; NONPSYCHOTIC RELATIVES; INTERHEMISPHERIC INTEGRATION; NEUROCOGNITIVE DEFICITS; COGNITIVE DEFICITS; DISTURBED PARENTS AB Siblings and offspring of persons with schizophrenia carry elevated genetic risk for the illness and manifest attentional and memory impairments. Because less is known about other neuropsychological functions and their specificity in adolescents, we conducted a genetic high-risk (HR) study of schizophrenia (HR-SCZ) and affective psychosis (HR-AFF). Participants (ages 12-25) were from the Harvard Adolescent High-Risk and Hillside Family studies, including 73 HR-SCZ, 18 HR-AFF, and 84 community controls (CCs) recruited in metropolitan Boston and New York. Groups were compared on overall neurocognitive functioning, 6 domains, and 13 test scores, controlling for age, parental education, and correlated data within families. The HR-SCZ group was significantly impaired overall, while the HR-AFF group demonstrated a trend toward overall impairment. HR-SCZ subjects showed significantly lower Verbal Ability (d = .73) and Executive Functioning/Working Memory (d = .47) than CCs. HR-AFF subjects showed reduced Verbal Ability (d = .64) compared to CCs. Excluding 12 CCs with a parental history of depression (without psychosis) led to larger differences between HR and CC groups across domains. Moreover, HR-SCZ and CC group differences in Verbal Memory (d = .39) and Visual-Spatial (d = .34) became statistically significant. There were no significant differences between HR-SCZ and HR-AFF groups. Data support a modest neuropsychological deficit in persons at genetic HR for psychosis, with a broader range of deficits in HR-SCZ. Future work should assess the relationship of neurocognition to adaptive functioning and possible onset of psychosis in HR samples. Ascertainment criteria for controls may markedly influence results and interpretation of group differences. C1 Harvard Univ, Sch Med, Beth Israel Deaconess Med Ctr, Masssachusetts Mental Hlth Ctr,Dept Psychiat,Div, Boston, MA 02115 USA. Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Psychiat, Boston, MA 02115 USA. Harvard Univ, Inst Psychiat Epidemiol & Genet, Boston, MA 02115 USA. NSLIJHS, Zucker Hillside Hosp, Dept Psychiat Res, Glen Oaks, NY USA. Univ Calif San Diego, Dept Psychiat, La Jolla, CA 92093 USA. Vet Med Res Fdn, San Diego, CA USA. SUNY Syracuse, Med Genet Res Ctr, Syracuse, NY 13210 USA. SUNY Syracuse, Dept Psychiat, Syracuse, NY 13210 USA. RP Seidman, LJ (reprint author), Harvard Univ, Sch Med, Beth Israel Deaconess Med Ctr, Masssachusetts Mental Hlth Ctr,Dept Psychiat,Div, Boston, MA 02115 USA. EM lseidman@bidmc.harvard.edu OI Glatt, Stephen/0000-0002-0360-7567; Faraone, Stephen/0000-0002-9217-3982 FU NIMH NIH HHS [MH 43518, MH 46318, MH 50203, MH 63951, MH 65562, R01 MH043518, R01 MH063951, R01 MH065562, R37 MH043518, U01 MH046318] NR 124 TC 84 Z9 87 U1 0 U2 7 PU OXFORD UNIV PRESS PI OXFORD PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND SN 0586-7614 J9 SCHIZOPHRENIA BULL JI Schizophr. Bull. PD JUL PY 2006 VL 32 IS 3 BP 507 EP 524 DI 10.1093/schbul/sbj078 PG 18 WC Psychiatry SC Psychiatry GA 061YE UT WOS:000238909500017 PM 16707777 ER PT J AU Seidman, LJ Thermenos, HW Poldrack, RA Peace, NK Koch, JK Faraone, SV Tsuang, MT AF Seidman, Larry J. Thermenos, Heidi W. Poldrack, Russell A. Peace, Nicole K. Koch, Jennifer K. Faraone, Stephen V. Tsuang, Ming T. TI Altered brain activation in dorsolateral prefrontal cortex in adolescents and young adults at genetic risk for schizophrenia: An fMRI study of working memory SO SCHIZOPHRENIA RESEARCH LA English DT Article DE schizophrenia; genetics; functional MRI; working memory; prefrontal cortex ID NONPSYCHOTIC RELATIVES; VULNERABILITY INDICATOR; 1ST-DEGREE RELATIVES; HIPPOCAMPAL VOLUME; PARIETAL CORTEX; FUNCTIONAL MRI; DYSFUNCTION; PERFORMANCE; SYMPTOMS; DEFICITS AB Objective: Adult first-degree relatives of persons with schizophrenia carry elevated genetic risk for the illness, demonstrate working memory (WM) impairments, and manifest alterations in dorsolateral prefrontal cortical (DLPFC) function during WM. Because substantially less is known about these phenotypes in adolescent subjects we sought to demonstrate that young relatives of persons with schizophrenia manifest impaired WM and altered prefrontal activation. Methods: Participants were 21 non-psychotic, unmedicated first-degree relatives of persons with a DSM-N diagnosis of schizophrenia or schizoaffective disorder, depressed type and 24 unmedicated controls, recruited from the community and hospitals in metropolitan Boston (ages 13-28). We compared groups on an auditory WM task with interference prior to scanning and used functional magnetic resonance imaging (fMRI) to compare groups while performing visual 2-back WM and control vigilance tasks. Blood oxygen level dependent signal change was measured using two whole-brain gradient echo EPI pulse acquisitions (21 contiguous. 5 mm axial slices), acquired on a Siemens 1.5T MR scanner. Data were analyzed using Statistical Parametric Mapping-99. Results: The high risk subjects were significantly impaired on the auditory WM task, had significantly greater Phobic Anxiety. and marginally greater Psychoticism than controls on the Symptom Checklist-90-Revised, and showed significantly greater task-elicited activation in the right DLPFC (BA 46). Psychopathology, IQ. and in-scanner WM performance did not account for group differences in brain activation. Conclusions: Data support a physiological difference (an exaggerated fMR1 response) in DLPFC in adolescents at genetic risk for schizophrenia, independent of psychosis. Future work can study the relationship of these measures to possible onset of schizophrenia. (c) 2006 Elsevier B.V. All rights reserved. C1 Harvard Univ, Dept Psychiat, Sch Med,Beth Israel Deaconess Med Ctr, Massachusetts Mental Hlth Ctr,Publ Psychiat Div, Boston, MA 02215 USA. Harvard Univ, Sch Med, Brockton W Roxbury VA Med Ctr, Dept Psychiat, Cambridge, MA 02140 USA. Harvard Univ, Sch Med, Massachusetts Gen Hosp, Dept Psychiat, Boston, MA 02114 USA. Harvard Univ, Inst Psychiat Epidemiol & Genet, Boston, MA 02115 USA. Harvard Univ, Sch Med, MIT, Martinos Ctr Biomed Imaging, Charlestown, MA 02129 USA. Massachusetts Gen Hosp, Charlestown, MA 02129 USA. Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA. Univ Calif Los Angeles, Dept Psychol, Los Angeles, CA 90095 USA. Univ Calif Los Angeles, Brain Res Inst, Los Angeles, CA 90095 USA. SUNY Upstate Med Univ, Dept Psychiat, Syracuse, NY 13210 USA. SUNY Genet Res Program, Syracuse, NY 13210 USA. Univ Calif San Diego, Dept Psychiat, Inst Behav Genom, La Jolla, CA 92093 USA. RP Seidman, LJ (reprint author), Harvard Univ, Dept Psychiat, Sch Med,Beth Israel Deaconess Med Ctr, Massachusetts Mental Hlth Ctr,Publ Psychiat Div, 401 Pk Dr, Boston, MA 02215 USA. EM lseidman@bidmc.harvard.edu; hthermen@bidmc.harvard.edu; poldrack@ucla.edu; Nicole.peace@gmail.com; jkk@nmr.mgh.harvard.edu; faraones@upstate.edu; mtsuang@ucsd.edu OI Faraone, Stephen/0000-0002-9217-3982 FU NCRR NIH HHS [P41RR14075]; NIMH NIH HHS [MH-43518, MH65562, R25 MH 60485] NR 74 TC 72 Z9 75 U1 1 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 JUL PY 2006 VL 85 IS 1-3 BP 58 EP 72 DI 10.1016/j.schres.2006.03.019 PG 15 WC Psychiatry SC Psychiatry GA 065AJ UT WOS:000239131500007 PM 16632333 ER PT J AU Subotnik, KL Nuechterlein, KH Green, MF Horan, WP Nienow, TM Ventura, J Nguyen, AT AF Subotnik, Kenneth L. Nuechterlein, Keith H. Green, Michael F. Horan, William P. Nienow, Tasha M. Ventura, Joseph Nguyen, Annie T. TI Neurocognitive and social cognitive correlates of formal thought disorder in schizophrenia patients SO SCHIZOPHRENIA RESEARCH LA English DT Article DE schizophrenia; proverbs; neurocognition; social cognition; formal thought disorder; concrete thinking ID PROVERB INTERPRETATION; COMMUNICATION DISTURBANCES; IDIOSYNCRATIC THINKING; GERIATRIC-PATIENTS; PARTIAL RECOVERY; ATTENTION; SYMPTOMS; LANGUAGE; DEFICIT; VULNERABILITY AB The neurocognitive and social cognitive correlates of two types of formal thought disorder (i.e., bizarre-idiosyncratic and concrete thinking) were examined in 47 stable outpatients with schizophrenia. Both types of thinking disturbance were related to impairments in verbal learning, intrusions in verbal memory, immediate auditory memory, sustained attention, and social schema knowledge. Distractibility during an immediate memory task was associated with more frequent bizarre verbalizations but not concreteness. Impaired verbal learning rate and intrusions in verbal memory independently contributed to the prediction of bizarre responses, whereas intrusions in verbal memory and impaired immediate memory independently contributed to concrete thinking. This pattern of findings is consistent with the view that neurocognitive and, possibly, social cognitive deficits underlie these two aspects of formal thinking disturbance in schizophrenia. (c) 2006 Elsevier B.V All rights reserved. C1 Univ Calif Los Angeles, Dept Psychiat & Biobehav Sci, Los Angeles, CA 90095 USA. Univ Calif Los Angeles, Dept Psychol, Los Angeles, CA 90095 USA. Vet Affairs Greater Los Angeles Healthcare Syst, Los Angeles, CA USA. RP Subotnik, KL (reprint author), Univ Calif Los Angeles, Dept Psychiat & Biobehav Sci, 300 UCLA Med Plaza,Room 2240, Los Angeles, CA 90095 USA. EM ksubotnik@mednet.ucla.edu FU NIMH NIH HHS [MH37705, MH30911, MH66286] NR 52 TC 30 Z9 30 U1 0 U2 2 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0920-9964 J9 SCHIZOPHR RES JI Schizophr. Res. PD JUL PY 2006 VL 85 IS 1-3 BP 84 EP 95 DI 10.1016/j.schres.2006.03.007 PG 12 WC Psychiatry SC Psychiatry GA 065AJ UT WOS:000239131500009 PM 16624529 ER PT J AU Byne, W Kidkardnee, S Tatusov, A Yiannoulos, G Buchsbaum, MS Haroutunian, V AF Byne, William Kidkardnee, Smith Tatusov, Alex Yiannoulos, Georgia Buchsbaum, Monte S. Haroutunian, Vahram TI Schizophrenia-associated reduction of neuronal and oligodendrocyte numbers in the anterior principal thalamic nucleus SO SCHIZOPHRENIA RESEARCH LA English DT Article DE schizophrenia; thalamus; anterior nucleus; oligodendrocyte; sex difference ID MULTIPLE BRAIN-REGIONS; CINGULATE CORTEX; EFFERENT CONNECTIONS; MEDIODORSAL NUCLEUS; GENE-EXPRESSION; MEDIAL THALAMUS; POSTMORTEM; VOLUME; ABNORMALITIES; MYELINATION AB The anterior principal thalamic nucleus provides a nodal link for intralimbic circuits involved in the execution of multiple complex functions that are impaired in schizophrenia (SZ). Using stereoloic sampling procedures. we assessed the volume and the number of neurons and oligodendrocytes in this nucleus in well-characterized postmortem material from 23 neuroleptic treated subjects with chronic SZ (SZs) and 12 comparison subjects (Cs) with no psychiatric history. Volume was decreased on average by 17% in SZ, but this difference was not statistically significant. For neuronal number. there was a signifcant sex by diagnosis interaction with neuronal number being lower in male (p = .002) but not female (p = .374) SZs relative to their respective Cs. For the number of oligodendrocytes, there was a main effect of diagnosis and a diagnosis by sex interaction such that number was significantly reduced in male SZs (p < .001) with a similar trend in female SZs (p = .051) relative to their respective controls. The ratio of oligodendrocytes to neurons was signifcantly decreased in SZs (p = .045) with no sex by diagnosis interaction. These findings are consistent with a previous report of reduced neuronal number in the anterior principal nucleus of finale SZs and add to a growing body of evidence implicating oligodendrocyte abnormalities in SZ. (c) 2006 Elsevier B.V. All rights reserved. C1 Bronx Vet Affairs Med Ctr, Div Bas & Lab Res, Bronx, NY 10468 USA. Mt Sinai Sch Med, Dept Psychiat, New York, NY 10029 USA. RP Byne, W (reprint author), Bronx Vet Affairs Med Ctr, Div Bas & Lab Res, 130 W Kingsbridge Rd,Rm 2F37,Res Bldg, Bronx, NY 10468 USA. EM william.byne@mssm.edu FU NIMH NIH HHS [MH45212, MH66998] NR 59 TC 49 Z9 49 U1 3 U2 4 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0920-9964 J9 SCHIZOPHR RES JI Schizophr. Res. PD JUL PY 2006 VL 85 IS 1-3 BP 245 EP 253 DI 10.1016/j.schres.2006.03.029 PG 9 WC Psychiatry SC Psychiatry GA 065AJ UT WOS:000239131500025 PM 16730162 ER PT J AU Bagby, GC AF Bagby, Grover C. TI Constitutional marrow failure: Introduction SO SEMINARS IN HEMATOLOGY LA English DT Editorial Material C1 Oregon Hlth Sci Univ, Inst Canc, Portland, OR 97201 USA. Portland VA Med Ctr, Portland, OR USA. RP Bagby, GC (reprint author), Oregon Hlth Sci Univ, Inst Canc, Portland, OR 97201 USA. OI Bagby, Grover/0000-0001-6830-2046 NR 0 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 0037-1963 J9 SEMIN HEMATOL JI Semin. Hematol. PD JUL PY 2006 VL 43 IS 3 BP 145 EP 146 DI 10.1053/j.seminhematol.2006.04.007 PG 2 WC Hematology SC Hematology GA 063BZ UT WOS:000238992300001 PM 16822456 ER PT J AU Hayes, TE Brandt, JT Chandler, WL Eby, CS Kottke-Marchant, K Krishnan, J Lefkowitz, JB Olson, JD Rund, CR Van Cott, EM Cunningham, MT AF Hayes, Timothy E. Brandt, John T. Chandler, Wayne L. Eby, Charles S. Kottke-Marchant, Kandice Krishnan, Jayashree Lefkowitz, Jerry B. Olson, John D. Rund, Chad R. Van Cott, Elizabeth M. Cunningham, Mark T. TI External peer review quality assurance testing in von Willebrand disease: The recent experience of the United States College of American Pathologists proficiency testing program SO SEMINARS IN THROMBOSIS AND HEMOSTASIS LA English DT Article DE von Willebrand factor (vWF); von Willebrand disease (vWD); hemostasis testing; quality control; quality assurance; proficiency testing ID CLASSIFICATION; DIAGNOSIS AB The U.S. College of American Pathologists (CAP) has conducted a focused studythe proficiency testing for von Willebrand disease (MID) analysis from 2003 to 2005. This report summarizes the findings regarding the accuracy and precision of the various assays at different analyte levels, as well as the influence of the reference material used to construct the assay standard curve. The results show that testing of von Willebrand factor (vWF):antigen (vWF:Ag) and ristocetin cofactor activity (v W:RCo) is reasonably accurate, with all-method mean values falling within 3.2 and 5.6%, respectively, of the International Society on Thrombosis and Haemostasis Secondary Coagulation Standard (lot 2) assigned values. vWF:Ag measurements are reasonably precise (all-method coefficients of variation [CVs] = 10.7 to 15.1%), even at lower levels,of vWF. The highest precision was observed for immunoturbidometric assays (CVs, 6.3 to 9.7%). V W:RCo measurements are less precise (all-method CVs, 23.3 to 30.9%). The reference materials used in the standard curves for immunoturbidometric vWF:Ag assays appear to have accurately assigned v W values for the majority of commercial suppliers. C1 Maine Med Ctr, Dept Pathol & Lab Med, Portland, ME 04102 USA. Eli Lilly & Co, Lilly Corp Ctr, Indianapolis, IN 46285 USA. Univ Washington, Dept Lab Med, Seattle, WA 98195 USA. Washington Univ, Sch Med, Dept Pathol, St Louis, MO 63110 USA. Cleveland Clin Fdn, Dept Clin Pathol, Cleveland, OH 44195 USA. Washington Hosp Ctr, Dept Pathol, Washington, DC 20010 USA. Univ Colorado, Hlth Sci Ctr, Dept Pathol, Denver, CO 80262 USA. Univ Texas, Hlth Sci Ctr, Dept Pathol, San Antonio, TX 78284 USA. Univ New Mexico, Dept Pathol, Hlth Sci Ctr, Albuquerque, NM 87131 USA. Massachusetts Gen Hosp, Dept Pathol, Boston, MA 02114 USA. Univ Kansas, Med Ctr, Dept Pathol, Kansas City, KS 66103 USA. RP Hayes, TE (reprint author), Maine Med Ctr, Dept Pathol & Lab Med, 22 Bramhall St, Portland, ME 04102 USA. EM hayest@mmc.org NR 7 TC 31 Z9 31 U1 0 U2 1 PU THIEME MEDICAL PUBL INC PI NEW YORK PA 333 SEVENTH AVE, NEW YORK, NY 10001 USA SN 0094-6176 J9 SEMIN THROMB HEMOST JI Semin. Thromb. Hemost. PD JUL PY 2006 VL 32 IS 5 BP 499 EP 504 DI 10.1055/s-2006-947864 PG 6 WC Hematology; Peripheral Vascular Disease SC Hematology; Cardiovascular System & Cardiology GA 068QF UT WOS:000239388800008 PM 16862523 ER PT J AU Patel, SR Malhotra, A Gottlieb, DJ White, DP Hu, FB AF Patel, Sanjay R. Malhotra, Atul Gottlieb, Daniel J. White, David P. Hu, Frank B. TI Correlates of long sleep duration SO SLEEP LA English DT Article DE sleep duration; long sleep; depression ID CORONARY-HEART-DISEASE; MORTALITY RISK; LEPTIN LEVELS; NHANES-I; WOMEN; DEPRIVATION; DEPRESSION; QUESTIONNAIRE; RESTRICTION; PREVENTION AB Study Objective: Sleeping more than 7 to 8 hours per day has been consistently associated with increased mortality. Whether this association is causal and what pathways explain this association are unknown. We sought to identify factors that could potentially explain the association between long sleep and mortality. Design: Cross-sectional epidemiologic survey. Participants: Middle-aged women (n = 60,028) participating in the Nurses Health Study II who reported a habitual sleep duration of 7 hours or more. Results: Multiple sclerosis (odds ratio [OR] = 3.7, 95% confidence interval [3.0-4.5]), antidepressant use (OR = 3.1, [2.9-3.3]), benzodiazepine use (OR = 3.0 [2.6-3.3]), and systemic lupus erythematosus (OR = 2.9, [2.3-3.61) were the factors most strongly associated with prolonged sleep. Combining these data with prevalence information and a range of plausible associations with mortality, the confounding rate ratio was estimated. This parameter is the ratio of the unadjusted long sleep-mortality rate ratio to the rate ratio adjusted for the factor and measures the extent that the factor can alter the long sleep-mortality association, either through confounding or as a causal intermediate. Based on this parameter, psychiatric and socioeconomic factors have the greatest potential to influence the long sleep-mortality relationship. Assuming each factor doubles mortality risk, the confounding rate ratios for depression, antidepressant use, and unemployment were 1.10, 1.18, and 1.12. Lesser influential factors were benzodiazepine use, poverty, low societal status, sedentary lifestyle, and obesity. Conclusion: Depression and low socioeconomic status are strong candidates for producing the statistical association between long sleep and mortality, either as confounders or as causal intermediates. Future causal research on the effects of long sleep should include a detailed assessment of psychiatric disease and socioeconomic status. C1 Case Western Reserve Univ, Div Pulm & Crit Care Med, Cleveland, OH 44106 USA. Brigham & Womens Hosp, Div Sleep Med, Boston, MA 02115 USA. Brigham & Womens Hosp, Dept Med, Channing Lab, Boston, MA 02115 USA. Harvard Univ, Sch Med, Boston, MA USA. Harvard Univ, Sch Publ Hlth, Dept Nutr, Boston, MA 02115 USA. Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA. Boston Univ, Div Pulm & Crit Care Med, Boston, MA 02215 USA. VA Boston Healthcare Syst, Boston, MA USA. RP Patel, SR (reprint author), Case Western Reserve Univ, Div Pulm & Crit Care Med, 11400 Euclid Ave,Room 260, Cleveland, OH 44106 USA. RI Loureiro, Nuno/I-6400-2012 OI Loureiro, Nuno/0000-0002-1166-3219 FU NCI NIH HHS [CA50385, R01 CA050385]; NHLBI NIH HHS [HL081385, K08 HL081385, K08 HL081385-02, R01 HL073146, R01 HL073146-02]; NIA NIH HHS [K23 AG024837-03, K23 AG024837] NR 41 TC 176 Z9 178 U1 1 U2 13 PU AMER ACADEMY SLEEP MEDICINE PI WESTCHESTER PA ONE WESTBROOK CORPORATE CENTER STE 920, WESTCHESTER, IL 60154 USA SN 0161-8105 J9 SLEEP JI Sleep PD JUL 1 PY 2006 VL 29 IS 7 BP 881 EP 889 PG 9 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA 062RF UT WOS:000238961500004 PM 16895254 ER PT J AU Gordon, MY Levicar, N Pai, M Bachellier, P Dimarakis, I Al-Allaf, F M'Hamdi, H Thalji, T Welsh, JP Marley, SB Davies, J Dazzi, F Marelli-Berg, F Tait, P Playford, R Jiao, L Jensen, S Nicholls, JP Ayav, A Nohandani, M Farzaneh, F Gaken, J Dodge, R Alison, M Apperley, JF Lechler, R Habib, NA AF Gordon, Myrtle Y. Levicar, Natasa Pai, Madhava Bachellier, Philippe Dimarakis, Ioannis Al-Allaf, Faisal M'Hamdi, Hanane Thalji, Tamara Welsh, Jonathan P. Marley, Stephen B. Davies, John Dazzi, Francesco Marelli-Berg, Federica Tait, Paul Playford, Raymond Jiao, Long Jensen, Steen Nicholls, Joanna P. Ayav, Ahmet Nohandani, Mahrokh Farzaneh, Farzin Gaken, Joop Dodge, Rikke Alison, Malcolm Apperley, Jane F. Lechler, Robert Habib, Nagy A. TI Characterization and clinical application of human CD34(+) stem/progenitor cell populations mobilized into the blood by granulocyte colony-stimulating factor SO STEM CELLS LA English DT Article DE stem cells; liver disease; transplantation; regenerative medicine ID MESENCHYMAL STEM-CELLS; MARROW STROMAL CELLS; PROGENITOR CELLS; CORD BLOOD; SUBPOPULATION AB A phase I study was performed to determine the safety and tolerability of injecting autologous CD34(+) cells into five patients with liver insufficiency. The study was based on the hypothesis that the CD34(+) cell population in granulocyte colony-stimulating factor (G-CSF)-mobilized blood contains a subpopulation of cells with the potential for regenerating damaged tissue. We separated a candidate CD34(+) stem cell population from the majority of the CD34(+) cells (99%) by adherence to tissue culture plastic. The adherent and nonadherent CD34(+) cells were distinct in morphology, immunophenotype, and gene expression profile. Reverse transcription-polymerase chain reaction-based gene expression analysis indicated that the adherent CD34(+) cells had the potential to express determinants consistent with liver, pancreas, heart, muscle, and nerve cell differentiation as well as hematopoiesis. Overall, the characteristics of the adherent CD34(+) cells identify them as a separate putative stem/progenitor cell population. In culture, they produced a population of cells exhibiting diverse morphologies and expressing genes corresponding to multiple tissue types. Encouraged by this evidence that the CD34(+) cell population contains cells with the potential to form hepatocyte-like cells, we gave G-CSF to five patients with liver insufficiency to mobilize their stem cells for collection by leukapheresis. Between 1 X 10(6) and 2 X 10(8) CD34(+) cells were injected into the portal vein (three patients) or hepatic artery (two patients). No complications or specific side effects related to the procedure were observed. Three of the five patients showed improvement in serum bilirubin and four of five in serum albumin. These observations warrant further clinical trials. C1 Univ London Imperial Coll Sci & Technol, Fac Med, Dept Surg Oncol & Technol, London W12 0NN, England. LiverCyte Ltd, London, England. Kings Coll London, Fac Med, Kings Guys & St Thomas Med Sch, London, England. Harvard Univ, Sch Med, Joslin Diabet Ctr, Boston, MA 02115 USA. Royal London Hosp Diabet & Metab Med, London, England. RP Habib, NA (reprint author), Univ London Imperial Coll Sci & Technol, Fac Med, Dept Surg Oncol & Technol, Hammersmith Campus,Du Cane Rd, London W12 0NN, England. EM nagy.habib@imperial.ac.uk RI Farzaneh, Farzin/B-4902-2009; OI Farzaneh, Farzin/0000-0002-9275-2415; AL-ALLAF, FAISAL/0000-0001-8430-3532 NR 26 TC 169 Z9 194 U1 0 U2 3 PU ALPHAMED PRESS PI DURHAM PA 318 BLACKWELL ST, STE 260, DURHAM, NC 27701-2884 USA SN 1066-5099 J9 STEM CELLS JI Stem Cells PD JUL PY 2006 VL 24 IS 7 BP 1822 EP 1830 DI 10.1634/stemcells.2005-0629 PG 9 WC Cell & Tissue Engineering; Biotechnology & Applied Microbiology; Oncology; Cell Biology; Hematology SC Cell Biology; Biotechnology & Applied Microbiology; Oncology; Hematology GA 085YE UT WOS:000240639500021 PM 16556705 ER PT J AU Salat, DH Smith, EE Tuch, DS Benner, T Pappu, V Schwab, KM Gurol, ME Rosas, D Rosand, J Greenberg, SM AF Salat, David H. Smith, Eric E. Tuch, David S. Benner, Thomas Pappu, Vasanth Schwab, Kristin M. Gurol, M. Edip Rosas, Diana Rosand, Jonathan Greenberg, Steven M. TI White matter alterations in cerebral amyloid angiopathy measured by diffusion tensor imaging SO STROKE LA English DT Article DE aging; amyloid; cerebral hemorrhage; dementia; diffusion ID INTRACEREBRAL HEMORRHAGE; MULTIPLE-SCLEROSIS; BRAIN IMAGES; LESIONS; MRI; OPTIMIZATION; REGISTRATION; DEMENTIA; ROBUST AB Background and Purpose-Cerebral amyloid angiopathy (CAA) represents beta-amyloid deposition in the small- and medium-sized vessels of the brain and meninges. CAA contributes to altered vessel function and is associated with white matter damage, cognitive impairment, and most salient, hemorrhagic stroke. We used diffusion tensor imaging to evaluate the anatomic distribution of white matter degeneration in participants diagnosed with advanced CAA. Methods-Diffusion tensor imaging was obtained from 11 participants dial-nosed with CAA-related intracerebral hemorrhage and 13 matched healthy control participants. Fractional anisotropy (FA) and diffusivity maps were compared using voxel based t test and region-of-interest analyses. Results-FA was reduced in CAA in temporal white matter and in the splenium of the corpus callosum (P < 0.001 with approximate to 17% reduction in temporal white matter and 15% reduction in the splenium). FA was marginally increased in CAA in the posterior limb of the internal capsule and subthalamic gray matter regions (approximate to 7% increase in subthalamic gray). FA changes were bilateral, remained significant in cluster analysis controlling for multiple comparisons, and did not depend on the hemisphere of the cerebral hemorrhage. Diffusivity was not substantially altered. Conclusions-These findings suggest that a pattern of regional brain tissue degeneration is a characteristic feature of advanced CAA. C1 Harvard Univ, Massachusetts Gen Hosp, Sch Med,Athinoula A Martinos Ctr Biomed Imaging, MIT,Dept Radiol,HMS, Charlestown, MA 02129 USA. Massachusetts Gen Hosp, Dept Neurol, Clin Trials Unit, Boston, MA 02114 USA. Massachusetts Gen Hosp, Dept Neurol, Memory Disorders Unit, Boston, MA 02114 USA. Massachusetts Gen Hosp, Ctr Human Genet Res, Boston, MA 02114 USA. RP Salat, DH (reprint author), Harvard Univ, Massachusetts Gen Hosp, Sch Med,Athinoula A Martinos Ctr Biomed Imaging, MIT,Dept Radiol,HMS, Bldg 149,13th St,Mail Code 149 2301, Charlestown, MA 02129 USA. EM salat@nmr.mgh.harvard.edu RI Smith, Eric/C-5443-2012; Gurol, Edip/J-2279-2014 OI Smith, Eric/0000-0003-3956-1668; Gurol, Edip/0000-0002-2169-4457 FU NCRR NIH HHS [P41RR14075]; NIA NIH HHS [K01 AG024898]; NIBIB NIH HHS [U54 EB005149]; NINDS NIH HHS [R01 NS041409] NR 25 TC 32 Z9 35 U1 1 U2 1 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0039-2499 J9 STROKE JI Stroke PD JUL PY 2006 VL 37 IS 7 BP 1759 EP 1764 DI 10.1161/01.STR.0000227328.86353.a7 PG 6 WC Clinical Neurology; Peripheral Vascular Disease SC Neurosciences & Neurology; Cardiovascular System & Cardiology GA 060HQ UT WOS:000238793700041 PM 16763176 ER PT J AU Wang, S Lee, SR Guo, SZ Kim, WJ Montaner, J Wang, XY Lo, EH AF Wang, Sophia Lee, Sun-Ryung Guo, Shu-Zhen Kim, Woo Jean Montaner, Joan Wang, Xiaoying Lo, Eng H. TI Reduction of tissue plasminogen activator-induced matrix metalloproteinase-9 by simvastatin in astrocytes SO STROKE LA English DT Article DE hemorrhage; stroke ID FOCAL CEREBRAL-ISCHEMIA; MATRIX-METALLOPROTEINASE; STROKE PROTECTION; THROMBOLYSIS; PROTEOLYSIS; SYNTHASE; STATINS; BRAIN; RAT; TPA AB Background and Purpose-Hemorrhagic conversion after tissue plasminogen activator (tPA) stroke therapy has been linked with elevations in matrix metalloproteinase-9 (MMP-9) at the neurovascular interface. Here, we test the idea that statins may directly ameliorate tPA-induced MMP-9 dysregulation. Methods-Recombinant human tPA (5 mu g/mL) was added to primary rat cortical astrocytes. Zymography was used to quantify MMP-9 levels in conditioned media. Effects of simvastatin or the Rho kinase inhibitor Y-27632 were assessed by pretreating cells before tPA exposure. Results-Sirrivastatin (1 to 10 mu mol/L) significantly reduced tPA-induced MMP-9 in cortical astrocytes. This effect may be mediated via the Rho kinase pathway because tPA-induced activation of Rho signaling was suppressed by simvastatin, and tPA-induced MMP-9 levels were similarly reduced by the Rho kinase inhibitor Y-27632 (I to 10 mu mol/L). Conclusions-Statins reduce tPA-induced MMP-9 dysregulation by inhibiting the Rho signaling pathway. Statins may ameliorate tPA-associated MMP imbalances in stroke. C1 Massachusetts Gen Hosp, Neuroprotect Res Lab, Dept Radiol, Boston, MA 02114 USA. Massachusetts Gen Hosp, Dept Neurol, Boston, MA 02114 USA. Harvard Univ, Sch Med, Program Neurosci, Boston, MA 02115 USA. Mt Sinai Sch Med, New York, NY USA. Valle Hebron Hosp, Barcelona, Spain. RP Lo, EH (reprint author), Neuroprotect Res Lab, MGH E 149-2401, Charlestown, MA 02129 USA. EM Lo@helix.mgh.harvard.edu RI Montaner, Joan/D-3063-2015; IBIS, NEUROVASCULAR/O-1855-2015 FU NINDS NIH HHS [P50-NS10828, R01-NS37074, R01-NS48422] NR 15 TC 43 Z9 45 U1 0 U2 6 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0039-2499 J9 STROKE JI Stroke PD JUL PY 2006 VL 37 IS 7 BP 1910 EP 1912 DI 10.1161/01.STR.0000226923.48905.39 PG 3 WC Clinical Neurology; Peripheral Vascular Disease SC Neurosciences & Neurology; Cardiovascular System & Cardiology GA 060HQ UT WOS:000238793700065 PM 16741180 ER PT J AU Fuchs, JR Nasseri, BA Vacanti, JP Fauza, DO AF Fuchs, Julie R. Nasseri, Boris A. Vacanti, Joseph P. Fauza, Dario O. TI Postnatal myocardial augmentation with skeletal myoblast-based fetal tissue engineering SO SURGERY LA English DT Article ID STEM-CELLS; CELLULAR CARDIOMYOPLASTY; CARDIAC-MUSCLE; MURINE HEART; TRANSPLANTATION; IMPLANTATION; REPAIR; CARDIOMYOCYTE; REGENERATION; PERFORMANCE AB Background. Cardiac anomalies constitute the most common birth defects, many of which involve variable myocardial deficiencies. Therapeutic options for structural myocardial repair remain limited in the neonatal population. This study was aimed at determining whether engineered fetal muscle constructs undergo milieu-dependent transdifferentiation after cardiac implantation, thus becoming a potential means to increase/support myocardial mass after birth. Methods. Myoblasts were isolated from skeletal muscle specimens harvested from fetal lambs, labeled by transduction with a retrovirus-expressing green fluorescent protein, expanded in vitro, and then seeded onto collagen hydrogels. After birth, animals underwent autologous implantation of the engineered constructs (n = 8) onto the myocardium as an onlay patch. Between 4 and 30 weeks postoperatively, implants were harvested for multiple analyses. Results. Fetal and postnatal survival rates were 89% and 100%, respectively. Labeled cells were identified within the implants at all time points by immunohistochemical staining for green fluorescent protein. At 24 and 30 weeks postimplantation, donor cells double-stained for green fluorescent protein and Troponin I, while losing skeletal (type II) myosin expression. Conclusions. Fetal skeletal myoblasts engraft in native myocardium up to 30 weeks after postnatal, autologous implantation as components of engineered onlay patches. These cells also display evidence of time-dependent transdifferentiation toward a cardiomyocyte-like lineage. Further analysis of fetal skeletal myoblast-based constructs for the repair of congenital myocardial defects is warranted. C1 Childrens Hosp Boston, Dept Surg, Boston, MA 02115 USA. Harvard Univ, Ctr Minimally Invas Surg, Cambridge, MA 02138 USA. Massachusetts Gen Hosp, Ctr Integrat Med & Innovat Technol, Boston, MA 02114 USA. RP Fauza, DO (reprint author), Childrens Hosp Boston, Dept Surg, Fegan 3,300 Longwood Ave, Boston, MA 02115 USA. EM dario.fauza@childrens.harvard.edu NR 30 TC 13 Z9 16 U1 1 U2 4 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 JUL PY 2006 VL 140 IS 1 BP 100 EP 107 DI 10.1016/j.surg.2006.01.016 PG 8 WC Surgery SC Surgery GA 068GW UT WOS:000239362100015 PM 16857447 ER PT J AU Stephen, AE Hodin, RA AF Stephen, Antonia E. Hodin, Richard A. TI Neuroendocrine tumors of the pancreas, excluding gastrinoma SO SURGICAL ONCOLOGY CLINICS OF NORTH AMERICA LA English DT Article ID ISLET-CELL TUMORS; PREOPERATIVE LOCALIZATION; LIVER-TRANSPLANTATION; GLUCAGONOMA SYNDROME; CLINICAL-FEATURES; INSULINOMAS; DIAGNOSIS; MANAGEMENT; SOMATOSTATINOMAS; SYMPTOMS AB Neuroendocrine tumors of the pancreas comprise a unique and relatively rare group of tumors, of which gastrinoma and insulinoma are the most common types. Insulinomas tend to be small, solitary and benign, with surgical resection curable in most cases. The remainder of the neuroendocrine tumors are usually large, and unlikely to be cured with surgery; their slow-growing nature, however, mandates aggressive surgical therapy, even in cases where metastatic disease is present. Somatostatin analogs, such as octreotide, are used to control the symptoms of hormone secretion; they are generally less effective in patients with insulinoma than in those with the other neuroendocrine tumors. Streptozocin, 5-fluorouracil, and doxorubicin are the most widely used chemotherapeutic agents in metastatic neuroendocrine tumors; their efficacy is limited, and significant side effects limit their use. Finally, liver transplantation in very select patients may prolong survival and alleviate debilitating symptoms. C1 Massachusetts Gen Hosp, Dept Surg, Boston, MA 02114 USA. RP Stephen, AE (reprint author), Massachusetts Gen Hosp, Dept Surg, 55 Fruit St, Boston, MA 02114 USA. EM astephen@partners.org NR 42 TC 18 Z9 19 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 1055-3207 EI 1558-5042 J9 SURG ONCOL CLIN N AM JI Surg. Oncol. Clin. N. Am. PD JUL PY 2006 VL 15 IS 3 BP 497 EP + DI 10.1016/j.soc.2006.05.012 PG 16 WC Oncology; Surgery SC Oncology; Surgery GA 101RL UT WOS:000241758000005 PM 16882494 ER PT J AU Haddad, S Chen, CA Santangelo, SL Seddon, JM AF Haddad, Stephen Chen, Clara A. Santangelo, Susan L. Seddon, Johanna M. TI The genetics of age-related macular degeneration: A review of progress to date SO SURVEY OF OPHTHALMOLOGY LA English DT Review DE age-related macular degeneration (AMD); age-related maculopathy (ARM); genetics; heritability; linkage; macula; retina ID COMPLEMENT FACTOR-H; BEAVER DAM EYE; APOLIPOPROTEIN-E GENE; C-REACTIVE PROTEIN; STARGARDT-DISEASE GENE; NONFAMILIAL JAPANESE PATIENTS; DIETARY-FAT; ALLELIC VARIATION; CANDIDATE GENE; CHOROIDAL NEOVASCULARIZATION AB Age-related macular degeneration (AMD) is the leading cause of vision loss and blindness among older adults in the USA and throughout the developed world. Etiological research suggests that AMD is a complex disease, caused by the actions and interactions of multiple genes and environmental factors. Familial aggregation studies, twin studies, and segregation analyses have provided strong evidence for the heritability of AMD, and linkage and association studies have been conducted to localize the disease-causing genes. Whole genome linkage scans have implicated nearly every chromosome in the human genome, with the most replicated signals residing on 1q25-31 and 10q26. Association studies have identified a major risk variant within the complement factor H gene (CFH), and recent reports suggest that PLEKHA1/LOC387715 and the BF/C2 regions may be major risk loci for AMD as well. Several other genes have had at least one positive association finding and deserve further exploration. Among these, apolipoprotein E (APOE) may be a minor risk locus. Additional genes will likely be identified, and future studies should explore the potential interactions of these genes with other genes as well as environmental factors. C1 Massachusetts Eye & Ear Infirm, Epidemiol Unit, Boston, MA 02114 USA. Massachusetts Eye & Ear Infirm, Psychiat & Neurodev Genet Unit, Boston, MA 02114 USA. Harvard Univ, Sch Med, Dept Psychiat, Boston, MA 02115 USA. Harvard Univ, Sch Med, Dept Ophthalmol, Boston, MA 02115 USA. Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA. RP Seddon, JM (reprint author), Massachusetts Eye & Ear Infirm, Epidemiol Unit, 243 Charles St, Boston, MA 02114 USA. EM Johanna_Seddon@meei.harvard.edu NR 138 TC 176 Z9 181 U1 1 U2 8 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0039-6257 J9 SURV OPHTHALMOL JI Surv. Ophthalmol. PD JUL-AUG PY 2006 VL 51 IS 4 BP 316 EP 363 DI 10.1016/j.survophthal.2006.05.001 PG 48 WC Ophthalmology SC Ophthalmology GA 068HN UT WOS:000239364100003 PM 16818082 ER PT J AU Norris, MM Aksan, A Sugimachi, K Toner, M AF Norris, Marlaina M. Aksan, Alptekin Sugimachi, Keishi Toner, Mehmet TI 3-O-methyl-D-glucose improves desiccation tolerance of keratinocytes SO TISSUE ENGINEERING LA English DT Article ID MAMMALIAN-CELLS; TREHALOSE; ANHYDROBIOSIS; PRESERVATION; EXPRESSION; MEMBRANES; EXPOSURE; GROWTH AB Transplantation of autologous skin grafts and tissue engineered skin replacements for the treatment of burns, trauma, and ulcerative wounds has been shown to restore a protective barrier to infection and fluid loss, reduce heat loss, provide mechanical strength, diminish pain, and dampen the hypermetabolic stress response to thermal injury. Patencies of these grafts depend mainly on the high viability and sustained function of the enmeshed keratinocytes. With growing demand in tissue replacement therapies, development of successful and economical preservation techniques for skin grafts and replacements becomes essential. In this regard, if attained, desiccated state storage offers an economical solution to availability, storage, and transportation problems. Recent studies indicate that carbohydrates are very efficient in stabilizing mammalian cells against various types of stresses, including those associated with cryopreservation and desiccation. In this study we introduce the use of 3-O-methyl-D-glucose (3-OMG), a nonmetabolizable glucose derivative, as a new means of providing protection for keratinocytes undergoing desiccation. We show that with decreasing water contents, viability of the cells decreases; however, at the same water content the immediate post-rehydration viability and long-term survival of the cells exposed to 3-OMG are much higher than those of controls. C1 Shriners Hosp Children, Boston, MA 02114 USA. Harvard Univ, Sch Med, Massachusetts Gen Hosp, Surg Serv, Boston, MA 02115 USA. Harvard Univ, Sch Med, Massachusetts Gen Hosp, Ctr Engn Med, Boston, MA 02115 USA. RP Toner, M (reprint author), Shriners Hosp Children, 51 Blossom St, Boston, MA 02114 USA. EM mtoner@hms.harvard.edu RI Aksan, Alptekin/A-7187-2008; Aksan, Alptekin/C-1579-2014 OI Aksan, Alptekin/0000-0001-9891-1715 FU NIBIB NIH HHS [EB022340] NR 26 TC 3 Z9 3 U1 0 U2 2 PU MARY ANN LIEBERT INC PI NEW ROCHELLE PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA SN 1076-3279 J9 TISSUE ENG JI Tissue Eng. PD JUL PY 2006 VL 12 IS 7 BP 1873 EP 1879 DI 10.1089/ten.2006.12.1873 PG 7 WC Cell & Tissue Engineering SC Cell Biology GA 071BK UT WOS:000239571800015 PM 16889517 ER PT J AU Manjunath, N Kumar, P Lee, SK Shankar, P AF Manjunath, N. Kumar, Priti Lee, Sang Kyung Shankar, Premlata TI Interfering antiviral immunity: application, subversion, hope? SO TRENDS IN IMMUNOLOGY LA English DT Review ID IMMUNODEFICIENCY-VIRUS TYPE-1; DOUBLE-STRANDED-RNA; PRIMARY HEMATOPOIETIC-CELLS; LENTIVIRAL VECTOR DELIVERY; GENE-EXPRESSION; IN-VIVO; MAMMALIAN-CELLS; T-CELLS; MEDIATED DELIVERY; HIV-1 INFECTION AB RNA interference (RNAi), initially recognized as a natural antiviral mechanism in plants, has rapidly emerged as an invaluable tool to suppress gene expression in a sequence-specific manner in all organisms, including mammals. Its potential to inhibit the replication of a variety of viruses has been demonstrated in vitro and in vivo in mouse and monkey models. These results have generated profound interest in the use of this technology as a potential treatment strategy for viral infections for which vaccines and drugs are unavailable or inadequate. In this review, we discuss the progress made within the past 2-3 years towards harnessing the potential of RNAi for clinical application in viral infections and the hurdles that have yet to be overcome. C1 Harvard Univ, Sch Med, CBR Inst Biomed Res, Boston, MA 02115 USA. Harvard Univ, Sch Med, Dept Pediat, Boston, MA 02115 USA. Hanyang Univ, Dept Bioengn, Seoul 133791, South Korea. RP Shankar, P (reprint author), Harvard Univ, Sch Med, CBR Inst Biomed Res, Boston, MA 02115 USA. EM shankar@cbr.rned.harvard.edu RI Kumar, Priti/C-5699-2009 FU NIAID NIH HHS [U19 AI 056900] NR 73 TC 17 Z9 18 U1 0 U2 1 PU ELSEVIER SCI LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND SN 1471-4906 J9 TRENDS IMMUNOL JI Trends Immunol. PD JUL PY 2006 VL 27 IS 7 BP 328 EP 335 DI 10.1016/j.it.2006.05.006 PG 8 WC Immunology SC Immunology GA 068JI UT WOS:000239369400006 PM 16753342 ER PT J AU Jones, R Capen, D Jacobson, M AF Jones, Rosemary Capen, Diane Jacobson, Margaretha TI PDGF and microvessel wall remodeling in adult lung: Imaging PDGF-R beta and PDGF-BB molecules in progenitor smooth muscle cells developing in pulmonary hypertension SO ULTRASTRUCTURAL PATHOLOGY LA English DT Article DE adult pulmonary hypertension; PDGF-BB; PDGF-R beta; progenitor smooth muscle cells ID ENDOTHELIAL GROWTH-FACTOR; ALVEOLAR MACROPHAGES; MURAL CELLS; HYPEROXIA; RECEPTOR; PROLIFERATION; RECRUITMENT; EXPRESSION; EXPOSURE; ALPHA AB Smooth muscle cells are relatively rare cells in the microvessels of the normal adult lung but develop in high numbers in the clinical pulmonary hypertensions (PHs). Understanding this cellular response has profound implications for determining the pathogenesis of PH, and for the development of therapeutic strategies, yet little is known of the angiogenic molecules responsible. The authors have previously shown that interstitial fibroblasts, and intermediate cells, are the progenitors of smooth muscle cells developing in adult lung microvessels in an in vivo model of experimental PH. The present study evaluates PDGF-R beta/PDGF-BB, an important angiogenic signaling pathway, using antibodies linked to protein A-gold (pA-AU) and quantitative high-resolution imaging techniques to detect expression by these cells. Each progenitor cell type in the control lung expressed PDGF-R beta and PDGF-BB. In the hypertensive lung, PDGF-R beta was highly expressed by fibroblasts developing as perivascular cells, the mean number of pA-AU labeled antigenic sites per cell profile, and their density (mu m(-2)), increasing with time: in intermediate cells the mean number of sites per cell profile, although not their density (mu m(-2)), also increased with time but less so than in the fibroblasts. In clear contrast to the RTK, constitutive expression levels of PDGF-BB were low in each progenitor cell type and remained restricted in the hypertensive lung. C1 Harvard Univ, Sch Med, Dept Anesthesia & Crit Care, Boston, MA 02129 USA. Massachusetts Gen Hosp, Dept Anesthesia & Crit Care, Boston, MA 02114 USA. RP Jones, R (reprint author), Harvard Univ, Sch Med, Dept Anesthesia & Crit Care, MGH East,Bldg 149,13th St, Charlestown, MA 02129 USA. EM jones@etherdome.mgh.harvard.edu FU NHLBI NIH HHS [5R01HL070866] NR 46 TC 17 Z9 17 U1 0 U2 2 PU TAYLOR & FRANCIS INC PI PHILADELPHIA PA 325 CHESTNUT ST, SUITE 800, PHILADELPHIA, PA 19106 USA SN 0191-3123 J9 ULTRASTRUCT PATHOL JI Ultrastruct. Pathol. PD JUL-AUG PY 2006 VL 30 IS 4 BP 267 EP 281 DI 10.1080/01913120600820336 PG 15 WC Microscopy; Pathology SC Microscopy; Pathology GA 083XD UT WOS:000240490600005 PM 16971352 ER PT J AU Cai, GP Sidhu, GS Wieczorek, R Gu, X Herrera, GA Cubukcu-Dimopulo, O Kahn, T AF Cai, Guoping Sidhu, Gurdip S. Wieczorek, Rosemary Gu, Xin Herrera, Guillermo A. Cubukcu-Dimopulo, Olcay Kahn, Thomas TI Plasma cell dyscrasia with kappa light-chain crystals in proximal tubular cells: A histological, immunofluorescent, and ultrastructural study SO ULTRASTRUCTURAL PATHOLOGY LA English DT Article DE crystal; immunoelectron microscopy; kappa light-chain; plasma cell dyscrasia; proximal tubulopathy; ultrastructure ID FANCONIS-SYNDROME; IMMUNOELECTRON MICROSCOPY; CYTOPLASMIC CRYSTALS; RENAL-DISEASE; MYELOMA; DEPOSITION AB This is a case report of a 56-year-old man with plasma cell dyscrasia who presented with proximal tubulopathy manifested as kappa light-chain crystal deposition in the proximal convoluted tubular cells. This was associated with mild cellular damage. The crystals were seen as negative images with the hematoxylin-eosin and periodic acid-Schiff (PAS) stains. They were identified as kappa light-chains by immunofluorescent imaging and confirmed by immunoelectron microscopy. Ultrastructurally, the crystals appear to be located within lysosomes. No deposits of light-chains were seen elsewhere in the kidney biopsy. C1 NY Harbor Healthcare Syst, Dept Pathol, New York, NY 10010 USA. NYU, Med Ctr, Dept Pathol, New York, NY 10016 USA. Louisiana State Univ, Ctr Hlth Sci, Dept Pathol, Shreveport, LA 71105 USA. Bronx Vet Adm Med Ctr, Dept Pathol, New York, NY USA. Bronx Vet Adm Med Ctr, Dept Med, New York, NY USA. RP Sidhu, GS (reprint author), NY Harbor Healthcare Syst, Dept Pathol, Manhattan Campus,423 East 23d St, New York, NY 10010 USA. EM deepsidhu@optonline.net NR 19 TC 12 Z9 13 U1 0 U2 0 PU TAYLOR & FRANCIS INC PI PHILADELPHIA PA 325 CHESTNUT ST, SUITE 800, PHILADELPHIA, PA 19106 USA SN 0191-3123 J9 ULTRASTRUCT PATHOL JI Ultrastruct. Pathol. PD JUL-AUG PY 2006 VL 30 IS 4 BP 315 EP 319 DI 10.1080/019131290945727 PG 5 WC Microscopy; Pathology SC Microscopy; Pathology GA 083XD UT WOS:000240490600010 PM 16971357 ER PT J AU Kim, M Gans, JD Nogueira, C Wang, A Paik, JH Feng, B Brennan, C Hahn, WC Cordon-Cardo, C Wagner, SN Flotte, TJ Duncan, LM Granter, SR Chin, L AF Kim, Minjung Gans, Joseph D. Nogueira, Cristina Wang, Audrey Paik, Ji-Hye Feng, Bin Brennan, Cameron Hahn, William C. Cordon-Cardo, Carlos Wagner, Stephan N. Flotte, Thomas J. Duncan, Lyn M. Granter, Scott R. Chin, Lynda TI Comparative oncogenomics identifies NEDD9 as a melanoma metastasis gene SO CELL LA English DT Article ID FOCAL-ADHESION KINASE; COMPARATIVE GENOMIC HYBRIDIZATION; OLIGONUCLEOTIDE MICROARRAY; MALIGNANT-MELANOMA; CANCER METASTASIS; DOCKING PROTEIN; CELL-MIGRATION; HEF1; LUNG; TRANSFORMATION AB Genomes of human cancer cells are characterized by numerous chromosomal aberrations of uncertain pathogenetic significance. Here, in an inducible mouse model of melanoma, we characterized metastatic variants with an acquired focal chromosomal amplification that corresponds to a much larger amplification in human metastatic melanomas. Further analyses identified Nedd9, an adaptor protein related to p130CAS, as the only gene within the minimal common region that exhibited amplification-associated overexpression. A series of functional, biochemical, and clinical studies established NEDD9 as a bona fide melanoma metastasis gene. NEDD9 enhanced invasion in vitro and metastasis in vivo of both normal and transformed melanocytes, functionally interacted with focal adhesion kinase and modulated focal contact formation, and exhibited frequent robust overexpression in human metastatic melanoma relative to primary melanoma. Thus, comparative oncogenomics has enabled the identification and facilitated the validation of a highly relevant cancer gene governing metastatic potential in human melanoma. C1 Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02115 USA. Univ Porto, Inst Mol Pathol & Immunol, Fac Med, P-4100 Oporto, Portugal. Dana Farber Canc Inst, Ctr Appl Canc Sci, Boston, MA 02115 USA. Mem Sloan Kettering Canc Ctr, Dept Surg, New York, NY 10021 USA. Mem Sloan Kettering Canc Ctr, Dept Pathol, New York, NY 10021 USA. MIT, Cambridge, MA 02142 USA. Harvard Univ, Broad Inst, Cambridge, MA 02142 USA. Austrian Acad Sci, Ctr Mol Med, A-1090 Vienna, Austria. Med Univ Vienna, Dept Dermatol, DIAID, A-1090 Vienna, Austria. Harvard Univ, Sch Med, Massachusetts Gen Hosp, Dept Pathol,Dermatopathol Unit, Boston, MA 02114 USA. Brigham & Womens Hosp, Dept Pathol, Boston, MA 02115 USA. Harvard Univ, Sch Med, Dept Dermatol, Boston, MA 02115 USA. RP Kim, M (reprint author), Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02115 USA. EM lynda_chin@dfci.harvard.edu RI Nogueira, Cristina/N-4574-2015; OI Nogueira, Cristina/0000-0002-0853-5304; Brennan, Cameron/0000-0003-4064-8891; Wagner, Stephan/0000-0003-4941-7029 FU NCI NIH HHS [P50 CA093683, P50 CA112962, P50 CA93683, R01 CA93947, U01 CA105423, U01 CA84313] NR 44 TC 262 Z9 271 U1 0 U2 10 PU CELL PRESS PI CAMBRIDGE PA 1100 MASSACHUSETTS AVE, CAMBRIDGE, MA 02138 USA SN 0092-8674 J9 CELL JI Cell PD JUN 30 PY 2006 VL 125 IS 7 BP 1269 EP 1281 DI 10.1016/j.cell.2006.06.008 PG 13 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA 064QP UT WOS:000239104500011 PM 16814714 ER PT J AU Walz, C Crowley, BJ Hudon, HE Gramlich, JL Neuberg, DS Podar, K Griffin, JD Sattler, M AF Walz, C Crowley, BJ Hudon, HE Gramlich, JL Neuberg, DS Podar, K Griffin, JD Sattler, M TI Activated Jak2 with the V617F point mutation promotes G(1)/S phase transition SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID TYROSINE KINASE JAK2; CELL-CYCLE ARREST; POLYCYTHEMIA-VERA; MYELOPROLIFERATIVE-DISORDERS; ERYTHROPOIETIN RECEPTOR; MYELOID-LEUKEMIA; N-ACETYLCYSTEINE; G1 PHASE; GROWTH; STAT5 AB Hematopoietic stem cells in myeloproliferative diseases mostly retain the potential to differentiate but are characterized by hyper-responsiveness to growth factors, as well as partial factor-independent growth. The V617F activating point mutation in Jak2 has recently been associated with myeloproliferative disorders. Using various cell line models, mechanisms that contribute to Jak2V617-mediated signaling were investigated. Treatment of the Jak2V617F mutant-expressing erythroid leukemia cell line HEL with a small molecule Jak2 inhibitor was associated with a dose-dependent G(1) cell cycle arrest. This inhibition correlated with decreased expression of cyclin D2 and increased expression of the cell cycle inhibitor p27(Kip). Inhibition of Jak2V617F with a Jak2-targeted small interfering RNA approach resulted in a similar phenotype. Mechanisms leading to altered p27(Kip) and cyclin D2 likely involve inhibition of STAT5, a major target of Jak2 in hematopoietic cells, because a constitutively active form of STAT5 reduced p27(Kip) and increased cyclin D2 expression. Jak2V617F and constitutively active STAT5 also induced high levels of reactive oxygen species, which are sufficient to promote G(1)/S phase transition. In contrast, treatment of HEL cells with the antioxidant N-acetylcysteine decreased cell growth or expression of cyclin D2 and increased expression of p27(Kip). Similar results were obtained in BaF3 cells transfected with Jak2V617F, but these cells required coexpression of the erythropoietin receptor for optimal signaling. These results suggest that regulation of cyclin D2 and p27(Kip) in combination with redox-dependent processes promotes G(1)/S phase transition downstream of Jak2V617F/STAT5 and therefore hint at potential novel targets for drug development that may aid traditional therapy. C1 Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02115 USA. Dana Farber Canc Inst, Dept Biostat & Computat Biol, Boston, MA 02115 USA. Brigham & Womens Hosp, Dept Med, Boston, MA 02115 USA. Harvard Univ, Sch Med, Boston, MA 02115 USA. RP Sattler, M (reprint author), Dana Farber Canc Inst, Dept Med Oncol, 44 Binney St, Boston, MA 02115 USA. EM martin_sattler@dfci.harvard.edu FU NIDDK NIH HHS [DK 66996] NR 42 TC 65 Z9 70 U1 0 U2 3 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD JUN 30 PY 2006 VL 281 IS 26 BP 18177 EP 18183 DI 10.1074/jbc.M600064200 PG 7 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA 055ZO UT WOS:000238490300069 PM 16632470 ER PT J AU Sekine, K Revzin, A Tompkins, RG Toner, M AF Sekine, Kazuhiko Revzin, Alexander Tompkins, Ronald G. Toner, Mehmet TI Panning of multiple subsets of leukocytes on antibody-decorated poly(ethylene) glycol-coated glass slides SO JOURNAL OF IMMUNOLOGICAL METHODS LA English DT Article DE CD4 T-cells; CD8 T-cells; monocytes; neutrophils; antibody; array ID LASER CAPTURE MICRODISSECTION; PERIPHERAL-BLOOD; DENDRITIC CELLS; CD14(+) MONOCYTES; LYMPHOCYTES; SEPARATION; SURFACE; CD4(+); CANCER; PHOTOLITHOGRAPHY AB The antibody (Ab) array format provides a unique opportunity to pan and characterize multiple leukocyte subsets in parallel. However, the questions of reproducibility and robustness of leukocyte panning on Ab arrays need to be answered for this technology to become an immunophenotyping tool. The present study sought to address several of these questions, including: (1) purity of leukocyte subsets captured on Ab regions, (2) dynamics of leukocyte binding, (3) elimination of non-specific cell adhesion, and (4) standardization of cell washing conditions. Abs for CD4 T-cells, CD8 T-cells, CD36 monocytes, and CD16b neutrophils were dispensed onto standard glass slides containing a thin film of poly(ethylene glycol) (PEG) hydrogel. PEG gel coating was highly effective in eliminated non-specific cell adhesion on the surface. Incubation of the Ab arrays with red blood cell (RBC) depleted whole blood resulting in antigen-specific panning of leukocyte subsets on the respective Ab domains. A flow through chamber was employed to determine optimal shear stress conditions for removal of non-specifically attached cells. The purity of the four subsets remaining on the surface after washing was determined by Wright staining and immunofluorescence, and was found to be as follows: CD4 T-cells (99.2 +/- 0.3%), CD8 T-cells (98.7 +/- 0.3%), CD36 monocytes (97.2 0.9%), and CD16b neutrophils (99.1 +/- 0.6%). In conclusion, the methods described in this study allow to separate whole blood into pure leukocyte subsets with minimal sample preparation and handling. These approaches will be valuable in the future development of Ab arrays as tools for quantitative immunophenotyping of leukocytes. (c) 2006 Elsevier B.V All rights reserved. C1 Shriners Hosp Children, Boston, MA 02114 USA. Harvard Univ, Massachusetts Gen Hosp, Sch Med, Ctr Engn Med, Boston, MA 02114 USA. Harvard Univ, Massachusetts Gen Hosp, Sch Med, Surg Serv, Boston, MA 02114 USA. Univ Calif Davis, Dept Biomed Engn, Davis, CA 95616 USA. RP Toner, M (reprint author), Shriners Hosp Children, 51 Blossom St, Boston, MA 02114 USA. EM mtoner@hms.harvard.edu RI Sekine, Kazuhiko/I-5835-2012 FU NIBIB NIH HHS [P41 EB002503] NR 31 TC 31 Z9 32 U1 1 U2 8 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 JUN 30 PY 2006 VL 313 IS 1-2 BP 96 EP 109 DI 10.1016/j.jim.2006.03.017 PG 14 WC Biochemical Research Methods; Immunology SC Biochemistry & Molecular Biology; Immunology GA 067HM UT WOS:000239292500010 PM 16822521 ER PT J AU Pettersen, KH Devor, A Ulbert, I Dale, AM Einevoll, GT AF Pettersen, KH Devor, A Ulbert, I Dale, AM Einevoll, GT TI Current-source density estimation based on inversion of electrostatic forward solution: Effects of finite extent of neuronal activity and conductivity discontinuities SO JOURNAL OF NEUROSCIENCE METHODS LA English DT Article DE local field potentials; current-source density; CSD; multielectrode; laminar electrode; barrel cortex ID FIELD POTENTIALS; SOMATOSENSORY CORTEX; ANURAN CEREBELLUM; CEREBRAL-CORTEX; VISUAL-CORTEX; RAT; ORGANIZATION; ACTIVATION; ENSEMBLES AB A new method for estimation of current-source density (CSD) from local field potentials is presented. This inverse CSD (iCSD) method is based on explicit inversion of the electrostatic forward solution and can be applied to data from multielectrode arrays with various geometries. Here, the method is applied to linear-array (laminar) electrode data. Three iCSD methods are considered: the CSD is assumed to have cylindrical symmetry and be (i) localized in infinitely thin discs, (ii) step-wise constant or (iii) continuous and smoothly varying (using cubic splines) in the vertical direction. For spatially confined CSD distributions the standard CSD method, involving a discrete double derivative, is seen in model calculations to give significant estimation errors when the lateral source dimension is comparable to the size of a cortical column (less than similar to 1 mm). Further, discontinuities in the extracellular conductivity are seen to potentially give sizable errors for even wider source distributions. The iCSD methods are seen to give excellent estimates when the correct lateral source dimension and spatial distribution of conductivity are incorporated. To illustrate the application to real data, iCSD estimates of stimulus-evoked responses measured with laminar electrodes in the rat somatosensory (barrel) cortex are compared to estimates from the standard CSD method. (c) 2006 Elsevier B.V. All rights reserved. C1 Norwegian Univ Life Sci, Dept Math Sci & Technol, N-1432 As, Norway. Massachusetts Gen Hosp, Athinoula A Martinos Ctr, Charlestown, MA 02129 USA. Univ Calif San Diego, Dept Radiol & Neurosci, La Jolla, CA 92093 USA. Hungarian Acad Sci, Inst Psychol, Budapest, Hungary. RP Einevoll, GT (reprint author), Norwegian Univ Life Sci, Dept Math Sci & Technol, POB 5003, N-1432 As, Norway. EM Gaute.Einevoll@umb.no RI Ulbert, Istvan/F-2213-2010; Dale, Anders/A-5180-2010 FU NIBIB NIH HHS [R01 EB000790, R01 EB00790]; NINDS NIH HHS [NS18741] NR 28 TC 89 Z9 89 U1 0 U2 5 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0165-0270 J9 J NEUROSCI METH JI J. Neurosci. Methods PD JUN 30 PY 2006 VL 154 IS 1-2 BP 116 EP 133 DI 10.1016/j.jneumeth.2005.12.005 PG 18 WC Biochemical Research Methods; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA 059LE UT WOS:000238733500014 PM 16436298 ER PT J AU Wolden-Hanson, T AF Wolden-Hanson, Tami TI Mechanisms of the anorexia of aging in the Brown Norway rat SO PHYSIOLOGY & BEHAVIOR LA English DT Article; Proceedings Paper CT Annual Meeting of the Society-for-the-Study-of-Ingestive-Behavior CY JUL 12-17, 2005 CL Pittsburgh, PA SP Soc Study Ingestive Behavior DE anorexia of aging; rat; aging; leptin; ghrelin; insulin; testosterone; neuropeptides; senescence; food intake; fasting ID HYPOTHALAMIC NEUROPEPTIDE-Y; AGOUTI-RELATED PROTEIN; REDUCED FEEDING RESPONSE; AGE-ASSOCIATED CHANGES; NPY GENE-EXPRESSION; BODY-COMPOSITION; ARCUATE NUCLEUS; FOOD-INTAKE; ENERGY HOMEOSTASIS; PARAVENTRICULAR NUCLEUS AB Aging is associated with a loss of the ability to maintain homeostasis in response to physiologic and environmental disturbances. Age-related dysregulation of food intake and energy balance appears to be the result of impaired responsiveness of hypothalamic integrative circuitry to metabolic cues, which can lead to lack of appropriate food intake (the anorexia of aging) and thus to inappropriate weight loss in response to acute or chronic illness or other stressors. Using the Brown Norway (BN) male rat model, we have shown that old animals fail to appropriately increase food intake after the metabolic challenge of a 72 h fast, resulting in the failure to re-gain lost body weight upon refeeding. Leptin levels increase with adiposity and age, and remain elevated above levels of young animals even after a 72 h fast, suggesting that hyperleptinemia may be influencing the energy balance dysregulation. It is unclear whether this age-related response is due to a failure of the network of hypothalamic neurons to appropriately integrate hormonal and neural inputs, or due to a failure of the neurons to produce the appropriate neuropeptides. We hypothesize that sequential, age-related alterations in the expression patterns of neuropeptides that maintain melanocortinergic tone, and in the hormone mediators that inform the system of the state of energy balance, result in a diminished ability to maintain energy homeostasis with increasing age. We have undertaken a number of interventional approaches to test this hypothesis, including manipulations of the hormones ghrelin, insulin and testosterone, and direct application of neuropeptides to the central nervous system in these animals. Published by Elsevier Inc. C1 VA Puget Sound Hlth Care Syst, Ctr Geriatr Res Educ & Clin, Seattle, WA 98108 USA. Univ Washington, Dept Med, Div Gerontol & Geriatr Med, Seattle, WA 98108 USA. RP Wolden-Hanson, T (reprint author), VA Puget Sound Hlth Care Syst, Ctr Geriatr Res Educ & Clin, S-182-GRECC,1660 S Columbian Way, Seattle, WA 98108 USA. EM twh@u.washington.edu NR 88 TC 27 Z9 27 U1 2 U2 2 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND SN 0031-9384 J9 PHYSIOL BEHAV JI Physiol. Behav. PD JUN 30 PY 2006 VL 88 IS 3 BP 267 EP 276 DI 10.1016/j.physbeh.2006.05.032 PG 10 WC Psychology, Biological; Behavioral Sciences SC Psychology; Behavioral Sciences GA 061JU UT WOS:000238868900008 PM 16781740 ER PT J AU Rubin, RT Miller, TH Rhodes, ME Czambel, RK AF Rubin, RT Miller, TH Rhodes, ME Czambel, RK TI Adrenal cortical responses to low- and high-dose ACTH(1-24) administration in major depressives vs. matched controls SO PSYCHIATRY RESEARCH LA English DT Article DE hypothalamo-pituitary-adrenocortical axis; cortisol; major depressive disorder ID DEXAMETHASONE SUPPRESSION TEST; ACTH STIMULATION TEST; GLAND VOLUME; ADRENOCORTICAL SENSITIVITY; HEALTHY-VOLUNTEERS; PITUITARY; CORTISOL; CORTICOTROPIN; WEIGHT; SUICIDE AB Increased hypothalamo-pituitary-adrenocortical (HPA) axis activity occurs in 30-50% of patients with major depression. This includes normal-to-increased adrenal cortical hormone (cortisol) secretion in spite of reduced corticotropin (ACTH) stimulation. A possible explanation is increased adrenal responsiveness to ACTH. Supporting this possibility is the finding of increased adrenal volume, which reverts to normal with successful treatment. Eight female and six male patients with major depression, and eight female and six male individually matched controls, underwent two test sessions 5-7 days apart. On the first day, a low ACTH, 24 dose (0.014 mu g/kg i.v.), equivalent to 1 mu g in a 70-kg individual, was given. On the second day, a supramaximal stimulating dose (250 mu g i.v.) was given. Serial blood samples were analyzed for immunoreactive (IR-)ACTH, ACTH(1-39), and cortisol. There were no significant sex or patient-control differences in IR-ACTH areas under the curve (AUCs) following low-dose ACTH(1-24), and the correlation between patient and matched control AUCs was +0.71, indicating good correspondence in the amount of circulating ACTH(1-24) available for adrenal stimulation. There were no significant sex or patient-control differences in cortisol response and no significant interaction between dose and subject group, indicating that patients did not differ from controls in their cortisol responses to either low- or high-dose ACTH(1-24). These findings do not indicate increased adrenal cortical responsiveness in patients with major depression. Neurochemical/neurohormonal and neural stimulatory factors other than ACTH might be responsible for the increased adrenal gland size and cortisol secretion, in spite of reduced pituitary ACTH secretion, that has been reported in this illness. Published by Elsevier Ireland Ltd. C1 VA Greater Los Angeles Healthcare Syst, Dept Psychiat & Mental Hlth 116, Los Angeles, CA 90073 USA. Univ Calif Los Angeles, Dept Psychiat & Biobehav Sci, Los Angeles, CA 90024 USA. Drexel Univ, Coll Med, Neurosci Res Ctr, Pittsburgh, PA 15212 USA. RP Rubin, RT (reprint author), VA Greater Los Angeles Healthcare Syst, Dept Psychiat & Mental Hlth 116, 11301 Wilshire Blvd, Los Angeles, CA 90073 USA. EM robert.rubin@med.va.gov FU NIMH NIH HHS [MH28380] NR 42 TC 12 Z9 12 U1 1 U2 1 PU ELSEVIER IRELAND LTD PI CLARE PA ELSEVIER HOUSE, BROOKVALE PLAZA, EAST PARK SHANNON, CO, CLARE, 00000, IRELAND SN 0165-1781 J9 PSYCHIAT RES JI Psychiatry Res. PD JUN 30 PY 2006 VL 143 IS 1 BP 43 EP 50 DI 10.1016/j.psychres.2005.10.003 PG 8 WC Psychiatry SC Psychiatry GA 059RD UT WOS:000238749000006 PM 16707164 ER PT J AU Denton, MD Digumarthy, SR Chua, S Colvin, RB Weisberg, AD Harris, NL Haupert, GT AF Denton, MD Digumarthy, SR Chua, S Colvin, RB Weisberg, AD Harris, NL Haupert, GT TI An 84-year-old man with staphylococcal bacteremia and renal failure - Henoch-Schonlein purpura associated with Staphylococcus aureus sepsis. Acute tubular necrosis. SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Editorial Material ID IGA NEPHROPATHY; SCHOENLEIN PURPURA; NEPHRITIS; GLOMERULONEPHRITIS; INFECTION; SUPERANTIGEN; ENDOCARDITIS; DEPOSITS; RECEPTOR; ADULTS C1 Derriford Hosp, Renal Unit, Plymouth PL6 8DH, Devon, England. Peninsula Med Sch, Dept Med, Plymouth, Devon, England. Massachusetts Gen Hosp, Dept Radiol, Boston, MA 02114 USA. Massachusetts Gen Hosp, Dept Cardiol, Boston, MA 02114 USA. Massachusetts Gen Hosp, Dept Pathol, Boston, MA 02114 USA. Harvard Univ, Sch Med, Dept Radiol, Boston, MA 02115 USA. Harvard Univ, Sch Med, Dept Med, Boston, MA 02115 USA. Harvard Univ, Sch Med, Dept Pathol, Boston, MA 02115 USA. RP Denton, MD (reprint author), Derriford Hosp, Renal Unit, Plymouth PL6 8DH, Devon, England. NR 23 TC 6 Z9 6 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 JUN 29 PY 2006 VL 354 IS 26 BP 2803 EP 2813 PG 11 WC Medicine, General & Internal SC General & Internal Medicine GA 057GQ UT WOS:000238584700010 PM 16807418 ER PT J AU Scadden, DT AF Scadden, DT TI The stem-cell niche as an entity of action SO NATURE LA English DT Article ID HEMATOPOIETIC STEM; BONE-MARROW; SELF-RENEWAL; DROSOPHILA OVARY; PROGENITOR CELLS; PERIPHERAL-BLOOD; VASCULAR NICHE; BETA-CATENIN; TENASCIN-C; GERM-CELLS AB Stem-cell populations are established in 'niches'-specific anatomic locations that regulate how they participate in tissue generation, maintenance and repair. The niche saves stem cells from depletion, while protecting the host from over-exuberant stem-cell proliferation. It constitutes a basic unit of tissue physiology, integrating signals that mediate the balanced response of stem cells to the needs of organisms. Yet the niche may also induce pathologies by imposing aberrant function on stem cells or other targets. The interplay between stem cells and their niche creates the dynamic system necessary for sustaining tissues, and for the ultimate design of stem-cell therapeutics. C1 Harvard Univ, Massachusetts Gen Hosp, Ctr Regenerat Med, Stem Cell Inst, Boston, MA 02114 USA. RP Scadden, DT (reprint author), Harvard Univ, Massachusetts Gen Hosp, Ctr Regenerat Med, Stem Cell Inst, 185 Cambridge St,CPZN-4265A, Boston, MA 02114 USA. EM scadden.david@mgh.harvard.edu NR 55 TC 962 Z9 1014 U1 4 U2 117 PU NATURE PUBLISHING GROUP PI LONDON PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND SN 0028-0836 J9 NATURE JI Nature PD JUN 28 PY 2006 VL 441 IS 7097 BP 1075 EP 1079 DI 10.1038/nature04957 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA 057SM UT WOS:000238615500034 PM 16810242 ER PT J AU Eggan, K Jurga, S Gosden, R Min, IM Wagers, AJ AF Eggan, K Jurga, S Gosden, R Min, IM Wagers, AJ TI Ovulated oocytes in adult mice derive from non-circulating germ cells SO NATURE LA English DT Article ID HEMATOPOIETIC STEM-CELLS; BONE-MARROW; FOLLICLE NUMBER; CYCLOPHOSPHAMIDE; OVARY; BLOOD AB Decades of research in reproductive biology have led to the generally accepted belief that in female mammals, all surviving germ cells enter meiosis at the end of fetal development and as a result, the postnatal ovary harbours a limited supply of oocytes that cannot be replenished or regenerated if lost to injury or disease. However, recent reports have challenged this view, suggesting instead that oocyte production is maintained through continual seeding of the ovary by circulating, bone-marrow-derived germ cells. To test directly the physiological relevance of circulating cells for female fertility, we established transplantation and parabiotic mouse models to assess the capacity of circulating bone marrow cells to generate ovulated oocytes, both in the steady state and after induced damage. Our studies showed no evidence that bone marrow cells, or any other normally circulating cells, contribute to the formation of mature, ovulated oocytes. Instead, cells that travelled to the ovary through the bloodstream exhibited properties characteristic of committed blood leukocytes. C1 Joslin Diabet Ctr, Sect Dev & Stem Cell Biol, Boston, MA 02215 USA. Harvard Univ, Stowers Med Inst, Harvard Stem Cell Inst, Cambridge, MA 02138 USA. Harvard Univ, Dept Mol & Cellular Biol, Cambridge, MA 02138 USA. Harvard Univ, Sch Med, Dept Pathol, Boston, MA 02215 USA. Cornell Univ, Weill Med Coll, Ctr Reprod Med & Infertil, New York, NY 10021 USA. RP Wagers, AJ (reprint author), Joslin Diabet Ctr, Sect Dev & Stem Cell Biol, Boston, MA 02215 USA. EM amy.wagers@joslin.harvard.edu NR 21 TC 154 Z9 163 U1 2 U2 16 PU NATURE PUBLISHING GROUP PI LONDON PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND SN 0028-0836 J9 NATURE JI Nature PD JUN 28 PY 2006 VL 441 IS 7097 BP 1109 EP 1114 DI 10.1038/nature04929 PG 6 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA 057SM UT WOS:000238615500041 PM 16799565 ER PT J AU Fox, CS Pencina, MJ Meigs, JB Vasan, RS Levitzky, YS D'Agostino, RB AF Fox, CS Pencina, MJ Meigs, JB Vasan, RS Levitzky, YS D'Agostino, RB TI Trends in the incidence of type 2 diabetes mellitus from the 1970s to the 1990s - The Framingham Heart Study SO CIRCULATION LA English DT Article DE diabetes mellitus; epidemiology; obesity; population; prevention ID BODY-MASS INDEX; US ADULTS; UNITED-STATES; INCREASING PREVALENCE; PHYSICAL-ACTIVITY; NATIONAL-HEALTH; RISK-FACTORS; WEIGHT-GAIN; OBESITY; WOMEN AB Background-Recent studies indicate that the prevalence of type 2 diabetes mellitus is increasing in the United States; less is known about trends in the incidence of type 2 diabetes mellitus. Methods and Results-Participants free of diabetes mellitus (n=3104; mean age 47 years; 1587 women) from the Framingham Offspring Study who attended a routine examination in the 1970s, 1980s, or 1990s were followed up for the 8-year incidence of diabetes mellitus. Diabetes was defined as a fasting plasma glucose >= 7.0 mmol/L or treatment with either insulin or a hypoglycemic agent. Pooled logistic regression was used to compare diabetes incidence across decades for participants between 40 and 55 years of age in each decade. The age-adjusted 8-year incidence rate of diabetes was 2.0%, 3.0%, and 3.7% among women and 2.7%, 3.6%, and 5.8% among men in the 1970s, 1980s, and 1990s, respectively. Compared with the 1970s, the age- and sex-adjusted odds ratio ( OR) for diabetes was 1.40 (95% confidence interval [CI], 0.89 to 2.22) in the 1980s and 2.05 ( 95% CI, 1.33 to 3.14) in the 1990s ( P for trend=0.0006). Among women, the OR was 1.50 ( 95% CI, 0.75 to 2.98) in the 1980s and 1.84 ( 95% CI, 0.95 to 3.55) in the 1990s ( P for trend=0.07) compared with the 1970s, whereas among men, the OR was 1.33 ( 95% CI, 0.72 to 2.47) in the 1980s and 2.21 ( 95% CI, 1.25 to 3.90) in the 1990s ( P for trend=0.003). Most of the increase in absolute incidence of diabetes occurred in individuals with body mass index >= 30 kg/m(2) ( P for trend=0.03). Conclusions-In the present community-based sample of middle-aged adults, we observed a doubling in the incidence of type 2 diabetes over the last 30 years. Careful surveillance of changes in diabetes incidence may be necessary if current trends of excess adiposity continue. C1 Framingham Heart Dis Epidemiol Study, Natl Heart & Lung Inst, Framingham, MA USA. Brigham & Womens Hosp, Dept Endocrinol Hypertens & Diabet, Boston, MA 02115 USA. Harvard Univ, Sch Med, Boston, MA 02115 USA. Boston Univ, Dept Math, Boston, MA 02215 USA. Massachusetts Gen Hosp, Div Gen Med, Boston, MA 02114 USA. Harvard Univ, Sch Med, Boston, MA 02115 USA. Boston Med Ctr, Div Cardiol, Boston, MA USA. NHLBI, Bethesda, MD 20892 USA. RP Fox, CS (reprint author), 73 Mt Wayte Ave,Suite 2, Framingham, MA 01702 USA. EM foxca@nhlbi.nih.gov OI Ramachandran, Vasan/0000-0001-7357-5970 FU NHLBI NIH HHS [2K24HL04334, N01-HC-25195] NR 32 TC 190 Z9 207 U1 1 U2 13 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0009-7322 J9 CIRCULATION JI Circulation PD JUN 27 PY 2006 VL 113 IS 25 BP 2914 EP 2918 DI 10.1161/CIRCULATIONAHA.106.613828 PG 5 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 057CG UT WOS:000238572100010 PM 16785337 ER PT J AU Lindsey, ML Escobar, P Mukherjee, R Goshorn, DK Sheats, NJ Bruce, JA Mains, IM Hendrick, JK Hewett, KW Gourdie, RG Matrisian, LM Spinale, FG AF Lindsey, ML Escobar, P Mukherjee, R Goshorn, DK Sheats, NJ Bruce, JA Mains, IM Hendrick, JK Hewett, KW Gourdie, RG Matrisian, LM Spinale, FG TI Matrix metalloproteinase-7 affects connexin-43 levels, electrical conduction, and survival after myocardial infarction SO CIRCULATION LA English DT Article DE infarction; leukocytes; metalloproteinases; myocardial infarction; remodeling ID SURFACE-PLASMON RESONANCE; HEART-FAILURE; GAP-JUNCTIONS; VENTRICULAR-TACHYCARDIA; IMPULSE PROPAGATION; BORDER ZONE; MATRILYSIN; MICE; MODEL; RAT AB Background-Matrix metalloproteinases ( MMPs) contribute to left ventricular remodeling after myocardial infarction (MI). Specific causative roles of particular MMPs, however, remain unclear. MMP-7 is abundant in cardiomyocytes and macrophages, but MMP-7 function after MI has not been defined. Methods and Results-Wild-type (WT; n=55) and MMP-7-null (MMP-7(-/-); n=32) mice underwent permanent coronary artery ligation for 7 days. MI sizes were similar, but survival was greatly improved in MMP-7(-/-) mice. The survival difference could not be attributed to differences in left ventricular dilation because end-diastolic volumes increased similarly. ECG analysis revealed a prolonged PR interval in WT but not in MMP-7(-/-) post-MI mice. Post-MI conduction velocity, determined by optically mapping electrical wavefront propagation, decreased to 78 +/- 6% of control for WT and was normalized in MMP-7(-/-) mice. In WT mice, slower conduction velocity correlated with a 53% reduction in the gap junction protein connexin-43. Direct binding of MMP-7 to connexin-43, determined by surface plasmon resonance technology, occurred in a dose-dependent manner. Connexin-43 processing by MMP-7 was confirmed by in silico and in vitro substrate analyses and MMP-7 infusion induced arrhythmias in vivo. Conclusions-MMP-7 deletion results in improved survival and myocardial conduction patterns after MI. This is the first report to implicate MMP-7 in post-MI remodeling and to demonstrate that connexin-43 is a novel MMP-7 substrate. C1 Univ Texas, Hlth Sci Ctr San Antonio, Dept Med, Div Cardiol, San Antonio, TX 78229 USA. Med Univ S Carolina, Div Cardiothorac Surg Res, Charleston, SC 29425 USA. Med Univ S Carolina, Dept Cell Biol & Anat, Charleston, SC 29425 USA. Vanderbilt Univ, Dept Canc Biol, Nashville, TN USA. Ralph H Johnson Vet Adm Med Ctr, Charleston, SC USA. RP Lindsey, ML (reprint author), Univ Texas, Hlth Sci Ctr San Antonio, Dept Med, Div Cardiol, 7703 Floyd Curl Dr,Mail Code 7872, San Antonio, TX 78229 USA. EM lindseym@uthscsa.edu RI Lindsey, Merry/B-2650-2012 FU NHLBI NIH HHS [HL-45024, HL-66029, HL-36059, HL-56728, HL-75360, HL-97012, R01 HL075360, HL-10337]; NICHD NIH HHS [HD-39946]; PHS HHS [P01-48788] NR 36 TC 76 Z9 81 U1 0 U2 5 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0009-7322 J9 CIRCULATION JI Circulation PD JUN 27 PY 2006 VL 113 IS 25 BP 2919 EP 2928 DI 10.1161/CIRCULATIONAHA.106.612960 PG 10 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 057CG UT WOS:000238572100011 PM 16769909 ER PT J AU Chin, PS Berg, AT Spencer, SS Lee, ML Shinnar, S Sperling, MR Langfitt, JT Walczak, TS Pacia, SV Bazil, CW Vassar, S Vickrey, BG AF Chin, PS Berg, AT Spencer, SS Lee, ML Shinnar, S Sperling, MR Langfitt, JT Walczak, TS Pacia, SV Bazil, CW Vassar, S Vickrey, BG TI Patient-perceived impact of resective epilepsy surgery SO NEUROLOGY LA English DT Article ID QUALITY-OF-LIFE; ANTERIOR TEMPORAL LOBECTOMY; TERM FOLLOW-UP; REFRACTORY EPILEPSY; SATISFACTION; MULTICENTER; OUTCOMES; ADJUSTMENT AB Objective: To evaluate the patient-perceived impact of resective epilepsy surgery, a key outcome to consider in evaluating such a highly invasive, elective procedure. Methods: Impact measures obtained from 396 patients in a multicenter cohort study of resective epilepsy surgery included (1) willingness to undergo surgery if that decision could be made again and (2) the overall impact of surgery on the patient's life. Predictors of impact were analyzed using multivariate ordinal logistic regression. Results: Of study participants, 73.8%, 77.4%, and 75.5% would definitely undergo surgery again and 78.2%, 80.2%, and 79.1% reported a very strong or strong positive overall impact of surgery at 3, 12, and 24 months. Multivariate ordinal logistic regression showed that seizure freedom predicted more positive perceptions at 3, 12, and 24 months (all p < 0.04). Becoming employed was uniquely associated with willingness to undergo surgery again and with overall impact at 24 months (all p < 0.05), but only a net 7% of the cohort improved their employment status. Right-sided resection (at 12 and 24 months, p < 0.005) and female gender ( at 3 and 12 months, p = 0.006) were each positively associated with perceived overall impact. Conclusions: Most epilepsy surgery patients report a positive overall impact of the procedure on their lives and a high willingness to undergo surgery again if that choice could be made. Seizure-free individuals express consistently more positive perceptions of the procedure. Findings suggest that it is important to make early efforts to reintegrate epilepsy surgery patients into employment. C1 Univ Calif Los Angeles, Robert Wood Johnson Clin Scholars Program, Dept Neurol, Los Angeles, CA USA. Univ Calif Los Angeles, Dept Med, Robert Wood Johnson Clin Scholars Program, Los Angeles, CA USA. Greater Los Angeles VA Hlth Care Syst, Los Angeles, CA USA. NIU, BIOS, De Kalb, IL USA. Yale Univ, Sch Med, Dept Neurol, New Haven, CT USA. Univ Calif Los Angeles, Sepulveda, CA USA. VA Med Ctr, HSR&D Field Program, Ctr Study Healthcare Provider Behav, Sepulveda, CA USA. Albert Einstein Coll Med, Montefiore Med Ctr, Dept Neurol, Bronx, NY 10467 USA. Albert Einstein Coll Med, Montefiore Med Ctr, Dept Pediat, Bronx, NY 10467 USA. Thomas Jefferson Univ, Sch Med, Dept Neurol, Philadelphia, PA 19107 USA. Univ Rochester, Dept Neurol, Rochester, NY USA. Minnesota Comprehens Epilepsy Program, Minneapolis, MN USA. NYU, Dept Neurol, New York, NY USA. Columbia Univ, Sch Med, Dept Neurol, New York, NY USA. Greater Los Angeles VA Hlth Care Syst, Los Angeles, CA USA. RP Chin, PS (reprint author), Genentech Inc, Hlth Econ & Outcomes Res, 1 DNA Way,MS 241A, San Francisco, CA 94080 USA. EM neuroepi@yahoo.com FU PHS HHS [R01 32375-06] NR 30 TC 27 Z9 29 U1 2 U2 3 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0028-3878 J9 NEUROLOGY JI Neurology PD JUN 27 PY 2006 VL 66 IS 12 BP 1882 EP 1887 DI 10.1212/01.wnl.0000219729.08924.54 PG 6 WC Clinical Neurology SC Neurosciences & Neurology GA 057CJ UT WOS:000238572400020 PM 16801655 ER PT J AU Arany, Z Novikov, M Chin, S Ma, YH Rosenzweig, A Spiegelman, BM AF Arany, Zoltan Novikov, Mikhail Chin, Sherry Ma, Yanhong Rosenzweig, Anthony Spiegelman, Bruce M. TI Transverse aortic constriction leads to accelerated heart failure in mice lacking PPAR-gamma coactivator 1 alpha SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE cardiac metabolism; mitochondria; transcription ID ACTIVATED RECEPTOR-ALPHA; MITOCHONDRIAL BIOGENESIS; NUCLEAR RECEPTORS; HEPATIC GLUCONEOGENESIS; TRANSCRIPTIONAL CONTROL; PRESSURE-OVERLOAD; TRAUMA-HEMORRHAGE; CARDIAC-FUNCTION; SKELETAL-MUSCLE; FAILING HEART AB Heart failure is accompanied by important defects in metabolism. The transcriptional coactivator peroxisome proliferator-activated receptor-gamma coactivator 1 alpha (PGC-1 alpha) is a powerful regulator of mitochondrial biology and metabolism. PGC-1 alpha and numerous genes regulated by PGC-1 alpha are repressed in models of cardiac stress, such as that generated by transverse aortic constriction (TAC). This finding has suggested that PGC-1 alpha repression may contribute to the maladaptive response of the heart to chronic hemodynamic loads. We show here that TAC in mice genetically engineered to lack PGC-1 alpha leads to accelerated cardiac dysfunction, which is accompanied by signs of significant clinical heart failure. Treating cardiac cells in tissue culture with the catecholamine epinephrine leads to repression of PGC-1a and many of its target genes, recapitulating the findings in vivo in response to TAC. Importantly, introduction of ectopic PGC-1 alpha can reverse the repression of most of these genes by epinephrine. Together, these data indicate that endogenous PGC-1 alpha serves a cardioprotective function and suggest that repression of PGC-1 alpha significantly contributes to the development of heart failure. Moreover, the data suggest that elevating PGC-1 alpha activity may have therapeutic potential in the treatment of heart failure. C1 Harvard Univ, Sch Med, Dana Farber Canc Inst, Boston, MA 02115 USA. Harvard Univ, Sch Med, Dept Cell Biol, Boston, MA 02115 USA. Harvard Univ, Sch Med, Beth Israel Deaconess Med Ctr, Div Cardiol, Boston, MA 02215 USA. RP Spiegelman, BM (reprint author), Harvard Univ, Sch Med, Dana Farber Canc Inst, Boston, MA 02115 USA. EM bruce_spiegelman@dfci.harvard.edu FU NHLBI NIH HHS [HL 079172, HL 077543, K08 HL079172, R01 HL077543]; NIDDK NIH HHS [DK 54477, DK 61562, R01 DK054477, R01 DK061562, R56 DK054477] NR 46 TC 174 Z9 180 U1 1 U2 7 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 JUN 27 PY 2006 VL 103 IS 26 BP 10086 EP 10091 DI 10.1073/pnas.0603615103 PG 6 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA 061LC UT WOS:000238872900061 PM 16775082 ER PT J AU Cina, RA Wikiel, K Lee, PW Cameron, AM Hettiarachy, S Rowland, H Goodrich, J Colby, C Spitzer, TR Neville, DM Huang, CA AF Cina, Robert A. Wikiel, Krzysztof J. Lee, Patricia W. Cameron, Andrew M. Hettiarachy, Shehan Rowland, Haley Goodrich, Jennifer Colby, Christine Spitzer, Thomas R. Neville, David M., Jr. Huang, Christene A. TI Stable multilineage chimerism without graft versus host disease following nonmyeloablative haploidentical hematopoietic cell transplantation SO TRANSPLANTATION LA English DT Article DE hematopoietic stem cells; transplantation; miniature swine ID BONE-MARROW-TRANSPLANTATION; LARGE-ANIMAL-MODEL; MINIATURE SWINE; MONOCLONAL-ANTIBODIES; MIXED CHIMERISM; NONHUMAN-PRIMATES; ENGRAFTMENT; STEM; LEUKEMIA; IRRADIATION AB Background. Hematopoictic cell transplantation may offer the only cure for patients with hematological diseases. The clinical application of this therapy has been limited by toxic conditioning and lack of matched donors. Haploidentical transplantation would serve to extend the potential donor pool; however, transplantation across major histocompatibility complex barriers is often associated with severe graft-versus-host disease. Here we evaluate a novel protocol to achieve engraftment across mismatch barriers without toxic conditioning or significant posttransplant complications. Methods. Nine major histocompatibility complex (MHC)-defined miniature swine received haploidentical hematopoietic cell transplantation following standard myeloablative conditioning. Nine additional animals received haploidentical hematopoietic cell transplantation following a minimally myelosuppressive regimen, consisting of 100 cGy total body irradiation, immunotoxin mediated T-cell depletion, and a short course of cyclosporine. Donor cell engraftment and peripheral chimerism was assessed by polymerase chain reaction and flow cytometry. Graft-versus-host disease was monitored by clinical grading and histology of skin biopsy specimens. Results. All animals conditioned for haploidentical hematopoietic cell transplantation using myeloablative conditioning were euthanized within 2 weeks due to engraftment failure or graft-versus-host disease. All animals conditioned with the nonmyeloablative regimen developed multilineage peripheral blood chimerism during the first 2 months following transplantation. Six animals evaluated beyond 100 days maintained multilineage chimerism in the peripheral blood and lymphoid tissues, showed evidence of progenitor cell engraftment in the bone marrow, and had minimal treatment-related complications. Conclusions. Here we report that stable multilineage chimerism and engraftment can be established across haploidentical major histocompatibility complex barriers with minimal treatment-related toxicity and without significant risk of graft-versus-host disease. C1 Massachusetts Gen Hosp, Transplantat Biol Res Ctr, Charlestown, MA 02129 USA. Beth Israel Deaconess Hosp, Dept Surg, Boston, MA USA. Georgetown Univ, Dept Surg, Washington, DC 20007 USA. Univ Calif Los Angeles, Dept Surg, Los Angeles, CA 90024 USA. Chelsea & Westminster NHS Trust, London, England. Massachusetts Gen Hosp, Dept Med, Bone Marrow Transplantat Program, Boston, MA 02114 USA. Harvard Univ, Sch Med, Boston, MA 02114 USA. NIMH, Mol Biol Lab, Bethesda, MD 20892 USA. RP Huang, CA (reprint author), Massachusetts Gen Hosp, Transplantat Biol Res Ctr, MGH E,Bldg 149-9019,13th St, Charlestown, MA 02129 USA. EM huangc@helix.mgh.harvard.edu NR 39 TC 31 Z9 31 U1 1 U2 2 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0041-1337 J9 TRANSPLANTATION JI Transplantation PD JUN 27 PY 2006 VL 81 IS 12 BP 1677 EP 1685 DI 10.1097/01.tp.0000226061.59196.84 PG 9 WC Immunology; Surgery; Transplantation SC Immunology; Surgery; Transplantation GA 058CX UT WOS:000238643200012 PM 16794534 ER PT J AU Lim, H de Boer, JF Park, BH Lee, ECW Yelin, R Yun, SH AF Lim, H de Boer, JF Park, BH Lee, ECW Yelin, R Yun, SH TI Optical frequency domain imaging with a rapidly swept laser in the 815-870 nm range SO OPTICS EXPRESS LA English DT Article ID COHERENCE TOMOGRAPHY; MOLECULAR CONTRAST; HUMAN RETINA; REFLECTOMETRY AB Optical frequency domain imaging (OFDI) in the 800-nm biological imaging window is demonstrated by using a novel wavelength-swept laser source. The laser output is tuned continuously from 815 to 870 nm at a 43.2-kHz repetition rate with 7-mW average power. Axial resolution of 10-mu m in biological tissue and peak sensitivity of 96 dB are achieved. In vivo imaging of Xenopus laevis is demonstrated with an acquisition speed of 84 frames per second (512 axial lines per frame). This new imaging technique may prove useful in comprehensive retinal screening for medical diagnosis and contrast-agent-based imaging for biological investigations. (c) 2006 Optical Society of America. C1 Harvard Univ, Sch Med, Boston, MA 02114 USA. Massachusetts Gen Hosp, Wellman Ctr Photomed, Boston, MA 02114 USA. RP Lim, H (reprint author), Harvard Univ, Sch Med, 50 Blossom st, Boston, MA 02114 USA. EM syun@hms.harvard.edu RI de Boer, Johannes/B-7590-2012 OI de Boer, Johannes/0000-0003-1253-4950 NR 30 TC 66 Z9 67 U1 1 U2 7 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 JUN 26 PY 2006 VL 14 IS 13 BP 5937 EP 5944 DI 10.1364/OE.14.005937 PG 8 WC Optics SC Optics GA 056VM UT WOS:000238553200011 PM 19516763 ER PT J AU Michaels, PJ Brachtel, EF Bounds, BC Brugge, WR Pitman, MB AF Michaels, PJ Brachtel, EF Bounds, BC Brugge, WR Pitman, MB TI Intraductal papillary mucinous neoplasm of the pancreas - Cytologic features predict histologic grade SO CANCER CYTOPATHOLOGY LA English DT Article DE intraductal papillary mucinous neoplasm; mucinous cysts; fine-needle aspiration biopsy; pancreas; pancreatic neoplasms; endoscopic ultrasound ID FINE-NEEDLE-ASPIRATION; SURGICAL RESECTION; CLINICOPATHOLOGICAL FEATURES; TUMORS; ADENOCARCINOMA; CARCINOMA; DIAGNOSIS; DUCT; PROGNOSIS; LESIONS AB BACKGROUND. Intraductal papillary mucinous neoplasm (IPMN) is an increasingly recognized cystic neoplasm of the pancreas, histologically classified by the degree of epithelial atypia and by the presence or absence of invasion of the cyst wall. To the authors' knowledge, the cytologic features of this neoplasm are poorly characterized, especially with respect to tumor grade. METHODS. Thirty-three endoscopic ultrasound (EUS)-guided pancreatic fine-needle aspiration biopsy (FNAB) samples and I pancreatic duct brush specimen from 25 patients with a histologically confirmed IPMN were retrospectively reviewed. Blinded to tumor grade, background mucin, inflammation, necrosis, overall cellularity, the presence of gastrointestinal-contaminating epithelium, architecture of cell clusters, and nuclear and cellular morphology were evaluated. in cases in which special stains for mucin were performed, the diagnostic utility of these stains was assessed. These cytologic features were subsequently correlated with the histologic diagnosis. RESULTS. The 34 cytology samples represented 4 adenomas, 15 IPMN-moderate dysplasias, 7 intraductal carcinomas, and 8 IPMNs with invasive carcinoma. Extracellular mucin was present in 97% of all cases; 53% had thick, viscous, "colloidlike" mucin. Special stains for mucin were positive in 6 of 11 cases (54%), helping to identify thin mucin in only 2 cases. Gastrointestinal contamination did not appear to create diagnostic difficulty due to an apparent dual (dysplastic-nondysplastic) epithelial population, but only 4 adenomas were evaluated in this study. Necrosis distinguished IPMN with carcinoma from IPMN-adenomas and IPMN with moderate dysplasia (P <.00001), and was more often observed with invasion than IPMN-carcinoma in situ (P <.05). Tight epithelial cell clusters with hyperchromatic nuclei and a high nuclear to cytoplasmic ratio was more significant in IPMN of at least moderate dysplasia (P =.03). Pale nuclei with parachromatin clearing was found to be a nuclear feature that was suspicious for at least carcinoma in situ (P <.001). In addition, significant background inflammation (neutrophils and histiocytes) was found to be more characteristic of IPMN with at least carcinoma in situ (P =.002). CONCLUSIONS. The presence of thick, "colloid-like" mucin is noted in half of the IPMN cases, but was not found to be specific to grade. The absence of such mucin does not exclude an IPMN. The presence of tight epithelial cell clusters is consistent with a neoplasm of at least moderate dysplasia, and abundant background inflammation and parachromatin clearing correlated with the presence of at least carcinoma in situ. Necrosis was the only feature found to be strongly suggestive of invasion. C1 Harvard Univ, Dept Pathol, Sch Med, Massachusetts Gen Hosp,James Homer Wright Pathol, Boston, MA 02114 USA. Harvard Univ, Cytopathol Lab, Sch Med, Massachusetts Gen Hosp, Boston, MA 02114 USA. Harvard Univ, Dept Gastroenterol, Sch Med, Massachusetts Gen Hosp, Boston, MA 02114 USA. RP Pitman, MB (reprint author), Harvard Univ, Dept Pathol, Sch Med, Massachusetts Gen Hosp,James Homer Wright Pathol, 55 Fruit St, Boston, MA 02114 USA. EM mpitman@partners.org NR 29 TC 75 Z9 80 U1 0 U2 2 PU JOHN WILEY & SONS INC PI HOBOKEN PA 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 0008-543X J9 CANCER CYTOPATHOL JI Cancer Cytopathol. PD JUN 25 PY 2006 VL 108 IS 3 BP 163 EP 173 DI 10.1002/cncr.21838 PG 11 WC Oncology; Pathology SC Oncology; Pathology GA 056CN UT WOS:000238498800005 PM 16550572 ER PT J AU Gupta, V Bei, M AF Gupta, V Bei, M TI Modification of Msx1 by SUMO-1 SO BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS LA English DT Article DE Msx1; sumoylation; post-translational modifications ID UBIQUITIN; NUCLEAR AB The small ubiquitin-related modifier SUMO reversibly modifies many proteins, including promoter-specific transcription factors. Genetic studies in both humans and mice indicate that the Msx1 transcription factor is associated with specific disorders, including cleft palate. We show that Msx1 conjugation to SUMO-1 in vivo is enhanced by an E3 SUMO ligase, PIAS1, suggesting that sumoylation of Msx1 is a new mechanism for modulating the molecular function of Msx1 during organogenesis. (c) 2006 Elsevier Inc. All rights reserved. C1 Massachusetts Gen Hosp, Cutaneous Biol Res Ctr, Charlestown, MA 02129 USA. Harvard Univ, Sch Med, Charlestown, MA 02129 USA. RP Bei, M (reprint author), Massachusetts Gen Hosp, Cutaneous Biol Res Ctr, 149 13th St, Charlestown, MA 02129 USA. EM marianna.bei@cbrc2.mgh.harvard.edu FU NIDCR NIH HHS [K22 DE 14230] NR 14 TC 18 Z9 21 U1 0 U2 0 PU ACADEMIC PRESS INC ELSEVIER SCIENCE PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA SN 0006-291X J9 BIOCHEM BIOPH RES CO JI Biochem. Biophys. Res. Commun. PD JUN 23 PY 2006 VL 345 IS 1 BP 74 EP 77 DI 10.1016/j.bbrc.2006.03.232 PG 4 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA 047KH UT WOS:000237877700011 PM 16678795 ER PT J AU Mehle, A Thomas, ER Rajendran, KS Gabuzda, D AF Mehle, A Thomas, ER Rajendran, KS Gabuzda, D TI A zinc-binding region in vif binds cul5 and determines cullin selection SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID IMMUNODEFICIENCY-VIRUS TYPE-1; UBIQUITIN LIGASE COMPLEXES; LARGE T-ANTIGEN; HIV-1 VIF; PROTEIN BINDS; V-PROTEIN; SOCS-BOX; CYTIDINE DEAMINATION; ANTIVIRAL ACTIVITY; VIRAL INFECTIVITY AB Human immunodeficiency virus-1 (HIV-1) Vif overcomes the antiviral activity of APOBEC3G by targeting it for ubiquitination via a Cullin 5-ElonginB-ElonginC (Cul5-EloBC) E3 ligase. Vif associates with Cul5-EloBC through a BC-box motif that binds EloC, but the mechanism by which Vif selectively recruits Cul5 is poorly understood. Here we report that a region of Vif (residues 100-142) upstream of the BC-box binds selectively to Cul5 in the absence of EloC. This region contains a zinc coordination site HX5CX17-18CX3-5H (HCCH), with His/Cys residues at positions 108, 114, 133, and 139 coordinating one zinc ion. The HCCH zinc coordination site, which is conserved among primate lentivirus Vif proteins, does not correspond to any known class of zinc-binding motif. Mutations of His/Cys residues in the HCCH motif impair zinc coordination, Cul5 binding, and APOBEC3G degradation. Mutations of conserved hydrophobic residues (Ile-120, Ala-123, and Leu-124) located between the two Cys residues in the HCCH motif disrupt binding of the zinc-coordinating region to Cul5 and inhibit APOBEC3G degradation. The Vif binding site maps to the first cullin repeat in the N terminus of Cul5. These data suggest that the zinc-binding region in Vif is a novel cullin interaction domain that mediates selective binding to Cul5. We propose that the HCCH zinc-binding motif facilitates Vif-Cul5 binding by playing a structural role in positioning hydrophobic residues for direct contact with Cul5. 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 Neurol, Boston, MA 02115 USA. RP Gabuzda, D (reprint author), Dana Farber Canc Inst, Dept Canc Immunol & AIDS, JF816,44 Binney St, Boston, MA 02115 USA. EM dana_gabuzda@dfci.harvard.edu FU NIAID NIH HHS [AI368186, AI62555] NR 58 TC 133 Z9 133 U1 1 U2 3 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD JUN 23 PY 2006 VL 281 IS 25 BP 17259 EP 17265 DI 10.1074/jbc.M602413200 PG 7 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA 053SV UT WOS:000238326300053 PM 16636053 ER PT J AU Xia, B Sheng, Q Nakanishi, K Ohashi, A Wu, JM Christ, N Liu, XG Jasin, M Couch, FJ Livingston, DM AF Xia, B Sheng, Q Nakanishi, K Ohashi, A Wu, JM Christ, N Liu, XG Jasin, M Couch, FJ Livingston, DM TI Control of BRCA2 cellular and clinical functions by a nuclear partner, PALB2 SO MOLECULAR CELL LA English DT Article ID CANCER SUSCEPTIBILITY PROTEIN; DNA-REPAIR DEFECT; FANCONI-ANEMIA; OVARIAN-CANCER; RECOMBINATIONAL REPAIR; GENE BRCA2; IN-VIVO; BREAST; RAD51; DAMAGE AB BRCA2 mutations predispose carriers to breast and ovarian cancer and can also cause other cancers and Fanconi anemia. BRCA2 acts as a "caretaker" of genome integrity by enabling homologous recombination (HR)-based, error-free DNA double-strand break repair (DSBR) and intra-S phase DNA damage checkpoint control. Described here is the identification of PALB2, a BRCA2 binding protein. PALB2 colocalizes with BRCA2 in nuclear foci, promotes its localization and stability in key nuclear structures (e.g., chromatin and nuclear matrix), and enables its recombinational repair and checkpoint functions. In addition, multiple, germline BRCA2 missense mutations identified in breast cancer patients but of heretofore unknown biological/clinical consequence appear to disrupt PALB2 binding and disable BRCA2 HR/DSBR function. Thus, PALB2 licenses key cellular biochemical properties of BRCA2 and ensures its tumor suppression function. C1 Dana Farber Canc Inst, Boston, MA 02115 USA. Harvard Univ, Sch Med, Boston, MA 02115 USA. Mem Sloan Kettering Canc Ctr, Program Mol Biol, New York, NY 10021 USA. Mayo Clin & Mayo Fdn, Coll Med, Dept Lab Med & Pathol, Rochester, MN 55905 USA. RP Livingston, DM (reprint author), Dana Farber Canc Inst, 44 Binney St, Boston, MA 02115 USA. EM david_livingston@dfci.harvard.edu NR 55 TC 340 Z9 350 U1 3 U2 16 PU CELL PRESS PI CAMBRIDGE PA 1100 MASSACHUSETTS AVE, CAMBRIDGE, MA 02138 USA SN 1097-2765 J9 MOL CELL JI Mol. Cell PD JUN 23 PY 2006 VL 22 IS 6 BP 719 EP 729 DI 10.1016/j.molcel.2006.05.022 PG 11 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA 059GT UT WOS:000238722000004 PM 16793542 ER PT J AU Qi, L Heredia, JE Altarejos, JY Screaton, R Goebel, N Niessen, S MacLeod, IX Liew, CW Kulkarni, RN Bain, J Newgard, C Nelson, M Evans, RM Yates, J Montminy, M AF Qi, L Heredia, JE Altarejos, JY Screaton, R Goebel, N Niessen, S MacLeod, IX Liew, CW Kulkarni, RN Bain, J Newgard, C Nelson, M Evans, RM Yates, J Montminy, M TI TRB3 links the E3 ubiquitin ligase COP1 to lipid metabolism SO SCIENCE LA English DT Article ID INSULIN-RESISTANCE; NEGATIVE REGULATOR; TRIBBLES HOMOLOG; GENE-EXPRESSION; ADIPOSE-TISSUE; ARABIDOPSIS; DROSOPHILA; PROTEIN; PHOTOMORPHOGENESIS; MORPHOGENESIS AB During fasting, increased concentrations of circulating catecholamines promote the mobilization of lipid stores from adipose tissue in part by phosphorylating and inactivating acetyl-coenzyme A carboxylase (ACC), the rate-limiting enzyme in fatty acid synthesis. Here, we describe a parallel pathway, in which the pseudokinase Tribbles 3 (TRB3), whose abundance is increased during fasting, stimulates lipolysis by triggering the degradation of ACC in adipose tissue. TRB3 promoted ACC ubiquitination through an association with the E3 ubiquitin ligase constitutive photomorphogenic protein 1 (COP1). Indeed, adipocytes deficient in TRB3 accumulated larger amounts of ACC protein than did wild-type cells. Because transgenic mice expressing TRB3 in adipose tissue are protected from diet-induced obesity due to enhanced fatty acid oxidation, these results demonstrate how phosphorylation and ubiquitination pathways converge on a key regulator of lipid metabolism to maintain energy homeostasis. C1 Salk Inst Biol Studies, Peptide Biol Lab, La Jolla, CA 92037 USA. Salk Inst Biol Studies, Gene Express Lab, La Jolla, CA 92037 USA. Scripps Res Inst, La Jolla, CA 92037 USA. Joslin Diabet Ctr, Boston, MA 02215 USA. Duke Univ, Med Ctr, Sarah W Stedman Nutr & Metab Ctr, Durham, NC 27704 USA. RP Montminy, M (reprint author), Salk Inst Biol Studies, Peptide Biol Lab, 10010 N Torrey Pines Rd, La Jolla, CA 92037 USA. EM montminy@salk.edu OI Bain, James/0000-0002-8917-9187 FU NIDDK NIH HHS [DK064142] NR 26 TC 157 Z9 166 U1 4 U2 10 PU AMER ASSOC ADVANCEMENT SCIENCE PI WASHINGTON PA 1200 NEW YORK AVE, NW, WASHINGTON, DC 20005 USA SN 0036-8075 J9 SCIENCE JI Science PD JUN 23 PY 2006 VL 312 IS 5781 BP 1763 EP 1766 DI 10.1126/science.1123374 PG 4 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA 055LS UT WOS:000238452800048 PM 16794074 ER PT J AU Chou, R Whelan, JP Zembowicz, A Harris, NL AF Chou, R Whelan, JP Zembowicz, A Harris, NL TI Case 19-2006: A 22-month-old boy with the rapid growth of subcutaneous nodules - Subcutaneous granuloma annulare, with secondary metaplastic synovial pseudocyst SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Editorial Material ID RHEUMATOID-ARTHRITIS; CHILDREN; CHILDHOOD; LYMPHOMA; TUMORS; SKIN C1 Massachusetts Gen Hosp, Pediat Rheumatol Serv, Boston, MA 02114 USA. Massachusetts Gen Hosp, Dept Pathol, Boston, MA 02114 USA. Harvard Univ, Sch Med, Dept Pediat, Cambridge, MA 02138 USA. Harvard Univ, Sch Med, Dept Pathol, Cambridge, MA 02138 USA. RP Chou, R (reprint author), Massachusetts Gen Hosp, Pediat Rheumatol Serv, Boston, MA 02114 USA. NR 28 TC 6 Z9 6 U1 1 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 JUN 22 PY 2006 VL 354 IS 25 BP 2697 EP 2704 PG 8 WC Medicine, General & Internal SC General & Internal Medicine GA 054ZJ UT WOS:000238416900010 ER PT J AU Carothers, JM Oestreich, SC Szostak, JW AF Carothers, JM Oestreich, SC Szostak, JW TI Aptamers selected for higher-affinity binding are not more specific for the target ligand SO JOURNAL OF THE AMERICAN CHEMICAL SOCIETY LA English DT Article ID IN-VITRO SELECTION; RNA APTAMER; MOLECULAR RECOGNITION; STRUCTURAL BASIS; ATP; STABILITY; COMPLEX; DISCRIMINATION; TETRAHYMENA; EVOLUTION AB Previous study of eleven different in vitro-selected RNA aptamers that bind guanosine triphosphate (GTP) with K(d)s ranging from 8 mu M to 9 nM showed that more information is required to specify the structures of the higher-affinity aptamers. We are interested in understanding how the more complex aptamers achieve higher affinities for the ligand. In vitro selection produces structural solutions to a functional problem that are are as simple as possible in terms of the information content needed to define them. It has long been assumed that the simplest way to improve the affinity of an aptamer is to increase the shape and functional group complementarity of the RNA binding pocket for the ligand. This argument underlies the hypothesis that selection for higher-affinity aptamers automatically leads to structures that bind more specifically to the target molecule. Here, we examined the binding specificities of the eleven GTP aptamers by carrying out competition binding studies with sixteen different chemical analogues of GTP. The aptamers have distinct patterns of specificity, implying that each RNA is a structurally unique solution to the problem of GTP binding. However, these experiments failed to provide evidence that higher-affinity aptamers bind more specifically to GTP. We suggest that the simplest way to improve aptamer K(d)s may be to increase the stability of the RNA tertiary structure with additional intramolecular RNA-RNA interactions; increasingly specific ligand binding may emerge only in response to direct selection for specificity. C1 Massachusetts Gen Hosp, Dept Mol Biol, Boston, MA 02114 USA. Massachusetts Gen Hosp, Ctr Computat & Integrat Biol 7215, Simches Res Ctr, Boston, MA 02114 USA. RP Szostak, JW (reprint author), Massachusetts Gen Hosp, Dept Mol Biol, 185 Cambridge St, Boston, MA 02114 USA. EM szostak@molbio.mgh.harvard.edu FU Howard Hughes Medical Institute; NIGMS NIH HHS [GM53936, R01 GM053936] NR 37 TC 63 Z9 65 U1 0 U2 25 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA SN 0002-7863 J9 J AM CHEM SOC JI J. Am. Chem. Soc. PD JUN 21 PY 2006 VL 128 IS 24 BP 7929 EP 7937 DI 10.1021/ja060952q PG 9 WC Chemistry, Multidisciplinary SC Chemistry GA 052TY UT WOS:000238258000048 PM 16771507 ER PT J AU Spertus, JA Kettelkamp, R Vance, C Decker, C Jones, PG Rumsfeld, JS Messenger, JC Khanal, S Peterson, ED Bach, RG Krumholz, HM Cohen, DJ AF Spertus, JA Kettelkamp, R Vance, C Decker, C Jones, PG Rumsfeld, JS Messenger, JC Khanal, S Peterson, ED Bach, RG Krumholz, HM Cohen, DJ TI Prevalence, predictors, and outcomes of premature discontinuation of thienopyridine therapy after drug-eluting stent placement results from the PREMIER registry SO CIRCULATION LA English DT Article DE angioplasty; anticoagulants; mortality; revascularization; stents ID PERCUTANEOUS CORONARY INTERVENTION; PRACTICE GUIDELINES COMMITTEE; ASSOCIATION TASK-FORCE; ST-SEGMENT ELEVATION; MYOCARDIAL-INFARCTION; ANTIPLATELET THERAPY; AMERICAN-COLLEGE; LATE THROMBOSIS; POOLED ANALYSIS; ARTERY-DISEASE AB Background - Although drug-eluting stents (DES) significantly reduce restenosis, they require 3 to 6 months of thienopyridine therapy to prevent stent thrombosis. The rate and consequences of prematurely discontinuing thienopyridine therapy after DES placement for acute myocardial infarction (MI) are unknown. Methods and Results - We used prospectively collected data from a 19-center study of MI patients to examine the prevalence and predictors of thienopyridine discontinuation 30 days after DES treatment. We then compared the mortality and cardiac hospitalization rates for the next 11 months between those who stopped and those who continued thienopyridine therapy. Among 500 DES-treated MI patients who were discharged on thienopyridine therapy, 68 (13.6%) stopped therapy within 30 days. Those who stopped were older, less likely to have completed high school or be married, more likely to avoid health care because of cost, and more likely to have had preexisting cardiovascular disease or anemia at presentation. They were also less likely to have received discharge instructions about their medications or a cardiac rehabilitation referral. Patients who stopped thienopyridine therapy by 30 days were more likely to die during the next 11 months (7.5% versus 0.7%, P < 0.0001; adjusted hazard ratio = 9.0; 95% confidence interval = 1.3 to 60.6) and to be rehospitalized (23% versus 14%, P = 0.08; adjusted hazard ratio = 1.5; 95% confidence interval = 0.78 to 3.0). Conclusions - Almost 1 in 7 MI patients who received a DES were no longer taking thienopyridines by 30 days. Prematurely stopping thienopyridine therapy was strongly associated with subsequent mortality. Strategies to improve the use of thienopyridines are needed to optimize the outcomes of MI patients treated with DES. C1 Mid Amer Heart Inst, Kansas City, MO 64111 USA. Univ Missouri, Kansas City, MO 64110 USA. Univ Colorado Hosp, Denver VA Med Ctr, Denver, CO USA. Univ Colorado, Hlth Sci Ctr, Denver, CO 80202 USA. Henry Ford Hlth Syst, Detroit, MI USA. Duke Univ, Durham, NC USA. Barnes Jewish Hosp, St Louis, MO 63110 USA. Washington Univ, Sch Med, St Louis, MO 63110 USA. Yale Univ, New Haven, CT USA. Beth Israel Deaconess Med Ctr, Boston, MA 02215 USA. RP Spertus, JA (reprint author), Mid Amer Heart Inst, 4401 Wornall Rd, Kansas City, MO 64111 USA. EM spertusj@umkc.edu NR 36 TC 558 Z9 594 U1 2 U2 16 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0009-7322 J9 CIRCULATION JI Circulation PD JUN 20 PY 2006 VL 113 IS 24 BP 2803 EP 2809 DI 10.1161/CIRCULATIONAHA.106.618066 PG 7 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 054NY UT WOS:000238385800008 PM 16769908 ER PT J AU Motzer, RJ Hutson, TE Tomczak, P Michaelson, MD Bukowski, RM Rixe, O Oudard, S Kim, ST Baum, CM Figlin, RA AF Motzer, R. J. Hutson, T. E. Tomczak, P. Michaelson, M. D. Bukowski, R. M. Rixe, O. Oudard, S. Kim, S. T. Baum, C. M. Figlin, R. A. TI Phase III randomized trial of sunitinib malate (SU1 1248) versus interferon-alfa (IFN-alpha) as first-line systemic therapy for patients with metastatic renal cell carcinoma (mRCC). SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Meeting Abstract CT 42nd Annual Meeting of the American-Society-of-Clinical-Oncology CY JUN 02-06, 2006 CL Atlanta, GA SP Amer Soc Clin Oncol C1 Mem Sloan Kettering Canc Ctr, New York, NY 10021 USA. Baylor Charles A Sammons Canc Ctr, Dallas, TX USA. Klin Oncol Oddzial Chemioterapii, Poznan, Poland. Massachusetts Gen Hosp, Boston, MA 02114 USA. Cleveland Clin Fdn, Cleveland, OH 44195 USA. Hop La Pitie Salpetriere, Paris, France. Georges Pompidou European Hosp, Paris, France. Pfizer Inc, La Jolla, CA USA. Univ Calif Los Angeles, Los Angeles, CA 90024 USA. NR 0 TC 21 Z9 21 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 JUN 20 PY 2006 VL 24 IS 18 SU S BP 2S EP 2S PN 1 PG 1 WC Oncology SC Oncology GA 063HN UT WOS:000239009400004 ER PT J AU Lin, NU Carey, LA Liu, MC Younger, J Come, SE Bullitt, E Van den Abbeele, AD Li, X Hochberg, FH Winer, EP AF Lin, N. U. Carey, L. A. Liu, M. C. Younger, J. Come, S. E. Bullitt, E. Van den Abbeele, A. D. Li, X. Hochberg, F. H. Winer, E. P. TI Phase II trial of lapatinib for brain metastases in patients with HER2+breast cancer. SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Meeting Abstract CT 42nd Annual Meeting of the American-Society-of-Clinical-Oncology CY JUN 02-06, 2006 CL Atlanta, GA SP Amer Soc Clin Oncol C1 Dana Farber Canc Inst, Boston, MA 02115 USA. Univ N Carolina, Chapel Hill, NC 27515 USA. Georgetown Univ, Washington, DC 20057 USA. Massachusetts Gen Hosp, Boston, MA 02114 USA. Beth Israel Deaconess Med Ctr, Boston, MA 02215 USA. NR 0 TC 20 Z9 20 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 JUN 20 PY 2006 VL 24 IS 18 SU S BP 3S EP 3S PN 1 PG 1 WC Oncology SC Oncology GA 063HN UT WOS:000239009400011 ER PT J AU Kandel, MJ Stadler, Z Masciari, S Collins, L Schnitt, S Harris, L Miron, A Richardson, A Garber, JE AF Kandel, M. J. Stadler, Z. Masciari, S. Collins, L. Schnitt, S. Harris, L. Miron, A. Richardson, A. Garber, J. E. TI Prevalence of BRCA1 mutations in triple negative breast cancer (BC). SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Meeting Abstract CT 42nd Annual Meeting of the American-Society-of-Clinical-Oncology CY JUN 02-06, 2006 CL Atlanta, GA SP Amer Soc Clin Oncol C1 Dana Farber Canc Inst, Boston, MA 02115 USA. Beth Israel Deaconess Med Ctr, Boston, MA 02215 USA. Brigham & Womens Hosp, Boston, MA 02115 USA. NR 0 TC 9 Z9 9 U1 0 U2 1 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 JUN 20 PY 2006 VL 24 IS 18 SU S BP 5S EP 5S PN 1 PG 1 WC Oncology SC Oncology GA 063HN UT WOS:000239009400016 ER PT J AU Partridge, AH Wolff, AC Marcom, PK Kaufman, PA Moore, C Lake, D Fleming, G Rugo, HS Collyar, D Winer, EP AF Partridge, A. H. Wolff, A. C. Marcom, P. K. Kaufman, P. A. Moore, C. Lake, D. Fleming, G. Rugo, H. S. Collyar, D. Winer, E. P. TI Study participants' perceptions of the process and impact of receiving results of N9831. SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Meeting Abstract CT 42nd Annual Meeting of the American-Society-of-Clinical-Oncology CY JUN 02-06, 2006 CL Atlanta, GA SP Amer Soc Clin Oncol C1 Dana Farber Canc Inst, Boston, MA 02115 USA. Sidney Kimmel Canc Ctr Johns Hopkins, Baltimore, MD USA. Duke Univ, Med Ctr, Durham, NC 27706 USA. Dartmouth Hitchcock Med Ctr, Lebanon, NH 03766 USA. Mem Sloan Kettering Canc Ctr, New York, NY 10021 USA. Univ Chicago, Chicago, IL 60637 USA. Univ Calif San Francisco, Ctr Comprehens Canc, San Francisco, CA 94143 USA. CALGB Patient Advocates Res, San Francisco, CA USA. NR 0 TC 0 Z9 0 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 JUN 20 PY 2006 VL 24 IS 18 SU S BP 7S EP 7S PN 1 PG 1 WC Oncology SC Oncology GA 063HN UT WOS:000239009400025 ER PT J AU Goss, PE Bondarenko, IN Manikhas, GN Pendergrass, KB Miller, WH AF Goss, P. E. Bondarenko, I. N. Manikhas, G. N. Pendergrass, K. B. Miller, W. H. CA 777 CLP-29 Study Grp TI Phase 3 study of atamestane plus toremifene vs. letrozole in advanced breast cancer. SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Meeting Abstract CT 42nd Annual Meeting of the American-Society-of-Clinical-Oncology CY JUN 02-06, 2006 CL Atlanta, GA SP Amer Soc Clin Oncol C1 Massachusetts Gen Hosp, Boston, MA 02114 USA. Dnepropetrovsk State Med Acad, Dnepropetrovsk, Ukraine. St Petersburg City Oncol Ctr, St Petersburg, Russia. Kansas City Canc Ctr, Kansas City, MO USA. McGill Univ, Montreal, PQ H3A 2T5, Canada. NR 0 TC 1 Z9 1 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 JUN 20 PY 2006 VL 24 IS 18 SU S BP 9S EP 9S PN 1 PG 1 WC Oncology SC Oncology GA 063HN UT WOS:000239009400034 ER PT J AU Ingle, J Tu, D Shepherd, L Palmer, M Pater, J Goss, P AF Ingle, J. Tu, D. Shepherd, L. Palmer, M. Pater, J. Goss, P. TI NCICCTG MA.17: Intent to treat analysis (ITT) of randomized patients after a median follow-up of 54 months. SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Meeting Abstract CT 42nd Annual Meeting of the American-Society-of-Clinical-Oncology CY JUN 02-06, 2006 CL Atlanta, GA SP Amer Soc Clin Oncol C1 Mayo Clin, Rochester, MN USA. NCI, Canada Clin Trials Grp, Kingston, ON, Canada. Massachusetts Gen Hosp, Ctr Canc, Boston, MA USA. NR 0 TC 10 Z9 10 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 JUN 20 PY 2006 VL 24 IS 18 SU S BP 15S EP 15S PN 1 PG 1 WC Oncology SC Oncology GA 063HN UT WOS:000239009400056 ER PT J AU Robert, NJ Goss, PE Ingle, JN Tu, D Shepherd, L Palmer, M Pater, J AF Robert, N. J. Goss, P. E. Ingle, J. N. Tu, D. Shepherd, L. Palmer, M. Pater, J. TI Updated analysis of NCICCTG MA.17 (letrozole vs. placebo to letrozole vs placebo) post unblinding. SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Meeting Abstract CT 42nd Annual Meeting of the American-Society-of-Clinical-Oncology CY JUN 02-06, 2006 CL Atlanta, GA SP Amer Soc Clin Oncol C1 Fairfax No Virginia Hematol Oncol, Fairfax, VA USA. Massachusetts Gen Hosp, Boston, MA 02114 USA. Mayo Clin, Coll Med, Rochester, MN USA. Queens Univ, Kingston, ON, Canada. Kingston Gen Hosp, Kingston, ON K7L 2V7, Canada. NR 0 TC 15 Z9 15 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 JUN 20 PY 2006 VL 24 IS 18 SU S BP 15S EP 15S PN 1 PG 1 WC Oncology SC Oncology GA 063HN UT WOS:000239009400058 ER PT J AU Muss, H Berry, D Cirrincione, C Budman, D Henderson, I Citron, M Norton, L Winer, E Hudis, C AF Muss, H. Berry, D. Cirrincione, C. Budman, D. Henderson, I. Citron, M. Norton, L. Winer, E. Hudis, C. TI Toxicity of older and younger patients (pts) treated (Rx) with intensive adjuvant chemotherapy (Cx) for node-positive (N plus ) breast cancer (BC): The CALGB experience. SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Meeting Abstract CT 42nd Annual Meeting of the American-Society-of-Clinical-Oncology CY JUN 02-06, 2006 CL Atlanta, GA SP Amer Soc Clin Oncol C1 Univ Vermont, Burlington, VT USA. Univ Texas, MD Anderson Canc Ctr, Houston, TX 77030 USA. CALGB Stat Ctr, Durham, NC USA. N Shore Univ Hosp, Manhasset, NY USA. Univ Calif San Francisco, San Francisco, CA 94143 USA. Pro Hlth Care Associates, Lake Success, NY USA. Mem Sloan Kettering Canc Ctr, New York, NY 10021 USA. Dana Farber Canc Inst, Boston, MA 02115 USA. NR 0 TC 0 Z9 0 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 JUN 20 PY 2006 VL 24 IS 18 SU S BP 17S EP 17S PN 1 PG 1 WC Oncology SC Oncology GA 063HN UT WOS:000239009400065 ER PT J AU Deprimo, SE Friece, C Huang, X Smeraglia, J Sherman, L Collier, M Baum, C Elias, AD Burstein, HJ Miller, KD AF Deprimo, S. E. Friece, C. Huang, X. Smeraglia, J. Sherman, L. Collier, M. Baum, C. Elias, A. D. Burstein, H. J. Miller, K. D. TI Effect of treatment with sunitinib malate, a multitargeted tyrosine kinase inhibitor, on circulating plasma levels of VEGF, soluble VEGF receptors 2 and 3, and soluble KIT in patients with metastatic breast cancer. SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Meeting Abstract CT 42nd Annual Meeting of the American-Society-of-Clinical-Oncology CY JUN 02-06, 2006 CL Atlanta, GA SP Amer Soc Clin Oncol C1 Pfizer Global Res & Dev, La Jolla, CA USA. Univ Colorado, Denver, CO 80202 USA. Dana Farber Canc Inst, Boston, MA 02115 USA. Indiana Univ, Ctr Canc, Indianapolis, IN 46204 USA. NR 0 TC 7 Z9 7 U1 0 U2 1 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 JUN 20 PY 2006 VL 24 IS 18 SU S BP 22S EP 22S PN 1 PG 1 WC Oncology SC Oncology GA 063HN UT WOS:000239009400086 ER PT J AU Chen, WY Colditz, GA Rosner, B AF Chen, W. Y. Colditz, G. A. Rosner, B. TI Breast cancer epidemiologic risk factors by HER2/neu status. SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Meeting Abstract CT 42nd Annual Meeting of the American-Society-of-Clinical-Oncology CY JUN 02-06, 2006 CL Atlanta, GA SP Amer Soc Clin Oncol C1 Dana Farber Canc Inst, Boston, MA 02115 USA. Brigham & Womens Hosp, Boston, MA 02115 USA. RI Colditz, Graham/A-3963-2009 OI Colditz, Graham/0000-0002-7307-0291 NR 0 TC 0 Z9 0 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 JUN 20 PY 2006 VL 24 IS 18 SU S BP 24S EP 24S PN 1 PG 1 WC Oncology SC Oncology GA 063HN UT WOS:000239009400092 ER PT J AU Ligibel, JA Chen, W Keshaviah, A Adloff, K Partridge, A Salinardi, T Winer, EP AF Ligibel, J. A. Chen, W. Keshaviah, A. Adloff, K. Partridge, A. Salinardi, T. Winer, E. P. TI The impact of an exercise intervention on body composition, fat distribution, and weight in breast cancer survivors. SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Meeting Abstract CT 42nd Annual Meeting of the American-Society-of-Clinical-Oncology CY JUN 02-06, 2006 CL Atlanta, GA SP Amer Soc Clin Oncol C1 Dana Farber Canc Inst, Boston, MA 02115 USA. NR 0 TC 1 Z9 1 U1 0 U2 1 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 JUN 20 PY 2006 VL 24 IS 18 SU S BP 25S EP 25S PN 1 PG 1 WC Oncology SC Oncology GA 063HN UT WOS:000239009400098 ER PT J AU Burstein, HJ Keshaviah, A Baron, A Hart, R Lambert-Falls, R Marcom, PK Gelman, R Winer, EP AF Burstein, H. J. Keshaviah, A. Baron, A. Hart, R. Lambert-Falls, R. Marcom, P. K. Gelman, R. Winer, E. P. TI Trastuzumab and vinorelbine or taxane chemotherapy for HER2+metastatic breast cancer: The TRAVIOTA study. SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Meeting Abstract CT 42nd Annual Meeting of the American-Society-of-Clinical-Oncology CY JUN 02-06, 2006 CL Atlanta, GA SP Amer Soc Clin Oncol C1 Dana Farber Canc Inst, Boston, MA 02115 USA. Calif Pacific Med Ctr, San Francisco, CA USA. Oncol Alliance, Milwaukee, WI USA. SC Oncol, Columbia, SC USA. Duke Univ, Med Ctr, Durham, NC USA. NR 0 TC 3 Z9 3 U1 0 U2 1 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 JUN 20 PY 2006 VL 24 IS 18 SU S BP 40S EP 40S PN 1 PG 1 WC Oncology SC Oncology GA 063HN UT WOS:000239009400158 ER PT J AU Naughton, MJ Gu, L Wang, XF Seidman, AD Winer, E Kornblith, AB AF Naughton, M. J. Gu, L. Wang, X. F. Seidman, A. D. Winer, E. Kornblith, A. B. TI Quality of life (QOL) companion to CALGB 9840: A phase III study of paclitaxel (P) via weekly 1 hour (hr) versus standard 3 hour infusion every 3 weeks with trastuzumab in the treatment of patients with/without HER-2/neu-overexpressing metastatic breast cancer. SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Meeting Abstract CT 42nd Annual Meeting of the American-Society-of-Clinical-Oncology CY JUN 02-06, 2006 CL Atlanta, GA SP Amer Soc Clin Oncol C1 Wake Forest Univ, Sch Med, Winston Salem, NC 27109 USA. CALGB Stat Ctr, Durham, NC USA. Mem Sloan Kettering Canc Ctr, New York, NY 10021 USA. Dana Farber Canc Inst, Boston, MA 02115 USA. NR 0 TC 1 Z9 1 U1 0 U2 1 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 JUN 20 PY 2006 VL 24 IS 18 SU S BP 46S EP 46S PN 1 PG 1 WC Oncology SC Oncology GA 063HN UT WOS:000239009400182 ER PT J AU Brenner, DE Su, Y Normolle, DP Syngal, S Bresalier, R Marcon, N Baron, J Block, T AF Brenner, D. E. Su, Y. Normolle, D. P. Syngal, S. Bresalier, R. Marcon, N. Baron, J. Block, T. TI Detection of colorectal neoplasia associated K-Ras mutations in human urine. SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Meeting Abstract CT 42nd Annual Meeting of the American-Society-of-Clinical-Oncology CY JUN 02-06, 2006 CL Atlanta, GA SP Amer Soc Clin Oncol C1 Univ Michigan, Ann Arbor, MI 48109 USA. Drexel Univ, Coll Med, Philadelphia, PA 19104 USA. Dana Farber Canc Inst, Boston, MA 02115 USA. MD Anderson Canc Ctr, Houston, TX USA. St Michaels Hosp, Toronto, ON M5B 1W8, Canada. Dartmouth Coll Sch Med, Hanover, NH USA. NR 0 TC 0 Z9 0 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 JUN 20 PY 2006 VL 24 IS 18 SU S BP 50S EP 50S PN 1 PG 1 WC Oncology SC Oncology GA 063HN UT WOS:000239009400195 ER PT J AU Lamon, EB Dias, LE AF Lamon, E. B. Dias, L. E. TI NSAIDs, osteoarthritis, and colorectal cancer risk: Can administrative data provide a window into the effectiveness of a cancer prevention? SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Meeting Abstract CT 42nd Annual Meeting of the American-Society-of-Clinical-Oncology CY JUN 02-06, 2006 CL Atlanta, GA SP Amer Soc Clin Oncol C1 Massachusetts Gen Hosp, Boston, MA 02114 USA. NR 0 TC 0 Z9 0 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 JUN 20 PY 2006 VL 24 IS 18 SU S BP 54S EP 54S PN 1 PG 1 WC Oncology SC Oncology GA 063HN UT WOS:000239009400213 ER PT J AU Chakravarti, A Berkey, B Robins, HI Guha, A Curran, WJ Brachman, D Shultz, C Mehta, M AF Chakravarti, A. Berkey, B. Robins, H. I. Guha, A. Curran, W. J. Brachman, D. Shultz, C. Mehta, M. TI An update of phase II results from RTOG 0211: A phase I/II study of gefitinib with radiotherapy in newly diagnosed glioblastorna. SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Meeting Abstract CT 42nd Annual Meeting of the American-Society-of-Clinical-Oncology CY JUN 02-06, 2006 CL Atlanta, GA SP Amer Soc Clin Oncol C1 Massachusetts Gen Hosp, Boston, MA 02114 USA. Amer Coll Radiol, Philadelphia, PA USA. Univ Wisconsin, Madison, WI USA. Univ Toronto, Toronto, ON, Canada. Thomas Jefferson Med Coll, Philadelphia, PA USA. Fdn Canc Res & Educ, Phoenix, AZ USA. Med Coll Wisconsin, Milwaukee, WI 53226 USA. NR 0 TC 4 Z9 4 U1 0 U2 1 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 JUN 20 PY 2006 VL 24 IS 18 SU S BP 64S EP 64S PN 1 PG 1 WC Oncology SC Oncology GA 063HN UT WOS:000239009400251 PM 27952272 ER PT J AU Glantz, MJ Chamberlain, MC Batchelor, T Eric, W Cavalli, F Shapiro, WR AF Glantz, M. J. Chamberlain, M. C. Batchelor, T. Eric, W. Cavalli, F. Shapiro, W. R. TI Interaction between route of intra-CSF chemotherapy administration and efficacy of therapy in patients wtih neoplastic meningitis. SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Meeting Abstract CT 42nd Annual Meeting of the American-Society-of-Clinical-Oncology CY JUN 02-06, 2006 CL Atlanta, GA SP Amer Soc Clin Oncol C1 Univ Massachusetts, Boston, MA 02125 USA. Moffitt Canc Ctr, Tampa, FL USA. Massachusetts Gen Hosp, Boston, MA 02114 USA. Beth Israel Deaconess Med Ctr, Boston, MA 02215 USA. Osped San Giovanni Bellinzona, Bellinzona, Switzerland. Barrow Neurol Inst, Phoenix, AZ 85013 USA. NR 0 TC 1 Z9 1 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 JUN 20 PY 2006 VL 24 IS 18 SU S BP 65S EP 65S PN 1 PG 1 WC Oncology SC Oncology GA 063HN UT WOS:000239009400253 ER PT J AU Grimm, S Pulido, J Jahnke, K Schiff, D Hall, A Shenkier, T Siegal, T Nancy, D Batchelor, T Abrey, L AF Grimm, S. Pulido, J. Jahnke, K. Schiff, D. Hall, A. Shenkier, T. Siegal, T. Nancy, D. Batchelor, T. Abrey, L. TI Primary intraocular lymphoma (PIOL): an international primary CNS Lymphoma Collaborative Group report. SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Meeting Abstract CT 42nd Annual Meeting of the American-Society-of-Clinical-Oncology CY JUN 02-06, 2006 CL Atlanta, GA SP Amer Soc Clin Oncol C1 Mem Sloan Kettering Canc Ctr, New York, NY 10021 USA. Mayo Clin Rochester, Rochester, MN USA. Charite Univ Med Berlin, Berlin, Germany. Univ Virginia, Charlottesville, VA USA. Royal Melbourne Hosp, Melbourne, Vic, Australia. British Columbia Canc Agcy, Vancouver, BC V5Z 4E6, Canada. Hadassah Hebrew Univ Hosp, IL-91120 Jerusalem, Israel. Oregon Hlth Sci Univ, Portland, OR 97201 USA. Massachusetts Gen Hosp, Boston, MA 02114 USA. NR 0 TC 0 Z9 0 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 JUN 20 PY 2006 VL 24 IS 18 SU S BP 66S EP 66S PN 1 PG 1 WC Oncology SC Oncology GA 063HN UT WOS:000239009400257 ER PT J AU Kilpatrick, MR Linn, NU Smith, JK Winer, EP Bullitt, E Carey, LA Ewend, MG AF Kilpatrick, M. R. Linn, N. U. Smith, J. K. Winer, E. P. Bullitt, E. Carey, L. A. Ewend, M. G. TI Superiority of bi-dimensional measurements compared to RECIST in measuring response of metastatic brain tumors. SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Meeting Abstract CT 42nd Annual Meeting of the American-Society-of-Clinical-Oncology CY JUN 02-06, 2006 CL Atlanta, GA SP Amer Soc Clin Oncol C1 Univ N Carolina, Chapel Hill, NC USA. Dana Farber Canc Inst, Boston, MA 02115 USA. NR 0 TC 2 Z9 2 U1 0 U2 1 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 JUN 20 PY 2006 VL 24 IS 18 SU S BP 68S EP 68S PN 1 PG 1 WC Oncology SC Oncology GA 063HN UT WOS:000239009400265 ER PT J AU Chang, SM Lamborn, K Wen, P Deangelis, L Fink, K Lieberman, F Yung, A Robins, I Cloughesy, T Junck, L Prados, M AF Chang, S. M. Lamborn, K. Wen, P. Deangelis, L. Fink, K. Lieberman, F. Yung, A. Robins, I. Cloughesy, T. Junck, L. Prados, M. TI Phase II study of POLY-ICLC in recurrent anaplastic glioma - A North American Brain Tumor Consortium study. SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Meeting Abstract CT 42nd Annual Meeting of the American-Society-of-Clinical-Oncology CY JUN 02-06, 2006 CL Atlanta, GA SP Amer Soc Clin Oncol C1 Dana Farber Canc Inst, Boston, MA 02115 USA. Mem Sloan Kettering Canc Ctr, New York, NY 10021 USA. Univ Texas, SW Med Ctr, Dallas, TX USA. Univ Pittsburgh, Pittsburgh, PA USA. MD Anderson Canc Ctr, Houston, TX USA. Univ Wisconsin, Madison, WI USA. Univ Calif Los Angeles, Los Angeles, CA USA. Univ Michigan, Ann Arbor, MI 48109 USA. Univ Calif San Francisco, Neurooncol Serv, San Francisco, CA 94143 USA. NR 0 TC 0 Z9 0 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 JUN 20 PY 2006 VL 24 IS 18 SU S BP 70S EP 70S PN 1 PG 1 WC Oncology SC Oncology GA 063HN UT WOS:000239009400273 ER PT J AU Olson, JJ Blakeley, JO Grossman, SA Weingart, J Rashid, A Supko, J AF Olson, J. J. Blakeley, J. O. Grossman, S. A. Weingart, J. Rashid, A. Supko, J. CA Nabtt CNS Consortium TI Differences in the distribution of methotrexate into high grade gliomas following intravenous administration, as monitored by microdialysis, are associated with blood brain barrier integrity. SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Meeting Abstract CT 42nd Annual Meeting of the American-Society-of-Clinical-Oncology CY JUN 02-06, 2006 CL Atlanta, GA SP Amer Soc Clin Oncol C1 Emory Univ, Nabtt CNS Consortium, Atlanta, GA 30322 USA. Massachusetts Gen Hosp, Boston, MA 02114 USA. Johns Hopkins Univ, Baltimore, MD USA. NR 0 TC 1 Z9 1 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 JUN 20 PY 2006 VL 24 IS 18 SU S BP 70S EP 70S PN 1 PG 1 WC Oncology SC Oncology GA 063HN UT WOS:000239009400272 ER PT J AU Hochberg, EH Supko, J Amato, A Salem, N Carminati, P Wen, P AF Hochberg, E. H. Supko, J. Amato, A. Salem, N. Carminati, P. Wen, P. TI Phase I trial and pharmacokinetic study of oral gimatecan in adults with malignant glioma. SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Meeting Abstract CT 42nd Annual Meeting of the American-Society-of-Clinical-Oncology CY JUN 02-06, 2006 CL Atlanta, GA SP Amer Soc Clin Oncol C1 Harvard Univ, Sch Med, Boston, MA 02115 USA. Sigma Tau Res Inc, Gaithersburg, MD USA. Sigmatau SpA Ind Farmaceut Riunite, Pomezia, Italy. Dana Farber Canc Inst, Boston, MA 02115 USA. NR 0 TC 0 Z9 0 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 JUN 20 PY 2006 VL 24 IS 18 SU S BP 72S EP 72S PN 1 PG 1 WC Oncology SC Oncology GA 063HN UT WOS:000239009400281 ER PT J AU Phuphanich, S Supko, J Carson, KA Grossman, SA Nabors, LB Mikkelsen, T Lesser, G Rosenfeld, M Desideri, S Olson, J AF Phuphanich, S. Supko, J. Carson, K. A. Grossman, S. A. Nabors, L. B. Mikkelsen, T. Lesser, G. Rosenfeld, M. Desideri, S. Olson, J. CA Nabtt CNS Consortium TI Phase I trial of bortezomib in adults with recurrent malignant glioma. SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Meeting Abstract CT 42nd Annual Meeting of the American-Society-of-Clinical-Oncology CY JUN 02-06, 2006 CL Atlanta, GA SP Amer Soc Clin Oncol C1 Nabtt CNS Consortium, Atlanta, GA USA. Winship Canc Inst, Atlanta, GA USA. Massachusetts Gen Hosp, Boston, MA 02114 USA. Johns Hopkins Univ, Baltimore, MD USA. Univ Alabama, Birmingham, AL USA. Henry Ford Hosp, Detroit, MI 48202 USA. Wake Forest Univ, Winston Salem, NC 27109 USA. Univ Penn, Philadelphia, PA 19104 USA. NR 0 TC 2 Z9 2 U1 0 U2 1 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 JUN 20 PY 2006 VL 24 IS 18 SU S BP 74S EP 74S PN 1 PG 1 WC Oncology SC Oncology GA 063HN UT WOS:000239009400289 ER PT J AU Kesari, S Schiff, D Doherty, L Gigas, D Batchelor, T Muzikansky, A O'Neill, A Drappatz, J Kieran, M Wen, PY AF Kesari, S. Schiff, D. Doherty, L. Gigas, D. Batchelor, T. Muzikansky, A. O'Neill, A. Drappatz, J. Kieran, M. Wen, P. Y. TI Phase II study of antiangiogenic (metronomic) chemotherapy for recurrent malignant gliomas. SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Meeting Abstract CT 42nd Annual Meeting of the American-Society-of-Clinical-Oncology CY JUN 02-06, 2006 CL Atlanta, GA SP Amer Soc Clin Oncol C1 Dana Farber Canc Inst, Boston, MA 02115 USA. Univ Virginia, Charlottesville, VA USA. Massachusetts Gen Hosp, Boston, MA 02114 USA. Childrens Hosp, Boston, MA 02115 USA. RI Kesari, Santosh/E-8461-2013 NR 0 TC 0 Z9 0 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 JUN 20 PY 2006 VL 24 IS 18 SU S BP 75S EP 75S PN 1 PG 1 WC Oncology SC Oncology GA 063HN UT WOS:000239009400292 ER PT J AU Heath, EI Alousi, A Eder, JP Valdivieso, M Vasist, LS Appleman, L Bhargava, P Colevas, AD Lorusso, PM Shapiro, G AF Heath, E. I. Alousi, A. Eder, J. P. Valdivieso, M. Vasist, L. S. Appleman, L. Bhargava, P. Colevas, A. D. Lorusso, P. M. Shapiro, G. TI A phase I dose escalation trial of ispinesib (SB-715992) administered days 1-3 of a 21-day cycle in patients with advanced solid tumors. SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Meeting Abstract CT 42nd Annual Meeting of the American-Society-of-Clinical-Oncology CY JUN 02-06, 2006 CL Atlanta, GA SP Amer Soc Clin Oncol C1 Dana Farber Canc Inst, Boston, MA 02115 USA. Karmanos Canc Inst, Detroit, MI USA. GlaxoSmithKline Inc, San Francisco, CA USA. Natl Canc Inst, Rockville, MD USA. NR 0 TC 2 Z9 2 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 JUN 20 PY 2006 VL 24 IS 18 SU S BP 85S EP 85S PN 1 PG 1 WC Oncology SC Oncology GA 063HN UT WOS:000239009400332 ER PT J AU Liebes, L Levy, DE Poplin, E Mendoza, S Fry, D Buckley, M Zoloratov, A Benson, A Hochster, H AF Liebes, L. Levy, D. E. Poplin, E. Mendoza, S. Fry, D. Buckley, M. Zoloratov, A. Benson, A., III Hochster, H. TI Gemcitabine (G) plamsa and intracellular pharmacokinetics in E6201: Greater metabolite levels using fixed dosing rate (FDR) delivery. SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Meeting Abstract CT 42nd Annual Meeting of the American-Society-of-Clinical-Oncology CY JUN 02-06, 2006 CL Atlanta, GA SP Amer Soc Clin Oncol C1 NYU, Med Ctr, New York, NY 10012 USA. Dana Farber Canc Inst, Boston, MA USA. Canc Inst New Jersey, New Brunswick, NJ USA. Northwestern Univ, Chicago, IL 60611 USA. NR 0 TC 1 Z9 1 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 JUN 20 PY 2006 VL 24 IS 18 SU S BP 85S EP 85S PN 1 PG 1 WC Oncology SC Oncology GA 063HN UT WOS:000239009400331 ER PT J AU Simon, GR Janne, PA Langer, C Clarie, V Dowlati, A Gadgeel, SM Kelly, K Ye, Z Obasaju, CK Hood, KE Kindler, HL AF Simon, G. R. Janne, P. A. Langer, C. Clarie, V. Dowlati, A. Gadgeel, S. M. Kelly, K. Ye, Z. Obasaju, C. K. Hood, K. E. Kindler, H. L. TI A finalized phase II report of pemetrexed (P) plus gemcitabine (G) as front-line chemotherapy for patients with peritoneal mesothelioma (PM). SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Meeting Abstract CT 42nd Annual Meeting of the American-Society-of-Clinical-Oncology CY JUN 02-06, 2006 CL Atlanta, GA SP Amer Soc Clin Oncol C1 Univ S Florida, H Lee Moffitt Canc Ctr, Tampa, FL 33682 USA. Dana Farber Canc Inst, Boston, MA 02115 USA. Fox Chase Canc Ctr, Philadelphia, PA 19111 USA. Univ New Mexico, Canc Res & Canc, Albuquerque, NM 87131 USA. Case Western Reserve Univ, Cleveland, OH 44106 USA. Wayne State Univ, Detroit, MI 48202 USA. Univ Colorado, Hlth Sci Ctr, Aurora, CO USA. Eli Lilly & Co, Indianapolis, IN 46285 USA. Univ Chicago, Chicago, IL 60637 USA. NR 0 TC 0 Z9 0 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 JUN 20 PY 2006 VL 24 IS 18 SU S BP 91S EP 91S PN 1 PG 1 WC Oncology SC Oncology GA 063HN UT WOS:000239009400356 ER PT J AU Supko, JG He, X Sao, N D'Amato, F Blaszkowsky, L Clark, JR Shapiro, GI Bhargava, P Appleman, LJ Eder, JP AF Supko, J. G. He, X. Sao, N. D'Amato, F. Blaszkowsky, L. Clark, J. R. Shapiro, G. I. Bhargava, P. Appleman, L. J. Eder, J. P. TI Pharmacokinetics of PT523, a novel aminopterin analogue, in patients with solid tumors. SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Meeting Abstract CT 42nd Annual Meeting of the American-Society-of-Clinical-Oncology CY JUN 02-06, 2006 CL Atlanta, GA SP Amer Soc Clin Oncol C1 Harvard Univ, Dana Farber Canc Inst, Ctr Canc, Boston, MA 02115 USA. Massachusetts Gen Hosp, Boston, MA 02115 USA. NR 0 TC 0 Z9 0 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 JUN 20 PY 2006 VL 24 IS 18 SU S BP 92S EP 92S PN 1 PG 1 WC Oncology SC Oncology GA 063HN UT WOS:000239009400359 ER PT J AU Kantoff, PW Glode, LM Tannenbaum, SI Bilhartz, DL Pittman, WG Schuetz, TJ AF Kantoff, P. W. Glode, L. M. Tannenbaum, S. I. Bilhartz, D. L. Pittman, W. G. Schuetz, T. J. TI Randomized, double-blind, vector-controlled study of targeted immunotherapy in patients (pts) with hormone-refractory prostate cancer (HRPC). SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Meeting Abstract CT 42nd Annual Meeting of the American-Society-of-Clinical-Oncology CY JUN 02-06, 2006 CL Atlanta, GA SP Amer Soc Clin Oncol C1 Dana Farber Canc Inst, Boston, MA 02115 USA. UCHSC Anschutz Canc Pavil, Aurora, CO USA. Urol Ctr, Greensboro, NC USA. Urol Associates, Nashville, TN USA. Urol Ctr Alabama, Homewood, AL USA. Therion Biol Corp, Cambridge, MA USA. NR 0 TC 5 Z9 5 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 JUN 20 PY 2006 VL 24 IS 18 SU S BP 100S EP 100S PN 1 PG 1 WC Oncology SC Oncology GA 063HN UT WOS:000239009400391 ER PT J AU Ho, AW Hatjiharissi, E Branagan, A Hunter, Z McEarchern, J Law, C Grewal, IS Santos, D Tai, Y Treon, SP AF Ho, A. W. Hatjiharissi, E. Branagan, A. Hunter, Z. McEarchern, J. Law, C. Grewal, I. S. Santos, D. Tai, Y. Treon, S. P. CA Bing Ctr for WM TI Therapeutic targeting of CD70 and CD27-CD70 interactions with the monoclonal antibody SGN-70 in Waldenstrom's Macroglobulinemia (WM). SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Meeting Abstract CT 42nd Annual Meeting of the American-Society-of-Clinical-Oncology CY JUN 02-06, 2006 CL Atlanta, GA SP Amer Soc Clin Oncol C1 Bing Ctr Waldenstroms Macroglobulinemia, Boston, MA USA. Dana Farber Canc Inst, Boston, MA 02115 USA. Seattle Genet Inc, Bothell, WA USA. RI Hunter, Zachary/H-3018-2013 OI Hunter, Zachary/0000-0002-1689-1691 NR 0 TC 2 Z9 2 U1 0 U2 0 PU AMER SOC 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 JUN 20 PY 2006 VL 24 IS 18 SU S BP 102S EP 102S PN 1 PG 1 WC Oncology SC Oncology GA 063HN UT WOS:000239009400399 ER PT J AU Rubin, EH Shapiro, GI Stein, MN Watson, P Bergstrom, D Xiao, A Clark, JB Freedman, SJ Eder, JP AF Rubin, E. H. Shapiro, G. I. Stein, M. N. Watson, P. Bergstrom, D. Xiao, A. Clark, J. B. Freedman, S. J. Eder, J. P. TI A phase I clinical and pharmacokinetic (PK) trial of the aurora kinase (AK) inhibitor MK-0457 in cancer patients. SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Meeting Abstract CT 42nd Annual Meeting of the American-Society-of-Clinical-Oncology CY JUN 02-06, 2006 CL Atlanta, GA SP Amer Soc Clin Oncol C1 Canc Inst New Jersey, New Brunswick, NJ USA. Dana Farber Canc Inst, Boston, MA 02115 USA. Merck Res Labs, Blue Bell, PA USA. NR 0 TC 7 Z9 7 U1 1 U2 2 PU AMER SOC CLINICAL ONCOLOGY PI ALEXANDRIA PA 330 JOHN CARLYLE ST, STE 300, ALEXANDRIA, VA 22314 USA SN 0732-183X J9 J CLIN ONCOL JI J. Clin. Oncol. PD JUN 20 PY 2006 VL 24 IS 18 SU S BP 123S EP 123S PN 1 PG 1 WC Oncology SC Oncology GA 063HN UT WOS:000239009400480 ER PT J AU Wong, KK Fracasso, PM Bukowski, RM Munster, PN Lynch, T Abbas, R Quinn, SE Zacharchuk, C Burris, H AF Wong, K. K. Fracasso, P. M. Bukowski, R. M. Munster, P. N. Lynch, T. Abbas, R. Quinn, S. E. Zacharchuk, C. Burris, H. TI HKI-272, an irreversible pan erbB receptor tyrosine kinase inhibitor: Preliminary phase 1 results in patients with solid tumors. SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Meeting Abstract CT 42nd Annual Meeting of the American-Society-of-Clinical-Oncology CY JUN 02-06, 2006 CL Atlanta, GA SP Amer Soc Clin Oncol C1 Dana Farber Canc Inst, Boston, MA 02115 USA. Washington Univ, Sch Med, St Louis, MO 63130 USA. Cleveland Clin Fdn, Cleveland, OH 44195 USA. Univ S Florida, H Lee Moffitt Canc Ctr, Tampa, FL 33682 USA. Massachusetts Gen Hosp, Boston, MA 02114 USA. Wyeth Ayerst Res, Collegeville, PA USA. Wyeth Ayerst Res, Cambridge, MA USA. Sarah Cannon Res Inst, Nashville, TN USA. NR 0 TC 9 Z9 9 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 JUN 20 PY 2006 VL 24 IS 18 SU S BP 125S EP 125S PN 1 PG 1 WC Oncology SC Oncology GA 063HN UT WOS:000239009400490 ER PT J AU Duda, DG Cohen, KS Di Tomaso, E Scadden, DT Willett, CG Jain, RK AF Duda, D. G. Cohen, K. S. Di Tomaso, E. Scadden, D. T. Willett, C. G. Jain, R. K. TI Differential circulation kinetics during antiangiogenic therapy of four distinct blood cell populations expressing endothelial markers. SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Meeting Abstract CT 42nd Annual Meeting of the American-Society-of-Clinical-Oncology CY JUN 02-06, 2006 CL Atlanta, GA SP Amer Soc Clin Oncol C1 Massachusetts Gen Hosp, Charlestown, MA USA. Massachusetts Gen Hosp, Boston, MA 02114 USA. Duke Univ, Med Ctr, Durham, NC USA. NR 0 TC 1 Z9 1 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 JUN 20 PY 2006 VL 24 IS 18 SU S BP 130S EP 130S PN 1 PG 1 WC Oncology SC Oncology GA 063HN UT WOS:000239009400510 ER PT J AU Eder, JP Appleman, L Heath, E Malburg, L Zhu, A Pilat, MJ Shapiro, G Lorusso, P AF Eder, J. P. Appleman, L. Heath, E. Malburg, L. Zhu, A. Pilat, M. J. Shapiro, G. Lorusso, P. TI A phase I study of a novel spectrum selective kinase inhibitor (SSKI), XL880, administered orally in patients (pts) with advanced solid tumors (STs). SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Meeting Abstract CT 42nd Annual Meeting of the American-Society-of-Clinical-Oncology CY JUN 02-06, 2006 CL Atlanta, GA SP Amer Soc Clin Oncol C1 Dana Farber Canc Inst, Boston, MA 02115 USA. Karmanos Canc Ctr, Detroit, MI USA. Massachusetts Gen Hosp, Boston, MA 02114 USA. Karmanos Canc Inst, Detroit, MI USA. NR 0 TC 0 Z9 0 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 JUN 20 PY 2006 VL 24 IS 18 SU S BP 131S EP 131S PN 1 PG 1 WC Oncology SC Oncology GA 063HN UT WOS:000239009400512 ER PT J AU Chanan-Khan, A Richardson, P Alsina, M Lonial, S Krishnan, A Carroll, M Albitar, M Hannah, AL Johnson, RG Anderson, K AF Chanan-Khan, A. Richardson, P. Alsina, M. Lonial, S. Krishnan, A. Carroll, M. Albitar, M. Hannah, A. L. Johnson, R. G. Anderson, K. TI Phase 1 clinical trial of KOS-953 plus bortezomib (BZ) in relapsed refractory multiple myeloma (MM). SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Meeting Abstract CT 42nd Annual Meeting of the American-Society-of-Clinical-Oncology CY JUN 02-06, 2006 CL Atlanta, GA SP Amer Soc Clin Oncol C1 Roswell Pk Canc Inst, Buffalo, NY 14263 USA. Dana Farber Canc Inst, Boston, MA USA. Univ S Florida, H Lee Moffitt Canc Ctr, Tampa, FL 33682 USA. Winship Canc Inst, Atlanta, GA USA. City Hope Natl Med Ctr, Duarte, CA 91010 USA. Univ Arizona, Arizona Canc Ctr, Tucson, AZ USA. Quest Diagnost, San Juan Capistrano, CA USA. Kosan Biosci Inc, Hayward, CA USA. NR 0 TC 0 Z9 0 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 JUN 20 PY 2006 VL 24 IS 18 SU S BP 137S EP 137S PN 1 PG 1 WC Oncology SC Oncology GA 063HN UT WOS:000239009400538 ER PT J AU Van den Abbeele, AD Barnes, AS De Vries, DJ Yap, JT Reichardt, P Casalli, PG Von Mehren, M O'Neel, J Hayes, W Demetri, GD AF Van den Abbeele, A. D. Barnes, A. S. De Vries, D. J. Yap, J. T. Reichardt, P. Casalli, P. G. Von Mehren, M. O'Neel, J. Hayes, W. Demetri, G. D. TI Assessment of response using FDG-PET and CT in a phase I study of AMN107 alone or in combination with imatinib (IM) in patients with imatinib-resistant (IM-R) gastrointestinal stromal tumors (GIST). SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Meeting Abstract CT 42nd Annual Meeting of the American-Society-of-Clinical-Oncology CY JUN 02-06, 2006 CL Atlanta, GA SP Amer Soc Clin Oncol C1 Dana Farber Canc Inst, Boston, MA 02115 USA. Ist Tumori, Milan, Italy. Fox Chase Canc Ctr, Philadelphia, PA 19111 USA. Novartis Pharmaceut Corp, E Hanover, NJ USA. NR 0 TC 1 Z9 1 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 JUN 20 PY 2006 VL 24 IS 18 SU S MA 3087 BP 142S EP 142S PN 1 PG 1 WC Oncology SC Oncology GA 063HN UT WOS:000239009401006 PM 27955213 ER PT J AU Fuchs, C Marshall, J Mitchell, E Wierzbicki, R Ganju, V Jeffery, M Schultz, J Richards, D Wang, B Morrison, M AF Fuchs, C. Marshall, J. Mitchell, E. Wierzbicki, R. Ganju, V. Jeffery, M. Schultz, J. Richards, D. Wang, B. Morrison, M. TI A randomized trial of first-line irinotecan/fluoropymidine combinations with or without celecoxib in metastatic colorectal cancer (BICC-C). SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Meeting Abstract CT 42nd Annual Meeting of the American-Society-of-Clinical-Oncology CY JUN 02-06, 2006 CL Atlanta, GA SP Amer Soc Clin Oncol C1 Dana Farber Canc Inst, Boston, MA 02115 USA. Vincent T Lombardi Canc Res Ctr, Washington, DC USA. Thomas Jefferson Univ, Med Ctr, Philadelphia, PA 19107 USA. Lakeridge Hlth Oshawa, Oshawa, ON, Canada. Frankston Hosp, Frankston, Vic, Australia. Christchurch Hosp, Christchurch, New Zealand. Virginia Oncol Associates, Newport News, VA USA. Tyler Canc Ctr, Tyler, TX USA. Pfizer Global Pharmaceut, New York, NY USA. NR 0 TC 18 Z9 18 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 JUN 20 PY 2006 VL 24 IS 18 SU S MA 3506 BP 147S EP 147S PN 1 PG 1 WC Oncology SC Oncology GA 063HN UT WOS:000239009401023 ER PT J AU Venook, A Niedzwiecki, D Hollis, D Sutherland, S Goldberg, R Alberts, S Benson, A Wade, J Schilsky, R Mayer, R AF Venook, A. Niedzwiecki, D. Hollis, D. Sutherland, S. Goldberg, R. Alberts, S. Benson, A. Wade, J. Schilsky, R. Mayer, R. TI Phase III study of irinotecan/5FU/LV (FOLFIRI) or oxaliplatin/5FU/LV (FOLFOX) +/- cetuximab for patients (pts) with untreated metastatic adenocarcinoma of the colon or rectum (MCRC): CALGB 80203 preliminary results. SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Meeting Abstract CT 42nd Annual Meeting of the American-Society-of-Clinical-Oncology CY JUN 02-06, 2006 CL Atlanta, GA SP Amer Soc Clin Oncol C1 Univ Calif San Francisco, San Francisco, CA 94143 USA. CALGB Stat Ctr, Durham, NC USA. Univ N Carolina, Chapel Hill, NC USA. Mayo Clin, Rochester, MN USA. Northwestern Univ, Chicago, IL 60611 USA. Cent Illinois CCOP, Decatur, IL USA. Univ Chicago, Chicago, IL 60637 USA. Dana Farber Canc Inst, Boston, MA 02115 USA. NR 0 TC 43 Z9 44 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 JUN 20 PY 2006 VL 24 IS 18 SU S MA 3509 BP 148S EP 148S PN 1 PG 1 WC Oncology SC Oncology GA 063HN UT WOS:000239009401028 PM 27953330 ER PT J AU Benson, AB Catalan, P Meropol, NJ Giantonio, BJ Sigurdson, ER Martenson, JA Whitehead, RP Sinicrope, F Mayer, RJ O'Dwyer, PJ AF Benson, A. B. Catalan, P. Meropol, N. J. Giantonio, B. J. Sigurdson, E. R. Martenson, J. A. Whitehead, R. P. Sinicrope, F. Mayer, R. J. O'Dwyer, P. J. TI ECOG E3201: Intergroup randomized phase III study of postoperative irinotecan, 5-fluorouracil (FU), leucovorin (LV) (FOLFIRI) vs oxaliplatin, FU/LV (FOLFOX) vs FU/LV for patients (pts) with stage II/III rectal cancer receiving either pre or postoperative radiation (RT)/FU. SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Meeting Abstract CT 42nd Annual Meeting of the American-Society-of-Clinical-Oncology CY JUN 02-06, 2006 CL Atlanta, GA SP Amer Soc Clin Oncol C1 Northwestern Univ, Chicago, IL 60611 USA. Dana Farber Canc Inst, Boston, MA 02115 USA. Fox Chase Canc Ctr, Philadelphia, PA 19111 USA. Univ Penn, Med Ctr, Philadelphia, PA 19104 USA. Mayo Clin, Rochester, MN USA. Univ Texas, Med Branch, Galveston, TX 77550 USA. NR 0 TC 1 Z9 1 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 JUN 20 PY 2006 VL 24 IS 18 SU S MA 3526 BP 152S EP 152S PN 1 PG 1 WC Oncology SC Oncology GA 063HN UT WOS:000239009401043 PM 27953298 ER PT J AU Giantonio, BJ Catalano, PJ O'Dwyer, PJ Meropol, NJ Benson, AB AF Giantonio, B. J. Catalano, P. J. O'Dwyer, P. J. Meropol, N. J. Benson, A. B., III TI Impact of bevacizumab dose reduction on clinical outcomes for patients treated on the Eastern Cooperative Oncology Group's Study E3200. SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Meeting Abstract CT 42nd Annual Meeting of the American-Society-of-Clinical-Oncology CY JUN 02-06, 2006 CL Atlanta, GA SP Amer Soc Clin Oncol C1 Northwestern Univ, Chicago, IL 60611 USA. Univ Penn, Philadelphia, PA 19104 USA. Dana Farber Canc Inst, Boston, MA 02115 USA. Fox Chase Canc Ctr, Philadelphia, PA 19111 USA. NR 0 TC 1 Z9 1 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 JUN 20 PY 2006 VL 24 IS 18 SU S MA 3538 BP 155S EP 155S PN 1 PG 1 WC Oncology SC Oncology GA 063HN UT WOS:000239009401055 ER PT J AU Meyerhardt, JA Stuart, K Zhu, A Fuchs, C Bhargava, P Earle, C Blaszkowsky, L Lawrence, C Battu, S Ryan, DP AF Meyerhardt, J. A. Stuart, K. Zhu, A. Fuchs, C. Bhargava, P. Earle, C. Blaszkowsky, L. Lawrence, C. Battu, S. Ryan, D. P. TI Phase II study of FOLFOX, bevacizumab and erlotinib as initial therapy for patients with metastatic colorectal cancer (MCRC). SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Meeting Abstract CT 42nd Annual Meeting of the American-Society-of-Clinical-Oncology CY JUN 02-06, 2006 CL Atlanta, GA SP Amer Soc Clin Oncol C1 Dana Farber Canc Inst, Boston, MA 02115 USA. Beth Israel Deaconess Med Ctr, Boston, MA 02215 USA. Massachusetts Gen Hosp, Boston, MA 02114 USA. NR 0 TC 2 Z9 2 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 JUN 20 PY 2006 VL 24 IS 18 SU S MA 3545 BP 157S EP 157S PN 1 PG 1 WC Oncology SC Oncology GA 063HN UT WOS:000239009401064 PM 27953263 ER PT J AU Ajani, JA Winter, KA Gunderson, LL Pedersen, J Benson, AB Thomas, C Mayer, RJ Haddock, MG Willett, C Willett, C Rich, TA AF Ajani, J. A. Winter, K. A. Gunderson, L. L. Pedersen, J. Benson, A. B. Thomas, C. Mayer, R. J. Haddock, M. G. Willett, C. Willett, C. Rich, T. A. TI Intergroup RTOG 98-11: A phase III randomized study of 5-fluorouracil (5-FU), mitomycin, and radiotherapy versus 5-fluorouracil, cisplatin and radiotherapy in carcinoma of the anal canal. SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Meeting Abstract CT 42nd Annual Meeting of the American-Society-of-Clinical-Oncology CY JUN 02-06, 2006 CL Atlanta, GA SP Amer Soc Clin Oncol C1 Univ Texas, MD Anderson Canc Ctr, Houston, TX 77030 USA. Radiat Therapy Oncol Grp, Philadelphia, PA USA. Mayo Clin Scottsdale, Scottsdale, AZ USA. Univ Alberta, Edmonton, AB, Canada. Northwestern Univ, Chicago, IL 60611 USA. Oregon Hlth Sci Univ, Portland, OR 97201 USA. Dana Farber Canc Inst, Boston, MA 02115 USA. Mayo Clin & Mayo Fdn, Rochester, MN 55905 USA. Duke Univ, Med Ctr, Durham, NC 27705 USA. Univ Virginia, Med Ctr, Charlottesville, VA USA. NR 0 TC 16 Z9 17 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 JUN 20 PY 2006 VL 24 IS 18 SU S MA 4009 BP 180S EP 180S PN 1 PG 1 WC Oncology SC Oncology GA 063HN UT WOS:000239009401157 PM 27953393 ER PT J AU Poplin, E Levy, DE Berlin, J Rothenberg, M Cella, D Mitchell, E Alberts, S Benson, A AF Poplin, E. Levy, D. E. Berlin, J. Rothenberg, M. Cella, D. Mitchell, E. Alberts, S. Benson, A., III TI Phase III trial of gemcitabine (30-minute infusion) versus gemcitabine (fixed-dose-rate infusion [FDR]) versus gemcitabine plus oxaliplatin (GEMOX) in patients with advanced pancreatic cancer (E6201). SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Meeting Abstract CT 42nd Annual Meeting of the American-Society-of-Clinical-Oncology CY JUN 02-06, 2006 CL Atlanta, GA SP Amer Soc Clin Oncol C1 Canc Inst New Jersey, New Brunswick, NJ USA. Dana Farber Canc Inst, Boston, MA 02115 USA. Vanderbilt Ingram Canc Ctr, Nashville, TN USA. Evanston NW Healthcare, Evanston, IL USA. Thomas Jefferson Univ, Philadelphia, PA 19107 USA. Mayo Clin, Rochester, MN USA. Northwestern Univ, Chicago, IL 60611 USA. NR 0 TC 39 Z9 40 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 JUN 20 PY 2006 VL 24 IS 18 SU S MA LBA4004 BP 180S EP 180S PN 1 PG 1 WC Oncology SC Oncology GA 063HN UT WOS:000239009401154 ER PT J AU Tepper, JE Krasna, M Niedzwiecki, D Hollis, D Reed, C Goldberg, R Rich, T Kiel, K Mayer, R AF Tepper, J. E. Krasna, M. Niedzwiecki, D. Hollis, D. Reed, C. Goldberg, R. Rich, T. Kiel, K. Mayer, R. TI Superiority of trimodality therapy to surgery alone in esophageal cancer: Results of CALGB 9781. SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Meeting Abstract CT 42nd Annual Meeting of the American-Society-of-Clinical-Oncology CY JUN 02-06, 2006 CL Atlanta, GA SP Amer Soc Clin Oncol C1 Univ N Carolina, Lineberger Comprehens Canc Ctr, Chapel Hill, NC USA. Univ Maryland, Baltimore, MD 21201 USA. CALGB Stat Ctr, Durham, NC USA. Med Univ S Carolina, Charleston, SC 29425 USA. Univ Virginia, Charlottesville, VA USA. Northwestern Univ, Chicago, IL 60611 USA. Dana Farber Canc Inst, Boston, MA 02115 USA. NR 0 TC 16 Z9 16 U1 1 U2 1 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 JUN 20 PY 2006 VL 24 IS 18 SU S MA 4012 BP 181S EP 181S PN 1 PG 1 WC Oncology SC Oncology GA 063HN UT WOS:000239009401159 ER PT J AU Bello, C Deprimo, SE Friece, C Smeraglia, J Sherman, L Tye, L Baum, C Meropol, NJ Lenz, H Kulke, MH AF Bello, C. Deprimo, S. E. Friece, C. Smeraglia, J. Sherman, L. Tye, L. Baum, C. Meropol, N. J. Lenz, H. Kulke, M. H. TI Analysis of circulating biomarkers of sunitinib malate in patients with unresectable neuroendocrine tumors (NET): VEGF, IL-8, and soluble VEGF receptors 2 and 3. SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Meeting Abstract CT 42nd Annual Meeting of the American-Society-of-Clinical-Oncology CY JUN 02-06, 2006 CL Atlanta, GA SP Amer Soc Clin Oncol C1 Pfizer Global Res & Dev, La Jolla, CA USA. Fox Chase Canc Ctr, Philadelphia, PA 19111 USA. USC Norris Comprehens Canc Ctr, Los Angeles, CA USA. Dana Farber Canc Inst, Boston, MA 02115 USA. NR 0 TC 9 Z9 9 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 JUN 20 PY 2006 VL 24 IS 18 SU S MA 4045 BP 189S EP 189S PN 1 PG 1 WC Oncology SC Oncology GA 063HN UT WOS:000239009401193 ER PT J AU Kulke, MH Stuart, K Earle, CC Bhargava, P Clark, JW Enzinger, PC Meyerhardt, J Attawia, M Lawrence, C Fuchs, CS AF Kulke, M. H. Stuart, K. Earle, C. C. Bhargava, P. Clark, J. W. Enzinger, P. C. Meyerhardt, J. Attawia, M. Lawrence, C. Fuchs, C. S. TI A phase II study of temozolomide and bevacizumab in patients with advanced neuroendocrine tumors. SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Meeting Abstract CT 42nd Annual Meeting of the American-Society-of-Clinical-Oncology CY JUN 02-06, 2006 CL Atlanta, GA SP Amer Soc Clin Oncol C1 Dana Farber Canc Inst, Boston, MA 02115 USA. Beth Israel Deaconess Med Ctr, Boston, MA 02215 USA. Massachusetts Gen Hosp, Boston, MA 02114 USA. NR 0 TC 31 Z9 31 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 JUN 20 PY 2006 VL 24 IS 18 SU S MA 4044 BP 189S EP 189S PN 1 PG 1 WC Oncology SC Oncology GA 063HN UT WOS:000239009401191 ER PT J AU Enzinger, PC Yock, T Suh, W Fidias, P Mamon, H Choi, N Lehman, N Lawrence, C Lynch, T Fuchs, C AF Enzinger, P. C. Yock, T. Suh, W. Fidias, P. Mamon, H. Choi, N. Lehman, N. Lawrence, C. Lynch, T. Fuchs, C. TI Phase II cisplatin, irinotecan, cetuximab and concurrent radiation therapy followed by surgery for locally advanced esophageal cancer. SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Meeting Abstract CT 42nd Annual Meeting of the American-Society-of-Clinical-Oncology CY JUN 02-06, 2006 CL Atlanta, GA SP Amer Soc Clin Oncol C1 Dana Farber Canc Inst, Boston, MA 02115 USA. NR 0 TC 8 Z9 8 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 JUN 20 PY 2006 VL 24 IS 18 SU S MA 4064 BP 194S EP 194S PN 1 PG 1 WC Oncology SC Oncology GA 063HN UT WOS:000239009401210 ER PT J AU O'Dwyer, PJ Giantonio, BJ Levy, DE Kauh, JS Fitzgerald, DB Benson, AB AF O'Dwyer, P. J. Giantonio, B. J. Levy, D. E. Kauh, J. S. Fitzgerald, D. B. Benson, A. B., III TI Gefitinib in advanced unresectable hepatocellular carcinoma: Results from the Eastern Cooperative Oncology Group's Study E1203. SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Meeting Abstract CT 42nd Annual Meeting of the American-Society-of-Clinical-Oncology CY JUN 02-06, 2006 CL Atlanta, GA SP Amer Soc Clin Oncol C1 Univ Penn, Philadelphia, PA 19104 USA. Dana Farber Canc Inst, Boston, MA 02115 USA. Emory Univ, Atlanta, GA 30322 USA. Riverview Reg Canc Ctr, Red Bank, NJ USA. Northwestern Univ, Chicago, IL 60611 USA. NR 0 TC 47 Z9 48 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 JUN 20 PY 2006 VL 24 IS 18 SU S MA 4143 BP 213S EP 213S PN 1 PG 1 WC Oncology SC Oncology GA 063HN UT WOS:000239009401288 ER PT J AU Sun, W Schwartz, J Zhu, A Philip, PA Metz, J Thomas, MB AF Sun, W. Schwartz, J. Zhu, A. Philip, P. A. Metz, J. Thomas, M. B. CA Liver Cancer Research Grp TI Feasibility of a multi-institutional liver cancer registry. SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Meeting Abstract CT 42nd Annual Meeting of the American-Society-of-Clinical-Oncology CY JUN 02-06, 2006 CL Atlanta, GA SP Amer Soc Clin Oncol C1 Univ Penn, Liver Canc Res Grp, Hlth Syst, Philadelphia, PA 19104 USA. Mt Sinai Sch Med, New York, NY USA. Massachusetts Gen Hosp, Boston, MA 02114 USA. Karmanos Canc Inst, Detroit, MI USA. Univ Texas, MD Anderson Canc Ctr, Houston, TX 77030 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CLINICAL ONCOLOGY PI ALEXANDRIA PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA SN 0732-183X J9 J CLIN ONCOL JI J. Clin. Oncol. PD JUN 20 PY 2006 VL 24 IS 18 SU S MA 4146 BP 214S EP 214S PN 1 PG 1 WC Oncology SC Oncology GA 063HN UT WOS:000239009401290 PM 27954197 ER PT J AU Chen, RC Clark, JA Mitchell, SP Talcott, JA AF Chen, R. C. Clark, J. A. Mitchell, S. P. Talcott, J. A. TI Long-term outcomes after local treatments for prostate cancer by functional categories: Late changes, different results. SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Meeting Abstract CT 42nd Annual Meeting of the American-Society-of-Clinical-Oncology CY JUN 02-06, 2006 CL Atlanta, GA SP Amer Soc Clin Oncol C1 Massachusetts Gen Hosp, Boston, MA 02114 USA. Boston Univ, Sch Publ Hlth, Boston, MA 02215 USA. NR 0 TC 0 Z9 0 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 JUN 20 PY 2006 VL 24 IS 18 SU S BP 218S EP 218S PN 1 PG 1 WC Oncology SC Oncology GA 063HN UT WOS:000239009401307 ER PT J AU Bajorin, DF Nichols, CR Margolin, KA Bacik, J Richardson, PG Vogelzang, NJ Einhorn, L Mazumdar, M Bosl, GJ Motzer, RJ AF Bajorin, D. F. Nichols, C. R. Margolin, K. A. Bacik, J. Richardson, P. G. Vogelzang, N. J. Einhorn, L. Mazumdar, M. Bosl, G. J. Motzer, R. J. TI Phase III trial of conventional-dose chemotherapy alone or with high-dose chemotherapy for metastatic germ cell tumors (GCT) patients (PTS): A cooperative group trial by Memorial Sloan-Kettering Cancer Center, ECOG, SWOG, and CALGB. SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Meeting Abstract CT 42nd Annual Meeting of the American-Society-of-Clinical-Oncology CY JUN 02-06, 2006 CL Atlanta, GA SP Amer Soc Clin Oncol C1 Mem Sloan Kettering Canc Ctr, New York, NY 10021 USA. Oregon Hlth Sci Univ, Portland, OR USA. City Hope Natl Med Ctr, Duarte, CA 91010 USA. Dana Farber Canc Inst, Boston, MA 02115 USA. Nevada Canc Inst, Las Vegas, NV USA. Indiana Univ, Indianapolis, IN 46204 USA. Cornell Univ, Weill Med Coll, Ithaca, NY 14853 USA. NR 0 TC 2 Z9 2 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 JUN 20 PY 2006 VL 24 IS 18 SU S BP 219S EP 219S PN 1 PG 1 WC Oncology SC Oncology GA 063HN UT WOS:000239009401309 ER PT J AU Michaelson, MD Lee, H Kaufman, DS Kantoff, PW Finkelstein, J Smith, MR AF Michaelson, M. D. Lee, H. Kaufman, D. S. Kantoff, P. W. Finkelstein, J. Smith, M. R. TI Annual zoledronic acid to prevent gonadotropin-releasing hormone agonist-induced bone loss in men with prostate cancer: A randomized placebo-controlled trial. SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Meeting Abstract CT 42nd Annual Meeting of the American-Society-of-Clinical-Oncology CY JUN 02-06, 2006 CL Atlanta, GA SP Amer Soc Clin Oncol C1 Massachusetts Gen Hosp, Boston, MA 02114 USA. Dana Farber Canc Inst, Boston, MA 02115 USA. NR 0 TC 1 Z9 1 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 JUN 20 PY 2006 VL 24 IS 18 SU S BP 220S EP 220S PN 1 PG 1 WC Oncology SC Oncology GA 063HN UT WOS:000239009401315 ER PT J AU Rini, BI George, DJ Michaelson, MD Rosenberg, JE Bukowski, RM Sosman, JA Stadler, WM Margolin, K Hutson, TE Baum, CM AF Rini, B. I. George, D. J. Michaelson, M. D. Rosenberg, J. E. Bukowski, R. M. Sosman, J. A. Stadler, W. M. Margolin, K. Hutson, T. E. Baum, C. M. TI Efficacy and safety of sunitinib malate (SU11248) in bevacizumab-refractory metastatic renal cell carcinoma (mRCC). SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Meeting Abstract CT 42nd Annual Meeting of the American-Society-of-Clinical-Oncology CY JUN 02-06, 2006 CL Atlanta, GA SP Amer Soc Clin Oncol C1 Cleveland Clin Fdn, Cleveland, OH 44195 USA. Duke Univ, Durham, NC USA. Massachusetts Gen Hosp, Boston, MA 02114 USA. Univ Calif San Francisco, San Francisco, CA 94143 USA. Vanderbilt Univ, Nashville, TN USA. Univ Chicago, Chicago, IL 60637 USA. Baylor Charles A Sammons Canc Ctr, Dallas, TX USA. Pfizer Inc, La Jolla, CA USA. NR 0 TC 8 Z9 8 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 JUN 20 PY 2006 VL 24 IS 18 SU S BP 222S EP 222S PN 1 PG 1 WC Oncology SC Oncology GA 063HN UT WOS:000239009401321 ER PT J AU Houk, BE Amantea, M Motzer, RJ Michaelson, MD Rini, BI George, DJ Redman, BG Hudes, GR Poland, B Bello, CL AF Houk, B. E. Amantea, M. Motzer, R. J. Michaelson, M. D. Rini, B. I. George, D. J. Redman, B. G. Hudes, G. R. Poland, B. Bello, C. L. TI Pharmacokinetics (PK) and efficacy of sunitinib in patients with metastatic renal cell carcinoma (mRCC). SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Meeting Abstract CT 42nd Annual Meeting of the American-Society-of-Clinical-Oncology CY JUN 02-06, 2006 CL Atlanta, GA SP Amer Soc Clin Oncol C1 Pfizer Global Res & Dev, La Jolla, CA USA. Mem Sloan Kettering Canc Ctr, New York, NY 10021 USA. Massachusetts Gen Hosp, Boston, MA 02114 USA. Cleveland Clin Fdn, Cleveland, OH USA. Duke Univ, Med Ctr, Durham, NC USA. Univ Michigan, Ann Arbor, MI 48109 USA. Fox Chase Canc Ctr, Philadelphia, PA 19111 USA. Pharsight Corp, Mountain View, CA USA. NR 0 TC 0 Z9 0 U1 1 U2 1 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 JUN 20 PY 2006 VL 24 IS 18 SU S BP 224S EP 224S PN 1 PG 1 WC Oncology SC Oncology GA 063HN UT WOS:000239009401330 ER PT J AU Dreicer, R Li, S Manola, J Haas, N Roth, B Wilding, G AF Dreicer, R. Li, S. Manola, J. Haas, N. Roth, B. Wilding, G. TI Phase II trial of epothilone B analogue BMS-247550 in advanced carcinoma of the urothelium (E3800): A trial of the Eastern Cooperative Oncology Group. SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Meeting Abstract CT 42nd Annual Meeting of the American-Society-of-Clinical-Oncology CY JUN 02-06, 2006 CL Atlanta, GA SP Amer Soc Clin Oncol C1 Cleveland Clin, Cleveland, OH 44106 USA. Dana Farber Canc Inst, Boston, MA 02115 USA. Fox Chase Canc Ctr, Philadelphia, PA 19111 USA. Vanderbilt Ingram Canc Ctr, Nashville, TN USA. Univ Wisconsin, Ctr Canc, Madison, WI USA. NR 0 TC 1 Z9 1 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 JUN 20 PY 2006 VL 24 IS 18 SU S BP 227S EP 227S PN 1 PG 1 WC Oncology SC Oncology GA 063HN UT WOS:000239009401342 ER PT J AU Smith, MR Chu, F Forrest, J Malkowicz, SB Price, D Sieber, P Barnette, KG Segal, S Steiner, MS AF Smith, M. R. Chu, F. Forrest, J. Malkowicz, S. B. Price, D. Sieber, P. Barnette, K. G. Segal, S. Steiner, M. S. TI Toremifene citrate increases bone mineral density in men receiving androgen deprivation therapy for prostate cancer. SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Meeting Abstract CT 42nd Annual Meeting of the American-Society-of-Clinical-Oncology CY JUN 02-06, 2006 CL Atlanta, GA SP Amer Soc Clin Oncol C1 Massachusetts Gen Hosp, Boston, MA 02114 USA. San Bernardino Urol Associates, San Bernardino, CA USA. Urol Specialists Oklahoma, Tulsa, OK USA. Univ Penn, Philadelphia, PA 19104 USA. Reg Urol, Shreveport, LA USA. Urol Associates Lancaster, Lancaster, PA USA. GTx Inc, Memphis, TN USA. NR 0 TC 0 Z9 0 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 JUN 20 PY 2006 VL 24 IS 18 SU S BP 229S EP 229S PN 1 PG 1 WC Oncology SC Oncology GA 063HN UT WOS:000239009401351 ER PT J AU Saad, F Coleman, RE Cook, R Smith, MR Brown, JE Hei, JY Chen, YM AF Saad, F. Coleman, R. E. Cook, R. Smith, M. R. Brown, J. E. Hei, J. Y. Chen, Y. M. TI Predictors of clinical outcome in patients with bone metastases from prostate cancer. SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Meeting Abstract CT 42nd Annual Meeting of the American-Society-of-Clinical-Oncology CY JUN 02-06, 2006 CL Atlanta, GA SP Amer Soc Clin Oncol C1 Ctr Hosp Univ Montreal, Montreal, PQ, Canada. Univ Waterloo, Waterloo, ON N2L 3G1, Canada. Massachusetts Gen Hosp, Boston, MA 02114 USA. Novartis Oncol, E Hanover, NJ USA. NR 0 TC 2 Z9 2 U1 0 U2 1 PU AMER SOC CLINICAL ONCOLOGY PI ALEXANDRIA PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA SN 0732-183X EI 1527-7755 J9 J CLIN ONCOL JI J. Clin. Oncol. PD JUN 20 PY 2006 VL 24 IS 18 SU S BP 230S EP 230S PN 1 PG 1 WC Oncology SC Oncology GA 063HN UT WOS:000239009401354 ER PT J AU Lin, AM Rosenberg, JE Weinberg, VK Kelly, WK Michaelson, MD Hussain, M Wilding, G Gross, ME Small, EJ AF Lin, A. M. Rosenberg, J. E. Weinberg, V. K. Kelly, W. K. Michaelson, M. D. Hussain, M. Wilding, G. Gross, M. E. Small, E. J. TI Clinical outcome of taxane-resistant (TR) hormone refractory prostate cancer (HRPC) patients (pts) treated with subsequent chemotherapy (ixabepilone (Ix) or mitoxantrone/prednisone (MP). SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Meeting Abstract CT 42nd Annual Meeting of the American-Society-of-Clinical-Oncology CY JUN 02-06, 2006 CL Atlanta, GA SP Amer Soc Clin Oncol C1 Univ Calif San Francisco, San Francisco, CA 94143 USA. Massachusetts Gen Hosp, Boston, MA 02114 USA. Univ Michigan, Ann Arbor, MI 48109 USA. Univ Wisconsin, Madison, WI USA. Cedars Sinai Med Ctr, Los Angeles, CA 90048 USA. NR 0 TC 5 Z9 5 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 JUN 20 PY 2006 VL 24 IS 18 SU S BP 231S EP 231S PN 1 PG 1 WC Oncology SC Oncology GA 063HN UT WOS:000239009401356 ER PT J AU Pomerantz, M Manola, J Taplin, M Bubley, G Inman, M Lowell, J Kantoff, P Oh, WK AF Pomerantz, M. Manola, J. Taplin, M. Bubley, G. Inman, M. Lowell, J. Kantoff, P. Oh, W. K. TI Phase II study of low dose (LD) and high dose (HD) premarin in androgen independent prostate cancer (AIPC). SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Meeting Abstract CT 42nd Annual Meeting of the American-Society-of-Clinical-Oncology CY JUN 02-06, 2006 CL Atlanta, GA SP Amer Soc Clin Oncol C1 Dana Farber Canc Inst, Boston, MA 02115 USA. Beth Israel Deaconess Med Ctr, Boston, MA 02215 USA. RI Oh, William/B-9163-2012 OI Oh, William/0000-0001-5113-8147 NR 0 TC 1 Z9 1 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 JUN 20 PY 2006 VL 24 IS 18 SU S BP 231S EP 231S PN 1 PG 1 WC Oncology SC Oncology GA 063HN UT WOS:000239009401357 ER PT J AU Taplin, M Xie, W Morganstern, D Bubley, G Ernstoff, M Regan, M AF Taplin, M. Xie, W. Morganstern, D. Bubley, G. Ernstoff, M. Regan, M. TI Chemo-hormonal therapy for biochemical progression of prostate cancer. SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Meeting Abstract CT 42nd Annual Meeting of the American-Society-of-Clinical-Oncology CY JUN 02-06, 2006 CL Atlanta, GA SP Amer Soc Clin Oncol C1 Dana Farber Canc Inst, Boston, MA 02115 USA. Faulkner Hosp, Boston, MA USA. Norris Cotton Canc Ctr, Lebanon, NH USA. NR 0 TC 0 Z9 0 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 JUN 20 PY 2006 VL 24 IS 18 SU S BP 231S EP 231S PN 1 PG 1 WC Oncology SC Oncology GA 063HN UT WOS:000239009401358 ER PT J AU Mathew, P Thall, PF Johnson, MM Oh, WK Meluch, AA Morris, MJ Troncoso, P Bucana, CD Fidler, IJ Logothetis, CJ AF Mathew, P. Thall, P. F. Johnson, M. M. Oh, W. K. Meluch, A. A. Morris, M. J. Troncoso, P. Bucana, C. D. Fidler, I. J. Logothetis, C. J. TI Preliminary results of a randomized placebo-controlled,double-blind trial of weekly docetaxel combined with imatinib in men with metastatic androgen-independent prostate cancer (AIPC) and bone metastases (BM). SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Meeting Abstract CT 42nd Annual Meeting of the American-Society-of-Clinical-Oncology CY JUN 02-06, 2006 CL Atlanta, GA SP Amer Soc Clin Oncol C1 Univ Texas, MD Anderson Canc Ctr, Houston, TX 77030 USA. Dana Farber Canc Inst, Boston, MA 02115 USA. Sarah Cannon Res Inst, Nashville, TN USA. Mem Sloan Kettering Canc Ctr, New York, NY 10021 USA. RI Oh, William/B-9163-2012 OI Oh, William/0000-0001-5113-8147 NR 0 TC 2 Z9 2 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 JUN 20 PY 2006 VL 24 IS 18 SU S BP 232S EP 232S PN 1 PG 1 WC Oncology SC Oncology GA 063HN UT WOS:000239009401360 ER PT J AU D'Amico, AV Cullen, J Chen, Y McLeod, DG AF D'Amico, A. V. Cullen, J. Chen, Y. McLeod, D. G. TI Prostate-specific antigen velocity and the odds of detecting gleason 8 to 10 prostate cancer at biopsy. SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Meeting Abstract CT 42nd Annual Meeting of the American-Society-of-Clinical-Oncology CY JUN 02-06, 2006 CL Atlanta, GA SP Amer Soc Clin Oncol C1 Dana Farber Canc Inst, Boston, MA 02115 USA. Walter Reed Army Med Ctr, Bethesda, MD USA. NR 0 TC 0 Z9 0 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 JUN 20 PY 2006 VL 24 IS 18 SU S BP 233S EP 233S PN 1 PG 1 WC Oncology SC Oncology GA 063HN UT WOS:000239009401366 ER PT J AU Srinivas, S Stadler, WM Bukowski, R Figlin, R Hayes, T Yankee, EW Jonasch, E AF Srinivas, S. Stadler, W. M. Bukowski, R. Figlin, R. Hayes, T. Yankee, E. W. Jonasch, E. TI Talactoferrin alfa may prolong progression-free survival in advanced renal carcinoma patients. SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Meeting Abstract CT 42nd Annual Meeting of the American-Society-of-Clinical-Oncology CY JUN 02-06, 2006 CL Atlanta, GA SP Amer Soc Clin Oncol C1 Stanford Med Ctr, Stanford, CA USA. Univ Chicago, Chicago, IL 60637 USA. Cleveland Clin, Cleveland, OH 44106 USA. Univ Calif Los Angeles, David Geffen Sch Med, Los Angeles, CA USA. VA Med Ctr, Houston, TX USA. Agennix, Houston, TX USA. Univ Texas, Houston, TX USA. NR 0 TC 0 Z9 0 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 JUN 20 PY 2006 VL 24 IS 18 SU S BP 241S EP 241S PN 1 PG 1 WC Oncology SC Oncology GA 063HN UT WOS:000239009401397 ER PT J AU Graff, J Mori, M Li, H Garzotto, M Penson, D Potosky, A Beer, TM AF Graff, J. Mori, M. Li, H. Garzotto, M. Penson, D. Potosky, A. Beer, T. M. TI Predictors of overall and cancer-specific survival in patients with clinically localized prostate cancer (PC) treated with primary androgen deprivation therapy (PADT): Results from the Prostate Cancer Outcomes Study. SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Meeting Abstract CT 42nd Annual Meeting of the American-Society-of-Clinical-Oncology CY JUN 02-06, 2006 CL Atlanta, GA SP Amer Soc Clin Oncol C1 Oregon Hlth Sci Univ, Portland, OR 97201 USA. Portland VA Med Ctr, Portland, OR 97201 USA. Univ So Calif, Los Angeles, CA 90089 USA. NCI, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 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 JUN 20 PY 2006 VL 24 IS 18 SU S BP 244S EP 244S PN 1 PG 1 WC Oncology SC Oncology GA 063HN UT WOS:000239009401408 ER PT J AU Daskivich, TJ Regan, MM Kantoft, PW Oh, WK AF Daskivich, T. J. Regan, M. M. Kantoft, P. W. Oh, W. K. TI Prostate specific antigen doubling time (PSA-DT) and velocity (PSA-V) provide independent prognostic information in androgen independent prostate cancer (AIPC) patients receiving chemotherapy. SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Meeting Abstract CT 42nd Annual Meeting of the American-Society-of-Clinical-Oncology CY JUN 02-06, 2006 CL Atlanta, GA SP Amer Soc Clin Oncol C1 Dana Farber Canc Inst, Boston, MA 02115 USA. RI Oh, William/B-9163-2012 OI Oh, William/0000-0001-5113-8147 NR 0 TC 0 Z9 0 U1 0 U2 1 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 JUN 20 PY 2006 VL 24 IS 18 SU S BP 245S EP 245S PN 1 PG 1 WC Oncology SC Oncology GA 063HN UT WOS:000239009401413 ER PT J AU Garzotto, M Mongoue-Tchokote, S Shannon, J Peters, L Sokoloff, MH Beer, TM Mori, M AF Garzotto, M. Mongoue-Tchokote, S. Shannon, J. Peters, L. Sokoloff, M. H. Beer, T. M. Mori, M. TI Effect of obesity on PSA density (PSAD): A new clinical predictor of prostate cancer. SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Meeting Abstract CT 42nd Annual Meeting of the American-Society-of-Clinical-Oncology CY JUN 02-06, 2006 CL Atlanta, GA SP Amer Soc Clin Oncol C1 Oregon Hlth Sci Univ, Portland, OR 97201 USA. Portland VA Med Ctr, Portland, OR USA. NR 0 TC 0 Z9 0 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 JUN 20 PY 2006 VL 24 IS 18 SU S BP 245S EP 245S PN 1 PG 1 WC Oncology SC Oncology GA 063HN UT WOS:000239009401415 ER PT J AU Liu, G Wang, W Dipaola, R Carducci, M Wilding, G AF Liu, G. Wang, W. Dipaola, R. Carducci, M. Wilding, G. TI A phase II study of a weekly schedule of BMS-247550 for patients with hormone-refractory prostate cancer: A trial of the Eastern Cooperative Oncology Group (E3803). SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Meeting Abstract CT 42nd Annual Meeting of the American-Society-of-Clinical-Oncology CY JUN 02-06, 2006 CL Atlanta, GA SP Amer Soc Clin Oncol C1 Univ Wisconsin, Ctr Comprehens Canc, Madison, WI 53706 USA. Dana Farber Canc Inst, Boston, MA 02115 USA. Canc Inst New Jersey, New Brunswick, NJ USA. Sidney Kimmel Comprehens Canc Ctr, Baltimore, MD USA. NR 0 TC 3 Z9 3 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 JUN 20 PY 2006 VL 24 IS 18 SU S BP 246S EP 246S PN 1 PG 1 WC Oncology SC Oncology GA 063HN UT WOS:000239009401416 ER PT J AU O'Brien, CA Mongoue-Tchokote, S Collins, L Spurgeon, S Peters, L Beer, TM Mori, M Garzotto, M AF O'Brien, C. A. Mongoue-Tchokote, S. Collins, L. Spurgeon, S. Peters, L. Beer, T. M. Mori, M. Garzotto, M. TI Assessment of PSA and digital rectal examination (DRE) for the detection of Gleason >= 7 prostate cancer in a referral population. SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Meeting Abstract CT 42nd Annual Meeting of the American-Society-of-Clinical-Oncology CY JUN 02-06, 2006 CL Atlanta, GA SP Amer Soc Clin Oncol C1 Oregon Hlth Sci Univ, Portland, OR 97201 USA. Portland VA Med Ctr, Portland, OR USA. NR 0 TC 0 Z9 0 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 JUN 20 PY 2006 VL 24 IS 18 SU S BP 249S EP 249S PN 1 PG 1 WC Oncology SC Oncology GA 063HN UT WOS:000239009401431 ER PT J AU Regan, MM Daskivich, TJ Kantoff, PW Oh, WK AF Regan, M. M. Daskivich, T. J. Kantoff, P. W. Oh, W. K. TI Utility of prostate specific antigen doubling time (PSA-DT) at the start of androgen independent prostate cancer (AIPC) and immediately before chemotherapy in predicting efficacy of taxane chemotherapy. SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Meeting Abstract CT 42nd Annual Meeting of the American-Society-of-Clinical-Oncology CY JUN 02-06, 2006 CL Atlanta, GA SP Amer Soc Clin Oncol C1 Dana Farber Canc Inst, Boston, MA 02115 USA. RI Oh, William/B-9163-2012 OI Oh, William/0000-0001-5113-8147 NR 0 TC 0 Z9 0 U1 0 U2 1 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 JUN 20 PY 2006 VL 24 IS 18 SU S BP 251S EP 251S PN 1 PG 1 WC Oncology SC Oncology GA 063HN UT WOS:000239009401437 ER PT J AU Nakabayashi, M Xie, W Regan, MM Jackman, DM Kantoff, PW Oh, WK AF Nakabayashi, M. Xie, W. Regan, M. M. Jackman, D. M. Kantoff, P. W. Oh, W. K. TI Response to low-dose ketoconazole and subsequent dose escalation to high-dose ketoconazole in patients with androgen-independent prostate cancer. SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Meeting Abstract CT 42nd Annual Meeting of the American-Society-of-Clinical-Oncology CY JUN 02-06, 2006 CL Atlanta, GA SP Amer Soc Clin Oncol C1 Dana Farber Canc Inst, Boston, MA 02115 USA. RI Oh, William/B-9163-2012 OI Oh, William/0000-0001-5113-8147 NR 0 TC 0 Z9 0 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 JUN 20 PY 2006 VL 24 IS 18 SU S BP 253S EP 253S PN 1 PG 1 WC Oncology SC Oncology GA 063HN UT WOS:000239009401444 ER PT J AU Bahary, J Bae, K Taussky, D Roach, M Sandler, HM Shipley, WU AF Bahary, J. Bae, K. Taussky, D. Roach, M., III Sandler, H. M. Shipley, W. U. TI Does timing of androgen deprivation influence radiation-induced toxicity? A secondary analysis of Radiation Therapy Oncology Group protocol 9413. SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Meeting Abstract CT 42nd Annual Meeting of the American-Society-of-Clinical-Oncology CY JUN 02-06, 2006 CL Atlanta, GA SP Amer Soc Clin Oncol C1 CHUM, Montreal, PQ, Canada. RTOG HQ, Philadelphia, PA USA. Univ Calif San Francisco, San Francisco, CA 94143 USA. Univ Michigan, Med Ctr, Ann Arbor, MI 48109 USA. Massachusetts Gen Hosp, Boston, MA 02114 USA. NR 0 TC 0 Z9 0 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 JUN 20 PY 2006 VL 24 IS 18 SU S BP 255S EP 255S PN 1 PG 1 WC Oncology SC Oncology GA 063HN UT WOS:000239009401454 ER PT J AU Cannistra, SA Matulonis, U Penson, R Wenham, R Armstrong, D Burger, RA Mackey, H Douglas, J Hambleton, J McGuire, W AF Cannistra, S. A. Matulonis, U. Penson, R. Wenham, R. Armstrong, D. Burger, R. A. Mackey, H. Douglas, J. Hambleton, J. McGuire, W. TI Bevacizumab in patients with advanced platinum-resistant ovarian cancer. SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Meeting Abstract CT 42nd Annual Meeting of the American-Society-of-Clinical-Oncology CY JUN 02-06, 2006 CL Atlanta, GA SP Amer Soc Clin Oncol C1 Beth Israel Deaconess Med Ctr, Boston, MA 02215 USA. Dana Farber Canc Inst, Boston, MA 02115 USA. Massachusetts Gen Hosp, Boston, MA 02114 USA. H Lee Moffitt Canc Ctr & Res Inst, Tampa, FL USA. Sidney Kimmel Comprehens Canc Ctr, Baltimore, MD USA. Univ Calif Irvine, Irvine, CA USA. Genentech Inc, San Francisco, CA USA. Franklin Sq Hosp Ctr, Baltimore, MD USA. NR 0 TC 13 Z9 14 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 JUN 20 PY 2006 VL 24 IS 18 SU S BP 257S EP 257S PN 1 PG 1 WC Oncology SC Oncology GA 063HN UT WOS:000239009401462 ER PT J AU Krasner, CN Seiden, MV Fuller, AF Roche, M Verrill, CL D'Amato, F Tretyakov, O Tyburski, K Matulonis, UA Supko, JG AF Krasner, C. N. Seiden, M. V. Fuller, A. F., Jr. Roche, M. Verrill, C. L. D'Amato, F. Tretyakov, O. Tyburski, K. Matulonis, U. A. Supko, J. G. TI Pharmacokinetic analysis of an all intraperitoneal carboplatin and paclitaxel regimen in ovarian cancer patients demonstrates favorable systemic bioavailability of both agents. SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Meeting Abstract CT 42nd Annual Meeting of the American-Society-of-Clinical-Oncology CY JUN 02-06, 2006 CL Atlanta, GA SP Amer Soc Clin Oncol C1 Harvard Univ, Dana Farber Canc Inst, Ctr Canc, Boston, MA 02115 USA. Massachusetts Gen Hosp, Boston, MA 02114 USA. NR 0 TC 2 Z9 2 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 JUN 20 PY 2006 VL 24 IS 18 SU S BP 257S EP 257S PN 1 PG 1 WC Oncology SC Oncology GA 063HN UT WOS:000239009401463 ER PT J AU Penson, RT Cannistra, SA Seiden, MV Krasner, CN Matulonis, UA Horowitz, NS Berlin, S Dizon, DS Lee, H Campos, SM AF Penson, R. T. Cannistra, S. A. Seiden, M. V. Krasner, C. N. Matulonis, U. A. Horowitz, N. S. Berlin, S. Dizon, D. S. Lee, H. Campos, S. M. TI Phase II study of carboplatin, paclitaxel and bevacizumab as first line chemotherapy and consolidation for advanced mullerian tumors. SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Meeting Abstract CT 42nd Annual Meeting of the American-Society-of-Clinical-Oncology CY JUN 02-06, 2006 CL Atlanta, GA SP Amer Soc Clin Oncol C1 Harvard Univ, Ctr Canc, Dana Farber Canc Inst, Boston, MA 02115 USA. Massachusetts Gen Hosp, Boston, MA 02114 USA. Beth Israel Deaconess Med Ctr, Boston, MA 02215 USA. Women & Infants Hosp Rhode Isl, Providence, RI USA. NR 0 TC 3 Z9 3 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 JUN 20 PY 2006 VL 24 IS 18 SU S BP 260S EP 260S PN 1 PG 1 WC Oncology SC Oncology GA 063HN UT WOS:000239009401475 ER PT J AU Matulonis, UA Kornblith, A Lee, H Bryan, J Gibson, C Wells, C Lee, J Sullivan, L Penson, RT AF Matulonis, U. A. Kornblith, A. Lee, H. Bryan, J. Gibson, C. Wells, C. Lee, J. Sullivan, L. Penson, R. T. TI Long-term impact of chemotherapy on early stage ovarian cancer patients. SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Meeting Abstract CT 42nd Annual Meeting of the American-Society-of-Clinical-Oncology CY JUN 02-06, 2006 CL Atlanta, GA SP Amer Soc Clin Oncol C1 Dana Farber Canc Inst, Boston, MA 02115 USA. Massachusetts Gen Hosp, Boston, MA 02114 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC 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 JUN 20 PY 2006 VL 24 IS 18 SU S BP 261S EP 261S PN 1 PG 1 WC Oncology SC Oncology GA 063HN UT WOS:000239009401477 ER PT J AU Mahoney, J Lee, H Foster, R Matulonis, U Duan, Z Seiden, MV AF Mahoney, J. Lee, H. Foster, R. Matulonis, U. Duan, Z. Seiden, M. V. TI Evaluation of serial serum IL-6 levels in women with newly diagnosed ovarian cancer on a prospective clinical trial. SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Meeting Abstract CT 42nd Annual Meeting of the American-Society-of-Clinical-Oncology CY JUN 02-06, 2006 CL Atlanta, GA SP Amer Soc Clin Oncol C1 Massachusetts Gen Hosp, 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 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 JUN 20 PY 2006 VL 24 IS 18 SU S BP 271S EP 271S PN 1 PG 1 WC Oncology SC Oncology GA 063HN UT WOS:000239009401519 ER PT J AU Roche, M Matulonis, U Krasner, C Penson, R Horowitz, N Berkenblit, A Findley, M Lee, J Horick, N Seiden, MV AF Roche, M. Matulonis, U. Krasner, C. Penson, R. Horowitz, N. Berkenblit, A. Findley, M. Lee, J. Horick, N. Seiden, M. V. TI Phase II trial of GM-CSF in women with asymptomatic mullerian cancer. SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Meeting Abstract CT 42nd Annual Meeting of the American-Society-of-Clinical-Oncology CY JUN 02-06, 2006 CL Atlanta, GA SP Amer Soc Clin Oncol C1 Dana Farber Harvard Canc Ctr, Boston, MA USA. Massachusetts Gen Hosp, Boston, MA 02114 USA. Dana Farber Canc Inst, Boston, MA 02115 USA. Beth Israel Deaconess Med Ctr, Boston, MA 02215 USA. NR 0 TC 0 Z9 0 U1 2 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 JUN 20 PY 2006 VL 24 IS 18 SU S BP 275S EP 275S PN 1 PG 1 WC Oncology SC Oncology GA 063HN UT WOS:000239009401535 ER PT J AU Campos, SM Parker, L Chen, W Bunnell, CA Atkinson, T Lee, J Matulonis, UA Harris, LN Krasner, CN AF Campos, S. M. Parker, L. Chen, W. Bunnell, C. A. Atkinson, T. Lee, J. Matulonis, U. A. Harris, L. N. Krasner, C. N. TI Phase I trial of liposomal doxorubicin and ZD 1839 in patients with refractory gynecological malignancies or metastatic breast cancer. SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Meeting Abstract CT 42nd Annual Meeting of the American-Society-of-Clinical-Oncology CY JUN 02-06, 2006 CL Atlanta, GA SP Amer Soc Clin Oncol C1 Dana Farber Canc Inst, Boston, MA 02115 USA. Massachusetts Gen Hosp, Boston, MA 02114 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC 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 JUN 20 PY 2006 VL 24 IS 18 SU S BP 276S EP 276S PN 1 PG 1 WC Oncology SC Oncology GA 063HN UT WOS:000239009401539 ER PT J AU Poeta, LM Goldwasser, MA Forastiere, A Benoit, N Califano, J Ridge, JA Goodwin, J Kenady, D Sidransky, D Koch, WM AF Poeta, L. M. Goldwasser, M. A. Forastiere, A. Benoit, N. Califano, J. Ridge, J. A. Goodwin, J. Kenady, D. Sidransky, D. Koch, W. M. TI Prognostic implication of p53 mutations in HNSCC: Results of intragroup margin study (E4393). SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Meeting Abstract CT 42nd Annual Meeting of the American-Society-of-Clinical-Oncology CY JUN 02-06, 2006 CL Atlanta, GA SP Amer Soc Clin Oncol C1 Johns Hopkins Univ, Baltimore, MD 21218 USA. Dana Farber Canc Inst, Boston, MA 02115 USA. Fox Chase Canc Ctr, Philadelphia, PA 19111 USA. Sylvester Comprehens Canc Ctr, Miami, FL USA. Univ Kentucky, Lexington, KY 40506 USA. NR 0 TC 0 Z9 0 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 JUN 20 PY 2006 VL 24 IS 18 SU S BP 281S EP 281S PN 1 PG 1 WC Oncology SC Oncology GA 063HN UT WOS:000239009401555 ER PT J AU Chambers, MS Welsh, DV Scrimger, RA Zehn, W Epstein, JB Troha, J Sonis, ST AF Chambers, M. S. Welsh, D. V. Scrimger, R. A. Zehn, W. Epstein, J. B. Troha, J. Sonis, S. T. TI RK-0202 for radiation-induced oral mucositis. SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Meeting Abstract CT 42nd Annual Meeting of the American-Society-of-Clinical-Oncology CY JUN 02-06, 2006 CL Atlanta, GA SP Amer Soc Clin Oncol C1 Univ Texas, MD Anderson Canc Ctr, Houston, TX 77030 USA. Univ Louisville, Louisville, KY 40292 USA. Cross Canc Inst, Edmonton, AB T6G 1Z2, Canada. Univ Nebraska, Coll Med, Omaha, NE 68182 USA. Univ Illinois, Chicago, IL USA. RxKinetix Inc, Louisville, CO USA. Dana Farber Canc Inst, Boston, MA 02115 USA. NR 0 TC 0 Z9 0 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 JUN 20 PY 2006 VL 24 IS 18 SU S BP 285S EP 285S PN 1 PG 1 WC Oncology SC Oncology GA 063HN UT WOS:000239009402012 ER PT J AU Cmelak, AJ Li, S Murphy, B Burkey, B Adams, GL Cannon, M Pinto, H Rosenthal, DI Ridge, JA Forastiere, AA AF Cmelak, A. J. Li, S. Murphy, B. Burkey, B. Adams, G. L. Cannon, M. Pinto, H. Rosenthal, D. I. Ridge, J. A. Forastiere, A. A. TI Locally advanced resectable larynx (L) or oropharynx (OP) cancer: Updated results of organ preservation trial ECOG 2399. SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Meeting Abstract CT 42nd Annual Meeting of the American-Society-of-Clinical-Oncology CY JUN 02-06, 2006 CL Atlanta, GA SP Amer Soc Clin Oncol C1 Vanderbilt Ingram Canc Ctr, Nashville, TN USA. Dana Farber Canc Inst, Boston, MA 02115 USA. Vanderbilt Univ, Med Ctr, Nashville, TN USA. Univ Minnesota, Minneapolis, MN USA. Canc Ctr Kansas, Wichita, KS USA. Stanford Univ, Palo Alto, CA 94304 USA. Univ Texas, MD Anderson Canc Ctr, Houston, TX 77030 USA. Fox Chase Canc Ctr, Philadelphia, PA 19111 USA. Johns Hopkins Univ, Baltimore, MD USA. NR 0 TC 1 Z9 1 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 JUN 20 PY 2006 VL 24 IS 18 SU S BP 286S EP 286S PN 1 PG 1 WC Oncology SC Oncology GA 063HN UT WOS:000239009402016 ER PT J AU Burtness, B Goldwasser, MA Axelrod, R Argiris, A Forastiere, AA AF Burtness, B. Goldwasser, M. A. Axelrod, R. Argiris, A. Forastiere, A. A. TI A randomized phase II study of BMS-247550 (ixabepilone) given daily x 5 days every 3 weeks or weekly in patients with metastatic or recurrent squamous cell cancer of the head and neck. SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Meeting Abstract CT 42nd Annual Meeting of the American-Society-of-Clinical-Oncology CY JUN 02-06, 2006 CL Atlanta, GA SP Amer Soc Clin Oncol C1 Fox Chase Canc Ctr, Philadelphia, PA 19111 USA. Dana Farber Canc Inst, Boston, MA 02115 USA. Thomas Jefferson Univ, Philadelphia, PA 19107 USA. Univ Pittsburgh, Pittsburgh, PA USA. Johns Hopkins Univ, Baltimore, MD USA. NR 0 TC 1 Z9 1 U1 0 U2 1 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 JUN 20 PY 2006 VL 24 IS 18 SU S BP 288S EP 288S PN 1 PG 1 WC Oncology SC Oncology GA 063HN UT WOS:000239009402021 ER PT J AU Argiris, A Goldwasser, MA Burtness, B Deconti, R Axelrod, R Van Waes, C Forastiere, A AF Argiris, A. Goldwasser, M. A. Burtness, B. Deconti, R. Axelrod, R. Van Waes, C. Forastiere, A. TI A phase II trial of PS-341 (bortezomib) followed by the addition of doxorubicin at progression in incurable adenoid cystic carcinoma of the head and neck: An Eastern Cooperative Oncology Group study. SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Meeting Abstract CT 42nd Annual Meeting of the American-Society-of-Clinical-Oncology CY JUN 02-06, 2006 CL Atlanta, GA SP Amer Soc Clin Oncol C1 Univ Pittsburgh, Pittsburgh, PA USA. Dana Farber Canc Inst, Boston, MA 02115 USA. Fox Chase Canc Ctr, Philadelphia, PA 19111 USA. Univ S Florida, H Lee Moffitt Canc Ctr, Tampa, FL 33682 USA. Thomas Jefferson Univ, Philadelphia, PA 19107 USA. Natl Canc Inst, Bethesda, MD USA. Johns Hopkins Univ, Baltimore, MD USA. NR 0 TC 3 Z9 3 U1 0 U2 1 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 JUN 20 PY 2006 VL 24 IS 18 SU S BP 298S EP 298S PN 1 PG 1 WC Oncology SC Oncology GA 063HN UT WOS:000239009402063 ER PT J AU Earle, CC Landrum, M Jeffrey, S Neville, B Weeks, J Ayanian, J AF Earle, C. C. Landrum, M. Jeffrey, S. Neville, B. Weeks, J. Ayanian, J. TI Consistency in regional trends of aggressiveness in cancer care near the end of life for elderly Americans, 1991-2000. SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Meeting Abstract CT 42nd Annual Meeting of the American-Society-of-Clinical-Oncology CY JUN 02-06, 2006 CL Atlanta, GA SP Amer Soc Clin Oncol C1 Dana Farber Canc Inst, Boston, MA 02115 USA. Harvard Univ, Sch Med, Boston, MA 02115 USA. NR 0 TC 0 Z9 0 U1 0 U2 1 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 JUN 20 PY 2006 VL 24 IS 18 SU S BP 302S EP 302S PN 1 PG 1 WC Oncology SC Oncology GA 063HN UT WOS:000239009402077 ER PT J AU Joffe, S Stumacher, M Clark, JW Weeks, JC AF Joffe, S. Stumacher, M. Clark, J. W. Weeks, J. C. TI Preferences for and expectations about experimental therapy among participants in randomized trials. SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Meeting Abstract CT 42nd Annual Meeting of the American-Society-of-Clinical-Oncology CY JUN 02-06, 2006 CL Atlanta, GA SP Amer Soc Clin Oncol C1 Univ Penn, Philadelphia, PA 19104 USA. Dana Farber Canc Inst, Boston, MA 02115 USA. Massachusetts Gen Hosp, Boston, MA 02114 USA. NR 0 TC 2 Z9 2 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 JUN 20 PY 2006 VL 24 IS 18 SU S BP 304S EP 304S PN 1 PG 1 WC Oncology SC Oncology GA 063HN UT WOS:000239009402087 ER PT J AU Moy, B Tu, D Shepherd, LE Pater, JL Whelan, TJ Ingle, JN Goss, PE AF Moy, B. Tu, D. Shepherd, L. E. Pater, J. L. Whelan, T. J. Ingle, J. N. Goss, P. E. TI NCICCTG MA.17: Tolerability of letrozole among ethnic minority women. SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Meeting Abstract CT 42nd Annual Meeting of the American-Society-of-Clinical-Oncology CY JUN 02-06, 2006 CL Atlanta, GA SP Amer Soc Clin Oncol C1 Massachusetts Gen Hosp, Boston, MA 02114 USA. Natl Canc Inst, Canada Clin Trials Grp, Kingston, ON, Canada. Queens Univ, Kingston, ON, Canada. Juravinski Canc Ctr, Hamilton, ON, Canada. Mayo Clin, Rochester, MN USA. RI Whelan, Timothy/D-3185-2017 NR 0 TC 0 Z9 0 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 JUN 20 PY 2006 VL 24 IS 18 SU S BP 305S EP 305S PN 1 PG 1 WC Oncology SC Oncology GA 063HN UT WOS:000239009402090 ER PT J AU Chen, AB D'Amico, AV Neville, BA Earle, CC AF Chen, A. B. D'Amico, A. V. Neville, B. A. Earle, C. C. TI Predictors of complications following prostate brachytherapy. SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Meeting Abstract CT 42nd Annual Meeting of the American-Society-of-Clinical-Oncology CY JUN 02-06, 2006 CL Atlanta, GA SP Amer Soc Clin Oncol C1 Harvard Univ, Radiat Oncol Program, Boston, MA 02115 USA. Dana Farber Canc Inst, Boston, MA 02115 USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU AMER SOC 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 JUN 20 PY 2006 VL 24 IS 18 SU S BP 306S EP 306S PN 1 PG 1 WC Oncology SC Oncology GA 063HN UT WOS:000239009402095 ER PT J AU Punglia, RS Weeks, JC Neville, BA Earle, CC AF Punglia, R. S. Weeks, J. C. Neville, B. A. Earle, C. C. TI Effect of distance to radiation treatment facility on use of radiation therapy after mastectomy in elderly women. SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Meeting Abstract CT 42nd Annual Meeting of the American-Society-of-Clinical-Oncology CY JUN 02-06, 2006 CL Atlanta, GA SP Amer Soc Clin Oncol C1 Dana Farber Canc Inst, Boston, MA 02115 USA. NR 0 TC 1 Z9 1 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 JUN 20 PY 2006 VL 24 IS 18 SU S MA 6030 BP 308S EP 308S PN 1 PG 1 WC Oncology SC Oncology GA 063HN UT WOS:000239009402102 PM 27954605 ER PT J AU Abel, GA Lee, SJ Viswanath, V Weeks, JC AF Abel, G. A. Lee, S. J. Viswanath, V. Weeks, J. C. TI Direct-to-consumer advertising in oncology: A content analysis of print media. SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Meeting Abstract CT 42nd Annual Meeting of the American-Society-of-Clinical-Oncology CY JUN 02-06, 2006 CL Atlanta, GA SP Amer Soc Clin Oncol C1 Dana Farber Canc Inst, Boston, MA 02115 USA. Fred Hutchinson Canc Res Ctr, Seattle, WA 98104 USA. NR 0 TC 0 Z9 0 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 JUN 20 PY 2006 VL 24 IS 18 SU S MA 6034 BP 309S EP 309S PN 1 PG 1 WC Oncology SC Oncology GA 063HN UT WOS:000239009402106 PM 27954603 ER PT J AU Mack, JW Cook, EF Wolfe, J Grier, HE Cleary, PD Weeks, JC AF Mack, J. W. Cook, E. F. Wolfe, J. Grier, H. E. Cleary, P. D. Weeks, J. C. TI Understanding of prognosis among parents of children with cancer: Parental optimism and the role of the parent-physician interaction. SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Meeting Abstract CT 42nd Annual Meeting of the American-Society-of-Clinical-Oncology CY JUN 02-06, 2006 CL Atlanta, GA SP Amer Soc Clin Oncol C1 Dana Farber Canc Inst, Boston, MA 02115 USA. Harvard Univ, Sch Publ Hlth, Boston, MA 02115 USA. Harvard Univ, Sch Med, Boston, MA 02115 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC 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 JUN 20 PY 2006 VL 24 IS 18 SU S MA 6033 BP 309S EP 309S PN 1 PG 1 WC Oncology SC Oncology GA 063HN UT WOS:000239009402107 PM 27954600 ER PT J AU Peppercorn, J Joffe, S Burstein, HJ Winer, E AF Peppercorn, J. Joffe, S. Burstein, H. J. Winer, E. TI Use of experimental therapy outside of clinical trials among US oncologists. SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Meeting Abstract CT 42nd Annual Meeting of the American-Society-of-Clinical-Oncology CY JUN 02-06, 2006 CL Atlanta, GA SP Amer Soc Clin Oncol C1 Univ N Carolina, Chapel Hill, NC 27515 USA. Dana Farber Canc Inst, Boston, MA 02115 USA. NR 0 TC 0 Z9 0 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 JUN 20 PY 2006 VL 24 IS 18 SU S MA 6047 BP 312S EP 312S PN 1 PG 1 WC Oncology SC Oncology GA 063HN UT WOS:000239009402120 PM 27954839 ER PT J AU Krzyzanowska, MK Regan, MM Powell, M Earle, CC Weeks, JC AF Krzyzanowska, M. K. Regan, M. M. Powell, M. Earle, C. C. Weeks, J. C. TI Impact of patient and physician factors on oncologists' recommendations for adjuvant chemotherapy in stage III colon cancer. SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Meeting Abstract CT 42nd Annual Meeting of the American-Society-of-Clinical-Oncology CY JUN 02-06, 2006 CL Atlanta, GA SP Amer Soc Clin Oncol C1 Princess Margaret Hosp, 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 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 JUN 20 PY 2006 VL 24 IS 18 SU S MA 6051 BP 313S EP 313S PN 1 PG 1 WC Oncology SC Oncology GA 063HN UT WOS:000239009402122 PM 27954834 ER PT J AU Gilligan, TD Kennedy, MW Olson, E Gerberick, A Wilson-Glover, A Allen, JD AF Gilligan, T. D. Kennedy, M. W. Olson, E. Gerberick, A. Wilson-Glover, A. Allen, J. D. TI Prostate-cancer (CaP) screening decision aid for black men designed to enhance shared decision-making. SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Meeting Abstract CT 42nd Annual Meeting of the American-Society-of-Clinical-Oncology CY JUN 02-06, 2006 CL Atlanta, GA SP Amer Soc Clin Oncol C1 Cleveland Clin, Cleveland, OH 44106 USA. Dana Farber Canc Inst, Boston, MA 02115 USA. Harvard Univ, Sch Publ Hlth, Boston, MA 02115 USA. NR 0 TC 0 Z9 0 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 JUN 20 PY 2006 VL 24 IS 18 SU S MA 6059 BP 315S EP 315S PN 1 PG 1 WC Oncology SC Oncology GA 063HN UT WOS:000239009402131 PM 27954807 ER PT J AU Friese, CR Aiken, LH AF Friese, C. R. Aiken, L. H. TI Surgical oncology outcomes: The role of nurse practice environments. SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Meeting Abstract CT 42nd Annual Meeting of the American-Society-of-Clinical-Oncology CY JUN 02-06, 2006 CL Atlanta, GA SP Amer Soc Clin Oncol C1 Dana Farber Canc Inst, Boston, MA 02115 USA. Univ Penn, Philadelphia, PA 19104 USA. NR 0 TC 0 Z9 0 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 JUN 20 PY 2006 VL 24 IS 18 SU S MA 6105 BP 326S EP 326S PN 1 PG 1 WC Oncology SC Oncology GA 063HN UT WOS:000239009402176 PM 27955232 ER PT J AU Patrice, SJ Patrice, JR Steinberg, JS Zietman, AL Smith, MR Hayman, JA AF Patrice, S. J. Patrice, J. R. Steinberg, J. S. Zietman, A. L. Smith, M. R. Hayman, J. A. TI A cost-effectiveness analysis of surveillance, radiotherapy, and carboplatin in the management of Stage I Testicular Seminoma. SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Meeting Abstract CT 42nd Annual Meeting of the American-Society-of-Clinical-Oncology CY JUN 02-06, 2006 CL Atlanta, GA SP Amer Soc Clin Oncol C1 Radiat Therapy Serv, Ft Myers, FL USA. Tulane Univ, Sch Publ Hlth, New Orleans, LA 70118 USA. Massachusetts Gen Hosp, Boston, MA 02114 USA. Univ Michigan, Ann Arbor, MI 48109 USA. NR 0 TC 1 Z9 1 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 JUN 20 PY 2006 VL 24 IS 18 SU S MA 6108 BP 327S EP 327S PN 1 PG 1 WC Oncology SC Oncology GA 063HN UT WOS:000239009402178 PM 27955226 ER PT J AU Oleynick, JU Albertsen, PC Barry, MM Walker-Corkery, EM Yao, S Lu-Yao, GL AF Oleynick, J. U. Albertsen, P. C. Barry, M. M. Walker-Corkery, E. M. Yao, S. Lu-Yao, G. L. TI Utility of the SEER-Medicare data to identify medical androgen deprivation therapy. SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Meeting Abstract CT 42nd Annual Meeting of the American-Society-of-Clinical-Oncology CY JUN 02-06, 2006 CL Atlanta, GA SP Amer Soc Clin Oncol C1 Canc Inst New Jersey, New Brunswick, NJ USA. Univ Connecticut, Farmington, CT USA. Massachusetts Gen Hosp, Boston, MA 02114 USA. NR 0 TC 2 Z9 2 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 JUN 20 PY 2006 VL 24 IS 18 SU S MA 6113 BP 328S EP 328S PN 1 PG 1 WC Oncology SC Oncology GA 063HN UT WOS:000239009402184 PM 27955168 ER PT J AU Nelson, EM Fraser, G Connors, AF Barry, MJ Krahn, M Conaway, MR Bashore, R Wolf, A Kilbridge, KL AF Nelson, E. M. Fraser, G. Connors, A. F., Jr. Barry, M. J. Krahn, M. Conaway, M. R. Bashore, R. Wolf, A. Kilbridge, K. L. TI Misunderstanding of prostate cancer (CaP) among African American (AA) men of lower socioeconomic status (Lo-SES). SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Meeting Abstract CT 42nd Annual Meeting of the American-Society-of-Clinical-Oncology CY JUN 02-06, 2006 CL Atlanta, GA SP Amer Soc Clin Oncol C1 Univ N Carolina, Chapel Hill, NC 27515 USA. Univ Virginia, Charlottesville, VA 22903 USA. Metro Hosp, Cleveland, OH USA. Massachusetts Gen Hosp, Boston, MA 02114 USA. Univ Toronto, Toronto, ON, Canada. Cent Virginia Community Hlth Ctr, New Canton, VA USA. NR 0 TC 0 Z9 0 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 JUN 20 PY 2006 VL 24 IS 18 SU S MA 6114 BP 329S EP 329S PN 1 PG 1 WC Oncology SC Oncology GA 063HN UT WOS:000239009402185 PM 27955166 ER PT J AU Grever, MR Dewald, GW Neuberg, DS Reed, JC Kitada, S Flinn, IW Appelbaum, FR Larson, RA Tallman, MS Gribben, JG Byrd, JC AF Grever, M. R. Dewald, G. W. Neuberg, D. S. Reed, J. C. Kitada, S. Flinn, I. W. Appelbaum, F. R. Larson, R. A. Tallman, M. S. Gribben, J. G. Byrd, J. C. TI Select high risk genetic features predict earlier progression following chemotherapy in chronic lymphocytic leukemia: Prospective randomized trial (Intergroup E2997) to evaluate justification for risk-adapted therapy. SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Meeting Abstract CT 42nd Annual Meeting of the American-Society-of-Clinical-Oncology CY JUN 02-06, 2006 CL Atlanta, GA SP Amer Soc Clin Oncol C1 Ohio State Univ, Columbus, OH 43210 USA. Mayo Clin & Mayo Fdn, Rochester, MN 55905 USA. Dana Farber Canc Inst, Boston, MA 02115 USA. Burnham Inst Med Res, La Jolla, CA USA. Johns Hopkins Univ, Baltimore, MD 21218 USA. Fred Hutchinson Canc Res Ctr, Seattle, WA 98104 USA. Univ Chicago, Chicago, IL 60637 USA. Northwestern Univ, Feinberg Sch Med, Chicago, IL 60611 USA. Inst Canc Barts, London, England. NR 0 TC 0 Z9 0 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 JUN 20 PY 2006 VL 24 IS 18 SU S BP 342S EP 342S PN 1 PG 1 WC Oncology SC Oncology GA 063HN UT WOS:000239009402239 ER PT J AU Silverman, LR Peterson, BL Holland, JF Stone, RM Powell, BL Larson, RA AF Silverman, L. R. Peterson, B. L. Holland, J. F. Stone, R. M. Powell, B. L. Larson, R. A. TI Transfusion independence in patients with myelodysplastic syndromes treated with azacitidine. SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Meeting Abstract CT 42nd Annual Meeting of the American-Society-of-Clinical-Oncology CY JUN 02-06, 2006 CL Atlanta, GA SP Amer Soc Clin Oncol C1 CUNY Mt Sinai Sch Med, New York, NY 10029 USA. Duke Univ, Med Ctr, Durham, NC USA. Dana Farber Canc Inst, Boston, MA 02115 USA. Wake Forest Univ, Sch Med, Winston Salem, NC 27109 USA. Univ Chicago, Chicago, IL 60637 USA. NR 0 TC 11 Z9 12 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 JUN 20 PY 2006 VL 24 IS 18 SU S BP 355S EP 355S PN 1 PG 1 WC Oncology SC Oncology GA 063HN UT WOS:000239009402292 ER PT J AU Deangelo, DJ Stone, RM Silverman, LB Stock, W Attar, EC Fearen, I Dallob, A Matthews, C Stone, J Freedman, SJ Aster, J AF Deangelo, D. J. Stone, R. M. Silverman, L. B. Stock, W. Attar, E. C. Fearen, I. Dallob, A. Matthews, C. Stone, J. Freedman, S. J. Aster, J. TI A phase I clinical trial of the notch inhibitor MK-0752 in patients with T-cell acute lymphoblastic leukemia/lymphoma (T-ALL) and other leukemias. SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Meeting Abstract CT 42nd Annual Meeting of the American-Society-of-Clinical-Oncology CY JUN 02-06, 2006 CL Atlanta, GA SP Amer Soc Clin Oncol C1 Dana Farber Canc Inst, Boston, MA 02115 USA. Univ Chicago, Chicago, IL 60637 USA. Massachusetts Gen Hosp, Boston, MA 02114 USA. Merck Res Labs, West Point, PA USA. Brigham & Womens Hosp, Boston, MA 02115 USA. NR 0 TC 78 Z9 82 U1 2 U2 8 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 JUN 20 PY 2006 VL 24 IS 18 SU S MA 6585 BP 357S EP 357S PN 1 PG 1 WC Oncology SC Oncology GA 063HN UT WOS:000239009402298 ER PT J AU Khan, KD O'Brien, S Rai, KR Brown, JR Abboud, C Hurd, DD Conkling, P Yang, Z Haltom, EJ Uprichard, MJ AF Khan, K. D. O'Brien, S. Rai, K. R. Brown, J. R. Abboud, C. Hurd, D. D. Conkling, P. Yang, Z. Haltom, E. J. Uprichard, M. J. TI Phase II study of talabostat and rituximab in fludarabine/rituximab-resistant or refractory patients with CLL. SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Meeting Abstract CT 42nd Annual Meeting of the American-Society-of-Clinical-Oncology CY JUN 02-06, 2006 CL Atlanta, GA SP Amer Soc Clin Oncol 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. James P Wilmot Canc Ctr, Rochester, NY USA. Wake Forest Univ, Winston Salem, NC 27109 USA. Virginia Oncol Associates, Norfolk, VA USA. Kendle Int Inc, Cincinnati, OH USA. Point Therapeut, Boston, MA USA. NR 0 TC 1 Z9 1 U1 1 U2 1 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 JUN 20 PY 2006 VL 24 IS 18 SU S BP 360S EP 360S PN 1 PG 1 WC Oncology SC Oncology GA 063HN UT WOS:000239009402311 ER PT J AU Heymach, JV Johnson, BE Prager, D Csada, E Roubec, J Pesek, M Spasova, I Hou, J Kennedy, S Herbst, RS AF Heymach, J. V. Johnson, B. E. Prager, D. Csada, E. Roubec, J. Pesek, M. Spasova, I. Hou, J. Kennedy, S. Herbst, R. S. TI A phase II trial of ZD6474 plus docetaxel in patients with previously treated NSCLC: Follow-up results. SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Meeting Abstract CT 42nd Annual Meeting of the American-Society-of-Clinical-Oncology CY JUN 02-06, 2006 CL Atlanta, GA SP Amer Soc Clin Oncol C1 Dana Farber Canc Inst, Boston, MA 02115 USA. Univ Calif Los Angeles, Med Ctr, Los Angeles, CA 90024 USA. Univ Szeged, Szeged, Hungary. Univ Ostrava, Univ Hosp Ostrava, Ostrava, Czech Republic. Charles Univ Prague, Plzen, Czech Republic. Charles Univ Prague, Prague, Czech Republic. AstraZeneca, Wilmington, DE USA. AstraZeneca, Macclesfield, Cheshire, England. Univ Texas, MD Anderson Canc Ctr, Houston, TX 77030 USA. NR 0 TC 15 Z9 15 U1 0 U2 3 PU AMER SOC CLINICAL ONCOLOGY PI ALEXANDRIA PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA SN 0732-183X J9 J CLIN ONCOL JI J. Clin. Oncol. PD JUN 20 PY 2006 VL 24 IS 18 SU S BP 368S EP 368S PN 1 PG 1 WC Oncology SC Oncology GA 063HN UT WOS:000239009402341 ER PT J AU Dowlati, A Gray, R Johnson, DH Schiller, JH Brahmer, J Sandler, AB AF Dowlati, A. Gray, R. Johnson, D. H. Schiller, J. H. Brahmer, J. Sandler, A. B. TI Prospective correlative assessment of biomarkers in E4599 randomized phase II/III trial of carboplatin and paclitaxel +/- bevacizumab in advanced non-small cell lung cancer (NSCLC). SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Meeting Abstract CT 42nd Annual Meeting of the American-Society-of-Clinical-Oncology CY JUN 02-06, 2006 CL Atlanta, GA SP Amer Soc Clin Oncol C1 Case Western Reserve Univ, Cleveland, OH 44106 USA. Dana Farber Canc Inst, Boston, MA 02115 USA. Vanderbilt Ingram Canc Ctr, Nashville, TN USA. Univ Wisconsin, Madison, WI 53706 USA. Johns Hopkins Univ, Baltimore, MD USA. RI Johnson, David/A-7437-2009 NR 0 TC 5 Z9 5 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 JUN 20 PY 2006 VL 24 IS 18 SU S BP 370S EP 370S PN 1 PG 1 WC Oncology SC Oncology GA 063HN UT WOS:000239009402352 ER PT J AU Janne, PA Rodriguez, LPA Gottfried, M Reaume, MN Kaukel, T Oh, YW Sykes, A Enas, N Brail, LH Von Pawel, J AF Janne, P. A. Rodriguez, L. Paz-Ares Gottfried, M. Reaume, M. N. Kaukel, T. Oh, Y. W. Sykes, A. Enas, N. Brail, L. H. Von Pawel, J. TI Randomized phase II trial of cisplatin/gemcitabine with or without LY293111, a multiple eicosonaid pathway modulator, in patients with chemotherapy naive advanced non-small cell lung carcinoma. SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Meeting Abstract CT 42nd Annual Meeting of the American-Society-of-Clinical-Oncology CY JUN 02-06, 2006 CL Atlanta, GA SP Amer Soc Clin Oncol C1 Dana Farber Canc Inst, Boston, MA 02115 USA. Univ Hosp, Madrid, Spain. Meir Hosp, Kefar Sava, Israel. Ottawa Reg Canc Ctr, Ottawa, ON K1Y 4K7, Canada. Thoraxzentrum, Hamburg, Germany. Univ Texas, MD Anderson Canc Ctr, Houston, TX 77030 USA. Eli Lilly & Co, Indianapolis, IN 46285 USA. Asklepios Fachklin, Gauting, Germany. NR 0 TC 1 Z9 1 U1 0 U2 1 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 JUN 20 PY 2006 VL 24 IS 18 SU S BP 370S EP 370S PN 1 PG 1 WC Oncology SC Oncology GA 063HN UT WOS:000239009402349 ER PT J AU Fidias, P Dakhil, SR Lyss, AP Loesch, DM Waterhouse, D Cunneen, J Ye, Z Tai, F Obasaju, CK Schiller, JH AF Fidias, P. Dakhil, S. R. Lyss, A. P. Loesch, D. M. Waterhouse, D. Cunneen, J. Ye, Z. Tai, F. Obasaju, C. K. Schiller, J. H. TI Updated report of a phase III study of induction therapy with gemcitabine plus carboplatin (GC) followed by either delayed vs. immediate second-line therapy with docetaxel (D) in advanced non-small cell lung cancer (NSCLC). SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Meeting Abstract CT 42nd Annual Meeting of the American-Society-of-Clinical-Oncology CY JUN 02-06, 2006 CL Atlanta, GA SP Amer Soc Clin Oncol C1 Stanford Univ, Stanford, CA 94305 USA. Massachusetts Gen Hosp, Boston, MA 02114 USA. Penrose Canc Ctr Kansas, Wichita, KS USA. Missouri Baptist Canc Ctr, St Louis, MO USA. Cent India Canc Ctr, Indianapolis, IN USA. Oncol Hematol Care Inc, Cincinnati, OH USA. Eli Lilly & Co, Indianapolis, IN 46285 USA. Univ Wisconsin Hosp, Madison, WI USA. NR 0 TC 2 Z9 2 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 JUN 20 PY 2006 VL 24 IS 18 SU S BP 372S EP 372S PN 1 PG 1 WC Oncology SC Oncology GA 063HN UT WOS:000239009402357 ER PT J AU Brahmer, JR Gray, R Schiller, JH Perry, M Sandler, A Johnson, D AF Brahmer, J. R. Gray, R. Schiller, J. H. Perry, M. Sandler, A. Johnson, D. TI ECOG 4599 phase III trial of carboplatin and paclitaxel +/- bevacizumab: Subset analysis of survival by gender. SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Meeting Abstract CT 42nd Annual Meeting of the American-Society-of-Clinical-Oncology CY JUN 02-06, 2006 CL Atlanta, GA SP Amer Soc Clin Oncol C1 Johns Hopkins Univ, Baltimore, MD USA. Dana Farber Canc Inst, Boston, MA 02115 USA. Univ Wisconsin, Madison, WI 53706 USA. Ellis Fischel Canc Ctr, Columbia, MO USA. Vanderbilt Univ, Nashville, TN USA. NR 0 TC 6 Z9 6 U1 0 U2 1 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 JUN 20 PY 2006 VL 24 IS 18 SU S BP 373S EP 373S PN 1 PG 1 WC Oncology SC Oncology GA 063HN UT WOS:000239009402361 ER PT J AU Ready, N Janne, P Herndon, J Bogart, J Crawford, J Edelman, M Wang, X Gu, L Green, MR Vokes, EE AF Ready, N. Janne, P. Herndon, J. Bogart, J. Crawford, J. Edelman, M. Wang, X. Gu, L. Green, M. R. Vokes, E. E. TI Chemoradiotherapy (CRT) and gefitinib (G) in stage III non-small cell lung cancer (NSCLC): A CALGB stratified phase II trial. SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Meeting Abstract CT 42nd Annual Meeting of the American-Society-of-Clinical-Oncology CY JUN 02-06, 2006 CL Atlanta, GA SP Amer Soc Clin Oncol C1 Rhode Isl Hosp, Providence, RI 02903 USA. Dana Farber Canc Inst, Boston, MA 02115 USA. Duke Univ, Med Ctr, Durham, NC 27706 USA. SUNY Upstate Med Ctr, Syracuse, NY USA. Univ Maryland, Baltimore, MD 21201 USA. Med Univ S Carolina, Charleston, SC 29425 USA. Univ Chicago, Chicago, IL 60637 USA. NR 0 TC 6 Z9 6 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 JUN 20 PY 2006 VL 24 IS 18 SU S BP 375S EP 375S PN 1 PG 1 WC Oncology SC Oncology GA 063HN UT WOS:000239009402370 ER PT J AU Merrick, DT Kittelson, J Winterhalder, R Kotantoulas, G Ingeberg, S Keith, RL Kennedy, TC Miller, YE Franklin, WA Hirsch, FR AF Merrick, D. T. Kittelson, J. Winterhalder, R. Kotantoulas, G. Ingeberg, S. Keith, R. L. Kennedy, T. C. Miller, Y. E. Franklin, W. A. Hirsch, F. R. TI Analysis of c-erb-1 (EGFR) and c-erb-2 (HER2) expression in bronchial dysplasia: Evaluation of potential targets for chemoprevention of lung cancer. SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Meeting Abstract CT 42nd Annual Meeting of the American-Society-of-Clinical-Oncology CY JUN 02-06, 2006 CL Atlanta, GA SP Amer Soc Clin Oncol C1 Univ Colorado, Denver VAMC, Denver, CO 80202 USA. Univ Zurich Hosp, CH-8091 Zurich, Switzerland. Athens Chest Hosp, Athens, Greece. Naestved Hosp, Naestved, Denmark. NR 0 TC 0 Z9 0 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 JUN 20 PY 2006 VL 24 IS 18 SU S MA 7070 BP 381S EP 381S PN 1 PG 1 WC Oncology SC Oncology GA 063HN UT WOS:000239009402394 PM 27953156 ER PT J AU Allen, AM Den, R Wong, JS Janne, PA Zurakowski, D Soto, R Bueno, R Sugarbaker, DJ Baldini, EH AF Allen, A. M. Den, R. Wong, J. S. Janne, P. A. Zurakowski, D. Soto, R. Bueno, R. Sugarbaker, D. J. Baldini, E. H. TI The influence of radiotherapy technique and dose on the patterns of failure for mesothelioma patients following extrapleural pneumonectomy. SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Meeting Abstract CT 42nd Annual Meeting of the American-Society-of-Clinical-Oncology CY JUN 02-06, 2006 CL Atlanta, GA SP Amer Soc Clin Oncol C1 Dana Farber Canc Inst, Boston, MA 02115 USA. Childrens Hosp Boston, Boston, MA USA. Brigham & Womens Hosp, Boston, MA 02115 USA. NR 0 TC 0 Z9 0 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 JUN 20 PY 2006 VL 24 IS 18 SU S BP 387S EP 387S PN 1 PG 1 WC Oncology SC Oncology GA 063HN UT WOS:000239009402418 ER PT J AU Kolesar, J Brahmer, J Li, S Guaglianone, P Patel, J Keppen, M Hidalgo, M Carbone, D Siegfried, J Schiller, J AF Kolesar, J. Brahmer, J. Li, S. Guaglianone, P. Patel, J. Keppen, M. Hidalgo, M. Carbone, D. Siegfried, J. Schiller, J. TI ECOG 3503: A pilot study to determine if downstream markers of EGFR linked signaling pathways predict response to erlotinib (OSI-774) in the first-line treatment of patients with advanced non-small cell lung cancer (NSCLC). SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Meeting Abstract CT 42nd Annual Meeting of the American-Society-of-Clinical-Oncology CY JUN 02-06, 2006 CL Atlanta, GA SP Amer Soc Clin Oncol C1 Univ Wisconsin, Madison, WI 53706 USA. Johns Hopkins, Baltimore, MD USA. Dana Farber Canc Inst, Boston, MA 02115 USA. Decatur Mem Hosp, Decatur, IL USA. Northwestern Univ, Chicago, IL 60611 USA. Siox Valley Clin Oncol, Sioux Falls, SD USA. Vanderbilt Univ, Nashville, TN USA. Univ Pittsburgh, Pittsburgh, PA 15260 USA. NR 0 TC 1 Z9 1 U1 0 U2 1 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 JUN 20 PY 2006 VL 24 IS 18 SU S MA 7162 BP 404S EP 404S PN 1 PG 1 WC Oncology SC Oncology GA 063HN UT WOS:000239009402486 PM 27953801 ER PT J AU Jackman, DM Yeap, B Lucca, J Ostler, PA Morse, LK Fidias, P Lynch, TJ Temel, J Johnson, BE Janne, PA AF Jackman, D. M. Yeap, B. Lucca, J. Ostler, P. A. Morse, L. K. Fidias, P. Lynch, T. J. Temel, J. Johnson, B. E. Janne, P. A. TI Phase II trial of erlotinib in elderly patients (age > 70) with previously untreated advanced non-small cell lung cancer (NSCLC): An analysis of quality of life and symptom response. SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Meeting Abstract CT 42nd Annual Meeting of the American-Society-of-Clinical-Oncology CY JUN 02-06, 2006 CL Atlanta, GA SP Amer Soc Clin Oncol C1 Dana Farber Canc Inst, Boston, MA 02115 USA. Massachusetts Gen Hosp, Boston, MA 02114 USA. NR 0 TC 4 Z9 5 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 JUN 20 PY 2006 VL 24 IS 18 SU S MA 7168 BP 406S EP 406S PN 1 PG 1 WC Oncology SC Oncology GA 063HN UT WOS:000239009402493 PM 27953799 ER PT J AU Sequist, LV Joshi, VA Janne, PA Fidias, P Muzikansky, A Meyerson, M Haber, DA Kucherlapati, R Johnson, BE Lynch, TJ AF Sequist, L. V. Joshi, V. A. Janne, P. A. Fidias, P. Muzikansky, A. Meyerson, M. Haber, D. A. Kucherlapati, R. Johnson, B. E. Lynch, T. J. TI Epidermal growth factor receptor (EGFR) mutation testingin non-small cell lung cancer (NSCLC) patients (pts). SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Meeting Abstract CT 42nd Annual Meeting of the American-Society-of-Clinical-Oncology CY JUN 02-06, 2006 CL Atlanta, GA SP Amer Soc Clin Oncol C1 Massachusetts Gen Hosp, Boston, MA 02114 USA. Mol Med Lab, Cambridge, MA USA. Dana Farber Canc Inst, Boston, MA 02115 USA. NR 0 TC 0 Z9 0 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 JUN 20 PY 2006 VL 24 IS 18 SU S MA 7177 BP 408S EP 408S PN 1 PG 1 WC Oncology SC Oncology GA 063HN UT WOS:000239009402503 PM 27953740 ER PT J AU Costa, DB Stephenson, P Kocher, O Tenen, DG Feins, RH Keller, SM Schiller, JH Johnson, DH Halmos, B AF Costa, D. B. Stephenson, P. Kocher, O. Tenen, D. G. Feins, R. H. Keller, S. M. Schiller, J. H. Johnson, D. H. Halmos, B. TI C/EBP alpha expression by immunohistochemistry lacks prognostic or predictive significance in primary resected non-small cell lung cancer. SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Meeting Abstract CT 42nd Annual Meeting of the American-Society-of-Clinical-Oncology CY JUN 02-06, 2006 CL Atlanta, GA SP Amer Soc Clin Oncol C1 Beth Israel Deaconess Med Ctr, Boston, MA 02215 USA. Dana Farber Canc Inst, Boston, MA 02115 USA. Univ Rochester, Rochester, NY USA. Montefiore Med Ctr, Bronx, NY 10467 USA. Univ Wisconsin, Madison, WI USA. Vanderbilt Univ, Sch Med, Nashville, TN 37212 USA. Case Western Reserve Univ, Cleveland, OH 44106 USA. RI Johnson, David/A-7437-2009 NR 0 TC 0 Z9 0 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 JUN 20 PY 2006 VL 24 IS 18 SU S MA 7202 BP 414S EP 414S PN 1 PG 1 WC Oncology SC Oncology GA 063HN UT WOS:000239009402526 PM 27954067 ER PT J AU Belinsky, SA Grimes, M Johnson, D Levy, D Schiller, J AF Belinsky, S. A. Grimes, M. Johnson, D. Levy, D. Schiller, J. TI Predicting gene promoter methylation in lung tumors through examination of sputum and serum. SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Meeting Abstract CT 42nd Annual Meeting of the American-Society-of-Clinical-Oncology CY JUN 02-06, 2006 CL Atlanta, GA SP Amer Soc Clin Oncol C1 Lovelace Resp Res Inst, Albuquerque, NM USA. Vanderbilt Univ, Nashville, TN USA. Dana Farber Canc Inst, Boston, MA 02115 USA. Univ Wisconsin, Madison, WI USA. NR 0 TC 0 Z9 0 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 JUN 20 PY 2006 VL 24 IS 18 SU S MA 7208 BP 416S EP 416S PN 1 PG 1 WC Oncology SC Oncology GA 063HN UT WOS:000239009402533 PM 27954063 ER PT J AU Heist, RS Zhou, W Cogan-Drew, T Liu, G Su, L Neuberg, D Lynch, TJ Wain, JC Christiani, DC AF Heist, R. Suk Zhou, W. Cogan-Drew, T. Liu, G. Su, L. Neuberg, D. Lynch, T. J. Wain, J. C. Christiani, D. C. TI MDM2 polymorphism and recurrence-free and overall survival in early stage non-small cell lung cancer (NSCLC). SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Meeting Abstract CT 42nd Annual Meeting of the American-Society-of-Clinical-Oncology CY JUN 02-06, 2006 CL Atlanta, GA SP Amer Soc Clin Oncol C1 Massachusetts Gen Hosp, Boston, MA 02114 USA. Harvard Univ, Sch Publ Hlth, Boston, MA 02115 USA. NR 0 TC 0 Z9 0 U1 1 U2 1 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 JUN 20 PY 2006 VL 24 IS 18 SU S MA 7221 BP 419S EP 419S PN 1 PG 1 WC Oncology SC Oncology GA 063HN UT WOS:000239009402547 ER PT J AU Smith, MR Chen, H Gordon, L Foran, J Kahl, B Advani, R Gascoyne, RD Weller, E Horning, SJ AF Smith, M. R. Chen, H. Gordon, L. Foran, J. Kahl, B. Advani, R. Gascoyne, R. D. Weller, E. Horning, S. J. TI Phase II study of rituximab plus CHOP followed by Y-90-ibritumomab tiuxetan in patients with previously untreated mantle cell lymphoma: An Eastern Cooperative Oncology Group Study (E1499). SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Meeting Abstract CT 42nd Annual Meeting of the American-Society-of-Clinical-Oncology CY JUN 02-06, 2006 CL Atlanta, GA SP Amer Soc Clin Oncol C1 Fox Chase Canc Ctr, Philadelphia, PA 19111 USA. Dana Farber Canc Inst, Boston, MA 02115 USA. Northwestern Univ, Chicago, IL 60611 USA. Univ Alabama, Birmingham, AL USA. Univ Wisconsin, Madison, WI 53706 USA. Stanford Univ, Stanford, CA 94305 USA. British Columbia Canc Agcy, Vancouver, BC V5Z 4E6, Canada. NR 0 TC 10 Z9 10 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 JUN 20 PY 2006 VL 24 IS 18 SU S MA 7503 BP 422S EP 422S PN 1 PG 1 WC Oncology SC Oncology GA 063HN UT WOS:000239009402559 PM 27955337 ER PT J AU Anderson, K Richardson, P Chanan-Khan, A Schlossman, R Munshi, N Oaklander, A Heffner, L Hassoun, H Avigan, D Amato, A AF Anderson, K. Richardson, P. Chanan-Khan, A. Schlossman, R. Munshi, N. Oaklander, A. Heffner, L. Hassoun, H. Avigan, D. Amato, A. TI Single-agent bortezomib in previously untreated multiple myeloma (MM): Results of a phase II multicenter study. SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Meeting Abstract CT 42nd Annual Meeting of the American-Society-of-Clinical-Oncology CY JUN 02-06, 2006 CL Atlanta, GA SP Amer Soc Clin Oncol C1 Dana Farber Canc Inst, Boston, MA 02115 USA. Roswell Pk Canc Inst, Buffalo, NY 14263 USA. Massachusetts Gen Hosp, Boston, MA 02114 USA. Emory Univ, Atlanta, GA 30322 USA. Mem Sloan Kettering Canc Ctr, New York, NY 10021 USA. Beth Israel Deaconess Med Ctr, Boston, MA 02215 USA. NR 0 TC 19 Z9 20 U1 0 U2 1 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 JUN 20 PY 2006 VL 24 IS 18 SU S MA 7504 BP 423S EP 423S PN 1 PG 1 WC Oncology SC Oncology GA 063HN UT WOS:000239009402560 PM 27955336 ER PT J AU Hunter, ZR Boxer, M Kahl, B Patterson, CJ Soumerai, JD Treon, SP AF Hunter, Z. R. Boxer, M. Kahl, B. Patterson, C. J. Soumerai, J. D. Treon, S. P. CA WMCTG TI Phase II study of alemtuzumab in lymphoplasmacytic lymphoma: Results of WMCTG trial 02-079. SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Meeting Abstract CT 42nd Annual Meeting of the American-Society-of-Clinical-Oncology CY JUN 02-06, 2006 CL Atlanta, GA SP Amer Soc Clin Oncol C1 Dana Farber Canc Inst, Boston, MA 02115 USA. Arizona Oncol Assoc, Tucson, AZ USA. Univ Wisconsin, Madison, WI 53706 USA. RI Hunter, Zachary/H-3018-2013 OI Hunter, Zachary/0000-0002-1689-1691 NR 0 TC 5 Z9 5 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 JUN 20 PY 2006 VL 24 IS 18 SU S BP 427S EP 427S PN 1 PG 1 WC Oncology SC Oncology GA 063HN UT WOS:000239009403012 ER PT J AU Vogl, DT Stadtmauer, EA Richardson, PG Sonneveld, P Schuster, MW Irwin, D Facon, T Harousseau, JM Boral, A Anderson, KC AF Vogl, D. T. Stadtmauer, E. A. Richardson, P. G. Sonneveld, P. Schuster, M. W. Irwin, D. Facon, T. Harousseau, J. M. Boral, A. Anderson, K. C. TI Impact of prior autologous stem cell transplant (ASCT) in patients receiving bortezomib or dexamethasone for relapsed/refractory multiple myeloma in the APEX trial. SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Meeting Abstract CT 42nd Annual Meeting of the American-Society-of-Clinical-Oncology CY JUN 02-06, 2006 CL Atlanta, GA SP Amer Soc Clin Oncol C1 Univ Penn, Sch Med, Philadelphia, PA 19104 USA. Dana Farber Canc Inst, Boston, MA 02115 USA. Erasmus MC, Rotterdam, Netherlands. Cornell Univ, Weill Med Coll, New York, NY USA. Alta Bates Comprehens Canc Ctr, Berkeley, CA USA. CHRU Lille, Serv Malad Sang, Lille, France. Univ Hosp, Nantes, France. Millennium Pharmaceut Inc, Cambridge, MA USA. RI FACON, THIERRY/M-9736-2014 OI FACON, THIERRY/0000-0001-7705-8460 NR 0 TC 0 Z9 0 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 JUN 20 PY 2006 VL 24 IS 18 SU S BP 433S EP 433S PN 1 PG 1 WC Oncology SC Oncology GA 063HN UT WOS:000239009403034 ER PT J AU Patterson, CJ Soumerai, J Hunter, Z Leleu, X Ghobrial, I Treon, SP AF Patterson, C. J. Soumerai, J. Hunter, Z. Leleu, X. Ghobrial, I. Treon, S. P. TI Sildenafil citrate suppresses disease progression in patients with Waldenstrom's macroglobulinemia. SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Meeting Abstract CT 42nd Annual Meeting of the American-Society-of-Clinical-Oncology CY JUN 02-06, 2006 CL Atlanta, GA SP Amer Soc Clin Oncol C1 Dana Farber Canc Inst, Boston, MA 02115 USA. RI Hunter, Zachary/H-3018-2013 OI Hunter, Zachary/0000-0002-1689-1691 NR 0 TC 3 Z9 3 U1 0 U2 1 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 JUN 20 PY 2006 VL 24 IS 18 SU S BP 435S EP 435S PN 1 PG 1 WC Oncology SC Oncology GA 063HN UT WOS:000239009403044 ER PT J AU Blum, KA Johnson, JL Niedzwiecki, D Cannellos, GP Cheson, BD Bartlett, NL AF Blum, K. A. Johnson, J. L. Niedzwiecki, D. Cannellos, G. P. Cheson, B. D. Bartlett, N. L. TI A phase II study of bortezomib in relapsed Hodgkin lymphoma: Preliminary results of CALGB 50206. SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Meeting Abstract CT 42nd Annual Meeting of the American-Society-of-Clinical-Oncology CY JUN 02-06, 2006 CL Atlanta, GA SP Amer Soc Clin Oncol C1 Ohio State Univ, Columbus, OH 43210 USA. CALGB Stat Ctr, Durham, NC USA. Dana Farber Canc Inst, Boston, MA 02115 USA. Georgetown Univ, Washington, DC USA. Washington Univ, St Louis, MO USA. RI Blum, Kristie/E-2768-2011 NR 0 TC 1 Z9 1 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 JUN 20 PY 2006 VL 24 IS 18 SU S BP 440S EP 440S PN 1 PG 1 WC Oncology SC Oncology GA 063HN UT WOS:000239009403064 ER PT J AU Issa, S Hwang, J Karch, J Fridlyand, J Prados, M Batchelor, T Aldape, K Haqq, C Damon, L Rubenstein, J AF Issa, S. Hwang, J. Karch, J. Fridlyand, J. Prados, M. Batchelor, T. Aldape, K. Haqq, C. Damon, L. Rubenstein, J. TI Treatment of primary CNS lymphoma with induction high-dose methotrexate, temozolomide, rituximab followed by consolidation cytarabine/etoposide: A pilot study with biomarker analysis. SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Meeting Abstract CT 42nd Annual Meeting of the American-Society-of-Clinical-Oncology CY JUN 02-06, 2006 CL Atlanta, GA SP Amer Soc Clin Oncol C1 Univ Calif San Francisco, San Francisco, CA 94143 USA. Massachusetts Gen Hosp, Boston, MA 02114 USA. MD Anderson Canc Ctr, Houston, TX USA. NR 0 TC 0 Z9 0 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 JUN 20 PY 2006 VL 24 IS 18 SU S BP 445S EP 445S PN 1 PG 1 WC Oncology SC Oncology GA 063HN UT WOS:000239009403083 ER PT J AU Breitkreutz, I Tai, Y Li, X Coffey, R Raab, MS Song, W Hideshima, T Chauhan, D Munshi, N Anderson, KC AF Breitkreutz, I. Tai, Y. Li, X. Coffey, R. Raab, M. S. Song, W. Hideshima, T. Chauhan, D. Munshi, N. Anderson, K. C. TI Lenalidomide and bortezomib induce osteoclast cytotoxicity and decrease BAFF secretion in osteoclasts in human multiple myeloma: Clinical implications. SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Meeting Abstract CT 42nd Annual Meeting of the American-Society-of-Clinical-Oncology CY JUN 02-06, 2006 CL Atlanta, GA SP Amer Soc Clin Oncol C1 Dana Farber Canc Inst, Boston, MA 02115 USA. NR 0 TC 0 Z9 0 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 JUN 20 PY 2006 VL 24 IS 18 SU S BP 448S EP 448S PN 1 PG 1 WC Oncology SC Oncology GA 063HN UT WOS:000239009403093 ER PT J AU Neri, EP Tassone, P Shammas, M Tai, Y Blotta, S Prabhala, R Catley, L Tagliaferri, P Venuta, S Anderson, KC Munshi, NC AF Neri, E. P. Tassone, P. Shammas, M. Tai, Y. Blotta, S. Prabhala, R. Catley, L. Tagliaferri, P. Venuta, S. Anderson, K. C. Munshi, N. C. TI Novel model to evaluate changes in gene expression profile of myeloma cells in vivo following interaction with human BM microenvironment. SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Meeting Abstract CT 42nd Annual Meeting of the American-Society-of-Clinical-Oncology CY JUN 02-06, 2006 CL Atlanta, GA SP Amer Soc Clin Oncol C1 Dana Farber Canc Inst, Boston, MA 02115 USA. VA Boston Healthcare Syst, Boston, MA USA. Univ Magna Graecia, Catanzaro, Italy. RI Catley, Laurence/E-5313-2013 NR 0 TC 0 Z9 0 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 JUN 20 PY 2006 VL 24 IS 18 SU S BP 449S EP 449S PN 1 PG 1 WC Oncology SC Oncology GA 063HN UT WOS:000239009403100 ER PT J AU Gajewski, TF Niedzwiecki, D Johnson, J Linette, G Bucher, C Blaskovich, M Sebti, S Haluska, F AF Gajewski, T. F. Niedzwiecki, D. Johnson, J. Linette, G. Bucher, C. Blaskovich, M. Sebti, S. Haluska, F. TI Phase II study of the farnesyltransferase inhibitor R115777 in advanced melanoma: CALGB 500104. SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Meeting Abstract CT 42nd Annual Meeting of the American-Society-of-Clinical-Oncology CY JUN 02-06, 2006 CL Atlanta, GA SP Amer Soc Clin Oncol C1 Univ Chicago, Chicago, IL 60637 USA. CALGB, Ctr Stat, Durham, NC USA. Washington Univ, St Louis, MO USA. Univ S Florida, H Lee Moffitt Canc Ctr, Tampa, FL 33682 USA. Massachusetts Gen Hosp, Boston, MA 02114 USA. NR 0 TC 4 Z9 4 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 JUN 20 PY 2006 VL 24 IS 18 SU S BP 456S EP 456S PN 1 PG 1 WC Oncology SC Oncology GA 063HN UT WOS:000239009403126 ER PT J AU Chang, C Knight, SJ Bennett, CL AF Chang, C. Knight, S. J. Bennett, C. L. TI Effects of depression on quality of life in Medicare beneficiaries with prostate cancer. SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Meeting Abstract CT 42nd Annual Meeting of the American-Society-of-Clinical-Oncology CY JUN 02-06, 2006 CL Atlanta, GA SP Amer Soc Clin Oncol C1 Northwestern Univ, Chicago, IL 60611 USA. San Francisco VA Med Ctr, San Francisco, CA USA. RI Bennett, Charles/C-2050-2008 NR 0 TC 0 Z9 0 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 JUN 20 PY 2006 VL 24 IS 18 SU S MA 8510 BP 470S EP 470S PN 1 PG 1 WC Oncology SC Oncology GA 063HN UT WOS:000239009403182 PM 27954170 ER PT J AU Temel, JS Jackson, VA Billings, A Prigerson, HG Fidias, P Lynch, TJ Pirl, W AF Temel, J. S. Jackson, V. A. Billings, A. Prigerson, H. G. Fidias, P. Lynch, T. J., Jr. Pirl, W. TI The effect of depression on survival in patients with newly diagnosed advanced non-small cell lung cancer (NSCLC). SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Meeting Abstract CT 42nd Annual Meeting of the American-Society-of-Clinical-Oncology CY JUN 02-06, 2006 CL Atlanta, GA SP Amer Soc Clin Oncol C1 Massachusetts Gen Hosp, 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 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 JUN 20 PY 2006 VL 24 IS 18 SU S MA 8511 BP 470S EP 470S PN 1 PG 1 WC Oncology SC Oncology GA 063HN UT WOS:000239009403183 PM 27954124 ER PT J AU Dias, L Lamont, E AF Dias, L. Lamont, E. TI Academic oncologists' attitudes and practices regarding the care of cancer patients at the end of life. SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Meeting Abstract CT 42nd Annual Meeting of the American-Society-of-Clinical-Oncology CY JUN 02-06, 2006 CL Atlanta, GA SP Amer Soc Clin Oncol C1 Massachusetts Gen Hosp, Boston, MA 02114 USA. NR 0 TC 0 Z9 0 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 JUN 20 PY 2006 VL 24 IS 18 SU S BP 486S EP 486S PN 1 PG 1 WC Oncology SC Oncology GA 063HN UT WOS:000239009403244 ER PT J AU Neus, MN Jacobson, JO Earle, C Desch, CE McNiff, K Thacker, L Simone, JV AF Neus, M. N. Jacobson, J. O. Earle, C. Desch, C. E. McNiff, K. Thacker, L. Simone, J. V. TI Evaluating end of life care: The Quality Oncology Practice Initiative (QOPI) Experience. SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Meeting Abstract CT 42nd Annual Meeting of the American-Society-of-Clinical-Oncology CY JUN 02-06, 2006 CL Atlanta, GA SP Amer Soc Clin Oncol C1 Oncol Hematol Care, Cincinnati, OH USA. N Shore Med Ctr, Salem, MA USA. Dana Farber Canc Inst, Boston, MA 02115 USA. Virginia Canc Inst, Richmond, VA USA. ASCO, Alexandria, VA USA. Virginia Hlth Qual Ctr, Richmond, VA USA. Simone Consulting, Dunwoody, GA USA. NR 0 TC 0 Z9 0 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 JUN 20 PY 2006 VL 24 IS 18 SU S BP 486S EP 486S PN 1 PG 1 WC Oncology SC Oncology GA 063HN UT WOS:000239009403245 ER PT J AU Ullrich, CK Hilden, JM Sheaffer, JW Moore, CL Berde, CB Weeks, JC Wolfe, J AF Ullrich, C. K. Hilden, J. M. Sheaffer, J. W. Moore, C. L. Berde, C. B. Weeks, J. C. Wolfe, J. TI Factors associated with fatigue in children with cancer at the end of life. SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Meeting Abstract CT 42nd Annual Meeting of the American-Society-of-Clinical-Oncology CY JUN 02-06, 2006 CL Atlanta, GA SP Amer Soc Clin Oncol C1 Dana Farber Canc Inst, Boston, MA 02115 USA. Childrens Hosp, Cleveland Clin, Cleveland, OH USA. Childrens Hosp & Clin Minnesota, St Paul, MN USA. Childrens Hosp, Boston, MA 02115 USA. NR 0 TC 0 Z9 0 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 JUN 20 PY 2006 VL 24 IS 18 SU S BP 486S EP 486S PN 1 PG 1 WC Oncology SC Oncology GA 063HN UT WOS:000239009403246 ER PT J AU Fox, S Berkey, B Knisely, J Chakravarti, A Yung, WA Curran, W Robins, H Brachmen, D Henderson, R Mehta, M Movas, B AF Fox, S. Berkey, B. Knisely, J. Chakravarti, A. Yung, W. A. Curran, W. Robins, H. Brachmen, D. Henderson, R. Mehta, M. Movas, B. TI Prospective neurocognitive effects and quality of life (QOL) in patients with multiple brain metastases receiving whole brain radiation (WBRT) +/- thalidomide on radiation therapy oncology group (RTOG) trial 0118. SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Meeting Abstract CT 42nd Annual Meeting of the American-Society-of-Clinical-Oncology CY JUN 02-06, 2006 CL Atlanta, GA SP Amer Soc Clin Oncol C1 Univ Virginia, Sch Nursing, Charlottesville, VA 22903 USA. Radiat Therapy Oncol Grp, Philadelphia, PA USA. Yale Univ, New Haven, CT USA. Massachusetts Gen Hosp, Boston, MA 02114 USA. Univ Texas, MD Anderson Canc Ctr, Houston, TX 77030 USA. Thomas Jefferson Univ Hosp, Philadelphia, PA 19107 USA. Univ Wisconsin, Madison, WI USA. Arizona Oncol Serv, Phoenix, AZ USA. Univ Florida, Shands Canc Ctr, Jacksonville, FL USA. Henry Ford Hlth Syst, Detroit, MI USA. NR 0 TC 0 Z9 0 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 JUN 20 PY 2006 VL 24 IS 18 SU S BP 490S EP 490S PN 1 PG 1 WC Oncology SC Oncology GA 063HN UT WOS:000239009403261 ER PT J AU Pirl, WF Muriel, A Schapia, L Hwang, V Moore, C Temel, J Kornblith, A Holland, JC AF Pirl, W. F. Muriel, A. Schapia, L. Hwang, V. Moore, C. Temel, J. Kornblith, A. Holland, J. C. TI Statewide survey on the management of psychosocial distress by oncologists. SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Meeting Abstract CT 42nd Annual Meeting of the American-Society-of-Clinical-Oncology CY JUN 02-06, 2006 CL Atlanta, GA SP Amer Soc Clin Oncol C1 Massachusetts Gen Hosp, Boston, MA 02114 USA. Dana Farber Canc Inst, Boston, MA 02115 USA. Mem Sloan Kettering Canc Ctr, New York, NY 10021 USA. NR 0 TC 0 Z9 0 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 JUN 20 PY 2006 VL 24 IS 18 SU S BP 493S EP 493S PN 1 PG 1 WC Oncology SC Oncology GA 063HN UT WOS:000239009403273 ER PT J AU Hesketh, PJ Younger, J Sanjay, R Trainor, B Sanz-Altamira, P Krentzin, M Hayden, M Hesketh, AM AF Hesketh, P. J. Younger, J. Sanjay, R. Trainor, B. Sanz-Altamira, P. Krentzin, M. Hayden, M. Hesketh, A. M. TI Aprepitant as salvage antiemetic therapy in breast cancer patients receiving doxorubicin and cyclophosphamide (AC). SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Meeting Abstract CT 42nd Annual Meeting of the American-Society-of-Clinical-Oncology CY JUN 02-06, 2006 CL Atlanta, GA SP Amer Soc Clin Oncol C1 Caritas St Elizabeths Med Ctr, Boston, MA USA. Massachusetts Gen Hosp, Boston, MA 02114 USA. Caritas Holy Family Hosp, Methuen, MA USA. NR 0 TC 0 Z9 0 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 JUN 20 PY 2006 VL 24 IS 18 SU S BP 497S EP 497S PN 1 PG 1 WC Oncology SC Oncology GA 063HN UT WOS:000239009403290 ER PT J AU Matthay, KK Quach, A Huberty, J Franc, B Groshen, S Shusterman, S Veatch, J Brophy, P Yanik, G Maris, J AF Matthay, K. K. Quach, A. Huberty, J. Franc, B. Groshen, S. Shusterman, S. Veatch, J. Brophy, P. Yanik, G. Maris, J. TI I-131-Metaiodobenzylguanidine (I-131-MIBG) double infusion with autologous stem cell transplant for neuroblastoma: A New Approaches to Neuroblastoma Therapy (NANT) study. SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Meeting Abstract CT 42nd Annual Meeting of the American-Society-of-Clinical-Oncology CY JUN 02-06, 2006 CL Atlanta, GA SP Amer Soc Clin Oncol C1 Univ Calif San Francisco, San Francisco, CA 94143 USA. Univ So Calif, Los Angeles, CA USA. Dana Farber Canc Inst, Boston, MA 02115 USA. Childrens Hosp Philadelphia, Philadelphia, PA 19104 USA. CS Mott Childrens Hosp, Ann Arbor, MI USA. NR 0 TC 0 Z9 0 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 JUN 20 PY 2006 VL 24 IS 18 SU S MA 9011 BP 504S EP 504S PN 1 PG 1 WC Oncology SC Oncology GA 063HN UT WOS:000239009403316 PM 27954209 ER PT J AU Barry, E Levy, DE Goldwasser, MA Loh, ML Deangelo, DJ Sallan, SE Silverman, LB AF Barry, E. Levy, D. E. Goldwasser, M. A. Loh, M. L. Deangelo, D. J. Sallan, S. E. Silverman, L. B. TI Outcome of adolescents with acute lymphoblastic leukemia (ALL) treated on Dana-Farber Cancer Institute (DFCI) ALL Consortium Protocols, 1991-2000. SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Meeting Abstract CT 42nd Annual Meeting of the American-Society-of-Clinical-Oncology CY JUN 02-06, 2006 CL Atlanta, GA SP Amer Soc Clin Oncol C1 Dana Farber Canc Inst, Boston, MA 02115 USA. Univ Calif San Francisco, San Francisco, CA 94143 USA. NR 0 TC 0 Z9 0 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 JUN 20 PY 2006 VL 24 IS 18 SU S MA 9023 BP 507S EP 507S PN 1 PG 1 WC Oncology SC Oncology GA 063HN UT WOS:000239009403328 PM 27954231 ER PT J AU Heinrich, MC Maki, RG Corless, CL Antonescu, CR Fletcher, JA Fletcher, CD Huang, X Baum, CM Demetri, GD AF Heinrich, M. C. Maki, R. G. Corless, C. L. Antonescu, C. R. Fletcher, J. A. Fletcher, C. D. Huang, X. Baum, C. M. Demetri, G. D. TI Sunitinib (SU) response in imatinib-resistant (IM-R) GIST correlates with KIT and PDGFRA mutation status. SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Meeting Abstract CT 42nd Annual Meeting of the American-Society-of-Clinical-Oncology CY JUN 02-06, 2006 CL Atlanta, GA SP Amer Soc Clin Oncol C1 OHSU Canc Inst, Portland, OR USA. Mem Sloan Kettering Canc Ctr, New York, NY 10021 USA. Brigham & Womens Hosp, Boston, MA 02115 USA. Pfizer, La Jolla, CA USA. Dana Farber Canc Inst, Boston, MA 02115 USA. NR 0 TC 31 Z9 33 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 JUN 20 PY 2006 VL 24 IS 18 SU S MA 9502 BP 520S EP 520S PN 1 PG 1 WC Oncology SC Oncology GA 063HN UT WOS:000239009403376 PM 27952818 ER PT J AU Chawla, SP Tolcher, AW Staddon, AP Schuetze, SM D'Amato, GZ Blay, JY Sankhala, KK Daly, ST Rivera, VM Demetri, GD AF Chawla, S. P. Tolcher, A. W. Staddon, A. P. Schuetze, S. M. D'Amato, G. Z. Blay, J. Y. Sankhala, K. K. Daly, S. T. Rivera, V. M. Demetri, G. D. TI Updated results of a phase II trial of AP23573, a novel mTOR inhibitor, in patients (pts) with advanced soft tissue or bone sarcomas. SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Meeting Abstract CT 42nd Annual Meeting of the American-Society-of-Clinical-Oncology CY JUN 02-06, 2006 CL Atlanta, GA SP Amer Soc Clin Oncol C1 John Wayne Canc Inst, Santa Monica, CA USA. Canc Therapy & Res Ctr S Texas, San Antonio, TX 78229 USA. Penn Oncol Hematol Associates, Philadelphia, PA USA. Univ Michigan, Ctr Canc, Ann Arbor, MI 48109 USA. Univ S Florida, H Lee Moffitt Canc Ctr, Tampa, FL 33682 USA. Ctr Leon Berard, F-69373 Lyon, France. ARIAD Pharmaceut Inc, Cambridge, MA USA. Dana Farber Canc Inst, Boston, MA 02115 USA. RI Blay, Jean-Yves/N-3966-2016 OI Blay, Jean-Yves/0000-0001-7190-120X NR 0 TC 27 Z9 28 U1 0 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 JUN 20 PY 2006 VL 24 IS 18 SU S MA 9505 BP 521S EP 521S PN 1 PG 1 WC Oncology SC Oncology GA 063HN UT WOS:000239009403379 ER PT J AU Grosso, F Demetri, GD Blay, JY Judson, I Le Cesne, A Spreafico, C Jimeno, J Pilotti, S D'Incalci, M Casali, PG AF Grosso, F. Demetri, G. D. Blay, J. Y. Judson, I. Le Cesne, A. Spreafico, C. Jimeno, J. Pilotti, S. D'Incalci, M. Casali, P. G. TI Patterns of tumor response to trabectedin (ET743) in myxoid liposarcomas. SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Meeting Abstract CT 42nd Annual Meeting of the American-Society-of-Clinical-Oncology CY JUN 02-06, 2006 CL Atlanta, GA SP Amer Soc Clin Oncol C1 Ist Nazl Tumori, I-20133 Milan, Italy. Dana Farber Canc Inst, Boston, MA 02115 USA. Ctr Leon Berard, F-69373 Lyon, France. Royal Marsden Hosp, London SW3 6JJ, England. Inst Gustave Roussy, Villejuif, France. PharmaMar, Madrid, Spain. Mario Negri Inst Pharmacol Res, I-20157 Milan, Italy. RI Blay, Jean-Yves/N-3966-2016 OI Blay, Jean-Yves/0000-0001-7190-120X NR 0 TC 9 Z9 9 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 JUN 20 PY 2006 VL 24 IS 18 SU S MA 9511 BP 522S EP 522S PN 1 PG 1 WC Oncology SC Oncology GA 063HN UT WOS:000239009403385 ER PT J AU Casali, PG Garrett, CR Blackstein, ME Shah, M Verweij, J McArthur, G Judson, I Li, J Baum, CM Demetri, GD AF Casali, P. G. Garrett, C. R. Blackstein, M. E. Shah, M. Verweij, J. McArthur, G. Judson, I. Li, J. Baum, C. M. Demetri, G. D. TI Updated results from a phase III trial of sunitinib in GIST patients (pts) for whom imatinib (IM) therapy has failed due to resistance or intolerance. SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Meeting Abstract CT 42nd Annual Meeting of the American-Society-of-Clinical-Oncology CY JUN 02-06, 2006 CL Atlanta, GA SP Amer Soc Clin Oncol C1 Ist Nazl Tumori, I-20133 Milan, Italy. H Lee Moffit Canc Ctr & Res Inst, Tampa, FL USA. Mt Sinai Hosp, Toronto, ON M5G 1X5, Canada. Univ Toronto, Toronto, ON, Canada. Ohio State Univ, Ctr Comprehens Canc, Columbus, OH 43210 USA. Erasmus Univ, Med Ctr, Rotterdam, Netherlands. Peter MacCallum Canc Ctr, Melbourne, Vic, Australia. Royal Marsden Hosp, London SW3 6JJ, England. Pfizer Global Res & Dev, La Jolla, CA USA. Dana Farber Canc Inst, Boston, MA 02115 USA. NR 0 TC 13 Z9 15 U1 0 U2 1 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 JUN 20 PY 2006 VL 24 IS 18 SU S MA 9513 BP 523S EP 523S PN 1 PG 1 WC Oncology SC Oncology GA 063HN UT WOS:000239009403386 ER PT J AU Albritton, KH Rankin, C Coffin, CM Ratner, N Budd, GT Schuetze, SM Randall, RL Declue, JE Borden, EC AF Albritton, K. H. Rankin, C. Coffin, C. M. Ratner, N. Budd, G. T. Schuetze, S. M. Randall, R. L. Declue, J. E. Borden, E. C. TI Phase II study of erlotinib in metastatic or unresectable malignant peripheral nerve sheath tumors (MPNST). SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Meeting Abstract CT 42nd Annual Meeting of the American-Society-of-Clinical-Oncology CY JUN 02-06, 2006 CL Atlanta, GA SP Amer Soc Clin Oncol C1 Dana Farber Canc Inst, Boston, MA 02115 USA. SW Oncol Grp, San Antonio, TX 78229 USA. Univ Utah, Salt Lake City, UT USA. Childrens Hosp, Cincinnati, OH 45229 USA. Cleveland Clin, Cleveland, OH 44106 USA. Natl Canc Inst, Bethesda, MD USA. Univ Michigan, Ann Arbor, MI 48109 USA. NR 0 TC 20 Z9 20 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 JUN 20 PY 2006 VL 24 IS 18 SU S MA 9518 BP 524S EP 524S PN 1 PG 1 WC Oncology SC Oncology GA 063HN UT WOS:000239009403391 PM 27952832 ER PT J AU Janeway, KA Matthews, DC Butrynski, JE D'Amato, GZ Agresta, S Garrett, C Corless, CL Albritton, KH Demetri, GD AF Janeway, K. A. Matthews, D. C. Butrynski, J. E. D'Amato, G. Z. Agresta, S. Garrett, C. Corless, C. L. Albritton, K. H. Demetri, G. D. TI Sunitinib treatment of pediatric metastatic GIST after failure of imatinib. SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Meeting Abstract CT 42nd Annual Meeting of the American-Society-of-Clinical-Oncology CY JUN 02-06, 2006 CL Atlanta, GA SP Amer Soc Clin Oncol C1 Dana Farber Canc Inst, Boston, MA 02115 USA. Univ Washington, Sch Med, Seattle, WA 98195 USA. H Lee Moffit Canc Ctr & Res Inst, Tampa, FL USA. Oregon Hlth Sci Univ, Inst Canc, Portland, OR 97201 USA. NR 0 TC 2 Z9 2 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 JUN 20 PY 2006 VL 24 IS 18 SU S MA 9519 BP 524S EP 524S PN 1 PG 1 WC Oncology SC Oncology GA 063HN UT WOS:000239009403392 ER PT J AU Blanke, CD Demetri, GD Von Mehren, M Heinrich, MC Eisenberg, BL Fletcher, J Corless, CL Wehrle, E Sandau, KB Joensuu, H AF Blanke, C. D. Demetri, G. D. Von Mehren, M. Heinrich, M. C. Eisenberg, B. L. Fletcher, J. Corless, C. L. Wehrle, E. Sandau, K. B. Joensuu, H. TI Long-term follow-up of a phase II randomized trial in advanced gastrointestinal stromal tumor (GIST) patients (pts) treated with imatinib mesylate. SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Meeting Abstract CT 42nd Annual Meeting of the American-Society-of-Clinical-Oncology CY JUN 02-06, 2006 CL Atlanta, GA SP Amer Soc Clin Oncol C1 OHSU Canc Inst, Portland, OR USA. Dana Farber Canc Inst, Boston, MA 02115 USA. Fox Chase Canc Ctr, Philadelphia, PA 19111 USA. Norris Cotton Canc Ctr, Lebanon, NH USA. Brigham & Womens Hosp, Boston, MA 02115 USA. Novart Pharma AG, Basel, Switzerland. Novartis Pharmaceut Corp, E Hanover, NJ USA. Univ Helsinki, Cent Hosp, FIN-00170 Helsinki, Finland. NR 0 TC 15 Z9 17 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 JUN 20 PY 2006 VL 24 IS 18 SU S MA 9528 BP 526S EP 526S PN 1 PG 1 WC Oncology SC Oncology GA 063HN UT WOS:000239009403401 ER PT J AU Bauer, S Demetri, GD Fletcher, JA AF Bauer, S. Demetri, G. D. Fletcher, J. A. TI Evaluation of SRC-family kinases in gastrointestinal stromal tumors. SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Meeting Abstract CT 42nd Annual Meeting of the American-Society-of-Clinical-Oncology CY JUN 02-06, 2006 CL Atlanta, GA SP Amer Soc Clin Oncol C1 Brigham & Womens Hosp, Boston, MA 02115 USA. Dana Farber Canc Inst, Boston, MA 02115 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC 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 JUN 20 PY 2006 VL 24 IS 18 SU S MA 9529 BP 527S EP 527S PN 1 PG 1 WC Oncology SC Oncology GA 063HN UT WOS:000239009403402 PM 27952790 ER PT J AU George, S Casali, PG Blay, J Le Cesne, A Tyler, AR Quigley, MT Tassell, V Baum, CM Demetri, GD AF George, S. Casali, P. G. Blay, J. Le Cesne, A. Tyler, A. R. Quigley, M. T. Tassell, V. Baum, C. M. Demetri, G. D. TI Phase II study of sunitinib administered in a continuous daily dosing regimen in patients (pts) with advanced GIST. SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Meeting Abstract CT 42nd Annual Meeting of the American-Society-of-Clinical-Oncology CY JUN 02-06, 2006 CL Atlanta, GA SP Amer Soc Clin Oncol C1 Dana Farber Canc Inst, Boston, MA 02115 USA. Ist Nazl Tumori, I-20133 Milan, Italy. Ctr Leon Berard, Lyon, France. Inst Gustave Roussy, F-94800 Villejuif, France. Pfizer Global Res & Dev, La Jolla, CA USA. RI Blay, Jean-Yves/N-3966-2016 OI Blay, Jean-Yves/0000-0001-7190-120X NR 0 TC 4 Z9 4 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 JUN 20 PY 2006 VL 24 IS 18 SU S MA 9532 BP 527S EP 527S PN 1 PG 1 WC Oncology SC Oncology GA 063HN UT WOS:000239009403405 ER PT J AU Morgan, JA Garrett, CR Schutte, HJ Hurwitz, H Rosen, LS Ruka, W Picus, J Kaiser, P Baum, CM Demetri, GD AF Morgan, J. A. Garrett, C. R. Schutte, H. J. Hurwitz, H. Rosen, L. S. Ruka, W. Picus, J. Kaiser, P. Baum, C. M. Demetri, G. D. TI Sunitinib for patients (pts) with advanced imatinib (IM)-refractory GIST: Early results from a "treatment-use" trial. SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Meeting Abstract CT 42nd Annual Meeting of the American-Society-of-Clinical-Oncology CY JUN 02-06, 2006 CL Atlanta, GA SP Amer Soc Clin Oncol C1 Dana Farber Canc Inst, Boston, MA 02115 USA. H Lee Moffit Canc Ctr & Res Inst, Tampa, FL USA. Marien Hosp, Dusseldorf, Germany. Duke Univ, Med Ctr, Durham, NC 27706 USA. Premiere Oncol, Santa Monica, CA USA. Canc Ctr Inst, Warsaw, Poland. Univ Washington, Sch Med, Siteman Canc Ctr, Seattle, WA 98195 USA. Oncol Specialists Sc, Park Ridge, IL USA. Pfizer Global Res & Dev, La Jolla, CA USA. NR 0 TC 0 Z9 0 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 JUN 20 PY 2006 VL 24 IS 18 SU S MA 9540 BP 529S EP 529S PN 1 PG 1 WC Oncology SC Oncology GA 063HN UT WOS:000239009403413 PM 27952801 ER PT J AU Raut, CP Van Den Abbeele, A Ramaiya, N Morgan, JA George, S Quigley, MT Dollard, AM Bertagnolli, MM Baum, C Demetri, GD AF Raut, C. P. Van Den Abbeele, A. Ramaiya, N. Morgan, J. A. George, S. Quigley, M. T. Dollard, A. M. Bertagnolli, M. M. Baum, C. Demetri, G. D. TI Patterns of PET response after long-term sunitinib therapy in patients (pts) with imatinib (IM)-resistant gastrointestinal stromal tumors (GIST). SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Meeting Abstract CT 42nd Annual Meeting of the American-Society-of-Clinical-Oncology CY JUN 02-06, 2006 CL Atlanta, GA SP Amer Soc Clin Oncol C1 Brigham & Womens Hosp, Boston, MA 02115 USA. Dana Farber Canc Inst, Boston, MA 02115 USA. Pfizer Inc, Cambridge, MA USA. NR 0 TC 1 Z9 1 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 JUN 20 PY 2006 VL 24 IS 18 SU S MA 9547 BP 531S EP 531S PN 1 PG 1 WC Oncology SC Oncology GA 063HN UT WOS:000239009403420 PM 27952946 ER PT J AU Reichardt, P Casali, PG Blay, J Von Mehren, M Schoffski, P Hosseinzadeh, S Tanaka, C Gsponer, T Veronese, ML Demetri, GD AF Reichardt, P. Casali, P. G. Blay, J. Von Mehren, M. Schoffski, P. Hosseinzadeh, S. Tanaka, C. Gsponer, T. Veronese, M. L. Demetri, G. D. TI A phase I study of AMN107 alone and in combination with imatinib in patients (pts) with imatinib-resistant gastrointestinal stromal tumors (GIST). SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Meeting Abstract CT 42nd Annual Meeting of the American-Society-of-Clinical-Oncology CY JUN 02-06, 2006 CL Atlanta, GA SP Amer Soc Clin Oncol C1 Charite Campus Buch, Berlin, Germany. Ist Nazl Tumori, I-20133 Milan, Italy. Hop Edouard Herriot, F-69374 Lyon, France. Ctr Leon Berard, F-69374 Lyon, France. Fox Chase Canc Ctr, Philadelphia, PA 19111 USA. Catholic Univ Louvain, Leuven Canc Inst, B-3000 Louvain, Belgium. Novartis Pharma AG, Basel, Switzerland. Novartis Pharma AG, E Hanover, NJ USA. Dana Farber Canc Inst, Boston, MA 02115 USA. RI Blay, Jean-Yves/N-3966-2016 OI Blay, Jean-Yves/0000-0001-7190-120X NR 0 TC 3 Z9 3 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 JUN 20 PY 2006 VL 24 IS 18 SU S MA 9545 BP 531S EP 531S PN 1 PG 1 WC Oncology SC Oncology GA 063HN UT WOS:000239009403418 ER PT J AU Bertagnolli, MM Compton, CC Niedzwiecki, D Warren, RS Jewell, S Bailey, GP Mayer, RJ Goldberg, R Saltz, L Redston, M AF Bertagnolli, M. M. Compton, C. C. Niedzwiecki, D. Warren, R. S. Jewell, S. Bailey, G. P. Mayer, R. J. Goldberg, R. Saltz, L. Redston, M. TI Microsatellite instability predicts improved response to adjuvant therapy with irinotecan, 5-fluorouracil and leucovorin in stage III colon cancer. SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Meeting Abstract CT 42nd Annual Meeting of the American-Society-of-Clinical-Oncology CY JUN 02-06, 2006 CL Atlanta, GA SP Amer Soc Clin Oncol C1 Canc & Leukemia Grp B, Boston, MA USA. Brigham & Womens Hosp, Boston, MA 02115 USA. NCI, Bethesda, MD 20892 USA. Duke Univ, Durham, NC 27706 USA. Univ Calif San Francisco, San Francisco, CA 94143 USA. Ohio State Univ, Columbus, OH 43210 USA. Dana Farber Canc Inst, Boston, MA 02115 USA. Univ N Carolina, Chapel Hill, NC 27515 USA. Mem Sloan Kettering Canc Ctr, New York, NY 10021 USA. NR 0 TC 4 Z9 4 U1 0 U2 1 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 JUN 20 PY 2006 VL 24 IS 18 SU S MA 10003 BP 541S EP 541S PN 1 PG 1 WC Oncology SC Oncology GA 063HN UT WOS:000239009403459 PM 27955350 ER PT J AU Lu-Yao, GL Albertsen, PC Stanford, JL Stukel, TA Walker-Corkery, ES Barry, MJ AF Lu-Yao, G. L. Albertsen, P. C. Stanford, J. L. Stukel, T. A. Walker-Corkery, E. S. Barry, M. J. TI Prostate cancer screening, treatment, and outcomes - A population-based study. SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Meeting Abstract CT 42nd Annual Meeting of the American-Society-of-Clinical-Oncology CY JUN 02-06, 2006 CL Atlanta, GA SP Amer Soc Clin Oncol C1 Canc Inst New Jersey, New Brunswick, NJ USA. Univ Connecticut, Farmington, CT 06269 USA. Fred Hutchinson Canc Res Ctr, Seattle, WA 98104 USA. Ctr Evaluat Clin Sci, Toronto, ON, Canada. Massachusetts Gen Hosp, Boston, MA 02114 USA. NR 0 TC 0 Z9 0 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 JUN 20 PY 2006 VL 24 IS 18 SU S MA 10017 BP 545S EP 545S PN 1 PG 1 WC Oncology SC Oncology GA 063HN UT WOS:000239009403473 PM 27955368 ER PT J AU Masciari, S Kandel, M Digianni, L Dillon, D Li, F Garber, J AF Masciari, S. Kandel, M. Digianni, L. Dillon, D. Li, F. Garber, J. TI Histopathological features of breast cancers in women with germline TP53 mutations. SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Meeting Abstract CT 42nd Annual Meeting of the American-Society-of-Clinical-Oncology CY JUN 02-06, 2006 CL Atlanta, GA SP Amer Soc Clin Oncol 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 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 JUN 20 PY 2006 VL 24 IS 18 SU S MA 10031 BP 548S EP 548S PN 1 PG 1 WC Oncology SC Oncology GA 063HN UT WOS:000239009403486 PM 27954107 ER PT J AU Borras, AM Kuang, Y Rogers, AM Holmes, AJ Ruiz, MG Joshi, VA Distel, RJ Giaccone, G Taron, M Janne, PA AF Borras, A. M. Kuang, Y. Rogers, A. M. Holmes, A. J. Ruiz, M. Gallegos Joshi, V. A. Distel, R. J. Giaccone, G. Taron, M. Janne, P. A. TI Detection of clinically significant mutations in the epidermal growth factor receptor missed by direct sequencing using a highly sensitive DNA endonuclease. SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Meeting Abstract CT 42nd Annual Meeting of the American-Society-of-Clinical-Oncology CY JUN 02-06, 2006 CL Atlanta, GA SP Amer Soc Clin Oncol C1 Dana Farber Canc Inst, Boston, MA 02115 USA. Virje Univ Med Ctr, Amsterdam, Netherlands. Brigham & Womens Hosp, Boston, MA 02115 USA. Hosp Germans Trias & Pujol, Barcelona, Spain. NR 0 TC 0 Z9 0 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 JUN 20 PY 2006 VL 24 IS 18 SU S MA 10054 BP 554S EP 554S PN 1 PG 1 WC Oncology SC Oncology GA 063HN UT WOS:000239009403508 PM 27954151 ER PT J AU Da Silva, M Flynn, KE Choppa, P Zhou, Z Bell, DW Iafrate, AJ Paler, RJ Allitto, BA Rohlfs, EM AF Da Silva, M. Flynn, K. E. Choppa, P. Zhou, Z. Bell, D. W. Iafrate, A. J. Paler, R. J. Allitto, B. A. Rohlfs, E. M. TI Detection of mutations in the EGFR tyrosine kinase domain by DNA sequencing. SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Meeting Abstract CT 42nd Annual Meeting of the American-Society-of-Clinical-Oncology CY JUN 02-06, 2006 CL Atlanta, GA SP Amer Soc Clin Oncol C1 Genzyme, Los Angeles, CA USA. Genzyme, Westborough, MA USA. Massachusetts Gen Hosp, Ctr Canc, Charlestown, MA USA. Massachusetts Gen Hosp, Boston, MA 02114 USA. NR 0 TC 0 Z9 0 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 JUN 20 PY 2006 VL 24 IS 18 SU S MA 10060 BP 555S EP 555S PN 1 PG 1 WC Oncology SC Oncology GA 063HN UT WOS:000239009403514 PM 27954179 ER PT J AU Berger, R Lin, DI Nieto, M Signoretti, S Hahn, WC Loda, M AF Berger, R. Lin, D. I. Nieto, M. Signoretti, S. Hahn, W. C. Loda, M. TI Androgen-dependent regulation of Her-2/neu in prostate cancer cells. SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Meeting Abstract CT 42nd Annual Meeting of the American-Society-of-Clinical-Oncology CY JUN 02-06, 2006 CL Atlanta, GA SP Amer Soc Clin Oncol C1 Sheba Med Ctr, Tel Hashomer, Israel. 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 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 JUN 20 PY 2006 VL 24 IS 18 SU S MA 10099 BP 565S EP 565S PN 1 PG 1 WC Oncology SC Oncology GA 063HN UT WOS:000239009403553 PM 27954046 ER PT J AU Motzer, RJ Hutson, TE Tomczak, P Michaelson, MD Bukowski, RM Rixe, O Oudard, S Kim, ST Baum, CM Figlin, RA AF Motzer, R. J. Hutson, T. E. Tomczak, P. Michaelson, M. D. Bukowski, R. M. Rixe, O. Oudard, S. Kim, S. T. Baum, C. M. Figlin, R. A. TI Phase III randomized trial of sunitinib malate (SU11248) versus interferon-alfa (IFN-alpha) as first-line systemic therapy for patients with metastatic renal cell carcinoma (mRCC) SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Meeting Abstract CT 42nd Annual Meeting of the American-Society-of-Clinical-Oncology CY JUN 02-06, 2006 CL Atlanta, GA SP Amer Soc Clin Oncol C1 Mem Sloan Kettering Canc Ctr, New York, NY 10021 USA. Baylor Sammons Texas Oncol PA, Dallas, TX USA. Klin Oncol Oddzial Chemioterapii, Poznan, Poland. Massachusetts Gen Hosp, Boston, MA 02114 USA. Cleveland Clin Fdn, Cleveland, OH 44195 USA. Grp Hosp Pitie Salpetriere, F-75634 Paris, France. Georges Pompidou European Hosp, Paris, France. Pfizer Inc, La Jolla, CA USA. Univ Calif Los Angeles, Los Angeles, CA USA. NR 0 TC 9 Z9 9 U1 0 U2 1 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 JUN 20 PY 2006 VL 24 IS 18 SU S BP 930S EP 930S PN 2 PG 1 WC Oncology SC Oncology GA 063HQ UT WOS:000239009700002 ER PT J AU Goss, PE Bondarenko, IN Manikhas, GN Pendergrass, KB Miller, WH Blanchett, D Lang, W Langecker, P AF Goss, P. E. Bondarenko, I. N. Manikhas, G. N. Pendergrass, K. B. Miller, W. H. Blanchett, D. Lang, W. Langecker, P. CA 777 CLP-29 Study Grp TI Phase 3 study of atamestane plus toremifene vs. letrozole in advanced breast cancer SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Meeting Abstract CT 42nd Annual Meeting of the American-Society-of-Clinical-Oncology CY JUN 02-06, 2006 CL Atlanta, GA SP Amer Soc Clin Oncol C1 Massachusetts Gen Hosp, Boston, MA 02114 USA. Dnepropetrovsk State Med Acad, Dnepropetrovsk, Ukraine. St Petersburg City Oncol Ctr, St Petersburg, Russia. Kansas City Canc Ctr, Kansas City, KS USA. McGill Univ, Montreal, PQ, Canada. Intarcia Therapeut Inc, Emeryville, CA USA. NR 0 TC 0 Z9 0 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 JUN 20 PY 2006 VL 24 IS 18 SU S BP 932S EP 932S PN 2 PG 1 WC Oncology SC Oncology GA 063HQ UT WOS:000239009700009 ER PT J AU Poplin, E Levy, DE Berlin, J Rothenberg, ML O'Dwyer, PJ Cella, D Mitchell, E Alberts, S Benson, A AF Poplin, E. Levy, D. E. Berlin, J. Rothenberg, M. L. O'Dwyer, P. J. Cella, D. Mitchell, E. Alberts, S. Benson, A., III TI Phase III trial of gemcitabine (30-minute infusion) versus gemcitabine (fixed-dose-rate infusion [FDR]) versus gemcitabine plus oxaliplatin (GEMOX) in patients with advanced pancreatic cancer (E6201) SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Meeting Abstract CT 42nd Annual Meeting of the American-Society-of-Clinical-Oncology CY JUN 02-06, 2006 CL Atlanta, GA SP Amer Soc Clin Oncol C1 Canc Inst New Jersey UMDNJ, New Brunswick, NJ USA. Dana Farber Canc Inst, Boston, MA 02115 USA. Vanderbilt Ingram Canc Ctr, Nashville, TN USA. Univ Penn, Philadelphia, PA 19104 USA. Evanston NW Healthcare, Evanston, IL USA. Thomas Jefferson Univ, Philadelphia, PA 19107 USA. Mayo Clin, Rochester, MN USA. Northwestern Univ, Chicago, IL 60611 USA. NR 0 TC 5 Z9 6 U1 0 U2 1 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 JUN 20 PY 2006 VL 24 IS 18 SU S BP 933S EP 933S PN 2 PG 1 WC Oncology SC Oncology GA 063HQ UT WOS:000239009700013 ER PT J AU Smith, MR Manola, J Kaufman, DS Oh, WK Bubley, GJ Kantoff, PW AF Smith, MR Manola, J Kaufman, DS Oh, WK Bubley, GJ Kantoff, PW TI Celecoxib versus placebo for men with prostate cancer and a rising serum prostate-specific antigen after radical prostatectomy and/or radiation therapy SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Article ID CYCLOOXYGENASE-2; CARCINOMA; EXPRESSION; TRIALS AB Purpose To assess the biologic activity of celecoxib, a selective cyclooxygenase-2 inhibitor, in men with recurrent prostate cancer using change in prostate-specific antigen (PSA) doubling time (PSADT) as the primary outcome variable. Patients and Methods Participants had histologically confirmed prostate cancer, no recent hormone therapy, rising serum PSA after radical prostatectomy and/or radiation therapy, and no radiographic evidence of metastases. Patients were randomly assigned to celecoxib (400 mg by mouth twice daily) or placebo. Treatment continued until disease progression or until adverse effects stopped treatment. A positive outcome was defined as post-treatment PSADT of more than 200% baseline PSADT with no new metastases. Results The study was terminated early after information about the cardiovascular safety of celecoxib prompted review of ongoing clinical studies. Before discontinuation of the study, 78 men were assigned randomly to either celecoxib or placebo. Eight (20%) of 40 men in the placebo group and 15 (40%) of 38 men in the celecoxib group had post-treatment PSADT of more than 200% of baseline PSADT with no new metastases (P =.08). Mean PSA velocity increased by 3.0% for the placebo group and decreased by 3.4% for the celecoxib group (P =.02). Conclusion Although the primary efficacy objective was not met, this study provides some evidence for biologic activity of celecoxib in prostate cancer. Compared with placebo, celecoxib significantly decreased mean PSA velocity and tended to increase the proportion of men who doubled their PSADT. C1 Massachusetts Gen Hosp, Ctr Canc, Boston, MA 02114 USA. Beth Israel Deaconess Med Ctr, Boston, MA 02215 USA. Dana Farber Canc Inst, Boston, MA 02115 USA. RP Smith, MR (reprint author), Massachusetts Gen Hosp, Ctr Canc, Yawkey 7038,55 Fruit St, Boston, MA 02114 USA. EM smith.matthew@mgh.harvard.edu RI Oh, William/B-9163-2012 OI Oh, William/0000-0001-5113-8147 NR 19 TC 88 Z9 89 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 JUN 20 PY 2006 VL 24 IS 18 BP 2723 EP 2728 DI 10.1200/JCO.2005.03.7804 PG 6 WC Oncology SC Oncology GA 056WU UT WOS:000238556600009 PM 16782912 ER PT J AU Berry, DL Moinpour, CM Jiang, CS Ankerst, DP Petrylak, DP Vinson, LV Lara, PN Jones, S Taplin, ME Burch, PA Hussain, MHA Crawford, ED AF Berry, DL Moinpour, CM Jiang, CS Ankerst, DP Petrylak, DP Vinson, LV Lara, PN Jones, S Taplin, ME Burch, PA Hussain, MHA Crawford, ED TI Quality of life and pain in advanced stage prostate cancer: Results of a Southwest Oncology Group randomized trial comparing docetaxel and estramustine to mitoxantrone and prednisone 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 PATTERN-MIXTURE-MODELS; PLUS PREDNISONE; PHASE-II; CLINICAL-TRIALS; CARCINOMA; QUESTIONNAIRE; MULTICENTER; INSTRUMENT; FLUTAMIDE; MEN AB Purpose Palliation of bone pain can be achieved in men with androgen-independent prostate cancer treated with docetaxel and estramustine (DE) or mitoxantrone and prednisone (MP). While Southwest Oncology Group trial 99-16 demonstrated a survival improvement of DE over MP, the study also was designed to compare the palliation of disease-related symptoms. Methods Pain palliation and global quality of life (QOL) were the two primary patient-reported outcomes. Pain was measured with the Present Pain Intensity scale of the McGill Pain Questionnaire-Short Form. The European Organisation for Research and Treatment of Cancer Core Quality of Life Questionnaire C30 (QLQ-C30) and its Prostate Cancer Module (PR25) measured QOL and symptom status. Pain and analgesic use were measured at random assignment, every cycle for eight cycles, and 1 year from random assignment; the QLQ-C30 and the PR25 were administered at random assignment, before cycle four (week 10) and cycle eight (month 6) and at 1 year. In addition to the primary intent-to-treat, missing at random analysis, sensitivity analyses were performed to assess robustness of global QOL conclusions under alternative informative missing data assumptions. Results Six hundred seventy four eligible patients received DE (n = 338) or MP (n = 336). In an intention-to-treat analysis, median overall survival was 17.5 months for the DE arm and 15.6 months for the MP arm (P = .02). There were no statistically significant differences in pain palliation between the treatment arms. The sensitivity analyses showed a consistent lack of statistically significant global QOL differences for the two arms. Conclusion DE had superior clinical efficacy (overall survival, time-to-progression, and prostate-specific antigen declines) with similar global QOL and pain palliation in the MP arm. C1 Univ Washington, Seattle, WA 98195 USA. Fred Hutchinson Canc Res Ctr, SW Oncol Grp, Ctr Stat, Seattle, WA 98104 USA. Columbia Presbyterian Med Ctr, New York, NY 10032 USA. Cent Arkansas Vet Affairs Healthcare Syst, Little Rock, AR USA. Univ Calif Davis, Ctr Canc, Sacramento, CA 95817 USA. SE Med Oncol Ctr, Goldsboro, NC USA. Dana Farber Canc Inst, Boston, MA 02115 USA. Mayo Clin, Rochester, MN USA. Univ Michigan, Ann Arbor, MI 48109 USA. Univ Colorado, Ctr Canc, Denver, CO 80262 USA. RP Berry, DL (reprint author), Univ Washington, Box 357266, Seattle, WA 98195 USA. EM donnalb@u.washington.edu NR 27 TC 57 Z9 59 U1 0 U2 1 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 JUN 20 PY 2006 VL 24 IS 18 BP 2828 EP 2835 DI 10.1200/JCO.2005.04.8207 PG 8 WC Oncology SC Oncology GA 056WU UT WOS:000238556600024 ER PT J AU George, RE Li, SL Medeiros-Nancarrow, C Neuberg, D Marcus, K Shamberger, RC Pulsipher, M Grupp, SA Diller, L AF George, RE Li, SL Medeiros-Nancarrow, C Neuberg, D Marcus, K Shamberger, RC Pulsipher, M Grupp, SA Diller, L TI High-risk neuroblastoma treated with tandem autologous peripheral-blood stem cell-supported transplantation: Long-term survival update SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Article ID BONE-MARROW-TRANSPLANTATION; UNTREATED DISSEMINATED NEUROBLASTOMA; II INVESTIGATIONAL WINDOW; PEDIATRIC-ONCOLOGY-GROUP; 2ND MALIGNANT NEOPLASMS; STAGE-IV NEUROBLASTOMA; CENTRAL-NERVOUS-SYSTEM; CHILDRENS CANCER GROUP; HIGH-DOSE THERAPY; RAPID-SEQUENCE AB Purpose To provide an update on long-term survival of patients with high-risk neuroblastoma treated with tandem cycles of myeloablative therapy and peripheral-blood stem-cell rescue (PBSCR). Patients and Methods Ninety-seven patients with high-risk neuroblastoma were treated between 1994 and 2002. Patients underwent induction therapy with five cycles of standard agents, resection of the primary tumor and local radiation, and two consecutive courses of myeloablative therapy (including total-body irradiation) with PBSCR. Results Fifty-one patients have experienced relapse or died. Median follow-up time among the 46 patients who remain alive without progression is 5.6 years (range, 15.1 months to 9.9 years). Progression-free survival (PFS) rate at 5 years from diagnosis was 47% (95% CI, 36% to 56%), and PFS rate at 7 years was 45% (95% CI, 34% to 55%). Overall survival rate was 60% (95% CI, 48% to 69%) and 53% (95% CI, 40% to 64%) at 5 and 7 years, respectively. The 5- and 7-year PFS rates from time of first transplantation for 82 patients who completed both transplants were 54% (95% CI, 42% to 64%) and 52% (95% CI, 40% to 63%), respectively. Five patients died from treatment-related toxicity after tandem transplantation. Relapse occurred in 37 (42%) of 89 patients, mainly within 3 years of transplantation and primarily in diffuse osseous sites. No primary CNS relapse or secondary leukemia was seen. One patient developed synovial cell sarcoma 8 years after therapy. Conclusion High-dose therapy with tandem autologous stem-cell rescue is effective for treating high-risk neuroblastoma, with encouraging long-term survival. CNS relapse and secondary malignancies are rare after this therapy. C1 Dana Farber Canc Inst, Dept Pediat Oncol, Boston, MA 02115 USA. Dana Farber Canc Inst, Dept Biostat, Boston, MA 02115 USA. Dana Farber Canc Inst, Dept Computat Biol, Boston, MA 02115 USA. Childrens Hosp Boston, Dept Med, Boston, MA USA. Childrens Hosp Boston, Dept Radiat Oncol, Boston, MA USA. Childrens Hosp Boston, Dept Surg, Boston, MA USA. Primary Childrens Med Ctr, Div Oncol, Salt Lake City, UT 84103 USA. Univ Penn, Childrens Hosp Philadelphia, Sch Med, Div Oncol, Philadelphia, PA 19104 USA. RP George, RE (reprint author), Dana Farber Canc Inst, Dept Pediat Oncol, Dana 322,44 Binney St, Boston, MA 02115 USA. EM rani_george@dfci.harvard.edu FU NCI NIH HHS [R21 CA110516] NR 33 TC 102 Z9 112 U1 0 U2 4 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 JUN 20 PY 2006 VL 24 IS 18 BP 2891 EP 2896 DI 10.1200/JCO.2006.05.6986 PG 6 WC Oncology SC Oncology GA 056WU UT WOS:000238556600033 PM 16782928 ER PT J AU Ferrone, CR Finkelstein, DM Thayer, SP Muzikansky, A Fernandez-del Castillo, C Warshaw, AL AF Ferrone, CR Finkelstein, DM Thayer, SP Muzikansky, A Fernandez-del Castillo, C Warshaw, AL TI Perioperative CA19-9 levels can predict stage and survival in patients with resectable pancreatic adenocarcinoma SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Article ID TUMOR-MARKERS; CA-19-9; CANCER; CARCINOMA; SERUM; ANTIGEN AB Purpose Different prognostic factors stratify patients with pancreatic adenocarcinoma. The purpose of this study was to determine whether preoperative CA19-9 levels can predict stage of disease or survival and whether a change in preoperative to postoperative CA19-9 or the postoperative CA19-9 predicts overall survival. Patients and Methods Four hundred twenty-four consecutive patients with pancreatic adenocarcinoma underwent resection between January 1, 1985 and January 1, 2004. Of the patients with a bilirubin less than 2 mg/dL, 176 had preoperative CA19-9 values, and 111 had pre- and postoperative CA19-9 values. Survival was measured from the first postoperative CA19-9 level measured (median, 39 days) until death or last follow-up. A multivariate failure time model was fit using clinical, operative, pathologic, and adjuvant treatment characteristics, and a categorization was defined by the values and changes in CA19-9 before and after surgery. Results Of the 176 patients, 128 (73%) had T3 lesions, and 99 (56 /0) had N1 disease; 138 patients (78%) underwent pancreaticoduodenectomy. Median preoperative CA19-9 levels were lower in NO patients compared with patients with positive nodes (nine v 164 U/mL, respectively; nonparametric P = .06) and in T1/T2 patients versus T3 patients (41 v162 U/mL, respectively; P = .03). Median follow-up time (n = 111) was 1.8 years (range, 1 to 12.9 years), with overall actuarial 1-, 3-, and 5-year survival rates of 70%, 36%, and 30%, respectively. Significant predictors of survival on multivariate analysis included a decrease in CA19-9 (P = .0005), negative lymph nodes (P = .001), lower T stage (P = .0008), and postoperative CA19-9 less than 200 U/mL (P = .0007). Conclusion In patients with pancreatic adenocarcinoma, preoperative CA19-9 correlates with stage of disease. Both a postoperative decrease in CA19-9 and a postoperative CA19-9 value of less than 200 U/mL are strong independent predictors of survival, even after adjusting for stage. CA19-9 levels should be included in a patient's perioperative care and should be considered for prognostic nomograms. C1 Massachusetts Gen Hosp, Dept Biostat, Boston, MA 02114 USA. Massachusetts Gen Hosp, Dept Surg, Boston, MA 02114 USA. Mem Sloan Kettering Canc Ctr, Dept Surg, New York, NY 10021 USA. RP Warshaw, AL (reprint author), Massachusetts Gen Hosp, Dept Biostat, 55 Fruit St,WHT506, Boston, MA 02114 USA. EM awarshaw@partners.org FU NIDDK NIH HHS [K08 DK071329] NR 17 TC 194 Z9 203 U1 1 U2 8 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 JUN 20 PY 2006 VL 24 IS 18 BP 2897 EP 2902 DI 10.1200/JCO.2005.05.3934 PG 6 WC Oncology SC Oncology GA 056WU UT WOS:000238556600034 PM 16782929 ER PT J AU Lee, SJ Schover, LR Partridge, AH Patrizio, P Wallace, WH Hagerty, K Beck, LN Brennan, LV Oktay, K AF Lee, SJ Schover, LR Partridge, AH Patrizio, P Wallace, WH Hagerty, K Beck, LN Brennan, LV Oktay, K TI American Society of Clinical Oncology recommendations on fertility preservation in cancer patients SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Review ID IN-VITRO FERTILIZATION; CRYOPRESERVED OVARIAN TISSUE; INTRACYTOPLASMIC SPERM INJECTION; VAGINAL RADICAL TRACHELECTOMY; BONE-MARROW TRANSPLANTATION; HORMONE-RELEASING HORMONE; LOW-TEMPERATURE STORAGE; BREAST-CANCER; CHILDHOOD-CANCER; HODGKINS-DISEASE AB Purpose To develop guidance to practicing oncologists about available fertility preservation methods and related issues in people treated for cancer. Methods An expert panel and a writing committee were formed. The questions to be addressed by the guideline were determined, and a systematic review of the literature from 1987 to 2005 was performed, and included a search of online databases and consultation with content experts. Results The literature review found many cohort studies, case series, and case reports, but relatively few randomized or definitive trials examining the success and impact of fertility preservation methods in people with cancer. Fertility preservation methods are used infrequently in people with cancer. Recommendations As part of education and informed consent before cancer therapy, oncologists should address the possibility of infertility with patients treated during their reproductive years and be prepared to discuss possible fertility preservation options or refer appropriate and interested patients to reproductive specialists. Clinician judgment should be employed in the timing of raising this issue, but discussion at the earliest possible opportunity is encouraged. Sperm and embryo cryopreservation are considered standard practice and are widely available; other available fertility preservation methods should be considered investigational and be performed in centers with the necessary expertise. Conclusion Fertility preservation is often possible in people undergoing treatment for cancer. To preserve the full range of options, fertility preservation approaches should be considered as early as possible during treatment planning. C1 Cornell Univ, Ctr Reprod Med & Infertil, Weill Med Coll, Fertil Preservat Program, New York, NY 10021 USA. Dana Farber Canc Inst, Boston, MA 02115 USA. Fertile Hope, New York, NY USA. Oncol Hematol Care, Crestview Hills, KY USA. Amer Soc Clin Oncol, Alexandria, VA USA. Yale Univ, Fertil Ctr, New Haven, CT USA. Univ Texas, MD Anderson Canc Ctr, Houston, TX 77030 USA. Royal Hosp Sick Children, Edinburgh EH9 1LF, Midlothian, Scotland. RP Oktay, K (reprint author), Cornell Univ, Ctr Reprod Med & Infertil, Weill Med Coll, Fertil Preservat Program, 505 F 70th St,HT-340, New York, NY 10021 USA. EM guidelines@asco.org OI wallace, william, hamish/0000-0001-8080-5674 NR 167 TC 868 Z9 903 U1 9 U2 50 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 JUN 20 PY 2006 VL 24 IS 18 BP 2917 EP 2931 DI 10.1200/JCO.2006.06.5888 PG 15 WC Oncology SC Oncology GA 056WU UT WOS:000238556600037 PM 16651642 ER PT J AU Ganz, PA Kwan, L Somerfield, MR Alberts, D Garber, JE Offit, K Lippman, SM AF Ganz, PA Kwan, L Somerfield, MR Alberts, D Garber, JE Offit, K Lippman, SM TI The role of prevention in oncology practice: Results from a 2004 survey of American Society of Clinical Oncology members SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Article ID CANCER SURVIVORS; TEACHABLE MOMENT; HEALTH; CARE AB Purpose In 2004, the American Society of Clinical Oncology (ASCO) Cancer Prevention Committee surveyed the members to describe involvement in clinical prevention activities. Methods A previously administered survey, with updated items on genetics, chemoprevention, and survivorship, was mailed to a stratified random sample of 2,000 domestic members and a convenience sample of 3,144 international members. Results A total of 49.7% of domestic members contacted and survey eligible responded (n = 851). Nonresponders were younger (50.5 v 51.7 years; P < .01); 465 international members responded. Overall, 35% had received formal instruction in cancer prevention and control, and most respondents expected increased use of prevention, screening/early detection, and risk reduction/genetic counseling in their practices in the next 5 years. Most reported caring for cancer survivors, including providing general medical care. They also either directly provide or refer patients for cancer prevention and control services (eg, cancer screening, tobacco and nutrition counseling, risk reduction, and chemoprevention). Multivariable modeling found fewer perceived barriers to inclusion of cancer prevention activities in clinical practice among those practicing in an academic setting, seeing a higher proportion of patients without a cancer diagnosis, having formal training in prevention and control, expecting an increase in prevention activities in the next 5 years, and providing community advice on prevention. Conclusion Barriers to the inclusion of cancer prevention and control activities in oncology clinical practice exist. Nevertheless, a substantial proportion of both domestic and international ASCO members report an interest in cancer prevention and control activities, with a desire for more specific educational programs in this emerging area of oncology practice. C1 Univ Calif Los Angeles, Jonsson Comprehens Canc Ctr, Div Canc Prevent & Control Res, Sch Med, Los Angeles, CA 90095 USA. Univ Calif Los Angeles, Jonsson Comprehens Canc Ctr, Div Canc Prevent & Control Res, Sch Publ Hlth, Los Angeles, CA 90095 USA. Amer Soc Clin Oncol, Alexandria, VA USA. Univ Arizona, Ctr Canc, Tucson, AZ USA. Dana Farber Canc Inst, Boston, MA 02115 USA. Mem Sloan Kettering Canc Ctr, Clin Genet Serv, New York, NY 10021 USA. Univ Texas, MD Anderson Canc Ctr, Dept Thorac Head & Neck Med Oncol, Houston, TX 77030 USA. RP Ganz, PA (reprint author), Univ Calif Los Angeles, Jonsson Comprehens Canc Ctr, Div Canc Prevent & Control Res, Sch Med, 650 Charles Young Dr S,Room A2-125 CHS, Los Angeles, CA 90095 USA. EM pganz@ucla.edu NR 9 TC 21 Z9 21 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 JUN 20 PY 2006 VL 24 IS 18 BP 2948 EP 2957 DI 10.1200/JCO.2006.05.8321 PG 10 WC Oncology SC Oncology GA 056WU UT WOS:000238556600039 ER PT J AU Nakabayashi, M Bartlett, RA Oh, WK AF Nakabayashi, M Bartlett, RA Oh, WK TI Treatment of bicalutamide-induced gynecomastia with breast-reduction surgery in prostate cancer SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Article ID MEDIAN FOLLOW-UP; TREATMENT OPTIONS; 150 MG; THERAPY C1 Dana Farber Canc Inst, Dept Med Oncol, Lank Ctr Genitourinary Oncol, Boston, MA 02115 USA. Harvard Univ, Childrens Hosp, Sch Med, Dept Surg, Boston, MA 02115 USA. RP Nakabayashi, M (reprint author), Dana Farber Canc Inst, Dept Med Oncol, Lank Ctr Genitourinary Oncol, Boston, MA 02115 USA. RI Oh, William/B-9163-2012 OI Oh, William/0000-0001-5113-8147 NR 8 TC 3 Z9 3 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 JUN 20 PY 2006 VL 24 IS 18 BP 2958 EP 2959 DI 10.1200/JCO.2005.03.8505 PG 2 WC Oncology SC Oncology GA 056WU UT WOS:000238556600040 PM 16782932 ER PT J AU Gibson, CM Morrow, DA Murphy, SA Palabrica, TM Jennings, LK Stone, PH Lui, HH Bulle, T Lakkis, N Kovach, R Cohen, DJ Fish, P McCabe, CH Braunwald, E AF Gibson, CM Morrow, DA Murphy, SA Palabrica, TM Jennings, LK Stone, PH Lui, HH Bulle, T Lakkis, N Kovach, R Cohen, DJ Fish, P McCabe, CH Braunwald, E CA TIMI Study Grp TI A Randomized trial to evaluate the relative protection against post-percutaneous coronary intervention microvascular dysfunction, ischemia, and inflammation among antiplatelet and antithrombotic agents - The PROTECT-TIMI-30 Trial SO JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY LA English DT Article ID GLYCOPROTEIN IIB/IIIA RECEPTOR; PLACEBO-CONTROLLED TRIAL; ACTIVATED CLOTTING TIME; MYOCARDIAL-INFARCTION; FRAME COUNT; UNFRACTIONATED HEPARIN; STENT IMPLANTATION; PERFUSION GRADE; UNSTABLE ANGINA; EPTIFIBATIDE AB OBJECTIVES The goal of this study was to evaluate glycoprotein IIb/IIIa inhibition with eptifibatide when administered with indirect thrombin inhibition as compared with monotherapy with direct thrombin inhibition with bivalirudin among patients with non-ST-segment elevation acute coronary syndromes (ACS). BACKGROUND The optimal combination of antiplatelet and antithrombin regimens that maximizes efficacy and minimizes bleeding among patients with non-ST-segment elevation ACS undergoing percutaneous coronary intervention (PCI) is unclear. METHODS A total of 857 patients with non-ST-segment elevation ACS were assigned randomly to c ifibatide + reduced dose unfractionated heparin (n 298), eptifibatide + reduced-dose enoxaparin (n = 275), or bivalirudin monotherapy (n 284). RESULTS Among angiographically evaluable patients (n = 754), the primary end point of post-PCI coronary flow reserve was significantly greater with bivalirudin (1.43 vs. 1.33 for pooled eptifibatide arms, p = 0.036). Thrombolysis In Myocardial Infarction (TIMI) myocardial perfusion grade more often was normal with eptifibatide treatment compared with bivalirudin (57.9% vs. 50.9%, p = 0.048). The duration of ischemia on continuous Holter monitoring after PCI was significantly longer among patients treated with bivalirudin (169 vs. 36 min, p = 0.013). There was no excess of TIMI major bleeding among patients treated with eptifibatide compared with bivalirudin (0.7%, n = 4 vs. 0%, p = NS), but TIMI minor bleeding was increased (2.5% vs. 0.4%, p = 0.027) as was transfusion (4.4% to 0.4%, p < 0.001). CONCLUSIONS Among moderate- to high-risk patients with ACS undergoing PCI, coronary flow reserve was greater with bivalirudin than eptifibatide. Eptifibatide improved myocardial perfusion and reduced the duration of post-PCI ischemia but was associated with higher minor bleeding and transfusion rates. Ischemic events and biomarkers for myonecrosis, inflammation, and thrombin generation did not differ between agents. C1 Brigham & Womens Hosp, TIMI Study Grp, Div Cardiovasc, Boston, MA 02115 USA. Harvard Univ, Sch Med, Dept Med, Boston, MA 02115 USA. Millennium Pharmaceut Inc, Cambridge, MA USA. Univ Tennessee, Knoxville, TN USA. APEX Cardiol, Jackson, TN USA. Cardiovasc Associates, Kingsport, TN USA. Ben Taub Gen Hosp, Houston, TX 77030 USA. Our Lady Lourdes Med Ctr, Camden, NJ USA. Beth Israel Deaconess Med Ctr, Boston, MA 02215 USA. RP Gibson, CM (reprint author), 350 Longwood Ave,1st Floor, Boston, MA 02115 USA. EM mgibson@timi.org NR 36 TC 81 Z9 89 U1 1 U2 3 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0735-1097 J9 J AM COLL CARDIOL JI J. Am. Coll. Cardiol. PD JUN 20 PY 2006 VL 47 IS 12 BP 2364 EP 2373 DI 10.1016/j.jacc.2005.12.077 PG 10 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA 053WT UT WOS:000238337500002 PM 16781360 ER PT J AU Clark, DJ Lessio, S O'Donoghue, M Tsalamandris, C Schainfeld, R Rosenfield, K AF Clark, DJ Lessio, S O'Donoghue, M Tsalamandris, C Schainfeld, R Rosenfield, K TI Mechanisms and predictors of carotid artery stent restenosis - A serial intravascular ultrasound study SO JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY LA English DT Article ID CORONARY-ARTERY; ELUTING STENTS; STENOSIS; IMPLANTATION; ANGIOGRAPHY; TRIAL; ENDARTERECTOMY; HYPERPLASIA; WALLSTENTS; IMMEDIATE AB OBJECTIVES The aim of this study was to determine the mechanisms and predictors of carotid artery restenosis after carotid artery stenting (CAS) using serial intravascular ultrasound (IVUS) imaging. BACKGROUND Carotid artery stenting is increasingly used to treat high-grade obstructive carotid disease, but our knowledge of carotid in-stent restenosis and remodeling remains limited. METHODS Post-procedural and 6-month (median 6 months) follow-up quantitative carotid angiography and IVUS were performed after self-expanding stent deployment in 50 internal carotid arteries (ICA). The IVUS measurements at multiple designated sites included minimal luminal diameter, lumen area, stent area (SA), and neointimal hyperplasia area (NIH). RESULTS Late stent enlargement at follow-up was found at all segments, and the percentage increase was greatest at the ICA lesion site (mean +/- SD, 48.9 +/- 35.3%). The NIH, expressed as a percentage of SA, was seen within all segments of the stent and was greatest at the ICA lesion site (37.3 +/- 23.3%). There was a strong positive correlation between the amount of NIH and late stent enlargement (r = 0.64; p < 0.001). Immediate post-procedural minimum ICA SA (r = -0.37; p < 0.01) and stent expansion (r = -0.44; p = 0.001) correlated negatively with the percentage restenotic area at follow-up. CONCLUSIONS Although self-expanding carotid stents generate considerable neointimal hyperplasia, the process is balanced by marked late stent enlargement. Small stent dimensions immediately post-procedure were associated with a higher risk of restenosis. C1 St Elizabeths Med Ctr Boston, Div Cardiovasc Med & Res, Boston, MA USA. Austin Hosp, Dept Cardiol, Melbourne, Vic 3084, Australia. Austin Hosp, Dept Med, Melbourne, Vic 3084, Australia. RP Rosenfield, K (reprint author), Massachusetts Gen Hosp, Div Cardiol, 55 Fruit St,Gray Bigelow 800,Mailstop 843, Boston, MA 02114 USA. EM krosenfield@fastmail.us NR 28 TC 48 Z9 50 U1 0 U2 2 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0735-1097 J9 J AM COLL CARDIOL JI J. Am. Coll. Cardiol. PD JUN 20 PY 2006 VL 47 IS 12 BP 2390 EP 2396 DI 10.1016/j.jacc.2006.01.076 PG 7 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA 053WT UT WOS:000238337500006 PM 16781364 ER PT J AU Goldfine, AB Beckman, JA Betensky, RA Devlin, H Hurley, S Varo, N Schonbeck, U Patti, ME Creager, MA AF Goldfine, AB Beckman, JA Betensky, RA Devlin, H Hurley, S Varo, N Schonbeck, U Patti, ME Creager, MA TI Family history of diabetes is a major determinant of endothelial function SO JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY LA English DT Article ID INSULIN-RESISTANCE; CARDIOVASCULAR-DISEASE; RISK-FACTOR; FOLLOW-UP; MELLITUS; GLUCOSE; INFLAMMATION; DYSFUNCTION; MORTALITY; PARENTS AB OBJECTIVES We evaluated whether endothelial dysfunction was present in nondiabetic persons with a family history (FH) of diabetes and assessed its relationship with insulin resistance and atherosclerosis risk factors. BACKGROUND Atherosclerosis is frequently present when type 2 diabetes (T2D) is first diagnosed. Endothelial dysfunction contributes to atherogenesis. METHODS Oral glucose tolerance and brachial artery flow-mediated, endothelium-dependent vasodilation (EDV) were assessed in 38 nondiabetic subjects; offspring of two parents with T2D (FH+) or with no first-degree relative with diabetes (FH-). RESULTS Although fasting glucose was higher in FH+ than FH- (5.3 +/- 0.1 mmol/l vs. 4.9 +/- 0.1 mmol/l, p < 0.03), glycemic burden assessed as 2-h or area-under-the-curve glucose after glucose load or glycosylated hemoglobin (HbA1c), and measures of insulin sensitivity or inflammation did not differ. Brachial artery flow-mediated EDV was reduced in FH + (7.1 +/- 0.9% vs. 11.7 +/- 1.6%, p < 0.02), with no difference in nitroglycerin-induced endothelium-independent vasodilatation. In the combined cohort, only FH+ (r(2) = 0.12, p < 0.02) and HbA1c (r(2) = 0.14, p < 0.02) correlated with EDV. Insulin resistance, assessed by tertile of homeostasis model assessment of insulin resistance (HOMA-IR), was associated with impaired endothelium-dependent vasodilatation in FH- (p < 0.03, analysis of variance), but not in FH+, as even the most insulin-sensitive FH+ ofspring had diminished endothelial function. In multiple regression analysis, including established cardiac risk factors, blood pressure and lipids, HbA1c, and HOMA-IR, FH remained a significant determinant of EDV (p = 0.04). CONCLUSIONS Bioavailability of nitric oxide is lower in persons with a strong FH of T2D. Glycemic burden, even in the nondiabetic range, can contribute to endothelial dysfunction. Abnormalities of endothelial function may contribute to atherosclerosis before development of overt diabetes. C1 Joslin Diabet Ctr, Boston, MA 02215 USA. Brigham & Womens Hosp, Boston, MA 02115 USA. Harvard Univ, Sch Publ Hlth, Dept Biostat, Boston, MA 02115 USA. RP Goldfine, AB (reprint author), Joslin Diabet Ctr, 1 Joslin Pl, Boston, MA 02215 USA. EM allison.goldfine@joslin.harvard.edu OI Beckman, Joshua/0000-0001-8332-8439 FU NCRR NIH HHS [M01 RR001032]; NHLBI NIH HHS [P01 HL48743]; NIDDK NIH HHS [K23-DK02795, P30 DK36836] NR 20 TC 51 Z9 56 U1 0 U2 1 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0735-1097 J9 J AM COLL CARDIOL JI J. Am. Coll. Cardiol. PD JUN 20 PY 2006 VL 47 IS 12 BP 2456 EP 2461 DI 10.1016/j.jacc.2066.02.045 PG 6 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA 053WT UT WOS:000238337500015 PM 16781373 ER PT J AU Weisberg, E Manley, P Mestan, J Cowan-Jacob, S Ray, A Griffin, JD AF Weisberg, E. Manley, P. Mestan, J. Cowan-Jacob, S. Ray, A. Griffin, J. D. TI AMN107 (nilotinib): a novel and selective inhibitor of BCR-ABL SO BRITISH JOURNAL OF CANCER LA English DT Review DE BCR-ABL; AMN107; nilotinib; dasatinib; imatinib-resistance ID CHRONIC MYELOID-LEUKEMIA; CHRONIC MYELOGENOUS LEUKEMIA; IN-VITRO ACTIVITY; TYROSINE KINASE; PHILADELPHIA-CHROMOSOME; C-ABL; IMATINIB; RESISTANCE; STI-571; GROWTH AB Chronic myelogenous leukaemia (CML) and Philadelphia chromosome positive (Ph+) acute lymphoblastic leukaemia ( ALL) are caused by the BCR-ABL oncogene. Imatinib inhibits the tyrosine kinase activity of the BCR-ABL protein and is an effective, frontline therapy for chronic-phase CML. However, accelerated or blast-crisis phase CML patients and Ph+ ALL patients often relapse due to drug resistance resulting from the emergence of imatinib-resistant point mutations within the BCR-ABL tyrosine kinase domain. This has stimulated the development of new kinase inhibitors that are able to over-ride resistance to imatinib. The novel, selective BCR-ABL inhibitor, AMN107, was designed to fit into the ATP-binding site of the BCR-ABL protein with higher affinity than imatinib. In addition to being more potent than imatinib (IC50 < 30 nM) against wild-type BCR-ABL, AMN107 is also significantly active against 32/33 imatinib-resistant BCR-ABL mutants. In preclinical studies, AMN107 demonstrated activity in vitro and in vivo against wild-type and imatinib-resistant BCR-ABL-expressing cells. In phase I/II clinical trials, AMN107 has produced haematological and cytogenetic responses in CML patients, who either did not initially respond to imatinib or developed imatinib resistance. Dasatinib (BMS-354825), which inhibits Abl and Src family kinases, is another promising new clinical candidate for CML that has shown good efficacy in CML patients. In this review, the early characterisation and development of AMN107 is discussed, as is the current status of AMN107 in clinical trials for imatinib-resistant CML and Ph+ ALL. Future trends investigating prediction of mechanisms of resistance to AMN107, and how and where AMN107 is expected to fit into the overall picture for treatment of early-phase CML and imatinib-refractory and late-stage disease are discussed. C1 Dana Farber Canc Inst, Dept Adult Oncol, Boston, MA 02115 USA. Novartis Inst Biomed Res, Basel, Switzerland. RP Griffin, JD (reprint author), Dana Farber Canc Inst, Dept Adult Oncol, 44 Binney St, Boston, MA 02115 USA. EM James_Griffin@dfci.harvard.edu NR 33 TC 247 Z9 261 U1 3 U2 24 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 JUN 19 PY 2006 VL 94 IS 12 BP 1765 EP 1769 DI 10.1039/sj.bjc.6603170 PG 5 WC Oncology SC Oncology GA 053EL UT WOS:000238288000001 PM 16721371 ER PT J AU Mueller, BU Pabst, T Hauser, P Gilliland, G Neuberg, D Tenen, DG AF Mueller, B. U. Pabst, T. Hauser, P. Gilliland, G. Neuberg, D. Tenen, D. G. TI Mutations of the transcription factor PU.1 are not associated with acute lymphoblastic leukaemia SO BRITISH JOURNAL OF CANCER LA English DT Article DE PU.1; ALL; transcription factor; mutation; leukaemia ID ACUTE MYELOID-LEUKEMIA; ETS ONCOGENE; EXPRESSION; MACROPHAGE; SPI-1; GENE; ERYTHROLEUKEMIAS; BINDING AB The transcription factor PU.I plays a crucial role during normal haematopoiesis in both myeloid cells and B-lymphocytes. Mice with a disruption in both alleles of the PU.I locus were found to lack macrophages and B cells and had delayed appearance of neutrophils. In addition, critical decrease of PU.I expression is sufficient to cause acute myeloid leukaemia (AML) and lymphomas in mice. Recently, we reported that heterozygous mutations in the PU.I gene are present in some patients with AML. Thus, we hypothesised that PU.I mutations might also contribute to the development of acute leukaemias of the B-cell lineage. Here, we screened 62 patients with B-cell acute lymphoblastic leukaemia (B-ALL) at diagnosis for genomic mutations by direct sequencing of all five exons of the PU.I gene. We found no genomic alteration of the PU.I gene suggesting that PU.I mutations are not likely to be common in B-ALL. C1 Univ Hosp Bern, Dept Internal Med, CH-3010 Bern, Switzerland. Univ Hosp Bern, Dept Clin Res, CH-3010 Bern, Switzerland. Univ Hosp Bern, Dept Med Oncol, CH-3010 Bern, Switzerland. Harvard Univ, Inst Med, Howard Hughes Med Inst, Boston, MA 02115 USA. Dana Farber Canc Inst, Dept Biostat, Boston, MA 02115 USA. Harvard Univ, Sch Med, Inst Med, Boston, MA 02115 USA. RP Mueller, BU (reprint author), Univ Hosp Bern, Dept Internal Med, CH-3010 Bern, Switzerland. EM beatrice.mueller@insel.ch OI Tenen, Daniel/0000-0002-6423-3888 NR 19 TC 5 Z9 5 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 JUN 19 PY 2006 VL 94 IS 12 BP 1918 EP 1920 DI 10.1038/sj.bjc.6603198 PG 3 WC Oncology SC Oncology GA 053EL UT WOS:000238288000023 PM 16735999 ER PT J AU Peer, D Margalit, R AF Peer, D Margalit, R TI Fluoxetine and reversal of multidrug resistance SO CANCER LETTERS LA English DT Review DE multidrug resistance (MDR); ABC transporters; chemosensitizers; fluoxetine; chemotherapy ID P-GLYCOPROTEIN; DRUG-RESISTANCE; BREAST-CANCER; VINCRISTINE RESISTANCE; TRANSPORTER PROTEINS; STEM-CELLS; IN-VITRO; INHIBITOR; MODULATION; PACLITAXEL AB This review centers on recent findings with respect to modulating cancer multidrug resistance (MDR) with the well-known antidepressant fluoxetine (prozac). The MDR phenomena and mechanisms are discussed, including the roles of ABC transporters as MDR-pumps and the potential involvement of cancer stem cells. The three generations of MDR reversal agents (chemosensitizers) are reviewed, introducing the concept of single-pump and multi-pump agents. The current status of chemosensitization is summarized, pointing-out the need for additional agents and outlining experimental criteria for testing novel candidates. Major in vitro and in vivo findings are summarized showing that fluoxetine is a chemosensitizer of the multipump type, and proposing it be considered a fourth-generation chemosensitizer. In concluding, we contemplate future prospects of modulating MDR in the clinic. (c) 2005 Elsevier Ireland Ltd. All rights reserved. C1 Tel Aviv Univ, George S Wise Fac Life Sci, Dept Biochem, IL-69978 Tel Aviv, Israel. Harvard Univ, Sch Med, CBR Inst Biomed Res, Boston, MA 02115 USA. RP Margalit, R (reprint author), Tel Aviv Univ, George S Wise Fac Life Sci, Dept Biochem, IL-69978 Tel Aviv, Israel. EM rimona@post.tau.ac.il RI Peer, Dan/A-1785-2011 OI Peer, Dan/0000-0001-8238-0673 NR 46 TC 39 Z9 41 U1 4 U2 16 PU ELSEVIER IRELAND LTD PI CLARE PA ELSEVIER HOUSE, BROOKVALE PLAZA, EAST PARK SHANNON, CO, CLARE, 00000, IRELAND SN 0304-3835 J9 CANCER LETT JI Cancer Lett. PD JUN 18 PY 2006 VL 237 IS 2 BP 180 EP 187 DI 10.1016/j.canlet.2005.06.003 PG 8 WC Oncology SC Oncology GA 056ZI UT WOS:000238563500003 PM 16014320 ER PT J AU Reddy, VB Iuga, AO Kounga, K Lerner, EA AF Reddy, VB Iuga, AO Kounga, K Lerner, EA TI Functional analysis of recombinant mutants of maxadilan with a PAC1 receptor-expressing melanophore cell line SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID CYCLASE-ACTIVATING POLYPEPTIDE; LUTZOMYIA-LONGIPALPIS; VASODILATORY PEPTIDE; I RECEPTOR; CLONING AB Maxadilan, a 61-amino-acid vasodilatory peptide, was initially isolated from the salivary glands of the sand fly Lutzomyia longipalpis. Although its primary sequence has no homology to that of pituitary adenylate cyclase-activating peptide, maxadilan is an agonist for the PAC1 receptor. A total of 58 substitution and deletion mutants was engineered in an effort to determine which residues were important for receptor activation. The mutants were characterized functionally using an assay based on pigment granule translocation in PAC1-expressing Xenopus laevis melanophores. Substitution of charged residues and proline 43 could alter ( but not eliminate) the agonist activity of the mutants. In contrast, we found that several multiple substitution mutants of the predicted beta-strand threonine residues became antagonists at the PAC1 receptor. The results suggest that these threonine residues are cooperatively involved in PAC1 activation. C1 Massachusetts Gen Hosp, Cutaneous Biol Res Ctr, Charlestown, MA 02129 USA. Harvard Univ, Sch Med, Charlestown, MA 02129 USA. RP Lerner, EA (reprint author), Massachusetts Gen Hosp, Cutaneous Biol Res Ctr, Bldg 149,13th St, Charlestown, MA 02129 USA. EM ethan.lerner@cbrc2.mgh.harvard.edu FU NIAID NIH HHS [U01 AI 61420-02]; NIAMS NIH HHS [R01 AR 2005] NR 11 TC 9 Z9 10 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 JUN 16 PY 2006 VL 281 IS 24 BP 16197 EP 16201 DI 10.1074/jbc.M509429200 PG 5 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA 051MR UT WOS:000238165700004 PM 16569645 ER PT J AU Xie, YM Massa, SM Ensslen-Craig, SE Major, DL Yang, T Tisi, MA Derevyanny, VD Runge, WO Mehta, BP Moore, LA Brady-Kalnay, SM Longo, FM AF Xie, YM Massa, SM Ensslen-Craig, SE Major, DL Yang, T Tisi, MA Derevyanny, VD Runge, WO Mehta, BP Moore, LA Brady-Kalnay, SM Longo, FM TI Protein-tyrosine phosphatase (PTP) wedge domain peptides - A novel approach for inhibition of PTP function and augmentation of protein-tyrosine kinase function SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID NERVE GROWTH-FACTOR; NEURITE OUTGROWTH; PC12 CELLS; SIGNAL-TRANSDUCTION; HOMOPHILIC BINDING; CATALYTIC-ACTIVITY; CRYSTAL-STRUCTURE; RECEPTOR; LAR; MU AB Inhibition of protein-tyrosine phosphatases (PTPs) counterbalancing protein-tyrosine kinases (PTKs) offers a strategy for augmenting PTK actions. Conservation of PTP catalytic sites limits development of specific PTP inhibitors. A number of receptor PTPs, including the leukocyte common antigen-related (LAR) receptor and PTP mu, contain a wedge-shaped helix-loop-helix located near the first catalytic domain. Helix-loop-helix domains in other proteins demonstrate homophilic binding and inhibit function; therefore, we tested the hypothesis that LAR wedge domain peptides would exhibit homophilic binding, bind to LAR, and inhibit LAR function. Fluorescent beads coated with LAR or PTP mu wedge peptides demonstrated PTP-specific homophilic binding, and LAR wedge peptide-coated beads precipitated LAR protein. Administration of LAR wedge Tat peptide to PC12 cells resulted in increased proliferation, decreased cell death, increased neurite outgrowth, and augmented Trk PTK-mediated responses to nerve growth factor (NGF), a phenotype matching that found in PC12 cells with reduced LAR levels. PTP mu wedge Tat peptide had no effect on PC12 cells but blocked the PTP mu-dependent phenotype of neurite outgrowth of retinal ganglion neurons on a PTP mu substrate, whereas LAR wedge peptide had no effect. The survival- and neurite-promoting effect of the LAR wedge peptide was blocked by the Trk inhibitor K252a, and reciprocal co-immunoprecipitation demonstrated LAR/ TrkA association. The addition of LAR wedge peptide inhibited LAR co-immunoprecipitation with TrkA, augmented NGF-induced activation of TrkA, ERK, and AKT, and in the absence of exogenous NGF, induced activation of TrkA, ERK, and AKT. PTP wedge domain peptides provide a unique PTP inhibition strategy and offer a novel approach for augmenting PTK function. C1 Stanford Univ, Dept Neurol & Neurol Sci, Stanford, CA 94305 USA. Univ N Carolina, Dept Neurol, Chapel Hill, NC 27599 USA. Univ Calif San Francisco, San Francisco Vet Affairs Med Ctr, Lab Computat Neurochem & Drug Discovery, San Francisco, CA 94121 USA. Univ Calif San Francisco, Dept Neurol, San Francisco, CA 94121 USA. Case Western Reserve Univ, Dept Neurosci, Cleveland, OH 44106 USA. Case Western Reserve Univ, Dept Mol Biol & Microbiol, Cleveland, OH 44106 USA. RP Longo, FM (reprint author), Stanford Univ, Dept Neurol & Neurol Sci, 300 Pasteur Dr, Stanford, CA 94305 USA. EM longo@stanford.edu FU NEI NIH HHS [R01 EY 12251, P01 EY 11373]; NIA NIH HHS [R01 AG 09873] NR 57 TC 37 Z9 38 U1 0 U2 4 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD JUN 16 PY 2006 VL 281 IS 24 BP 16482 EP 16492 DI 10.1074/jbc.M603131200 PG 11 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA 051MR UT WOS:000238165700038 PM 16613844 ER PT J AU Qiu, ZH Norflus, F Singh, B Swindell, MK Buzescu, R Bejarano, M Chopra, R Zucker, B Benn, CL DiRocco, DP Cha, JHJ Ferrante, RJ Hersch, SM AF Qiu, ZH Norflus, F Singh, B Swindell, MK Buzescu, R Bejarano, M Chopra, R Zucker, B Benn, CL DiRocco, DP Cha, JHJ Ferrante, RJ Hersch, SM TI Sp1 is up-regulated in cellular and transgenic models of Huntington disease, and its reduction is neuroprotective SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID TRANSCRIPTION FACTOR SP1; ENDOTHELIAL-CELLS; GENE-EXPRESSION; SYNERGISTIC ACTIVATION; CORTICAL-NEURONS; RECEPTOR GENE; MOUSE MODEL; MICE; INHIBITORS; PROMOTER AB Interactions between mutant huntingtin (Htt) and a variety of transcription factors including specificity proteins (Sp) have been suggested as a central mechanism in Huntington disease (HD). However, the transcriptional activity induced by Htt in neurons that triggers neuronal death has yet to be fully elucidated. In the current study, we characterized the relationship of Sp1 to Htt protein aggregation and neuronal cell death. We found increased levels of Sp1 in neuronal-like PC12 cells expressing mutant Htt, primary striatal neurons, and brain tissue of HD transgenic mice. Sp1 levels were also elevated when 3-nitropropionate (3-NP) was used to induce cell death in PC12 cells. To assess the effects of knocking down Sp1 in HD pathology, we used Sp1 siRNA, a heterozygous Sp1 knock-out mouse, and mithramycin A, a DNA-intercalating agent that inhibits Sp1 function. The three approaches consistently yielded reduced levels of Sp1 which ameliorated toxicity caused by either mutant Htt or 3-NP. In addition, when HD mice were crossed with Sp1 heterozygous knock-out mice, the resulting offspring did not experience the loss of dopamine D2 receptor mRNA characteristic of HD mice, and survived longer than their HD counterparts. Our data suggest that enhancement of transcription factor Sp1 contributes to the pathology of HD and demonstrates that its suppression is beneficial. C1 Harvard Univ, Massachusetts Gen Hosp, Sch Med, Massachussets Gen Inst Neurodegenerat Dis,Dept Ne, Charlestown, MA 02129 USA. Bedford Vet Affairs Med Ctr, Ctr Geriatr Res Educ & Clin, Bedford, MA 01730 USA. Boston Univ, Sch Med, Dept Neurol, Boston, MA 02118 USA. Boston Univ, Sch Med, Dept Anat & Neurobiol, Boston, MA 02118 USA. Boston Univ, Sch Med, Dept Pathol, Boston, MA 02118 USA. Boston Univ, Sch Med, Dept Psychiat, Boston, MA 02118 USA. RP Hersch, SM (reprint author), Mass Gen Inst Neurodegenerat Dis MGH E, Bldg 114,Suite 2001,114 16th St, Charlestown, MA 02129 USA. EM hersch@helix.mgh.harvard.edu FU NCCIH NIH HHS [AT 00613]; NINDS NIH HHS [NS 038106, NS 045242, NS 045806, NS 35255] NR 46 TC 63 Z9 65 U1 0 U2 3 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD JUN 16 PY 2006 VL 281 IS 24 BP 16672 EP 16680 DI 10.1074/jbc.M511648200 PG 9 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA 051MR UT WOS:000238165700061 PM 16595660 ER PT J AU Sabeti, PC Schaffner, SF Fry, B Lohmueller, J Varilly, P Shamovsky, O Palma, A Mikkelsen, TS Altshuler, D Lander, ES AF Sabeti, P. C. Schaffner, S. F. Fry, B. Lohmueller, J. Varilly, P. Shamovsky, O. Palma, A. Mikkelsen, T. S. Altshuler, D. Lander, E. S. TI Positive natural selection in the human lineage SO SCIENCE LA English DT Review ID BLOOD-GROUP LOCUS; HUMAN GENOME; LINKAGE DISEQUILIBRIUM; DARWINIAN SELECTION; NUCLEOTIDE SUBSTITUTION; MOLECULAR EVOLUTION; POPULATION-GENETICS; HAPLOTYPE STRUCTURE; ADAPTIVE EVOLUTION; PROTEIN EVOLUTION AB Positive natural selection is the force that drives the increase in prevalence of advantageous traits, and it has played a central role in our development as a species. Until recently, the study of natural selection in humans has largely been restricted to comparing individual candidate genes to theoretical expectations. The advent of genome-wide sequence and polymorphism data brings fundamental new tools to the study of natural selection. It is now possible to identify new candidates for selection and to reevaluate previous claims by comparison with empirical distributions of DNA sequence variation across the human genome and among populations. The flood of data and analytical methods, however, raises many new challenges. Here, we review approaches to detect positive natural selection, describe results from recent analyses of genomewide data, and discuss the prospects and challenges ahead as we expand our understanding of the role of natural selection in shaping the human genome. C1 Harvard Univ, Cambridge, MA 02138 USA. Harvard Univ, Sch Med, Dept Genet, Boston, MA USA. Harvard Univ, Sch Med, Dept Med, Boston, MA USA. Brown Univ, Providence, RI 02912 USA. Massachusetts Gen Hosp, Dept Mol Biol, Ctr Human Genet Res, Boston, MA 02114 USA. Massachusetts Gen Hosp, Diabet Unit, Boston, MA 02114 USA. MIT, Dept Biol, Cambridge, MA USA. Whitehead Inst Biomed Res, Cambridge, MA 02142 USA. Harvard Univ, Sch Med, Dept Syst Biol, Boston, MA USA. RP Schaffner, SF (reprint author), MIT, Broad Inst, 77 Massachusetts Ave, Cambridge, MA 02139 USA. EM sfs@broad.mit.edu RI Mikkelsen, Tarjei/A-1306-2007; Altshuler, David/A-4476-2009; Schaffner, Stephen/D-1189-2011; Phelps, Steve/H-2263-2011; Varilly, Patrick/C-8118-2013 OI Mikkelsen, Tarjei/0000-0002-8133-3135; Altshuler, David/0000-0002-7250-4107; Varilly, Patrick/0000-0003-4619-8174 NR 73 TC 547 Z9 564 U1 14 U2 138 PU AMER ASSOC ADVANCEMENT SCIENCE PI WASHINGTON PA 1200 NEW YORK AVE, NW, WASHINGTON, DC 20005 USA SN 0036-8075 J9 SCIENCE JI Science PD JUN 16 PY 2006 VL 312 IS 5780 BP 1614 EP 1620 DI 10.1126/science.1124309 PG 7 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA 053EO UT WOS:000238288600035 PM 16778047 ER PT J AU Heist, EK Taub, C Fan, D Arzola-Castaner, D Alabiad, CR Reddy, VY Mansour, M Mela, T Picard, MH Ruskin, JN Singh, JP AF Heist, EK Taub, C Fan, D Arzola-Castaner, D Alabiad, CR Reddy, VY Mansour, M Mela, T Picard, MH Ruskin, JN Singh, JP TI Usefulness of a novel "response score" to predict hemodynamic and clinical outcome from cardiac resynchronization therapy SO AMERICAN JOURNAL OF CARDIOLOGY LA English DT Article ID CONGESTIVE-HEART-FAILURE; SYSTOLIC FUNCTION; DELAY; SITE AB Cardiac resynchronization therapy (CRT) is an important treatment for patients with congestive heart failure and ventricular dyssynchrony, but response to CRT is highly variable. We assessed whether a scoring system that encompasses a combination of patient selection and procedural variables would improve prediction of CRT response. Thirty-nine patients who underwent CRT with echocardiographic assessment of baseline contractility and left ventricular (LV) dyssynchrony, intraprocedural assessment of LV lead electrical delay, and postprocedural chest radiography were included. Baseline LV dyssynchrony was measured by Doppler tissue velocity imaging as the maximum time difference between peak systolic velocity of anterior, lateral, posterior, and septal walls. The hemodynamic effect of CRT was measured by Doppler analysis of mitral regurgitation as percent change in maximal +dP/dt (Delta dP/dt) with CRT on versus off. Acute responders to CRT were defined as Delta dp/dt; >= 25%. Clinical response was measured as a combined end point of hospitalization for heart failure and all-cause mortality. A 4-point response score was generated using variables associated with Delta dP/dt and assigning 1 point for a dorsoventral LV/right ventricular interlead distance > 10 cm, 1 point for a LV lead electrical delay >= 50%, 1 point for a baseline maximum +dP/dt < 600 mm Hg/s, and 1 point for a maximum time difference > 100 ms. In conclusion, there was a significant association between response score (0 to 4 points) and acute hemodynamic response to CRT (p < 0.0001). Kaplan-Meier analysis associated a higher response score with improved 12-month event-free survival after CRT implantation (p = 0.0019). (c) 2006 Elsevier Inc. All rights reserved. C1 Harvard Univ, Sch Med, Massachusetts Gen Hosp, Cardiac Arrhythmia Serv, Boston, MA 02115 USA. Harvard Univ, Sch Med, Massachusetts Gen Hosp, Echocardiog Serv, Boston, MA 02115 USA. Harvard Univ, Sch Med, Massachusetts Gen Hosp, Dept Med, Boston, MA 02115 USA. RP Singh, JP (reprint author), Harvard Univ, Sch Med, Massachusetts Gen Hosp, Cardiac Arrhythmia Serv, Boston, MA 02115 USA. EM jsingh@partners.org OI Picard, Michael/0000-0002-9264-3243 NR 20 TC 9 Z9 12 U1 0 U2 0 PU EXCERPTA MEDICA INC PI NEW YORK PA 650 AVENUE OF THE AMERICAS, NEW YORK, NY 10011 USA SN 0002-9149 J9 AM J CARDIOL JI Am. J. Cardiol. PD JUN 15 PY 2006 VL 97 IS 12 BP 1732 EP 1736 DI 10.1016/j.amjcard.2006.01.035 PG 5 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA 055EZ UT WOS:000238434100011 PM 16765123 ER PT J AU Tedrow, UB Kramer, DB Stevenson, LW Stevenson, WG Baughman, KL Epstein, LM Lewis, EF AF Tedrow, UB Kramer, DB Stevenson, LW Stevenson, WG Baughman, KL Epstein, LM Lewis, EF TI Relation of right ventricular peak systolic pressure to major adverse events in patients undergoing cardiac resynchronization therapy SO AMERICAN JOURNAL OF CARDIOLOGY LA English DT Article ID PULMONARY-HYPERTENSION; DYSFUNCTION; MORTALITY; RISK AB The degree to which increased right-sided heart pressures influence outcome in cardiac resynchronization therapy (CRT) is unclear. High right ventricular (RV) pressures may contribute to septal malpositioning, thus hindering effective resynchronization. We hypothesized that Patients with high RV systolic pressures before CRT implantation would have poorer outcome. We evaluated echocardiograms, electrocardiograms, and clinical records from 75 consecutive patients with CRT. RV systolic pressure was calculated from the peak tricuspid regurgitant, time-velocity profile. The primary end point was a composite of mortality, cardiac transplantation, or need for a left ventricular assist device. Events were evaluated by Kaplan-Meier curves and Cox proportional hazard ratios. Patients grouped by RV systolic pressure divided at the median of 35 mm Hg were similar except for more renal insufficiency and RV dysfunction when RV systolic pressure was > 35 mm Hg. Univariate analysis identified RV systolic pressure > 35 mm Hg (hazard ratio [HR] 3.32), diabetes (FIR 2.45), renal insufficiency (HR 3.52), atrial fibrillation (HR 3.07), use of nonamiodarone antiarrhythmic medications (HR 2.86), atrial pacing (HR 2.57), and prolonged PR interval (HR 1.009) as associated with poorer outcome. Normal sinus rhythm at implantation (HR 0.34), baseline left bundle branch block (HR 0.44), and P-blocker use (HR 0.47) were associated with improved outcome. In a multivariable model, high RV systolic pressure (HR 3.71, 95% confidence interval 1.31 to 10.4), renal insufficiency (HR 3.18, 95% confidence interval 1.29 to 7.86), and atrial fibrillation (HR 4.22;95% confidence interval 1.54 to 11.6) remained significant. In conclusion, despite resynchronization, patients with high RV pressures have significantly decreased survival after adjusting for significant contributing influences. (c) 2006 Elsevier Inc. All rights reserved. C1 Brigham & Womens Hosp, Div Cardiovasc, Boston, MA 02115 USA. Massachusetts Gen Hosp, Dept Med, Boston, MA 02114 USA. RP Tedrow, UB (reprint author), Brigham & Womens Hosp, Div Cardiovasc, 75 Francis St, Boston, MA 02115 USA. EM utedrow@partners.org NR 7 TC 20 Z9 21 U1 0 U2 1 PU EXCERPTA MEDICA INC PI NEW YORK PA 650 AVENUE OF THE AMERICAS, NEW YORK, NY 10011 USA SN 0002-9149 J9 AM J CARDIOL JI Am. J. Cardiol. PD JUN 15 PY 2006 VL 97 IS 12 BP 1737 EP 1740 DI 10.1016/j.amjcard.2006.01.033 PG 4 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA 055EZ UT WOS:000238434100012 PM 16765124 ER PT J AU Kloner, RA Jackson, G Hutter, AM Mittleman, MA Chan, M Warner, MR Costigan, TM Vail, GM AF Kloner, RA Jackson, G Hutter, AM Mittleman, MA Chan, M Warner, MR Costigan, TM Vail, GM TI Cardiovascular safety update of tadalafil: Retrospective analysis of data from placebo-controlled and open-label clinical trials of tadalafil with as needed, three times-per-week or once-a-day dosing SO AMERICAN JOURNAL OF CARDIOLOGY LA English DT Article ID ERECTILE DYSFUNCTION; MYOCARDIAL-INFARCTION; SILDENAFIL-CITRATE; ORAL SILDENAFIL; RISK-FACTORS; EFFICACY; MEN; HYPERTENSION; IMPOTENCE AB Because most men with erectile dysfunction have underlying vascular disease, it is important to update the cardiovascular safety profile of medications used in the treatment of erectile dysfunction. This retrospective analysis evaluated serious cardiovascular treatment-emergent adverse events (CVTEAEs) reported in 36 clinical trials of tadalafil, a phosphodiesterase-5 inhibitor used for the treatment of erectile dysfunction. A serious CVTEAE was defined as myocardial infarction, cardiovascular death, or cerebrovascular death. In the 36 trials, 12,487 men (mean age 55 years) with erectile dysfunction received tadalafil, with 5,771 patient-years (PYs) of exposure, and 2,047 men (mean age 56 years) received placebo, with 460 PYs of exposure. Tadalafil 2 to 50 mg was taken as needed, 3 times/week, or once a day. Co-morbidities at baseline included hypertension (31%), diabetes (21%), hyperlipidemia (17%), and coronary artery disease (5%). Across all trials, the incidence rate of serious CVTEAEs was 0.40/100 PYs in tadalafil-treated patients and 0.43/100 PYs in placebo-treated patients. In patients taking tadalafil as needed, 3 times/week, or once a day, the incidence rates of serious CVTEAEs ranged from 0.17 to 0.54/100 PYs across placebo-controlled and open-label trials. In conclusion, the incidence rates of serious CVTEAEs were comparable among men with erectile dysfunction taking tadalafil as needed, 3 times/week, or once a day, and these rates were also comparable with those in placebo-treated patients. In this clinical trial population of men with erectile dysfunction, tadalafil was not associated with an increased risk for serious cardiovascular adverse events. (c) 2006 Elsevier Inc. All rights reserved. C1 Univ Calif Los Angeles, Inst Heart, Hosp Good Samaritan, Cardiovasc Div,Keck Sch Med, Los Angeles, CA 90024 USA. Guys & St Thomas Hosp, London SE1 9RT, England. Harvard Univ, Sch Med, Massachusetts Gen Hosp, Boston, MA 02115 USA. Harvard Univ, Sch Med, Cardiol Epidemiol Res Unit, Beth Israel Deaconess Med Ctr, Boston, MA 02115 USA. Eli Lilly & Co, Lilly Res Labs, Danforth, ON, Canada. Eli Lilly & Co, Lilly Res Labs, Indianapolis, IN 46285 USA. RP Kloner, RA (reprint author), Univ Calif Los Angeles, Inst Heart, Hosp Good Samaritan, Cardiovasc Div,Keck Sch Med, Los Angeles, CA 90024 USA. EM rkloner@goodsam.org RI Kloner, Robert/B-2971-2012 NR 20 TC 35 Z9 37 U1 0 U2 0 PU EXCERPTA MEDICA INC PI NEW YORK PA 650 AVENUE OF THE AMERICAS, NEW YORK, NY 10011 USA SN 0002-9149 J9 AM J CARDIOL JI Am. J. Cardiol. PD JUN 15 PY 2006 VL 97 IS 12 BP 1778 EP 1784 DI 10.1016/j.amjcard.2005.12.073 PG 7 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA 055EZ UT WOS:000238434100022 PM 16765134 ER PT J AU Berrios-Rivera, JP Street, RL Popa-Lisseanu, MGG Kallen, MA Richardson, MN Janssen, NM Marcus, DM Reveille, JD Warner, NB Suarez-Almazor, ME AF Berrios-Rivera, JP Street, RL Popa-Lisseanu, MGG Kallen, MA Richardson, MN Janssen, NM Marcus, DM Reveille, JD Warner, NB Suarez-Almazor, ME TI Trust in physicians and elements of the medical interaction in patients with rheumatoid arthritis and systemic lupus erythematosus SO ARTHRITIS & RHEUMATISM-ARTHRITIS CARE & RESEARCH LA English DT Article DE physician trust; communication; rheumatoid arthritis; systemic lupus erythematosus ID QUALITY-OF-LIFE; PRIMARY-CARE; PREVENTIVE SERVICES; ETHNIC DISPARITIES; HEALTH-CARE; RACE; SCALE; SATISFACTION; PERCEPTIONS; PROFESSION AB Objective. To identify components of the patient-doctor relationship associated with trust in physicians. Methods. We assessed 102 patients with systemic lupus erythematosus (SLE) or rheumatoid arthritis (RA) seen at publicly funded hospitals in Houston, Texas. Patients completed a self-response survey examining patient perceptions of the medical encounter and trust in their physicians. Evaluated components of physicians' behaviors included: informativeness, sensitivity to concerns, reassurance and support, patient-centeredness, and participatory decision-making style. Scales were scored 0 to 10, with higher numbers indicating more positive perceptions of communication. Results. Seventy patients had RA and 32 SLE; 25% were white, 43% Latino, 31% African American, and 75% were female. Mean scores for the medical interaction and trust scales ranged from 6.2-7.1, indicating moderate degrees of positive perceptions. All components were highly and positively correlated with each other, and with trust, suggesting that these traits are all elements of a positive style of doctor-patient communication. In multivariate analysis, ethnicity, physicians' informativeness, physicians' sensitivity to concerns, patient-centeredness, disease activity, and patient trust in the US health care system were independent predictors of trust in physicians. A separate model examined the predictors of patient disclosure of information. Patient perceptions of physicians' patient-centeredness and severity of disease activity were independently predictive of patient disclosure of information. Conclusion. In patients with SLE and RA, trust in physicians is significantly associated with patients' ethnicity and their perceptions about specific components of physicians' communication style. Trust in physicians can be improved by using a patient-centered approach, being sensitive to patient concerns, and providing adequate clinical information. Furthermore, patients appear to be more willing to disclose concerns when physicians use a patient-centered communication style. C1 Michael E DeBakey Vet Affairs Med Ctr, Houston, TX 77030 USA. Baylor Coll Med, Houston, TX 77030 USA. Texas A&M Univ, College Stn, TX USA. Univ Texas, Hlth Sci Ctr, Houston, TX USA. RP Suarez-Almazor, ME (reprint author), Michael E DeBakey Vet Affairs Med Ctr, 2002 Holcombe Blvd, Houston, TX 77030 USA. EM mes@bcm.tmc.edu FU NIAMS NIH HHS [R01 AR 47858] NR 47 TC 58 Z9 59 U1 3 U2 11 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 0004-3591 J9 ARTHRIT RHEUM-ARTHR JI Arthritis Rheum-Arthritis Care Res. PD JUN 15 PY 2006 VL 55 IS 3 BP 385 EP 393 DI 10.1002/art.21988 PG 9 WC Rheumatology SC Rheumatology GA 051PL UT WOS:000238172900008 PM 16739207 ER PT J AU Quackenbush, J Salzberg, SL AF Quackenbush, J Salzberg, SL TI It is time to end the patenting of software SO BIOINFORMATICS LA English DT Editorial Material C1 Harvard Univ, Sch Publ Hlth, Dana Farber Canc Inst, Dept Biostat, Boston, MA 02115 USA. Univ Maryland, Ctr Bioinformat & Computat Biol, College Pk, MD 20742 USA. RP Quackenbush, J (reprint author), Harvard Univ, Sch Publ Hlth, Dana Farber Canc Inst, Dept Biostat, 665 Huntington Ave, Boston, MA 02115 USA. EM johnq@jimmy.harvard.edu; salzberg@umd.edu RI Salzberg, Steven/F-6162-2011 OI Salzberg, Steven/0000-0002-8859-7432 FU NLM NIH HHS [R01 LM007938, R01 LM006845, R01 LM006845-08, R01 LM007938-04] NR 2 TC 0 Z9 0 U1 0 U2 0 PU OXFORD UNIV PRESS PI OXFORD PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND SN 1367-4803 J9 BIOINFORMATICS JI Bioinformatics PD JUN 15 PY 2006 VL 22 IS 12 BP 1416 EP 1417 DI 10.1093/bioinformatics/btl167 PG 2 WC Biochemical Research Methods; Biotechnology & Applied Microbiology; Computer Science, Interdisciplinary Applications; Mathematical & Computational Biology; Statistics & Probability SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Computer Science; Mathematical & Computational Biology; Mathematics GA 059YQ UT WOS:000238768500002 PM 16766564 ER PT J AU Massey, GV Zipursky, A Chang, MN Doyle, JJ Nasim, S Taub, JW Ravindranath, Y Dahl, G Weinstein, HJ AF Massey, GV Zipursky, A Chang, MN Doyle, JJ Nasim, S Taub, JW Ravindranath, Y Dahl, G Weinstein, HJ TI A prospective study of the natural history of transient leukemia (TL) in neonates with Down syndrome (DS): Children's Oncology Group (COG) study POG-9481 SO BLOOD LA English DT Article ID ACUTE MYELOID-LEUKEMIA; ACUTE MEGAKARYOBLASTIC LEUKEMIA; MYELOPROLIFERATIVE DISORDER; ABNORMAL MYELOPOIESIS; PRENATAL-DIAGNOSIS; MYELODYSPLASTIC SYNDROME; MEGAKARYOCYTIC LEUKEMIA; GATA1 MUTATIONS; CLONAL ANALYSIS; BLAST CELLS AB A unique transient leukemia (TL) has been described in newborns with Down syndrome (DS; or trisomy 21 mosaics). This leukemia has a high incidence of spontaneous remission; however, early death and subsequent development of acute megakaryoblastic leukemia (AMKL) have been reported. We prospectively evaluated 48 infants with DS and TL to determine the natural history and biologic characteristics of this disease, identify the clinical characteristics associated with early death or subsequent leukemia, and assess the incidence of subsequent leukemia. Blast cells associated with TL in DS infants exhibited FAB M-7 morphology and phenotype. Most infants (74%) had trisomy 21 (or mosaicism) as the only cytogenetic abnormality in the blast cells. Most children were able to spontaneously clear peripheral blasts (89%), normalize blood counts (74%), and maintain a complete remission (64%). Early death occurred in 17% of infants and was significantly correlated with higher white blood cell count at diagnosis (P <.001), increased bilirubin and liver enzymes (P <.005), and a failure to normalize the blood count (P=.001). Recurrence of leukemia occurred in 19% of infants at a mean of 20 months. Development of leukemia was significantly correlated with karyotypic abnormalities in addition to trisomy 21 (P=.037). Ongoing collaborative clinical studies are needed to determine the optimal role of chemotherapy for infants at risk for increased mortality or disease recurrence and to further the knowledge of the unique biologic features of this TL. C1 Virginia Commonwealth Univ, Med Coll Virginia, Richmond, VA 23298 USA. Hosp Sick Children, Toronto, ON M5G 1X8, Canada. Stat Off, Childrens Oncol Grp, Gainesville, FL USA. Childrens Hosp Michigan, Detroit, MI 48201 USA. Stanford Univ, Sch Med, Stanford, CA 94305 USA. Massachusetts Gen Hosp, Boston, MA 02114 USA. RP Massey, GV (reprint author), POB 980121, Richmond, VA 23298 USA. EM gvmassey@hsc.vcu.edu NR 58 TC 129 Z9 133 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 JUN 15 PY 2006 VL 107 IS 12 BP 4606 EP 4613 DI 10.1182/blood-2005-06-2448 PG 8 WC Hematology SC Hematology GA 053LA UT WOS:000238305400013 PM 16469874 ER PT J AU Schenten, D Egert, A Pasparakis, M Rajewsky, K AF Schenten, D Egert, A Pasparakis, M Rajewsky, K TI M17, a gene specific for germinal center (GC) B cells and a prognostic marker for GC B-cell lymphomas, is dispensable for the GC reaction in mice SO BLOOD LA English DT Article ID CLASS-SWITCH RECOMBINATION; STRONGLY PREDICTS SURVIVAL; SOMATIC HYPERMUTATION; IMMUNE-RESPONSE; PRIMARY IMMUNIZATION; AFFINITY MATURATION; ANTIBODY DIVERSITY; HAPTEN NP; EXPRESSION; INTERLEUKIN-4 AB In T-cell-dependent antibody responses, antigen-specific B cells undergo a phase of secondary antibody diversification in germinal centers (GCs). Somatic hypermutation (SHM) introduces mutations into the rearranged immunoglobulin (Ig) variable (V) region genes, and class-switch recombination (CSR) alters the Ig heavy (H) chain constant region. Aberrant SHM or CSR is thought to contribute to the development of GC-derived B-cell malignancies. Diffuse large B-cell lymphomas (DLBCLs) are a heterogeneous group of such GC-derived tumors. Based on their gene expression profile, DLBCLs can be divided into activated B-cell-like and GC-like subgroups. The human gene HGAL is predominantly expressed in GCs. It is also part of the gene expression signature of GC-like DLBCL, and its high expression in DLBCL has been associated with a better clinical prognosis. We have generated mice deficient of the HGAL homologue M17 in order to investigate its functional significance. The mutant animals form normal GCs, undergo efficient CSR and SHM, and mount T-cell-dependent antibody responses similar to wildtype controls. Thus, M17 is dispensable for the GC reaction, and its potential function in the pathogenesis of DLBCL remains elusive. C1 CBR Inst Biomed Res, Boston, MA 02115 USA. Harvard Univ, Sch Med, Boston, MA USA. Univ Cologne, Genet Inst, D-5000 Cologne 41, Germany. EMBL, Mouse Biol Unit, Monterotondo, Italy. RP Rajewsky, K (reprint author), CBR Inst Biomed Res, 200 Longwood Ave,WAB, Boston, MA 02115 USA. EM rajewsky@cbr.med.harvard.edu OI Pasparakis, Manolis/0000-0002-9870-0966 FU NIAID NIH HHS [AI 054636] NR 47 TC 12 Z9 13 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 JUN 15 PY 2006 VL 107 IS 12 BP 4849 EP 4856 DI 10.1182/blood-2005-10-4154 PG 8 WC Hematology SC Hematology GA 053LA UT WOS:000238305400046 PM 16493007 ER PT J AU Eapen, M Raetz, E Zhang, MJ Muehlenbein, C Devidas, M Abshire, T Billett, A Homans, A Camitta, B Carroll, WL Davies, SM AF Eapen, M Raetz, E Zhang, MJ Muehlenbein, C Devidas, M Abshire, T Billett, A Homans, A Camitta, B Carroll, WL Davies, SM CA Childrens Oncology Grp Ctr Int Blood Marrow Transplant R TI Outcomes after HLA-matched sibling transplantation or chemotherapy in children with B-precursor acute lymphoblastic leukemia in a second remission: a collaborative study of the Children's Oncology Group and the Center for International Blood and Marrow Transplant Research SO BLOOD LA English DT Article ID STEM-CELL TRANSPLANTATION; UNRELATED DONORS; FOLLOW-UP; EXPERIENCE; THERAPY; RELAPSE; TIME AB The best treatment approach for children with B-precursor acute lymphoblastic leukemia (ALL) in second clinical remission (CR) after a marrow relapse is controversial. To address this question, we compared outcomes in 188 patients enrolled in chemotherapy trials and 186 HLA-matched sibling transplants, treated between 1991 and 1997. Groups were similar except that chemotherapy recipients were younger (median age, 5 versus 8 years) and less likely to have combined marrow and extramedullary relapse (19% versus 30%). To adjust for time-to-transplant bias, treatment outcomes were compared using left-truncated Cox regression models. The relative efficacy of chemotherapy and transplantation depended on time from diagnosis to first relapse and the transplant conditioning regimen used. For children with early first relapse (< 36 months), risk of a second relapse was significantly lower after total body irradiation (TBI)-containing transplant regimens (relative risk [RR], 0.49; 95% confidence interval [CI] 0.33-0.71, P < .001) than chemotherapy regimens. In contrast, for children with a late first relapse (>= 36 months), risks of second relapse were similar after TBI-containing regimens and chemotherapy (FIR, 0.92; 95% CI, 0.49-1.70, P = .78). These data support HLA-matched sibling donor transplantation using a TBI-containing regimen in second CR for children with ALL and early relapse. C1 Med Coll Wisconsin, Ctr Int Blood & Marrow Transplant Res, Ctr Stat, Milwaukee, WI 53226 USA. Stat Ctr Childrens Oncol Grp, Arcadia, CA USA. NYU, Med Ctr, New York, NY 10016 USA. Univ Florida, Gainesville, FL 32611 USA. Emory Univ, Atlanta, GA 30322 USA. Dana Farber Canc Inst, Boston, MA 02115 USA. Univ Vermont, Coll Med, Burlington, VT 05405 USA. Childrens Hosp, Med Ctr, Cincinnati, OH 45229 USA. RP Eapen, M (reprint author), Med Coll Wisconsin, Ctr Int Blood & Marrow Transplant Res, Ctr Stat, 8701 Watertown Plank Rd,POB 26509, Milwaukee, WI 53226 USA. EM meapen@mcw.edu FU NCI NIH HHS [U24 CA076518, U24-CA76518-08, U10-CA098543] NR 25 TC 82 Z9 83 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD JUN 15 PY 2006 VL 107 IS 12 BP 4961 EP 4967 DI 10.1182/blood-2005-12-4942 PG 7 WC Hematology SC Hematology GA 053LA UT WOS:000238305400060 PM 16493003 ER PT J AU Punglia, RS Kuntz, KM Winer, EP Weeks, JC Burstein, HJ AF Punglia, RS Kuntz, KM Winer, EP Weeks, JC Burstein, HJ TI The impact of tumor progesterone receptor status on optimal adjuvant endocrine therapy for postmenopausal patients with early-stage breast cancer - A decision analysis SO CANCER LA English DT Article DE breast cancer; tamoxifen; aromatase inhibitor; decision analysis; postmenopausal; progesterone receptor ID RANDOMIZED-TRIAL; TAMOXIFEN THERAPY; WOMEN; ANASTROZOLE; COMBINATION; LETROZOLE AB BACKGROUND. Emerging data suggest that treatment outcomes with aromatase inhibitors (AIs) and/or tarnoxifen may differ for tumors that express both the estrogen receptor (ER) and the progesterone receptor (PR) (ER+/PR+) compared with those that lack PR expression (ER+/PR-). However, the optimal sequencing of AIs and tamoxifen as adjuvant therapy is not known and may differ for biologic subsets of cancers. METHODS. Markov models were used to simulate disease-free survival (DFS) separately among postmenopausal women with ER+/PR+ cancers and women with ER+/PR- cancers. By using risk estimates reported from randomized clinical trials, treatment with 5 years of an At alone with sequential treatment consisting of tamoxifen with crossover to an At at 2 years was compared. RESULTS. For women with ER+/PR+ cancers, sequential therapy with tarnoxifen followed by crossover to an At at 2 years yielded modest improvements in 10-year DFS estimates compared with planned At monotherapy (84.3% vs. 82.2% and 68.8% vs. 64.8% for lymph node-negative and lymph node-positive patients, respectively). However, for women with ER+/PR- cancers, upfront treatment with an AI yielded improved outcomes with 10-year DFS rates of 90.5% and 80.1% for the lymph node-negative and node-positive groups, respectively, compared with 88.2% and 76.1%, respectively, for sequential treatment with tarnoxifen followed by an AI. CONCLUSIONS. Modeling estimates suggested that the optimal endocrine treatment strategy may differ based on the biologic features of breast cancer tumors. Patients with ER+/PR+ tumors achieved optimal 10-year DFS estimates with tamoxifen followed by a crossover to AI therapy, whereas patients with ER+/PR- tumors fared best when they initiated treatment with AI. C1 Dana Farber Canc Inst, Div Med Oncol, Boston, MA 02115 USA. Dana Farber Canc Inst, Dept Radiat Oncol, Boston, MA 02115 USA. Brigham & Womens Hosp, Boston, MA 02115 USA. Harvard Univ, Sch Publ Hlth, Dept Hlth Policy & Management, Boston, MA USA. Brigham & Womens Hosp, Dept Med, Boston, MA USA. Harvard Univ, Sch Med, Boston, MA USA. RP Burstein, HJ (reprint author), Dana Farber Canc Inst, Div Med Oncol, 44 Binney St, Boston, MA 02115 USA. EM hburstein@partners.org NR 16 TC 17 Z9 19 U1 0 U2 0 PU JOHN WILEY & SONS INC PI HOBOKEN PA 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 0008-543X J9 CANCER JI Cancer PD JUN 15 PY 2006 VL 106 IS 12 BP 2576 EP 2582 DI 10.1002/cncr.21919 PG 7 WC Oncology SC Oncology GA 051OR UT WOS:000238170900007 PM 16703595 ER PT J AU Wang, Q Diskin, S Rappaport, E Attiyeh, E Mosse, Y Shue, D Seiser, E Jagannathan, J Shusterman, S Bansal, M Khazi, D Winter, C Okawa, E Grant, G Cnaan, A Zhao, HQ Cheung, NK Gerald, W London, W Matthay, KK Brodeur, GM Maris, JM AF Wang, Q Diskin, S Rappaport, E Attiyeh, E Mosse, Y Shue, D Seiser, E Jagannathan, J Shusterman, S Bansal, M Khazi, D Winter, C Okawa, E Grant, G Cnaan, A Zhao, HQ Cheung, NK Gerald, W London, W Matthay, KK Brodeur, GM Maris, JM TI Integrative genomics identifies distinct molecular classes of neuroblastoma and shows that multiple genes are targeted by regional alterations in DNA copy number SO CANCER RESEARCH LA English DT Article; Proceedings Paper CT Symposium on Amorphous and Nanocrystalline Silicon Science and Technology held at the 2005 MRS Spring Meeting CY MAR 28-APR 01, 2005 CL San Francisco, CA SP Mat Res Soc ID CHILDRENS-CANCER-GROUP; ARTIFICIAL NEURAL-NETWORKS; PEDIATRIC-ONCOLOGY-GROUP; HIGH-RISK NEUROBLASTOMA; TUMOR-SUPPRESSOR GENE; N-MYC; PATHOLOGY CLASSIFICATION; CHILDHOOD NEUROBLASTOMA; MICROARRAY ANALYSIS; 17Q GAIN AB Neuroblastoma is remarkable for its clinical heterogeneity and is characterized by genomic alterations that are strongly correlated with tumor behavior. The specific genes that influence neuroblastoma biology and are targeted by genomic alterations remain largely unknown. We quantified mRNA expression in a highly annotated series of 101 prospectively collected diagnostic neuroblastoma primary tumors using an oligonucleotide-based microarray. Genomic copy number status at the prognostically relevant loci 1P36, 2p24 (MYCN), 11q23, and 17q23 was determined by PCR and was aberrant in 26, 20, 40, and 38 cases, respectively. In addition, 72 diagnostic neuroblastoma primary tumors assayed in a different laboratory were used as an independent validation set. Unsupervised hierarchical clustering showed that gene expression was highly correlated with genomic alterations and clinical markers of tumor behavior. The vast majority of samples with MYCN amplification and 1p36 loss of heterozygosity (LOH) clustered together on a terminal node of the sample dendrogram, whereas the majority of samples with 11q deletion clustered separately and both of these were largely distinct from the copy number neutral group of tumors. Genes involved in neurodevelopment were broadly overrepresented in the more benign tumors, whereas genes involved in RNA processing and cellular proliferation were highly represented in the most malignant cases. By combining transcriptomic and genomic data, we showed that LOH at 1p and 11q was associated with significantly decreased expression of 122 (61%) and 88 (27%) of the genes mapping to 1p35-36 and all of 11q, respectively, suggesting that multiple genes may be targeted by LOH events. A total of 71 of the 1p35-36 genes were also differentially expressed in the independent validation data set, providing a prioritized list of candidate neuroblastoma suppressor genes. Taken together, these data are consistent with the hypotheses that the neuroblastoma transcriptome is a sensitive marker of underlying tumor biology and that chromosomal deletion events in this cancer likely target multiple genes through alteration in mRNA dosage. Lead positional candidates for neuroblastoma suppressor genes can be inferred from these data, but the potential multiplicity of transcripts involved has significant implications for ongoing gene discovery strategies. C1 Childrens Hosp Philadelphia, Div Oncol, Philadelphia, PA 19104 USA. Childrens Hosp Philadelphia, Div Biostat, Philadelphia, PA 19104 USA. Univ Penn, Sch Med, Dept Pediat, Philadelphia, PA 19104 USA. Univ Penn, Sch Med, Abramson Family Canc Res Inst, Philadelphia, PA 19104 USA. Univ Penn, Ctr Bioinformat, Philadelphia, PA 19104 USA. Dana Farber Canc Inst, Dept Pediat Oncol, Boston, MA 02115 USA. Harvard Univ, Sch Med, Dept Pediat, Boston, MA 02115 USA. Mem Sloan Kettering Canc Ctr, New York, NY 10021 USA. Univ Florida, Dept Stat, Gainesville, FL 32611 USA. Childrens Oncol Grp, Gainesville, FL 32611 USA. Univ Calif San Francisco, Sch Med, San Francisco, CA 94143 USA. RP Maris, JM (reprint author), Childrens Hosp Philadelphia, Div Oncol, 34th St & Civ Ctr Blvd, Philadelphia, PA 19104 USA. EM maris@chop.edu FU NCI NIH HHS [P01-CA106450, P01-CA97323, R01-CA39771, R01-CA78545, R01-CA87847, U10-CA98543] NR 79 TC 131 Z9 132 U1 0 U2 3 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA SN 0008-5472 J9 CANCER RES JI Cancer Res. PD JUN 15 PY 2006 VL 66 IS 12 BP 6050 EP 6062 DI 10.1158/0008-5472.CAN-05-4618 PG 13 WC Oncology SC Oncology GA 054LX UT WOS:000238379500014 PM 16778177 ER PT J AU Diederichs, S Haber, DA AF Diederichs, Sven Haber, Daniel A. TI Sequence variations of microRNAs in human cancer: Alterations in predicted secondary structure do not affect processing SO CANCER RESEARCH LA English DT Article ID CHRONIC LYMPHOCYTIC-LEUKEMIA; RNA-INTERFERENCE; BLADDER-CANCER; LUNG-CANCER; C-ELEGANS; EXPRESSION; GENE; REGIONS; TARGET; DROSHA AB Expression levels of microRNAs (miRNAs) are globally reduced in cancer compared with matched normal tissues, and miRNA function has recently been implicated in tumorigenesis. To test whether epigenetic silencing contributes to miRNA suppression in tumors, lung cancer cells were treated with inhibitors of DNA methylation or histone deacetylation. No significant alteration in miRNA expression was detected using microarray profiling. To search for tumor-associated mutations that could affect processing and expression of mature miRNAs, a panel of 91 cancer-derived cell lines was analyzed for sequence variations in 15 miRNAs implicated in tumorigenesis by virtue of their known target transcripts (let-7 family targeting oncogenic Ras) or their localization to sites of frequent chromosomal instability (miR-143, miR-145, miR-26a-1, and miR-21). No mutations were detected within any of the short mature miRNA sequences. In addition to previously reported polymorphisms, I sequence variant in a precursor miRNA and 15 variants in primary miRNA (pri-miRNA) transcripts were identified. Despite pri-miRNAs having dramatic changes in the predicted secondary folding structure Ranking putative cleavage sites, processing and miRNA maturation were not affected in vivo. Thus, genetic variants in miRNA precursors are common in cancer cells but are unlikely to have physiologic significance. C1 Harvard Univ, Sch Med, Massachusetts Gen Hosp, Ctr Canc, Charlestown, MA 02129 USA. RP Haber, DA (reprint author), Harvard Univ, Sch Med, Massachusetts Gen Hosp, Ctr Canc, Bldg 149,13th St, Charlestown, MA 02129 USA. EM haber@helix.mgh.harvard.edu RI Diederichs, Sven/J-6237-2012 OI Diederichs, Sven/0000-0001-7901-4752 FU PHS HHS [NIH01 95281] NR 42 TC 126 Z9 135 U1 0 U2 10 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA SN 0008-5472 J9 CANCER RES JI Cancer Res. PD JUN 15 PY 2006 VL 66 IS 12 BP 6097 EP 6104 DI 10.1158/0008-5472.CAN-06-0537 PG 8 WC Oncology SC Oncology GA 054LX UT WOS:000238379500019 PM 16778182 ER PT J AU Crawford, LJA Walker, B Ovaa, H Chauhan, D Anderson, KC Morris, TCM Irvine, AE AF Crawford, Lisa J. A. Walker, Brian Ovaa, Huib Chauhan, Dharminder Anderson, Kenneth C. Morris, Treen C. M. Irvine, Alexandra E. TI Comparative selectivity and specificity of the proteasome inhibitors BzLLLCOCHO, PS-341, and MG-132 SO CANCER RESEARCH LA English DT Article ID MULTIPLE-MYELOMA CELLS; DEXAMETHASONE; BORTEZOMIB; APOPTOSIS; THERAPY; SITES; COMBINATION; MECHANISMS; MATURATION; ALDEHYDES AB The 26S proteasome is a multicatalytic protease responsible for regulated intracellular protein degradation. Its function is mediated by three main catalytic activities: (a) chymotrypsinlike (CT-L), (b) trypsin-like, and (c) peptidylglutamyl peptide hydrolysing (PGPH). Proteasome inhibition is an emerging therapy for many cancers and is a novel treatment for multiple myeloma. Here, we profile the contributions of the three catalytic activities in multiple myeloma cell lines and compare the specificity and cytotoxicity of the novel proteasome inhibitor BzLLLCOCHO and inhibitors PS-341 (Velcade, bortezomib) and MG-132. Using fluorogenic substrates and an active site-directed probe specific for proteasome catalytic subunits, we show differential subunit specificity for each of the inhibitors. Addition of BzLLLCOCHO strongly inhibited all three catalytic activities, treatment with PS-341 completely inhibited CT-L and PGPH activities, and treatment with MG132 resulted in weak inhibition of the CT-L and PGPH activities. Multiple myeloma cells were more sensitive to induction of apoptosis by PS-341 and MG-132 than BzLLLCOCHO. This study emphasizes the need for further investigation of the effects of these compounds on gene and protein expression in the cell to allow for the development of more specific and targeted inhibitors. C1 Queens Univ Belfast, Ctr Canc Res & Cell Biol, Belfast, Antrim, North Ireland. Belfast City Hosp, Dept Haematol, Belfast BT9 7AD, Antrim, North Ireland. Harvard Univ, Sch Med, Boston, MA 02115 USA. Dana Farber Canc Inst, Boston, MA 02115 USA. Netherlands Canc Inst, Div Cellular Biochem, NL-1066 CX Amsterdam, Netherlands. RP Irvine, AE (reprint author), Queens Univ Belfast, Belfast City Hosp, Haematol U Floor,Tower Block,Lisburn Rd, Belfast BT9 7AB, Antrim, North Ireland. EM s.irvine@qub.ac.uk RI IRVINE, ALEXANDRA/B-3497-2009 NR 26 TC 83 Z9 86 U1 0 U2 16 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA SN 0008-5472 J9 CANCER RES JI Cancer Res. PD JUN 15 PY 2006 VL 66 IS 12 BP 6379 EP 6386 DI 10.1158/0008-5472.CAN-06-0605 PG 8 WC Oncology SC Oncology GA 054LX UT WOS:000238379500053 PM 16778216 ER PT J AU Mitsiades, CS Poulaki, V Fanourakis, G Sozopoulos, E McMillin, D Wen, ZQ Voutsinas, G Tseleni-Balafouta, S Mitsiades, N AF Mitsiades, CS Poulaki, V Fanourakis, G Sozopoulos, E McMillin, D Wen, ZQ Voutsinas, G Tseleni-Balafouta, S Mitsiades, N TI Fas signaling in thyroid carcinomas is diverted from apoptosis to proliferation SO CLINICAL CANCER RESEARCH LA English DT Article ID NF-KAPPA-B; MULTIPLE-MYELOMA CELLS; INDUCED-PROXIMITY MODEL; MEDIATED APOPTOSIS; UP-REGULATION; THERAPEUTIC IMPLICATIONS; PROTEIN EXPRESSION; DEATH RECEPTORS; ACTIVATION; LIGAND AB Purpose: The death receptor Fas is present in thyroid carcinomas, yet fails to trigger apoptosis. Interestingly, Fas has been reported to be actually overexpressed in papillary thyroid carcinomas, suggesting that it may confer a survival advantage. Experimental Design: We investigated the expression and activation status of Fas pathway mediators in thyroid carcinoma cell lines and tumor specimens. Results: All cell lines tested express Fas-associated death domain, procaspase-8, procaspase-9, and procaspase-3; resistance to Fas-mediated apoptosis could not be attributed to lack of any of these apoptosis mediators. Moreover, Fas death domain mutations were not found in our study. The proteasome inhibitors MG132 and PS-341 (bortezomib,Velcade), which lead to accumulation of the nuclear factor kappa B (NF-kappa B) inhibitor I kappa B, did not sensitize SW579 cells to Fas-mediated apoptosis, suggesting that resistance to Fas-mediated apoptosis is not due to proteasome or NF-kappa B activity. Cross-linking of Fas in vitro induced recruitment of Fas-associated death domain - like interleukin-1 beta - converting enzyme inhibitory protein (FLIP) instead of procaspase-8. Inhibition of FLIP expression with a FLIP antisense oligonucleotide resulted in significant sensitization to Fas-mediated apoptosis. Fas cross-linking promoted BrdUrd incorporation; activated the mitogen-activated protein kinase/extracellular signal - regulated kinase kinase/extracellular signal -regulated kinase, NF-kappa B, and activator protein-1 pathways in thyroid carcinoma cells in vitro; and protected cells from tumor necrosis factor - related apoptosis-inducing ligand - induced apoptosis. We also found that good prognosis papillary thyroid carcinoma specimens exhibited higher immunoreactivity for cleaved (activated) caspase-8 than poor prognosis tumors. Conclusions: In thyroid carcinomas, the proteolytic cleavage and activation of caspase-8 depends on the balance between expression levels for procaspase-8 and FLIP and correlates with favorable clinical prognosis. Fas may actually stimulate proliferation and confer a survival advantage to thyroid cancer cells. C1 Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02115 USA. Harvard Univ, Massachusetts Eye & Ear Infirm, Sch Med, Boston, MA USA. Harvard Univ, Sch Med, Dept Med, Boston, MA USA. Univ Athens, Dept Pathol, GR-10679 Athens, Greece. NCSR Demokritos, Inst Biol, Lab Environm Mutagenesis & Carcinogenesis, GR-15310 Athens, Greece. RP Mitsiades, CS (reprint author), Dana Farber Canc Inst, Dept Med Oncol, Room M555,Mayer Bldg,44 Binney St, Boston, MA 02115 USA. EM Constantine_Mitsiades@dfci.harvard.edu NR 49 TC 43 Z9 51 U1 0 U2 1 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA SN 1078-0432 J9 CLIN CANCER RES JI Clin. Cancer Res. PD JUN 15 PY 2006 VL 12 IS 12 BP 3705 EP 3712 DI 10.1158/1078-0432.CCR-05-2493 PG 8 WC Oncology SC Oncology GA 054YS UT WOS:000238415100008 PM 16778096 ER PT J AU McGovern, BH Wurcel, A Kim, AY zur Wiesch, JS Bica, I Zaman, MT Timm, J Walker, BD Lauer, GM AF McGovern, BH Wurcel, A Kim, AY zur Wiesch, JS Bica, I Zaman, MT Timm, J Walker, BD Lauer, GM TI Acute hepatitis C virus infection in incarcerated injection drug users SO CLINICAL INFECTIOUS DISEASES LA English DT Article; Proceedings Paper CT 41st Annual Meeting of the Infectious-Diseases-Society-of-America CY OCT 09-12, 2003 CL San Diego, CA SP Infect Dis Soc Amer ID CORRECTIONAL HEALTH-CARE; VIRAL CLEARANCE; RIBAVIRIN; SEROCONVERSION; PERSISTENCE; PREVALENCE; THERAPY; INMATES; PRISONS; VIREMIA AB Background. The Centers for Disease Control and Prevention has emphasized the need for interventional programs regarding hepatitis C virus (HCV) infection for injection drug users, the group of persons who are at highest risk of acquiring acute infection. Methods. We designed a pilot study to assess the feasibility of identifying injection drug users with acute HCV infection in correctional and detoxification facilities. On-site medical providers were educated regarding risk factors and signs and symptoms of infection and were instructed to refer all patients with hepatitis to our specialty clinic. Results. Over a 30-month period, 21 patients received a diagnosis of acute hepatitis C, 3 received a diagnosis of hepatitis B, and 1 received a diagnosis of hepatitis A. Of the 21 patients with acute hepatitis C, 19 were identified in the prison setting shortly after incarceration. Of the 17 patients who were observed serially (mean duration of observation, 6.3 months), 8 had spontaneous virologic clearance. Early therapy with pegylated interferon was initiated for 5 patients with persistent viremia and led to a sustained virologic response in 2 individuals. All patients agreed to undergo human immunodeficiency virus counseling and testing, as well as to receive immunization for hepatitis A and B. Conclusions. Incarceration presents a unique opportunity to identify injection drug users with acute HCV infection, to initiate counseling regarding other bloodborne pathogens, and to facilitate immunizations and HCV treatment. C1 Lemuel Shattuck Hosp, Boston, MA USA. Tufts Univ, Sch Med, Boston, MA 02111 USA. Massachusetts Gen Hosp, Partners AIDS Res Ctr, Div Infect Dis, Boston, MA 02114 USA. Harvard Univ, Sch Med, Boston, MA 02115 USA. Howard Hughes Med Inst, Chevy Chase, MD USA. RP McGovern, BH (reprint author), Lemuel Shattuck Hosp, 170 Morton St, Jamaica Plain, MA 02130 USA. EM bmcgovern@tufts-nemc.org FU NCRR NIH HHS [M01-RR00054]; NIAID NIH HHS [AI31563, R01 AI031563, U19 AI066345] NR 30 TC 29 Z9 29 U1 0 U2 3 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 1058-4838 J9 CLIN INFECT DIS JI Clin. Infect. Dis. PD JUN 15 PY 2006 VL 42 IS 12 BP 1663 EP 1670 DI 10.1086/504327 PG 8 WC Immunology; Infectious Diseases; Microbiology SC Immunology; Infectious Diseases; Microbiology GA 043TO UT WOS:000237624800001 PM 16705568 ER PT J AU Holmes, CB Zheng, H Martinson, NA Freedberg, KA Walensky, RP AF Holmes, CB Zheng, H Martinson, NA Freedberg, KA Walensky, RP TI Optimizing treatment for HIV-infected South African women exposed to single-dose nevirapine: Balancing efficacy and cost SO CLINICAL INFECTIOUS DISEASES LA English DT Article; Proceedings Paper CT 26th Annual Meeting of the Society-for-Medical-Decision-Making CY OCT 17-20, 2004 CL Atlanta, GA SP Soc Med Decis Making ID IMMUNODEFICIENCY-VIRUS TYPE-1; ACTIVE ANTIRETROVIRAL THERAPY; TO-CHILD TRANSMISSION; INTRAPARTUM; TRIAL; RESISTANCE; LAMIVUDINE; COMBINATION; PREVENTION; ZIDOVUDINE AB Introduction. Nevirapine (NVP) resistance may decrease the effectiveness of viral suppression with NVP-based antiretroviral therapy (ART) in women infected with human immunodeficiency virus (HIV) with previous exposure to single-dose NVP. However, the alternative lopinavir-ritonavir-based ART regimen is more expensive. Our objectives were to project the tradeoffs regarding life expectancy, cost, and cost-effectiveness of these ART regimens for NVP-exposed, HIV-infected women in South Africa. Methods. We developed a simulation model in which NVP-exposed, HIV-infected South African women received 1 of 5 treatment strategies: HIV care without ART, NVP-based ART, lopinavir-ritonavir-based ART, NVP-based ART followed by lopinavir-ritonavir-based ART, or lopinavir-ritonavir-based ART followed by NVP-based ART. The prevalence of NVP resistance was 39%; other data were obtained from the published literature. Results. Projected life expectancy was 43.7 months for women who did not receive ART, 77.4 months for women who received a single NVP-based regimen, and 84.5 months for women who received a single lopinavir-ritonavir-based regimen. NVP resistance reduced survival time by up to 11.6 months among women who received NVP-based ART. The cost-effectiveness of NVP-based ART was $800 (US dollars) per year of life saved, compared with no ART, and the cost-effectiveness of lopinavir-ritonavir-based therapy was $4400 per year of life saved, compared with NVP-based ART. Lopinavir-ritonavir followed by NVP-based ART yielded the greatest life expectancy (105.4 months), had a cost-effectiveness of $2300 per year of life saved, and, if the efficacy of NVP-based regimens improved 16 months postpartum, further increased survival. Conclusions. NVP resistance substantially decreased the projected survival time associated with NVP-based ART, and lopinavir-ritonavir-based ART resulted in a superior survival time but at higher cost. A sequential regimen starting with lopinavir-ritonavir-based ART followed by NVP-based ART maximized projected survival and was cost effective in South Africa. C1 Massachusetts Gen Hosp, Div Gen Med, Dept Med, Boston, MA 02114 USA. Massachusetts Gen Hosp, Div Infect Dis, Boston, MA 02114 USA. Harvard Univ, Sch Med, AIDS Res Ctr, Boston, MA 02115 USA. Johns Hopkins Univ, Baltimore, MD USA. Univ Witwatersrand, Perinatal HIV Res Unit, Johannesburg, South Africa. RP Holmes, CB (reprint author), Massachusetts Gen Hosp, Div Gen Med, Dept Med, 50 Staniford St,9th Fl, Boston, MA 02114 USA. EM cbholmes@partners.org OI Walensky, Rochelle P./0000-0002-8795-379X FU NIAID NIH HHS [P30 AI60354, K23 AI01794, P30 AI060354, K23 AI001794, K01 AI062440, K24 AI062476, T32 AI07433]; PHS HHS [CCU/U64 119525] NR 37 TC 7 Z9 7 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 1058-4838 J9 CLIN INFECT DIS JI Clin. Infect. Dis. PD JUN 15 PY 2006 VL 42 IS 12 BP 1772 EP 1780 DI 10.1086/504382 PG 9 WC Immunology; Infectious Diseases; Microbiology SC Immunology; Infectious Diseases; Microbiology GA 043TO UT WOS:000237624800020 PM 16705586 ER PT J AU Zhan, Y Fujino, A MacLaughlin, DT Manganaro, TF Szotek, PP Arango, NA Teixeira, J Donahoe, PK AF Zhan, Y Fujino, A MacLaughlin, DT Manganaro, TF Szotek, PP Arango, NA Teixeira, J Donahoe, PK TI Mullerian inhibiting substance regulates its receptor/SMAD signaling and causes mesenchymal transition of the coelomic epithelial cells early in Mullerian duct regression SO DEVELOPMENT LA English DT Article DE MIS; MIS type 1/ II receptor; SMAD; epithelial-to-mesenchymal transition; RNA interference; organ culture; rat ID NF-KAPPA-B; FEMALE REPRODUCTIVE-TRACT; BETA-CATENIN; II RECEPTOR; OVARIAN-CANCER; DEVELOPMENTAL EXPRESSION; BRANCHING MORPHOGENESIS; TRANSDUCTION PATHWAY; SEXUAL DEVELOPMENT; GENE-EXPRESSION AB Examination of Mullerian inhibiting substance (MIS) signaling in the rat in vivo and in vitro revealed novel developmental stage- and tissue-specific events that contributed to a window of MIS responsiveness in Mullerian duct regression. The MIS type II receptor (MISRII)-expressing cells are initially present in the coelomic epithelium of both male and female urogenital ridges, and then migrate into the mesenchyme surrounding the male Mullerian duct under the influence of MIS. Expression of the genes encoding MIS type I receptors, Alk2 and Alk3, is also spatiotemporally controlled; Alk2 expression appears earlier and increases predominantly in the coelomic epithelium, whereas Alk3 expression appears later and is restricted to the mesenchyme, suggesting sequential roles in Mullerian duct regression. MIS induces expression of Alk2, Alk3 and Smad8, but downregulates Smad5 in the urogenital ridge. Alk2-specific small interfering RNA (siRNA) blocks both the transition of MISRII expression from the coelomic epithelium to the mesenchyme and Mullerian duct regression in organ culture. Mullerian duct regression can also be inhibited or accelerated by siRNA targeting Smad8 and Smad5, respectively. Thus, the early action of MIS is to initiate an epithelial-to-mesenchymal transition of MISRII-expressing cells and to specify the components of the receptor/SMAD signaling pathway by differentially regulating their expression. C1 Massachusetts Gen Hosp, Dept Surg, Pediat Surg Res Labs, Boston, MA 02114 USA. Harvard Univ, Sch Med, Boston, MA 02114 USA. RP Donahoe, PK (reprint author), Massachusetts Gen Hosp, Dept Surg, Pediat Surg Res Labs, Boston, MA 02114 USA. EM donahoe.patricia@mgh.harvard.edu OI Teixeira, Jose/0000-0002-6438-5064 FU NCI NIH HHS [CA-17393]; NICHD NIH HHS [HD-32112] NR 62 TC 48 Z9 49 U1 0 U2 1 PU COMPANY OF BIOLOGISTS LTD PI CAMBRIDGE PA BIDDER BUILDING CAMBRIDGE COMMERCIAL PARK COWLEY RD, CAMBRIDGE CB4 4DL, CAMBS, ENGLAND SN 0950-1991 J9 DEVELOPMENT JI Development PD JUN 15 PY 2006 VL 133 IS 12 BP 2359 EP 2369 DI 10.1242/dev.02383 PG 11 WC Developmental Biology SC Developmental Biology GA 055TY UT WOS:000238474600008 PM 16687449 ER PT J AU Lloret, A Dragileva, E Teed, A Espinola, J Fossale, E Gillis, T Lopez, E Myers, RH MacDonald, ME Wheeler, VC AF Lloret, A Dragileva, E Teed, A Espinola, J Fossale, E Gillis, T Lopez, E Myers, RH MacDonald, ME Wheeler, VC TI Genetic background modifies nuclear mutant huntingtin accumulation and HD CAG repeat instability in Huntington's disease knock-in mice SO HUMAN MOLECULAR GENETICS LA English DT Article ID AGE-OF-ONSET; TRINUCLEOTIDE REPEAT; MOUSE MODEL; SOMATIC MOSAICISM; TRANSGENIC MICE; EARLY MOTOR; EXPANSION; LENGTH; MUTATION; REPAIR AB Genetically precise models of Huntington's disease (HD), Hdh CAG knock-in mice, are powerful systems in which phenotypes associated with expanded HD CAG repeats are studied. To dissect the genetic pathways that underlie such phenotypes, we have generated Hdh(Q111) knock-in mouse lines that are congenic for C57BL/6, FVB/N and 129Sv inbred genetic backgrounds and investigated four Hdh(Q111) phenotypes in these three genetic backgrounds: the intergenerational instability of the HD CAG repeat and the striatal-specific somatic HD CAG repeat expansion, nuclear mutant huntingtin accumulation and intranuclear inclusion formation. Our results reveal increased intergenerational and somatic instability of the HD CAG repeat in C57BL/6 and FVB/N backgrounds compared with the 129Sv background. The accumulation of nuclear mutant huntingtin and the formation of intranuclear inclusions were fastest in the C57BU6 background, slowest in the 129Sv background and intermediate in the FVB/N background. Inbred strain-specific differences were independent of constitutive HD CAG repeat size and did not correlate with Hdh mRNA levels. These data provide evidence for genetic modifiers of both intergenerational HD CAG repeat instability and striatal-specific phenotypes. Different relative contributions of C57BU6 and 129Sv genetic backgrounds to the onset of nuclear mutant huntingtin and somatic HD CAG repeat expansion predict that the initiation of each of these two phenotypes is modified by different genes. Our findings set the stage for defining disease-related genetic pathways that will ultimately provide insight into disease mechanism. C1 Massachusetts Gen Hosp, Ctr Human Genet Res, Mol Neurogenet Unit, Boston, MA 02114 USA. Boston Univ, Sch Med, Dept Neurol, Boston, MA 02118 USA. RP Wheeler, VC (reprint author), Massachusetts Gen Hosp, Ctr Human Genet Res, Mol Neurogenet Unit, 185 Cambridge St, Boston, MA 02114 USA. EM wheeler@helix.mgh.harvard.edu OI Myers, Richard/0000-0002-8365-2674 FU NINDS NIH HHS [NS032765, NS049206, P50NS016367, R01 NS049206] NR 53 TC 49 Z9 49 U1 0 U2 4 PU OXFORD UNIV PRESS PI OXFORD PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND SN 0964-6906 J9 HUM MOL GENET JI Hum. Mol. Genet. PD JUN 15 PY 2006 VL 15 IS 12 BP 2015 EP 2024 DI 10.1093/hmg/ddl125 PG 10 WC Biochemistry & Molecular Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Genetics & Heredity GA 057RW UT WOS:000238613900009 PM 16687439 ER PT J AU Maertens, GN Cherepanov, P Engelman, A AF Maertens, GN Cherepanov, P Engelman, A TI Transcriptional co-activator p75 binds and tethers the Myc-interacting protein JPO2 to chromatin SO JOURNAL OF CELL SCIENCE LA English DT Article DE LEDGF/p75; JPO2; Myc; chromatin tethering; HIV-1; integrase ID HUMAN-IMMUNODEFICIENCY-VIRUS; RETROVIRAL DNA INTEGRATION; ACUTE MYELOID-LEUKEMIA; STRESS-RELATED GENES; HIV-1 INTEGRASE; GROWTH-FACTOR; TYPE-1 INTEGRASE; HUMAN-CELLS; TRANSFORMING ACTIVITY; NUCLEAR-LOCALIZATION AB Transcriptional co-activator p75 is implicated in human cancer, autoimmunity and replication of human immunodeficiency virus type 1 (HIV-1) as a dominant integrase-interacting protein. Although characterized as chromatin associated, the normal biological role(s) of p75 remains fairly unclear. To gain insight into p75 function, we have characterized its cellular binding partners and report that JPO2, a recently identified Myc-binding protein, associates with p75 in vitro and in vivo. The pseudo HEAT repeat analogous topology (PHAT) domain of p75, which mediates its interaction with integrase, also mediates the interaction with JPO2, and recombinant integrase protein competes with JPO2 protein for binding to p75 in vitro. JPO2 binds p75 through a 61-residue (amino acids 58-119) region that is distinct from its Myc-interacting domain. In cells, JPO2 and p75 co-localize throughout the cell cycle, and both proteins concentrate on condensed chromosomes during mitosis. Strikingly, the association of JPO2 with chromatin strictly depends upon p75, similar to that of ectopically expressed integrase. Also similar to its effect on integrase, p75 stabilizes intracellular steady-state levels of JPO2 protein. Our results suggest a role for p75 in the Myc regulatory network, and indicate that p75 is a general adaptor protein tethering divergent factors to chromatin through its versatile integrase-binding domain. C1 Harvard Univ, Sch Med, Dept Canc Immunol & AIDS, Dana Farber Canc Inst, Boston, MA 02115 USA. Harvard Univ, Sch Med, Dept Pathol, Boston, MA 02115 USA. RP Engelman, A (reprint author), Harvard Univ, Sch Med, Dept Canc Immunol & AIDS, Dana Farber Canc Inst, Boston, MA 02115 USA. EM alan_engelman@dfci.harvard.edu RI Cherepanov, Peter/F-6859-2010; Maertens, Goedele/D-8628-2015 OI Cherepanov, Peter/0000-0002-0634-538X; Maertens, Goedele/0000-0002-1963-8026 FU NIAID NIH HHS [AI39394, AI52014, AI60354] NR 54 TC 76 Z9 80 U1 1 U2 2 PU COMPANY OF BIOLOGISTS LTD PI CAMBRIDGE PA BIDDER BUILDING CAMBRIDGE COMMERCIAL PARK COWLEY RD, CAMBRIDGE CB4 4DL, CAMBS, ENGLAND SN 0021-9533 J9 J CELL SCI JI J. Cell Sci. PD JUN 15 PY 2006 VL 119 IS 12 BP 2563 EP 2571 DI 10.1242/jcs.02995 PG 9 WC Cell Biology SC Cell Biology GA 054YC UT WOS:000238413500017 PM 16735438 ER PT J AU Shaw, MH Freeman, GJ Scott, MF Fox, BA Bzik, DJ Belkaid, Y Yap, GS AF Shaw, MH Freeman, GJ Scott, MF Fox, BA Bzik, DJ Belkaid, Y Yap, GS TI Tyk2 negatively regulates adaptive Th1 immunity by mediating IL-10 signaling and promoting IFN-gamma-dependent IL-10 reactivation SO JOURNAL OF IMMUNOLOGY LA English DT Article ID CD4(+) T-CELLS; TOXOPLASMA-GONDII; TYK2-DEFICIENT MICE; INTERFERON-GAMMA; LEISHMANIA-MAJOR; B10.Q/J MICE; ACTIVATED MACROPHAGES; HERITABLE DEFECT; ABSENCE; INTERLEUKIN-10 AB The Jak, Tyk2, is activated in response to IL-12 and IFN-alpha beta and promotes IFN-gamma production by Th1-type CD4 cells. Mice deficient in Tyk2 function have been previously shown to be resistant to autoimmune arthritis and septic shock but are acutely susceptible to opportunistic pathogens such as Toxoplasma gondii. In this study, we show that Tyk2, in addition to mediating the biological effects of IL-12 and IFN-alpha beta, is an important regulator for the signaling and expression of the immunosuppressive cytokine IL-10. In the absence of Tyk2, Ag-reactive CD4 cells exhibit impaired IL-10 synthesis following rechallenge of T. gondii vaccine-primed mice. The impaired IL-10 reactivation leads to unopposed antimicrobial effector mechanisms which results in a paradoxically superior protection of immune Tyk2(-/-) mice against virulent T. gondii challenge. We further demonstrate that Tyk2 indirectly controls CD4 IL-10 reactivation by signaling for maximal IFN-gamma secretion. The unexpected role of IFN-gamma in mediating IL-10 reactivation by Th1 cells provides compelling evidence that conditions driving Th1 responses establish a negative feedback loop, which will ultimately lead to its autoregulation. Thus, Tyk2 can be viewed as a dual-function Jak, mediating both pro and anti-inflammatory cytokine responses. C1 Brown Univ, Dept Mol Microbiol & Immunol, Div Biol & Med, Providence, RI 02912 USA. Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02215 USA. Dartmouth Coll Sch Med, Dept Microbiol & Immunol, Hanover, NH 03756 USA. NIAID, Parasit Dis Lab, NIH, Bethesda, MD 20892 USA. RP Yap, GS (reprint author), Brown Univ, Dept Mol Microbiol & Immunol, Div Biol & Med, Box GB-6, Providence, RI 02912 USA. EM George_Yap@Brown.edu FU NCI NIH HHS [CA84500]; NIAID NIH HHS [R01 AI050618, AI 50618, AI39671, R01 AI041930, R01 AI041930-07, R21 AI052026] NR 35 TC 61 Z9 66 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 JUN 15 PY 2006 VL 176 IS 12 BP 7263 EP 7271 PG 9 WC Immunology SC Immunology GA 050QA UT WOS:000238101800015 PM 16751369 ER PT J AU Medoff, BD Seed, B Jackobek, R Zora, J Yang, Y Luster, AD Xavier, R AF Medoff, BD Seed, B Jackobek, R Zora, J Yang, Y Luster, AD Xavier, R TI CARMA1 is critical for the development of allergic airway inflammation in a murine model of asthma SO JOURNAL OF IMMUNOLOGY LA English DT Article ID NF-KAPPA-B; T-CELL-RECEPTOR; IMMUNE-RESPONSES; ACTIVATION; RECRUITMENT; ANTIGEN; PHOSPHORYLATION; KINASE; CARD11; BCL10 AB CARMA1 has been shown to be important for Ag-stimulated activation of NF-kappa B in lymphocytes in vitro and thus could be a novel therapeutic target in inflammatory diseases such as asthma. In the present study, we demonstrate that mice with deletion in the CARMA1 gene (CARMA1(-/-)) do not develop inflammation in a murine model of asthma. Compared with wild-type controls, CARMA1(-/-) mice did not develop airway eosinophilia, had no significant T cell recruitment into the airways, and had no evidence for T cell activation in the lung or draining lymph nodes. In addition, the CARMA1(-/-) mice had significantly decreased levels of IL-4, IL-5, and IL-13, did not produce IgE, and did not develop airway hyperresponsiveness or mucus cell hypertrophy. However, adoptive transfer of wild-type Th2 cells into CARMA1(-/-) mice restored eosinophilic airway inflammation, cytokine production, airway hyperresponsiveness, and mucus production. This is the first demonstration of an in vivo role for CARMA1 in a disease process. Furthermore, the data clearly show that CARMA1 is essential for the development of allergic airway inflammation through its role in T lymphocytes, and may provide a novel means to inhibit NF-kappa B for therapy in asthma. C1 Massachusetts Gen Hosp, Ctr Computat & Integrat Biol, Boston, MA 02114 USA. Massachusetts Gen Hosp, Gastrointestinal Unit, Boston, MA 02114 USA. Harvard Univ, Sch Med, Boston, MA 02114 USA. Massachusetts Gen Hosp, Ctr Immunol & Inflammatory Dis, Div Rheumatol Allergy & Immunol, Charlestown, MA 02129 USA. Harvard Univ, Sch Med, Charlestown, MA 02129 USA. Massachusetts Gen Hosp, Pulm & Crit Care Unit, Boston, MA 02114 USA. RP Xavier, R (reprint author), Massachusetts Gen Hosp, Ctr Computat & Integrat Biol, Simches Res Bldg,Room 7222,185 Cambridge St, Boston, MA 02114 USA. EM xavier@molbio.mgh.harvard.edu FU NHLBI NIH HHS [K08 HL072775, R01 HL088297]; NIAID NIH HHS [AI27849, AI46731]; NIDDK NIH HHS [DK43351, P30 DK040561-11, P30 DK040561] NR 34 TC 25 Z9 25 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 JUN 15 PY 2006 VL 176 IS 12 BP 7272 EP 7277 PG 6 WC Immunology SC Immunology GA 050QA UT WOS:000238101800016 PM 16751370 ER PT J AU Shimizu, M Shimamura, M Owaki, T Asakawa, M Fujita, K Kudo, M Iwakura, Y Takeda, Y Luster, AD Mizuguchi, J Yoshimoto, T AF Shimizu, M Shimamura, M Owaki, T Asakawa, M Fujita, K Kudo, M Iwakura, Y Takeda, Y Luster, AD Mizuguchi, J Yoshimoto, T TI Antiangiogenic and antitumor activities of IL-27 SO JOURNAL OF IMMUNOLOGY LA English DT Article ID CD4(+) T-CELLS; ANGIOGENESIS IN-VIVO; IFN-GAMMA; INDUCIBLE PROTEIN-10; ENDOTHELIAL-CELLS; INNATE RESISTANCE; ADAPTIVE IMMUNITY; TUMOR-REGRESSION; IL-12 FAMILY; INTERLEUKIN-12 AB IL-27 is a novel IL-6/IL-12 family cytokine playing an important role in the early regulation of Th1 responses. We have recently demonstrated that IL-27 has potent antitumor activity, which is mainly mediated through CD8(+) T cells, against highly immunogenic murine colon carcinoma. In this study, we further evaluated the antitumor and antiangiogenic activities of IL-27, using poorly immunogenic murine melanoma B16F10 tumors, which were engineered to overexpress single-chain IL-27 (B16F10 + IL-27). B16F10 + IL-27 cells exerted antitumor activity against not only s.c. tumor but also experimental pulmonary metastasis. Similar antitumor and antimetastatic activities of IL-27 were also observed in IFN-gamma knockout mice. In NOD-SCID mice, these activities were decreased, but were still fairly well-retained, suggesting that different mechanisms other than the immune response are also involved in the exertion of these activities. Immunohistochemical analyses with Abs against vascular endothelial growth factor and CD31 revealed that B16F10 + IL-27 cells markedly suppressed tumor-induced neovascularization in lung metastases. Moreover, B16F10 + IL-27 cells clearly inhibited angiogenesis by dorsal air sac method, and IL-27 exhibited dose-dependent inhibition of angiogenesis on chick embryo chorioallantoic membrane. IL-27 was revealed to directly act on HUVECs and induce production of the antiangiogenic chemokines, IFN-gamma-inducible protein (IP-10) and monokine induced by IFN-gamma. Finally, augmented mRNA expression of IP-10 and monokine induced by IFN-gamma was detected at the s.c. B16F10 + IL-27 tumor site, and antitumor activity of IL-27 was partially inhibited by the administration of anti-IP-10. These results suggest that IL-27 possesses potent antiangiogenic activity, which plays an important role in its antitumor and antimetastatic activities. C1 Tokyo Med Univ, Intractable Immune Syst Dis Res Ctr, Shinjuku Ku, Tokyo 1608402, Japan. Tokyo Med Univ, Dept Pathol, Shinjuku Ku, Tokyo 1608402, Japan. Tokyo Med Univ, Dept Immunol, Shinjuku Ku, Tokyo 1608402, Japan. Tokyo Metropolitan Inst Med Sci, Med R&D Ctr, Tokyo Metropolitan Org Med Res, Bunkyo Ku, Tokyo, Japan. Tokyo Univ Sci, Fac Pharmaceut Sci, Noda, Chiba 278, Japan. Univ Tokyo, Inst Med Sci, Ctr Med Expt, Minato Ku, Tokyo, Japan. Japan Anti TB Assoc, Breast Surg Oncol Ctr, Double Barres Cross Hosp, Tokyo, Japan. Harvard Univ, Massachusetts Gen Hosp, Sch Med, Ctr Immunol & Inflammatory Dis,Div Rheumatol Alle, Charlestown, MA 02129 USA. RP Yoshimoto, T (reprint author), Tokyo Med Univ, Intractable Immune Syst Dis Res Ctr, Shinjuku Ku, 6-1-1 Shinjuku, Tokyo 1608402, Japan. EM yoshimot@tokyo-med.ac.jp RI Iwakura, Yoichiro/E-5457-2011 OI Iwakura, Yoichiro/0000-0002-9934-5775 NR 47 TC 107 Z9 123 U1 1 U2 4 PU AMER ASSOC IMMUNOLOGISTS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA SN 0022-1767 J9 J IMMUNOL JI J. Immunol. PD JUN 15 PY 2006 VL 176 IS 12 BP 7317 EP 7324 PG 8 WC Immunology SC Immunology GA 050QA UT WOS:000238101800021 PM 16751375 ER PT J AU Shen, KZ Johnson, SW AF Shen, Ke-Zhong Johnson, Steven W. TI Subthalamic stimulation evokes complex EPSCs in the rat substantia nigra pars reticulata in vitro SO JOURNAL OF PHYSIOLOGY-LONDON LA English DT Article ID BASAL GANGLIA CIRCUITRY; GABAERGIC INHIBITION; MICROSCOPIC ANALYSIS; PARKINSONS-DISEASE; NEURONS; NUCLEUS; TRANSMISSION; RESPONSES; LESIONS; RECEPTORS AB The subthalamic nucleus (STN) plays an important role in movement control by exerting its excitatory influence on the substantia nigra pars reticulata (SNR), a major output structure of the basal ganglia. Moreover, excessive burst firing of SNR neurons seen in Parkinson's disease has been attributed to excessive transmission in the subthalamonigral pathway. Using the 'blind' whole-cell patch clamp recording technique in rat brain slices, we found that focal electrical stimulation of the STN evoked complex, long-duration excitatory postsynaptic currents (EPSCs) in SNR neurons. Complex EPSCs lasted 200-500 ms and consisted of an initial monosynaptic EPSC followed by a series of late EPSCs superimposed on a slow inward shift in holding current. Focal stimulation of regions outside the STN failed to evoke complex EPSCs. The late component of complex EPSCs was markedly reduced by ionotropic glutamate receptor antagonists (2-amino-5-phosphonopentanoic acid and 6-cyano-7-nitro-quinoxalone) and by a GABA(A) receptor agonist (isoguvacine) when these agents were applied directly to the STN using a fast-flow microapplicator. Moreover, the complex EPSC was greatly enhanced by bath application of the GABAA receptor antagonists picrotoxin or bicuculline. These data suggest that recurrent glutamate synapses in the STN generate polysynaptic, complex EPSCs that are under tonic inhibition by GABA. Because complex EPSCs are expected to generate bursts of action potentials in SNR neurons, we suggest that complex EPSCs may contribute to the pathological burst firing that is associated with the symptoms of Parkinson's disease. C1 Portland VA Med Ctr, R&D 61, Portland, OR 97207 USA. Oregon Hlth & Sci Univ, Dept Neurol, Portland, OR 97239 USA. RP Johnson, SW (reprint author), Portland VA Med Ctr, R&D 61, 3710 SW US Vet Hosp Rd, Portland, OR 97207 USA. EM johnsost@ohsu.edu FU NINDS NIH HHS [NS 38175, R01 NS038175] NR 46 TC 25 Z9 25 U1 0 U2 4 PU BLACKWELL PUBLISHING PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DQ, OXON, ENGLAND SN 0022-3751 J9 J PHYSIOL-LONDON JI J. Physiol.-London PD JUN 15 PY 2006 VL 573 IS 3 BP 697 EP 709 DI 10.1113/jphysiol.2006.110031 PG 13 WC Neurosciences; Physiology SC Neurosciences & Neurology; Physiology GA 065IU UT WOS:000239154200008 PM 16613871 ER PT J AU Mizumori, M Meyerowitz, J Takeuchi, T Lim, S Lee, P Supuran, CT Guth, PH Engel, E Kaunitz, JD Akiba, Y AF Mizumori, Misa Meyerowitz, Justin Takeuchi, Tetsu Lim, Shu Lee, Paul Supuran, Claudiu T. Guth, Paul H. Engel, Eli Kaunitz, Jonathan D. Akiba, Yasutada TI Epithelial carbonic anhydrases facilitate P-CO2 and pH regulation in rat duodenal mucosa SO JOURNAL OF PHYSIOLOGY-LONDON LA English DT Article ID ZOLLINGER-ELLISON SYNDROME; APICAL CL-/HCO3-EXCHANGER; NA+/H+ EXCHANGER; BICARBONATE SECRETION; ACID LOSS; INTRACELLULAR PH; HCO3-SECRETION; ISOZYME-IX; GASTROINTESTINAL-TRACT; ALKALINE SECRETION AB The duodenum is the site of mixing of massive amounts of gastric H+ with secreted HCO3-, generating CO2 and H2O accompanied by the neutralization of H+. We examined the role of membrane-bound and soluble carbonic anhydrases (CA) by which H+ is neutralized, CO2 is absorbed, and HCO3- is secreted. Rat duodena were perfused with solutions of different pH and P-CO2 with or without a cell-permeant CA inhibitor methazolamide (MTZ) or impermeant CA inhibitors. Flow-through pH and P-CO2 electrodes simultaneously measured perfusate and effluent pH and P-CO2. High CO2 (34.7 kPa) perfusion increased net CO2 loss from the perfusate compared with controls (pH 6.4 saline, P-CO2 approximate to 0) accompanied by portal venous (PV) acidification and P-CO2 increase. Impermeant CA inhibitors abolished net perfusate CO2 loss and increased net HCO3- gain, whereas all CA inhibitors inhibited PV acidification and PCO2 increase. The changes in luminal and PV pH and [CO2] were also inhibited by the Na+-H+ exchanger-1 (NHE1) inhibitor dimethylamiloride, but not by the NHE3 inhibitor S3226. Luminal acid decreased total CO2 output and increased H+ loss with PV acidification and P-CO2 increase, all inhibited by all CA inhibitors. During perfusion of a 30% CO2 buffer, loss Of CO2 from the lumen was CA dependent as was transepithelial transport of perfused (CO2)-C-13. H+ and CO2 loss from the perfusate were accompanied by increases of PV H+ and tracer CO2, but unchanged PV total CO2, consistent with CA-dependent transmucosal. H+ and CO2 movement. Inhibition of membrane-bound CAs augments the apparent rate of net basal HCO3- secretion. Luminal H+ traverses the apical membrane as CO2, is converted back to cytosolic H+, which is extruded via NHE1. Membrane-bound and cytosolic CAs cooperatively facilitate secretion of HCO3 into the lumen and CO2 diffusion into duodenal mucosa, serving as important acid-base regulators. C1 Univ Calif Los Angeles, Greater Los Angeles Vet Affairs Healthcare Syst, Los Angeles, CA USA. Univ Calif Los Angeles, Sch Med, Dept Med, Los Angeles, CA 90024 USA. Univ Calif Los Angeles, Sch Med, Dept Biomath, Los Angeles, CA 90024 USA. Brentwood Biomed Res Inst, Los Angeles, CA 90073 USA. Harvard Westlake Sch, Los Angeles, CA 90073 USA. Harbor UCLA Med Ctr, Stable Isotope Facil, Torrance, CA 90509 USA. Univ Florence, Dipartimento Chim, Lab Chim Bioinorgan, Florence, Italy. RP Kaunitz, JD (reprint author), W Los Angeles VA Med Ctr, Bldg 114,Suite 217,11301 Wilshire Blvd, Los Angeles, CA 90073 USA. EM jake@ucla.edu RI Supuran, Claudiu/A-5151-2008; OI Meyerowitz, Justin/0000-0001-7194-8286 FU BLRD VA [I01 BX001245]; NIDDK NIH HHS [P30 DK0413, R01 DK054221, R01 DK54221] NR 59 TC 37 Z9 40 U1 0 U2 1 PU BLACKWELL PUBLISHING PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DQ, OXON, ENGLAND SN 0022-3751 J9 J PHYSIOL-LONDON JI J. Physiol.-London PD JUN 15 PY 2006 VL 573 IS 3 BP 827 EP 842 DI 10.1113/jphysiol.2006.107581 PG 16 WC Neurosciences; Physiology SC Neurosciences & Neurology; Physiology GA 065IU UT WOS:000239154200018 PM 16556652 ER PT J AU Roostaeian, J Carlsen, B Simhaee, D Jarrahy, R Huang, WB Ishida, K Rudkin, GH Yamaguchi, DT Miller, TA AF Roostaeian, J Carlsen, B Simhaee, D Jarrahy, R Huang, WB Ishida, K Rudkin, GH Yamaguchi, DT Miller, TA TI Characterization of growth and osteogenic differentiation of rabbit bone marrow stromal cells SO JOURNAL OF SURGICAL RESEARCH LA English DT Article DE rabbit; bone marrow stromal cells; growth; differentiation; BNW; TGF-beta; osteogenesis; tissue engineering ID MESENCHYMAL STEM-CELLS; FACTOR-BETA; OSTEOBLASTIC CELLS; GENE-EXPRESSION; IN-VITRO; TISSUE; REGENERATION; OSTEOPONTIN; DEFECTS; PROLIFERATION AB Background. The rabbit is recognized as an excellent model to study the repair of bony defects with tissue engineered constructs. However, the use of rabbit bone marrow stromal. cells (RBMSCs) has been limited despite the proven benefits of autologous BMSCs in the formation of bone. The purpose of this study was to characterize the growth and differentiation pattern of RBMSCs and their response to growth factors. Material and methods. BMSCs were isolated from New Zealand White rabbits and cultured. Serial cell counts of parallel cultures were taken daily to determine cell growth. Response of RBMSCs to varying doses of recombinant human BMP-2 (rhBMP-2) and their time course was gauged by alkaline phosphatase (ALP) activity. The osteoblastic differentiation potential of RBMSCs in response to rhBMP-2 treatment was determined by evaluating the expression pattern of various genes involved with osteogensis using northern analysis. Von Kossa staining was performed to determine the effect of rhBMP-2 on the mineralization capabilities of RBMSCs. Results. The growth rate of RBMSCs severely declined after first passage and this rate was further suppressed by TGF-ss 1. The optimal dose response of rhBMP-2 was determined to be 50 ng/ml and its time course displayed increasing alkaline phosphatase activity over time. Two osteogenic markers, collagen I and osteopontin, were up regulated by rhBMP-2 treatment. Finally, the mineralization capability of RBMSCs was determined to be enhanced by rhBMP-2 treatment. Conclusion. Our work indicates that RBMSCs possess strong osteogenic potential and can be successfully applied toward bone tissue engineering in a rabbit model. (c) 2006 Elsevier Inc. All rights reserved. C1 VA Greater LA Healthcare Syst, Plast Surg Lab, Plast Surg Sect, Los Angeles, CA 90073 USA. Univ Calif Los Angeles, Dept Surg, Div Plast Surg, Los Angeles, CA USA. RP Miller, TA (reprint author), VA Greater LA Healthcare Syst, Plast Surg Lab, Plast Surg Sect, Room 221,Bldg 114,11301 Whilshire Blvd, Los Angeles, CA 90073 USA. EM millerlab@hotmail.com NR 53 TC 19 Z9 23 U1 3 U2 10 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 JUN 15 PY 2006 VL 133 IS 2 BP 76 EP 83 DI 10.1016/j.jss.2005.09.026 PG 8 WC Surgery SC Surgery GA 052OM UT WOS:000238243000003 PM 16360178 ER EF