FN Thomson Reuters Web of Science™ VR 1.0 PT J AU Compas, BE Beckjord, E Agocha, B Sherman, ML Langrock, A Grossman, CI Dausch, B Glinder, J Kaiser, C Anderson-Hanley, C Luecken, L AF Compas, Bruce E. Beckjord, Ellen Agocha, Bede Sherman, Marne L. Langrock, Adela Grossman, Cynthia I. Dausch, Barbara Glinder, Judith Kaiser, Cheryl Anderson-Hanley, Cay Luecken, Linda TI Measurement of coping and stress responses in women with breast cancer SO PSYCHO-ONCOLOGY LA English DT Article DE coping; breast cancer; measurement; cancer; oncology ID PSYCHOLOGICAL ADJUSTMENT; EMOTIONAL DISTRESS; PSYCHOMETRIC PROPERTIES; SECONDARY CONTROL; FIT; ADOLESCENCE; HYPOTHESIS; STRATEGIES; PATTERNS; GOODNESS AB The development of the Responses to Stress Questionnaire-cancer version (RSQ-CV) to assess coping with and responses to the stress of breast cancer is described. The RSQ-CV was completed by 232 women with breast cancer near the time of their diagnosis. Confirmatory factor analyses verified a model that includes three voluntary coping factors (primary control engagement coping, secondary control engagement coping, disengagement coping) and two involuntary stress response factors (involuntary engagement, involuntary disengagement). Internal consistency reliability, and stability over 12 weeks for the five factors were adequate to excellent. Convergent and discriminant validity was examined through correlations with measures of intrusive thoughts, avoidance, and dimensions of perceived control. Significant correlations with symptoms of anxiety and depression are also reported. Applications of the RSQ-CV for research with breast cancer patients are discussed. Copyright (C) 2006 John Wiley & Sons, Ltd. C1 Vanderbilt Univ, Dept Psychol & Human Dev, Nashville, TN 37203 USA. NCI, Canc Prevent Fellowship Program, Div Canc Prevent, NIH, Bethesda, MD 20892 USA. Univ Connecticut, Storrs, CT 06269 USA. Univ Missouri, Kansas City, MO 64110 USA. Middlebury Coll, Middlebury, VT 05753 USA. Univ Vermont, Burlington, VT 05405 USA. Glen Falls Hosp, Canc Ctr Res Off, Glens Falls, NY USA. Arizona State Univ, Tempe, AZ 85287 USA. RP Compas, BE (reprint author), Vanderbilt Univ, Dept Psychol & Human Dev, Peabody 512,230 Appleton Pl, Nashville, TN 37203 USA. EM bruce.compas@vanderbilt.edu RI Luecken, Linda/K-6891-2013 FU NCI NIH HHS [R01CA67936] NR 50 TC 22 Z9 22 U1 0 U2 5 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 DEC PY 2006 VL 15 IS 12 BP 1038 EP 1054 DI 10.1002/pon.999 PG 17 WC Oncology; Psychology; Psychology, Multidisciplinary; Social Sciences, Biomedical SC Oncology; Psychology; Biomedical Social Sciences GA 126VL UT WOS:000243543500002 PM 17009343 ER PT J AU Hasin, DS Liu, XH Alderson, D Grant, BF AF Hasin, Deborah S. Liu, Xinhua Alderson, Donald Grant, Bridget F. TI DSM-IV alcohol dependence: a categorical or dimensional phenotype? SO PSYCHOLOGICAL MEDICINE LA English DT Article ID INTERVIEW SCHEDULE AUDADIS; JUVENILE MYOCLONIC EPILEPSY; GENERAL-POPULATION SAMPLE; SUBSTANCE USE DISORDERS; DRUG MODULES; MAJOR DEPRESSION; RELIABILITY; ABUSE; ASSOCIATION; DIAGNOSES AB Background. Etiologic research on complex disorders including alcohol dependence requires informative phenotypes. Information is lost when categorical variables represent inherently dimensional conditions. We investigated the validity of DSM-IV alcohol dependence Lis a dimensional phenotype by examining evidence for linearity and thresholds in associations with validating variables. Method. Current drinkers in the National Longitudinal Alcohol Epidemiologic Survey (NLAES) (n = 18 352) and National Epidemiologic Survey of Alcohol and Related Conditions (NESA RC) (n=20836) were analyzed. Validating variables included family alcoholism, early-onset drinking, and alcohol treatment. Logistic or Poisson regression modeled the relationships between the validating variables and dependence in categorical, dimensional or hybrid forms, with severity defined as number Of Current DSM-IV alcohol-dependence criteria. Wald tests assessed differences between models. Results. No evidence was found for boundaries between categories. Instead, the association of alcohol dependence with the validating variables generally increased in linear fashion as the number of alcohol-dependence criteria increased. For NLAES models of family alcoholism, early-onset drinking and treatment, the lines had zero intercepts, with slopes of 0-18, 0-27, 0-70, respectively. For NESARC models of family history and early-onset drinking, the zero intercept lines had slopes of 0(.)20, 0(.)33, and 0(.)77, respectively. Wald tests indicated that models representing alcohol dependence as a dimensional linear predictor best described the association between dependence criteria and the validating variables. Conclusions. The sample sizes allowed strong tests. Diagnoses are necessary for clinical decision-making, but a dimensional alcohol-dependence indicator Should provide more information for research purposes. C1 NIAAA, Div Intramural Clin & Biol Res, Lab Epidemiol & Biometry, NIH, Bethesda, MD 20892 USA. Columbia Univ, Mialman Sch Publ Hlth, Dept Epidemiol, New York, NY 10027 USA. Columbia Univ, Coll Phys & Surg, Dept Psychiat, New York, NY 10027 USA. New York State Psychiat Inst & Hosp, New York, NY 10032 USA. Columbia Univ, Mailman Sch Publ Hlth, Dept Biostat, New York, NY 10027 USA. RP Grant, BF (reprint author), NIAAA, Div Intramural Clin & Biol Res, Lab Epidemiol & Biometry, NIH, MS 9304,5635 Fishers Lane, Bethesda, MD 20892 USA. EM bgrant@willco.niaaa.nih.gov FU Intramural NIH HHS; NIAAA NIH HHS [AA K05 AA014223, R01AA8159] NR 37 TC 39 Z9 39 U1 2 U2 3 PU CAMBRIDGE UNIV PRESS PI NEW YORK PA 32 AVENUE OF THE AMERICAS, NEW YORK, NY 10013-2473 USA SN 0033-2917 J9 PSYCHOL MED JI Psychol. Med. PD DEC PY 2006 VL 36 IS 12 BP 1695 EP 1705 DI 10.1017/S0033291706009068 PG 11 WC Psychology, Clinical; Psychiatry; Psychology SC Psychology; Psychiatry GA 129XU UT WOS:000243764200005 PM 17038207 ER PT J AU Rogers, J Viding, E Blair, RJ Frith, U Happe, F AF Rogers, John Viding, Essi Blair, R. James Frith, Uta Happe, Francesca TI Autism spectrum disorder and psychopathy: shared cognitive underpinnings or double hit? SO PSYCHOLOGICAL MEDICINE LA English DT Article ID ASPERGERS SYNDROME; EXECUTIVE DYSFUNCTION; CHILDREN; RESPONSES; VIOLENCE; OTHERS; QUESTIONNAIRE; IMPAIRMENT; TENDENCIES; CHILDHOOD AB Background. We measured psychopathic traits in boys with autism spectrum disorder (ASD) selected for difficult and aggressive behaviour. We asked (1) whether psychopathic tendencies can be measured in ASD independent of the severity of autistic behaviour; (ii) whether individuals with ASD with callous-unemotional (CU) traits differ in their cognitive profile from those without such traits; and (iii) how the cognitive data from this study compare with previous data of Youngsters with psychopathic tendencies. Method. Twenty-eight ASD boys were rated on psychopathic tendencies, autistic traits and a range of cognitive measures assessing mentalizing ability, executive functions, emotion recognition and ability to make moral-conventional distinction. Results. Our results indicate that psychopathic tendencies are not related to severity of ASD. In addition., such tendencies do not seem to be related to core autistic cognitive deficits, specifically in 'mind-reading' or executive function. Boys with co-occurring ASD and CU tendencies share some behaviours and aspects of cognitive profile with boys who have psychopathic tendencies alone. Conclusions. Callous/psychopathic acts in a small number of individuals with ASD probably reflect a 'double hit' involving an additional impairment of empathic response to distress Cues, which is not part and parcel of ASD itself. C1 UCL, Dept Psychol, London WC1E 6BT, England. Kings Coll London, Inst Psychiat, London WC2R 2LS, England. NIMH, Mood & Anxiety Disorders Program, Bethesda, MD 20892 USA. RP Viding, E (reprint author), UCL, Dept Psychol, Gower St, London WC1E 6BT, England. EM e.viding@ucl.ac.uk RI Frith, Uta/C-1757-2008; Happe, Francesca/D-5544-2012; OI Frith, Uta/0000-0002-9063-4466; Happe, Francesca/0000-0001-9226-4000 FU Medical Research Council [G9617036] NR 44 TC 56 Z9 57 U1 4 U2 22 PU CAMBRIDGE UNIV PRESS PI NEW YORK PA 32 AVENUE OF THE AMERICAS, NEW YORK, NY 10013-2473 USA SN 0033-2917 J9 PSYCHOL MED JI Psychol. Med. PD DEC PY 2006 VL 36 IS 12 BP 1789 EP 1798 DI 10.1017/S0033291706008853 PG 10 WC Psychology, Clinical; Psychiatry; Psychology SC Psychology; Psychiatry GA 129XU UT WOS:000243764200014 PM 17018169 ER PT J AU Sperling, AJ Lu, ZL Manis, FR Seidenberg, MS AF Sperling, Anne J. Lu, Zhong-Lin Manis, Franklin R. Seidenberg, Mark S. TI Motion-perception deficits and reading impairment: It's the noise, not the motion SO PSYCHOLOGICAL SCIENCE LA English DT Article ID SPEECH-PERCEPTION; VISUAL PATHWAYS; DYSLEXIA; SENSITIVITY; ATTENTION; SKILLS AB We tested the hypothesis that deficits on sensory-processing tasks frequently associated with poor reading and dyslexia are the result of impairments in external-noise exclusion, rather than motion perception or magnocellular processing. We compared the motion-direction discrimination thresholds of adults and children with good or poor reading performance, using coherent-motion displays embedded in external noise. Both adults and children who were poor readers had higher thresholds than their respective peers in the presence of high external noise, but not in the presence of low external noise or when the signal was clearly demarcated. Adults' performance in high external noise correlated with their general reading ability, whereas children's performance correlated with their language and verbal abilities. The results support the hypothesis that noise-exclusion deficits impair reading and language development and suggest that the impact of such deficits on the development of reading skills changes with age. C1 Georgetown Univ, Med Ctr, Madison, WI USA. Univ So Calif, Madison, WI USA. Univ Wisconsin, Madison, WI USA. RP Sperling, AJ (reprint author), NIMH, Off Sci Policy Planning & Commun, 6001 Execut Blvd, Bethesda, MD 20892 USA. EM sperlinga@mail.nih.gov FU NICHD NIH HHS [HD29891] NR 34 TC 61 Z9 62 U1 4 U2 12 PU BLACKWELL PUBLISHING PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DQ, OXON, ENGLAND SN 0956-7976 J9 PSYCHOL SCI JI Psychol. Sci. PD DEC PY 2006 VL 17 IS 12 BP 1047 EP 1053 DI 10.1111/j.1467-9280.2006.01825.x PG 7 WC Psychology, Multidisciplinary SC Psychology GA 117IL UT WOS:000242866500008 PM 17201786 ER PT J AU Sabino, V Cottone, P Koob, GF Steardo, L Lee, MJ Rice, KC Zorrilla, EP AF Sabino, Valentina Cottone, Pietro Koob, George F. Steardo, Luca Lee, Mei J. Rice, Kenner C. Zorrilla, Eric P. TI Dissociation between opioid and CRF1 antagonist sensitive drinking in Sardinian alcohol-preferring rats SO PSYCHOPHARMACOLOGY LA English DT Article DE Sardinian alcohol-preferring or sP rat; ethanol or alcohol intake; genetic or selectively bred animal model; anxiety or stress; Corticotropin-releasing factor or Corticotropin-releasing hormone or CRF or CRH; CRF1 receptor antagonist or CRH1 receptor antagonist; opioids; naltrexone; withdrawal or abstinence; dependence ID CORTICOTROPIN-RELEASING-FACTOR; ANXIETY-LIKE BEHAVIOR; HORMONE-RECEPTOR 1; ETHANOL WITHDRAWAL; ENDOCRINE RESPONSES; LOCOMOTOR-ACTIVITY; ANIMAL-MODEL; DEPENDENCE; NALTREXONE; STRESS AB Rationale The role of positive vs negative ethanol reinforcement in ethanol intake of Sardinian alcohol-preferring (sP) rats is unclear. Objectives To test the hypothesis that spontaneous ethanol self-administration of sP rats was sensitive to the opioid receptor antagonist naltrexone, whereas withdrawal-induced, but not spontaneous, ethanol self-administration would be sensitive to corticotropin-releasing factor(1) (CRF1) antagonists, implicating differential roles for positive and negative reinforcement, respectively. Methods Male sP rats operantly (FR1, 30 min/day) self-administered ethanol (10% v/v) until responding stabilized. One group (n=11) was made ethanol dependent through intermittent ethanol vapor exposure. Both nondependent (n=10) and dependent rats received the CRF1 antagonist LWH-63 (5, 10, and 20 mg/kg, s.c.). Separate nondependent sP rats (n=10) received the opioid antagonist naltrexone (16, 50, 150, and 450 mu g/kg, s.c.). Finally, CRF1 antagonists (MJL-1-109-2, LWH-63, and R121919) were studied for their actions on home-cage ethanol drinking in nondependent sP rats (n=6-8/group) under continuous, limited-access, or stressed conditions. Results Naltrexone potently reduced ethanol self-administration in nondependent sP rats. LWH-63 reduced heightened ethanol self-administration of vapor-sensitive, dependent sP rats. CRF1 antagonists did not reduce ethanol intake in nondependent sP rats. R121919 (10 mg/kg, s.c.) retained antistress activity in sP rats, blunting novelty stress-induced suppression of ethanol intake. Conclusions Spontaneous ethanol self-administration of sP rats was opioid dependent with CRF1 receptors implicated in withdrawal-induced drinking. Opioid and CRF1 receptors play different roles in ethanol reinforcement and perhaps the ethanol addiction cycle. Such distinctions may apply to subtypes of alcoholic patients who differ in their motivation to drink and ultimately treatment response. C1 Scripps Res Inst, Mol & Integrat Neurosci Dept, La Jolla, CA 92037 USA. Univ Roma La Sapienza, Dept Human Physiol & Pharmacol, I-00185 Rome, Italy. NIDDKD, Med Chem Lab, Bethesda, MD 20892 USA. Scripps Res Inst, Harold L Dorris Neurol Res Inst, La Jolla, CA 92037 USA. RP Sabino, V (reprint author), Scripps Res Inst, Mol & Integrat Neurosci Dept, SP30-2400,10550 N Torrey Pines Rd, La Jolla, CA 92037 USA. EM vsabino@scripps.edu; ezorrilla@scripps.edu RI Cottone, Pietro/F-5291-2012; Sabino, Valentina/F-5290-2012; koob, george/P-8791-2016; OI Cottone, Pietro/0000-0003-1320-1672; Sabino, Valentina/0000-0002-6680-1279; Steardo, Luca/0000-0003-3570-2195 FU NIAAA NIH HHS [P60AA000642-21] NR 54 TC 57 Z9 57 U1 0 U2 0 PU SPRINGER PI NEW YORK PA 233 SPRING STREET, NEW YORK, NY 10013 USA SN 0033-3158 J9 PSYCHOPHARMACOLOGY JI Psychopharmacology PD DEC PY 2006 VL 189 IS 2 BP 175 EP 186 DI 10.1007/s00213-006-0546-5 PG 12 WC Neurosciences; Pharmacology & Pharmacy; Psychiatry SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry GA 102FV UT WOS:000241797300005 PM 17047935 ER PT J AU Roma, PG Flint, WW Higley, JD Riley, AL AF Roma, Peter G. Flint, Wesley W. Higley, J. Dee Riley, Anthony L. TI Assessment of the aversive and rewarding effects of alcohol in Fischer and Lewis rats SO PSYCHOPHARMACOLOGY LA English DT Article DE Fischer; Lewis; alcohol; conditioned taste aversion; conditioned place preference; blood alcohol; hypothermia; ethanol; strain differences; behavioral genetics ID CONDITIONED TASTE-AVERSION; PLACE PREFERENCE; STRAIN DIFFERENCES; LOCOMOTOR-ACTIVITY; APPARATUS BIAS; ETHANOL; MORPHINE; BEHAVIOR; COCAINE; DRINKING AB Rationale Application of the Fischer-Lewis genetic model of drug abuse to the study of alcohol's motivational properties has been limited. Objectives To assess the aversive and rewarding effects of ethanol in Fischer and Lewis rats. Materials and methods Fischer and Lewis rats underwent a four-trial combined conditioned taste aversion/conditioned place preference procedure (CTA/CPP; 0, 1, 1.25, or 1.5 g/kg IP ethanol). Others received 0, 1, or 1.5 g/kg followed by tail blood sampling at 15-, 60- and 180-min post-injection. In additional groups, hypothermia to 0, 1.5, and 3 g/kg was assessed before and 30- and 60-min post-injection. Results All alcohol-treated groups except low-dose Lewis acquired CTA after one trial. Fischer rats developed stronger CTAs than Lewis at 1.25 and 1.5 g/kg. Ethanol-induced reward in taste or place conditioning was not evident in either strain. Lewis animals showed overall higher peak blood alcohol concentrations, but hypothermia did not vary by strain. Conclusion Compared to Fischer, Lewis rats are less sensitive to alcohol's aversive effects as assessed in the CTA paradigm. The behavioral differences observed are not due to hypothermia, but pharmacokinetic differences may contribute. These data underscore the importance of genetic factors and the aversive effects of initial drug exposures in modeling vulnerability to abuse. In addition to its application with other drugs, the Fischer-Lewis model may be useful for investigating the biobehavioral bases of alcohol abuse. C1 American Univ, Psychopharmacol Lab, Dept Psychol, Washington, DC 20016 USA. NIAAA, Lab Clin & Translat Studies, Sect Primate Studies, Poolesville, MD 20837 USA. RP Roma, PG (reprint author), American Univ, Psychopharmacol Lab, Dept Psychol, 4400 Massachusetts Ave NW, Washington, DC 20016 USA. EM PeteRoma@gmail.com FU Intramural NIH HHS NR 66 TC 38 Z9 39 U1 1 U2 1 PU SPRINGER PI NEW YORK PA 233 SPRING STREET, NEW YORK, NY 10013 USA SN 0033-3158 J9 PSYCHOPHARMACOLOGY JI Psychopharmacology PD DEC PY 2006 VL 189 IS 2 BP 187 EP 199 DI 10.1007/s00213-006-0553-6 PG 13 WC Neurosciences; Pharmacology & Pharmacy; Psychiatry SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry GA 102FV UT WOS:000241797300006 PM 17013639 ER PT J AU Grakalic, I Schindler, CW Baumann, MH Rice, KC Riley, AL AF Grakalic, Ivana Schindler, Charles W. Baumann, Michael H. Rice, Kenner C. Riley, Anthony L. TI Effects of stress modulation on morphine-induced conditioned place preferences and plasma corticosterone levels in Fischer, Lewis, and Sprague-Dawley rat strains SO PSYCHOPHARMACOLOGY LA English DT Article DE stress; F344; LEW; morphine; conditioned place preference; methyl-6; 7-dimethoxy-4-ethyl-beta-carboline-3-carboxylate; antalarmin; corticosterone ID CORTICOTROPIN-RELEASING-FACTOR; CRH RECEPTOR ANTAGONIST; INDUCED RELAPSE; BEHAVIORAL SENSITIZATION; PERIPHERAL INFLAMMATION; INDUCED REINSTATEMENT; LOCOMOTOR-ACTIVITY; OPIATE WITHDRAWAL; D-2 RECEPTORS; DOPAMINE D-1 AB Rationale There is a direct relationship between hypothalamic-pituitary-adrenal axis (HPA) reactivity and susceptibility to drug use in outbred rats. Specifically, manipulations that increase or decrease HPA activity also increase or decrease drug intake, respectively. Interestingly, this relationship has not been established in the inbred Fischer (F344) and Lewis (LEW) rat strains that are often used as animal models of susceptibility to drug use. Objective The present study investigated the effects of manipulations known to affect HPA activity on morphine-induced conditioned place preference (CPP) in male LEW, F344, and Sprague-Dawley (SD) rats. Materials and methods In experiment 1, animals were exposed to an injection of methyl-6,7-dimethoxy-4-ethyl-beta-carboline-3-carboxylate (DMCM) and 2-h restraint stress prior to the conditioning of a morphine-induced place preference (1, 4, or 10 mg/kg subcutaneous). In experiment 2, animals were chronically exposed to corticotropin-releasing hormone type 1 receptor antagonist, antalarmin, prior to CPP training. The effects of DMCM/restraint and antalarmin on corticosterone levels were examined in experiments 3 and 4. Results In outbred rats, DMCM/restraint increased both HPA activity and morphine-induced CPP, while antalarmin decreased CPP and produced a slight, but nonsignificant, decrease in corticosterone levels. In the inbred rats, however, DMCM/restraint increased plasma corticosterone yet decreased place preferences in the LEW strain, and antalarmin treatment decreased plasma corticosterone but increased place preferences in the F344 strain. Conclusions These data suggest that the relationship between stress and drug use may be nonmonotonic. The use of these inbred strains in genetic analysis of drug addiction may require reexamination. C1 NIDA, Preclin Pharmacol Sect, Behav Neurol Branch, DHSS,NIH,Intramural Res Program, Baltimore, MD 21224 USA. NIDDKD, DHHD, NIH, Bethesda, MD 20892 USA. NIDA, Clin Psychopharmacol Sect, DHHS, NIH,Intramural Res Program, Baltimore, MD 21224 USA. American Univ, Washington, DC 20016 USA. RP Grakalic, I (reprint author), NIDA, Preclin Pharmacol Sect, Behav Neurol Branch, DHSS,NIH,Intramural Res Program, 5500 Nathan Shock Dr, Baltimore, MD 21224 USA. EM igrakalic@intra.nida.nih.gov FU Intramural NIH HHS NR 49 TC 27 Z9 27 U1 0 U2 1 PU SPRINGER PI NEW YORK PA 233 SPRING STREET, NEW YORK, NY 10013 USA SN 0033-3158 J9 PSYCHOPHARMACOLOGY JI Psychopharmacology PD DEC PY 2006 VL 189 IS 3 BP 277 EP 286 DI 10.1007/s00213-006-0562-5 PG 10 WC Neurosciences; Pharmacology & Pharmacy; Psychiatry SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry GA 107DP UT WOS:000242151200002 PM 17016707 ER PT J AU Marsh, AA Finger, EC Buzas, B Soliman, N Richell, RA Vythilingham, M Pine, DS Goldman, D Blair, RJR AF Marsh, Abigail A. Finger, Elizabeth C. Buzas, Beata Soliman, Niveen Richell, Rebecca A. Vythilingham, Meena Pine, Daniel S. Goldman, David Blair, R. J. R. TI Impaired recognition of fear facial expressions in 5-HTTLPR S-polymorphism carriers following tryptophan depletion SO PSYCHOPHARMACOLOGY LA English DT Article DE tryptophan depletion; fear; serotonin; 5-HTTLPR; amygdala ID SEROTONIN TRANSPORTER GENE; HUMAN AMYGDALA; FUNCTIONAL POLYMORPHISM; SELECTIVE IMPAIRMENT; BEHAVIORAL-RESPONSES; UNMEDICATED PATIENTS; HEALTHY-VOLUNTEERS; NEURAL RESPONSES; PANIC DISORDER; THREAT CUES AB Rationale Genotype at the 5' promoter region (5-HTTLPR) of the serotonin transporter has been implicated in moderating the effects of acute tryptophan depletion on neurocognitive functioning. Acute tryptophan depletion has been associated with the processing of fear-relevant cues, such as emotional expressions, but the effect of genotype at the 5-HTTLPR has not been assessed. Objective The present study investigated the effects of acute tryptophan depletion on the recognition of standardized facial expressions of emotions in healthy volunteers classified as ll homozygotes or s carriers. Materials and methods A double-blind between-groups design was used with volunteers randomly selected to ingest capsules containing an amino acid mixture specifically lacking tryptophan, or placebo capsules containing lactose. 5 h after capsule ingestion, subjects were required to identify anger, disgust, fear, happiness, sadness, and surprise expressions that progressed from neutral to each full emotional expression in 5% steps. Results Tryptophan depletion significantly impaired the recognition of fearful facial expressions in s carriers but not ll homozygotes. This impairment was specific to fear expressions. No significant differences in the recognition of other expressions were found. Free tryptophan levels were correlated with fear recognition in s carriers but not ll homozygotes. Conclusions The effects of acute tryptophan depletion on the processing of emotional expressions varies as a function of genotype at the 5-HTTLPR. Depletion impairs the recognition of fear in s carriers but not ll homozygotes. This finding reinforces the importance of considering genotype when assessing the behavioral effects of pharmacologic modulation. C1 NIMH, Mood & Anxiety Program, NIH, Bethesda, MD 20892 USA. NIAAA, Neurogenet Lab, NIH, Bethesda, MD USA. RP Marsh, AA (reprint author), NIMH, Mood & Anxiety Program, NIH, 15K,North Dr,MSC 2670, Bethesda, MD 20892 USA. EM amarsh@post.harvard.edu RI Finger, Elizabeth/B-6453-2015; Goldman, David/F-9772-2010 OI Goldman, David/0000-0002-1724-5405 FU Intramural NIH HHS NR 50 TC 31 Z9 32 U1 2 U2 8 PU SPRINGER PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA SN 0033-3158 J9 PSYCHOPHARMACOLOGY JI Psychopharmacology PD DEC PY 2006 VL 189 IS 3 BP 387 EP 394 DI 10.1007/s00213-006-0581-2 PG 8 WC Neurosciences; Pharmacology & Pharmacy; Psychiatry SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry GA 107DP UT WOS:000242151200011 PM 17013635 ER PT J AU Kwon, DW Ko, K Vannucci, M Reddy, ALN Kim, S AF Kwon, D. W. Ko, K. Vannucci, M. Reddy, A. L. N. Kim, S. TI Wavelet methods for the detection of anomalies and their application to network traffic analysis SO QUALITY AND RELIABILITY ENGINEERING INTERNATIONAL LA English DT Article DE change point detection; network traffic; statistical hypothesis testing; wavelet transforms ID CONSERVATIVE CASCADES; TIME-SERIES; VARIANCE; MODEL AB Here we develop an integrated tool for the online detection of network anomalies. We consider statistical change point detection algorithms, for both local changes in the variance and for the detection of jumps, and propose modified versions of these algorithms based on moving window techniques. We investigate performances on simulated data and on network traffic data with several superimposed attacks. All detection methods are based on wavelet packet transforms. Copyright (C) 2006 John Wiley & Sons, Ltd. C1 Texas A&M Univ, Dept Stat, College Stn, TX 77843 USA. Texas A&M Univ, Dept Elect Engn, College Stn, TX 77843 USA. NCI, Radiat Epidemiol Branch, Div Canc Epidemiol & Genet, Rockville, MD 20852 USA. Boise State Univ, Dept Math, Boise, ID 83725 USA. RP Vannucci, M (reprint author), Texas A&M Univ, Dept Stat, College Stn, TX 77843 USA. EM mvannucci@stat.tamu.edu NR 22 TC 9 Z9 9 U1 1 U2 1 PU JOHN WILEY & SONS LTD PI CHICHESTER PA THE ATRIUM, SOUTHERN GATE, CHICHESTER PO19 8SQ, W SUSSEX, ENGLAND SN 0748-8017 J9 QUAL RELIAB ENG INT JI Qual. Reliab. Eng. Int. PD DEC PY 2006 VL 22 IS 8 BP 953 EP 969 DI 10.1002/qre.781 PG 17 WC Engineering, Multidisciplinary; Engineering, Industrial; Operations Research & Management Science SC Engineering; Operations Research & Management Science GA 114VQ UT WOS:000242694100008 ER PT J AU Sokolov, M Panyutin, IG Neumann, R AF Sokolov, M. Panyutin, I. G. Neumann, R. TI Genome-wide gene expression changes in normal human fibroblasts in response to low-let gamma-radiation and high-let-like (125)IUdR exposures SO RADIATION PROTECTION DOSIMETRY LA English DT Article; Proceedings Paper CT 14th International Symposium on Microdosimetry CY NOV 13-18, 2005 CL Venezia-Isola di San Servo, ITALY SP INFN Lab Nazl Legnaro, Legnaro Padova, INFN Sezione Pavia, Univ Pavia Dipartimento Fis Nucl Teor, NASA Johnson Space Ctr, CERN, Med Res Council ID DOUBLE-STRAND BREAKS; IONIZING-RADIATION; MAMMALIAN-CELLS; FOCUS FORMATION; DNA-DAMAGE; IN-VIVO; RADIOTOXICITY; I-125; REPAIR; IRRADIATION AB Functional genomics studies were carried out to characterize the transcriptional response of normal human fibroblasts to ionizing radiation (IR) of different types. To this end, lung fibroblast IMR-90 cultures were exposed either to external beam gamma-radiation or to internal irradiation from decay of I-125-labeled deoxyuridine ((125)IUdR) incorporated into the cellular DNA. A relatively small dose of 1 Gy of gamma-radiation was delivered to cell cultures either at a high dose-rate (HDR, 1 Gy, 1 min) or at a low dose-rate (LDR, 1 Gy, 22 h). More than 41,000 transcripts were assayed by oligo DNA microarray featuring all known and predicted genes in human genome. Gene expression profiles following gamma-radiation and decays of high-linear energy transfer (LET)-like I-125 share the majority of genes in common, indicating the involvement of similar pathways in signal transduction after IR exposures of different modalities. Gene Ontology (GO) analysis revealed that the oxidative phosphorylation, metabolism of nt, protein kinase cascade and cell cycle are among the up-regulated biological processes mostly affected by gamma-radiation in IMR-90 cells. The translational elongation, negative regulation of cell growth, antigen processing and protein targeting are down-regulated following IR exposures. About one-third of genes differentially expressed following either HDR or LDR gamma-radiation exposures in the same absorbed dose were different, indicating the involvement of distinct transcriptional programs in cellular response to irradiation delivered with the different dose rates. C1 NIH, Dept Nucl Med, Warren G Magnuson Clin Ctr, Bethesda, MD 20892 USA. RP Panyutin, IG (reprint author), NIH, Dept Nucl Med, Warren G Magnuson Clin Ctr, Bethesda, MD 20892 USA. EM igorp@helix.nih.gov NR 30 TC 20 Z9 21 U1 1 U2 2 PU OXFORD UNIV PRESS PI OXFORD PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND SN 0144-8420 J9 RADIAT PROT DOSIM JI Radiat. Prot. Dosim. PD DEC PY 2006 VL 122 IS 1-4 BP 195 EP 201 DI 10.1093/rpd/nlc423 PG 7 WC Environmental Sciences; Public, Environmental & Occupational Health; Nuclear Science & Technology; Radiology, Nuclear Medicine & Medical Imaging SC Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Nuclear Science & Technology; Radiology, Nuclear Medicine & Medical Imaging GA 162YR UT WOS:000246125900043 PM 17145729 ER PT J AU Smilenov, LB Hall, EJ Bonner, WM Sedelnikova, OA AF Smilenov, L. B. Hall, E. J. Bonner, W. M. Sedelnikova, O. A. TI A microbeam study of DNA double-strand breaks in bystander primary human fibroblasts SO RADIATION PROTECTION DOSIMETRY LA English DT Article; Proceedings Paper CT 14th International Symposium on Microdosimetry CY NOV 13-18, 2005 CL Venezia-Isola di San Servo, ITALY SP INFN Lab Nazl Legnaro, Legnaro Padova, INFN Sezione Pavia, Univ Pavia Dipartimento Fis Nucl Teor, NASA Johnson Space Ctr, CERN, Med Res Council ID RADIATION ONCOGENESIS; H2AX PHOSPHORYLATION; CELLS; IRRADIATION; CANCER AB Radiation-induced bystander effect has been well documented. However, the mechanisms are poorly understood. How we incorporate this effect into the classical models of risk assessment remains an open question. Here, the induction of bystander effect was studied by assessing DNA double-strand break (DSB) formation in situ with the rapid and sensitive gamma-H2AX focus formation assay. Utilising the Columbia University single-cell microbeam system to deliver 2 or 20 individual alpha particles to selected cell nuclei in a precisely known proportion of cells in a population, the induced DNA DSB incidences were quantified 30 min and 18 h post-IR. The increase in DNA DSB incidence in bystander cells lacked of a linear dose response indicating that neither the dose of irradiation nor proportion of irradiated cells in a population, is a critical parameter. This study confirms a binary all-or-nothing model of triggering the bystander response. The delay and persistence of the bystander response suggests a different mechanism of DSB induction in bystander cells than in directly irradiated cells. C1 NCI, Mol Pharmacol Lab, Canc Res Ctr, NIH, Bethesda, MD 20892 USA. Columbia Univ, Coll Phys & Surg, Mol Pharmacol Lab, NIH, New York, NY 10032 USA. RP Sedelnikova, OA (reprint author), NCI, Mol Pharmacol Lab, Canc Res Ctr, NIH, 9000 Rockville Pike, Bethesda, MD 20892 USA. EM sedelnio@mail.nih.gov FU Intramural NIH HHS; NIBIB NIH HHS [P41-EB002033] NR 19 TC 28 Z9 29 U1 0 U2 3 PU OXFORD UNIV PRESS PI OXFORD PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND SN 0144-8420 J9 RADIAT PROT DOSIM JI Radiat. Prot. Dosim. PD DEC PY 2006 VL 122 IS 1-4 BP 256 EP 259 DI 10.1093/rpd/ncl461 PG 4 WC Environmental Sciences; Public, Environmental & Occupational Health; Nuclear Science & Technology; Radiology, Nuclear Medicine & Medical Imaging SC Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Nuclear Science & Technology; Radiology, Nuclear Medicine & Medical Imaging GA 162YR UT WOS:000246125900053 PM 17164279 ER PT J AU Becker, GJ AF Becker, Gary J. TI RSNA takes another step in support of imaging research SO RADIOLOGY LA English DT Editorial Material C1 NCI, Canc Imaging Program, Bethesda, MD 20892 USA. RP Becker, GJ (reprint author), NCI, Canc Imaging Program, 6130 Execut Blvd,Suite 3007,MSC 7319, Bethesda, MD 20892 USA. EM becker@rsna.org NR 5 TC 1 Z9 1 U1 0 U2 0 PU RADIOLOGICAL SOC NORTH AMERICA PI OAK BROOK PA 820 JORIE BLVD, OAK BROOK, IL 60523 USA SN 0033-8419 J9 RADIOLOGY JI Radiology PD DEC PY 2006 VL 241 IS 3 BP 653 EP 656 DI 10.1148/radiol.2413060666 PG 4 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA 109BM UT WOS:000242282900004 PM 17114616 ER PT J AU Yeshwant, SC Summers, RM Yao, JH Brickman, DS Choi, JR Pickhardt, PJ AF Yeshwant, Srinath C. Summers, Ronald M. Yao, Jianhua Brickman, Daniel S. Choi, J. Richard Pickhardt, Perry J. TI Polyps: Linear and volumetric measurement at CT colonography SO RADIOLOGY LA English DT Article ID COLONIC POLYPS; IN-VITRO; COLONOSCOPY; SIZE; SEGMENTATION AB Purpose: To retrospectively determine which of several computed tomographic (CT) colongraphy-based polyp measurements is most compatible with the linear measurement at optical colonoscopy and which is best for assessing change in polyp size. Materials and Methods: This HIPAA-compliant study had institutional review board approval; informed consent was obtained. Prone and supine CT colonography with same-day optical colonoscopy was performed in 216 patients (147 men and 69 women; age range, 46-79 years; mean age, 59.2 years) with 338 polyps detected at CT colonography. Polyp size was measured with three linear measurements and two volume measurements. One linear measurement and one volume measurement were preformed by using automated segmentation; remaining measurements were performed manually. Compatibility with linear size at optical colonoscopy and measurement reproducibility were assessed three ways; variation from size measurement at optical colonoscopy, change between prone and supine scans, and variability between observers. Confidence analysis assess the ability of each measurement of 1 cm or greater. Results; Two hundred fifty-one segmentable polyps were present on both supine and prone scans. Linear polyp diameter manually measured on a three-dimensional endoluminally viewed surface (L-M3D) indicated with 95% confidence that a polyp measured as 0.8 cm or smaller was less than 1.0 cm at optical colonoscopy. Prone and supine polyp size difference was smallest for L-M3D and the linear diameter computed from manual and automated volume measurements, with interquartile ranges smaller than or equal to 0.3, 0.2 and 0.5 cm, respectively. Interobserver and intraobserver variability was smallest for linear polyp diameter measurements on a two-dimensional display, with a mean percentage difference of 2.8% (95% Bland-Altman limits of agreement: -17.8%, 23.4%) and 5.0% (95% Bland-Altman limits of agreement: -25.3%, 38.3%), respectively. Conclusion: L-M3D best approximated polyp size measurements at optical colonoscopy. Linear diameter calculated from automated volume measurements showed the smallest variation between supine and prone scans while avoiding observer variability and may be best for assessing polyp size changes with serial examinations. C1 NIH, Dept Diagnost Radiol, Ctr Clin, Bethesda, MD 20892 USA. Uniformed Serv Univ Hlth Sci, Bethesda, MD 20814 USA. Walter Reed Army Med Ctr, Washington, DC 20307 USA. Natl Naval Med Ctr, Bethesda, MD USA. RP Summers, RM (reprint author), NIH, Dept Diagnost Radiol, Ctr Clin, Bldg 10,Room 1C351,10 Ctr Dr,MSC 1182, Bethesda, MD 20892 USA. EM rms@nih.gov FU Intramural NIH HHS NR 22 TC 27 Z9 29 U1 1 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 DEC PY 2006 VL 241 IS 3 BP 802 EP 811 DI 10.1148/radiol.2413051534 PG 10 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA 109BM UT WOS:000242282900022 PM 17114627 ER PT J AU Coffey, M Engel-Hills, P El-Gantiry, M Benjaafar, N Wilkinson, K Vikram, B AF Coffey, Mary Engel-Hills, Penelope El-Gantiry, Mahmoud Benjaafar, Noureddine Wilkinson, Kate Vikram, Bhadrasanin TI A core curriculum for RTTs (radiation therapists/radiotherapy radiographers) designed for developing countries under the auspices of the international atomic energy agency (IAEA) SO RADIOTHERAPY AND ONCOLOGY LA English DT Article C1 Univ Dublin Trinity Coll, Sch Med, Div Radiat Therapy, Dublin 2, Ireland. Natl Canc Inst, Cairo, Egypt. Inst Natl Oncol, Rabat, Morocco. Peter MacCallum Canc Ctr, Melbourne, Vic, Australia. NCI, Washington, DC USA. RP Coffey, M (reprint author), Trinity Ctr Hlth Sci, Div Radiat Therapy, St James Hosp, Dublin 8, Ireland. NR 2 TC 2 Z9 2 U1 0 U2 0 PU ELSEVIER IRELAND LTD PI CLARE PA ELSEVIER HOUSE, BROOKVALE PLAZA, EAST PARK SHANNON, CO, CLARE, 00000, IRELAND SN 0167-8140 J9 RADIOTHER ONCOL JI Radiother. Oncol. PD DEC PY 2006 VL 81 IS 3 BP 324 EP 325 DI 10.1016/j.radonc.2006.08.026 PG 2 WC Oncology; Radiology, Nuclear Medicine & Medical Imaging SC Oncology; Radiology, Nuclear Medicine & Medical Imaging GA 122FI UT WOS:000243210700016 PM 17126433 ER PT J AU Robey, RW Fetsch, PA Polgar, O Dean, M Bates, SE AF Robey, Robert W. Fetsch, Patricia A. Polgar, Orsolya Dean, Michael Bates, Susan E. TI The livestock photosensitizer, phytoporphyrin (phylloerythrin), is a substrate of the ATP-binding cassette transporter ABCG2 SO RESEARCH IN VETERINARY SCIENCE LA English DT Article DE ABCG2; ABCB1; phytoporphyrin/phylloerythrin; photosensitization; transporter ID MULTIDRUG-RESISTANCE; PHOTO-SENSITIZATION; CANCER; SHEEP; MUTATION; PROBE AB Hepatogenous photosensitization occurs in livestock following damage to the liver or biliary apparatus that results in impaired excretion of phytoporphyrin (phylloerythrin), a photo sensitizer. Based on earlier observations that porphyrin-based photosensitizers are substrates of the ATP-binding cassette transporter ABCG2, we examined the ability of the hepatic transporters ABCB1 (P-glycoprotein) and ABCG2 to transport phytoporphyrin. Transport of phytoporphyrin was blocked by the ABCG2-specific inhibitor fumitremorgin C (FTC) in human embryonic kidney cells transfected with full length human ABCG2, while no transport by cells transfected with human ABCB1 was noted. FTC-inhibited transport of phytoporphyrin was also demonstrated in ABCG2-expressing LLC-PK1 pig kidney cells, consistent with the idea that the pig orthologue, like human ABCG2, transports the photo sensitizer. ABCG2 expression was confirmed by immunohistochemistry in the hepatocytes of cow, pig and sheep livers. We conclude that phytoporphyrin is a substrate for ABCG2 and that the transporter is likely responsible for its biliary excretion. Published by Elsevier Ltd. C1 NCI, Med Oncol Branch, Canc Res Ctr, Bethesda, MD 20892 USA. NCI, Pathol Lab, Canc Res Ctr, Bethesda, MD 20892 USA. NCI, Human Genet Sect, Lab Genom Divers, Frederick, MD 21702 USA. RP Robey, RW (reprint author), NCI, Med Oncol Branch, Canc Res Ctr, Bldg 10,Room 13N240B,10 Ctr Dr,MSC 1903, Bethesda, MD 20892 USA. EM robeyr@mail.nih.gov RI Dean, Michael/G-8172-2012 OI Dean, Michael/0000-0003-2234-0631 FU Intramural NIH HHS NR 22 TC 14 Z9 14 U1 0 U2 8 PU W B SAUNDERS CO LTD PI LONDON PA 32 JAMESTOWN RD, LONDON NW1 7BY, ENGLAND SN 0034-5288 J9 RES VET SCI JI Res. Vet. Sci. PD DEC PY 2006 VL 81 IS 3 BP 345 EP 349 DI 10.1016/j.rvsc.2006.04.003 PG 5 WC Veterinary Sciences SC Veterinary Sciences GA 090KU UT WOS:000240951000009 PM 16808938 ER PT J AU Lodde, BM Sankar, V Kok, MR Leakan, RA Tak, PP Pillemer, SR AF Lodde, B. M. Sankar, V. Kok, M. R. Leakan, R. A. Tak, P. P. Pillemer, S. R. TI Re: Traditional cardiovascular risk factors in primary Sjogren's syndrome: role of dyslipidaemia SO RHEUMATOLOGY LA English DT Letter ID CLASSIFICATION; PATHOGENESIS; PREVALENCE; CRITERIA C1 NIDCR, GTTB, NIH, Bethesda, MD 20892 USA. Univ Amsterdam, Acad Med Ctr, Div Clin Immunol & Rheumatol, Amsterdam, Netherlands. RP Lodde, BM (reprint author), NIDCR, GTTB, NIH, 10 Ctr Dr,Room 1N114,MSC, Bethesda, MD 20892 USA. EM blodde@mail.nih.gov NR 9 TC 0 Z9 0 U1 0 U2 0 PU OXFORD UNIV PRESS PI OXFORD PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND SN 1462-0324 J9 RHEUMATOLOGY JI RHEUMATOLOGY PD DEC PY 2006 VL 45 IS 12 BP 1581 EP 1582 DI 10.1093/rheumatology/kel350 PG 3 WC Rheumatology SC Rheumatology GA 108NV UT WOS:000242247400030 ER PT J AU Insel, TR AF Insel, Thomas R. TI Tribute to Wayne Fenton, MD (1953-2006) SO SCHIZOPHRENIA RESEARCH LA English DT Biographical-Item C1 NIMH, NIH, Bethesda, MD USA. RP Insel, TR (reprint author), NIMH, NIH, Bethesda, MD USA. EM insel@mail.nih.gov FU Intramural NIH HHS [Z99 MH999999] NR 0 TC 2 Z9 2 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0920-9964 J9 SCHIZOPHR RES JI Schizophr. Res. PD DEC PY 2006 VL 88 IS 1-3 BP 1 EP 2 DI 10.1016/j.schres.2006.09.019 PG 2 WC Psychiatry SC Psychiatry GA 115FJ UT WOS:000242719900001 PM 17097473 ER PT J AU Yin, XB Liu, XD Sun, LG Zhu, RB Xie, ZQ Wang, YH AF Yin, Xuebin Liu, Xiaodong Sun, Liguang Zhu, Renbin Xie, Zhouqing Wang, Yuhong TI A 1500-year record of lead, copper, arsenic, cadmium, zinc level in Antarctic seal hairs and sediments SO SCIENCE OF THE TOTAL ENVIRONMENT LA English DT Article DE Antarctica; seal hair; excrement; heavy metal; anthropogenic source; natural source ID ARCTIC LAKE-SEDIMENTS; HEAVY-METALS; SNOW RECORD; MERCURY; POLLUTION; ICE; DEPOSITION; CIVILIZATIONS; HEMISPHERE; AEROSOL AB To reconstruct the profiles of heavy metal levels in the South Ocean ecosystem of Antarctica, the concentrations of lead (Pb), copper (Cu), arsenic (As), cadmium (Cd), and zinc (Zn) in seal hairs and lake sediments spanning the past 1500 years from Fildes Peninsula of King George Island and in weathering lake sediments from Nelson Island of West Antarctica were determined. The lead contents in the seal hairs and the weathering sediments show a sharp increase since the late 1800s, very likely due to anthropogenic contamination from modem industries. After the 1980s, the Ph content in seal hairs dropped by one-third, apparently due to the reduced usage of leaded gasoline in the Southern Hemisphere. Copper arises mainly from the weathering process, and its level may be substantially affected by climatic conditions. The concentrations of Cd, As, and Zn do not show any clear temporal trends. (c) 2006 Published by Elsevier B.V. C1 Univ Sci & Technol China, Inst Polar Environm, Hefei 230026, Anhui, Peoples R China. Chinese Acad Sci, Inst Soil Sci, State Key Lab Soil & Sustainable Agr, Nanjing 210008, Jiangsu, Peoples R China. Univ Sci & Technol China, Sch Earth & Space Sci, CAS Key Lab Crust Mantle Mat & Environm, Hefei 230026, Anhui, Peoples R China. NIH, Bethesda, MD 20892 USA. RP Sun, LG (reprint author), Univ Sci & Technol China, Inst Polar Environm, Hefei 230026, Anhui, Peoples R China. EM slg@ustc.edu.cn NR 24 TC 15 Z9 22 U1 7 U2 29 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0048-9697 J9 SCI TOTAL ENVIRON JI Sci. Total Environ. PD DEC 1 PY 2006 VL 371 IS 1-3 BP 252 EP 257 DI 10.1016/j.scitotenv.2006.07.022 PG 6 WC Environmental Sciences SC Environmental Sciences & Ecology GA 111DH UT WOS:000242431100025 PM 16928392 ER PT J AU Hawk, E Viner, JL AF Hawk, Ernest Viner, Jaye L. TI What is the future of oncology? National Cancer Institute initiatives to improve research, development, and implementation in cancer prevention and treatment SO SEMINARS IN ONCOLOGY LA English DT Article; Proceedings Paper CT 2nd Annual International-Society-of-Gastrointestinal-Oncology Conference CY JUL 14-16, 2005 CL Arlington, VA SP Int* Soc* Gasrointestinal Oncol C1 NCI, Off Ctr Training & Resources, OD, Bethesda, MD 20892 USA. RP Hawk, E (reprint author), NCI, Off Ctr Training & Resources, OD, 6116 Execut Blvd,Room 700, Bethesda, MD 20892 USA. EM eh51p@nih.gov NR 1 TC 4 Z9 4 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 0093-7754 J9 SEMIN ONCOL JI Semin. Oncol. PD DEC PY 2006 VL 33 IS 6 SU 11 BP S6 EP S9 DI 10.1053/j.seminoncol.2006.10.012 PG 4 WC Oncology SC Oncology GA 125DD UT WOS:000243421000003 PM 17178278 ER PT J AU Trimble, EL AF Trimble, Edward L. TI Concluding remarks: Optimal treatment for women with ovarian cancer SO SEMINARS IN ONCOLOGY LA English DT Editorial Material ID CARE C1 NCI, Bethesda, MD 20892 USA. RP Trimble, EL (reprint author), NCI, 6130 Execut Blvd,Suite 7025, Bethesda, MD 20892 USA. EM tt6m@nih.gov NR 8 TC 3 Z9 3 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 0093-7754 J9 SEMIN ONCOL JI Semin. Oncol. PD DEC PY 2006 VL 33 IS 6 SU 12 BP S25 EP S26 DI 10.1053/j.seminoncol.2006.11.004 PG 2 WC Oncology SC Oncology GA 130IW UT WOS:000243794300005 PM 17223447 ER PT J AU Garantziotis, S Schwartz, DA AF Garantziotis, Stavros Schwartz, David A. TI Host-environment interactions in pulmonary fibrosis SO SEMINARS IN RESPIRATORY AND CRITICAL CARE MEDICINE LA English DT Review DE idiopathic pulmonary fibrosis; host susceptibility; environmental triggers ID BRONCHOALVEOLAR LAVAGE FLUID; SURFACTANT PROTEIN-C; ACID GASTROESOPHAGEAL-REFLUX; INTERSTITIAL LUNG-DISEASE; HUMAN-DIPLOID FIBROBLASTS; NIEMANN-PICK-DISEASE; HEPATITIS-C; THORACOABDOMINAL MECHANICS; OCCUPATIONAL EXPOSURE; SYSTEMIC-SCLEROSIS AB Idiopathic pulmonary fibrosis (IPF) is a progressive scarring disease of the pulmonary parenchyma, leading to respiratory failure and death. Several epidemiological and theoretical observations link the pathogenesis of this disease to environmental injury to the lungs. We discuss the theoretical framework of this hypothesis and we present data in support of the concept that genetic and nongenetic host susceptibility may interact with repetitive environmental injury to lead to IPF. C1 NIEHS, Res Triangle Pk, NC 27709 USA. Duke Univ, Med Ctr, Div Allergy Pulm & Crit Care Med, Durham, NC USA. RP Schwartz, DA (reprint author), NIEHS, POB 12233,MD B2-01, Res Triangle Pk, NC 27709 USA. EM schwartzd@niehs.nih.gov RI Garantziotis, Stavros/A-6903-2009 OI Garantziotis, Stavros/0000-0003-4007-375X NR 75 TC 8 Z9 10 U1 0 U2 2 PU THIEME MEDICAL PUBL INC PI NEW YORK PA 333 SEVENTH AVE, NEW YORK, NY 10001 USA SN 1069-3424 J9 SEMIN RESP CRIT CARE JI Semin. Respir. Crit. Care Med. PD DEC PY 2006 VL 27 IS 6 BP 574 EP 580 DI 10.1055/s-2006-957329 PG 7 WC Critical Care Medicine; Respiratory System SC General & Internal Medicine; Respiratory System GA 121YZ UT WOS:000243194200003 PM 17195134 ER PT J AU Cassard, L Cohen-Solal, J Camilleri-Broet, S Fournier, E Fridman, WH Sautes-Fridman, C AF Cassard, Lydie Cohen-Solal, Joel Camilleri-Broet, Sophie Fournier, Emilie Fridman, Wolf Herman Sautes-Fridman, Catherine TI Fc gamma receptors and cancer SO SPRINGER SEMINARS IN IMMUNOPATHOLOGY LA English DT Review DE melanoma; B cell lymphoma; prognostic value; antibody therapy; anti-tumor immunity ID B-CELL LYMPHOMA; ANTI-CD20 MONOCLONAL-ANTIBODY; IMMUNE-COMPLEXES; TUMOR-CELLS; SOLUBLE RECEPTOR; IMMUNOGLOBULIN-G; EXPRESSION; RIIB; MELANOMA; GENE AB Fc gamma Rs are a family of heterogeneous molecules that play opposite roles in immune response and control the effector functions of IgG antibodies. In many cancers, IgG antibodies are produced that recognize cancer cells, form immune complexes and therefore, activate Fc gamma R. The therapeutic efficacy of monoclonal IgG antibodies against hematopoietic and epithelial tumors also argue for an important role of IgG antibodies in anti-tumor defenses. Since the 1980s, a series of lines of evidence in experimental models and in humans strongly suggest that Fc gamma R are involved in the therapeutic activity of monoclonal IgG antibodies by activating the cytotoxic activity of Fc gamma R-positive cells such as NK cells, monocytes, macrophages and neutrophils and by increasing antigen presentation by dendritic cells. Since many cell types co-express activating and inhibitory Fc gamma R, the Fc gamma R-dependent effector functions of IgG anti-tumor antibodies are counterbalanced by the inhibitory Fc gamma RIIB. In addition, some tumor cells express Fc gamma R either constitutively, such as B cell lymphomas or ectopically, such as 40% of human metastatic melanoma. The tumor Fc gamma R isoform is preferentially Fc gamma RIIB, which is functional at least in human metastatic melanoma. This review summarizes these data and discusses how Fc gamma RIIB expression may influence the anti-tumor immune reaction and how beneficial or deleterious this expression could be for the efficiency of therapeutics based on monoclonal anti-tumor antibodies. C1 Univ Paris 06, INSERM, UMRs255, Univ Paris 05,Ctr Rech Cordeliers, F-75270 Paris 06, France. Univ Paris 06, AP HP, Serv Anat Pathol, Hotel Dieu, F-75181 Paris, France. NCI, Surg Branch, Bethesda, MD 20812 USA. Columbia Univ, Dept Med, New York, NY 10032 USA. RP Sautes-Fridman, C (reprint author), Univ Paris 06, INSERM, UMRs255, Univ Paris 05,Ctr Rech Cordeliers, 15 Rue Ecole Med, F-75270 Paris 06, France. EM catherine.fridman@u255.bhdc.jussieu.fr NR 74 TC 4 Z9 5 U1 0 U2 1 PU SPRINGER PI NEW YORK PA 233 SPRING STREET, NEW YORK, NY 10013 USA SN 0344-4325 J9 SPRINGER SEMIN IMMUN JI Springer Semin. Immunopathol. PD DEC PY 2006 VL 28 IS 4 BP 321 EP 328 DI 10.1007/s00281-006-0058-8 PG 8 WC Immunology; Pathology SC Immunology; Pathology GA 111PN UT WOS:000242465800003 PM 17096153 ER PT J AU Gurevich, G Vexler, A AF Gurevich, Gregory Vexler, Albert TI Guaranteed maximum likelihood splitting tests of a linear regression model SO STATISTICS LA English DT Article DE change point; Martingale structure; maximum likelihood; threshold; two-phase linear model ID CHANGE-POINT PROBLEM; 2 SEPARATE REGIMES; ASYMPTOTICS; TIME AB We propose and examine a class of generalized maximum likelihood asymptotic power one tests for detection of various types of changes in a linear regression model. In economic and epidemiologic studies, such segmented regression models often occur as threshold models, where it is assumed that the exposure has no influence on the response up to a possible unknown threshold. An important task of such studies is testing the existence and estimation of this threshold. Guaranteed non-asymptotic upper bounds for the significance levels of these tests are presented. We demonstrate how the proposed tests were applied toward solving an actual problem encountered with real data. C1 Sami Shamoon Coll Engn, Dept Ind Engn & Management, IL-84100 Beer Sheva, Israel. NICHHD, Div Epidemiol Stat & Prevent Res, NIH, DHHS, Rockville, MD 20852 USA. RP Gurevich, G (reprint author), Sami Shamoon Coll Engn, Dept Ind Engn & Management, Bialik Basel Sts, IL-84100 Beer Sheva, Israel. EM gregoryg@sce.ac.il NR 25 TC 3 Z9 3 U1 0 U2 0 PU TAYLOR & FRANCIS LTD PI ABINGDON PA 4 PARK SQUARE, MILTON PARK, ABINGDON OX14 4RN, OXON, ENGLAND SN 0233-1888 J9 STATISTICS JI Statistics PD DEC PY 2006 VL 40 IS 6 BP 465 EP 484 DI 10.1080/02331880601013874 PG 20 WC Statistics & Probability SC Mathematics GA 118KB UT WOS:000242940100001 ER PT J AU Letterio, J Rudikoff, E Voong, N Bauer, SR AF Letterio, John Rudikoff, Eva Voong, Nga Bauer, Steven R. TI Transforming growth factor-beta 1 sensitivity is altered in abl-myc- and raf-myc-induced mouse pre-B-cell tumors SO STEM CELLS LA English DT Article DE transforming growth factor-beta 1; pre-B tumors; myc; abl; raf ID GROWTH-FACTOR-BETA; TGF-BETA; RECEPTOR EXPRESSION; APOPTOSIS; MICE; TGF-BETA-1; LYMPHOCYTES; LINES; PLASMACYTOMAS; ACTIVATION AB Understanding the mechanisms leading to transformation of early B-lineage precursors is an important step leading to rational design of new treatments for precursor (pre)-B-cell leukemia. We used normal mouse pre-B cells to determine if and how transforming growth factor (TGF)-beta 1 affects these precursors to the B-cell lineage and whether transformed pre-B cells respond to TGF-beta 1. We found that normal pre-B cells proliferating in the presence of interleukin (IL)-7 enter cell-cycle arrest after exposure to TGF-beta 1. However, clonally related IL-7-independent tumors induced by oncogenes abl + myc or raf + myc have reduced sensitivity to TGF-beta 1. In contrast, tumor cells induced by myc alone remain sensitive to TGF-beta 1 growth suppression. These results suggest that lesions in different molecular signaling pathways can lead to loss of TGF-beta 1 sensitivity in a single cell type. The approach of using normal pre-B-cell lines and transformation by overexpression of different oncogenes provides a system to compare and contrast molecular pathways that lead to full malignancy. C1 US FDA, Ctr Biol Evaluat & Res, Cell & Tissue Therapy Branch, Rockville, MD 20852 USA. Case Western Reserve Univ, Div Pediat Hematol Oncol, Ireland Canc Ctr, Cleveland, OH 44106 USA. NCI, NIH, Lab Cell Regulat & Carcinogenesis, Bethesda, MD 20892 USA. RP Bauer, SR (reprint author), US FDA, Ctr Biol Evaluat & Res, Cell & Tissue Therapy Branch, NIH Bldg 29B,Room 2NN10,HFM-740,1401 Rockville Pi, Rockville, MD 20852 USA. EM Steven.Bauer@fda.hhs.gov RI Bauer, Steven/G-5559-2012; OI Bauer, Steven/0000-0003-2831-846X FU Intramural NIH HHS NR 27 TC 2 Z9 3 U1 0 U2 0 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 DEC PY 2006 VL 24 IS 12 BP 2611 EP 2617 DI 10.1634/stemcells.2005-0623 PG 7 WC Cell & Tissue Engineering; Biotechnology & Applied Microbiology; Oncology; Cell Biology; Hematology SC Cell Biology; Biotechnology & Applied Microbiology; Oncology; Hematology GA 114WL UT WOS:000242696200002 PM 16945999 ER PT J AU Zhang, JW He, XC Tong, WG Johnson, T Wiedemann, LM Mishina, Y Feng, JQ Li, LH AF Zhang, Jiwang He, Xi C. Tong, Wei-Gang Johnson, Teri Wiedemann, Leanne M. Mishina, Yuji Feng, Jian Q. Li, Linheng TI Bone morphogenetic protein signaling inhibits hair follicle anagen induction by restricting epithelial stem/progenitor cell activation and expansion SO STEM CELLS LA English DT Article DE hair follicle; stem cells; BMP; beta-catenin; Wnt; PTEN; Akt ID FORKHEAD TRANSCRIPTION FACTOR; GLYCOGEN-SYNTHASE KINASE; MULTIPOTENT STEM-CELLS; LABEL-RETAINING CELLS; BETA-CATENIN; MESENCHYMAL INTERACTIONS; TUMOR-SUPPRESSOR; MOUSE EPIDERMIS; GROWTH-PHASE; SELF-RENEWAL AB Epithelial stem cells (EP-SCs) located in the bulge region of a hair follicle (HF) have the potential to give rise to hair follicle stem/progenitor cells that migrate down to regenerate HFs. Bone morphogenetic protein (BMP) signaling has been shown to regulate the HF cycle by inhibiting anagen induction. Here we show that active BMP signaling functions to prevent EP-SC activation and expansion. Dynamic expression of Noggin, a BMP antagonist, releases EP-SCs from BMP-mediated restriction, leading to EP-SC activation and initiation of the anagen phase. Experimentally induced conditional inactivation of the BMP type IA receptor ( Bmpr1a) in EP-SCs leads to overproduction of HF stem/ progenitor cells and the eventual formation of matricomas. This genetic manipulation of the BMP signaling pathway also reveals unexpected activation of beta-catenin, a major mediator of Wnt signaling. We propose that BMP activity controls the HF cycle by antagonizing Wnt/beta-catenin activity. This is at least partially achieved by BMP- mediated enhancement of transforming growth factor-beta-regulated epithelial cell-specific phosphatase ( PTEN) function. Subsequently, PTEN, through phosphatidyl inositol 3-kinase-Akt, inhibits the activity of beta-catenin, the convergence point of the BMP and Wnt signaling pathways. C1 Stowers Inst Med Res, Kansas City, MO 64110 USA. Natl Inst Environm Hlth Sci, Lab Reprod & Dev Toxicol, Res Triangle Pk, NC USA. Univ Missouri, Sch Dent, Dept Oral Biol, Kansas City, MO 64110 USA. Univ Kansas, Med Ctr, Dept Pathol & Lab Med, Kansas City, KS 66103 USA. RP Li, LH (reprint author), Stowers Inst Med Res, 1000 E 50th St, Kansas City, MO 64110 USA. EM lil@stowers-institute.org NR 70 TC 86 Z9 91 U1 1 U2 15 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 DEC PY 2006 VL 24 IS 12 BP 2826 EP 2839 DI 10.1634/stemcells.2005-0544 PG 14 WC Cell & Tissue Engineering; Biotechnology & Applied Microbiology; Oncology; Cell Biology; Hematology SC Cell Biology; Biotechnology & Applied Microbiology; Oncology; Hematology GA 114WL UT WOS:000242696200024 PM 16960130 ER PT J AU Luby, M Bykowski, JL Schellinger, PD Merino, J'G Warach, S AF Luby, Marie Bykowski, Julie L. Schellinger, Peter D. Merino, Jose G. Warach, Steven TI Intra- and interrater reliability of ischemic lesion volume measurements on diffusion-weighted, mean transit time and fluid-attenuated inversion recovery MRI SO STROKE LA English DT Article DE acute stroke; brain imaging; magnetic resonance; neuroradiology; thrombolysis ID ACUTE STROKE; INFARCT VOLUME; PREDICTION; PERFUSION; TRIAL AB Background and Purpose - We investigated the intra- and interrater reliability of ischemic lesion volumes measurements assessed by different MRI sequences at various times from onset. Methods - Ischemic lesion volumes were measured for intrarater reliability using diffusion-weighted (DWI), mean transit time (MTT) perfusion and fluid-attenuated inversion recovery (FLAIR) MRI at chronic (> 3 days from stroke onset) time points. A single intrarater reader, blind to clinical information and time point, repeated the volume measurements on two occasions separated by at least 1 week. Interrater reliability was also obtained in the second set of patients using acute DWI, MTT and chronic FLAIR MRI. Four blinded readers performed these volume measurements. Average deviations across repeat measurements per lesion and differences between sample means between the two measurements were calculated globally, ie, across all sequences and time points, and per reader type for each sequence at each time point. Results - There was good concordance of the mean sample volumes of the 2 intrarater readings (deviations were < 4% and 2 mL globally, < 2% and 2 mL for DWI, < 6% and 7 mL for MTT, and < 2% and 1 mL for FLAIR). There was also good concordance of the interrater readings (< 5% and 2 mL globally). Conclusions - Repeat measurements of stroke lesion volumes show excellent intra- and interrater concordance for DWI, MTT and FLAIR at acute through chronic time points. C1 Natl Inst Neurol Disorders & Stroke, Sect Stroke Diagnost & Therapeut, NIH, Bethesda, MD 20892 USA. Univ Klinikum Erlangen, Neurol Klin, Erlangen, Germany. RP Luby, M (reprint author), Natl Inst Neurol Disorders & Stroke, Sect Stroke Diagnost & Therapeut, NIH, 10 Ctr Dr,Rm B1D733,MSC 1063, Bethesda, MD 20892 USA. EM lubym@ninds.nih.gov OI Merino, Jose/0000-0002-6676-0008 FU Intramural NIH HHS [Z99 NS999999] NR 16 TC 55 Z9 55 U1 0 U2 3 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0039-2499 J9 STROKE JI Stroke PD DEC PY 2006 VL 37 IS 12 BP 2951 EP 2956 DI 10.1161/01.STR.0000249416.77132.1a PG 6 WC Clinical Neurology; Peripheral Vascular Disease SC Neurosciences & Neurology; Cardiovascular System & Cardiology GA 124ZO UT WOS:000243411500027 PM 17082470 ER PT J AU Hallenbeck, J del Zoppo, G Jacobs, T Hakim, A Goldman, S Utz, U Hasan, A AF Hallenbeck, John del Zoppo, Gregory Jacobs, Tom Hakim, Antoine Goldman, Stephen Utz, Ursula Hasan, Ahmed CA Immunomodulation Workshop Particip TI Immunomodulation strategies for preventing vascular disease of the brain and heart - Workshop summary SO STROKE LA English DT Article DE acute stroke; cerebrovascular disease; immunology; inflammation; ischemia; stroke ID CORONARY-ARTERY-DISEASE; COA REDUCTASE INHIBITOR; ATHEROSCLEROTIC PLAQUE; CEREBRAL-ISCHEMIA; MUCOSAL TOLERANCE; HYPERTENSIVE-RATS; IMMUNE-RESPONSES; STROKE SIZE; T-CELLS; INFLAMMATION AB This workshop examined the opportunities for translational research directed at immune and inflammatory mechanisms. This summary presents the background data in 3 general areas: (1) inflammation and hemostasis in cerebrovascular and cardiovascular disease, (2) immune interactions in the central nervous system and heart, and (3) translation of immune modulation in the brain and heart, all of which supported a consensus derivation of the opportunities for future research in these areas. The summary concludes with 11 recommendations. C1 Natl Inst Neurol Disorders & Stroke, NIH, Stroke Branch, Bethesda, MD 20892 USA. Scripps Res Inst, Dept Mol & Expt Med, La Jolla, CA 92037 USA. Natl Inst Neurol Disorders & Stroke, NIH, Bethesda, MD USA. Canadian Stroke Network, Ottawa, ON, Canada. NHLBI, NIH, Bethesda, MD 20892 USA. RP Hallenbeck, J (reprint author), Natl Inst Neurol Disorders & Stroke, NIH, Stroke Branch, 49 Convent Dr,MSC 4476, Bethesda, MD 20892 USA. EM hallenbj@ninds.nih.gov FU Intramural NIH HHS [Z99 NS999999] NR 61 TC 12 Z9 13 U1 0 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 DEC PY 2006 VL 37 IS 12 BP 3035 EP 3042 DI 10.1161/01.STR.0000248836.82538.ee PG 8 WC Clinical Neurology; Peripheral Vascular Disease SC Neurosciences & Neurology; Cardiovascular System & Cardiology GA 124ZO UT WOS:000243411500041 PM 17082471 ER PT J AU Liu, J Pan, YP Ma, BY Nussinov, R AF Liu, Jin Pan, Yongping Ma, Buyong Nussinov, Ruth TI "Similarity trap" in protein-protein interactions could be carcinogenic: Simulations of p53 core domain complexed with 53BP1 and BRCA1 BRCT domains SO STRUCTURE LA English DT Article ID CRYSTAL-STRUCTURE; STRUCTURAL BASIS; DNA-REPAIR; CANCER; BREAST; DYNAMICS; REGION; RECOGNITION; MUTATIONS; REPEATS AB Similar binding sites often imply similar protein-protein interactions and similar functions; however, similar binding sites may also constitute traps for nonfunctional associations. How are similar sites distinguished to prevent misassociations? BRCT domains from breast cancer-susceptibility gene product BRCA1 and protein 5313131 have similar structures yet different binding behaviors with p53 core domain. 53BP1-BRCT domain forms a stable complex with p53. In contrast, BRCA1-p53 interaction is weak or other mechanisms operate. To delineate the difference, we designed 13 BRCA1-BRCT mutants and computationally investigated the structural and stability changes compared to the experimental p53-53BP1 structure. Interestingly, of the 13, the 2 mutations that are cancerous and involve nonconserved residues are those that enforced p53 core domain binding with BRCA1-BRCT in a way similar to p53-53BP1 binding. Hence, falling into the "similarity trap" may disrupt normal BRCA1 and p53 functions. Our results illustrate how this trap is avoided in the native state. C1 SAIC Frederick Inc, Basic Res Program, Ctr Canc Res Nanobiol Program, NCI, Frederick, MD 21702 USA. Tel Aviv Univ, Sackler Sch Med, Sackler Inst Mol Med, Dept Human Genet & Mol Med, IL-69978 Tel Aviv, Israel. RP Ma, BY (reprint author), SAIC Frederick Inc, Basic Res Program, Ctr Canc Res Nanobiol Program, NCI, Frederick, MD 21702 USA. EM mab@ncifcrf.gov; ruthn@ncifcrf.gov RI Ma, Buyong/F-9491-2011 OI Ma, Buyong/0000-0002-7383-719X FU Intramural NIH HHS [Z01 BC010441-04, Z01 BC010440-04]; NCI NIH HHS [N01-CO-12400, N01 CO012400, N01CO12400] NR 33 TC 8 Z9 8 U1 0 U2 0 PU CELL PRESS PI CAMBRIDGE PA 1100 MASSACHUSETTS AVE, CAMBRIDGE, MA 02138 USA SN 0969-2126 J9 STRUCTURE JI Structure PD DEC PY 2006 VL 14 IS 12 BP 1811 EP 1821 DI 10.1016/j.str.2006.10.009 PG 11 WC Biochemistry & Molecular Biology; Biophysics; Cell Biology SC Biochemistry & Molecular Biology; Biophysics; Cell Biology GA 117QS UT WOS:000242888600009 PM 17161371 ER PT J AU Wyatt, K White, HE Wang, LC Bateman, OA Slingsby, C Orlova, EV Wistow, G AF Wyatt, Keith White, Helen E. Wang, Luchun Bateman, Orval A. Slingsby, Christine Orlova, Elena V. Wistow, Graeme TI Lengsin is a survivor of an ancient family of class I glutamine synthetases re-engineered by evolution for a role in the vertebrate lens SO STRUCTURE LA English DT Article ID BETA-GAMMA-CRYSTALLIN; SEQUENCE TAG ANALYSIS; 3-DIMENSIONAL RECONSTRUCTION; RHIZOBIUM-MELILOTI; ALPHA-CRYSTALLIN; NEIBANK PROJECT; EYE TISSUES; PROTEIN; GENE; MODEL AB Lengsin is a major protein of the vertebrate eye lens. It belongs to the hitherto purely prokaryotic GS I branch of the glutamine synthetase (GS) superfamily, but has no enzyme activity. Like the taxon-specific crystallins, Lengsin is the result of the recruitment of an ancient enzyme to a noncatalytic role in the vertebrate lens. Cryo-EM and modeling studies of Lengsin show a dodecamer structure with important similarities and differences with prokaryotic GS I structures. GS homology regions of Lengsin are well conserved, but the N-terminal domain shows evidence of dynamic evolutionary changes. Compared with birds and fish, most mammals have an additional exon corresponding to part of the N-terminal domain; however, in human, this is a nonfunctional pseudoexon. Genes related to Lengsin are also present in the sea urchin, suggesting that this branch of the GS I family, supplanted by GS II enzymes in vertebrates, has an ancient role in metazoans. C1 NEI, NIH, Sect Mol Struct & Funct Genom, Bethesda, MD 20892 USA. Univ London Birkbeck Coll, Dept Crystallog, Inst Struct Mol Biol, London WC1E 7HX, England. RP Wistow, G (reprint author), NEI, NIH, Sect Mol Struct & Funct Genom, Bethesda, MD 20892 USA. EM graeme@helix.nih.gov FU NEI NIH HHS [Z01 EY000320-07, Z01 EY000433] NR 59 TC 17 Z9 18 U1 0 U2 3 PU CELL PRESS PI CAMBRIDGE PA 1100 MASSACHUSETTS AVE, CAMBRIDGE, MA 02138 USA SN 0969-2126 J9 STRUCTURE JI Structure PD DEC PY 2006 VL 14 IS 12 BP 1823 EP 1834 DI 10.1016/j.str.2006.10.008 PG 12 WC Biochemistry & Molecular Biology; Biophysics; Cell Biology SC Biochemistry & Molecular Biology; Biophysics; Cell Biology GA 117QS UT WOS:000242888600010 PM 17161372 ER PT J AU Yasuno, F Zoghbi, SS McCarron, JA Hong, J Ichise, M Brown, AK Gladding, RL Bacher, JD Pike, VW Innis, RB AF Yasuno, Fumihiko Zoghbi, Sami S. McCarron, Julie A. Hong, Jinsoo Ichise, Masanori Brown, Amira K. Gladding, Robert L. Bacher, John D. Pike, Victor W. Innis, Robert B. TI Quantification of serotonin 5-HT1A receptors in monkey brain with [C-11](R)-(-)-RWAY SO SYNAPSE LA English DT Article DE serotonin 5-HT1A; [C-11](R)-(-)-RWAY; kinetic analysis; P-glycoprotein; PET ID MEDIATED MULTIDRUG-RESISTANCE; P-GLYCOPROTEIN; IN-VIVO; PET; BINDING; RADIOLIGAND; MODEL; TOMOGRAPHY; REVERSAL; BARRIER AB [C-11](R)-(-)-RWAY ([C-11]2, 3, 4, 5, 6, 7-hexahydro-1{4-[1[4-(2-methoxyphenyl)-piperazinyl]]-2-phenylbutyry}-1H-azepine) is a new radioligand for imaging brain 5-HT1A receptors with positron emission tomography. In [C-11](R)-(-)-RWAY, the direction of the amide bond is expected to reduce metabolism by hydrolysis while allowing easy C-11-labeling at the methoxy position. The purposes of this study were to evaluate different tracer kinetic models in nonhuman primates to quantify 5-HT1A receptors with [C-11](R)-(-)-RWAY and to test for the possible action of P-glycoprotein (P-gp), one of the known efflux pumps at the blood-brain barrier. The brain uptake of radioactivity from [C-11](R)-(-)-RWAY into 5-HT1A receptor-rich brain regions was severalfold greater than for its antipode ([C-11](S)-(+)-RWAY) and could be displaced by receptor saturating doses of the selective 5-HT1A antagonist, WAY-100635. Pretreatment with tariquidar, a potent inhibitor of P-gp, increased brain uptake of [C-11])-(-)-RWAY about 1.5-fold and the plasma free fraction about 1.8-fold. Thus, the effect of tariquidar on brain uptake may have been caused by displacement of the radioligand binding to plasma proteins. Mathematical modeling showed that the estimated values of regional binding potential were correlated strongly between two-tissue compartment model and multilinear reference tissue model, and thus, supported the use of the cerebellum as a reference region. Published 2006 Wiley-Liss, Inc. C1 NIMH, Mol Imaging Branch, Bethesda, MD 20892 USA. NIMH, Div Vet Resources, Off Res Serv, Bethesda, MD 20892 USA. RP Yasuno, F (reprint author), NIMH, Mol Imaging Branch, Bldg 1,Room B3-10,1 Ctr Dr, Bethesda, MD 20892 USA. EM yasunof@mail.nih.gov FU NIMH NIH HHS [Z01-MH002795-04] NR 35 TC 29 Z9 30 U1 0 U2 1 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 0887-4476 J9 SYNAPSE JI Synapse PD DEC 1 PY 2006 VL 60 IS 7 BP 510 EP 520 DI 10.1002/syn.20327 PG 11 WC Neurosciences SC Neurosciences & Neurology GA 093FI UT WOS:000241153000004 PM 16952161 ER PT J AU Huang, SX Podsypanina, K Chen, YD Cai, WY Tsimelzon, A Hilsenbeek, S Li, Y AF Huang, Shixia Podsypanina, Katrina Chen, Yidong Cai, Weiyan Tsimelzon, Anna Hilsenbeek, Susan Li, Yi TI Wnt-1 is dominant over Neu in specifying mammary tumor expression profiles SO TECHNOLOGY IN CANCER RESEARCH & TREATMENT LA English DT Article DE gene expression profiling; mouse model; and breast cancer ID TRANSGENIC MOUSE MODELS; HUMAN BREAST-CANCER; GENE-EXPRESSION; MOLECULAR PORTRAITS; PROGENITOR CELLS; MICE; CLASSIFICATION; GLAND; GENERATION; NEOPLASIA AB Wnt-1 and Neu collaborate to induce mammary tumors in bitransgenic mice carrying both MMTV-Wnt-1 and MMTV-Neu. In this report, gene expression profiles were determined for tumors from these bitransgenic mice, and compared with expression profiles of tumors from mice singly transgenic for MMTV-Wnt-1 or MMTV-Neu. While very different from tumors arising in MMTV-Neu transgenic mice, tumors from these bitransgenic mice were found not to have identifiable differences from tumors from MMTV-Wnt-1 transgenic mice, using clustering and multidimensional scaling analyses (unsupervised and supervised), One-way Analysis of Variance (ANOVA), and two sample t test (the later two of which were combined with false discovery rate computation). These observations suggest that Wnt-1 is dominant over Neu in specifying mammary tumor expression profiles. C1 Baylor Coll Med, Breast Ctr, Houston, TX 77030 USA. Baylor Coll Med, Dan L Duncan Canc Ctr, Houston, TX 77030 USA. Baylor Coll Med, Dept Mol & Cell Biol, Houston, TX 77030 USA. Mem Sloan Kettering Canc Ctr, Sloan Kettering Inst, Program Canc Biol & Genet, New York, NY USA. NHGRI, NIH, Bethesda, MD 20892 USA. RP Huang, SX (reprint author), Baylor Coll Med, Breast Ctr, Houston, TX 77030 USA. EM shixiah@bcm.tmc.edu OI Li, Yi/0000-0002-9976-518X FU NCI NIH HHS [R01CA113869-01] NR 32 TC 11 Z9 11 U1 0 U2 0 PU ADENINE PRESS PI SCHENECTADY PA 2066 CENTRAL AVE, SCHENECTADY, NY 12304 USA SN 1533-0346 J9 TECHNOL CANCER RES T JI Technol. Cancer Res. Treat. PD DEC PY 2006 VL 5 IS 6 BP 565 EP 571 PG 7 WC Oncology SC Oncology GA 123RF UT WOS:000243312400003 PM 17121432 ER PT J AU Svensson, AM Whiteley, GR Callas, PW Bovill, EG AF Svensson, Annika M. Whiteley, Gordon R. Callas, Peter W. Bovill, Edwin G. TI SELDI-TOF plasma profiles distinguish individuals in a protein C-deficient family with thrombotic episodes occuring before age 40 SO THROMBOSIS AND HAEMOSTASIS LA English DT Article DE venous thrombosis; SELDI-TOF; mass spectrometry; proteomics; protein C deficiency ID VENOUS THROMBOSIS; CLINICAL PROTEOMICS; MASS-SPECTROMETRY; OVARIAN-CANCER; SERUM; DISEASE; RISK; PATTERNS AB We tested the hypothesis that differences in the low-molecular-weight (500-20,000 Da) proteomic profile of plasma may be detectable between members of a protein C-deficient family who have suffered thrombotic events before age 40 compared to family members without a history of venous thrombosis. Unfractionated plasma samples from members of a previously described large thrombophilic kindred with type I protein C deficiency were applied to ProteinChip weak cation exchange interaction arrays (WCX2; Ciphergen Biosystems, Fremont, CA, USA) and subjected to SELDI-TOF (surface-enhanced laser desorption/ionization time-of-flight) mass spectrometry using the Ciphergen PBSII ProteinChip System (Ciphergen Biosystems). Profiles were analyzed by a boosted decision-tree algorithm. When individuals who had presented with deep venous thrombosis (DVT) before the age of 40 (n = 21) were compared to age-matched, healthy family members (n = 50), the proteomic patterns defined by the decision-tree analysis could classify the entity of DVT before age 40 with 67% sensitivity, at a specificity of 86%. When a small group of cases with history of superficial venous thrombosis (n = 6) was added to the case group, the sensitivity was 87.5% at a specificity of 80%. These data support the hypothesis that members of the protein C deficient Vermont kindred 11 who suffer a thrombotic event before age 40 display significant differences in low-molecular-weight proteomics profile compared to those who remain disease-free. This is the first study to apply SELDI-TOF technology in conjunction with a bioinformatics tool to analyze low-molecular-weight proteomic patterns in patients with venous thrombosis. C1 Univ Vermont, Coll Med, Dept Pathol, Burlington, VT 05405 USA. NCI Frederick, Clin Prote Reference Lab, SAIC Frederick Inc, Gaithersburg, MD USA. Univ Vermont, Coll Med, Dept Biostat, Burlington, VT USA. RP Bovill, EG (reprint author), Univ Vermont, Coll Med, Dept Pathol, Burlington, VT 05405 USA. EM Edwin.Bovill@uvm.edu FU NCI NIH HHS [N01-CO-12400]; NHLBI NIH HHS [P01 HL 4703] NR 19 TC 11 Z9 11 U1 0 U2 0 PU SCHATTAUER GMBH-VERLAG MEDIZIN NATURWISSENSCHAFTEN PI STUTTGART PA HOLDERLINSTRASSE 3, D-70174 STUTTGART, GERMANY SN 0340-6245 J9 THROMB HAEMOSTASIS JI Thromb. Haemost. PD DEC PY 2006 VL 96 IS 6 BP 725 EP 730 DI 10.1160/TH06-05-0273 PG 6 WC Hematology; Peripheral Vascular Disease SC Hematology; Cardiovascular System & Cardiology GA 117SI UT WOS:000242893200006 PM 17139365 ER PT J AU Jonklaas, J Sarlis, NJ Litofsky, D Ain, KB Bigos, ST Brierley, JD Cooper, DS Haugen, BR Ladenson, PW Magner, J Robbins, J Ross, DS Skarulis, M Maxon, HR Sherman, SI AF Jonklaas, Jacqueline Sarlis, Nicholas J. Litofsky, Danielle Ain, Kenneth B. Bigos, S. Thomas Brierley, James D. Cooper, David S. Haugen, Bryan R. Ladenson, Paul W. Magner, James Robbins, Jacob Ross, Douglas S. Skarulis, Monica Maxon, Harry R. Sherman, Steven I. TI Outcomes of patients with differentiated thyroid carcinoma following initial therapy SO THYROID LA English DT Article ID HIGH-RISK PAPILLARY; RADIOACTIVE IODINE; THYROTROPIN SUPPRESSION; DEATH CERTIFICATES; OBSERVER VARIATION; PROGNOSTIC FACTORS; I-131 THERAPY; CANCER; SURVIVAL; DISEASE AB This analysis was performed to determine the effect of initial therapy on the outcomes of thyroid cancer patients. The study setting was a prospectively followed multi-institutional registry. Patients were stratified as low risk (stages I and II) or high risk (stages III and IV). Treatments employed included near-total thyroidectomy, administration of radioactive iodine, and thyroid hormone suppression therapy. Outcome measures were overall survival, disease-specific survival, and disease-free survival. Near-total thyroidectomy, radioactive iodine, and aggressive thyroid hormone suppression therapy were each independently associated with longer overall survival in high-risk patients. Near-total thyroidectomy followed by radioactive iodine therapy, and moderate thyroid hormone suppression therapy, both predicted improved overall survival in stage II patients. No treatment modality, including lack of radioactive iodine, was associated with altered survival in stage I patients. Based on our overall survival data, we confirm that near-total thyroidectomy is indicated in high-risk patients. We also conclude that radioactive iodine therapy is beneficial for stage II, III, and IV patients. Importantly, we show for the first time that superior outcomes are associated with aggressive thyroid hormone suppression therapy in high-risk patients, but are achieved with modest suppression in stage II patients. We were unable to show any impact, positive or negative, of specific therapies in stage I patients. C1 Georgetown Univ, Ctr Med, Washington, DC 20007 USA. Univ Texas, MD Anderson Canc Ctr, Houston, TX USA. Univ Kentucky, Ctr Med, Lexington, KY USA. Maine Med Ctr, Portland, ME USA. Princess Margaret Hosp, Toronto, ON M4X 1K9, Canada. Sinai Hosp, Baltimore, MD 21215 USA. Univ Colorado, Denver, CO USA. Hlth Sci Ctr, Aurora, CO USA. Johns Hopkins Univ, Sch Med, Baltimore, MD USA. Genzyme Corp, Cambridge, MA USA. NIH, Bethesda, MD USA. Massachusetts Gen Hosp, Boston, MA 02114 USA. Univ Cincinnati, Ctr Med, Cincinnati, OH USA. RP Jonklaas, J (reprint author), Georgetown Univ, Ctr Med, 4000 Reservoir Rd,NW Bldg D,Ste 230, Washington, DC 20007 USA. EM jj@bc.georgetown.edu RI Jonklaas, Jacqueline/G-2807-2010; OI Jonklaas, Jacqueline/0000-0002-2238-2666; Ain, Kenneth/0000-0002-2668-934X; Sherman, Steven/0000-0002-3079-5153 FU NCRR NIH HHS [K23 RR16524] NR 61 TC 263 Z9 285 U1 1 U2 11 PU MARY ANN LIEBERT INC PI NEW ROCHELLE PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA SN 1050-7256 J9 THYROID JI Thyroid PD DEC PY 2006 VL 16 IS 12 BP 1229 EP 1242 DI 10.1089/thy.2006.16.1229 PG 14 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA 123RD UT WOS:000243312200006 PM 17199433 ER PT J AU Soto, J Berman, J AF Soto, J. Berman, J. TI Treatment of New World cutaneous leishmaniasis with miltefosine SO TRANSACTIONS OF THE ROYAL SOCIETY OF TROPICAL MEDICINE AND HYGIENE LA English DT Article DE cutaneous leishmaniasis; Leishmania panamensis; drug therapy; miltefosine ID CONTROLLED CLINICAL-TRIAL; MEGLUMINE ANTIMONATE; TOPICAL TREATMENT; GUATEMALA; HEXADECYLPHOSPHOCHOLINE; IDENTIFICATION AB Miltefosine (2.5 mg/kg/day for 28 days) was investigated for treatment of New World cutaneous leishmaniasis in Colombia and Guatemala. The data from a controlled study was remarkably similar to the data of a prior uncontrolled pilot study. In the controlled study, the per-protocol 6-month cure rate for Leishmania panamensis disease was 91% compared with a concomitant placebo cure rate of 38%. In Guatemala, the cure rate for L. braziliensis and L. mexicana disease was similar to 50% compared with similar to 20% for placebo. In both countries, nausea but not 'motion sickness' and vomiting but not diarrhoea were experienced by approximately 30% more miltefosine patients than placebo patients. Mild elevation of creatinine, but not of aspartate aminotransferase or alanine aminotransferase, was also more frequently seen in the miltefosine group than in the placebo group. Miltefosine was well tolerated, and as effective as historic values of antimony for treatment of L. panamensis disease. (c) 2006 Royal Society of Tropical Medicine and Hygiene. Published by Elsevier Ltd. All rights reserved. C1 NIH, Natl Ctr Complementary & Alternative Med, Bethesda, MD 20892 USA. Consorcio Invest Bioclin, Bogota, Colombia. RP Berman, J (reprint author), NIH, Natl Ctr Complementary & Alternative Med, 6707 Democracy Blvd,Suite 401, Bethesda, MD 20892 USA. EM bermanjo@mail.nih.gov NR 17 TC 51 Z9 51 U1 1 U2 2 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0035-9203 J9 T ROY SOC TROP MED H JI Trans. Roy. Soc. Trop. Med. Hyg. PD DEC PY 2006 VL 100 SU 1 BP S34 EP S40 DI 10.1016/j.trstmh.2006.02.022 PG 7 WC Public, Environmental & Occupational Health; Tropical Medicine SC Public, Environmental & Occupational Health; Tropical Medicine GA 106YV UT WOS:000242138800007 PM 16930649 ER PT J AU Khuu, HM Patel, N Carter, CS Murray, PR Read, EJ AF Khuu, Hanh M. Patel, Nayana Carter, Charles S. Murray, Patrick R. Read, Elizabeth J. TI Sterility testing of cell therapy products: parallel comparison of automated methods with a CFR-compliant method SO TRANSFUSION LA English DT Article ID PLASTIC CULTURE BOTTLES; BACTERIAL-CONTAMINATION; MICROBIAL-CONTAMINATION; BONE-MARROW; PERIPHERAL-BLOOD; MICROBIOLOGIC CONTAMINATION; CLINICAL-SIGNIFICANCE; POTENTIAL SOURCE; COMPONENTS; TRANSPLANTATION AB BACKGROUND: Automated blood culture systems are not FDA-approved for sterility testing of human cells, tissues, or cellular- or tissue-based products. It was previously demonstrated that BacT/ALERT (bioMerieux) and Bactec (Becton Dickinson) were superior to the manual CFR method described in the general biologics regulations, in rates of detection and time to detection of organisms seeded into mock mononuclear cell products with a variety of background media and antibiotics. In this study, the two automated systems were compared to the CFR method for sterility testing of actual cell therapy products manufactured in our facility. STUDY DESIGN AND METHODS: Over a 36-month period, in-process and final product samples from all cell therapy products manufactured in our facility were tested for sterility both by the CFR method and by either BacT/ALERT or Bactec. Products were categorized according to collection and processing variables for analysis of results. RESULTS: For 1617 samples of a broad range of cell therapy products, rates of true-positive tests were comparable for the automated and CFR methods (2.3% vs. 2.1%), but the CFR method had higher rates of false-positive results (7.3% vs. 0.2%). For automated systems, time to detection of organisms was equivalent to, or faster than, the CFR method. CONCLUSION: Compared to the CFR method, both BacT/ALERT and Bactec are more sensitive, faster in time to detection, less prone to false-positive results, and less labor-intensive. Both of these automated systems are suitable for sterility testing of cell therapy products after site-specific validation has been performed. C1 NIH, Ctr Clin, Dept Transfus Med, NIH, Bethesda, MD 20892 USA. NIH, Ctr Clin, Dept Lab Med, NIH, Bethesda, MD 20892 USA. RP Khuu, HM (reprint author), NIH, Ctr Clin, Dept Transfus Med, NIH, Bldg 10,Room 3C720 MSC 1288, Bethesda, MD 20892 USA. EM hkhuu@mail.cc.nih.gov NR 33 TC 18 Z9 19 U1 0 U2 1 PU BLACKWELL PUBLISHING PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DQ, OXON, ENGLAND SN 0041-1132 J9 TRANSFUSION JI Transfusion PD DEC PY 2006 VL 46 IS 12 BP 2071 EP 2082 DI 10.1111/j.1537-2995.2006.01041.x PG 12 WC Hematology SC Hematology GA 108LT UT WOS:000242242000007 PM 17176318 ER PT J AU Hansen, BJ Robbins, FM Adams, S Byrne, KM Lee, H Stroncek, DF AF Hansen, B. J. Robbins, F. -M. Adams, S. Byrne, K. M. Lee, H. Stroncek, D. F. TI Identification of a KEL7 subtype: implications for genotyping red blood cell Js(a) and Js(b) antigens SO TRANSFUSION MEDICINE LA English DT Letter ID MOLECULAR-BASIS; PHENOTYPE C1 NIH, Dept Transfus Med, Warren G Magnuson Clin Ctr, Bethesda, MD 20892 USA. RP Hansen, BJ (reprint author), NIH, Dept Transfus Med, Warren G Magnuson Clin Ctr, Bldg 10, Bethesda, MD 20892 USA. NR 6 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL PUBLISHING PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DQ, OXON, ENGLAND SN 0958-7578 J9 TRANSFUSION MED JI Transfus. Med. PD DEC PY 2006 VL 16 IS 6 BP 445 EP 446 DI 10.1111/j.1365-3148.2006.00689.x PG 2 WC Hematology SC Hematology GA 108LL UT WOS:000242241200009 PM 17163877 ER PT J AU Shah, BH Catt, KJ AF Shah, Bukhtiar H. Catt, Kevin J. TI Protein phosphatase 5 as a negative key regulator of Raf-1 activation SO TRENDS IN ENDOCRINOLOGY AND METABOLISM LA English DT Editorial Material ID PROTEIN PHOSPHATASE-5; SIGNAL-TRANSDUCTION; RECEPTOR ACTIVATION; KINASE; CANCER; TRANSACTIVATION; APOPTOSIS; PATHWAY AB Growth factors such as the epidermal growth factor cause sequential activation of receptor tyrosine kinases, adaptor molecules and the Raf-MEK-ERK pathway. The kinetics and intensity of these signals are dependent on the balance between phosphorylation and dephosphorylation of these molecules by numerous kinases and phosphatases, respectively. Recently, protein phosphatase 5 has been characterized as a key dephosphoryllation regulator of Raf-1 activation in growth factor-mediated signaling, leading to attenuation of the MEK-ERK cascade. C1 NICHD, Sect Hormonal Regulat, NIH, Bethesda, MD 20892 USA. RP Shah, BH (reprint author), NICHD, Sect Hormonal Regulat, NIH, Bethesda, MD 20892 USA. EM shahb@mail.nih.gov NR 14 TC 6 Z9 7 U1 0 U2 0 PU ELSEVIER SCIENCE LONDON PI LONDON PA 84 THEOBALDS RD, LONDON WC1X 8RR, ENGLAND SN 1043-2760 J9 TRENDS ENDOCRIN MET JI Trends Endocrinol. Metab. PD DEC PY 2006 VL 17 IS 10 BP 382 EP 384 DI 10.1016/j.tem.2006.10.013 PG 3 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA 119ZY UT WOS:000243054200003 PM 17084641 ER PT J AU Baler, RD Volkow, ND AF Baler, Ruben D. Volkow, Nora D. TI Drug addiction: the neurobiology of disrupted self-control SO TRENDS IN MOLECULAR MEDICINE LA English DT Review ID CORTICOTROPIN-RELEASING-FACTOR; COCAINE-SEEKING BEHAVIOR; PLACEBO-CONTROLLED TRIAL; PREFRONTAL CORTEX; NUCLEUS-ACCUMBENS; BRAIN ACTIVATION; ORBITOFRONTAL CORTEX; SYNAPTIC PLASTICITY; DOPAMINE RESPONSES; LOCOMOTOR-ACTIVITY AB The nature of addiction is often debated along moral versus biological lines. However, recent advances in neuroscience offer insights that might help bridge the gap between these opposing views. Current evidence shows that most drugs of abuse exert their initial reinforcing effects by inducing dopamine surges in limbic regions, affecting other neurotransmitter systems and leading to characteristic plastic adaptations. Importantly, there seem to be intimate relationships between the circuits disrupted by abused drugs and those that underlie self-control. Significant changes can be detected in circuits implicated in reward, motivation and/or drive, salience attribution, inhibitory control and memory consolidation. Therefore, addiction treatments should attempt to reduce the rewarding properties of drugs while enhancing those of alternative reinforcers, inhibit conditioned memories and strengthen cognitive control. We posit that the time has come to recognize that the process of addiction erodes the same neural scaffolds that enable self-control and appropriate decision making. C1 NIDA, NIH, Bethesda, MD 20892 USA. RP Volkow, ND (reprint author), NIDA, NIH, Bethesda, MD 20892 USA. EM nvolkow@nida.nih.gov NR 84 TC 189 Z9 204 U1 10 U2 55 PU ELSEVIER SCI LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND SN 1471-4914 J9 TRENDS MOL MED JI Trends Mol. Med PD DEC PY 2006 VL 12 IS 12 BP 559 EP 566 DI 10.1016/j.molmed.2006.10.005 PG 8 WC Biochemistry & Molecular Biology; Cell Biology; Medicine, Research & Experimental SC Biochemistry & Molecular Biology; Cell Biology; Research & Experimental Medicine GA 119YO UT WOS:000243050600002 PM 17070107 ER PT J AU Lu, L Koya, E Zhai, HF Hope, BT Shaham, Y AF Lu, Lin Koya, Eisuke Zhai, Haifeng Hope, Bruce T. Shaham, Yavin TI Role of ERK in cocaine addiction SO TRENDS IN NEUROSCIENCES LA English DT Review ID SIGNAL-REGULATED KINASE; MESOLIMBIC DOPAMINE SYSTEM; BEHAVIORAL SENSITIZATION; NUCLEUS-ACCUMBENS; SEEKING BEHAVIOR; PLACE PREFERENCE; GENE-EXPRESSION; MAP KINASE; TRANSDUCTION CASCADE; NEOSTRIATAL NEURONS AB Cocaine addiction is characterized by compulsive drug-taking behavior and high rates of relapse. According to recent theories, this addiction is due to drug-induced adaptations in the cellular mechanisms that underlie normal learning and memory. Such mechanisms involve signaling by extracellular signal-regulated kinase (ERK). As we review here, evidence from rodent studies also implicates ERK in cocaine psychomotor sensitization, cocaine reward, consolidation and reconsolidation of memories for cocaine cues, and time-dependent increases in cocaine seeking after withdrawal (incubation of cocaine craving). The role of ERK in these behaviors involves long-term stable alterations in synaptic plasticity that result from repeated cocaine exposure, and also rapidly induced alterations in synaptic transmission events that acutely control cocaine-seeking behaviors. Pharmacological manipulations that decrease the extent to which cocaine and cocaine cues induce ERK activity might therefore be considered as potential treatments for cocaine addiction. C1 Peking Univ, Natl Inst Drug Dependence, Dept Neuropharmacol, Beijing 100083, Peoples R China. NIDA, Behav Neurosci Branch, IRP, NIH,DHHS, Baltimore, MD 21224 USA. RP Lu, L (reprint author), Peking Univ, Natl Inst Drug Dependence, Dept Neuropharmacol, Beijing 100083, Peoples R China. EM linlu@bjmu.edu.cn; yshaham@intra.nida.nih.gov RI Hope, Bruce/A-9223-2010; shaham, yavin/G-1306-2014 OI Hope, Bruce/0000-0001-5804-7061; FU Intramural NIH HHS NR 70 TC 169 Z9 172 U1 0 U2 16 PU ELSEVIER SCIENCE LONDON PI LONDON PA 84 THEOBALDS RD, LONDON WC1X 8RR, ENGLAND SN 0166-2236 J9 TRENDS NEUROSCI JI Trends Neurosci. PD DEC PY 2006 VL 29 IS 12 BP 695 EP 703 DI 10.1016/j.tins.2006.10.005 PG 9 WC Neurosciences SC Neurosciences & Neurology GA 118NK UT WOS:000242948800006 PM 17084911 ER PT J AU Rothman, RB Blough, BE Baumann, MH AF Rothman, Richard B. Blough, Bruce E. Baumann, Michael H. TI Dual dopamine-5-HT releasers: potential treatment agents for cocaine addiction SO TRENDS IN PHARMACOLOGICAL SCIENCES LA English DT Review ID D-AMPHETAMINE TREATMENT; D-FENFLURAMINE; PSYCHOSTIMULANT WITHDRAWAL; STIMULANT DEPENDENCE; INTRAVENOUS COCAINE; NUCLEUS-ACCUMBENS; 5-HT2B RECEPTORS; SEEKING BEHAVIOR; RHESUS-MONKEYS; AGONIST-LIKE AB Biogenic amine transporters (BATs) are integral membrane proteins that translocate biogenic amine neurotransmitters [norepinephrine, dopamine (DA) and 5-hydroxytryptamine (5-HT)] across cell membranes. BATs are the principal sites of action for many psychotropic drugs, including abused stimulants such as cocaine and methamphetamine. Preclinical and human data demonstrate that withdrawal from long-term cocaine administration produces a dual deficit of synaptic DA and 5-HT in the brain, indicating the advantage of developing medications that normalize impairments in both neurotransmitter systems. In this article, we review data supporting the notion that stimulant effects normally produced by increased levels of extracellular DA can be antagonized by concurrent increases in levels of extracellular 5-HT. Accordingly, nonselective BAT substrates that can release both DA and 5-HT, such as the novel compound PAL287, have low abuse potential while maintaining the ability to suppress drug-seeking behavior. The collective findings indicate that such drugs will provide neurochemical normalization therapy for cocaine addiction and might also be useful for treating depression, obsessive-compulsive disorder, attention deficit disorder and obesity. C1 NIDA, Clin Psychopharmacol Sect, Intramural Res Program, NIH, Baltimore, MD 21224 USA. Res Triangle Inst Int, Chem & Life Sci Grp, Res Triangle Pk, NC 27709 USA. RP Rothman, RB (reprint author), NIDA, Clin Psychopharmacol Sect, Intramural Res Program, NIH, POB 5180,5500 Nathan Shock Dr, Baltimore, MD 21224 USA. EM rrothman@mail.nih.gov FU Intramural NIH HHS; NIDA NIH HHS [R01 DA 12970] NR 61 TC 28 Z9 28 U1 0 U2 3 PU ELSEVIER SCIENCE LONDON PI LONDON PA 84 THEOBALDS RD, LONDON WC1X 8RR, ENGLAND SN 0165-6147 J9 TRENDS PHARMACOL SCI JI Trends Pharmacol. Sci. PD DEC PY 2006 VL 27 IS 12 BP 612 EP 618 DI 10.1016/j.tips.2006.10.006 PG 7 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA 114QJ UT WOS:000242680400002 PM 17056126 ER PT J AU Szabo, C Pacher, P Swanson, RA AF Szabo, Csaba Pacher, Pal Swanson, Raymond A. TI Novel modulators of poly(ADP-ribose) polymerase SO TRENDS IN PHARMACOLOGICAL SCIENCES LA English DT Review ID FOCAL CEREBRAL-ISCHEMIA; ENDOTHELIAL DYSFUNCTION; CELL-DEATH; IN-VITRO; MICROGLIAL ACTIVATION; PARP-1 INHIBITION; OXIDATIVE STRESS; GENE DISRUPTION; MOUSE MODEL; MINOCYCLINE AB The nuclear enzyme poly(ADP-ribose) polymerase (PARP)-1 has an important role in regulating cell death and cellular responses to DNA repair. Pharmacological inhibitors of PARP have entered clinical testing as cytoprotective agents in cardiovascular diseases and as adjunct antitumor therapeutics. Initially, it was assumed that the regulation of PARP occurs primarily at the level of DNA breakage: recognition of DNA breaks was considered to be the primary regulator (activator) or the catalytic activity of PARK Recent studies have provided evidence that PARP-1 activity can also be modulated by several endogenous factors, including various kinases, purines and caffeine metabolites. There is a gender difference in the contribution of PARP-1 to stroke and inflammatory responses, which is due, at least in part, to endogenous estrogen levels. Several tetracycline antibiotics are also potent PARP-1 inhibitors. In this article, we present an overview of novel PARP-1 modulators. C1 Univ Med & Dent New Jersey, New Jersey Med Sch, Dept Surg, Newark, NJ 07103 USA. NIH, Sect Oxidate Stress tissue Injury, Lab Physiol Studies, Bethesda, MD 20892 USA. NIAAA, Bethesda, MD 20892 USA. RP Szabo, C (reprint author), Univ Med & Dent New Jersey, New Jersey Med Sch, Dept Surg, 185 S Orange Ave,Univ Hts, Newark, NJ 07103 USA. EM szabocsaba@aol.com RI Pacher, Pal/B-6378-2008; OI Pacher, Pal/0000-0001-7036-8108; Swanson, Raymond/0000-0002-3664-5359 FU Intramural NIH HHS [Z01 AA000375-02]; NIGMS NIH HHS [R01 GM060915, R01 GM060915-01] NR 57 TC 42 Z9 44 U1 0 U2 3 PU ELSEVIER SCIENCE LONDON PI LONDON PA 84 THEOBALDS RD, LONDON WC1X 8RR, ENGLAND SN 0165-6147 J9 TRENDS PHARMACOL SCI JI Trends Pharmacol. Sci. PD DEC PY 2006 VL 27 IS 12 BP 626 EP 630 DI 10.1016/j.tips.2006.10.003 PG 5 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA 114QJ UT WOS:000242680400004 PM 17055069 ER PT J AU Chulada, PC Corey, LA Vannappagari, V Whitehead, NS Blackshear, PJ AF Chulada, Patricia C. Corey, Linda A. Vannappagari, Vani Whitehead, Nedra S. Blackshear, Perry J. TI The feasibility of creating a population-based national twin registry in the United States SO TWIN RESEARCH AND HUMAN GENETICS LA English DT Article ID COMPLEX TRAITS; HEALTH AB Between 4 to 6 million twins exist in the US today who offer scientists a valuable potential resource for conducting behavioral and biomedical research. However, unlike many other countries, there is no national system in the US for identifying twins and eliciting their participation in these important research programs. Therefore, the National Institute of Environmental Health Sciences (NIEHS) is conducting a study to determine the feasibility of creating a national, population-based twin registry in the US. The major goal is to estimate the potential size and characteristics of a national twin registry based on the current twin population in the US, our ability to ascertain and enrol them, and their willingness to participate. Existing US twin cohorts are also being examined in this study as well as alternatives for improving US twin resources should a national twin registry be deemed infeasible. The various options will be compared in terms of possible source populations, generalizability and adequacy for statistically powering various types of etiological studies. Two expert advisory panels have been assembled to assist in the conduct of this study. The Scientific Advisory Panel is charged with providing expertise concerning study goals, design and methodology, and evaluating the study's conclusion. A separate Ethics Advisory Panel is charged with providing expertise on the ethical, legal, and social issues that might be encountered if a national twin registry is ultimately pursued. Having a national population-based twin registry in the US would be advantageous to US scientists and those worldwide. It would provide ample numbers of twin pairs to conduct various types of environmental genomic studies currently not possible with existing US twin resources. It would also allow US scientists to select for characteristics (race, ethnicity, environments, and so on) inherent in our own population. Finally and foremost, it would help to meet the worldwide demand for twin resources which is expected to increase over time, as new genomic and analytical tools become available and new hypotheses emerge concerning the complex interplay between genes, lifestyles and environment. C1 NIEHS, Program Clin Res, Res Triangle Pk, NC 27709 USA. Virginia Commonwealth Univ, Virginia Inst Psychiat & Behav Genet, Richmond, VA USA. GlaxoSmithKline Inc, Res & Dev, Res Triangle Pk, NC USA. Res Triangle Inst, Atlanta, GA USA. RP Chulada, PC (reprint author), NIEHS, Program Clin Res, POB 12233, Res Triangle Pk, NC 27709 USA. EM chulada@niehs.nih.gov FU Intramural NIH HHS [Z99 ES999999, 001-0038-895] NR 10 TC 1 Z9 3 U1 1 U2 3 PU AUSTRALIAN ACAD PRESS PI BOWEN HILLS PA 32 JEAYS ST, BOWEN HILLS, QLD 4006, AUSTRALIA SN 1832-4274 J9 TWIN RES HUM GENET JI Twin Res. Hum. Genet. PD DEC PY 2006 VL 9 IS 6 BP 919 EP 926 DI 10.1375/183242706779462705 PG 8 WC Genetics & Heredity; Obstetrics & Gynecology SC Genetics & Heredity; Obstetrics & Gynecology GA 122HO UT WOS:000243216600038 PM 17254431 ER PT J AU Anderson, JM Swanson, KI Schwartz, TR Glass, GE Norris, DE AF Anderson, Jennifer M. Swanson, Katherine I. Schwartz, Timothy R. Glass, Gregory E. Norris, Douglas E. TI Mammal diversity and infection prevalence in the maintenance of enzootic Borrelia burgdorferi along the western coastal plains of Maryland SO VECTOR-BORNE AND ZOONOTIC DISEASES LA English DT Article DE Lyme disease; Ixodes scapularis; Peromyscus leucopus; Borrelia burgdorferi ID IXODES-DAMMINI ACARI; SOUTHERN UNITED-STATES; LYME-DISEASE; PEROMYSCUS-LEUCOPUS; SCAPULARIS ACARI; PHYLOGENETIC-RELATIONSHIPS; MICROTUS-PENNSYLVANICUS; DERMACENTOR-VARIABILIS; SPATIAL-DISTRIBUTION; EASTERN CHIPMUNK AB The primary vector of Borrelia burgdorferi in North America, Ixodes scapularis, feeds on various mammalian, avian, and reptilian hosts. Several small mammal hosts; Peromyscus leucopus, Tamias striatus, Microtus pennsylvanicus, and Blarina spp. can serve as reservoirs in an enzootic cycle of Lyme disease. The primary reservoir in the northeast United States is the white-footed mouse, P. leucopus. The infection prevalence of this reservoir as well as the roles of potential secondary reservoirs has not been established in southern Maryland, a region of low to moderate Borrelia infection in humans. Intensive trapping at 96 locations throughout the western Coastal Plains of Maryland was conducted and we found that 31.6% of P. leucopus were infected with B. burgdorferi. Sequence and phylogenetic analysis revealed that only B. burgdorferi sensu stricto circulated in southern Maryland, Feral house mice and voles also were infected and may serve as secondary hosts. Peromyscus gender, age and month of capture were significantly associated with infection status. Larval I. scapularis were the dominant ectoparasite collected from captured rodents even though host seeking A. americanum and D. variabilis were collected in greater numbers across the sampling region. Our findings illustrate that the enzootic cycle of LD is maintained in the western Coastal Plains region of southern Maryland between I. scapularis and P. leucopus as the dominant reservoir. C1 Johns Hopkins Bloomberg Sch Publ Hlth, W Harry Feinstone Dept Mol Microbiol & Immunol, Baltimore, MD USA. RP Anderson, JM (reprint author), NIAID, LMVR, NIH, 12735 Twinbrook Pkwy,Rm 2E-22, Rockville, MD 20852 USA. EM jenanderson@niaid.nih.gov FU NIAID NIH HHS [T32 AI007417]; NIEHS NIH HHS [T32 ES007141, T32ES07141]; PHS HHS [U50/CCU319554] NR 57 TC 4 Z9 4 U1 5 U2 13 PU MARY ANN LIEBERT INC PI NEW ROCHELLE PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA SN 1530-3667 J9 VECTOR-BORNE ZOONOT JI Vector-Borne Zoonotic Dis. PD WIN PY 2006 VL 6 IS 4 BP 411 EP 422 DI 10.1089/vbz.2006.6.411 PG 12 WC Public, Environmental & Occupational Health; Infectious Diseases SC Public, Environmental & Occupational Health; Infectious Diseases GA 123AB UT WOS:000243267600013 PM 17187577 ER PT J AU De Waal, L Suzer, Y Wyatt, LS Sintnicolaas, K Sutter, G Moss, B Osterhaus, ADME De Swart, RL AF De Waal, Leon Suzer, Yasemin Wyatt, Linda S. Sintnicolaas, Kees Sutter, Gerd Moss, Bernard Osterhaus, Albert D. M. E. De Swart, Rik L. TI T cell responses to respiratory syncytial virus fusion and attachment proteins in human peripheral blood mononuclear cells SO VIRAL IMMUNOLOGY LA English DT Article ID RSV INFECTION; LYMPHOCYTE EPITOPE; GLYCOPROTEIN-G; VACCINE; IMMUNITY; INFANTS; IDENTIFICATION; RECOGNIZE; MACAQUES; CHILDREN AB The cellular immune response to respiratory syncytial virus (RSV) is considered important in both protection and immunopathogenesis. We have studied the HLA class I- and class II-restricted T cell responses to RSV fusion (F) and attachment (G) proteins in peripheral blood mononuclear cells (PBMCs) obtained from healthy young adults. PBMCs were stimulated with autologous cells infected with recombinant modified vaccinia virus Ankara (rMVA) expressing RSV F (rMVA-F) or G (rMVA-G). In rMVA-F-stimulated bulk cultures F-specific CD4(=) and CD8(+) T cell responses were demonstrated, whereas in rMVA-G-stimulated cultures only G-specific CD4(+) T cell responses were detected. Using a set of overlapping peptides spanning the F protein, a number of the F-specific T cell responses could be mapped to different antigenic regions, whereas for the G protein only CD4(+) T cell responses recognizing the central conserved domain could be detected. These results suggest that the RSV glycoprotein-specific T cell response is directed to a number of different epitopes. Further studies must be performed to confirm the apparent inability of the RSV G protein to induce CD8(+) T cell responses. The rMVA-based in vitro stimulation protocol will be useful to define protein-specific T cell responses in different viral systems. C1 Erasmus MC, Dept Virol, NL-3015 CE Rotterdam, Netherlands. Paul Ehrlich Inst, Dept Virol, D-6070 Langen, Germany. NIAID, Viral Dis Lab, NIH, Bethesda, MD 20892 USA. Sanquin Blood Bank S W Reg, Rotterdam, Netherlands. RP De Waal, L (reprint author), Erasmus MC, Dept Virol, S Gravendykwal 230, NL-3015 CE Rotterdam, Netherlands. EM l.dewaal@erasmusmc.nl OI De Swart, Rik/0000-0003-3599-8969 NR 38 TC 8 Z9 8 U1 1 U2 1 PU MARY ANN LIEBERT INC PI NEW ROCHELLE PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA SN 0882-8245 J9 VIRAL IMMUNOL JI Viral Immunol. PD WIN PY 2006 VL 19 IS 4 BP 669 EP 678 DI 10.1089/vim.2006.0061 PG 10 WC Immunology; Virology SC Immunology; Virology GA 124DD UT WOS:000243346600009 PM 17201662 ER PT J AU Moniuszko, M Edghill-Smith, Y Venzon, D Stevceva, L Nacsa, J Tryniszewska, E Tsai, WP Franchini, G AF Moniuszko, Marcin Edghill-Smith, Yvette Venzon, David Stevceva, Liljana Nacsa, Janos Tryniszewska, Elzbieta Tsai, Wen-Po Franchini, Genoveffa TI Decreased number of CD4(+) and CD8(+) T cells that express the interleukin-7 receptor in blood and tissues of SIV-infected macaques SO VIROLOGY LA English DT Article DE SIV; IL-7/IL-7R; T cells ID VIRUS SIVMAC251 CHALLENGE; SIMIAN IMMUNODEFICIENCY; ANTIRETROVIRAL THERAPY; RHESUS MACAQUES; IL-7 RECEPTOR; IN-VIVO; HOMEOSTATIC PROLIFERATION; CD127 EXPRESSION; MEMORY CELLS; HIV AB Acute HIV/SIV (human/simian immunodeficiency virus) infection results in severe CD4(+) T cell depletion in lymphoid compartments. During the chronic phase of infection, CD4+ T cell numbers rebound in blood but remain low in the gut-associated lymphoid tissue (GALT), even when viral replication is suppressed by antiretroviral therapy (ART). Thus, strategies to repopulate lymphoid compartments may ameliorate the clinical outcome of HIV/SIV infection. Interleukin (IL)-7 is a key cytokine for the maintenance of homeostatic proliferation of T cells. In HIV/SIV infection, IL-7 expression is increased, likely to compensate for T cell loss, suggesting that supraphysiological administration of IL-7 could provide additional benefit. However, the ability of T cells to respond to IL-7 is dependent on the level of expression of the IL-7 receptor (IL-7R) in T cells in various body compartments. In here, we investigated the proportion of IL-7R(+) T cells in blood, spleen, gut, and genitourinary tract of healthy and SIV-infected macaques with various degrees of CD4+ T cell depletion. We found that the percentage of T cells expressing IL-7R was significantly lower in both CD4(+) and CD8(+) T cell subsets in SIV-infected macaques than in healthy animals and this decrease directly correlated with the CD4+ T cell number. Importantly, the proportion of CD4+ and CD8+ T cells expressing IL-7R in blood paralleled that found in tissues. IL-7R(+) T cells within the SIV-specific CD8(+) T cells varied and were lowest in most tissues of viremic macaques, likely reflecting continuous antigen stimulation of effector cells. C1 NCI, Anin Models & Retroviral Vaccines Sect, Bethesda, MD 20892 USA. Med Univ Bialystok, Bialystok, Poland. NCI, Biostat & Data Management Sect, Bethesda, MD 20892 USA. RP Franchini, G (reprint author), NCI, Anin Models & Retroviral Vaccines Sect, 41-D804, Bethesda, MD 20892 USA. EM franchig@mail.nih.gov OI Stevceva, Liljana/0000-0002-3761-2460 FU Intramural NIH HHS NR 42 TC 19 Z9 19 U1 0 U2 2 PU ACADEMIC PRESS INC ELSEVIER SCIENCE PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA SN 0042-6822 J9 VIROLOGY JI Virology PD DEC PY 2006 VL 356 IS 1-2 BP 188 EP 197 DI 10.1016/j.virol.2006.07.031 PG 10 WC Virology SC Virology GA 111BD UT WOS:000242424800021 PM 16934309 ER PT J AU Li, F Zoumplis, D Matallana, C Kilgore, NR Reddick, M Yunus, AS Adamson, CS Salzwedel, K Martin, DE Allaway, GP Freed, EO Wild, CT AF Li, Feng Zoumplis, Dorian Matallana, Claudia Kilgore, Nicole R. Reddick, Mary Yunus, Abdul S. Adamson, Catherine S. Salzwedel, Karl Martin, David E. Allaway, Graham P. Freed, Eric O. Wild, Carl T. TI Determinants of activity of the HIV-1 maturation inhibitor PA-457 SO VIROLOGY LA English DT Article DE PA-457; HIV; maturation inhibitor; CA-SP1 cleavage; viral determinants ID IMMUNODEFICIENCY-VIRUS TYPE-1; ROUS-SARCOMA-VIRUS; DIMERIZATION INITIATION SITE; LATE ASSEMBLY DOMAIN; GAG PRECURSOR; DELETION MUTATIONS; HELICAL STRUCTURE; VIRAL PROTEASE; MATRIX PROTEIN; LIFE-CYCLE AB 3-0-(3',3'-dimethylsuccinyl) betulinic acid, also termed PA-457 or DSB, is a novel HIV-1 inhibitor that blocks virus maturation by disrupting cleavage of the capsid precursor, CA-SP1. To better define the molecular target for PA-457, we prepared a panel of mutant viruses with point deletions spanning the CA-SP1 cleavage domain and characterized each of these viruses for PA-457 sensitivity. Our results indicate that amino acid residues in the N-terminal half of SP1 serve as determinants of PA-457 activity, while residues in the C-terminal half of SP1 were not involved in compound activity. These findings support and extend previous observations that PA-457 is a specific inhibitor of CA-SP1 cleavage and identify the CA-SP1 domain as the primary viral determinant for this novel inhibitor of HIV-1 replication. (c) 2006 Elsevier Inc. All rights reserved. C1 Panacos Pharmaceut, Gaithersburg, MD 20877 USA. NCI, HIV Drug Resistance Program, Frederick, MD 21702 USA. RP Wild, CT (reprint author), 19008 Oxcart Pl, Gaithersburg, MD 20886 USA. EM cwild@aol.com FU NIAID NIH HHS [5 R44 AI051047-03] NR 41 TC 47 Z9 51 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 0042-6822 J9 VIROLOGY JI Virology PD DEC PY 2006 VL 356 IS 1-2 BP 217 EP 224 DI 10.1016/j.virol.2006.07.023 PG 8 WC Virology SC Virology GA 111BD UT WOS:000242424800024 PM 16930665 ER PT J AU Shewmaker, F Wickner, RB AF Shewmaker, Frank Wickner, Reed B. TI Ageing in yeast does not enhance prion generation SO YEAST LA English DT Article DE [URE3]; [PSI+]; Ure2p; Sup35p ID SACCHAROMYCES-CEREVISIAE; LIFE-SPAN; PROTEIN; CHAPERONE; URE3; PROPAGATION; GUANIDINE; HSP104; CELLS; GENE AB The yeast prions [URE3] and [PSI+] are self-propagating amyloids of Ure2p and Sup35p, respectively. The analogous transmissible spongiform encephalopathies of mammals and other amyloidoses are largely diseases of later life. From normal strains lacking the prions, we isolated old cells and measured the frequency of de novo [URE3] and [PSI I] prion generation. We find no evidence that ageing of yeast increases the frequency of prion occurrence. Copyright (c) 2006 John Wiley & Sons, C1 NIDDKD, Lab Biochem & Genet, NIH, Bethesda, MD 20892 USA. RP Wickner, RB (reprint author), NIDDKD, Lab Biochem & Genet, NIH, Bldg 8,Room 225,8 Ctr Dr,MSC 0830, Bethesda, MD 20892 USA. EM wickner@helix.nih.gov FU Intramural NIH HHS NR 19 TC 4 Z9 4 U1 0 U2 1 PU JOHN WILEY & SONS LTD PI CHICHESTER PA THE ATRIUM, SOUTHERN GATE, CHICHESTER PO19 8SQ, W SUSSEX, ENGLAND SN 0749-503X J9 YEAST JI Yeast PD DEC PY 2006 VL 23 IS 16 BP 1123 EP 1128 DI 10.1002/yea.1425 PG 6 WC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Microbiology; Mycology SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Microbiology; Mycology GA 121RC UT WOS:000243173700001 PM 17133618 ER PT J AU Needham, PG Trumbly, RJ AF Needham, Patrick G. Trumbly, Robert J. TI In vitro characterization of the Mig1 repressor from Saccharomyces cerevisiae reveals evidence for monomeric and higher molecular weight forms SO YEAST LA English DT Article DE Mig1; Saccharomyces cerevisiae; yeast; glucose repression ID TRANSCRIPTION FACTOR PHO4; GLUCOSE REPRESSION; GEL-ELECTROPHORESIS; GENE-EXPRESSION; REGULATED EXPRESSION; COREPRESSOR COMPLEX; SUC2 GENE; YEAST; PROTEIN; BINDING AB The Mig1 DNA-binding protein of Saccharomyces cerevisiae was expressed and purified from yeast and the physical properties were characterized by several methods, including gel filtration, sucrose gradient sedimentation and native gel electrophoresis. Purified Mig1 exists as a monomer with a Stokes' radius of 48 A and a sedimentation coefficient of 3.55 S. Mig1 has an elongated shape with a frictional coefficient of 1.83. The K-d of purified Mig1 for the SUC2 A site is 2.8 nM and for SUC2 B site 25.8 nM; these values were similar for Mig1 purified from repressed and derepressed cells. Full-length Mig1 expressed in yeast binds more tightly to SUC2 B than bacterially expressed GST-Mig1. Sucrose gradient sedimentation resolved a larger molecular weight form of Mig1 in whole-cell extracts that was not seen in purified samples and may represent a complex with another protein. This complex is found within the nucleus and is seen only in repressed cells. Mig1 exists in multiple phosphorylation states and only less phosphorylated forms of Mig1 are associated with this complex. Copyright (c) 2006 John Wiley & Sons, Ltd. C1 Univ Toledo, Coll Med, Dept Biochem & Canc Biol, Toledo, OH 43614 USA. RP Needham, PG (reprint author), NIH, Bldg 8,Rm 407,9000 Rockville Pike, Bethesda, MD 20892 USA. EM needhamp@niddk.nih.gov NR 58 TC 2 Z9 2 U1 0 U2 0 PU JOHN WILEY & SONS LTD PI CHICHESTER PA THE ATRIUM, SOUTHERN GATE, CHICHESTER PO19 8SQ, W SUSSEX, ENGLAND SN 0749-503X J9 YEAST JI Yeast PD DEC PY 2006 VL 23 IS 16 BP 1151 EP 1166 DI 10.1002/yea.1429 PG 16 WC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Microbiology; Mycology SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Microbiology; Mycology GA 121RC UT WOS:000243173700004 PM 17133623 ER PT J AU Eling, TE Baek, SJ Shim, M Lee, CH AF Eling, Thomas E. Baek, Seung Joon Shim, Minsub Lee, Chang Ho TI NSAID activated gene (NAG-1), a modulator of tumorigenesis SO JOURNAL OF BIOCHEMISTRY AND MOLECULAR BIOLOGY LA English DT Review DE anti-tumorigenic; cancer; Cox inhibitor; Min mice; NAG-1; tumor suppressor ID TGF-BETA SUPERFAMILY; GROWTH-FACTOR-BETA; CYCLOOXYGENASE INHIBITORS INDUCE; COLORECTAL-CANCER CELLS; PROSTATE-CANCER; P53-DEPENDENT MECHANISM; TUMOR-DEVELOPMENT; CYTOKINE-1 MIC-1; H6D POLYMORPHISM; CARCINOMA-CELLS AB The NSAID activated gene (NAG-1), a member of the TGF-beta superfamily, is involved in tumor progression and development. The over-expression of NAG-1 in cancer cells results in growth arrest and increase in apoptosis, suggesting that NAG-1 has anti-tumorigenic activity. This conclusion is further supported by results of experiments with transgenic mice that ubiquitously express human NAG-1. These transgenic mice are resistant to the development of intestinal tumors following treatment with azoxymethane or by introduction of a mutant APC gene. In contrast, other data suggest a pro-tumorigenic role for NAG-1, for example, high expression of NAG-1 is frequently observed in tumors. NAG-1 may be like other members of the TGF-beta superfamily, acting as a tumor suppressor in the early stages, but acting pro-tumorigenic at the later stages of tumor progression. The expression of NAG-1 can be increased by treatment with drugs and chemicals documented to prevent tumor formation and development. Most notable is the increase in NAG-1 expression by the inhibitors of cyclooxygenases that prevent human colorectal cancer development. The regulation of NAG-1 is complex, but these agents act through either p53 or EGR-1 related pathways. In addition, an increase in NAG-1 is observed in inhibition of the AKT/GSK-3(3 pathway, suggesting NAG-1 alters cell survival. Thus, NAG-1 expression is regulated by tumor suppressor pathways and appears to modulate tumor progression. C1 NIEHS, NIH, Res Triangle Pk, NC 27709 USA. Univ Tennessee, Coll Vet Med, Dept Pathobiol, Knoxville, TN 37996 USA. Kangnung Natl Univ, Dept Biol, Kangnung 210702, South Korea. RP Eling, TE (reprint author), NIEHS, NIH, Res Triangle Pk, NC 27709 USA. EM eling@niehs.nih.gov OI Baek, Seung/0000-0001-7866-7778 NR 45 TC 64 Z9 67 U1 0 U2 1 PU SPRINGER SINGAPORE PTE LTD PI SINGAPORE PA #04-01 CENCON I, 1 TANNERY RD, SINGAPORE 347719, SINGAPORE SN 1225-8687 J9 J BIOCHEM MOL BIOL JI J. Biochem. Mol. Biol. PD NOV 30 PY 2006 VL 39 IS 6 BP 649 EP 655 PG 7 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA 110EH UT WOS:000242360600001 PM 17129398 ER PT J AU El-Sadr, WM Lundgren, JD Neaton, JD Gordin, F Abrams, D Arduino, RC Babiker, A Burman, W Clumeck, N Cohen, CJ Cohn, D Cooper, D Darbyshire, J Emery, S Fatkenheuer, G Gazzard, B Grund, B Hoy, J Klingman, K Losso, M Mejia, JMR Markowitz, N Neuhaus, J Phillips, A Rappoport, C AF El-Sadr, W. M. Lundgren, J. D. Neaton, J. D. Gordin, F. Abrams, D. Arduino, R. C. Babiker, A. Burman, W. Clumeck, N. Cohen, C. J. Cohn, D. Cooper, D. Darbyshire, J. Emery, S. Faetkenheuer, G. Gazzard, B. Grund, B. Hoy, J. Klingman, K. Losso, M. Mejia, J. M. Ramos Markowitz, N. Neuhaus, J. Phillips, A. Rappoport, C. CA Strategies Management Antiretrovir TI CD4+count-guided interruption of antiretroviral treatment SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Article ID CLINICAL-TRIALS; RANDOMIZED-TRIAL; COMBINATION THERAPY; AIDS EVENTS; T-CELLS; HIV; MORTALITY; INFECTION; VIRUS; DEATH AB BACKGROUND: Despite declines in morbidity and mortality with the use of combination antiretroviral therapy, its effectiveness is limited by adverse events, problems with adherence, and resistance of the human immunodeficiency virus (HIV). METHODS: We randomly assigned persons infected with HIV who had a CD4+ cell count of more than 350 per cubic millimeter to the continuous use of antiretroviral therapy (the viral suppression group) or the episodic use of antiretroviral therapy (the drug conservation group). Episodic use involved the deferral of therapy until the CD4+ count decreased to less than 250 per cubic millimeter and then the use of therapy until the CD4+ count increased to more than 350 per cubic millimeter. The primary end point was the development of an opportunistic disease or death from any cause. An important secondary end point was major cardiovascular, renal, or hepatic disease. RESULTS: A total of 5472 participants (2720 assigned to drug conservation and 2752 to viral suppression) were followed for an average of 16 months before the protocol was modified for the drug conservation group. At baseline, the median and nadir CD4+ counts were 597 per cubic millimeter and 250 per cubic millimeter, respectively, and 71.7% of participants had plasma HIV RNA levels of 400 copies or less per milliliter. Opportunistic disease or death from any cause occurred in 120 participants (3.3 events per 100 person-years) in the drug conservation group and 47 participants (1.3 per 100 person-years) in the viral suppression group (hazard ratio for the drug conservation group vs. the viral suppression group, 2.6; 95% confidence interval [CI], 1.9 to 3.7; P<0.001). Hazard ratios for death from any cause and for major cardiovascular, renal, and hepatic disease were 1.8 (95% CI, 1.2 to 2.9; P=0.007) and 1.7 (95% CI, 1.1 to 2.5; P=0.009), respectively. Adjustment for the latest CD4+ count and HIV RNA level (as time-updated covariates) reduced the hazard ratio for the primary end point from 2.6 to 1.5 (95% CI, 1.0 to 2.1). CONCLUSIONS: Episodic antiretroviral therapy guided by the CD4+ count, as used in our study, significantly increased the risk of opportunistic disease or death from any cause, as compared with continuous antiretroviral therapy, largely as a consequence of lowering the CD4+ cell count and increasing the viral load. Episodic antiretroviral therapy does not reduce the risk of adverse events that have been associated with antiretroviral therapy. C1 Harlem Hosp Med Ctr, Div Infect Dis, New York, NY 10037 USA. Columbia Univ, New York, NY USA. Hvidovre Univ Hosp, DK-2650 Hvidovre, Denmark. Univ Minnesota, Minneapolis, MN USA. Washington Vet Affairs Med Ctr, Washington, DC USA. Univ Calif San Francisco, San Francisco, CA 94143 USA. Univ Texas, Sch Med, Houston, TX USA. MRC, London, England. Denver Publ Hlth Dept, Denver, CO USA. Ctr Hosp Univ St Pierre, Brussels, Belgium. Community Res Initiat New England, Boston, MA USA. Natl Ctr HIV Epidemiol & Clin Res, Sydney, NSW, Australia. Univ Hosp, Cologne, Germany. Natl Ctr HIV Epidemiol & Clin Res, Melbourne, Vic, Australia. NIAID, Bethesda, MD 20892 USA. Hosp Gen de Agudos JM Ramos Mejia, Buenos Aires, DF, Argentina. Henry Ford Hosp, Detroit, MI 48202 USA. Royal Free Hosp, Sch Med, London NW3 2QG, England. RP El-Sadr, WM (reprint author), Harlem Hosp Med Ctr, Div Infect Dis, Rm 3107,506 Lenox Ave, New York, NY 10037 USA. EM wme1@columbia.edu RI Phillips, Andrew/B-4427-2008; OI Phillips, Andrew/0000-0003-2384-4807; Lundgren, Jens/0000-0001-8901-7850 NR 41 TC 1257 Z9 1274 U1 2 U2 32 PU MASSACHUSETTS MEDICAL SOC PI WALTHAM PA WALTHAM WOODS CENTER, 860 WINTER ST,, WALTHAM, MA 02451-1413 USA SN 0028-4793 J9 NEW ENGL J MED JI N. Engl. J. Med. PD NOV 30 PY 2006 VL 355 IS 22 BP 2283 EP 2296 PG 14 WC Medicine, General & Internal SC General & Internal Medicine GA 110CG UT WOS:000242355300004 ER PT J AU Hampson, LA Agrawal, M Joffe, S Gross, CP Verter, J Emanuel, EJ AF Hampson, Lindsay A. Agrawal, Manish Joffe, Steven Gross, Cary P. Verter, Joel Emanuel, Ezekiel J. TI Patients' views on financial conflicts of interest in cancer research trials SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Article ID POTENTIAL RESEARCH PARTICIPANTS; ACADEMIC MEDICAL-CENTERS; INFORMED CONSENT; TRUST; PHYSICIANS; DISCLOSURE; PROFESSION AB BACKGROUND: Financial ties between researchers or medical centers and companies whose drugs are being tested have come under increasing scrutiny. METHODS: We conducted in-person interviews with 253 patients in cancer-research trials (a 93% response rate) at five U.S. medical centers to determine their attitudes regarding potential financial conflicts of interest among researchers and medical centers. RESULTS: More than 90% of patients expressed little or no worry about financial ties that researchers or institutions might have with drug companies. Most patients said they would have enrolled in the trial even if the drug company had paid the researcher for speaking (82% of those interviewed) or consulting (75%) or if the researcher had received royalty payments (70%) or owned stock in the company (76%). Similarly, most patients would have enrolled in the trial if their cancer center had owned stock in the drug company (77%) or received royalty payments from the company (79%). Most patients believed it was ethical for researchers to receive speaking fees (81%) or consulting fees (82%) from the company. However, a substantial minority of patients wanted disclosure of the oversight system for researchers (40%) and of researchers' financial interests (31%); 17% thought no disclosure to patients was necessary. CONCLUSIONS: Most patients in cancer-research trials were not worried about financial ties between researchers or medical centers and drug companies and would still have enrolled in the trial if they had known about such financial ties. A substantial minority wanted to be informed about the oversight system to protect against financial conflicts of interest and about researchers' financial interests. C1 NIH, Dept Clin Bioeth, Ctr Clin, Bethesda, MD 20892 USA. Univ Michigan, Sch Med, Ann Arbor, MI USA. Dana Farber Canc Inst, Dept Pediat Oncol, Boston, MA 02115 USA. Yale Univ, Sch Med, Yale Canc Ctr, New Haven, CT USA. Yale Univ, Sch Med, Gen Internal Med Sect, New Haven, CT USA. Stat Collaborat, Washington, DC USA. RP Emanuel, EJ (reprint author), NIH, Dept Clin Bioeth, Ctr Clin, Bldg 10,Rm 1C118, Bethesda, MD 20892 USA. EM eemanuel@nih.gov OI Joffe, Steven/0000-0002-0667-7384 NR 33 TC 70 Z9 71 U1 0 U2 7 PU MASSACHUSETTS MEDICAL SOC PI WALTHAM PA WALTHAM WOODS CENTER, 860 WINTER ST,, WALTHAM, MA 02451-1413 USA SN 0028-4793 J9 NEW ENGL J MED JI N. Engl. J. Med. PD NOV 30 PY 2006 VL 355 IS 22 BP 2330 EP 2337 DI 10.1056/NEJMsa064160 PG 8 WC Medicine, General & Internal SC General & Internal Medicine GA 110CG UT WOS:000242355300008 PM 17135586 ER PT J AU Nabel, EG AF Nabel, Elizabeth G. TI Conflict of interest - or conflict of priorities? SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Editorial Material C1 NHLBI, Bethesda, MD 20892 USA. RP Nabel, EG (reprint author), NHLBI, Bldg 10, Bethesda, MD 20892 USA. NR 3 TC 6 Z9 6 U1 0 U2 0 PU MASSACHUSETTS MEDICAL SOC PI WALTHAM PA WALTHAM WOODS CENTER, 860 WINTER ST,, WALTHAM, MA 02451-1413 USA SN 0028-4793 J9 NEW ENGL J MED JI N. Engl. J. Med. PD NOV 30 PY 2006 VL 355 IS 22 BP 2365 EP 2367 DI 10.1056/NEJMe068238 PG 3 WC Medicine, General & Internal SC General & Internal Medicine GA 110CG UT WOS:000242355300016 PM 17135592 ER PT J AU Solomon, S Wittes, J Arber, N Bertagnolli, M Hawk, E Levin, B AF Solomon, Scott Wittes, Janet Arber, Nadir Bertagnolli, Monica Hawk, Ernest Levin, Bernard CA APC PreSAP Trial Investigators TI Risks and benefits of celecoxib to prevent colorectal adenomas - Reply SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Letter C1 Brigham & Womens Hosp, Boston, MA 02115 USA. Stat Collaborat, Washington, DC 20036 USA. Tel Aviv Sourasky Med Ctr, IL-64239 Tel Aviv, Israel. NCI, Bethesda, MD 20892 USA. Univ Texas, MD Anderson Canc Ctr, Houston, TX 77030 USA. RP Solomon, S (reprint author), Brigham & Womens Hosp, 75 Francis St, Boston, MA 02115 USA. NR 1 TC 0 Z9 0 U1 0 U2 0 PU MASSACHUSETTS MEDICAL SOC PI WALTHAM PA WALTHAM WOODS CENTER, 860 WINTER ST,, WALTHAM, MA 02451-1413 USA SN 0028-4793 J9 NEW ENGL J MED JI N. Engl. J. Med. PD NOV 30 PY 2006 VL 355 IS 22 BP 2371 EP 2372 PG 2 WC Medicine, General & Internal SC General & Internal Medicine GA 110CG UT WOS:000242355300025 ER PT J AU Kulldorff, M Huang, L Pickle, L Duczmal, L AF Kulldorff, Martin Huang, Lan Pickle, Linda Duczmal, Luiz TI An elliptic spatial scan statistic SO STATISTICS IN MEDICINE LA English DT Article DE disease surveillance; clusters; clustering; spatial statistics; eccentricity penalty; statistical power ID UNITED-STATES; CLUSTERS; CANCER; SURVEILLANCE; DISEASE; BREAST AB The spatial scan statistic is commonly used for geographical disease cluster detection, cluster evaluation and disease surveillance. The most commonly used shape of the scanning window is circular. In this paper we explore an elliptic version of the spatial scan statistic, using a scanning window of variable location, shape (eccentricity), angle and size, and with and without an eccentricity penalty. The method is applied to breast cancer mortality data from Northeastern United States and female oral cancer mortality in the United States. Power comparisons are made with the circular scan statistic. Copyright (c) 2006 John Wiley & Sons, Ltd. C1 Harvard Univ, Sch Med, Dept Ambulatory Care & Prevent, Boston, MA 02215 USA. Harvard Pilgrim Hlth Care, Boston, MA 02215 USA. Univ Connecticut, Dept Stat, Storrs, CT 06269 USA. NCI, Stat Applicat & Res Branch, Div Canc Control & Populat Studies, Bethesda, MD 20892 USA. Univ Fed Minas Gerais, Dept Estatist, Belo Horizonte, MG, Brazil. RP Kulldorff, M (reprint author), Harvard Univ, Sch Med, Dept Ambulatory Care & Prevent, 133 Brookline Ave,6th Floor, Boston, MA 02215 USA. EM martin_kulldorff@hms.harvard.edu; huangla@mail.nih.gov; picklel@mail.nih.gov; duczmal@est.ufmg.br RI Kulldorff, Martin/H-4282-2011; OI Kulldorff, Martin/0000-0002-5284-2993 NR 21 TC 188 Z9 202 U1 1 U2 17 PU JOHN WILEY & SONS LTD PI CHICHESTER PA THE ATRIUM, SOUTHERN GATE, CHICHESTER PO19 8SQ, W SUSSEX, ENGLAND SN 0277-6715 J9 STAT MED JI Stat. Med. PD NOV 30 PY 2006 VL 25 IS 22 BP 3929 EP 3943 DI 10.1002/sim.2490 PG 17 WC Mathematical & Computational Biology; Public, Environmental & Occupational Health; Medical Informatics; Medicine, Research & Experimental; Statistics & Probability SC Mathematical & Computational Biology; Public, Environmental & Occupational Health; Medical Informatics; Research & Experimental Medicine; Mathematics GA 111CT UT WOS:000242429400011 PM 16435334 ER PT J AU Roberts, A Wood, J Subbarao, K Ferguson, M Wood, D Cherian, T AF Roberts, Anjeanette Wood, John Subbarao, Kanta Ferguson, Morag Wood, David Cherian, Thomas TI Animal models and antibody assays for evaluating candidate SARS vaccines: Summary of a technical meeting 25-26 August 2005, London, UK SO VACCINE LA English DT Article DE SARS virus; animal models; vaccines; guidelines ID ACUTE-RESPIRATORY-SYNDROME; HUMAN MONOCLONAL-ANTIBODY; INFECTIOUS PERITONITIS VIRUS; CORONAVIRUS SPIKE PROTEIN; ENHANCED PULMONARY PATHOLOGY; 2ND INTERNATIONAL STANDARD; GOLDEN SYRIAN-HAMSTERS; DEPENDENT ENHANCEMENT; NEUTRALIZING ANTIBODIES; BALB/C MICE AB Severe acute respiratory syndrome (SARS) emerged in the Guangdong province of China in late 2002 and spread to 29 countries. By the end of the outbreak in July 2003, the CDC and WHO reported 8437 cases with a 9.6% case fatality rate. The disease was caused by a previously unrecognized coronavirus, SARS-CoV. Drawing on experience with animal coronavirus vaccines, several vaccine candidates have been developed and evaluated in pre-clinical trials. Available data suggest that vaccines should be based on the the 180 kDa viral spike protein, S, the only significant neutralization antigen capable of inducing protective immune responses in animals. In the absence of clinical cases of SARS, candidate vaccines should be evaluated for efficacy in animal models, and although it is uncertain whether the United States Food and Drug Administration's "animal rule" would apply to licensure of a SARS vaccine, it is important to develop standardized animal models and immunological assays in preparation for this eventuality. This report summarizes the recommendations from a WHO Technical Meeting on Animal Models and Antibody Assays for Evaluating Candidate SARS Vaccines held on 25-26 August 2005 in South Mimms, UK, provides guidance on the use of animal models, and outlines the steps to develop standard reagents and assays for immunological evaluation of candidate SARS vaccines. (c) 2006 Elsevier Ltd. All rights reserved. C1 WHO, Dept Immunizat Vaccines & Biol, CH-1211 Geneva 27, Switzerland. NIAID, Bethesda, MD 20892 USA. Natl Inst Biol Stand & Controls, Potters Bar EN6 3QG, Herts, England. RP Cherian, T (reprint author), WHO, Dept Immunizat Vaccines & Biol, 20 Ave Appia, CH-1211 Geneva 27, Switzerland. EM cheriant@who.int FU Intramural NIH HHS NR 81 TC 9 Z9 9 U1 0 U2 0 PU ELSEVIER SCI LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND SN 0264-410X EI 1873-2518 J9 VACCINE JI Vaccine PD NOV 30 PY 2006 VL 24 IS 49-50 BP 7056 EP 7065 DI 10.1016/j.vaccine.2006.07.009 PG 10 WC Immunology; Medicine, Research & Experimental SC Immunology; Research & Experimental Medicine GA 114OA UT WOS:000242674300008 PM 16930781 ER PT J AU Hu, N Wang, CY Hu, Y Yang, HH Kong, LH Lu, N Su, H Wang, QH Goldstein, AM Buetow, KH Emmert-Buck, MR Taylor, PR Lee, MP AF Hu, Nan Wang, Chaoyu Hu, Ying Yang, Howard H. Kong, Li-Hui Lu, Ning Su, Hua Wang, Quan-Hong Goldstein, Alisa M. Buetow, Kenneth H. Emmert-Buck, Michael R. Taylor, Philip R. Lee, Maxwell P. TI Genome-wide loss of heterozygosity and copy number alteration in esophageal squamous cell carcinoma using the Affymetrix GeneChip Mapping 10 K array SO BMC GENOMICS LA English DT Article ID NUCLEOTIDE POLYMORPHISM ARRAY; ALLELIC LOSS; NORTHERN CHINA; FAMILY-HISTORY; CANCER; IDENTIFICATION; PROGRESSION; POPULATION; IMBALANCES; DEFINES AB Background: Esophageal squamous cell carcinoma (ESCC) is a common malignancy worldwide. Comprehensive genomic characterization of ESCC will further our understanding of the carcinogenesis process in this disease. Results: Genome-wide detection of chromosomal changes was performed using the Affymetrix GeneChip 10 K single nucleotide polymorphism (SNP) array, including loss of heterozygosity (LOH) and copy number alterations (CNA), for 26 pairs of matched germ-line and micro-dissected tumor DNA samples. LOH regions were identified by two methods -using Affymetrix's genotype call software and using Affymetrix's copy number alteration tool (CNAT) software -and both approaches yielded similar results. Non-random LOH regions were found on 10 chromosomal arms (in decreasing order of frequency: 17p, 9p, 9q, 13q, 17q, 4q, 4p, 3p, 15q, and 5q), including 20 novel LOH regions (10 kb to 4.26 Mb). Fifteen CNA-loss regions (200 kb to 4.3 Mb) and 36 CNA-gain regions (200 kb to 9.3 Mb) were also identified. Conclusion: These studies demonstrate that the Affymetrix 10 K SNP chip is a valid platform to integrate analyses of LOH and CNA. The comprehensive knowledge gained from this analysis will enable improved strategies to prevent, diagnose, and treat ESCC. C1 NCI, Genet Epidemiol Branch, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA. NCI, Lab Populat Genet, Ctr Canc Res, Bethesda, MD 20892 USA. Shanxi Canc Hosp, Taiyuan 030013, Shanxi, Peoples R China. Chinese Acad Med Sci, Canc Inst & Hosp, Beijing 100021, Peoples R China. NCI, Pathol Lab, Ctr Canc Res, Bethesda, MD 20892 USA. RP Hu, N (reprint author), NCI, Genet Epidemiol Branch, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA. EM nh38k@nih.gov; wangc@mail.nih.gov; yhu@mail.nih.gov; hy43h@nih.gov; han_xiaoyou@yahoo.com.cn; nlu03@126.com; hs98@georgetown.edu; zhongmeiketi@yahoo.com.cn; ag29o@nih.gov; buetowke@mail.nih.gov; buckm@mail.nih.gov; ptaylor@mail.nih.gov; maxlee@mail.nih.gov FU Intramural NIH HHS NR 27 TC 24 Z9 25 U1 0 U2 1 PU BIOMED CENTRAL LTD PI LONDON PA MIDDLESEX HOUSE, 34-42 CLEVELAND ST, LONDON W1T 4LB, ENGLAND SN 1471-2164 J9 BMC GENOMICS JI BMC Genomics PD NOV 29 PY 2006 VL 7 AR 299 DI 10.1186/1471-2164-7-299 PG 16 WC Biotechnology & Applied Microbiology; Genetics & Heredity SC Biotechnology & Applied Microbiology; Genetics & Heredity GA 115IH UT WOS:000242727500001 PM 17134496 ER PT J AU Hines, LM Hoffman, PL Bhave, S Saba, L Kaiser, A Snell, L Goncharov, I LeGault, L Dongier, M Grant, B Pronko, S Martinez, L Yoshimura, M Tabakoff, B AF Hines, Lisa M. Hoffman, Paula L. Bhave, Sanjiv Saba, Laura Kaiser, Alan Snell, Larry Goncharov, Igor LeGault, Lucie Dongier, Maurice Grant, Bridget Pronko, Sergey Martinez, Larry Yoshimura, Masami Tabakoff, Boris CA WHO Int Soc Biomed Res Alcoholism Stud Trait Markers Alcohol Dependence I TI A sex-specific role of type VII adenylyl cyclase in depression SO JOURNAL OF NEUROSCIENCE LA English DT Article DE adenylyl cyclase; association study; depression; haplotype; human; mouse models; genetic polymorphisms ID TAIL SUSPENSION TEST; FAMILY-HISTORY INFORMATION; EMBRYONIC STEM-CELLS; ALCOHOL-USE DISORDER; PROTEIN-KINASE-C; MAJOR DEPRESSION; PSYCHIATRIC-DISORDERS; BEHAVIORAL DESPAIR; CANDIDATE GENES; HAPLOTYPE RECONSTRUCTION AB Major depression represents a complex mental disorder. The identification of biological markers that define subtypes of major depressive disorder would greatly facilitate appropriate medical treatments, as well as provide insight into etiology. Reduced activity of the cAMP signaling system has been implicated in the etiology of major depression. Previous work has shown low adenylyl cyclase activity in platelets and postmortem brain tissue of depressed individuals. Here, we investigate the role of the brain type VII isoform of adenylyl cyclase (AC7) in the manifestation of depressive symptoms in genetically modified animals, using a combination of in vivo behavioral experiments, gene expression profiling, and bioinformatics. We also completed studies with humans on the association of polymorphisms in the AC7 gene with major depressive illness (unipolar depression) based on Diagnostic and Statistical Manual of Mental Disorders IV criteria. Collectively, our results demonstrate a sex-specific influence of the AC7 gene on a heritable form of depressive illness. C1 Univ Colorado Denver, Sch Med, Dept Pharmacol, Aurora, CO 80045 USA. McGill Univ, Dept Psychiat, Verdun, PQ H4H 1R3, Canada. NIAAA, Div Epidemiol, Rockville, MD 20852 USA. Louisiana State Univ, Sch Vet Med, Dept Comparat Biomed Sci, Baton Rouge, LA 70803 USA. RP Tabakoff, B (reprint author), Univ Colorado Denver, Sch Med, Dept Pharmacol, Mail Stop F-8303,POB 6511, Aurora, CO 80045 USA. EM boris.tabakoff@uchsc.edu OI Saba, Laura/0000-0001-9649-1294 FU NIAAA NIH HHS [R01 AA013148-06, R01 AA009014, U01 AA 13489, K01 AA000240, K01 AA000240-05, R01 AA 13162, R01 AA013148] NR 77 TC 30 Z9 30 U1 0 U2 1 PU SOC NEUROSCIENCE PI WASHINGTON PA 11 DUPONT CIRCLE, NW, STE 500, WASHINGTON, DC 20036 USA SN 0270-6474 J9 J NEUROSCI JI J. Neurosci. PD NOV 29 PY 2006 VL 26 IS 48 BP 12609 EP 12619 DI 10.1523/JNEUROSCI.1040-06.2006 PG 11 WC Neurosciences SC Neurosciences & Neurology GA 110OJ UT WOS:000242387900025 PM 17135423 ER PT J AU Szyld, EG Warley, EM Freimanis, L Gonin, R Cahn, PE Calvet, GA Duarte, G Melo, VH Read, JS AF Szyld, Edgardo G. Warley, Eduardo M. Freimanis, Laura Gonin, Rene Cahn, Pedro E. Calvet, Guilherme A. Duarte, Geraldo Melo, Victor H. Read, Jennifer S. CA NISDI Perinatal Study Grp TI Maternal antiretroviral drugs during pregnancy and infant low birth weight and preterm birth SO AIDS LA English DT Article; Proceedings Paper CT 12th Conference on Retroviruses and Opportunistic Infections CY FEB 22-25, 2005 CL Boston, MA DE HIV-1; HAART; low birth weight; preterm; pregnancy ID IMMUNODEFICIENCY-VIRUS INFECTION; GESTATIONAL-AGE; INCREASED RISK; NEWBORN-INFANT; HIV-INFECTION; THERAPY; WOMEN; TRANSMISSION; PREECLAMPSIA; MORTALITY AB Objective: To determine the relationship between maternal antiretroviral regimens during pregnancy and adverse infant outcomes [low birth weight (LBW) and preterm birth]. The a priori hypothesis was that protease inhibitor (PI)-containing regimens are associated with an increased risk of LBW and preterm birth. Design: Prospective cohort study of HIV-1-infected women and their infants (NISDI Perinatal Study). Methods: Data were analysed from 681 women receiving at least one antiretroviral drug [in order of increasing complexity: one or two nucleoside reverse transcriptase inhibitors (1-2 NRTI), two NRTI plus one non-nucleoside reverse transcriptase inhibitor (NNRTI) (HAART/NNRTI), or two NRTI plus one PI (HAART/PI)] for at least 28 days during pregnancy, and who delivered live born, singleton infants with known birth weight and gestational age by 1 March 2005. Multivariable logistic regression modeling was used to assess the relationship of maternal ART with LBW and with preterm birth, adjusting for covariates. Results: The incidence of LBW and preterm birth, respectively, was 9.6% and 7.4% (1-2 NRTI), 7.4% and 5.8% (HAART/NNRTI), and 16.7% and 10.6% (HAART/PI). There was no statistically significant increased risk of LBW [adjusted odds ratio (AOR), 1.5; 95% confidence interval (95% CI), 0.7-3.2] or preterm birth (AOR, 1.1; 95% CI, 0.5-2.8) among women who received HAART/PI compared with women receiving 1-2 NRTI. Conclusions: Among a population of HIV-1-infected women in Latin America and the Caribbean, maternal receipt of PI-containing ART regimens during pregnancy was not associated with a statistically significant increase in risk of LBW or preterm birth. (c) 2006 Lippincott Williams & Wilkins. C1 Hosp Juan Fernandez, Buenos Aires, DF, Argentina. Hosp Diego Paroissien, Buenos Aires, DF, Argentina. Hosp Servidores Estado Rio De Janeiro, Ribeirao Preto, Brazil. Univ Sao Paulo, Sch Med, BR-14049 Ribeirao Preto, Brazil. Univ Fed Minas Gerais, Sch Med, Belo Horizonte, MG, Brazil. WESTAT Corp, Rockville, MD 20850 USA. NICHD, Pediat Adolescent & Maternal AIDS Branch, NIH, DHHS, Bethesda, MD USA. RP Szyld, EG (reprint author), Gavilan 1086, RA-1046 Buenos Aires, DF, Argentina. EM ezyld@fibertel.com.ar RI Mussi-Pinhata, Marisa/G-6568-2012; Duarte, Geraldo/J-7906-2012; Calvet, Guilherme/G-6959-2013 OI Calvet, Guilherme/0000-0002-3545-5238 FU NICHD NIH HHS [N01-HD-3-3345] NR 43 TC 63 Z9 64 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0269-9370 J9 AIDS JI Aids PD NOV 28 PY 2006 VL 20 IS 18 BP 2345 EP 2353 DI 10.1097/01.aids.0000253362.01696.9d PG 9 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA 119UM UT WOS:000243039400011 PM 17117021 ER PT J AU Chaturvedi, AK Goedert, JJ AF Chaturvedi, Anil K. Goedert, James J. TI Human papillomavirus genotypes among women with HIV: implications for research and prevention SO AIDS LA English DT Editorial Material ID HUMAN-IMMUNODEFICIENCY-VIRUS; SQUAMOUS INTRAEPITHELIAL LESIONS; PARTICLE VACCINE; INFECTED WOMEN; CONTROLLED-TRIAL; NEGATIVE WOMEN; HPV GENOTYPES; YOUNG-WOMEN; HIGH-RISK; TYPE-16 C1 NCI, Div Canc Epidemiol & Genet, Rockville, MD USA. RP Chaturvedi, AK (reprint author), NCI, Div Canc Epidemiol & Genet, Rockville, MD USA. EM chaturva@mail.nih.gov RI Chaturvedi, Anil/J-2024-2015 OI Chaturvedi, Anil/0000-0003-2696-8899 NR 28 TC 7 Z9 7 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0269-9370 J9 AIDS JI Aids PD NOV 28 PY 2006 VL 20 IS 18 BP 2381 EP 2383 DI 10.1097/01.aids.0000253366.94072.b4 PG 3 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA 119UM UT WOS:000243039400015 PM 17117025 ER PT J AU McGruder, BM Atha, DH Wang, W Huppi, K Wei, WQ Abnet, CC Qiao, YL Dawsey, SM Taylor, PR Jakupciak, JP AF McGruder, Brenna M. Atha, Donald H. Wang, Wendy Huppi, Konrad Wei, Wen-Qiang Abnet, Christian C. Qiao, You-Lin Dawsey, Sanford M. Taylor, Philip R. Jakupciak, John P. TI Real-time telomerase assay of less-invasively collected esophageal cell samples SO CANCER LETTERS LA English DT Article DE real-time TRAP; telomerase activity; diagnostics; biomarkers; telomerase candidate reference material; esophageal squamous cell carcinoma; esophageal balloon cytology ID QUANTITATIVE-ANALYSIS; SQUAMOUS DYSPLASIA; MOLECULAR MARKERS; CANCER PREVENTION; COLORECTAL-CANCER; CARCINOMA; EXPRESSION; TUMOR; CHINA; PROLIFERATION AB Genomic and proteomic efforts have discovered a complex list of biomarkers that identify human disease, stratify risk of disease within populations, and monitor drug or therapy responses for treatment. Attention is needed to characterize these biomarkers and to develop high-throughput technologies to evaluate their accuracy and precision. Telomerase activity is correlated with tumor progression, indicating cells that express telomerase possess aggressive clinical behavior and that telomerase activity could be a clinically important cancer biomarker. Traditionally, the detection of cancer has involved invasive procedures to procure samples. There is a need for less invasive approaches suitable for population- and clinic-based assays for cancer early detection. Esophageal balloon cytology (EBC) is a low-invasive screening technique, which samples superficial epithelial cells from the esophagus. Since telomerase activity is absent in superficial cells of normal esophageal squamous epithelium but is often present in superficial cells from dysplastic lesions and ESCCs, measuring telomerase activity in EBC samples may be a good way to screen for these lesions. The development of rapid real-time telomerase activity assays raises the possibility of extending such screening to high-risk populations. In this study, we evaluate the feasibility of using rapid Real-Time Telomerase Repeat Amplification Protocol (RTTRAP) for the analysis of NIST telomerase candidate reference material and esophageal clinical samples. The telomerase activity of eight EBC samples was also measured by capillary electrophoresis of RTTRAP products, RApidTRAP, and hTERT mRINIA RT-PCR assays. These findings demonstrate the feasibility of using the RTTRAP assay in EBC samples and suggest that individuals from high-risk populations can be screened for telomerase activity. (c) 2006 Elsevier Ireland Ltd. All rights reserved. C1 Natl Inst Stand & Technol, Div Biochem Sci, Gaithersburg, MD 20899 USA. NCI, Canc Biomarkers Res Grp, Rockville, MD USA. NCI, Ctr Adv Technol, Gaithersburg, MD USA. NCI, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA. Chinese Acad Med Sci, Inst Canc, Dept Canc Epidemiol, Beijing 100021, Peoples R China. RP Jakupciak, JP (reprint author), Natl Inst Stand & Technol, Div Biochem Sci, 100 Bur Dr,MS 8311, Gaithersburg, MD 20899 USA. EM johnj@nist.gov RI Qiao, You-Lin/B-4139-2012; Abnet, Christian/C-4111-2015 OI Qiao, You-Lin/0000-0001-6380-0871; Abnet, Christian/0000-0002-3008-7843 FU CCR NIH HHS [N01-RC-91019]; Intramural NIH HHS NR 41 TC 8 Z9 9 U1 1 U2 5 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 NOV 28 PY 2006 VL 244 IS 1 BP 91 EP 100 DI 10.1016/j.canlet.2005.12.012 PG 10 WC Oncology SC Oncology GA 118OR UT WOS:000242952100013 PM 16569479 ER PT J AU de Silva, R Gutierrez, LF Raval, AN McVeigh, ER Ozturk, C Lederman, RJ AF de Silva, Ranil Gutierrez, Luis F. Raval, Amish N. McVeigh, Elliot R. Ozturk, Cengizhan Lederman, Robert J. TI X-ray fused with magnetic resonance imaging (XFM) to target endomyocardial injections - Validation in a swine model of myocardial infarction SO CIRCULATION LA English DT Article DE catheterization; interventional magnetic resonance imaging; mapping; myocardial infarction; stem cell therapy; stereotaxic techniques; radiography ID ISCHEMIC-HEART FAILURE; COMPUTED TOMOGRAPHIC-IMAGES; GENE-TRANSFER; CATHETER ABLATION; THERAPEUTIC ANGIOGENESIS; PORCINE HEART; DOUBLE-BLIND; REAL-TIME; MR-IMAGES; REGISTRATION AB Background - Magnetic resonance imaging (MRI) permits 3-dimensional (3D) cardiac imaging with high soft tissue contrast. X-ray fluoroscopy provides high-resolution, 2-dimensional (2D) projection imaging. We have developed real-time x-ray fused with MRI (XFM) to guide invasive procedures that combines the best features of both imaging modalities. We tested the accuracy of XFM using external fiducial markers to guide endomyocardial cell injections in infarcted swine hearts. Methods and Results - Endomyocardial injections of iron-labeled mesenchymal stromal cells admixed with tissue dye were performed in previously infarcted hearts of 12 Yucatan miniswine (weight, 33 to 67 kg). Features from cardiac MRI were displayed combined with x-ray in real time to guide injections. During 130 injections, operators were provided with 3D surfaces of endocardium, epicardium, myocardial wall thickness (range, 2.6 to 17.7 mm), and infarct registered with live x-ray images to facilitate device navigation and choice of injection location. XFM-guided injections were compared with postinjection MRI and with necropsy specimens obtained 24 hours later. Visual inspection of the pattern of dye staining on 2,3,5-triphenyltetrazolium chloride-stained heart slices agreed (kappa = 0.69) with XFM-derived injection locations mapped onto delayed hyperenhancement MRI and the susceptibility artifacts seen on the postinjection T2*-weighted gradient echo MRI. The distance between the predicted and actual injection locations in vivo was 3.2 +/- 2.6 mm (n = 64), and 75% of injections were within 4.1 mm of the predicted location. Conclusions - Three-dimensional to two-dimensional registration of x-ray and MR images with the use of external fiducial markers accurately targets endomyocardial injection in a swine model of myocardial infarction. C1 NHLBI, NIH, Cardiovasc Branch, Bethesda, MD 20892 USA. NHLBI, NIH, Lab Cardiac Energet, Div Intramural Res, Bethesda, MD 20892 USA. Johns Hopkins Univ, Sch Med, Dept Biomed Engn, Baltimore, MD 21205 USA. RP Lederman, RJ (reprint author), NHLBI, NIH, Cardiovasc Branch, Bldg 10,Room 2C713, Bethesda, MD 20892 USA. EM ledermar@nhlbi.nih.gov RI Ozturk, Cengizhan/A-6177-2016 OI Ozturk, Cengizhan/0000-0002-6966-0774 FU Intramural NIH HHS [Z01 HL004608-08]; NHLBI NIH HHS [Z01 HL004608, Z01 HL005062, Z01-HL004608-06, Z01-HL005062-04] NR 39 TC 40 Z9 40 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0009-7322 J9 CIRCULATION JI Circulation PD NOV 28 PY 2006 VL 114 IS 22 BP 2342 EP 2350 DI 10.1161/CIRCULATIONAHA.105.598524 PG 9 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 125XS UT WOS:000243477400010 PM 17101858 ER PT J AU Babin, V Roland, C Darden, TA Sagui, C AF Babin, Volodymyr Roland, Christopher Darden, Thomas A. Sagui, Celeste TI The free energy landscape of small peptides as obtained from metadynamics with umbrella sampling corrections SO JOURNAL OF CHEMICAL PHYSICS LA English DT Article ID MOLECULAR-DYNAMICS METHOD; PARTICLE MESH EWALD; COMPLEX-SYSTEMS; CAR-PARRINELLO; AVERAGE FORCE; BETA-HAIRPIN; SIMULATIONS; ALGORITHM; WATER; PATH AB There is considerable interest in developing methodologies for the accurate evaluation of free energies, especially in the context of biomolecular simulations. Here, we report on a reexamination of the recently developed metadynamics method, which is explicitly designed to probe "rare events" and areas of phase space that are typically difficult to access with a molecular dynamics simulation. Specifically, we show that the accuracy of the free energy landscape calculated with the metadynamics method may be considerably improved when combined with umbrella sampling techniques. As test cases, we have studied the folding free energy landscape of two prototypical peptides: Ace-(Gly)(2)-Pro-(Gly)(3)-Nme in vacuo and trialanine solvated by both implicit and explicit water. The method has been implemented in the classical biomolecular code AMBER and is to be distributed in the next scheduled release of the code. (c) 2006 American Institute of Physics. C1 N Carolina State Univ, CHiPS, Raleigh, NC 27695 USA. N Carolina State Univ, Dept Phys, Raleigh, NC 27695 USA. NIEHS, Res Triangle Pk, NC 27709 USA. RP Babin, V (reprint author), N Carolina State Univ, CHiPS, Raleigh, NC 27695 USA. EM sagui@ncsu.edu FU Intramural NIH HHS [Z01 ES043010-21] NR 43 TC 50 Z9 50 U1 4 U2 27 PU AMER INST PHYSICS PI MELVILLE PA 1305 WALT WHITMAN RD, STE 300, MELVILLE, NY 11747-4501 USA SN 0021-9606 EI 1089-7690 J9 J CHEM PHYS JI J. Chem. Phys. PD NOV 28 PY 2006 VL 125 IS 20 AR 204909 DI 10.1063/1.2393236 PG 9 WC Chemistry, Physical; Physics, Atomic, Molecular & Chemical SC Chemistry; Physics GA 110UZ UT WOS:000242408100063 PM 17144742 ER PT J AU Dumstorf, CA Clark, AB Lin, QC Kissling, GE Yuan, T Kucherlapati, R McGregor, WG Kunkel, TA AF Dumstorf, Chad A. Clark, Alan B. Lin, Qingcong Kissling, Grace E. Yuan, Tao Kucherlapati, Raju McGregor, W. Glenn Kunkel, Thomas A. TI Participation of mouse DNA polymerase iota in strand-biased mutagenic bypass of UV photoproducts and suppression of skin cancer SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE translesion synthesis; UV mutagenesis; Y family polymerase; polymerase eta ID PIGMENTOSUM VARIANT CELLS; CHINESE-HAMSTER CELLS; XERODERMA-PIGMENTOSUM; INDUCED MUTATIONS; INCREASED SUSCEPTIBILITY; TRANSLESION SYNTHESIS; EXCISION REPAIR; THYMINE DIMER; HPRT GENE; Y-FAMILY AB DNA polymerase iota (pol iota) is a conserved Y family enzyme that is implicated in translesion DNA synthesis (TLS) but whose cellular functions remain uncertain. To test the hypothesis that pol L performs TLS in cells, we compared UV-induced mutagenesis in primary fibroblasts derived from wild-type mice to mice lacking functional pol eta, pol iota, or both. A deficiency in mouse DNA polymerase eta (pol eta) enhanced UV-induced Hprt mutant frequencies. This enhanced UV-induced mutagenesis and UV-induced mutagenesis in wild-type cells were strongly diminished in cells deficient in pol iota, indicating that pol t participates in the bypass of UV photoproducts in cells. Moreover, a clear strand bias among UV-induced base substitutions was observed in wild-type cells that was diminished in pol eta- and pol iota-deficient mouse cells and abolished in cells deficient in both enzymes. These data suggest that these enzymes bypass UV photoproducts in an asymmetric manner. To determine whether pol iota status affects cancer susceptibility, we compared the UV-induced skin cancer susceptibility of wild-type mice to mice lacking functional pol eta, pol iota, or both. Although pol iota deficiency alone had no effect, UV-induced skin tumors in pol eta-deficient mice developed 4 weeks earlier in mice concomitantly deficient in pol iota. Collectively, these data reveal functions for Pot L in bypassing UV photoproducts and in delaying the onset of UV-induced skin cancer. C1 NIEHS, Mol Genet Lab, NIH, Dept Hlth & Human Serv, Res Triangle Pk, NC 27709 USA. NIEHS, Struct Biol Lab, NIH, Dept Hlth & Human Serv, Res Triangle Pk, NC 27709 USA. NIEHS, Biostat Branch, NIH, Dept Hlth & Human Serv, Res Triangle Pk, NC 27709 USA. Univ Louisville, Dept Pharmacol & Toxicol, Louisville, KY 40202 USA. Univ Louisville, James Graham Brown Canc Ctr, Louisville, KY 40202 USA. Harvard Univ, Sch Med, Partners Healthcare Ctr Genet & Genom, Boston, MA 02115 USA. RP Kunkel, TA (reprint author), NIEHS, Mol Genet Lab, NIH, Dept Hlth & Human Serv, Res Triangle Pk, NC 27709 USA. EM kunkel@niehs.nih.gov FU Intramural NIH HHS; NCEH CDC HHS [EH 11040]; NCI NIH HHS [CA112197, CA112664, CA84301, R01 CA112197, R03 CA112664, U01 CA084301] NR 53 TC 68 Z9 70 U1 1 U2 2 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD NOV 28 PY 2006 VL 103 IS 48 BP 18083 EP 18088 DI 10.1073/pnas.0605247103 PG 6 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA 111PJ UT WOS:000242465200012 PM 17114294 ER PT J AU Zhu, JF Jankovic, D Grinberg, A Guo, LY Paul, WE AF Zhu, Jinfang Jankovic, Dragana Grinberg, Alex Guo, Liying Paul, William E. TI Gfi-1 plays an important role in IL-2-mediated Th2 cell expansion SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE cytokine; GATA-3; Schistosome; T cell differentiation ID TRANSCRIPTIONAL REPRESSOR GFI1; CD4+ T-CELLS; INTERFERON-GAMMA PRODUCTION; HEMATOPOIETIC STEM-CELLS; GENE-EXPRESSION; FACTOR GATA-3; DIFFERENTIATION; IL-4; STAT5; INHIBITION AB Enforced expression of growth factor independent 1 (Gfi-1), a transcription repressor induced by T cell activation and IL-4/Stat6 signaling, strikingly enhances Th2 cell expansion. Using conditionally Gfi1-deficient mice prepared for this study, we show that in vitro or in vivo deletion of this factor dramatically reduces Th2, but not Th1, cell expansion in response to IL-2. Both increased cell apoptosis and reduced cell proliferation resulted from Gfi1 deletion. IL-2-Stat5 signaling was partially reduced in Gfi1-deficient Th2 cells, but overexpression of Stat5 failed to restore normal Th2 expansion in these cells, suggesting that Gfi-1 also functioned downstream of, or in parallel with, Stat5 signaling. Reduced Th2 cell expansion in the absence of Gfi-1 was confirmed by the diminished frequency of IL-4-producing cells when these mice were infected with Schistosoma mansoni. C1 NIAID, Immunol Lab, NIH, Bethesda, MD 20892 USA. NIAID, Parasit Dis Lab, NIH, Bethesda, MD 20892 USA. NICHHD, Lab Mammalian Genes & Dev, NIH, Bethesda, MD 20892 USA. RP Zhu, JF (reprint author), NIAID, Immunol Lab, NIH, Bldg 10,Room 11N311,10 Ctr Dr,MSC 1892, Bethesda, MD 20892 USA. EM jfzhu@niaid.nih.gov; wpaul@niaid.nih.gov RI Zhu, Jinfang/B-7574-2012 FU Intramural NIH HHS NR 49 TC 57 Z9 59 U1 0 U2 0 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD NOV 28 PY 2006 VL 103 IS 48 BP 18214 EP 18219 DI 10.1073/pnas.0608981103 PG 6 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA 111PJ UT WOS:000242465200034 PM 17116877 ER PT J AU Wu, YM Przysiecki, C Flanagan, E Bello-Irizarry, SN Ionescu, R Muratova, O Dobrescu, G Lambert, L Keister, D Rippeon, Y Long, CA Shi, L Caulfield, M Shaw, A Saul, A Shiver, J Miller, LH AF Wu, Yimin Przysiecki, Craig Flanagan, Elizabeth Bello-Irizarry, Sheila N. Ionescu, Roxana Muratova, Olga Dobrescu, Gelu Lambert, Lynn Keister, David Rippeon, Yvette Long, Carole A. Shi, Li Caulfield, Michael Shaw, Alan Saul, Allan Shiver, John Miller, Louis H. TI Sustained high-titer antibody responses induced by conjugating a malarial vaccine candidate to outer-membrane protein complex SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE malaria; Pfs25; transmission-blocking vaccine ID TRANSMISSION-BLOCKING VACCINE; PLASMODIUM-FALCIPARUM; IMMUNOGENICITY; ENHANCEMENT; TRIAL AB The development of protein subunit vaccines to combat some of the world's deadliest pathogens such as a malaria parasite, Plasmodium, falciparum, is stalled, due in part to the inability to induce and sustain high-titer antibody responses. Here, we show the induction of persistent, high-titer antibody responses to recombinant Pfs25H, a human malarial transmission-blocking protein vaccine candidate, after chemical conjugation to the outer-membrane protein complex (OMPC) of Neisseria meningitidis serogroup B and adsorption to aluminum hydroxyphosphate. In mice, the Pfs25HOMPC conjugate vaccine was > 1,000 times more potent in generating anti-Pfs25H ELISA reactivity than a similar 0.5-mu g dose of Pfs25H alone in Montanide ISA720, a water-in-oil adjuvant. The immune enhancement requires covalent conjugation between Pfs25H and the OMPC, given that physically mixed Pfs25H and OMPC on aluminum hydroxyphosphate failed to induce greater activity than the nonconjugated Pfs25H on aluminum hydroxyphosphate. The conjugate vaccine Pfs25H-OMPC also was highly immunogenic in rabbits and rhesus monkeys. In rhesus monkeys, the antibody responses were sustained over 18 months, at which time another vaccination with nonconjugated Pfs25H induced strong anamnestic responses. The vaccine-induced anti-Pfs25-specific antibodies in all animal species blocked the transmission of parasites to mosquitoes. Protein antigen conjugation to OMPC or other protein carrier may have general application to a spectrum of protein subunit vaccines to increase immunogenicity without the need for potentially reactogenic adjuvants. C1 NIAID, Malaria Vaccine Dev Branch, NIH, Rockville, MD 20852 USA. Merck Res Labs, West Point, PA 19486 USA. RP Wu, YM (reprint author), NIAID, Malaria Vaccine Dev Branch, NIH, 5640 Fishers Lane, Rockville, MD 20852 USA. EM yiwu@niaid.nih.gov; lmiller@niaid.nih.gov RI Saul, Allan/I-6968-2013 OI Saul, Allan/0000-0003-0665-4091 FU Intramural NIH HHS NR 24 TC 71 Z9 75 U1 1 U2 3 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD NOV 28 PY 2006 VL 103 IS 48 BP 18243 EP 18248 DI 10.1073/pnas.0608545103 PG 6 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA 111PJ UT WOS:000242465200039 PM 17110440 ER PT J AU Barbour, AG Dai, QY Restrepo, BI Stoenner, HG Frank, SA AF Barbour, Alan G. Dai, Qiyuan Restrepo, Blanca I. Stoenner, Herbert G. Frank, Steven A. TI Pathogen escape from host immunity by a genome program for antigenic variation SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE antibody; Borrelia; recombination; relapsing fever; vector-borne ID BACTERIUM BORRELIA-HERMSII; SEGMENTAL GENE CONVERSION; PLASMODIUM-FALCIPARUM; RELAPSING FEVER; TRYPANOSOMA-BRUCEI; LINEAR PLASMIDS; EXPRESSION; RECOMBINATION; TRANSCRIPTION; VARIANTS AB The vector-borne bacterium Borrelia hermsii, a relapsing fever agent, switches gene expression of a surface protein between different antigenic variants, thereby causing sequential waves of immune escape within hosts and increasing the likelihood of transmission. Analogous programmed systems of antigenic variation occur in African trypanosomes and Plasmodium falciparum. In these examples, switch rates to individual variants differ over a wide range. We studied how B. hermsii determines switch rates in two experimental infections: one where variants were identified by specific antisera and one based on identification by DNA sequence. Unexpressed loci of variant antigens copy into a single expression site at rates determined by extragenic features of silent loci rather than similarity between coding sequences of variants at silent sites and the single expression site. Two elements, in particular, determine switch rates. one set of elements overlaps the 5' ends of the expressed gene and the silent loci; greater sequence identity between elements was associated with a higher switch rate. The second set of elements flanks the expression site on the 3' side and occurs at variable distances downstream from silent loci; the nearer an element to a silent locus, the greater the switch rate of that locus into the expression site. In combination, these two features of the genome provide a simple mechanism to modulate switch rate whereby silent loci form a hierarchy of switch rates into the expression site. Although the switching hierarchy causes changes in individual cells that are stochastic, ordering of variants within hosts is semipredictable. C1 Univ Calif Irvine, Pacific SW Ctr, Dept Microbiol, Irvine, CA 92697 USA. Univ Calif Irvine, Pacific SW Ctr, Dept Mol Genet, Irvine, CA 92697 USA. Univ Calif Irvine, Pacific SW Ctr, Dept Med, Irvine, CA 92697 USA. Univ Texas, Hlth Sci Ctr, Dept Microbiol, San Antonio, TX 78229 USA. Univ Texas, Hlth Sci Ctr, Sch Publ Hlth, Brownsville, TX 78520 USA. NIAID, Rocky Mt Lab, NIH, Hamilton, MT 59840 USA. Univ Calif Irvine, Dept Ecol & Evolut Biol, Irvine, CA 92697 USA. RP Barbour, AG (reprint author), Univ Calif Irvine, Pacific SW Ctr, Dept Microbiol, 3012 Hewitt Hall, Irvine, CA 92697 USA. EM abarbour@uci.edu RI Barbour, Alan/B-3160-2009; OI Barbour, Alan/0000-0002-0719-5248; Frank, Steven/0000-0001-7348-7794 FU NIAID NIH HHS [AI24424, R01 AI024424, R37 AI024424]; NIGMS NIH HHS [GM076499, U01 GM076499] NR 39 TC 66 Z9 66 U1 0 U2 3 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD NOV 28 PY 2006 VL 103 IS 48 BP 18290 EP 18295 DI 10.1073/pnas.0605302103 PG 6 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA 111PJ UT WOS:000242465200047 PM 17101971 ER PT J AU Jazii, FR Najafi, Z Malekzadeh, R Conrads, TP Ziaee, AA Abnet, C Yazdznbod, M Karkhane, AA Salekdeh, GH AF Jazii, Ferdous Rastgar Najafi, Zahra Malekzadeh, Reza Conrads, Thomas P. Ziaee, Abed Ali Abnet, Christian Yazdznbod, Mansour Karkhane, Ali Asghar Salekdeh, Ghasem H. TI Identification of squamous cell carcinoma associated proteins by proteomics and loss of beta tropomyosin expression in esophageal cancer SO WORLD JOURNAL OF GASTROENTEROLOGY LA English DT Article DE squamous cell carcinoma; esophagus; esophageal; proteomics; two dimensional electrophoresis; polypeptide marker ID HEPATOCELLULAR-CARCINOMA; BREAST-CANCER; GEL-ELECTROPHORESIS; HYDROGEN-PEROXIDE; MASS-SPECTROMETRY; INDUCED APOPTOSIS; EPITHELIAL-CELLS; GENE-EXPRESSION; DOWN-REGULATION; FACTOR-ALPHA AB AIM: To assess the proteome of normal versus tumor tissue in squamous cell carcinoma of the esophagus (SCCE) in Iranian patients and compare our results with former reports by using proteomics. METHODS: Protein was extracted from normal and tumor tissues. Two dimensional electrophoresis was carried out and spots with differential expression were identified with mass spectrometry. RNA extraction and RT-PCR along with immunodetection were performed. RESULTS: Fourteen proteins were found whose expression levels differed in tumor compared to normal tissues. Mass spectrometric analysis resulted in the identification of beta-tropomyosin (TM beta), myosin light chain 2 (and its isoform), myosin regulatory light chain 2, peroxyredoxin 2, annexin I and an unknown polypeptide as the down regulated polypeptides in tumor tissue. Heat shock protein 70 (HSP70), TPM4-ALK fusion oncoprotein 2, myosin light polypeptide 6, keratin I, GH16431p and calreticulin were the up-regulated polypeptides found in tumor tissue. Several of these proteins, such as TM beta, HSP70, annexin I, calreticulin, TPM4-ALK and isoforms of myosins, have been well recognized in tumorigenesis of esophageal or other types of cancers. CONCLUSION: Our study not only supports the involvement of some of the formerly reported proteins in SCCE but also introduces additional proteins found to be lost in SCCE, including TM beta. (C) 2006 The WJG Press. All rights reserved. C1 Natl Inst Genet Engn & Biotechnol, Tehran, Iran. Med Univ, Shariati Hosp, Digest Dis Res Ctr, Tehran, Iran. SAIC Frederick B, Lab Proteom & Analyt Technol, Frederick, MD 21702 USA. Univ Tehran, Inst Biochem & Biophys, Tehran, Iran. Med Univ, Shariati Hosp, Dept Surg, Tehran, Iran. NCI, Ctr Canc Res, Canc Prevent Studies Branch, Bethesda, MD 20892 USA. Agr Biotechnol Res Inst Iran, Karaj, Iran. RP Jazii, FR (reprint author), Natl Inst Genet Engn & Biotechnol, POB 14155 6343, Tehran, Iran. EM rastgar_jazii@yahoo.com RI Salekdeh, Ghasem Hosseini/E-4198-2012; Abnet, Christian/C-4111-2015; Salekdeh, Ghasem Hosseini/R-8716-2016; OI Abnet, Christian/0000-0002-3008-7843; Malekzadeh, Reza/0000-0003-1043-3814 NR 57 TC 87 Z9 95 U1 1 U2 3 PU BAISHIDENG PUBL GRP CO LTD PI BEIJING PA RM 903, BLDG D, OCEAN INTERNATIONAL CTR, NO 62 DONGSIHUAN ZHONGLU, BEIJING, CHAOYANG DISTRICT 100025, PEOPLES R CHINA SN 1007-9327 J9 WORLD J GASTROENTERO JI World J. Gastroenterol. PD NOV 28 PY 2006 VL 12 IS 44 BP 7104 EP 7112 PG 9 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA 112LO UT WOS:000242527600006 PM 17131471 ER PT J AU Bartali, B Semba, RD Frongillo, EA Varadhan, R Ricks, MO Blaum, CS Ferrucci, L Guralnik, JM Fried, LP AF Bartali, Benedetta Semba, Richard D. Frongillo, Edward A. Varadhan, Ravi Ricks, Michelle O. Blaum, Caroline S. Ferrucci, Luigi Guralnik, Jack M. Fried, Linda P. TI Low micronutrient levels as a predictor of incident disability in older women SO ARCHIVES OF INTERNAL MEDICINE LA English DT Article ID OXIDATIVE STRESS; HOMOCYSTEINE; ATHEROSCLEROSIS; ANTIOXIDANTS; PERFORMANCE; COMPONENT; SELENIUM; FRAILTY; DISEASE; HEALTH AB Background: The role of nutritional status in the disablement process is still unclear. The objective of this study was to assess whether low concentrations of nutrients predict the development and course of disability. Methods: Longitudinal study including community-dwelling women 65 years or older enrolled in the Women's Health and Aging Study I. In total, 643 women were assessed prospectively at 6-month intervals from 1992 to 1995. Results: Incidence rates of disability in activities of daily living (ADLs) during 3 years of follow-up. Incidence rates in the lowest quartile of each selected nutrient were compared with those in the upper quartiles. The hazard ratios were estimated from Cox models adjusted for potential confounders. Women in the lowest quartile of serum concentrations of vitamin B-6 ( hazard ratio [HR], 1.31; 95% confidence interval [CI], 1.03-1.67), vitamin B-12 ( HR, 1.40; 95% CI, 1.12-1.74), and selenium ( HR, 1.38; 95% CI, 1.12-1.71) had significantly higher risk of disability in ADLs during 3 years of follow-up compared with women in the upper 3 quartiles. Conclusions: Low serum concentrations of vitamins B6 and B12 and selenium predict subsequent disability in ADLs in older women living in the community. Nutritional status is one of the key factors to be considered in the development of strategies aimed at preventing or delaying the disablement process. C1 Cornell Univ, Div Nutrit Sci, Ithaca, NY 14853 USA. Johns Hopkins Med Inst, Dept Ophthalmol, Baltimore, MD 21205 USA. Johns Hopkins Med Inst, Ctr Aging & Hlth, Div Geriatr Med & Gerontol, Baltimore, MD 21205 USA. Univ Michigan, Dept Med, Ann Arbor, MI 48109 USA. NIA, Longitudinal Studies Sect, Clin Res Branch, NIH, Baltimore, MD USA. NIA, Lab Epidemiol Demog & Biometry, NIH, Bethesda, MD USA. RP Bartali, B (reprint author), Cornell Univ, Div Nutrit Sci, Savage Hall, Ithaca, NY 14853 USA. EM bb232@cornell.edu FU Intramural NIH HHS [Z99 AG999999]; NCRR NIH HHS [M01 RR000722]; NIA NIH HHS [N01 AG012112, N01-AG12112, R01 AG011703, R01 AG027012, R01 AG11703-01A1, R37 AG019905]; NIAID NIH HHS [R01 AI041956, R01 AI41956] NR 24 TC 39 Z9 41 U1 1 U2 3 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610-0946 USA SN 0003-9926 J9 ARCH INTERN MED JI Arch. Intern. Med. PD NOV 27 PY 2006 VL 166 IS 21 BP 2335 EP 2340 DI 10.1001/archinte.166.21.2335 PG 6 WC Medicine, General & Internal SC General & Internal Medicine GA 109MQ UT WOS:000242312700006 PM 17130386 ER PT J AU Tsai, CJ Leitzmann, MF Willett, WC Giovannucci, EL AF Tsai, Chung-Jyi Leitzmann, Michael F. Willett, Walter C. Giovannucci, Edward L. TI Weight cycling and risk of gallstone disease in men SO ARCHIVES OF INTERNAL MEDICINE LA English DT Article ID CATCH-UP GROWTH; HEALTH-PROFESSIONALS; METABOLIC SYNDROME; PROSPECTIVE COHORT; UNSATURATED FATS; CHOLELITHIASIS; HAMSTERS; OBESITY; PREVALENCE; STRATEGIES AB Background: The long-term effect of repeated intentional weight loss and weight regain on the risk of gallstone disease in men is not clear. Methods: Participants in the Health Professionals Followup Study provided information on intentional weight loss during the previous 4 years in 1992. Weight cyclers were men who had intentional weight loss and weight regain. Men free of gallstone disease at baseline were followed from 1992 to 2002. On biennial questionnaires the participants reported newly diagnosed gallstone disease. Results: During 264 760 person-years of follow-up we ascertained 1222 cases of symptomatic gallstones. We examined the effect of weight cycling on the risk of gallstone disease. The multivariate relative risk of weight cyclers, compared with weight maintainers, after adjusting for potential confounding variables, including body mass index, was 1.11 (95% confidence interval [CI], 0.94-1.31) in light cyclers, 1.18 ( 95% CI, 0.97-1.43) in moderate cyclers, and 1.42 ( 95% CI, 1.11-1.81) in severe cyclers. We further examined the effect of number of cycling episodes. Among weight cyclers, the relative risk associated with having more than 1 weight cycle, compared with weight maintainers, was 1.10 ( 95% CI, 0.88-1.37) in light cyclers, 1.28 ( 95% CI, 1.03-1.59) in moderate cyclers, and 1.51(95% CI, 1.13-2.02) in severe cyclers. Conclusions: Our findings suggest that weight cycling, independent of body mass index, may increase the risk of gallstone disease in men. Larger weight fluctuation and more weight cycles are associated with greater risk. C1 Univ Kentucky, Div Digest Dis & Nutr, Med Ctr, Lexington, KY 40536 USA. Brigham & Womens Hosp, Channing Lab, Dept Med, Boston, MA 02115 USA. Harvard Univ, Sch Med, Boston, MA 02115 USA. Harvard Univ, Dept Nutr, Sch Publ Hlth, Boston, MA 02115 USA. Harvard Univ, Dept Epidemiol, Sch Publ Hlth, Boston, MA 02115 USA. NCI, Div Canc Epidemiol & Genet, Dept Hlth & Human Serv, NIH, Bethesda, MD 20892 USA. RP Tsai, CJ (reprint author), Univ Kentucky, Div Digest Dis & Nutr, Med Ctr, 800 Rose St, Lexington, KY 40536 USA. FU NCI NIH HHS [CA55075]; NIDDK NIH HHS [DK46200] NR 39 TC 27 Z9 27 U1 0 U2 0 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610-0946 USA SN 0003-9926 J9 ARCH INTERN MED JI Arch. Intern. Med. PD NOV 27 PY 2006 VL 166 IS 21 BP 2369 EP 2374 DI 10.1001/archinte.166.21.2369 PG 6 WC Medicine, General & Internal SC General & Internal Medicine GA 109MQ UT WOS:000242312700011 PM 17130391 ER PT J AU Kupelian, V Wei, JT O'Leary, MP Kusek, JW Litman, HJ Link, CL McKinlay, JB AF Kupelian, Varant Wei, John T. O'Leary, Michael P. Kusek, John W. Litman, Heather J. Link, Carol L. McKinlay, John B. CA BACH Survey Investigators TI Prevalence of lower urinary tract symptoms and effect on quality of life in a racially and ethnically diverse random sample - The Boston Area Community Health (BACH) Survey SO ARCHIVES OF INTERNAL MEDICINE LA English DT Article ID BENIGN PROSTATIC HYPERPLASIA; CARE-SEEKING BEHAVIOR; NATURAL-HISTORY; MEN; INDEX; WOMEN; POPULATION; SPECIFICITY; VALIDATION; COUNTRIES AB Background: Previous studies of lower urinary tract symptoms (LUTS) have focused on men, with few studies including minority populations. The Boston Area Community Health (BACH) Survey is designed to study the prevalence and impact of LUTS among both men and women in a racially, ethnically, and socioeconomically diverse population. Methods: The BACH Survey used a stratified 2-stage cluster design to randomly sample 5506 adults aged 30 to 79 from the city of Boston, Mass ( 2301 men, 3205 women, 1770 blacks, 1877 Hispanics, and 1859 whites). Data were obtained using interviewer and self-administered questionnaires. The presence of LUTS was defined as an American Urological Association symptom index score of 8 or above. Quality of life was assessed using the Medical Outcomes Study 12-Item Short Form Survey (SF-12), and a measure of bother was based on the interference of urinary symptoms with various activities. Analyses were weighted to the Boston population using SUDAAN version 9.0 statistical software. Results: The overall prevalence of LUTS was 18.7% and increased with age (10.5% at age 30-39 years to 25.5% at age 70-79 years) but did not differ by sex or race/ethnicity. Quality of life was significantly reduced among those with LUTS, as measured by the bother of symptoms and the SF-12 component scores. Prevalence of prescription medication use for urinary symptoms was low even among participants with LUTS, with more than 90% of participants reporting no medication use. Conclusions: In this population-based, racially and ethnically diverse random sample, LUTS were common among both men and women and increased substantially with age. Lower urinary tract symptoms had a negative impact on quality of life across age, sex, and race/ethnic groups. C1 New England Res Inst, Inst Community Hlth Studies, Watertown, MA 02472 USA. Univ Michigan, Med Ctr, Dept Urol, Ann Arbor, MI 48109 USA. Brigham & Womens Hosp, Div Urol, Boston, MA 02115 USA. NIDDK, NIH, Bethesda, MD USA. RP Kupelian, V (reprint author), New England Res Inst, Inst Community Hlth Studies, 9 Galen St, Watertown, MA 02472 USA. EM vkupelian@neriscience.com RI Wei, John/E-8967-2012 FU NIDDK NIH HHS [DK56842] NR 35 TC 154 Z9 165 U1 0 U2 2 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610-0946 USA SN 0003-9926 J9 ARCH INTERN MED JI Arch. Intern. Med. PD NOV 27 PY 2006 VL 166 IS 21 BP 2381 EP 2387 DI 10.1001/archinte.166.21.2381 PG 7 WC Medicine, General & Internal SC General & Internal Medicine GA 109MQ UT WOS:000242312700013 PM 17130393 ER PT J AU Gauduin, MC Yu, Y Barabasz, A Carville, A Piatak, M Lifson, JD Desrosiers, RC Johnson, RP AF Gauduin, Marie-Claire Yu, Yi Barabasz, Amy Carville, Angela Piatak, Mike Lifson, Jeffrey D. Desrosiers, Ronald C. Johnson, R. Paul TI Induction of a virus-specific effector-memory CD4(+) T cell response by attenuated SIV infection SO JOURNAL OF EXPERIMENTAL MEDICINE LA English DT Article ID SIMIAN-IMMUNODEFICIENCY-VIRUS; PLASMA VIRAL LOAD; HIV-1 INFECTION; RHESUS-MACAQUES; INVERSE RELATIONSHIP; CD8(+) LYMPHOCYTES; HELPER RESPONSES; IN-VITRO; EX-VIVO; LIVE AB We investigated simian immunodeficiency virus (SIV)-specific CD4(+) T cell responses in rhesus macaques chronically infected with attenuated or pathogenic SIV strains. Analysis of SIV Delta nef-infected animals revealed a relatively high frequency of SIV-specific CD4+ T cells representing 4-10% of all CD4+ T lymphocytes directed against multiple SIV proteins. Gag-specific CD4+ T cells in wild-type SIV-infected animals were 5-10-fold lower in frequency and inversely correlated with the level of plasma viremia. SIV-specific CD4+ cells from SIV Delta nef animals were predominantly CD27(-)CD28(-)CD45RA(low)CCR7(-)CCR5(-), consistent with an effector-memory subset, and included a fully differentiated CD45RA(+)CCR7(-) subpopulation. In contrast, SIV-specific CD4(+) T cells from SIV-infected animals were mostly CD27(+)C D28(+)CD45RA(-)CCR7(+)CCR5(+), consistent with an early central memory phenotype. The CD45RA(+)CCR7(-)CD(4+) subset from SIV Delta nef animals was highly enriched for effector CD4(+) T cells, as indicated by the perforin expression and up- regulation of the lysosomal membrane protein CD107a after SIV Gag stimulation. SIV-specific CD4(+) T cells in attenuated SIV-infected animals were increased in frequency in bronchioalveolar lavage and decreased in lymph nodes, consistent with an effector-memory T cell population. The ability of SIV Delta nef to induce a high frequency virus-specific CD4(+)T cell response with direct effector function may play a key role in protective immunity produced by vaccination with attenuated SIV strains. C1 Harvard Univ, New England Reg Primate Res Ctr, Sch Med, Div Immunol, Southborough, MA 01772 USA. Harvard Univ, New England Reg Primate Res Ctr, Sch Med, Div Microbiol, Southborough, MA 01772 USA. Harvard Univ, New England Reg Primate Res Ctr, Sch Med, Div Primate Med, Southborough, MA 01772 USA. Inst Appl Int Corp Frederick Inc, AIDS Vaccine Program, NCI, Frederick, MD 21702 USA. Massachusetts Gen Hosp, Infect Dis Unit, Partners AIDS Res Ctr, Boston, MA 02115 USA. RP Gauduin, MC (reprint author), Harvard Univ, New England Reg Primate Res Ctr, Sch Med, Div Immunol, Southborough, MA 01772 USA. EM mcgauduin@sfbr.org FU NCI NIH HHS [N01-CO-12400, N01CO12400]; NCRR NIH HHS [K26 RR000168, P51 RR000168, RR00168]; NIAID NIH HHS [AI45314, AI62412, R01 AI043890, R01 AI062412, AI43890] NR 47 TC 51 Z9 52 U1 0 U2 2 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 1114 FIRST AVE, 4TH FL, NEW YORK, NY 10021 USA SN 0022-1007 J9 J EXP MED JI J. Exp. Med. PD NOV 27 PY 2006 VL 203 IS 12 BP 2661 EP 2672 DI 10.1084/jem.20060134 PG 12 WC Immunology; Medicine, Research & Experimental SC Immunology; Research & Experimental Medicine GA 109WG UT WOS:000242339700009 PM 17116733 ER PT J AU Kabashima, K Haynes, NM Xu, Y Nutt, SL Allende, ML Proia, RL Cyster, JG AF Kabashima, Kenji Haynes, Nicole M. Xu, Ying Nutt, Stephen L. Allende, Maria L. Proia, Richard L. Cyster, Jason G. TI Plasma cell S1P(1) expression determines secondary lymphoid organ retention versus bone marrow tropism SO JOURNAL OF EXPERIMENTAL MEDICINE LA English DT Article ID SPHINGOSINE 1-PHOSPHATE RECEPTORS; ANTIBODY-PRODUCTION; IMMUNE-RESPONSE; T-CELLS; B-CELLS; HUMORAL IMMUNITY; DENDRITIC CELLS; SPHINGOSINE-1-PHOSPHATE; MEMORY; RESPONSIVENESS AB After induction in secondary lymphoid organs, a subset of antibody-secreting cells (ASCs) homes to the bone marrow (BM) and contributes to long-term antibody production. The factors determining secondary lymphoid organ residence versus BM tropism have been unclear. Here we demonstrate that in mice treated with FTY720 or that lack sphingosine-1-phosphate (S1P) receptor-1 (S1P(1)) in B cells, IgG ASCs are induced and localize normally in secondary lymphoid organs but they are reduced in numbers in blood and BM. Many IgG ASCs home to BM on day 3 of the secondary response and day 3 splenic ASCs exhibit S1P responsiveness, whereas the cells remaining at day 5 are unable to respond. S1P(1) mRNA abundance is higher in ASCs isolated from blood compared to spleen, whereas CXCR4 expression is lower. Blood ASCs also express higher amounts of Kruppel-like factor (KLF)2, a regulator of S1P(1) gene expression. These findings establish an essential role for S1P(1) in IgG plasma cell homing and they suggest that differential regulation of S1P(1) expression in differentiating plasma cells may determine whether they remain in secondary lymphoid organs or home to BM. C1 Univ Calif San Francisco, HHMI, San Francisco, CA 94143 USA. Univ Calif San Francisco, Dept Microbiol & Immunol, San Francisco, CA 94143 USA. Walter & Eliza Hall Inst Med Res, Parkville, Vic 3050, Australia. NIDDKD, Genet Dev & Dis Branch, NIH, Bethesda, MD 20892 USA. RP Cyster, JG (reprint author), Univ Calif San Francisco, HHMI, San Francisco, CA 94143 USA. EM Jason.Cyster@ucsf.edu RI Proia, Richard/A-7908-2012; Kabashima, Kenji/G-2521-2014; OI Kabashima, Kenji/0000-0002-0773-0554; Nutt, Stephen/0000-0002-0020-6637 FU NIAID NIH HHS [AI45073, N01AI40098, R01 AI045073] NR 42 TC 101 Z9 102 U1 0 U2 3 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 1114 FIRST AVE, 4TH FL, NEW YORK, NY 10021 USA SN 0022-1007 J9 J EXP MED JI J. Exp. Med. PD NOV 27 PY 2006 VL 203 IS 12 BP 2683 EP 2690 DI 10.1084/jem.20061289 PG 8 WC Immunology; Medicine, Research & Experimental SC Immunology; Research & Experimental Medicine GA 109WG UT WOS:000242339700011 PM 17101733 ER PT J AU Orlova, VV Economopoulou, M Lupu, F Santoso, S Chavakis, T AF Orlova, Valeria V. Economopoulou, Matina Lupu, Florea Santoso, Sentot Chavakis, Triantafyllos TI Junctional adhesion molecule-C regulates vascular endothelial permeability by modulating VE-cadherin-mediated cell-cell contacts SO JOURNAL OF EXPERIMENTAL MEDICINE LA English DT Article ID JAM FAMILY-MEMBERS; BARRIER FUNCTION; IMMUNOGLOBULIN SUPERFAMILY; P21-ACTIVATED KINASE; RAP1; MIGRATION; BINDING; NEOVASCULARIZATION; HETEROGENEITY; INFLAMMATION AB We recently reported that junctional adhesion molecule (JAM)-C plays a role in leukocyte transendothelial migration. Here, the role of JAM-C in vascular permeability was investigated in vitro and in vivo. As opposed to macrovascular endothelial cells that constitutively expressed JAM-C in cell-cell contacts, in quiescent microvascular endothelial cells, JAM-C localized mainly intracellularly,and was recruited to junctions upon short-term stimulation with vascular endothelial growth factor (VEGF) or histamine. Strikingly, disruption of JAM-C function decreased basal permeability and prevented the VEGF-and histamine-induced increases in human dermal microvascular endothelial cell permeability in vitro and skin permeability in mice. Permeability increases are essential in angiogenesis, and JAM-C blockade reduced hyperpermeability and neovascularization in hypoxia-induced retinal angiogenesis in mice. The underlying mechanisms of the JAM-C-mediated increase in endothelial permeability were studied. JAM- C was essential for the regulation of endothelial actomyosin, as revealed by decreased F-actin, reduced myosin light chain phosphorylation, and actin stress fiber formation due to JAM-C knockdown. Moreover, the loss of JAM-C expression resulted in stabilization of VE-cadherin-mediated interendothelial adhesion in a manner dependent on the small GTPase Rap1. Together, through modulation of endothelial contractility and VE-cadherin-mediated adhesion, JAM-C helps to regulate vascular permeability and pathologic angiogenesis. C1 NCI, Expt Immunol Branch, NIH, Bethesda, MD 20892 USA. Oklahoma Med Res Fdn, Cardiovasc Biol Res Program, Oklahoma City, OK 73104 USA. Univ Heidelberg, Dept Med 1, D-69120 Heidelberg, Germany. Univ Giessen, Inst Clin Immunol & Transfus Med, D-35392 Giessen, Germany. RP Chavakis, T (reprint author), NCI, Expt Immunol Branch, NIH, Bethesda, MD 20892 USA. EM chavakist@mail.nih.gov RI Lupu, Florea/C-3162-2009; Orlova, Valeria/C-6065-2014 OI Lupu, Florea/0000-0003-1249-9278; Orlova, Valeria/0000-0002-1169-2802 FU Intramural NIH HHS NR 47 TC 109 Z9 115 U1 1 U2 3 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 1114 FIRST AVE, 4TH FL, NEW YORK, NY 10021 USA SN 0022-1007 J9 J EXP MED JI J. Exp. Med. PD NOV 27 PY 2006 VL 203 IS 12 BP 2703 EP 2714 DI 10.1084/jem.20051730 PG 12 WC Immunology; Medicine, Research & Experimental SC Immunology; Research & Experimental Medicine GA 109WG UT WOS:000242339700013 PM 17116731 ER PT J AU DeVoss, J Hou, YF Johannes, K Lu, W Liou, GI Rinn, J Chang, H Caspi, R Fong, L Anderson, MS AF DeVoss, Jason Hou, Yafei Johannes, Kellsey Lu, Wen Liou, Gregory I. Rinn, John Chang, Howard Caspi, Rachel Fong, Lawrence Anderson, Mark S. TI Spontaneous autoimmunity prevented by thymic expression of a single self-antigen SO JOURNAL OF EXPERIMENTAL MEDICINE LA English DT Article ID T-CELL TOLERANCE; PROMISCUOUS GENE-EXPRESSION; RETINOID-BINDING PROTEIN; AIRE-DEFICIENT MICE; EPITHELIAL-CELLS; NOD MICE; TRANSGENIC MICE; IDENTIFICATION; AUTOANTIGENS; MECHANISMS AB The expression of self-antigen in the thymus is believed to be responsible for the deletion of autoreactive T lymphocytes, a critical process in the maintenance of unresponsiveness to self. The Autoimmune regulator (Aire) gene, which is defective in the disorder autoimmune polyglandular syndrome type 1, has been shown to promote the thymic expression of self-antigens. A clear link, however, between specific thymic self-antigens and a single autoimmune phenotype in this model has been lacking. We show that autoimmune eye disease in aire-deficient mice develops as a result of loss of thymic expression of a single eye antigen, interphotoreceptor retinoid-binding protein (IRBP). In addition, lack of IRBP expression solely in the thymus, even in the presence of aire expression, is sufficient to trigger spontaneous eye-specific autoimmunity. These results suggest that failure of thymic expression of selective single self-antigens can be sufficient to cause organ-specific autoimmune disease, even in otherwise self-tolerant individuals. C1 Univ Calif San Francisco, Ctr Diabet, San Francisco, CA 94143 USA. Univ Calif San Francisco, Dept Med, San Francisco, CA 94143 USA. Med Coll Georgia, Dept Ophthalmol, Augusta, GA 30912 USA. Stanford Univ, Sch Med, Canc Biol Program, Stanford, CA 94305 USA. NEI, Immunol Lab, NIH, Bethesda, MD 20892 USA. RP Anderson, MS (reprint author), Univ Calif San Francisco, Ctr Diabet, San Francisco, CA 94143 USA. EM manderson@diabetes.ucsf.edu OI Caspi, Rachel/0000-0002-7140-7671 FU NEI NIH HHS [EY016408, R01 EY016408]; NIDDK NIH HHS [DK59958, K08 DK059958] NR 41 TC 162 Z9 166 U1 0 U2 6 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 1114 FIRST AVE, 4TH FL, NEW YORK, NY 10021 USA SN 0022-1007 J9 J EXP MED JI J. Exp. Med. PD NOV 27 PY 2006 VL 203 IS 12 BP 2727 EP 2735 DI 10.1084/jem.20061864 PG 9 WC Immunology; Medicine, Research & Experimental SC Immunology; Research & Experimental Medicine GA 109WG UT WOS:000242339700015 PM 17116738 ER PT J AU Chin, YW Mdee, LK Mbwambo, ZH Mi, QW Chai, HB Cragg, GM Swanson, SM Kinghorn, AD AF Chin, Young-Won Mdee, Ladislaus K. Mbwambo, Zakaria H. Mi, Qiuwen Chai, Hee-Byung Cragg, Gordon M. Swanson, Steven M. Kinghorn, A. Douglas TI Prenylated flavonoids from the root bark of Berchemia discolor, a Tanzanian medicinal plant SO JOURNAL OF NATURAL PRODUCTS LA English DT Article AB Five new prenylated flavonoids (1-5) were isolated from the root bark of Berchemia discolor, collected in Tanzania, along with 10 known compounds, by bioactivity-guided fractionation. The structures of compounds 1-5 were elucidated using various spectroscopic techniques. Of these isolates, compound 4, and the known compounds nitidulin (6), amorphigenin (7), and dabinol (8), exhibited cytotoxic activity when evaluated against a small panel of human cancer cells. Nitidulin (6) was further tested in an in vivo hollow fiber assay and found to be active against LNCaP (human hormone-dependent prostate cancer) cells implanted intraperitoneally, at doses of 10, 20, and 40 mg/kg. C1 Ohio State Univ, Coll Pharm, Div Med Chem & Pharmacognosy, Columbus, OH 43210 USA. Univ Illinois, Coll Pharm, Program Collaborat Res Pharmaceut Sci, Chicago, IL 60612 USA. Univ Illinois, Coll Pharm, Dept Med Chem & Pharmacognosy, Chicago, IL 60612 USA. NCI, Frederick, MD 21702 USA. Muhimbili Univ, Coll Hlth Sci, Inst Tradit Med, Dar Es Salaam, Tanzania. RP Kinghorn, AD (reprint author), Ohio State Univ, Coll Pharm, Div Med Chem & Pharmacognosy, Columbus, OH 43210 USA. EM kinghorn.4@osu.edu OI Kinghorn, A. Douglas/0000-0002-6647-8707 FU NCI NIH HHS [U19 CA052956, U19 CA052956-15, U19-CA-52956] NR 12 TC 19 Z9 20 U1 1 U2 9 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA SN 0163-3864 J9 J NAT PROD JI J. Nat. Prod. PD NOV 27 PY 2006 VL 69 IS 11 BP 1649 EP 1652 DI 10.1021/np060418w PG 4 WC Plant Sciences; Chemistry, Medicinal; Pharmacology & Pharmacy SC Plant Sciences; Pharmacology & Pharmacy GA 109HH UT WOS:000242298300026 PM 17125241 ER PT J AU Mandruzzato, S Callegaro, A Turcatel, G Francescato, S Montesco, MC Chiarion-Sileni, V Mocellin, S Rossi, CR Bicciato, S Wang, E Marincola, FM Zanovello, P AF Mandruzzato, Susanna Callegaro, Andrea Turcatel, Gianluca Francescato, Samuela Montesco, Maria C. Chiarion-Sileni, Vanna Mocellin, Simone Rossi, Carlo R. Bicciato, Silvio Wang, Ena Marincola, Francesco M. Zanovello, Paola TI A gene expression signature associated with survival in metastatic melanoma SO JOURNAL OF TRANSLATIONAL MEDICINE LA English DT Article ID CUTANEOUS MALIGNANT-MELANOMA; AMERICAN JOINT COMMITTEE; SQUAMOUS-CELL CARCINOMA; HEPATOCELLULAR-CARCINOMA; PREDICT SURVIVAL; BREAST-CANCER; CLASS-II; PROGNOSIS; LUNG; CLASSIFICATION AB Background: Current clinical and histopathological criteria used to define the prognosis of melanoma patients are inadequate for accurate prediction of clinical outcome. We investigated whether genome screening by means of high-throughput gene microarray might provide clinically useful information on patient survival. Methods: Forty-three tumor tissues from 38 patients with stage III and stage IV melanoma were profiled with a 17,500 element cDNA microarray. Expression data were analyzed using significance analysis of microarrays (SAM) to identify genes associated with patient survival, and supervised principal components (SPC) to determine survival prediction. Results: SAM analysis revealed a set of 80 probes, corresponding to 70 genes, associated with survival, i.e. 45 probes characterizing longer and 35 shorter survival times, respectively. These transcripts were included in a survival prediction model designed using SPC and cross-validation which allowed identifying 30 predicting probes out of the 80 associated with survival. Conclusion: The longer-survival group of genes included those expressed in immune cells, both innate and acquired, confirming the interplay between immunological mechanisms and the natural history of melanoma. Genes linked to immune cells were totally lacking in the poor-survival group, which was instead associated with a number of genes related to highly proliferative and invasive tumor cells. C1 Univ Padua, Dept Oncol & Surg Sci, Oncol Sect, Padua, Italy. Univ Padua, Dept Chem Proc Engn, Padua, Italy. Univ Padua, Dept Oncol & Surg Sci, Pathol Sect, Padua, Italy. Ist Oncol Veneto, Padua, Italy. Univ Padua, Dept Oncol & Surg Sci, Surg Sect, Padua, Italy. NIH, Dept Transfus Med, Ctr Clin, Bethesda, MD 20892 USA. RP Mandruzzato, S (reprint author), Univ Padua, Dept Oncol & Surg Sci, Oncol Sect, Padua, Italy. EM susanna.mandruzzato@unipd.it; acallegaro@yahoo.it; gianlucaturcatel@virgilio.it; samuela.francescato@unipd.it; maria.montesco@sanita.padova.it; vanna.chiarionsileni@sanita.padova.it; simone.mocellin@unipd.it; carlor.rossi@unipd.it; silvio.bicciato@unipd.it; Ewang@mail.cc.nih.gov; FMarincola@cc.nih.gov; paola.zanovello@unipd.it RI Rossi, Carlo Riccardo/A-7685-2010; Bicciato, Silvio/C-9825-2009; Montesco, Maria/L-5693-2016; OI Rossi, Carlo Riccardo/0000-0001-7875-5655; Bicciato, Silvio/0000-0002-1944-7078; Montesco, Maria/0000-0002-2095-2557; MANDRUZZATO, SUSANNA/0000-0002-0707-995X NR 40 TC 53 Z9 55 U1 0 U2 2 PU BIOMED CENTRAL LTD PI LONDON PA MIDDLESEX HOUSE, 34-42 CLEVELAND ST, LONDON W1T 4LB, ENGLAND SN 1479-5876 J9 J TRANSL MED JI J. Transl. Med. PD NOV 27 PY 2006 VL 4 AR 50 DI 10.1186/1479-5876-4-50 PG 11 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA 119CV UT WOS:000242990700001 PM 17129373 ER PT J AU Maestripieri, D McCormack, K Lindell, SG Higley, JD Sanchez, MM AF Maestripieri, Dario McCormack, Kai Lindell, Stephen G. Higley, J. Dee Sanchez, Mar M. TI Influence of parenting style on the offspring's behaviour and CSF monoamine metabolite levels in crossfostered and noncrossfostered female rhesus macaques SO BEHAVIOURAL BRAIN RESEARCH LA English DT Article DE parenting style; early experience; behavioural development; brain monoamines; primates ID CEREBROSPINAL-FLUID MONOAMINE; MOTHER-INFANT RELATIONSHIPS; JAPANESE MACAQUES; INDIVIDUAL-DIFFERENCES; STRESS REACTIVITY; NONHUMAN-PRIMATES; MATERNAL-CARE; MONKEYS; TRANSMISSION; EXPERIENCE AB We investigated the association between variation in parenting style and the offspring's behaviour and CSF monoantine metabolite (5-HIAA, HVA, and MHPG) levels in rhesus monkeys. Study subjects were 25 two-year-old females reared by their biological mothers and 15 same-aged females that were crossfostered at birth and reared by unrelated mothers. Subjects that were rejected more by their mothers in the first 6 months of life engaged in more solitary play and had lower CSF concentrations of 5-HIAA than subjects that were rejected less. The relation between these variables was generally similar in crossfostered and noncrossfostered females. CSF levels of 5-HIAA were negatively correlated with rates of scratching, a behavioural indicator of anxiety. These results suggest that that early exposure to high rates of maternal rejection can result in higher anxiety later in life, and that this effect may be mediated by serotonergic mechanisms. Variation in maternal protectiveness did not affect offspring behaviour and neither protectiveness nor rejection affected CSF levels of HVA and MHPG. CSF levels of MHPG, however, were negatively correlated with solitary play behaviour and avoidance of other individuals, suggesting that individuals with lower CSF MHPG were more fearful and socially phobic than those with higher CSF MHPG. Taken together, these findings suggest that individual differences in anxiety and fearfulness in young rhesus monkeys are accounted for, at least in part, by variation in CSF levels of monoamine metabolites, and that the development of brain monoamine systems, particularly serotonin, can be affected by early exposure to variable maternal behaviour. (c) 2006 Elsevier B.V. All rights reserved. C1 Univ Chicago, Dept Comparat Human Dev, Chicago, IL 60637 USA. Emory Univ, Yerkes Natl Primate Res Ctr, Atlanta, GA 30322 USA. Spelman Coll, Dept Psychol, Atlanta, GA 30314 USA. NIAAA, Sect Study Primate Models Psychopathol, Poolesville, MD USA. Emory Univ, Dept Psychiat, Atlanta, GA 30322 USA. RP Maestripieri, D (reprint author), Univ Chicago, Dept Comparat Human Dev, 5730 S Woodlawn Ave, Chicago, IL 60637 USA. EM dario@uchicago.edu FU NCRR NIH HHS [RR-00165]; NIMH NIH HHS [R01-MH62577, K02-MH63097, R01-MH57249, R21-MH01005] NR 30 TC 39 Z9 39 U1 0 U2 8 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0166-4328 J9 BEHAV BRAIN RES JI Behav. Brain Res. PD NOV 25 PY 2006 VL 175 IS 1 BP 90 EP 95 DI 10.1016/j.bbr.2006.08.002 PG 6 WC Behavioral Sciences; Neurosciences SC Behavioral Sciences; Neurosciences & Neurology GA 109KY UT WOS:000242308200010 PM 16971003 ER PT J AU Wang, W Parker, GE Skurat, AV Raben, N DePaoli-Roach, AA Roach, PJ AF Wang, Wei Parker, Gretchen E. Skurat, Alexander V. Raben, Nina DePaoli-Roach, Anna A. Roach, Peter J. TI Relationship between glycogen accumulation and the laforin dual specificity phosphatase SO BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS LA English DT Article DE laforin; Lafora disease; glycogen; protein phosphatase ID PROGRESSIVE MYOCLONUS EPILEPSY; CARBOHYDRATE-BINDING DOMAIN; PROTEIN PHOSPHATASE; STORAGE-DISEASE; EPM2A GENE; MUSCLE; SYNTHASE; UBIQUITINATION; DYSFUNCTION; MUTATIONS AB Laforin, encoded by the EPM2A gene, is a dual specificity protein phosphatase that has a functional glycogen-binding domain. Mutations in the EPM2A gene account for around half of the cases of Lafora disease, an autosomal recessive neurodegenerative disorder, characterized by progressive myoclonus epilepsy. The hallmark of the disease is the presence of Lafora bodies, which contain polyglucosan, a poorly branched form of glycogen, in neurons and other tissues. We examined the level of laforin protein in several mouse models in which muscle glycogen accumulation has been altered genetically. Mice with elevated muscle glycogen have increased laforin as judged by Western analysis. Mice completely lacking muscle glycogen or with 10% normal muscle glycogen had reduced laforin. Mice defective in the GAA gene encoding lysosomal alpha-glucosidase (acid maltase) overaccumulate glycogen in the lysosome but did not have elevated laforin. We propose, therefore, that laforin senses cytosolic glycogen accumulation which in turn determines the level of laforin protein. (c) 2006 Elsevier Inc. All rights reserved. C1 Indiana Univ, Sch Med, Dept Biochem & Mol Biol, Indianapolis, IN 46202 USA. Indiana Univ, Diabet Res Ctr, Bloomington, IN 47405 USA. NIAMSD, NIH, Bethesda, MD 20892 USA. RP Roach, PJ (reprint author), Indiana Univ, Sch Med, Dept Biochem & Mol Biol, Indianapolis, IN 46202 USA. EM proach@iupui.edu FU NIDDK NIH HHS [R01 DK036569, DK27221, R37 DK027221, DK36569, F32 DK066983, F32 DK66983, R01 DK027221, R56 DK027221] NR 35 TC 16 Z9 16 U1 0 U2 0 PU ACADEMIC PRESS INC ELSEVIER SCIENCE PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA SN 0006-291X J9 BIOCHEM BIOPH RES CO JI Biochem. Biophys. Res. Commun. PD NOV 24 PY 2006 VL 350 IS 3 BP 588 EP 592 DI 10.1016/j.bbrc.2006.09.091 PG 5 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA 099HN UT WOS:000241584300014 PM 17022935 ER PT J AU Sidorova, NY Muradymov, S Rau, DC AF Sidorova, Nina Y. Muradymov, Shakir Rau, Donald C. TI Differences in hydration coupled to specific and nonspecific competitive binding and to specific DNA binding of the restriction endonuclease BamHI SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID PREFERENTIAL HYDRATION; OSMOTIC-STRESS; WATER RELEASE; MACROMOLECULAR HYDRATION; PROTEIN STABILITY; RECOGNITION SITE; ECORI; COMPLEXES; REPRESSOR; EXCLUSION AB Using the osmotic stress technique together with a self-cleavage assay we measure directly differences in sequestered water between specific and nonspecific DNA-BamHI complexes as well as the numbers of water molecules released coupled to specific complex formation. The difference between specific and nonspecific binding free energy of the BamHI scales linearly with solute osmolal concentration for seven neutral solutes used to set water activity. The observed osmotic dependence indicates that the nonspecific DNA-BamHI complex sequesters some 120-150 more water molecules than the specific complex. The weak sensitivity of the difference in number of waters to the solute identity suggests that these waters are sterically inaccessible to solutes. This result is in close agreement with differences in the structures determined by x-ray crystallography. We demonstrate additionally that when the same solutes that were used in competition experiments are used to probe changes accompanying the binding of free BamHI to its specific DNA sequence, the measured number of water molecules released in the binding process is strikingly solute-dependent ( with up to 10-fold difference between solutes). This result is expected for reactions resulting in a large change in a surface exposed C1 NICHD, Lab Phys & Struct Biol, NIH, Bethesda, MD 20892 USA. RP Sidorova, NY (reprint author), Bldg 9,Rm 1E-108, Bethesda, MD 20892 USA. EM sidorova@mail.nih.gov FU Intramural NIH HHS NR 43 TC 22 Z9 23 U1 0 U2 4 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD NOV 24 PY 2006 VL 281 IS 47 BP 35656 EP 35666 DI 10.1074/jbc.M608018200 PG 11 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA 106KX UT WOS:000242100500010 PM 17008319 ER PT J AU Nicolas, E Lee, MG Hakimi, MA Cam, HP Grewal, SIS Shiekhattar, R AF Nicolas, Estelle Lee, Min Gyu Hakimi, Mohamed-Ali Cam, Hugh P. Grewal, Shiv I. S. Shiekhattar, Ramin TI Fission yeast homologs of human histone H3 lysine 4 demethylase regulate a common set of genes with diverse functions SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID ARGININE METHYLATION; ANDROGEN-RECEPTOR; SWIRM DOMAIN; COMPLEX; COMPONENT; FAMILY; LSD1; COREST; TRANSCRIPTION; REPRESSION AB Schizosaccharomyces pombe contains two proteins, SWIRM1 and SWIRM2, with close homology to human histone H3 lysine 4 demethylase. Both proteins contain the amino oxidase catalytic domain and a recently described DNA interaction SWIRM domain. Here we describe the biochemical isolation and the functional characterization of SWIRM1 and SWIRM2. Our results indicate that while SWIRM2 is an essential gene, cells lacking SWIRM1 are viable. We found that SWIRM1 and SWIRM2 are stably associated in a multiprotein complex, but intriguingly, unlike their human counterpart, S. pombe SWIRM complex contains neither a histone deacetylase nor any detectable demethylase activity. Genome-wide chromatin immunoprecipitation unexpectedly showed the absence of both SWIRM proteins from heterochromatic domains. Instead, consistent with biochemical analyses, SWIRM1 and SWIRM2 co-localize to a common set of target gene promoters whose functions are implicated in diverse processes including mitochondrial metabolism and transcriptional regulation. Importantly, we show that SWIRM1 is not only required for optimum transcription of its target genes but also display a global role in regulation of antisense transcription. C1 NCI, Mol Cell Biol Lab, NIH, Bethesda, MD 20892 USA. Wistar Inst Anat & Biol, Philadelphia, PA 19104 USA. RP Grewal, SIS (reprint author), NCI, Mol Cell Biol Lab, NIH, Bethesda, MD 20892 USA. EM grewals@mail.nih.gov; shiekhattar@wistar.org RI Nicolas, Estelle/C-4425-2008; HAKIMI, Mohamed-Ali/F-9806-2014; OI Nicolas, Estelle/0000-0003-0412-8477; HAKIMI, Mohamed-ali/0000-0002-2547-8233 FU Intramural NIH HHS; NIGMS NIH HHS [GM61204] NR 33 TC 17 Z9 22 U1 0 U2 2 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD NOV 24 PY 2006 VL 281 IS 47 BP 35983 EP 35988 DI 10.1074/jbc.M606349200 PG 6 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA 106KX UT WOS:000242100500045 PM 16990277 ER PT J AU Kuznetsova, E Proudfoot, M Gonzales, CF Brown, G Omelchenko, MV Borozan, I Carmel, L Wolf, YI Mori, H Savchenko, AV Arrowsmith, CH Koonin, EV Edwards, AM Yakunin, AF AF Kuznetsova, Ekaterina Proudfoot, Michael Gonzales, Claudio F. Brown, Greg Omelchenko, Marina V. Borozan, Ivan Carmel, Liran Wolf, Yuri I. Mori, Hirotada Savchenko, Alexei V. Arrowsmith, Cheryl H. Koonin, Eugene V. Edwards, Aled M. Yakunin, Alexander F. TI Genome-wide analysis of substrate specificities of the Escherichia coli haloacid dehalogenase-like phosphatase family SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID GENERAL ENZYMATIC SCREENS; CATALYTIC PROMISCUITY; CRYSTAL-STRUCTURE; NONENZYMATIC GLYCOSYLATION; L-2-HALOACID DEHALOGENASE; PHOSPHOSERINE PHOSPHATASE; BETA-PHOSPHOGLUCOMUTASE; ALKALINE-PHOSPHATASE; ACID DEHALOGENASE; MOLECULAR-CLONING AB Haloacid dehalogenase (HAD)-like hydrolases are a vast superfamily of largely uncharacterized enzymes, with a few members shown to possess phosphatase, beta-phosphoglucomutase, phosphonatase, and dehalogenase activities. Using a representative set of 80 phosphorylated substrates, we characterized the substrate specificities of 23 soluble HADs encoded in the Escherichia coli genome. We identified small molecule phosphatase activity in 21 HADs and beta-phosphoglucomutase activity in one protein. The E. coli HAD phosphatases show high catalytic efficiency and affinity to a wide range of phosphorylated metabolites that are intermediates of various metabolic reactions. Rather than following the classical "one enzyme-one substrate" model, most of the E. coli HADs show remarkably broad and overlapping substrate spectra. At least 12 reactions catalyzed by HADs currently have no EC numbers assigned in Enzyme Nomenclature. Surprisingly, most HADs hydrolyzed small phosphodonors ( acetyl phosphate, carbamoyl phosphate, and phosphoramidate), which also serve as substrates for autophosphorylation of the receiver domains of the two-component signal transduction systems. The physiological relevance of the phosphatase activity with the preferred substrate was validated in vivo for one of the HADs, YniC. Many of the secondary activities of HADs might have no immediate physiological function but could comprise a reservoir for evolution of novel phosphatases. C1 Univ Toronto, Banting & Best Dept Med Res, Toronto, ON M5G 1L6, Canada. Univ Toronto, Dept Med Biophys, Toronto, ON M5G 1L6, Canada. Ontario Canc Inst, Ontario Ctr Struct Proteom, Toronto, ON M5G 2C4, Canada. Natl Lib Med, Natl Ctr Biotechnol Informat, NIH, Bethesda, MD 20894 USA. Nara Inst Sci & Technol, Grad Sch Biol Sci, Nara 6300101, Japan. Univ Toronto, Struct Genom Consortium, Toronto, ON M5G 1L6, Canada. RP Edwards, AM (reprint author), Univ Toronto, Banting & Best Dept Med Res, 112 Coll St,Rm 024, Toronto, ON M5G 1L6, Canada. EM aled.edwards@utoronto.ca; a.iakounine@utoronto.ca RI Carmel, Liran/A-9681-2008; Mori, Hirotada/B-4934-2011; Yakunin, Alexander/J-1519-2014; OI Yakunin, Alexander/0000-0003-0813-6490 FU NIGMS NIH HHS [GM62414-01] NR 80 TC 120 Z9 141 U1 0 U2 12 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD NOV 24 PY 2006 VL 281 IS 47 BP 36149 EP 36161 DI 10.1074/jbc.M605449200 PG 13 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA 106KX UT WOS:000242100500065 PM 16990279 ER PT J AU Li, TW Santockyte, R Shen, RF Tekle, E Wang, GH Yang, DCH Chock, PB AF Li, Tianwei Santockyte, Rasa Shen, Rong-Fong Tekle, Ephrem Wang, Guanghui Yang, David C. H. Chock, P. Boon TI Expression of SUMO-2/3 induced senescence through p53- and pRB-mediated pathways SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID CELLULAR SENESCENCE; HUMAN HOMOLOG; TUMOR-CELLS; P53; UBIQUITIN; APOPTOSIS; PROTEINS; SUPPRESSOR; MODIFIERS; NUCLEAR AB Three highly homologous small ubiquitin-related modifier ( SUMO) proteins have been identified in mammals. Modifications of proteins by SUMO-1 have been shown to regulate transcription, nucleocytoplasmic transport, protein stability, and protein-protein interactions. Relative to SUMO-1, little is known about the functions of SUMO-2 or SUMO-3 ( referred to as SUMO-2/3). Here, stable cell lines overexpressing processed forms of SUMO-2/3 (SUMO-2/3GG) as well as their non-conjugatable derivatives, SUMO-2/3 Delta GG, were established. Cells overexpressing SUMO-2/3GG showed a premature senescence phenotype as revealed by cellular morphology and senescence-associated galactosidase activity. The senescence pathway protein p21 was up-regulated in cells overexpressing SUMO-2/3GG. In contrast, cells overexpressing non-conjugatable forms of SUMO-2/3 Delta GG showed neither an apparent senescent phenotype nor elevated p21. Both p53 and pRB were found to be modified by SUMO-2/3. Site-directed mutagenesis studies showed that Lys-386 of p53, the SUMO- 1 modification site, is also the modification site for SUMO-2/3. In addition, H2O2 treatment of untransfected cells caused an increase in p53 sumoylation by SUMO-2/3, whereas that by SUMO- 1 remained unchanged. Moreover, knocking down tumor suppressor proteins p53 or pRB using small interfering RNA significantly alleviated the premature senescence phenotypes in SUMO-2/3GG overexpressing cells. Together, our results reveal that p53 and pRB can be sumoylated by SUMO-2/3 in vivo, and such modification of p53 and pRB may play roles in premature senescence and stress response. C1 NHLBI, Biochem Lab, NIH, Bethesda, MD 20892 USA. NHLBI, Proteom Core Facil, NIH, Bethesda, MD 20892 USA. Georgetown Univ, Dept Chem, Washington, DC 20057 USA. RP Chock, PB (reprint author), NHLBI, Biochem Lab, NIH, Bldg 50,Rm 2134,50 S Dr,MSC-8012, Bethesda, MD 20892 USA. EM bchock@nih.gov RI Yang, David/A-7294-2009 NR 28 TC 58 Z9 64 U1 0 U2 1 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD NOV 24 PY 2006 VL 281 IS 47 BP 36221 EP 36227 DI 10.1074/jbc.M608236200 PG 7 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA 106KX UT WOS:000242100500073 PM 17012228 ER PT J AU Toth, B Balla, A Ma, H Knight, ZA Shokat, KM Balla, T AF Toth, Balazs Balla, Andras Ma, Hui Knight, Zachary A. Shokat, Kevan M. Balla, Tamas TI Phosphatidylinositol 4-kinase III beta regulates the transport of ceramide between the endoplasmic reticulum and Golgi SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID OXYSTEROL-BINDING-PROTEIN; PLECKSTRIN HOMOLOGY DOMAINS; PLASMA-MEMBRANE; SACCHAROMYCES-CEREVISIAE; MOLECULAR MACHINERY; 4-KINASE ACTIVITY; CELL-SURFACE; GENE ENCODES; YEAST; SECRETION AB The recently identified ceramide transfer protein, CERT, is responsible for the bulk of ceramide transport from the endoplasmic reticulum ( ER) to the Golgi. CERT has a C-terminal START domain for ceramide binding and an N-terminal pleckstrin homology domain that binds phosphatidylinositol 4-phosphate suggesting that phosphatidylinositol ( PI) 4-kinases are involved in the regulation of CERT-mediated ceramide transport. In the present study fluorescent analogues were used to follow the ER to Golgi transport of ceramide to determine which of the four mammalian PI 4-kinases are involved in this process. Overexpression of pleckstrin homology domains that bind phosphatidylinositol 4-phosphate strongly inhibited the transport of C5-BODIPY-ceramide to the Golgi. A newly identified PI3-kinase inhibitor, PIK93 that selectively inhibits the type III PI4-kinase beta enzyme, and small interfering RNA-mediated down-regulation of the individual PI4-kinase enzymes, revealed that PI4-kinase beta has a dominant role in ceramide transport between the ER and Golgi. Accordingly, inhibition of PI4-kinase III beta either by wortmannin or PIK93 inhibited the conversion of [H-3] serine-labeled endogenous ceramide to sphingomyelin. Therefore, PI4-kinase beta is a key enzyme in the control of spingomyelin synthesis by controlling the flow of ceramide from the ER to the Golgi compartment. C1 NICHD, Sect Mol Signal Transduct, NIH, Bethesda, MD 20892 USA. Univ Calif San Francisco, Program Chem & Chem Biol, San Francisco, CA 94143 USA. Univ Calif San Francisco, Howard Hughes Med Inst, San Francisco, CA 94143 USA. Univ Calif San Francisco, Dept Cellular & Mol Pharmacol, San Francisco, CA 94143 USA. RP Balla, T (reprint author), Bldg 49,Rm 6A35,49 Convent Dr, Bethesda, MD 20892 USA. EM ballat@mail.nih.gov RI Toth, Balazs/B-4252-2012; OI Balla, Tamas/0000-0002-9077-3335; Balla, Andras/0000-0002-6450-2793 FU Intramural NIH HHS; NIAID NIH HHS [AI044009] NR 39 TC 80 Z9 81 U1 1 U2 7 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD NOV 24 PY 2006 VL 281 IS 47 BP 36369 EP 36377 DI 10.1074/jbc.M604935200 PG 9 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA 106KX UT WOS:000242100500088 PM 17003043 ER PT J AU Thera, MA Doumbo, OK Coulibaly, D Diallo, DA Sagara, I Dicko, A Diemert, DJ Heppner, DG Stewart, VA Angov, E Soisson, L Leach, A Tucker, K Lyke, KE Plowe, CV AF Thera, Mahamadou A. Doumbo, Ogobara K. Coulibaly, Drissa Diallo, Dapa A. Sagara, Issaka Dicko, Alassane Diemert, David J. Heppner, D. Gray, Jr. Stewart, V. Ann Angov, Evelina Soisson, Lorraine Leach, Amanda Tucker, Kathryn Lyke, Kirsten E. Plowe, Christopher V. CA Mali FMP1 Working Grp TI Safety and allele-specific immunogenicity of a malaria vaccine in Malian adults: Results of a phase I randomized trial SO PLOS CLINICAL TRIALS LA English DT Article ID MEROZOITE SURFACE PROTEIN-1; PLASMODIUM-FALCIPARUM; BANDIAGARA; CHILDREN; EFFICACY; DISEASE AB Objectives: The objectives were to evaluate the safety, reactogenicity, and allele-specific immunogenicity of the blood-stage malaria vaccine FMP1/AS02A in adults exposed to seasonal malaria and the impact of natural infection on vaccine-induced antibody levels. Design: We conducted a randomized, double-blind, controlled phase I clinical trial. Setting: Bandiagara, Mali, West Africa, is a rural town with intense seasonal transmission of Plasmodium falciparum malaria. Participants: Forty healthy, malaria-experienced Malian adults aged 18-55 y were enrolled. Interventions: The FMP1/AS02A malaria vaccine is a 42-kDa recombinant protein based on the carboxy-terminal end of merozoite surface protein-1 (MSP-1(42)) from the 3D7 clone of P. falciparum, adjuvanted with AS02A. The control vaccine was a killed rabies virus vaccine (Imovax). Participants were randomized to receive either FMP1/AS02A or rabies vaccine at 0, 1, and 2 mo and were followed for 1 y. Outcome Measures: Solicited and unsolicited adverse events and allele-specific antibody responses to recombinant MSP-1(42) and its subunits derived from P. falciparum strains homologous and heterologous to the 3D7 vaccine strain were measured. Results: Transient local pain and swelling were more common in the malaria vaccine group than in the control group (11/20 versus 3/20 and 10/20 versus 6/20, respectively). MSP-1(42) antibody levels rose during the malaria transmission season in the control group, but were significantly higher in malaria vaccine recipients after the second immunization and remained higher after the third immunization relative both to baseline and to the control group. Immunization with the malaria vaccine was followed by significant increases in antibodies recognizing three diverse MSP-1(42) alleles and their subunits. Conclusions: FMP1/AS02A was well tolerated and highly immunogenic in adults exposed to intense seasonal malaria transmission and elicited immune responses to genetically diverse parasite clones. Anti-MSP-1(42) antibody levels followed a seasonal pattern that was significantly augmented and prolonged by the malaria vaccine. C1 Univ Maryland, Sch Med, Ctr Vaccine Dev, Baltimore, MD 21201 USA. Stat Collaborat, Washington, DC USA. GlaxoSmithKline Biol, Rixensart, Belgium. US Agcy Int Dev, Washington, DC 20523 USA. Walter Reed Army Inst Res, Dept Immunol, Silver Spring, MD USA. NIAID, Malaria Vaccine Dev branch, NIH, Bethesda, MD 20892 USA. Univ Bamako, Malaria Res & Training Ctr, Bamako, Mali. RP Plowe, CV (reprint author), Univ Maryland, Sch Med, Ctr Vaccine Dev, Baltimore, MD 21201 USA. EM cplowe@medicine.umaryland.edu OI Diemert, David/0000-0002-2789-0512 FU FIC NIH HHS [D43 TW001589]; NIAID NIH HHS [N01AI85346] NR 17 TC 47 Z9 49 U1 0 U2 5 PU PUBLIC LIBRARY SCIENCE PI SAN FRANCISCO PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA SN 1555-5887 J9 PLOS CLIN TRIALS JI PLos Clin. Trials PD NOV 24 PY 2006 VL 1 IS 7 AR e34 DI 10.1371/journal.pctr.0010034 PG 8 WC Medicine, Research & Experimental; Pharmacology & Pharmacy SC Research & Experimental Medicine; Pharmacology & Pharmacy GA 150SU UT WOS:000245239100002 PM 17124530 ER PT J AU Faustman, DL Tran, SD Kodama, S Lodde, BM Szalayova, I Key, S Toth, ZE Mezey, E AF Faustman, Denise L. Tran, Simon D. Kodama, Shohta Lodde, Beatrijs M. Szalayova, Ildiko Key, Sharon Toth, Zsuzsanna E. Mezey, Eva TI Comment on papers by Chong et al., Nishio et al., and Suri et al. on diabetes reversal in NOD mice SO SCIENCE LA English DT Editorial Material ID REGENERATION; CELLS C1 Massachusetts Gen Hosp, Charlestown, MA 02129 USA. McGill Univ, Montreal, PQ, Canada. Brigham & Womens Hosp, Boston, MA 02215 USA. NIH, Bethesda, MD 20892 USA. RP Faustman, DL (reprint author), Massachusetts Gen Hosp, Charlestown, MA 02129 USA. EM faustman@helix.mgh.harvard.edu; mezeye@mail.nih.gov NR 10 TC 0 Z9 0 U1 0 U2 1 PU AMER ASSOC ADVANCEMENT SCIENCE PI WASHINGTON PA 1200 NEW YORK AVE, NW, WASHINGTON, DC 20005 USA SN 0036-8075 J9 SCIENCE JI Science PD NOV 24 PY 2006 VL 314 IS 5803 DI 10.1126/science.1129811 PG 2 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA 108BR UT WOS:000242215800019 ER PT J AU Bloom, SL Spong, CY Thom, E Varner, MW Rouse, DJ Weininger, S Ramin, SM Caritis, SN Peaceman, A Sorokin, Y Sciscione, A Carpenter, M Mercer, B Thorp, J Malone, F Harper, M Iams, J Anderson, G AF Bloom, Steven L. Spong, Catherine Y. Thom, Elizabeth Varner, Michael W. Rouse, Dwight J. Weininger, Sandy Ramin, Susan M. Caritis, Steve N. Peaceman, Alan Sorokin, Yoram Sciscione, Anthony Carpenter, Marshall Mercer, Brian Thorp, John Malone, Fergal Harper, Margaret Iams, Jay Anderson, Garland CA Natl Inst Child Hlth Human Dev Mat TI Fetal pulse oximetry and cesarean delivery SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Article; Proceedings Paper CT 26th Annual Meeting of the Society-for-Maternal-Fetal-Medicine CY FEB 02, 2006 CL Miami, FL SP Soc Maternal Fetal Med AB Background: Knowledge of fetal oxygen saturation, as an adjunct to electronic fetal monitoring, may be associated with a significant change in the rate of cesarean deliveries or the infant's condition at birth. Methods: We randomly assigned 5341 nulliparous women who were at term and in early labor to either "open" or "masked" fetal pulse oximetry. In the open group, fetal oxygen saturation values were displayed to the clinician. In the masked group, the fetal oxygen sensor was inserted and the values were recorded by computer, but the data were hidden. Labor complicated by a nonreassuring fetal heart rate before randomization was documented for subsequent analysis. Results: There was no significant difference in the overall rates of cesarean delivery between the open and masked groups (26.3% and 27.5%, respectively; P=0.31). The rates of cesarean delivery associated with the separate indications of a nonreassuring fetal heart rate (7.1% and 7.9%, respectively; P=0.30) and dystocia (18.6% and 19.2%, respectively; P=0.59) were similar between the two groups. Similar findings were observed in the subgroup of 2168 women in whom a nonreassuring fetal heart rate was detected before randomization. The condition of the infants at birth did not differ significantly between the two groups. Conclusions: Knowledge of the fetal oxygen saturation is not associated with a reduction in the rate of cesarean delivery or with improvement in the condition of the newborn. (ClinicalTrials.gov number, NCT00098709.). C1 Univ Texas, SW Med Ctr, Dept Obstet & Gynecol, Dallas, TX 75390 USA. NICHHD, Bethesda, MD 20892 USA. George Washington Univ, Ctr Biostat, Washington, DC USA. Univ Utah, Salt Lake City, UT USA. Univ Alabama, Birmingham, AL USA. US FDA, Rockville, MD 20857 USA. Univ Texas, Hlth Sci Ctr, Houston, TX USA. Univ Pittsburgh, Pittsburgh, PA USA. Northwestern Univ, Chicago, IL 60611 USA. Wayne State Univ, Detroit, MI USA. Drexel Univ, Philadelphia, PA 19104 USA. Brown Univ, Providence, RI 02912 USA. Case Western Reserve Univ, Cleveland, OH 44106 USA. Univ N Carolina, Chapel Hill, NC USA. Columbia Univ, New York, NY USA. Wake Forest Univ, Winston Salem, NC 27109 USA. Ohio State Univ, Columbus, OH 43210 USA. Univ Texas, Med Branch, Galveston, TX 77550 USA. RP Bloom, SL (reprint author), Univ Texas, SW Med Ctr, Dept Obstet & Gynecol, 5323 Harry Hines Blvd, Dallas, TX 75390 USA. EM steven.bloom@utsouthwestern.edu RI Varner, Michael/K-9890-2013; OI caritis, steve/0000-0002-2169-0712; Varner, Michael/0000-0001-9455-3973; Peaceman, Alan/0000-0002-4515-4850 FU NICHD NIH HHS [HD27915, HD27869, HD27860, HD27917, HD21410, HD34116, HD34136, HD34208, HD36801, HD40485, HD40500, HD40512, HD40544, HD40545, HD40560] NR 14 TC 50 Z9 52 U1 0 U2 2 PU MASSACHUSETTS MEDICAL SOC PI WALTHAM PA WALTHAM WOODS CENTER, 860 WINTER ST,, WALTHAM, MA 02451-1413 USA SN 0028-4793 J9 NEW ENGL J MED JI N. Engl. J. Med. PD NOV 23 PY 2006 VL 355 IS 21 BP 2195 EP 2202 DI 10.1056/NEJMoa061170 PG 8 WC Medicine, General & Internal SC General & Internal Medicine GA 107KQ UT WOS:000242170900006 PM 17124017 ER PT J AU Lauriat, TL Dracheva, S Kremerskothen, J Duning, K Haroutunian, V Buxbaum, JD Hyde, TM Kleinman, JE McInnes, LA AF Lauriat, Tara L. Dracheva, Stella Kremerskothen, Joachim Duning, Kerstin Haroutunian, Vahram Buxbaum, Joseph D. Hyde, Thomas M. Kleinman, Joel E. McInnes, L. Alison TI Characterization of KIAA0513, a novel signaling molecule that interacts with modulators of neuroplasticity, apoptosis, and the cytoskeleton SO BRAIN RESEARCH LA English DT Article DE yeast two-hybrid; RT-PCR; gene expression; KIBRA; cerebellum; schizophrenia ID HS1-ASSOCIATED PROTEIN X-1; PREFRONTAL CORTEX; ELDERLY-PATIENTS; EBNA-LP; SCHIZOPHRENIA; HAX-1; EXPRESSION; GENE; KIBRA; CEREBELLUM AB KIAA0513 was previously identified as upregulated in the dorsolateral prefrontal cortex of subjects with schizophrenia by microarray analysis. In the present study, the differential expression in the schizophrenic subjects was confirmed by quantitative RT-PCR. The limited homology to proteins of known function and lack of functional domains in the encoded protein have made it difficult to predict a function for KIAA0513. We used in situ hybridization, RNA blots, western blots, and immunocytochemistry to examine KIAA0513 expression in normal brain and peripheral tissues. The gene is ubiquitously expressed but is enriched in the brain, particularly in the cerebellum. Finally, interacting proteins were identified using a yeast two-hybrid screen to functionally characterize the protein. KIAA0513 interacts with KIBRA, HAX-1, and INTS4, which also interact with proteins involved in neuroplasticity, apoptosis, and cytoskeletal regulation. Therefore, KIAA0513 is likely to be involved in signaling pathways related to these processes. (c) 2006 Elsevier B.V. All rights reserved. C1 CUNY Mt Sinai Sch Med, Dept Psychiat, New York, NY 10029 USA. Brockton W Roxbury Vet Affairs Med Ctr, Bronx, NY USA. Univ Clin Munster, Dept Med, Div Nephrol, Munster, Germany. NIMH, Clin Brain Disorders Branch, Bethesda, MD 20892 USA. Mt Sinai Sch Med, Dept Human Genet, New York, NY USA. RP McInnes, LA (reprint author), CUNY Mt Sinai Sch Med, Dept Psychiat, 1 Gustave L Levy Pl,Box 1229, New York, NY 10029 USA. EM alison.mcinnes@mssm.edu OI Lauriat, Tara/0000-0003-0729-9386; Buxbaum, Joseph/0000-0001-8898-8313 FU NCI NIH HHS [1 R24 CA095823] NR 37 TC 9 Z9 11 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0006-8993 J9 BRAIN RES JI Brain Res. PD NOV 22 PY 2006 VL 1121 BP 1 EP 11 DI 10.1016/j.brainres.2006.08.099 PG 11 WC Neurosciences SC Neurosciences & Neurology GA 114LT UT WOS:000242668400001 PM 17010949 ER PT J AU Lawrence, JJ Saraga, F Churchill, JF Statland, JM Travis, KE Skinner, FK McBain, CJ AF Lawrence, J. Josh Saraga, Fernanda Churchill, Joseph F. Statland, Jeffrey M. Travis, Katherine E. Skinner, Frances K. McBain, Chris J. TI Somatodendritic Kv7/KCNQ/M channels control interspike interval in hippocampal interneurons SO JOURNAL OF NEUROSCIENCE LA English DT Article DE antiepileptic; action potential; hippocampus; interneuron; M-current; neuromodulation; potassium channel ID GATED K+ CHANNELS; KCNQ2/KCNQ3 POTASSIUM CHANNELS; STRATUM-ORIENS INTERNEURONS; SYNAPTIC-TRANSMISSION; PYRAMIDAL CELLS; RAT HIPPOCAMPUS; FAST-SPIKING; NETWORK OSCILLATIONS; SUBUNIT COMPOSITION; MOUSE-BRAIN AB The M-current (I-M), comprised of Kv7 channels, is a voltage-activated K+ conductance that plays a key role in the control of cell excitability. In hippocampal principal cells, I-M controls action potential (AP) accommodation and contributes to the medium-duration after hyperpolarization, but the role of I-M in control of interneuron excitability remains unclear. Here, we investigated I-M in hippocampal stratum oriens (SO) interneurons, both from wild-type and transgenic mice in which green fluorescent protein (GFP) was expressed in somatostatin-containing interneurons. Somatodendritic expression of Kv7.2 or Kv7.3 subunits was colocalized in a subset of GFP + SO interneurons, corresponding to oriens-lacunosum moleculare (O-LM) cells. Under voltage clamp (VC) conditions at -30 mV, the Kv7 channel antagonists linopirdine/XE-991 abolished the I-M amplitude present during relaxation from -30 to -50 mV and reduced the holding current (I-hold). In addition, 0.5 mM tetraethylammonium reduced I-M, suggesting that I-M was composed of Kv7.2-containing channels. In contrast, the Kv7 channel opener retigabine increased I-M amplitude and Ihold. When strongly depolarized in VC, the linopirdine-sensitive outward current activated rapidly and comprised up to 20% of the total current. In current-clamp recordings from GFP + SO cells, linopirdine induced depolarization and increased AP frequency, whereas retigabine induced hyperpolarization and arrested firing. In multicompartment O-LM interneuron models that incorporated I-M, somatodendritic placement of Kv7 channels best reproduced experimentally measured I-M. The models suggest that Kv3- and Kv7-mediated channels both rapidly activate during single APs; however, Kv3 channels control rapid repolarization of the AP, whereas Kv7 channels primarily control the interspike interval. C1 NICHHD, Lab Cellular & Synapt Neurophysiol, NIH, Bethesda, MD 20892 USA. Univ Hlth Network, Toronto Western Res Inst, Toronto, ON M5T 2S8, Canada. Univ Toronto, Dept Med, Toronto, ON M5T 2S8, Canada. Univ Toronto, Dept Physiol, Toronto, ON M5T 2S8, Canada. Univ Toronto, Inst Biomat & Biomed Engn, Toronto, ON M5T 2S8, Canada. RP Lawrence, JJ (reprint author), NICHHD, Lab Cellular & Synapt Neurophysiol, NIH, Bethesda, MD 20892 USA. EM lawrenjo@mail.nih.gov; fernanda.saraga@utoronto.ca FU Intramural NIH HHS NR 66 TC 77 Z9 80 U1 0 U2 4 PU SOC NEUROSCIENCE PI WASHINGTON PA 11 DUPONT CIRCLE, NW, STE 500, WASHINGTON, DC 20036 USA SN 0270-6474 J9 J NEUROSCI JI J. Neurosci. PD NOV 22 PY 2006 VL 26 IS 47 BP 12325 EP 12338 DI 10.1523/JNEUROSCI.3521-06.2006 PG 14 WC Neurosciences SC Neurosciences & Neurology GA 110OI UT WOS:000242387800026 PM 17122058 ER PT J AU Soler-Llavina, GJ Chang, TH Swartz, KJ AF Soler-Llavina, Gilberto J. Chang, Tsg-Hui Swartz, Kenton J. TI Functional interactions at the interface between voltage-sensing and pore domains in the shaker K-v channel SO NEURON LA English DT Article ID GATED POTASSIUM CHANNELS; GATING CURRENTS; OPEN-STATE; HELICAL STRUCTURE; CHARGE MOVEMENT; ACTIVATION GATE; ION CHANNELS; S4 SEGMENT; SENSOR; PROTEIN AB Voltage-activated potassium (K-v) channels contain a central pore domain that is partially surrounded by four voltage-sensing domains. Recent X-ray structures suggest that the two domains lack extensive protein-protein contacts within presumed transmembrane regions, but whether this is the case for functional channels embedded in lipid membranes remains to be tested. We investigated domain interactions in the Shaker Kv channel by systematically mutating the pore domain and assessing tolerance by examining channel maturation, S4 gating charge movement, and channel opening. When mapped onto the X-ray structure of the K(v)1.2 channel the large number of permissive mutations support the notion of relatively independent domains, consistent with crystallographic studies. Inspection of the maps also identifies portions of the interface where residues are sensitive to mutation, an external cluster where mutations hinder voltage sensor activation, and an internal cluster where domain interactions between S4 and S5 helices from adjacent subunits appear crucial for the concerted opening transition. C1 NINDS, Mol Physiol & Biophys Sect, Porter Neurosci Res Ctr, NIH, Bethesda, MD 20892 USA. RP Swartz, KJ (reprint author), NINDS, Mol Physiol & Biophys Sect, Porter Neurosci Res Ctr, NIH, Bldg 36,Rm 4D04, Bethesda, MD 20892 USA. EM swartzk@ninds.nih.gov FU Intramural NIH HHS [ZIA NS002945-13] NR 66 TC 65 Z9 65 U1 0 U2 2 PU CELL PRESS PI CAMBRIDGE PA 1100 MASSACHUSETTS AVE, CAMBRIDGE, MA 02138 USA SN 0896-6273 J9 NEURON JI Neuron PD NOV 22 PY 2006 VL 52 IS 4 BP 623 EP 634 DI 10.1016/j.neuron.2006.10.005 PG 12 WC Neurosciences SC Neurosciences & Neurology GA 110WX UT WOS:000242413100010 PM 17114047 ER PT J AU Belle, SH Burgio, L Burns, R Coon, D Czaja, SJ Gallagher-Thompson, D Gitlin, LN Klinger, J Koepke, KM Lee, CC Martindale-Adam, J Nichols, L Schulz, R Stahl, S Stevens, A Winter, L Zhang, S AF Belle, Steven H. Burgio, Louis Burns, Robert Coon, David Czaja, Sara J. Gallagher-Thompson, Dolores Gitlin, Laura N. Klinger, Julie Koepke, Kathy Mann Lee, Chin Chin Martindale-Adam, Jennifer Nichols, Linda Schulz, Richard Stahl, Sidney Stevens, Alan Winter, Laraine Zhang, Song CA Resources Enhancing Alzheimers TI Enhancing the quality of life of dementia caregivers from different ethnic or racial groups - A randomized, controlled trial SO ANNALS OF INTERNAL MEDICINE LA English DT Article ID SOCIAL SUPPORT; OLDER ADULTS; INTERVENTIONS; DEPRESSION; METAANALYSIS; DESIGN; BURDEN; SCALE; REACH AB Background: Caring for a family member with dementia is extremely stressful, contributes to psychiatric and physical illness among caregivers, and increases the risk for caregiver death. Finding better ways to support family caregivers is a major public health challenge. Objective: To test the effects of a structured multicomponent intervention on quality of life and clinical depression in caregivers and on rates of institutional placement of care recipients in 3 diverse racial or ethnic groups. Design: Randomized, controlled trial. Setting: In-home caregivers in 5 U.S. cities. Participants: 212 Hispanic or Latino, 219 white or Caucasian, and 211 black or African-American caregivers and their care recipients with Alzheimer disease or related disorders. Intervention: Caregivers within each racial or ethnic group were randomly assigned to an intervention or to a control group. The intervention addressed caregiver depression, burden, self-care, and social support and care recipient problem behaviors through 12 in-home and telephone sessions over 6 months. Caregivers in the control group received 2 brief "check-in" telephone calls during the 6-month intervention. Measurements: The primary outcome was a quality-of-life indicator comprising measures of 6-month caregiver depression, burden, self-care, and social support and care recipient problem behaviors. Secondary outcomes were caregiver clinical depression and institutional placement of the care recipient at 6 months. Results: Hispanic or Latino and white or Caucasian caregivers in the intervention group experienced significantly greater improvement in quality of life than those in the control group (P < 0.001 and P = 0.037, respectively). Black or African-American spouse caregivers also improved significantly more (P = 0.003). Prevalence of clinical depression was lower among caregivers in the intervention group (12.6% vs. 22.7%; P = 0.001). There were no statistically significant differences in institutionalization at 6 months. Limitations: The study used only a single 6-month follow-up assessment, combined heterogeneous cultures and ethnicities into a single group, and excluded some ethnic groups. Conclusions: A structured multicomponent intervention adapted to individual risk profiles can increase the quality of life of ethnically diverse dementia caregivers. C1 Univ Pittsburgh, Pittsburgh, PA 15260 USA. Univ Alabama, Tuscaloosa, AL USA. Univ Tennessee, Ctr Hlth Sci, Memphis, TN 38163 USA. Geriatr Grp Memphis, Memphis, TN USA. Arizona State Univ, Tempe, AZ USA. Univ Miami, Miami, FL 33152 USA. Stanford Univ, Sch Med, Palo Alto, CA 94304 USA. Vet Affairs Palo Alto Hlth Care Syst, Palo Alto, CA USA. Thomas Jefferson Univ, Philadelphia, PA 19107 USA. NINR, Bethesda, MD 20892 USA. NIH, Bethesda, MD 20892 USA. Scott & White Mem Hosp & Clin, Temple, TX 76508 USA. RP Schulz, R (reprint author), Univ Pittsburgh, 121 Univ Pl,6th Floor, Pittsburgh, PA 15260 USA. EM schulz@pitt.edu FU NIA NIH HHS [U01 AG020274, AG13265, AG13289, AG13305, AG13313, AG20277, U01 AG013265, U01 AG013289, U01 AG013305, U01 AG013313, U01 AG020274-03]; NINR NIH HHS [NR004261, U01 NR004261, U01 NR004261-07] NR 28 TC 286 Z9 287 U1 11 U2 44 PU AMER COLL PHYSICIANS PI PHILADELPHIA PA INDEPENDENCE MALL WEST 6TH AND RACE ST, PHILADELPHIA, PA 19106-1572 USA SN 0003-4819 J9 ANN INTERN MED JI Ann. Intern. Med. PD NOV 21 PY 2006 VL 145 IS 10 BP 727 EP 738 PG 12 WC Medicine, General & Internal SC General & Internal Medicine GA 110OB UT WOS:000242387100002 PM 17116917 ER PT J AU Gorelick, D AF Gorelick, DavidA. TI Health insurance portability and accountability act privacy rule and research consent documents SO ANNALS OF INTERNAL MEDICINE LA English DT Letter C1 NIDA, Baltimore, MD 21224 USA. RP Gorelick, D (reprint author), NIDA, POB 5180, Baltimore, MD 21224 USA. NR 1 TC 0 Z9 0 U1 0 U2 0 PU AMER COLL PHYSICIANS PI PHILADELPHIA PA INDEPENDENCE MALL WEST 6TH AND RACE ST, PHILADELPHIA, PA 19106-1572 USA SN 0003-4819 J9 ANN INTERN MED JI Ann. Intern. Med. PD NOV 21 PY 2006 VL 145 IS 10 BP 790 EP 790 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA 110OB UT WOS:000242387100015 PM 17116932 ER PT J AU Wendler, D Shalowitz, D AF Wendler, David Shalowitz, David TI Health insurance portability and accountability act privacy rule and research consent documents - Response SO ANNALS OF INTERNAL MEDICINE LA English DT Letter C1 NIH, Bethesda, MD 20892 USA. RP Wendler, D (reprint author), NIH, Bldg 10, Bethesda, MD 20892 USA. RI Shalowitz, David/A-7432-2009 NR 0 TC 1 Z9 1 U1 0 U2 0 PU AMER COLL PHYSICIANS PI PHILADELPHIA PA INDEPENDENCE MALL WEST 6TH AND RACE ST, PHILADELPHIA, PA 19106-1572 USA SN 0003-4819 J9 ANN INTERN MED JI Ann. Intern. Med. PD NOV 21 PY 2006 VL 145 IS 10 BP 790 EP 791 PG 2 WC Medicine, General & Internal SC General & Internal Medicine GA 110OB UT WOS:000242387100016 ER PT J AU Brewer, BY Ballin, JD Fialcowitz-White, EJ Blackshear, PJ Wilson, GM AF Brewer, Brandy Y. Ballin, Jeff D. Fialcowitz-White, Elizabeth J. Blackshear, Perry J. Wilson, Gerald M. TI Substrate dependence of conformational changes in the RNA-binding domain of tristetraprolin assessed by fluorescence spectroscopy of tryptophan mutants SO BIOCHEMISTRY LA English DT Article ID AU-RICH ELEMENTS; CONTAINING MESSENGER-RNAS; ZINC-FINGER PROTEINS; MAMMALIAN-CELLS; DECAY PATHWAY; DEADENYLATION; DEGRADATION; ANISOTROPY; IDENTIFICATION; RECOGNITION AB Association of tristetraprolin ( TTP) with mRNAs containing selected AU-rich mRNA-destabilizing elements ( AREs) initiates rapid cytoplasmic degradation of these transcripts. The RNA-binding activity of TTP is mediated by an internal tandem zinc finger domain that preferentially recognizes U-rich RNA ligands containing adjacent UUAU half-sites and is accompanied by conformational changes within the peptide. Here, we have used analogues of the TTP RNA-binding domain containing specific tryptophan substitutions to probe the Zn2+ and RNA substrate dependence of conformational events within individual zinc fingers. Fluorescence methods demonstrate that the N-terminal, but not C-terminal, zinc finger domain adopts a stably folded conformation in the presence of Zn2+. Denaturant titrations suggest that both the N- and C-terminal zinc fingers exhibit limited structural heterogeneity in the absence of RNA substrates, although this is more pronounced for the C-terminal finger. Binding to a cognate ARE substrate induced significant conformational changes within each zinc finger, which also included increased resistance to chemical denaturation. Studies with mutant ARE ligands revealed that a single UUAU half-site was sufficient to induce structural modulation of the N- terminal finger. However, RNA-dependent folding of the C-terminal zinc finger was only observed in the presence of tandem UUAU half-sites, suggesting that the conformation of this domain is linked not only to RNA substrate recognition but also to the ligand occupancy and/or conformational status of the N- terminal finger. Coupled with previous structural and thermodynamic analyses, these data provide a mechanistic framework for discrimination of RNA substrates involving ligand-dependent conformational adaptation of both zinc fingers within the TTP RNA-binding domain. C1 Univ Maryland, Sch Med, Dept Biochem & Mol Biol, Baltimore, MD 21201 USA. Univ Maryland, Sch Med, Marlene & Stewart Greenebaum Canc Ctr, Baltimore, MD 21201 USA. Natl Inst Environm Hlth Sci, Lab Signal Transduct, NIH, Dept Hlth & Human Serv, Res Triangle Pk, NC 27709 USA. Natl Inst Environm Hlth Sci, Off Clin Res, NIH, Dept Hlth & Human Serv, Res Triangle Pk, NC 27709 USA. RP Wilson, GM (reprint author), Univ Maryland, Sch Med, Dept Biochem & Mol Biol, Baltimore, MD 21201 USA. EM gwils001@umaryland.edu RI Ballin, Jeff/D-3752-2011 OI Ballin, Jeff/0000-0002-2712-130X FU NCI NIH HHS [CA102428, R01 CA102428, R56 CA102428] NR 47 TC 15 Z9 15 U1 0 U2 4 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA SN 0006-2960 J9 BIOCHEMISTRY-US JI Biochemistry PD NOV 21 PY 2006 VL 45 IS 46 BP 13807 EP 13817 DI 10.1021/bi061320j PG 11 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA 105HN UT WOS:000242021100013 PM 17105199 ER PT J AU Dawson, HD Collins, G Pyle, R Key, M Weeraratna, A Deep-Dixit, V Nadal, CN Taub, DD AF Dawson, Harry D. Collins, Gary Pyle, Robert Key, Michael Weeraratna, Ashani Deep-Dixit, Vishwa Nadal, Celeste N. Taub, Dennis D. TI Direct and indirect effects of retinoic acid on human Th2 cytokine and chemokine expression by human T lymphocytes SO BMC IMMUNOLOGY LA English DT Article ID VITAMIN-A-DEFICIENCY; ACUTE PROMYELOCYTIC LEUKEMIA; IFN-GAMMA; IN-VITRO; INTERLEUKIN-12 PRODUCTION; GENE-EXPRESSION; X-RECEPTOR; ANTIBODY-RESPONSE; CELL-DEVELOPMENT; IL-4 PRODUCTION AB Background: Vitamin A (VA) deficiency induces a type 1 cytokine response and exogenously provided retinoids can induce a type 2 cytokine response both in vitro and in vivo. The precise mechanism(s) involved in this phenotypic switch are inconsistent and have been poorly characterized in humans. In an effort to determine if retinoids are capable of inducing Th2 cytokine responses in human T cell cultures, we stimulated human PBMCs with immobilized anti-CD3 mAb in the presence or absence of all-trans retinoic acid (ATRA) or 9-cis-RA. Results: Stimulation of human PBMCs and purified T cells with ATRA and 9-cis-RA increased mRNA and protein levels of IL-4, IL-5, and IL-13 and decreased levels of IFN-gamma, IL-2, IL-12p70 and TNF-alpha upon activation with anti-CD3 and/or anti-CD28 mAbs. These effects were dose-dependent and evident as early as 12 hr post stimulation. Real time RT-PCR analysis revealed a dampened expression of the Th1-associated gene, T-bet, and a time-dependent increase in the mRNA for the Th2-associated genes, GATA-3, c-MAF and STAT6,upon treatment with ATRA. Besides Th1 and Th2 cytokines, a number of additional proinflammatory and regulatory cytokines including several chemokines were also differentially regulated by ATRA treatment. Conclusion: These data provide strong evidence for multiple inductive roles for retinoids in the development of human type-2 cytokine responses. C1 NIA, Immunol Lab, Gerontol Res Ctr, NIH, Baltimore, MD 21224 USA. USDA, Nutrient Requirement & Funct Lab, Beltsville, MD 20705 USA. RP Taub, DD (reprint author), NIA, Immunol Lab, Gerontol Res Ctr, NIH, Baltimore, MD 21224 USA. EM harry.dawson@ars.usda.gov; collinsg@grc.nia.nih.gov; pyleb@grc.nia.nih.gov; keym@grc.nia.nih.gov; weerarat@grc.nia.nih.gov; vishwa.dixit@pbrc.edu; cnadal@ufl.edu; taubd@grc.nia.nih.gov RI Dawson, Harry/H-8242-2013 FU Intramural NIH HHS NR 66 TC 58 Z9 63 U1 0 U2 3 PU BIOMED CENTRAL LTD PI LONDON PA MIDDLESEX HOUSE, 34-42 CLEVELAND ST, LONDON W1T 4LB, ENGLAND SN 1471-2172 J9 BMC IMMUNOL JI BMC Immunol. PD NOV 21 PY 2006 VL 7 AR 27 DI 10.1186/1471-2172-7-27 PG 15 WC Immunology SC Immunology GA 110VO UT WOS:000242409600001 PM 17118196 ER PT J AU Berezhkovskii, AM Makhnovskii, YA Zitserman, VY AF Berezhkovskii, Alexander M. Makhnovskii, Yurii A. Zitserman, Vladimir Yu. TI Escape from a cavity through a small window: Turnover of the rate as a function of friction constant SO JOURNAL OF CHEMICAL PHYSICS LA English DT Article ID PERIODIC POROUS MATERIALS; DYNAMIC DISORDER; BROWNIAN-MOTION; DIFFUSIVITY; LANGEVIN; KRAMERS; MODEL AB To escape from a cavity through a small window the particle has to overcome a high entropy barrier to find the exit. As a consequence, its survival probability in the cavity decays as a single exponential and is characterized by the only parameter, the rate constant. We use simulations to study escape of Langevin particles from a cubic cavity through a small round window in the center of one of the cavity walls with the goal of analyzing the friction dependence of the escape rate. We find that the rate constant shows the turnover behavior as a function of the friction constant, zeta: The rate constant grows at very small zeta, reaches a maximum value which is given by the transition-state theory (TST), and then decreases approaching zero as zeta ->infinity. Based on the results found in simulations and some general arguments we suggest a formula for the rate constant that predicts a turnover of the escape rate for ergodic cavities in which collisions of the particle with the cavity walls are defocusing. At intermediate-to-high friction the formula describes transition between two known results for the rate constant: the TST estimation and the high friction limiting behavior that characterizes escape of diffusing particles. In this range of friction the rate constants predicted by the formula are in good agreement with those found in simulations. At very low friction the rate constants found in simulations are noticeably smaller than those predicted by the formula. This happens because the simulations were run in the cubic cavity which is not ergodic. (c) 2006 American Institute of Physics. C1 NIH, Math & Stat Comp Lab, Div Comparat Biosci, Ctr Informat Technol, Bethesda, MD 20892 USA. Russian Acad Sci, AV Topchiev Petrochem Synth Inst, Moscow 119991, Russia. Russian Acad Sci, Thermophys Ctr, Inst High Temp, Moscow 125412, Russia. RP Berezhkovskii, AM (reprint author), NIH, Math & Stat Comp Lab, Div Comparat Biosci, Ctr Informat Technol, Bldg 10, Bethesda, MD 20892 USA. EM berezh@mail.nih.gov RI Makhnovskii, Yurii/B-1223-2014 OI Makhnovskii, Yurii/0000-0002-1517-536X FU Intramural NIH HHS NR 19 TC 4 Z9 4 U1 0 U2 2 PU AMER INST PHYSICS PI MELVILLE PA 1305 WALT WHITMAN RD, STE 300, MELVILLE, NY 11747-4501 USA SN 0021-9606 EI 1089-7690 J9 J CHEM PHYS JI J. Chem. Phys. PD NOV 21 PY 2006 VL 125 IS 19 AR 194501 DI 10.1063/1.2374893 PG 7 WC Chemistry, Physical; Physics, Atomic, Molecular & Chemical SC Chemistry; Physics GA 107OV UT WOS:000242181800037 PM 17129117 ER PT J AU Pustovoit, MA Berezhkovskii, AM Bezrukov, SM AF Pustovoit, M. A. Berezhkovskii, A. M. Bezrukov, S. M. TI Analytical theory of hysteresis in ion channels: Two-state model SO JOURNAL OF CHEMICAL PHYSICS LA English DT Article ID SCALING LAWS; DYNAMICAL HYSTERESIS; CURRENT FLUCTUATIONS; MEMBRANE CHANNELS; GATING KINETICS; CELL MEMBRANE; ISING-MODEL; SYSTEM; DRIVEN; EXCITABILITY AB Channel-forming proteins in a lipid bilayer of a biological membrane usually respond to variation of external voltage by changing their conformations. Periodic voltages with frequency comparable with the inverse relaxation time of the protein produce hysteresis in the occupancies of the protein conformations. If the channel conductance changes when the protein jumps between these conformations, hysteresis in occupancies is observed as hysteresis in ion current through the channel. We develop an analytical theory of this phenomenon assuming that the channel conformational dynamics can be described in terms of a two-state model. The theory describes transient behavior of the channel after the periodic voltage is switched on as well as the shape and area of the hysteretic loop as functions of the frequency and amplitude of the applied voltage. The area vanishes as the voltage period T tends to zero and infinity. Asymptotic behaviors of the loop area A in the high- and low-frequency regimes, respectively, are A similar to T and A similar to T-1. (c) 2006 American Institute of Physics. C1 St Petersburg Nucl Phys Inst, Gatchina 188300, Russia. NIH, Math & Stat Comp Lab, Div Computat Biosci, Bethesda, MD 20892 USA. NICHHD, Lab Phys & Struct Biol, NIH, Bethesda, MD 20892 USA. RP Pustovoit, MA (reprint author), St Petersburg Nucl Phys Inst, Gatchina 188300, Russia. EM bezrukos@mail.nih.gov RI Pustovoit, Mark/B-5249-2008 FU Intramural NIH HHS NR 29 TC 13 Z9 13 U1 0 U2 4 PU AMER INST PHYSICS PI MELVILLE PA 1305 WALT WHITMAN RD, STE 300, MELVILLE, NY 11747-4501 USA SN 0021-9606 EI 1089-7690 J9 J CHEM PHYS JI J. Chem. Phys. PD NOV 21 PY 2006 VL 125 IS 19 AR 194907 DI 10.1063/1.2364898 PG 8 WC Chemistry, Physical; Physics, Atomic, Molecular & Chemical SC Chemistry; Physics GA 107OV UT WOS:000242181800087 PM 17129167 ER PT J AU Dan, N Shimoni, K Pata, V Danino, D AF Dan, Nily Shimoni, Karin Pata, Veena Danino, Dganit TI Effect of mixing on the morphology of cylindrical micelles SO LANGMUIR LA English DT Article ID NONIONIC SURFACTANT; AQUEOUS-SOLUTIONS; MEMBRANE SOLUBILIZATION; TEMPERATURE-DEPENDENCE; CRYO-TEM; DETERGENT; VESICLES; MICROSTRUCTURE; CHOLESTEROL; COPOLYMERS AB Increasing the spontaneous curvature of an amphiphile can lead to a first-order morphology transition from threadlike micelles to a branched network. The two morphologies were linked to entropy-driven topological defects; networks are dominated by Y-junctions, while linear threadlike structures are dominated by spherical end-caps. In this paper we investigate the effect of mixing on the morphological transitions in nonionic amphiphilic systems. We find that mixed equilibrium structures are obtained within seconds; these mixed cylindrical structures display comparable numbers of end-caps and branch points, resulting in a novel 'short armed' branched (SAB) morphology. Quite surprisingly, the probability of either defect (end-caps or branch points) is independent of composition, so that neither a first-order nor a second-order morphological transition is observed. A possible explanation may be local demixing of the two amphiphilic components, which adds a degree of freedom and thus enables the formation of a unique morphology that cannot be obtained in single-component systems. We further find that within a relatively large composition range phase equilibrium exists between vesicles, SAB micelles, and spherical micelles. C1 Drexel Univ, Dept Biol & Chem Engn, Philadelphia, PA 19104 USA. Technion Israel Inst Technol, Dept Food Engn & Biotechnol, IL-32000 Haifa, Israel. Technion Israel Inst Technol, Russell Berrie Nanotechnol Inst, IL-32000 Haifa, Israel. NICHHD, Lab Cellular & Mol Biophys, Bethesda, MD 20892 USA. RP Dan, N (reprint author), Drexel Univ, Dept Biol & Chem Engn, Philadelphia, PA 19104 USA. EM dan@coe.drexel.edu; dganitd@techunix.technion.ac.il RI Danino, Dganit/D-6832-2016 OI Danino, Dganit/0000-0002-9782-4940 NR 31 TC 25 Z9 25 U1 0 U2 18 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA SN 0743-7463 J9 LANGMUIR JI Langmuir PD NOV 21 PY 2006 VL 22 IS 24 BP 9860 EP 9865 DI 10.1021/la061254m PG 6 WC Chemistry, Multidisciplinary; Chemistry, Physical; Materials Science, Multidisciplinary SC Chemistry; Materials Science GA 105HX UT WOS:000242022100012 PM 17106974 ER PT J AU Binzoni, T Leung, TS Gandjbakhche, AH Rufenacht, D Delpy, DT AF Binzoni, T. Leung, T. S. Gandjbakhche, A. H. Rufenacht, D. Delpy, D. T. TI Comment on 'The use of the Henyey - Greenstein phase function in Monte Carlo simulations in biomedical optics' SO PHYSICS IN MEDICINE AND BIOLOGY LA English DT Article AB In this letter the authors highlight the presence of an error appearing in the discussion of the note 'The use of the Henyey-Greenstein phase function in Monte Carlo simulations in biomedical optics' previously published by them ( Binzoni et al 2006 Phys. Med. Biol. 51 N313). In the light of this error, the discussion and conclusions in the original paper are revised in this letter and the role of the use of the phase functions in MC simulations, interpreted in probabilistic terms, is better clarified. The exact definition for the probability density function for the deflection angle, in the case of the Henyey-Greenstein model, is also given. C1 Univ Geneva, Med Ctr, Dept Neurosci Fondamentales, Geneva, Switzerland. Univ Hosp Geneva, Dept Radiol & Informat Med, Geneva, Switzerland. UCL, Dept Med Phys & Bioengn, London WC1E 6BT, England. NICHHD, Lab Integrat & Med Biophys, NIH, Bethesda, MD 20892 USA. RP Binzoni, T (reprint author), Univ Geneva, Med Ctr, Dept Neurosci Fondamentales, 1 R Michel Servet, Geneva, Switzerland. EM Tiziano.Binzoni@medecine.unige.ch NR 1 TC 10 Z9 10 U1 0 U2 0 PU IOP PUBLISHING LTD PI BRISTOL PA TEMPLE CIRCUS, TEMPLE WAY, BRISTOL BS1 6BE, ENGLAND SN 0031-9155 J9 PHYS MED BIOL JI Phys. Med. Biol. PD NOV 21 PY 2006 VL 51 IS 22 BP L39 EP L41 DI 10.1088/0031-9155/51/22/L01 PG 3 WC Engineering, Biomedical; Radiology, Nuclear Medicine & Medical Imaging SC Engineering; Radiology, Nuclear Medicine & Medical Imaging GA 113RR UT WOS:000242615500017 PM 17068360 ER PT J AU Johnson, ME Cheng, Z Morrison, VA Scherer, S Ventura, M Gibbs, RA Green, ED Eichler, EE AF Johnson, Matthew E. Cheng, Ze Morrison, V. Anne Scherer, Steven Ventura, Mario Gibbs, Richard A. Green, Eric D. Eichler, Evan E. CA NISC Comparat Sequencing Program TI Recurrent duplication-driven transposition of DNA during hominoid evolution SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE duplicons; LCR16 elements; lineage-specific duplications; segmental duplication ID HUMAN SEGMENTAL DUPLICATIONS; HUMAN-GENOME; L1 RETROTRANSPOSITION; PRIMATE EVOLUTION; GENE FAMILY; GREAT-APE; SEQUENCE; EXPANSION; CHIMPANZEE; RECOMBINATION AB The underlying mechanism by which the interspersed pattern of human segmental duplications has evolved is unknown. Based on a comparative analysis of primate genomes, we show that a particular segmental duplication (LCR16a) has been the source locus for the formation of the majority of intrachromosomal duplications blocks on human chromosome 16. We provide evidence that this particular segment has been active independently in each great ape and human lineage at different points during evolution. Euchromatic sequence that flanks sites of LCIR16a integration are frequently lineage-specific duplications. This process has mobilized duplication blocks (15-200 kb in size) to new genomic locations in each species. Breakpoint analysis of lineage-specific insertions suggests coordinated deletion of repeat-rich DNA at the target site, in some cases deleting genes in that species. Our data support a model of duplication where the probability that a segment of DNA becomes duplicated is determined by its proximity to core duplicons, such as LCR16a. C1 Univ Washington, Dept Genome Sci, Seattle, WA 98195 USA. Univ Washington, Howard Hughes Med Inst, Seattle, WA 98195 USA. Case Western Reserve Univ, Sch Med, Dept Genet, Cleveland, OH 44106 USA. Case Western Reserve Univ, Sch Med, Ctr Human Genet, Cleveland, OH 44106 USA. Univ Hosp Cleveland, Cleveland, OH 44106 USA. NISC, Natl Human Genome Res Inst, NIH, Bethesda, MD 20892 USA. NISC, Genome Technol Branch, Bethesda, MD 20892 USA. Baylor Coll Med, Human Genome Sequencing Ctr, Houston, TX 77030 USA. Univ Bari, Sez Genet, Dipartimento Anat Patol & Genet, I-70126 Bari, Italy. RP Eichler, EE (reprint author), Univ Washington, Dept Genome Sci, Seattle, WA 98195 USA. EM eee@gs.washington.edu RI Ventura, Mario/E-6420-2011 OI Ventura, Mario/0000-0001-7762-8777 FU Intramural NIH HHS; NIGMS NIH HHS [GM58815, R01 GM058815] NR 42 TC 40 Z9 40 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 NOV 21 PY 2006 VL 103 IS 47 BP 17626 EP 17631 DI 10.1073/pnas.0605426103 PG 6 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA 111PG UT WOS:000242464900011 PM 17101969 ER PT J AU Weldon, PJ Kramer, M Gordon, S Spande, TF Daly, JW AF Weldon, Paul J. Kramer, Matthew Gordon, Scott Spande, Thomas F. Daly, John W. TI A common pumiliotoxin from poison frogs exhibits enantioselective toxicity against mosquitoes SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE alkaloids; chemical defense; dendrobatid poison frogs; insecticidal activity; skin secretions ID DENDROBATES-PUMILIO; ALKALOIDS; SKIN AB Neotropical poison frogs (Dendrobatidae) contain a variety of lipophilic alkaloids in their diffusely distributed cutaneous glands, including a major class of compounds known as pumiliotoxins. Pumiliotoxins are highly toxic and are believed to protect frogs against predators. Their potential activity against ectoparasites, however, has not been investigated. We tested female yellow fever mosquitoes (Aedes aegypti) for responses to 8-hydroxy-8methyl-6-(2'-methyl-hexylidene)-1-azabicyclo[4.3.0]nonane, designated pumiliotoxin 251 D [PTX (+)-251 D], a skin alkaloid present in all genera of dendrobatids and in other anurans, and to its unnatural enantiomer, PTX (-)-251D. Both enantiomers of PTX 251D presented on silicone feeding membranes reduced landing and feeding by A. aegypti, but PTX (+)-251D did so at lower concentrations. PTX (+)-251 D also induced toxicosis, shown when mosquitoes failed to fly off membranes. Similarly, mosquitoes confined with copper wires coated with PTX (+)-251D exhibited greater latencies to fly off the substrate and a higher incidence of leg autotomy than did those confined with the (-)-enantiomer. Our results on the contact toxicities of PTX 251D enantiomers parallel those reported for mice injected with them. The presentation of serial dilutions of PTX (+)-251 D to A. aegypti revealed a minimum toxic concentration of 0.1 mu g/cm(2). This value is substantially lower than that estimated for the cutaneous abundance of this compound in some frogs, an observation consistent the function of PTX 251D in anuran chemical defense against ectoparasitic arthropods. C1 Smithsonian Inst, Conservat & Res Ctr, Front Royal, VA 22630 USA. USDA ARS, Biometr Consulting Serv, Beltsville Agr Res Ctr, Beltsville, MD 20705 USA. Walter Reed Army Inst Res, Dept Entomol, Div Communicable Dis & Immunol, Washington, DC 20307 USA. NIDDK, Bioorgan Chem Lab, NIH, Dept Hlth & Human Serv, Bethesda, MD 20892 USA. RP Weldon, PJ (reprint author), Smithsonian Inst, Conservat & Res Ctr, 1500 Remount Rd, Front Royal, VA 22630 USA. EM weldonp@si.edu; jdaly@nih.gov RI Gordon, Scott/B-8875-2011 FU Intramural NIH HHS NR 26 TC 25 Z9 27 U1 1 U2 10 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD NOV 21 PY 2006 VL 103 IS 47 BP 17818 EP 17821 DI 10.1073/pnas.0608646103 PG 4 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA 111PG UT WOS:000242464900044 PM 17095598 ER PT J AU Lee, Y Ise, T Ha, D Saint Fleur, A Hahn, Y Liu, XF Nagata, S Lee, B Bera, TK Pastan, I AF Lee, Yoomi Ise, Tomoko Ha, Duc Saint Fleur, Ashley Hahn, Yoonsoo Liu, Xiu-Fen Nagata, Satoshi Lee, Byungkook Bera, Tapan K. Pastan, Ira TI Evolution and expression of chimeric POTE-actin genes in the human genome SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE ANKRD26; cancer; primate; retroposon; testis ID ORIGIN; RETROTRANSPOSITION; DROSOPHILA; PROTEINS; PROSTATE; PARALOGS; CELLS; YOUNG AB We previously described a primate-specific gene family, POTE, that is expressed in many cancers but in a limited number of normal organs. The 13 POTE genes are dispersed among eight different chromosomes and evolved by duplications and remodeling of the human genome from an ancestral gene, ANKRD26. Based on sequence similarity, the POTE gene family members can be divided into three groups. By genome database searches, we identified an actin retroposon insertion at the carboxyl terminus of one of the ancestral POTE paralogs. By Northern blot analysis, we identified the expected 7.5-kb POTE-actin chimeric transcript in a breast cancer cell line. The protein encoded by the POTE-actin transcript is predicted to be 120 kDa in size. Using anti-POTE mAbs that recognize the amino-terminal portion of the POTE protein, we detected the 120-kDa POTE-actin fusion protein in breast cancer cell lines known to express the fusion transcript. These data demonstrate that insertion of a retroposon produced an altered functional POTE gene. This example indicates that new functional human genes can evolve by insertion of retroposons. C1 NCI, Mol Biol Lab, Canc Res Ctr, NIH, Bethesda, MD 20892 USA. RP Pastan, I (reprint author), NCI, Mol Biol Lab, Canc Res Ctr, NIH, 37 Convent Dr,Room 5106, Bethesda, MD 20892 USA. EM pastani@mail.nih.gov FU Intramural NIH HHS NR 21 TC 19 Z9 20 U1 0 U2 2 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD NOV 21 PY 2006 VL 103 IS 47 BP 17885 EP 17890 DI 10.1073/pnas.0608344103 PG 6 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA 111PG UT WOS:000242464900056 PM 17101985 ER PT J AU Zhou, QB Xie, H Zhang, L Stewart, JK Gu, XX Ryan, JJ AF Zhou, Qibing Xie, Hang Zhang, Lin Stewart, Jennifer K. Gu, Xing-Xing Ryan, John J. TI cis-terpenones as an effective chemopreventive agent against aflatoxin B1-induced cytotoxicity and TCDD-induced P450 1A/B activity in HepG2 cells SO CHEMICAL RESEARCH IN TOXICOLOGY LA English DT Article ID REPUBLIC-OF-CHINA; HEPATOCELLULAR-CARCINOMA; CYTOCHROME-P450 1B1; DAMAGE; B-1; DNA; INDIVIDUALS; INHIBITION; ACTIVATION; APOPTOSIS AB Aflatoxin B1 (AFB1) is a potent carcinogen, which can significantly increase the risk of hepatocellular carcinoma development through food contamination. In past decades, chemopreventive agents, such as oltipraz and chlorophyllins, have demonstrated that chemo-intervention is an effective approach to reduce hepatotoxicity by AFB1. However, because of the potential adverse effects of these agents, alternative novel mechanism-based chemopreventive agents are needed. We report here that novel cis-terpenones 1-3, which were synthesized as the precursors of natural product analogues in our laboratory, showed promising protective effects against AFB1-induced cytotoxicity in HepG2 cells. Chemo-protection was observed with increasing concentrations of cis-terpenones in the co-treatment of AFB1, and no cytotoxicity was observed with cis-terpenones alone. In addition, cis-terpenones 1-3 at 10 mu M effectively inhibited induced cytochrome P450 1A/1B activity by 50% in HepG2 cells, as indicated by an EROD assay. P450 1A/B is involved in the activation of many pre-carcinogens and is highly inducible in liver cells. These results suggested that novel terpenones 1-3 are candidates for the development of novel mechanism-based chemopreventive agents against AFB1 and other carcinogenic stimuli. C1 Virginia Commonwealth Univ, Dept Chem, Richmond, VA 23284 USA. Natl Inst Deafness & Other Commun Disorders, NIH, Rockville, MD 20850 USA. Virginia Commonwealth Univ, Dept Biol, Richmond, VA 23284 USA. RP Zhou, QB (reprint author), Virginia Commonwealth Univ, Dept Chem, 1001 W Main St, Richmond, VA 23284 USA. EM qzhou@vcu.edu FU NIAID NIH HHS [R01 AI059638, R01 AI059638-02] NR 28 TC 9 Z9 9 U1 0 U2 6 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA SN 0893-228X J9 CHEM RES TOXICOL JI Chem. Res. Toxicol. PD NOV 20 PY 2006 VL 19 IS 11 BP 1415 EP 1419 DI 10.1021/tx0601307 PG 5 WC Chemistry, Medicinal; Chemistry, Multidisciplinary; Toxicology SC Pharmacology & Pharmacy; Chemistry; Toxicology GA 106TK UT WOS:000242124100003 PM 17112227 ER PT J AU Song, L Li, JX Zhang, DY Liu, ZG Ye, JP Zhan, QM Shen, HM Whiteman, M Huang, CS AF Song, Lun Li, Jingxia Zhang, Dongyun Liu, Zheng-Gang Ye, Jianping Zhan, Qimin Shen, Han-Ming Whiteman, Matt Huang, Chuanshu TI IKK beta programs to turn on the GADD45 alpha-MKK4-JNK apoptotic cascade specifically via p50 NF-kappa B in arsenite response SO JOURNAL OF CELL BIOLOGY LA English DT Article ID INDUCED CELL-TRANSFORMATION; MOLECULAR MECHANISMS; SIGNAL-TRANSDUCTION; GADD45 INDUCTION; T-LYMPHOCYTES; KINASE ALPHA; FAS-LIGAND; JNK; ACTIVATION; PATHWAY AB Cross talk between NF-kappa B and c-Jun N-terminal kinases (JNKs) has been implicated in the cell life and death decision under various stresses. Functional suppression of JNK activation by NF-kappa B has recently been proposed as a key cellular survival mechanism and contributes to cancer cells escaping from apoptosis. We provide a novel scenario of the proapoptotic role of I kappa B kinase beta (IKK beta)-NF-K kappa B, which can act as the activator of the JNK pathway through the induction of GADD45 alpha for triggering MKK4/JNK activation, in response to the stimulation of arsenite, a cancer therapeutic reagent. This effect of IKK beta-NF-kappa B is dependent on p50 but not the p65/relA NF-kappa B subunit, which can Increase the stability of GADD45 alpha protein through suppressing its ubiquitination and proteasome-dependent degradation. IKK beta-NF-kappa B can therefore either activate or suppress the JNK cascade and consequently mediate pro- or antiapoptotic effects, depending on the manner of its induction. Furthermore, the NF-kappa B p50 subunit can exert a novel regulatory function on protein modification independent of the classical NF-kappa B transcriptional activity. C1 NYU, Sch Med, Nelson Inst Environm Med, Tuxedo Pk, NY 10987 USA. NCI, Ctr Canc Res, Cell & Canc Biol Branch, NIH, Bethesda, MD 20892 USA. Louisiana State Univ, Pennington Biomed Res Ctr, Baton Rouge, LA 70808 USA. Chinese Acad Med Sci, Natl Key Lab Mol Oncol, Inst Canc, Peking Union Med Coll, Beijing 100021, Peoples R China. Natl Univ Singapore, Yong Loo Lin Sch Med, Dept Community Occupat & Family Med, Singapore 117597, Singapore. Natl Univ Singapore, Yong Loo Lin Sch Med, Dept Biochem, Singapore 117597, Singapore. RP Huang, CS (reprint author), NYU, Sch Med, Nelson Inst Environm Med, Tuxedo Pk, NY 10987 USA. EM chuanshu@env.med.nyu.edu RI Whiteman, Matthew/C-6079-2009; SHEN, Han-Ming/B-5942-2011; OI Whiteman, Matthew/0000-0002-6583-6779; SHEN, Han-Ming/0000-0001-7369-5227; Huang, Chuanshu/0000-0003-4133-5096 FU NCI NIH HHS [CA112557, CA094964, CA103180, R01 CA094964, R01 CA103180, R01 CA112557]; NIEHS NIH HHS [ES000260, ES012451, P30 ES000260, R01 ES012451] NR 43 TC 64 Z9 67 U1 0 U2 3 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 1114 FIRST AVE, 4TH FL, NEW YORK, NY 10021 USA SN 0021-9525 J9 J CELL BIOL JI J. Cell Biol. PD NOV 20 PY 2006 VL 175 IS 4 BP 607 EP 617 DI 10.1083/jcb.200602149 PG 11 WC Cell Biology SC Cell Biology GA 109ER UT WOS:000242291200011 PM 17116751 ER PT J AU Strong, CD Wertz, PW Wang, CW Yang, F Meltzer, PS Andl, T Millar, SE Ho, IC Pai, SY Segre, JA AF Strong, Cristina de Guzman Wertz, Philip W. Wang, Chenwei Yang, Fan Meltzer, Paul S. Andl, Thomas Millar, Sarah E. Ho, I-Cheng Pai, Sung-Yun Segre, Julia A. TI Lipid defect underlies selective skin barrier impairment of an epidermal-specific deletion of Gata-3 SO JOURNAL OF CELL BIOLOGY LA English DT Article ID STEM-CELL NICHE; TRANSCRIPTION FACTOR; PERMEABILITY BARRIER; ATOPIC-DERMATITIS; GAUCHER-DISEASE; REGULATES DIFFERENTIATION; ANTIMICROBIAL PEPTIDES; CAENORHABDITIS-ELEGANS; TARGETED DISRUPTION; CORNIFIED ENVELOPE AB Skin lies at the interface between the complex physiology of the body and the external environment. This essential epidermal barrier, composed of cornified proteins encased in lipids, prevents both water loss and entry of infectious or toxic substances. We uncover that the transcription factor GATA-3 is required to establish the epidermal barrier and survive in the ex utero environment. Analysis of Gata-3 mutant transcriptional profiles at three critical developmental stages identifies a specific defect in lipid biosynthesis and a delay in differentiation. Genomic analysis identifies highly conserved GATA-3 binding sites bound in vivo by GATA-3 in the first intron of the lipid acyltransferase gene AGPAT5. Skin from both Gata-3-/- and previously characterized barrier-deficient Kruppel-like factor 4-/- newborns up-regulate antimicrobial peptides, effectors of innate immunity. Comparison of these animal models illustrates how impairment of the skin barrier by two genetically distinct mechanisms leads to innate immune responses, as observed in the common human skin disorders psoriasis and atopic dermatitis. C1 NHGRI, Bethesda, MD 20892 USA. NCI, NIH, Bethesda, MD 20892 USA. Univ Iowa, Iowa City, IA 52242 USA. Univ Penn, Dept Dermatol, Philadelphia, PA 19104 USA. Harvard Univ, Sch Med, Brigham & Womens Hosp, Div Rheumatol Immunol & Allergy, Boston, MA 02115 USA. Harvard Univ, Sch Med, Dana Farber Canc Inst, Boston, MA 02115 USA. Harvard Univ, Sch Med, Childrens Hosp, Dept Pediat Hematol Oncol, Boston, MA 02115 USA. RP Segre, JA (reprint author), NHGRI, Bethesda, MD 20892 USA. EM jsegre@nhgri.nih.gov NR 55 TC 42 Z9 43 U1 0 U2 0 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 1114 FIRST AVE, 4TH FL, NEW YORK, NY 10021 USA SN 0021-9525 J9 J CELL BIOL JI J. Cell Biol. PD NOV 20 PY 2006 VL 175 IS 4 BP 661 EP 670 DI 10.1083/jcb.200605057 PG 10 WC Cell Biology SC Cell Biology GA 109ER UT WOS:000242291200015 ER PT J AU Weinberg, S Davies, P Brenner, S Wolpert, L Barrow, JD Collins, F Hooft, GT De Waal, F Tegmark, M Wilson, EO AF Weinberg, Steven Davies, Paul Brenner, Sydney Wolpert, Lewis Barrow, John D. Collins, Francis Hooft, Gerard T. De Waal, Frans Tegmark, Max Wilson, Edward O. TI What is reality? Roger Penrose SO NEW SCIENTIST LA English DT Editorial Material C1 Univ Texas, S Josey Welch Fdn Chair Sci & Regental, Austin, TX 78712 USA. Arizona State Univ, Tempe, AZ USA. Crick Jacobs Ctr, Salk Inst, La Jolla, CA USA. UCL, London WC1E 6BT, England. Univ Cambridge, Cambridge CB2 1TN, England. US Natl Human Gen Res Inst, Bethesda, MD USA. Univ Utrecht, Spinoza Inst, NL-3508 TC Utrecht, Netherlands. MIT, Cambridge, MA 02139 USA. Emory Univ, Atlanta, GA 30322 USA. Harvard Univ, Cambridge, MA 02138 USA. RP Weinberg, S (reprint author), Univ Texas, S Josey Welch Fdn Chair Sci & Regental, Austin, TX 78712 USA. NR 0 TC 0 Z9 0 U1 1 U2 10 PU REED BUSINESS INFORMATION LTD PI SUTTON PA QUADRANT HOUSE THE QUADRANT, SUTTON SM2 5AS, SURREY, ENGLAND SN 0262-4079 J9 NEW SCI JI New Sci. PD NOV 18 PY 2006 VL 192 IS 2578 BP 32 EP 38 PG 7 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA 110DH UT WOS:000242358000024 ER PT J AU Rajesh, M Mukhopadhyay, P Batkai, S Godlewski, G Hasko, G Liaudet, L Pacher, P AF Rajesh, Mohanraj Mukhopadhyay, Partha Batkai, Sandor Godlewski, Grzegorz Hasko, Gyorgy Liaudet, Lucas Pacher, Pal TI Pharmacological inhibition of poly(ADP-ribose) polymerase inhibits angiogenesis SO BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS LA English DT Article DE poly(ADP-ribose) polymerase (PARP); angiogenesis; proliferation; migration; tube formation; HUVEC; 3-AB; PJ-34 ID DIABETIC ENDOTHELIAL DYSFUNCTION; MISMATCH REPAIR-DEFICIENT; HEART-FAILURE; CELLS; TEMOZOLOMIDE; GROWTH; ACTIVATION; MINOCYCLINE; AG14361 AB Poly(ADP-ribose) polymerase (PARP) is a nuclear enzyme which plays an important role in regulating cell death and cellular responses to DNA repair. Pharmacological inhibitors of PARP are being considered as treatment for cancer both in monotherapy as well as in combination with chemotherapeutic agents and radiation, and were also reported to be protective against untoward effects exerted by certain anticancer drugs. Here we show that pharmacological inhibition of PARP with 3-aminobenzamide or PJ-34 dose-dependently reduces VEGF-induced proliferation, migration, and tube formation of human umbilical vein endothelial cells in vitro. These results suggest that treatment with PARP inhibitors may exert additional benefits in various cancers and retinopathies by decreasing angiogenesis. (c) 2006 Elsevier Inc. All rights reserved. C1 NIAAA, Sect Oxidat Stress Tissue Injury, Lab Physiol Studies, NIH, Bethesda, MD 20892 USA. Univ Med & Dent New Jersey, New Jersey Med Sch, Dept Surg, Newark, NJ 07103 USA. CHU Vaudois, Dept Intens Care Med, CH-1011 Lausanne, Switzerland. RP Pacher, P (reprint author), NIAAA, Sect Oxidat Stress Tissue Injury, Lab Physiol Studies, NIH, 5625 Fishers Lane,MSC-9413, Bethesda, MD 20892 USA. EM pacher@mail.nih.gov RI Batkai, Sandor/G-3889-2010; MUKHOPADHYAY, PARTHA/G-3890-2010; Pacher, Pal/B-6378-2008; Batkai, Sandor/H-7983-2014; Liaudet, Lucas/E-1322-2017 OI MUKHOPADHYAY, PARTHA/0000-0002-1178-1274; Pacher, Pal/0000-0001-7036-8108; Liaudet, Lucas/0000-0003-2670-4930 FU Intramural NIH HHS [Z99 AA999999] NR 31 TC 48 Z9 49 U1 0 U2 2 PU ACADEMIC PRESS INC ELSEVIER SCIENCE PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA SN 0006-291X J9 BIOCHEM BIOPH RES CO JI Biochem. Biophys. Res. Commun. PD NOV 17 PY 2006 VL 350 IS 2 BP 352 EP 357 DI 10.1016/j.bbrc.2006.09.049 PG 6 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA 096PS UT WOS:000241389900015 PM 17007818 ER PT J AU Sugiyama, E Tanaka, N Nakajima, T Kamijo, Y Yokoyama, S Li, YF Gonzalez, FJ Aoyama, T AF Sugiyama, Elko Tanaka, Naoki Nakajima, Tamie Kamijo, Yuji Yokoyama, Shin Li, Yufeng Gonzalez, Frank J. Aoyama, Toshifumi TI Haploinsufficiency in the PPAR alpha and LDL receptor genes leads to gender- and age-specific obesity and hyperinsulinemia SO BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS LA English DT Article DE peroxisome proliferator-activated receptor alpha; low-density lipoprotein receptor; gender- and age-specific obesity; hyperinsulinemia; hyperglycemia; hyperlipidemia; insulin resistance; constitutive condition ID INSULIN-RESISTANCE; DEFICIENT MICE; NULL MICE; LIPID-METABOLISM; PROLIFERATOR; DIET; ATHEROSCLEROSIS; GAMMA; MACROPHAGES; ACTIVATION AB When preparing peroxisome proliferator-activated receptor (PPAR)alpha:low-density lipoprotein receptor (LDLR) (-/-) double knockout mice, we unexpectedly found a unique gender- and age-specific obesity in the F1 generation, PPAR alpha (+/-):LDLR (+/-), even in mice fed standard chow. Body weights of the male heterozygous mice increased up to about 60 g at 75 weeks of age, then decreased by about 30g at 100 weeks of age. More than 95% of the heterozygous mice between 35- and 75-week-olds were overweight. Of interest, the obese heterozygous mice also exhibited hyperinsulinemia correlating with moderate insulin resistance. Hepatic gene expression of LDLR was lower than expected in the heterozygous mice, particularly at 50 and 75 weeks of age. In contrast, the hepatic expression of PPAR alpha was higher than expected in obese heterozygous mice, but decreased in non-obese older heterozygous mice. Modulated expression of these genes may be partially associated with the onset of the hyperinsulinemia. (c) 2006 Elsevier Inc. All rights reserved. C1 Shinshu Univ, Grad Sch Med, Inst Aging & Adaptat, Dept Metab Regulat, Matsumoto, Nagano 3908621, Japan. Nagano Prefectural Coll, Dept Nutr Sci, Nagano 3808525, Japan. Shinshu Univ, Sch Med, Dept Internal Med 2, Matsumoto, Nagano 3908621, Japan. Shinshu Univ, Sch Med, Dept Hyg & Med Genet, Matsumoto, Nagano 3908621, Japan. Shinshu Univ, Sch Med, Dept Psychiat, Matsumoto, Nagano 3908621, Japan. NCI, Lab Metab, Bethesda, MD 20892 USA. RP Sugiyama, E (reprint author), Shinshu Univ, Grad Sch Med, Inst Aging & Adaptat, Dept Metab Regulat, Matsumoto, Nagano 3908621, Japan. EM eikoyoko@nagano-kentan.ac.jp NR 29 TC 4 Z9 4 U1 0 U2 0 PU ACADEMIC PRESS INC ELSEVIER SCIENCE PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA SN 0006-291X J9 BIOCHEM BIOPH RES CO JI Biochem. Biophys. Res. Commun. PD NOV 17 PY 2006 VL 350 IS 2 BP 370 EP 376 DI 10.1016/j.bbrc.2006.09.048 PG 7 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA 096PS UT WOS:000241389900018 PM 17011521 ER PT J AU Sheng, Y Tsai-Morris, CH Gutti, R Maeda, Y Dufau, ML AF Sheng, Yi Tsai-Morris, Chon-Hwa Gutti, Ravi Maeda, Yuji Dufau, Maria L. TI Gonadotropin-regulated testicular RNA helicase (GRTH/Ddx25) is a transport protein involved in gene-specific mRNA export and protein translation during spermatogenesis SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID DEAD-BOX PROTEINS; NUCLEAR-EXPORT; PGK-2 ISOZYMES; PROLACTIN GENE; EXPRESSION; FAMILY; TESTIS; MOUSE; PORE; TRANSCRIPTION AB Gonadotropin-regulated testicular RNA helicase (GRTH/Ddx25), a member of the DEAD-box protein family, is essential for completion of spermatogenesis. GRTH is present in the cytoplasm and nucleus of meiotic spermatocytes and round spermatids and functions as a component of mRNP particles, implicating its post-transcriptional regulatory roles in germ cells. In this study, GRTH antibodies specific to N- or C- terminal sequences showed differential subcellular expression of GRTH 56- and 61-kDa species in nucleus and cytoplasm, respectively, of rodent testis and transfected COS1 cells. The 56-kDa nuclear species interacted with CRM1 and participated in mRNA transport. The phosphorylated cytoplasmic 61-kDa species was associated with polyribosomes. Confocal studies on COS-1 cells showed that GRTH-GFP was retained in the nucleus by treatment with a RNA polymerase inhibitor or the nuclear protein export inhibitor. This indicated that GRTH is a shuttling protein associated with RNA export. The N- terminal leucine-rich region (61-74 amino acids) was identified as the nuclear export signal that participated in CRM1-dependent nuclear export pathway. Deletion analysis identified a 14-amino acid GRTH sequence (100-114 amino acids) as a nuclear localization signal. GRTH selectively regulated the translation of specific genes including histone 4 and HMG2 in germ cells. In addition, GRTH participated in the nuclear export of RNA messages (PGK2, tACE, and TP2) in a gene-specific manner. These studies strongly indicate that the mammalian GRTH/Ddx25 gene is a multifunctional RNA helicase that is an essential regulator of sperm maturation. C1 NICHD, Sect Mol Endocrinol, ERRB, NIH, Bethesda, MD 20892 USA. RP Dufau, ML (reprint author), NICHD, Sect Mol Endocrinol, ERRB, NIH, Bldg 49,Rm 6A-36,49 Convent Dr,MSC 4510, Bethesda, MD 20892 USA. EM dufaum@mail.nih.gov OI Gutti, Ravi/0000-0002-0912-5796 FU Intramural NIH HHS NR 34 TC 40 Z9 43 U1 0 U2 2 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD NOV 17 PY 2006 VL 281 IS 46 BP 35048 EP 35056 DI 10.1074/jbc.M605086200 PG 9 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA 104CN UT WOS:000241933700038 PM 16968703 ER PT J AU Hoe, HS Tran, TS Matsuoka, Y Howell, BW Rebeck, GW AF Hoe, Hyang-Sook Tran, Tracy S. Matsuoka, Yasuji Howell, Brian W. Rebeck, G. William TI DAB1 and Reelin effects on amyloid precursor protein and apoE receptor 2 trafficking and processing SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID RECEPTOR-RELATED PROTEIN; ADAPTER PROTEIN; DISABLED 1; MICE LACKING; F-SPONDIN; FE65; BINDING; METABOLISM; DOMAINS; LIGAND AB Numerous cytoplasmic adaptor proteins, including JIP1, FE65, and X11 alpha, affect amyloid precursor protein (APP) processing and A beta production. Dab1 is another adaptor protein that interacts with APP as well as with members of the apoE receptor family. We examined the effect of Dab1 on APP and apoEr2 processing in transfected cells and primary neurons. Dab1 interacted with APP and apoEr2 and increased levels of their secreted extracellular domains and their cytoplasmic C-terminal fragments. These effects depended on the NPXY domains of APP and apoEr2 and on the phosphotyrosine binding domain of Dab1 but did not depend on phosphorylation of Dab1. Dab1 decreased the levels of APP beta-C-terminal fragment and secreted A beta. Full-length Dab1 or its phosphotyrosine binding domain alone increased surface levels of APP, as determined by surface protein biotinylation and live cell staining. A ligand for apoEr2, the extracellular matrix protein Reelin, significantly increased the interaction of apoEr2 with Dab1. Surprisingly, we also found that Reelin treatment significantly increased the interaction of APP and Dab1. Moreover, Reelin treatment increased cleavage of APP and apoEr2 and decreased production of the beta-C-terminal fragment of APP and A beta. Together, these data suggest that Dab1 alters trafficking and processing of APP and apoEr2, and this effect is influenced by extracellular ligands. C1 Georgetown Univ, Med Ctr, Dept Neurosci, Washington, DC 20057 USA. Georgetown Univ, Med Ctr, Dept Neurol, Washington, DC 20057 USA. NINDS, Neurogenet Branch, Porter Neurosci Res Ctr, NIH, Bethesda, MD 20892 USA. RP Rebeck, GW (reprint author), Georgetown Univ, Med Ctr, Dept Neurosci, 3970 Reservoir Rd NW, Washington, DC 20057 USA. EM gwr2@georgetown.edu OI Howell, Brian/0000-0002-0204-0773 FU NIA NIH HHS [K01 AG022455, R01 AG14473] NR 35 TC 101 Z9 108 U1 1 U2 1 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD NOV 17 PY 2006 VL 281 IS 46 BP 35176 EP 35185 DI 10.1074/jbc.M602162200 PG 10 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA 104CN UT WOS:000241933700051 PM 16951405 ER PT J AU Verzijl, D Pardo, L van Dijk, M Gruijthuijsen, YK Jongejan, A Timmerman, H Nicholas, J Schwarz, M Murphy, PM Leurs, R Smit, MJ AF Verzijl, Dennis Pardo, Leonardo van Dijk, Marie Gruijthuijsen, Yvonne K. Jongejan, Aldo Timmerman, Henk Nicholas, John Schwarz, Mario Murphy, Philip M. Leurs, Rob Smit, Martine J. TI Helix 8 of the viral chemokine receptor ORF74 directs chemokine binding SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID PROTEIN-COUPLED RECEPTOR; KAPOSIS-SARCOMA; CONSTITUTIVE ACTIVITY; INVERSE AGONISTS; CARBOXYL-TERMINUS; CHARGED RESIDUES; ACTIVATION; RHODOPSIN; LIGAND; IDENTIFICATION AB The constitutively active G-protein-coupled receptor and viral oncogene ORF74, encoded by Kaposi sarcoma-associated herpesvirus (human herpesvirus 8), binds a broad range of chemokines, including CXCL1 (agonist), CXCL8 ( neutral ligand), and CXCL10 (inverse agonist). Although chemokines interact with the extracellular N terminus and loops of the receptor, we demonstrate that helix 8 (Hx8) in the intracellular carboxyl tail (C-tail) of ORF74 directs chemokine binding. Partial deletion of the C-tail resulted in a phenotype with reduced constitutive activity but intact regulation by ligands. Complete deletion of the C-tail, including Hx8, resulted in an inactive phenotype that lacks CXCL8 binding sites and has an increased number of binding sites for CXCL10. Similar effects were obtained with the single R7.61(322)W or Q7.62(323)P mutations in Hx8. We propose that the conserved charged or polar side chain at position 7.61 has a specific role in stabilizing the end of transmembrane domain 7 (TM7). Disruption of Hx8 by deletion or mutation distorts an H-bonding network, involving highly conserved amino acids within TM2, TM7, and Hx8, that is crucial for positioning of the TM domains, coupling to G alpha q, and CXCL8 binding. Thus, Hx8 appears to exert a key role in receptor stabilization through the conserved residue R7.61, directing the ligand binding profile of ORF74 and likely also that of other class A G-protein-coupled receptors. C1 Vrije Univ Amsterdam, Div Med Chem, Leiden Amsterdam Ctr Drug Res, NL-1081 HV Amsterdam, Netherlands. Univ Autonoma Barcelona, Fac Med, Unidad Bioestadist, Lab Med Computac, E-08193 Barcelona, Spain. Univ Maastricht, Cardiovasc Res Inst Maastricht, Dept Med Microbiol, NL-6202 AZ Maastricht, Netherlands. Johns Hopkins Univ, Mol Virol Labs, Sidney Kimmel Comprehens Canc Ctr, Baltimore, MD 21231 USA. NIAID, Lab Mol Immunol, NIH, Bethesda, MD 20892 USA. RP Smit, MJ (reprint author), Vrije Univ Amsterdam, Div Med Chem, Leiden Amsterdam Ctr Drug Res, Boelelaan 1083, NL-1081 HV Amsterdam, Netherlands. EM MJ.Smit@few.vu.nl RI van Dijk, Marie/L-1901-2014; OI Pardo, Leonardo/0000-0003-1778-7420; Verzijl, Dennis/0000-0002-7716-9838; Pardo, Luis/0000-0003-1375-4349 FU NCI NIH HHS [CA113239, CA119887, CA76445, P01 CA113239, R01 CA076445, R21 CA119887] NR 44 TC 20 Z9 20 U1 0 U2 1 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD NOV 17 PY 2006 VL 281 IS 46 BP 35327 EP 35335 DI 10.1074/jbc.M606877200 PG 9 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA 104CN UT WOS:000241933700067 PM 16997914 ER PT J AU Yi, L Fang, J Isik, N Chim, J Jin, T AF Yi, Ling Fang, Jun Isik, Nilgun Chim, Jimmy Jin, Tian TI HIV gp120-induced interaction between CD4 and CCR5 requires cholesterol-rich microenvironments revealed by live cell fluorescence resonance energy transfer imaging SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID IMMUNODEFICIENCY-VIRUS TYPE-1; CHEMOKINE RECEPTORS; T-CELLS; MEMBRANE MICRODOMAINS; LIPID RAFTS; GP120; ENTRY; INFECTION; SURFACE; GLYCOPROTEIN AB Binding of the human immunodeficiency virus (HIV) envelope gp120 glycoprotein to CD4 and CCR5 receptors on the plasma membrane initiates the viral entry process. Although plasma membrane cholesterol plays an important role in HIV entry, its modulating effect on the viral entry process is unclear. Using fluorescence resonance energy transfer imaging, we have provided evidence here that CD4 and CCR5 localize in different microenvironments on the surface of resting cells. Binding of the third variable region V3-containing gp120 core to CD4 and CCR5 induced association between these receptors, which could be directly monitored by fluorescence resonance energy transfer on the plasma membrane of live cells. Depletion of cholesterol from the plasma membrane abolished the gp120 core-induced associations between CD4 and CCR5, and reloading cholesterol restored the associations in live cells. Our studies suggest that, during the first step of the HIV entry process, gp120 binding alters the microenvironments of unbound CD4 and CCR5, with plasma membrane cholesterol required for the formation of the HIV entry complex. C1 NIAID, Lab Immunogenet, Twinbrook Facil 2, NIH, Rockville, MD 20852 USA. RP Jin, T (reprint author), NIAID, Lab Immunogenet, Twinbrook Facil 2, NIH, Rockville, MD 20852 USA. EM tjin@niaid.nih.gov FU Intramural NIH HHS NR 40 TC 21 Z9 23 U1 0 U2 0 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD NOV 17 PY 2006 VL 281 IS 46 BP 35446 EP 35453 DI 10.1074/jbc.M607302200 PG 8 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA 104CN UT WOS:000241933700078 PM 16963439 ER PT J AU Leifer, CA Brooks, JC Hoelzer, K Lopez, J Kennedy, MN Mazzoni, A Segal, DM AF Leifer, Cynthia A. Brooks, James C. Hoelzer, Karin Lopez, Jody Kennedy, Margaret N. Mazzoni, Alessandra Segal, David M. TI Cytoplasmic targeting motifs control localization of toll-like receptor 9 SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID BACTERIAL CPG-DNA; INTRACELLULAR COMPARTMENTS; SUBCELLULAR-LOCALIZATION; SIGNAL-TRANSDUCTION; DENDRITIC CELLS; CUTTING EDGE; DOMAIN; TLR9; RECOGNITION; ACTIVATION AB Toll-like receptors (TLRs) are essential for host defense. Although several TLRs reside on the cell surface, nucleic acid recognition of TLRs occurs intracellularly. For example, the receptor for CpG containing bacterial and viral DNA, TLR9, is retained in the endoplasmic reticulum. Recent evidence suggests that the localization of TLR9 is critical for appropriate ligand recognition. Here we have defined which structural features of the TLR9 molecule control its intracellular localization. Both the cytoplasmic and ectodomains of TLR9 contain sufficient information, whereas the transmembrane domain plays no role in intracellular localization. We identify a 14-amino acid stretch that directs TLR9 intracellularly and confers intracellular localization to the normally cell surface-expressed TLR4. Truncation or mutation of the cytoplasmic tail of TLR9 reveals a vesicle localization motif that targets early endosomes. We propose a model whereby modification of the cytoplasmic tail of TLR9 results in trafficking to early endosomes where it encounters CpG DNA. C1 Cornell Univ, Coll Vet Med, Ithaca, NY 14853 USA. NCI, Expt Immunol Branch, NIH, Bethesda, MD 20892 USA. RP Leifer, CA (reprint author), Cornell Univ, Coll Vet Med, VMC C5-153, Ithaca, NY 14853 USA. EM cal59@cornell.edu RI Hoelzer, Karin/A-8230-2010 FU Intramural NIH HHS; NCI NIH HHS [K22 CA113705, K22 CA113705-03]; NIAID NIH HHS [T32 AI007643] NR 31 TC 61 Z9 64 U1 1 U2 4 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD NOV 17 PY 2006 VL 281 IS 46 BP 35585 EP 35592 DI 10.1074/jbc.M607511200 PG 8 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA 104CN UT WOS:000241933700091 PM 16990271 ER PT J AU Sambe, H Hoshina, K Moaddel, R Wainer, IW Haginaka, J AF Sambe, Haruyo Hoshina, Kaori Moaddel, Ruin Wainer, Irving W. Haginaka, Jun TI Uniformly-sized, molecularly imprinted polymers for nicotine by precipitation polymerization SO JOURNAL OF CHROMATOGRAPHY A LA English DT Article DE molecularly imprinted polymer; nicotine; precipitation polymerization; chiral separation; molecular recognition; cigarette smoke extract ID SOLID-PHASE EXTRACTION; STATIONARY-PHASE; RECOGNITION ABILITY; BIOLOGICAL SAMPLES; MICROSPHERES; RETENTION; CHROMATOGRAPHY; MONODISPERSE; TOBACCO; SMOKE AB Uniformly-sized, molecularly imprinted polymers (MIPs) for (S)-nicotine have been prepared by a precipitation polymerization method using methacrylic acid (MAA) or 2-(trifluoromethyl)acrylic acid (TFMAA) as a functional monomer and divinylbenzene (DVB) as a cross-linker in a mixture of toluene and acetonitrile. The (S)-nicotine-imprinted MAA-co-DVB polymers were monodispersed microspheres of about 4 mu m in diameter, while the TFMAA-co-DVB ones were gel-like. Molecular recognition abilities of the former MIPs were evaluated for nicotine and its structurally related compounds in liquid chromatography using a mixture of sodium phosphate buffer and acetonitrile as the eluent. Enantioseparation of nicotine was attained using the (S)-nicotine-imprinted MAA-co-DVB polymers. Furthermore, they could selectively trap nicotine in cigarette smoke extracts. (c) 2006 Elsevier B.V. All rights reserved. C1 Mukogawa Womens Univ, Fac Pharmaceut Sci, Nishinomiya, Hyogo 6638179, Japan. NIA, Ctr Gerontol Res, Baltimore, MD 21224 USA. RP Haginaka, J (reprint author), Mukogawa Womens Univ, Fac Pharmaceut Sci, 11-68 Koshien Kyuban Cho, Nishinomiya, Hyogo 6638179, Japan. EM haginaka@mukogawa-u.ac.jp NR 28 TC 61 Z9 71 U1 4 U2 23 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0021-9673 J9 J CHROMATOGR A JI J. Chromatogr. A PD NOV 17 PY 2006 VL 1134 IS 1-2 BP 88 EP 94 DI 10.1016/j.chroma.2006.08.073 PG 7 WC Biochemical Research Methods; Chemistry, Analytical SC Biochemistry & Molecular Biology; Chemistry GA 105VC UT WOS:000242059400012 PM 16978633 ER PT J AU Zerhouni, EA AF Zerhouni, Elias A. TI Research funding - NIH in the post-doubling era: Realities and strategies SO SCIENCE LA English DT Editorial Material C1 NIH, Bethesda, MD 20892 USA. RP Zerhouni, EA (reprint author), NIH, Bldg 10, Bethesda, MD 20892 USA. EM zerhounidirect@nih.gov NR 4 TC 64 Z9 64 U1 0 U2 4 PU AMER ASSOC ADVANCEMENT SCIENCE PI WASHINGTON PA 1200 NEW YORK AVE, NW, WASHINGTON, DC 20005 USA SN 0036-8075 J9 SCIENCE JI Science PD NOV 17 PY 2006 VL 314 IS 5802 BP 1088 EP 1090 DI 10.1126/science.1136931 PG 3 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA 105PW UT WOS:000242045800023 PM 17110557 ER PT J AU Blanchard, J Grosell, M AF Blanchard, Jonathan Grosell, Martin TI Copper toxicity across salinities from freshwater to seawater in the euryhaline fish Fundulus heteroclitus: Is copper an ionoregulatory toxicant in high salinities? SO AQUATIC TOXICOLOGY LA English DT Article DE Cu toxicity; ionoregulation; nitrogen excretion; marine fishy; killifish ID ATOMIC-ABSORPTION SPECTROMETRY; TROUT ONCORHYNCHUS-MYKISS; PLATICHTHYS-FLESUS L; RAINBOW-TROUT; IONIC REGULATION; SALMO-GAIRDNERI; CARBONIC-ANHYDRASE; SEA-WATER; EXPOSURE; GILL AB Two waterborne Cu. exposures were performed to investigate if Cu is an ionoregulatory toxicant at all salinities in the killifish, Fundulus heteroclitus. A 30-day flow through exposure in 0 (FW), 5, 11, 22, and 28 ppt (SW) and three [Cu]'s (nominal 0, 30, and 150 jig Cu L-1) revealed no apparent Cu. induced mortality at the intermediate salinities and high mortality in FW and SW. Fish were sampled at 4, 12, and 30 days after the start of the exposure and both Na+/K+ adenosine triphosphatase (Na+/K+ ATPase) and carbonic anhydrase (CA) activity in the gill and intestine as well as whole body [Na+], and [Cl-] were measured. At the high [Cu] a reduction of whole body [Na+] after 4 days of exposure in FW was the only physiological parameter influenced. A second static 24 h Cu exposure was performed in FW, 5, 13, and 29 ppt (SW) and two (Cu]'s (nominal 0 and 110 mu g Cu L-1). In addition to the parameters listed above, ammonia flux was measured at all salinities and Na+ flux was measured in FW fish. Cu affected ionoregulation in FW where decreased Na+ uptake associated with inhibition of Na+/K+ ATPase led to decreased whole body [Na+]) after 24 h. The only affected parameter in SW was net ammonia excretion suggesting that Cu is not an ionoregulatory toxicant in SW at the concentrations employed. We propose that physiology rather than chemistry explain much of the variation in Cu toxicity seen across salinities. (c) 2006 Elsevier B.V. All rights reserved. C1 Univ Miami, Rosenstiel Sch Marine & Atmospher Sci, Div Marine Biol & Fisheries, NIEHS Marine & Freshwater Biomed Sci Ctr, Miami, FL 33149 USA. RP Blanchard, J (reprint author), Univ Miami, Rosenstiel Sch Marine & Atmospher Sci, Div Marine Biol & Fisheries, NIEHS Marine & Freshwater Biomed Sci Ctr, 4600 Rickenbacker Causeway, Miami, FL 33149 USA. EM jblanchard@rsmas.miami.edu FU NIEHS NIH HHS [ES05705] NR 33 TC 68 Z9 70 U1 0 U2 26 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0166-445X J9 AQUAT TOXICOL JI Aquat. Toxicol. PD NOV 16 PY 2006 VL 80 IS 2 BP 131 EP 139 DI 10.1016/j.aquatox.2006.08.001 PG 9 WC Marine & Freshwater Biology; Toxicology SC Marine & Freshwater Biology; Toxicology GA 105WX UT WOS:000242064100004 PM 16996624 ER PT J AU Mayr, FB Jilma-Stohlawetz, P Firbas, C Suffredini, AF Derendorf, H Jilma, B AF Mayr, Florian B. Jilma-Stohlawetz, Petra Firbas, Christa Suffredini, Anthony F. Derendorf, Hartmut Jilma, Bernd TI Functional role of the chemokine binding duffy antigen receptor complex (DARC) in human inflammation in vivo. SO BLOOD LA English DT Meeting Abstract CT 48th Annual Meeting of the American-Society-of-Hematology CY DEC 09-12, 2006 CL Orlando, FL SP Amer Soc Hematol C1 Med Univ Vienna, Vienna, 20892, Austria. Med Univ Vienna, Blood Grp Serol & Transfus Med, Vienna, Austria. NIH, Dept Crit Care Med, Ctr Clin, Bethesda, MD USA. Coll Pharm, Gainesville, FL USA. RI Derendorf, Hartmut/B-4628-2012 OI Derendorf, Hartmut/0000-0003-4016-1370 NR 0 TC 0 Z9 0 U1 0 U2 1 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2006 VL 108 IS 11 MA 20 BP 10A EP 10A PN 1 PG 1 WC Hematology SC Hematology GA 111GS UT WOS:000242440000021 ER PT J AU Nemeth, M Bodine, D AF Nemeth, Michael Bodine, David TI beta-catenin expression in cultured bone marrow stromal cells is required to maintain production of osteoblasts and hematopoietic progenitor cells. SO BLOOD LA English DT Meeting Abstract CT 48th Annual Meeting of the American-Society-of-Hematology CY DEC 09-12, 2006 CL Orlando, FL SP Amer Soc Hematol C1 NHGRI, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2006 VL 108 IS 11 MA 85 BP 29A EP 29A PN 1 PG 1 WC Hematology SC Hematology GA 111GS UT WOS:000242440000086 ER PT J AU Pilon, AM Arcasoy, MO Vayda, SE Dressman, HK Bieker, JJ Bodine, DM Gallagher, PG AF Pilon, Andre M. Arcasoy, Murat O. Vayda, Serena E. Dressman, Holly K. Bieker, James J. Bodine, David M. Gallagher, Patrick G. TI Defects in E2F1/2 expression are associated with abnormalities in cell cycle and differentiation in EKLF-deficient erythroid cells. SO BLOOD LA English DT Meeting Abstract CT 48th Annual Meeting of the American-Society-of-Hematology CY DEC 09-12, 2006 CL Orlando, FL SP Amer Soc Hematol C1 NHGRI, NIH, Bethesda, MD 20892 USA. Duke Univ, Durham, NC USA. Mt Sinai Sch Med, MCDB, New York, NY USA. Yale Univ, New Haven, CT USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2006 VL 108 IS 11 MA 84 BP 29A EP 29A PN 1 PG 1 WC Hematology SC Hematology GA 111GS UT WOS:000242440000085 ER PT J AU Arepally, GM Qi, R Hollingsworth, J Suvarna, S AF Arepally, Gowthami M. Qi, Rui Hollingsworth, John Suvarna, Shayela TI Determinants of PF4/heparin immunogenicity in a murine model of HIT. SO BLOOD LA English DT Meeting Abstract CT 48th Annual Meeting of the American-Society-of-Hematology CY DEC 09-12, 2006 CL Orlando, FL SP Amer Soc Hematol C1 Duke Univ, Med Ctr, Durham, NC USA. Natl Inst Environm Hlth Sci, Environm Dis Med, Res Triangle Pk, NC USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2006 VL 108 IS 11 MA 96 BP 32A EP 33A PN 1 PG 2 WC Hematology SC Hematology GA 111GS UT WOS:000242440000097 ER PT J AU Longo, DL Glatstein, E Duffey, PL Young, RC Fiem, S Jaffe, ES Camphausen, K Wilson, W DeVita, VT AF Longo, Dan L. Glatstein, Eli Duffey, Patricia L. Young, Robert C. Fiem, Shelby Jaffe, Elaine S. Camphausen, Kevin Wilson, Wyndham DeVita, Vincent T. TI A prospective trial of radiation alone vs combination chemotherapy alone for early-stage Hodgkin's disease: Implications of 25-year follow-up to current combined modality therapy. SO BLOOD LA English DT Meeting Abstract CT 48th Annual Meeting of the American-Society-of-Hematology CY DEC 09-12, 2006 CL Orlando, FL SP Amer Soc Hematol C1 Natl Canc Inst, Pathol Branch, Bethesda, MD USA. Natl Inst Aging, Intramural Res Program, Baltimore, MD USA. Univ Penn, Dept Radiat Oncol, Philadelphia, PA 19104 USA. Fox Chase Canc Ctr, Off President, Philadelphia, PA 19111 USA. Yale Canc Ctr, Off Director, New Haven, CT USA. NR 0 TC 7 Z9 7 U1 1 U2 1 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2006 VL 108 IS 11 MA 98 BP 33A EP 33A PN 1 PG 1 WC Hematology SC Hematology GA 111GS UT WOS:000242440000099 ER PT J AU Chen, JC Young, NS AF Chen, Jichun Young, Neal S. TI Reduced regulatory T cell to activated T cell ratio in a mouse model of immune-mediated bone marrow failure and prevention of aplastic anemia by infusion of T regulatory cells. SO BLOOD LA English DT Meeting Abstract CT 48th Annual Meeting of the American-Society-of-Hematology CY DEC 09-12, 2006 CL Orlando, FL SP Amer Soc Hematol C1 NHLBI, Hematol Branch, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2006 VL 108 IS 11 MA 121 BP 40A EP 40A PN 1 PG 1 WC Hematology SC Hematology GA 111GS UT WOS:000242440000122 ER PT J AU Hillmen, P Muus, P Duhrsen, U Risitano, AM Schubert, J Young, NS Schrezenmeier, H Szer, J Brodsky, RA Hill, A Socie, G Rollins, SA Rother, RP Bell, L Luzzatto, L AF Hillmen, Peter Muus, Petra Duehrsen, Ulrich Risitano, Antonio M. Schubert, Joerg Young, Neal S. Schrezenmeier, Hubert Szer, Jeffrey Brodsky, Robert A. Hill, Anita Socie, Gerard Rollins, Scott A. Rother, Russell P. Bell, Leonard Luzzatto, Lucio TI The terminal complement inhibitor eculizumab reduces thrombosis in patients with paroxysmal nocturnal hemoglobinuria. SO BLOOD LA English DT Meeting Abstract CT 48th Annual Meeting of the American-Society-of-Hematology CY DEC 09-12, 2006 CL Orlando, FL SP Amer Soc Hematol C1 Leeds Gen Infirm, Leeds, W Yorkshire, England. Radboud Univ Nijmegen, Nijmegen, Netherlands. Univ Hosp, Sch Med, Essen, Germany. Mediche Federico Univ 2, NIH, Naples, Italy. Saarland Univ, Homburg, Germany. NHLBI, Bethesda, MD USA. Inst Clin Transfusionmedizi & Immungenetikn, Helmholtzstr, Germany. Royal Hosp, INSERM, Melbourne, Vic, Australia. Sidney Kimmel Comprehens Canc Ctr, Baltimore, MD USA. Hop St Louis, Paris, France. Alexion Pharmaceut Inc, Cheshire, CT USA. Ins Toscano Tumori, Florence, Italy. RI Muus, P./L-4539-2015 NR 0 TC 4 Z9 4 U1 1 U2 2 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2006 VL 108 IS 11 MA 123 BP 40A EP 41A PN 1 PG 2 WC Hematology SC Hematology GA 111GS UT WOS:000242440000124 ER PT J AU Schubert, J Hillmen, P Duhrsen, U Young, NS Elebute, M Szer, J Gianfaldoni, G Socie, G Browne, P Mojcik, CF Rother, RP Muus, P AF Schubert, Joerg Hillmen, Peter Duehrsen, Ulrich Young, Neal S. Elebute, Modupe Szer, Jeffrey Gianfaldoni, Giacomo Socie, Gerard Browne, Paul Mojcik, Christopher F. Rother, Russell P. Muus, Petra TI Treatment with the terminal complement inhibitor eculizumab improves anemia in patients with paroxysmal nocturnal hemoglobinuria: Phase III triumph study results. SO BLOOD LA English DT Meeting Abstract CT 48th Annual Meeting of the American-Society-of-Hematology CY DEC 09-12, 2006 CL Orlando, FL SP Amer Soc Hematol C1 Univ Saarland, Sch Med, D-6650 Homburg, Germany. Leeds Gen Infirmary, Leeds, W Yorkshire, England. Univ Hosp Essen, Essen, Germany. NHLBI, NIH, Bethesda, MD USA. St George Hosp, London, England. Royal Melbourne Hosp, Melbourne, Vic, Australia. Azienda Ospedaliera Univ Careggi, Florence, Italy. Hosp St Louis, INSERM, Paris, France. St James Hosp, Dublin 8, Ireland. Alexion Pharmaceut Inc, Cheshire, CT USA. Radboud Univ Nijmegen, Nijmegen, Netherlands. RI Muus, P./L-4539-2015 NR 0 TC 1 Z9 1 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2006 VL 108 IS 11 MA 124 BP 41A EP 41A PN 1 PG 1 WC Hematology SC Hematology GA 111GS UT WOS:000242440000125 ER PT J AU Wang, HS Feng, JX Qi, CF Morse, H AF Wang, Hongsheng Feng, Jianxun Qi, Chenfeng Morse, Herbert TI Identification and characterization of a novel lymphotoxin alpha mutant recovered from an ENU mutagenesis screen. SO BLOOD LA English DT Meeting Abstract CT 48th Annual Meeting of the American-Society-of-Hematology CY DEC 09-12, 2006 CL Orlando, FL SP Amer Soc Hematol C1 NIAID, Immunopathol Lab, Rockville, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2006 VL 108 IS 11 MA 3868 BP 44B EP 44B PN 2 PG 1 WC Hematology SC Hematology GA 111GW UT WOS:000242440400149 ER PT J AU Buchner, DA Shavit, JA Su, FY Yamaoka, JS Kamei, M Mcgee, B Hanosh, AW Weinstein, BM Ginsburg, D Lyons, SE AF Buchner, David A. Shavit, Jordan A. Su, Fengyun Yamaoka, Jennifer S. Kamei, Makoto Mcgee, Beth Hanosh, Andrew W. Weinstein, Brant M. Ginsburg, David Lyons, Susan E. TI pak2a mutations cause cerebral hemorrhage in redhead zebrafish. SO BLOOD LA English DT Meeting Abstract CT 48th Annual Meeting of the American-Society-of-Hematology CY DEC 09-12, 2006 CL Orlando, FL SP Amer Soc Hematol C1 Univ Michigan, Howard Hughes Med Inst, Inst Life Sci, Ann Arbor, MI 48109 USA. NICHD, Mol Genet Lab, Bethesda, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2006 VL 108 IS 11 MA 142 BP 46A EP 46A PN 1 PG 1 WC Hematology SC Hematology GA 111GS UT WOS:000242440000143 ER PT J AU Dowdell, KC Niemela, J Dale, JK Puck, J Rao, VK Fleisher, T Straus, SE AF Dowdell, Kennichi C. Niemela, Julie Dale, Janet K. Puck, Jennifer Rao, V. Koneti Fleisher, Thomas Straus, Stephen E. TI Role of somatic Fas mutations in the pathogenesis of autoimmune lymphoproliferative syndrome (ALPS). SO BLOOD LA English DT Meeting Abstract CT 48th Annual Meeting of the American-Society-of-Hematology CY DEC 09-12, 2006 CL Orlando, FL SP Amer Soc Hematol C1 NIH, NIAID, LCID, Bethesda, MD 20892 USA. NIH, CC, DLM, Bethesda, MD 20892 USA. NIH, NHGRI, GMBB, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2006 VL 108 IS 11 MA 3900 BP 52B EP 52B PN 2 PG 1 WC Hematology SC Hematology GA 111GW UT WOS:000242440400181 ER PT J AU Pulsipher, M Chitphakdithai, P Klein, J Kurian, S Leitman, S Anderlini, P Logan, B Horowitz, MM Confer, DL AF Pulsipher, Michael Chitphakdithai, Pintip Klein, John Kurian, Seira Leitman, Susan Anderlini, Paolo Logan, Brent Horowitz, Mary M. Confer, Dennis L. TI Volunteer unrelated donor PBSC collection efficacy and recipient outcomes: Results of a prospective national marrow donor program (NMDP) trial, 1999-2003. SO BLOOD LA English DT Meeting Abstract CT 48th Annual Meeting of the American-Society-of-Hematology CY DEC 09-12, 2006 CL Orlando, FL SP Amer Soc Hematol C1 Univ Utah, Salt Lake City, UT 20892 USA. Nat Marrow Donor Prog, Minneapolis, MN 77030 USA. Ctr Int Blood & Marrow Transplantat Res, Milwaukee, WI USA. NIH, Bethesda, MD USA. Univ Texas, MD Anderson Canc Ctr, Houston, TX USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2006 VL 108 IS 11 MA 169 BP 54A EP 54A PN 1 PG 1 WC Hematology SC Hematology GA 111GS UT WOS:000242440000170 ER PT J AU Alter, BP Baerlocher, G Savage, SA Chanock, SJ Weksler, BB Willner, JP Peters, JA Lansdorp, PM AF Alter, Blanche P. Baerlocher, Gabriela Savage, Sharon A. Chanock, Stephen Jacob Weksler, Babette B. Willner, Judith P. Peters, June A. Lansdorp, Peter M. TI Telomere length measurement by flow-FISH distinguishes Dyskeratosis congenita from other bone marrow failure syndromes. SO BLOOD LA English DT Meeting Abstract CT 48th Annual Meeting of the American-Society-of-Hematology CY DEC 09-12, 2006 CL Orlando, FL SP Amer Soc Hematol C1 NCI, Div Canc Epidemiol & Genet, Clin Genet Branch, Bethesda, MD 20892 USA. Univ Hosp Bern, CH-3010 Bern, Switzerland. NCI, Pediat Oncol Branch, Bethesda, MD 20892 USA. Weill Med Coll, New York, NY USA. Mt Sinai Sch Med, New York, NY USA. British Columbia Canc Res Ctr, Terry Fox Lab, Vancouver, BC V5Z 1L3, Canada. RI Savage, Sharon/B-9747-2015 OI Savage, Sharon/0000-0001-6006-0740 NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2006 VL 108 IS 11 MA 183 BP 58A EP 59A PN 1 PG 2 WC Hematology SC Hematology GA 111GS UT WOS:000242440000184 ER PT J AU Calado, RT Yewdell, WT Wilkerson, KL Regal, JA Kajigaya, S Young, NS AF Calado, Rodrigo T. Yewdell, William T. Wilkerson, Keisha L. Regal, Joshua A. Kajigaya, Sachiko Young, Neal S. TI Sex hormones modulate the length of telomeres of normal and telomerase-mutant leukocytes through the estrogen receptor pathway. SO BLOOD LA English DT Meeting Abstract CT 48th Annual Meeting of the American-Society-of-Hematology CY DEC 09-12, 2006 CL Orlando, FL SP Amer Soc Hematol C1 NHLBI, Hematol Branch, Bethesda, MD 20892 USA. RI Calado, Rodrigo/G-2619-2011 NR 0 TC 0 Z9 0 U1 0 U2 2 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2006 VL 108 IS 11 MA 182 BP 58A EP 58A PN 1 PG 1 WC Hematology SC Hematology GA 111GS UT WOS:000242440000183 ER PT J AU Gomes, T Sellers, S Donahue, RE Adler, R La Rochelle, A Dunbar, CE AF Gomes, Theo Sellers, Stephanie Donahue, Robert E. Adler, Rima La Rochelle, Andre Dunbar, Cynthia E. TI Ex vivo expansion of retrovirally-transduced primate CD34+cells results in preferential engraftment and persistence of clones with MDS1/EVI1 insertion sites. SO BLOOD LA English DT Meeting Abstract CT 48th Annual Meeting of the American-Society-of-Hematology CY DEC 09-12, 2006 CL Orlando, FL SP Amer Soc Hematol C1 NIH, NHLBI, Hematol Branch, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2006 VL 108 IS 11 MA 203 BP 64A EP 64A PN 1 PG 1 WC Hematology SC Hematology GA 111GS UT WOS:000242440000204 ER PT J AU Shaheed, G Malkovska, V Horne, M Mendoza, J Patel, M Rees, J Wesley, R Merryman, P AF Shaheed, Gurvinder Malkovska, Vera Horne, McDonald Mendoza, Jose Patel, Mehool Rees, John Wesley, Robert Merryman, Paula TI Clinical scoring, the PF4 ENHANCED assay, and the (14) C-serotinin release assay for the diagnosis of heparin induced thrombocytopenia (HIT) in complex medical and surgical patients. SO BLOOD LA English DT Meeting Abstract CT 48th Annual Meeting of the American-Society-of-Hematology CY DEC 09-12, 2006 CL Orlando, FL SP Amer Soc Hematol C1 Washington Hosp Ctr, Inst Canc, Washington, DC 20010 USA. WG Magnuson Clin Ctr, Natl Inst Hlth, Dept Lab Med, Hematol Serv, Bethesda, MD USA. Washington Hosp Ctr, Dept Pathol, Sect Coagulat & Flow Cytometry, Washington, DC 20010 USA. Washington Hosp Ctr, Dept Pathol, Sect Coagulat & Flow Cytometry, Washington, DC 20010 USA. WG Magnuson Clin Ctr, Natl Inst Hlth, Biostat & Clin Epidemiol Serv, Off Director, Bethesda, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 2021 L ST NW, SUITE 900, WASHINGTON, DC 20036 USA SN 0006-4971 EI 1528-0020 J9 BLOOD JI Blood PD NOV 16 PY 2006 VL 108 IS 11 MA 3949 BP 64B EP 64B PN 2 PG 1 WC Hematology SC Hematology GA 111GW UT WOS:000242440400230 ER PT J AU Wilson, WH Dunleavy, K Pittaluga, S Grant, N Shovlin, M Steinberg, S Raffeld, M Staudt, L Jaffe, ES Janik, J AF Wilson, Wyndham H. Dunleavy, Kieron Pittaluga, Stefania Grant, Nicole Shovlin, Margaret Steinberg, Seth Raffeld, Mark Staudt, Louis Jaffe, Elaine S. Janik, John TI DA-EPOCH-R is highly effective in both BCL-6+ and BCL-6-untreated de novo diffuse large B-cell lymphoma (DLBCL): Study update and analysis of survival outcomes for multiple biomarkers. SO BLOOD LA English DT Meeting Abstract CT 48th Annual Meeting of the American-Society-of-Hematology CY DEC 09-12, 2006 CL Orlando, FL SP Amer Soc Hematol C1 Canc Res Ctr, Natl Canc Inst, Bethesda, MD USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2006 VL 108 IS 11 MA 206 BP 65A EP 65A PN 1 PG 1 WC Hematology SC Hematology GA 111GS UT WOS:000242440000207 ER PT J AU Dunleavy, K Pittaluga, S Janik, J Grant, N Shovlin, M Steinberg, S Raffeld, M Staudt, L Jaffe, ES Wilson, WH AF Dunleavy, Kieron Pittaluga, Stefania Janik, John Grant, Nicole Shovlin, Margaret Steinberg, Seth Raffeld, Mark Staudt, Louis Jaffe, Elaine S. Wilson, Wyndham H. TI Primary mediastinal large B-cell lymphoma (PMBL) outcome may be significantly improved by the addition of rituximab to dose-adjusted (DA)-EPOCH and obviates the need for radiation: Results from a prospective study of 44 patients. SO BLOOD LA English DT Meeting Abstract CT 48th Annual Meeting of the American-Society-of-Hematology CY DEC 09-12, 2006 CL Orlando, FL SP Amer Soc Hematol C1 Canc Res Ctr, Natl Canc Inst, Bethesda, MD USA. NR 0 TC 4 Z9 4 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2006 VL 108 IS 11 MA 209 BP 66A EP 66A PN 1 PG 1 WC Hematology SC Hematology GA 111GS UT WOS:000242440000210 ER PT J AU Pasqualucci, L Compagno, M Mo, TW Smith, P Morse, HC Murty, VVVS Dalla-Favera, R AF Pasqualucci, Laura Compagno, Mara Mo, Tongwei Smith, Paula Morse, Herbert C., III Murty, V. V. V. S. Dalla-Favera, Riccardo TI Activation induced cytidine deaminase (AID) is required for germinal center derived lymphomagenesis. SO BLOOD LA English DT Meeting Abstract CT 48th Annual Meeting of the American-Society-of-Hematology CY DEC 09-12, 2006 CL Orlando, FL SP Amer Soc Hematol C1 Columbia Univ, Herbert Irving Comprehens Canc Ctr, Inst Canc Genet, New York, NY USA. Natl Inst Hlth, NIAID, Immunopathol Lab, Rockville, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2006 VL 108 IS 11 MA 223 BP 70A EP 70A PN 1 PG 1 WC Hematology SC Hematology GA 111GS UT WOS:000242440000224 ER PT J AU Rollison, DE Hayat, M Smith, M Strom, SS Merritt, WD Ries, L Edwards, BK List, AF AF Rollison, Dana E. Hayat, Matthew Smith, Martyn Strom, Sara S. Merritt, William D. Ries, Lynn Edwards, Brenda K. List, Alan F. TI First report of national estimates of the incidence of myelodysplastic syndromes and chronic myeloproliferative disorders from the USSEER program. SO BLOOD LA English DT Meeting Abstract CT 48th Annual Meeting of the American-Society-of-Hematology CY DEC 09-12, 2006 CL Orlando, FL SP Amer Soc Hematol C1 H Lee Moffitt Canc Ctr & Res Inst, Surveillance Res Program, Tampa, FL 94720 USA. Natl Canc Inst, Canc Therapy Evaluat Program, Bethesda, MD USA. Natl Canc Inst, Mol Epidemiol & Toxicol Lab, Bethesda, MD USA. Univ Calif Berkeley, Berkeley, CA USA. MD Anderson Canc Ctr, Houston, TX USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2006 VL 108 IS 11 MA 247 BP 77A EP 77A PN 1 PG 1 WC Hematology SC Hematology GA 111GS UT WOS:000242440000248 ER PT J AU Lin, TS Heerema, NA Fischer, B Blum, KA Moran, ME McEldowney, MB Broering, S Lozanski, G Colevas, D Grever, MR Byrd, JC AF Lin, Thomas S. Heerema, Nyla A. Fischer, Beth Blum, Kristie A. Moran, Mollie E. McEldowney, Michelle B. Broering, Sara Lozanski, Gerard Colevas, Dimitrios Grever, Michael R. Byrd, John C. TI Flavopiridol is active in genetically high-risk, relapsed chronic lymphocytic leukemia (CLL): Analysis of 56 patients by cytogenetic abnormality. SO BLOOD LA English DT Meeting Abstract CT 48th Annual Meeting of the American-Society-of-Hematology CY DEC 09-12, 2006 CL Orlando, FL SP Amer Soc Hematol C1 Ohio State Univ, Columbus, OH USA. Ohio State Univ, Dept Pathol, Columbus, OH 43210 USA. Natl Canc Inst, Canc Therapy Evaluat Program, Rockville, MD USA. RI Blum, Kristie/E-2768-2011 NR 0 TC 3 Z9 3 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2006 VL 108 IS 11 MA 302 BP 93A EP 93A PN 1 PG 1 WC Hematology SC Hematology GA 111GS UT WOS:000242440000303 ER PT J AU Mielke, S Rezvani, K Solomon, SR Savani, BN Nunes, R Yong, A Schindler, J Read, EJ Vitetta, ES Barrett, AJ AF Mielke, Stephan Rezvani, Katayoun Solomon, Scott R. Savani, Bipin N. Nunes, Raquel Yong, Agnes Schindler, John Read, Elizabeth J. Vitetta, Ellen S. Barrett, A. John TI Selective depletion of CD25+ host-reactive donor lymphocytes from allografts preserves a CD25-CD4+foxp3+ fraction of T cells and thereby provides a source for efficient reconstitution of regulatory T cells and additional GVHD control. SO BLOOD LA English DT Meeting Abstract CT 48th Annual Meeting of the American-Society-of-Hematology CY DEC 09-12, 2006 CL Orlando, FL SP Amer Soc Hematol C1 NIH, NHLBI, Stem Cell Allogen Transplant Sect, Hematol Branch, Bethesda, MD 20892 USA. Univ Texas, SW Med Ctr, Canc Immunobiol Ctr, Dept Microbiol, Dallas, TX USA. Natl Inst Hlth, Ctr Clin, Dept Transfus Med, Cell Processing Sect, Bethesda, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2006 VL 108 IS 11 MA 308 BP 95A EP 95A PN 1 PG 1 WC Hematology SC Hematology GA 111GS UT WOS:000242440000309 ER PT J AU Fry, TJ Roger, AR Hakim, F Love, C Layton, P Fowler, D Bishop, MR Gress, R Mackall, CL Wayne, AS AF Fry, Terry J. Roger, Alison R. Hakim, Frances Love, Cynthia Layton, Paula Fowler, Daniel Bishop, Michael R. Gress, Ronald Mackall, Crystal L. Wayne, Alan S. TI Early recovery of thymus-derived naive T cells in pediatric patients (pts) treated with non-myeloablative allogeneic peripheral blood stem cell transplantation (NMSCT) for cancer. SO BLOOD LA English DT Meeting Abstract CT 48th Annual Meeting of the American-Society-of-Hematology CY DEC 09-12, 2006 CL Orlando, FL SP Amer Soc Hematol C1 NIH, Ctr Canc Res, NCI, Pediat Oncol Branch, Bethesda, MD 20892 USA. Duke Univ, Sch Med, Durham, NC USA. NIH, NCI, Ctr Canc Res, Expt Transplantat & Immunol Branch, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2006 VL 108 IS 11 MA 310 BP 96A EP 96A PN 1 PG 1 WC Hematology SC Hematology GA 111GS UT WOS:000242440000311 ER PT J AU Dean, RM Fowler, D Wilson, WH Hakim, F Steinberg, S Odom, J Chow, C Sportes, C Gea-Banacloche, J Pavletic, SZ Hardy, NM Gress, R Bishop, MR AF Dean, Robert M. Fowler, Daniel Wilson, Wyndham H. Hakim, Frances Steinberg, Seth Odom, Jeanne Chow, Catherine Sportes, Claude Gea-Banacloche, Juan Pavletic, Steven Z. Hardy, Nancy M. Gress, Ronald Bishop, Michael R. TI Phase II clinical experience with dose-adjusted EPOCH-Fludarabine, a novel regimen for targeted immune depletion (TID) and disease control in patients with lymphoid malignancies prior to reduced-intensity allogeneic hematopoietic stem cell transplantation (RIST). SO BLOOD LA English DT Meeting Abstract CT 48th Annual Meeting of the American-Society-of-Hematology CY DEC 09-12, 2006 CL Orlando, FL SP Amer Soc Hematol C1 Taussig Canc Ctr, Cleveland Clin, Cleveland, Qld, Australia. Ctr Canc Res, Natl Canc Inst, Bethesda, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2006 VL 108 IS 11 MA 317 BP 98A EP 98A PN 1 PG 1 WC Hematology SC Hematology GA 111GS UT WOS:000242440000318 ER PT J AU Srinivasan, R Carrington, M Suffredini, D Smith, A Martin, M Berg, M Barrett, AJ Srivastava, S Lundqvist, A Yokoyoma, H Savani, BN Childs, RW AF Srinivasan, Ramaprasad Carrington, Mary Suffredini, Dante Smith, Aleah Martin, Maureen Berg, Maria Barrett, A. John Srivastava, Shivani Lundqvist, Andreas Yokoyoma, Hisayuki Savani, Bipin N. Childs, Richard W. TI Impact of KIR and HLA genotypes on outcome in nonmyeloablative hematopoietic cell transplantation (HCT) using HLA matched related donors. SO BLOOD LA English DT Meeting Abstract CT 48th Annual Meeting of the American-Society-of-Hematology CY DEC 09-12, 2006 CL Orlando, FL SP Amer Soc Hematol C1 NCI, Urol Oncol Branch, Bethesda, MD USA. NCI, SAIC, Frederick, MD USA. NHLBI, Hematol Branch, Bethesda, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2006 VL 108 IS 11 MA 323 BP 100A EP 100A PN 1 PG 1 WC Hematology SC Hematology GA 111GS UT WOS:000242440000324 ER PT J AU Sabaawy, HE Embree, LJ Azuma, M Hickstein, DD AF Sabaawy, Hatem E. Embree, Lisa J. Azuma, Mizuki Hickstein, Dennis D. TI Transplantation of hematopoietic and endothelial stem cell progenitors in transgenic zebrafish. SO BLOOD LA English DT Meeting Abstract CT 48th Annual Meeting of the American-Society-of-Hematology CY DEC 09-12, 2006 CL Orlando, FL SP Amer Soc Hematol C1 Natl Canc Inst, Expt Transplantat & Immunol Branch, Bethesda, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2006 VL 108 IS 11 MA 337 BP 105A EP 105A PN 1 PG 1 WC Hematology SC Hematology GA 111GS UT WOS:000242440000338 ER PT J AU Caudell, DL Zhang, ZH Chung, YJ Aplan, PD AF Caudell, David L. Zhang, Zhenhau Chung, Yangjo Aplan, Peter D. TI The CALM-AF10 fusion gene expressed in transgenic mice produces acute leukemia. SO BLOOD LA English DT Meeting Abstract CT 48th Annual Meeting of the American-Society-of-Hematology CY DEC 09-12, 2006 CL Orlando, FL SP Amer Soc Hematol C1 Natl Canc Inst, Genet Branch, Bethesda, MD USA. RI Aplan, Peter/K-9064-2016 NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2006 VL 108 IS 11 MA 358 BP 110A EP 110A PN 1 PG 1 WC Hematology SC Hematology GA 111GS UT WOS:000242440000359 ER PT J AU Lenz, G Nagel, I Siebert, R Sanger, W Wright, GW Zhao, H Rosenwald, A Muller-Hermelink, HK Gascoyne, RD Campo, E Jaffe, ES Smeland, EB Fisher, RI Michael Kuehl, W Chan, WC Staudt, LM AF Lenz, Georg Nagel, Inga Siebert, Reiner Sanger, Warren Wright, George W. Zhao, Hong Rosenwald, Andreas Muller-Hermelink, Hans-Konrad Gascoyne, Randy D. Campo, Elias Jaffe, Elaine S. Smeland, Erlend B. Fisher, Richard I. Michael Kuehl, W. Chan, Wing C. Staudt, Louis M. TI Aberrant immunoglobulin class switch recombination and switch translocations in activated B cell-like diffuse large B-Cell lymphoma. SO BLOOD LA English DT Meeting Abstract CT 48th Annual Meeting of the American-Society-of-Hematology CY DEC 09-12, 2006 CL Orlando, FL SP Amer Soc Hematol C1 NIH, Natl Canc Inst, Metab Branch, Bethesda, MD 20892 USA. Univ Hosp Schleswig Holstein, Inst Human Genet, Kiel, Germany. Univ Nebraska Med Ctr, Omaha, NE USA. NIH, Natl Canc Inst, Biometr Res Branch, Bethesda, MD 20892 USA. Univ Wurzburg, Dept Pathol, D-8700 Wurzburg, Germany. British Columbia Canc Agcy, Vancouver, BC V5Z 4E6, Canada. Univ Barcelona, Hosp Clin, Barcelona, Spain. NIH, Pathol Lab, Natl Canc Inst, Bethesda, MD 20892 USA. Rikshospitalet Radiumhospitalet Med Ctr, Dept Immunol, Oslo, Norway. Univ Rochester, Sch Med, James P Wilmot Canc Ctr, SW Oncol Grp, Rochester, NY USA. NIH, Ctr Canc Res, Natl Canc Inst, Genet Branch, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2006 VL 108 IS 11 MA 356 BP 110A EP 110A PN 1 PG 1 WC Hematology SC Hematology GA 111GS UT WOS:000242440000357 ER PT J AU Devlin, EE Horton, CL Garrett-Beal, LJ Gallagher, PG Bodine, DM AF Devlin, Emily E. Horton, Cheryl Lynn Garrett-Beal, Lisa J. Gallagher, Patrick G. Bodine, David M. TI A transgenic mouse assay to compare the barrier activities of the chicken beta-globin 5'HS4, human beta-globin 5'HS5 and mouse 3'HS1. SO BLOOD LA English DT Meeting Abstract CT 48th Annual Meeting of the American-Society-of-Hematology CY DEC 09-12, 2006 CL Orlando, FL SP Amer Soc Hematol C1 NHGRI, Hematopoiesis Sect, Bethesda, MD 20892 USA. NHGRI, Transgen Mouse Cre Fac, Bethesda, MD 20892 USA. Yale Univ, New Haven, CT USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2006 VL 108 IS 11 MA 362 BP 111A EP 112A PN 1 PG 2 WC Hematology SC Hematology GA 111GS UT WOS:000242440000363 ER PT J AU Bryant, BJ Hopkins, JA Leitman, SF AF Bryant, Barbara J. Hopkins, Julie A. Leitman, Susan F. TI Evaluation of low mean corpuscular volume in an apheresis donor population. SO BLOOD LA English DT Meeting Abstract CT 48th Annual Meeting of the American-Society-of-Hematology CY DEC 09-12, 2006 CL Orlando, FL SP Amer Soc Hematol C1 Natl Inst Hlth, Dept Transfus Med, Bethesda, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2006 VL 108 IS 11 MA 4136 BP 114B EP 114B PN 2 PG 1 WC Hematology SC Hematology GA 111GW UT WOS:000242440400417 ER PT J AU Bashey, A Medina, B Corringham, S Pasek, M Carrier, E Streicher, H Lowy, I Mason, JR Soiffer, RJ Ball, ED AF Bashey, Asad Medina, Bridget Corringham, Sue Pasek, Mildred Carrier, Ewa Streicher, Howard Lowy, Israel Mason, James R. Soiffer, Robert J. Ball, Edward D. TI Phase I study of ipilimumab (neutralizing monoclonal anti-CTLA4 antibody) to treat relapse of malignancy after allogeneic hematopoietic stem cell transplantation: Evidence of tumor regression without induction of GVHD. SO BLOOD LA English DT Meeting Abstract CT 48th Annual Meeting of the American-Society-of-Hematology CY DEC 09-12, 2006 CL Orlando, FL SP Amer Soc Hematol C1 Univ Calif San Diego, Moores Canc Ctr, La Jolla, CA 92093 USA. NCI, Pharmaceut Management Branch, Bethesda, MD 20892 USA. Medarex Inc, Bloomsbury, NJ USA. Scripps Clin, La Jolla, CA USA. Northside Hosp, BMT Grp Georgia, Atlanta, GA USA. Dana Farber Canc Inst, Hematol Malignancies Program, Boston, MA 02115 USA. NR 0 TC 1 Z9 1 U1 0 U2 1 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2006 VL 108 IS 11 MA 410 BP 125A EP 126A PN 1 PG 2 WC Hematology SC Hematology GA 111GS UT WOS:000242440000411 ER PT J AU Kantarjian, HM Sawyers, C Hochhaus, A Schiffer, CA Guilhot, F Niederwieser, DW Gambacorti, C Stone, RM Fischer, T Goldman, J Krahnke, T Mone, M Talpaz, M Druker, BJ AF Kantarjian, Hagop M. Sawyers, Charles Hochhaus, Andreas Schiffer, Charles A. Guilhot, Francois Niederwieser, Dietger W. Gambacorti, Carlo Stone, Richard M. Fischer, Thomas Goldman, John Krahnke, T. Mone, M. Talpaz, Moshe Druker, Brian J. TI Six year follow-up results of a phase II study of imatinib in late chronic phase (L-CP) chronic myeloid leukemia (CML) post interferon-a (IFN) Refractoriness/Intolerance. SO BLOOD LA English DT Meeting Abstract CT 48th Annual Meeting of the American-Society-of-Hematology CY DEC 09-12, 2006 CL Orlando, FL SP Amer Soc Hematol C1 MD Anderson Canc Ctr, Houston, TX USA. Univ Calif Los Angeles, Los Angeles, CA USA. Univ Heidelberg, D-6800 Mannheim, Germany. Karmanos Canc Inst, Detroit, MI USA. CHU La Miletrie, Poitiers, France. Univ Leipzig, D-7010 Leipzig, Germany. Inst Natl Tumori, Milan, Italy. Dana Farber Canc Inst, Boston, MA USA. Univ Mainz, D-6500 Mainz, Germany. NHLBI, Bethesda, MD 20892 USA. Univ Michigan, Ann Arbor, MI 48109 USA. Oregon Hlth Sci Univ, Portland, OR 97201 USA. RI Sawyers, Charles/G-5327-2016 NR 0 TC 2 Z9 2 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2006 VL 108 IS 11 MA 428 BP 130A EP 131A PN 1 PG 2 WC Hematology SC Hematology GA 111GS UT WOS:000242440000429 ER PT J AU Karp, JE Feldman, EJ Morris, L Greer, J Ironside, V Smith, BD Ritchie, E Gore, SD Levis, MJ Kaufmann, SH Malek, S Wright, JJ AF Karp, Judith E. Feldman, Eric J. Morris, Lawrence Greer, Jacqueline Ironside, Valerie Smith, B. Douglas Ritchie, Ellen Gore, Steven D. Levis, Mark J. Kaufmann, Scott H. Malek, Sami Wright, John J. TI Active oral regimen for elderly adults with newly diagnosed acute myelogenous leukemia (AML): Phase I trial of oral tipifarnib (T) combined with oral etoposide (E) for adults >= Age 70 who are not candidates for traditional cytotoxic chemotherapy (TCC). SO BLOOD LA English DT Meeting Abstract CT 48th Annual Meeting of the American-Society-of-Hematology CY DEC 09-12, 2006 CL Orlando, FL SP Amer Soc Hematol C1 Johns Hopkins Univ, Sidney Kimmel Canc Ctr, Baltimore, MD USA. Cornell Univ, New York Presbyterian Hosp, New York, NY USA. Bone Marrow Transplant Grp Georgia, Atlanta, GA USA. Mayo Clin, Rochester, MN USA. Univ Michigan, Ctr Comprehens Canc, Ann Arbor, MI 48109 USA. Natl Canc Inst, Canc Therapy Evaluat Program, Rockville, MD USA. NR 0 TC 2 Z9 2 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2006 VL 108 IS 11 MA 426 BP 130A EP 130A PN 1 PG 1 WC Hematology SC Hematology GA 111GS UT WOS:000242440000427 ER PT J AU Mealiffe, ME Kirchhoff, T Wiernik, PH Lynch, HT Daibata, M Gerdes, AM Offit, K Goldin, LR Horwitz, MS AF Mealiffe, Mathew E. Kirchhoff, Tomas Wiernik, Peter H. Lynch, Henry T. Daibata, Masanori Gerdes, Anne-Marie Offit, Kenneth Goldin, Lynn R. Horwitz, Marshall S. TI KLHDC8B is a novel, mitotically-regulated classical Hodgkin's lymphoma candidate susceptibility gene. SO BLOOD LA English DT Meeting Abstract CT 48th Annual Meeting of the American-Society-of-Hematology CY DEC 09-12, 2006 CL Orlando, FL SP Amer Soc Hematol C1 Univ Washington, Sch Med, Seattle, WA USA. Mem Sloan Kettering Canc Ctr, New York, NY USA. New York Med Coll, Our Lady Mercy Canc Ctr, New York, NY USA. Creighton Univ, Omaha, NE 68178 USA. Kochi Med Sch, Kochi, Japan. Odense Univ Hosp, DK-5000 Odense, Denmark. Natl Canc Inst, Div Canc Epidemol & Genet, Bethesda, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2006 VL 108 IS 11 MA 473 BP 143A EP 144A PN 1 PG 2 WC Hematology SC Hematology GA 111GS UT WOS:000242440000474 ER PT J AU Zhang, X Wang, JF Kunos, G Jerome, EG AF Zhang, Xuefeng Wang, Jian Feng Kunos, George Jerome, E. Groopman TI Delta (9)-tetrahydrocannabinol contributes to the development of Kaposi's sarcoma. SO BLOOD LA English DT Meeting Abstract CT 48th Annual Meeting of the American-Society-of-Hematology CY DEC 09-12, 2006 CL Orlando, FL SP Amer Soc Hematol C1 Beth Israel Deaconess Med Ctr, Harvard Med Sch, Div Expt Med, Boston, MA 02215 USA. Beth Israel Deaconess Med Ctr, Harvard Med Sch, Dept Surg, Boston, MA 02215 USA. Natl Inst Hlth, NIAAA, Bethesda, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2006 VL 108 IS 11 MA 492 BP 149A EP 149A PN 1 PG 1 WC Hematology SC Hematology GA 111GS UT WOS:000242440000493 ER PT J AU Rosenberg, PS Stein, S Rodger, E Bolyard, AA Bonilla, MA Dror, Y Kannourakis, G Newburger, PE Boxer, LA Alter, BP Dale, DC AF Rosenberg, Philip S. Stein, Steven Rodger, Elin Bolyard, Audrey Anna Bonilla, Mary Ann Dror, Yigal Kannourakis, George Newburger, Peter E. Boxer, Laurence A. Alter, Blanche P. Dale, David C. TI Genotype-phenotype associations in patients with severe congenital neutropenia. SO BLOOD LA English DT Meeting Abstract CT 48th Annual Meeting of the American-Society-of-Hematology CY DEC 09-12, 2006 CL Orlando, FL SP Amer Soc Hematol C1 Natl Canc Inst, Div Canc Epidemiol & Genet, Biostat Branch, Bethesda, MD USA. Univ Washington, Dept Med, Seattle, WA USA. St Josephs Childrens Hosp, Pediat Hematol Oncol, Paterson, NJ USA. Univ Toronto, Hosp Sick Children, Toronto, ON M5G 1X8, Canada. Ballarat Onc & Haem Serv, Wendoure, Vic, Australia. Univ Massachusetts, Med Ctr, Worcester, MA USA. Univ Michigan, Ann Arbor, MI 48109 USA. Div Canc Epidemiol & Genet, Clin Genet Branch, Bethesda, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2006 VL 108 IS 11 MA 502 BP 152A EP 152A PN 1 PG 1 WC Hematology SC Hematology GA 111GS UT WOS:000242440000503 ER PT J AU Gore, SD Jiemjit, A Silverman, LB Aucott, T Baylin, S Carraway, H Douses, T Fandy, T Herman, J Karp, JE Licht, JD Murgo, AJ Odchimar-Reissig, R Smith, BD Zwiebel, JA Sugar, E AF Gore, Steven D. Jiemjit, Anchalee Silverman, Lewis B. Aucott, Timothy Baylin, Stephen Carraway, Hetty Douses, Tianna Fandy, Tamer Herman, James Karp, Judith E. Licht, Jonathan D. Murgo, Anthony J. Odchimar-Reissig, Rosalie Smith, B. Douglas Zwiebel, James A. Sugar, Elizabeth TI Combined Methyltransferase/Histone deacetylase inhibition with 5Azacitidine and MS-275 in patients with MDS, CMMoL and AML: Clinical response, Histone Acetylation and DNA damage. SO BLOOD LA English DT Meeting Abstract CT 48th Annual Meeting of the American-Society-of-Hematology CY DEC 09-12, 2006 CL Orlando, FL SP Amer Soc Hematol C1 Sidney Kimmel Comprehens Canc Ctr, Baltimore, MD USA. Mt Sinai Sch Med, New York, NY USA. Northwestern Univ, Chicago, IL 60611 USA. Natl Canc Inst, Canc Therapy Evaluat Program, Bethesda, MD USA. NR 0 TC 12 Z9 12 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2006 VL 108 IS 11 MA 517 BP 156A EP 157A PN 1 PG 2 WC Hematology SC Hematology GA 111GS UT WOS:000242440000518 ER PT J AU Alter, BP Rosenberg, PS Brody, LC AF Alter, Blanche P. Rosenberg, Philip S. Brody, Lawrence C. TI Biallelic mutations in FANCD1/BRCA2 are associated with extraordinary risks of cancer. SO BLOOD LA English DT Meeting Abstract CT 48th Annual Meeting of the American-Society-of-Hematology CY DEC 09-12, 2006 CL Orlando, FL SP Amer Soc Hematol C1 Natl Canc Inst, Div Canc Epidemiol & Genet, Clin Genet Branch, Bethesda, MD USA. Natl Canc Inst, Div Canc Epidemiol & Genet, Biostat Branch, Bethesda, MD USA. Natl Inst Hlth, NHGRI, Genome Technol Branch, Bethesda, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 2 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2006 VL 108 IS 11 MA 4326 BP 160B EP 160B PN 2 PG 1 WC Hematology SC Hematology GA 111GW UT WOS:000242440401013 ER PT J AU Owen, AN Wolfsberg, T Laflamme, K Wong, C Maksimova, Y Elnitski, L Gallagher, PG Bodine, DM AF Owen, Ashley N. Wolfsberg, Tyra Laflamme, Karina Wong, Clara Maksimova, Yelena Elnitski, Laura Gallagher, Patrick G. Bodine, David M. TI A 200 kb survey of chromatin in the ANK-1 locus demonstrates an erythroid-specific chromatin hub that activates the erythrocyte ankyrin (ANK-1E) promoter. SO BLOOD LA English DT Meeting Abstract CT 48th Annual Meeting of the American-Society-of-Hematology CY DEC 09-12, 2006 CL Orlando, FL SP Amer Soc Hematol C1 NHGRI, Hematol Sect, Bethesda, MD USA. NHGRI, Gen Technol Branch, Bethesda, MD USA. Yale Univ, New Haven, CT USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2006 VL 108 IS 11 MA 536 BP 162A EP 162A PN 1 PG 1 WC Hematology SC Hematology GA 111GS UT WOS:000242440000537 ER PT J AU Tanno, T Bhanu, NV Oneal, PA Goh, SH Staker, P Lee, YT Luban, NLC Childs, R Leitman, SF Miller, JL AF Tanno, Toshihiko Bhanu, Natarajan V. Oneal, Patricia A. Goh, Sung-Ho Staker, Pamela Lee, Y. Terry Luban, Naomi L. C. Childs, Richard Leitman, Susan F. Miller, Jeffery L. TI Discovery of growth differentiation factor 15 as an erythroblast-secreted regulator of hepcidin with very high level expression in patients with thalassemia. SO BLOOD LA English DT Meeting Abstract CT 48th Annual Meeting of the American-Society-of-Hematology CY DEC 09-12, 2006 CL Orlando, FL SP Amer Soc Hematol C1 NIH, NIDDK, Mol Med Branch, Bethesda, MD 20892 USA. Childrens Natl Med Ctr, Lab Med & Pathol, Washington, DC 20010 USA. NIH, NHLBI, Hematol Branch, Bethesda, MD 20892 USA. NIH, Dept Transfus Med, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2006 VL 108 IS 11 MA 553 BP 167A EP 167A PN 1 PG 1 WC Hematology SC Hematology GA 111GS UT WOS:000242440000554 ER PT J AU Powell, BL Moser, B Stock, W Gallagher, RE Willman, CL Stone, RM Rowe, JM Coutre, S Feusner, JH Gregory, J Couban, S Appelbaum, FR Tallman, MS Larson, RA AF Powell, Bayard L. Moser, Barry Stock, Wendy Gallagher, Robert E. Willman, Cheryl L. Stone, Richard M. Rowe, Jacob M. Coutre, Steven Feusner, James H. Gregory, John Couban, Stephen Appelbaum, Frederick R. Tallman, Martin S. Larson, Richard A. TI Preliminary results from the north American acute promyelocytic leukemia (APL) study C9710. SO BLOOD LA English DT Meeting Abstract CT 48th Annual Meeting of the American-Society-of-Hematology CY DEC 09-12, 2006 CL Orlando, FL SP Amer Soc Hematol C1 Canc & Leukemia Grp B, Chicago, IL USA. Eastern Oncol Grp, Philadelphia, PA USA. SW Oncol Grp, San Antonio, TX USA. Childrens Oncol Grp, Arcadia, CA USA. NCI, Kingston, ON, Canada. NR 0 TC 3 Z9 3 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2006 VL 108 IS 11 MA 566 BP 171A EP 171A PN 1 PG 1 WC Hematology SC Hematology GA 111GS UT WOS:000242440000567 ER PT J AU Rizzatti, EG Mora-Jensen, H Lee, E Miura, Y Lai, R Daibata, M Wiestner, A AF Rizzatti, Edgar G. Mora-Jensen, Helena Lee, Elinor Miura, Yuji Lai, Raymond Daibata, Masanori Wiestner, Adrian TI Bortezomib activity against mantle cell lymphoma overcomes classic mechanisms of drug resistance and targets cell cycle control. SO BLOOD LA English DT Meeting Abstract CT 48th Annual Meeting of the American-Society-of-Hematology CY DEC 09-12, 2006 CL Orlando, FL SP Amer Soc Hematol C1 NHLBI, Hematol Branch, Bethesda, MD 20892 USA. Univ Alberta, Dept Lab Med & Pathol, Edmonton, AB, Canada. Kochi Med Sch, Dept Hematol & Resp Med, Kochi, Japan. NR 0 TC 0 Z9 0 U1 1 U2 3 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2006 VL 108 IS 11 MA 4393 BP 176B EP 176B PN 2 PG 1 WC Hematology SC Hematology GA 111GW UT WOS:000242440401077 ER PT J AU Miura, YJ Lee, E Gibellini, F White, T Marti, G Wilson, W Wiesmer, A AF Miura, Yuji Lee, Elinor Gibellini, Federica White, Therese Marti, Gerald Wilson, Wyndham Wiesmer, Adrian TI ZAP-70 expression is associated with increased migration to SDF-1 in chronic lymphocytic leukemia. SO BLOOD LA English DT Meeting Abstract CT 48th Annual Meeting of the American-Society-of-Hematology CY DEC 09-12, 2006 CL Orlando, FL SP Amer Soc Hematol C1 NIH, NHLBI, Hematol Branch, Bethesda, MD 20892 USA. NIH, NCI, Canc Res Ctr, Bethesda, MD 20892 USA. US FDA, Ctr Biol Evaluat & Res, Bethesda, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2006 VL 108 IS 11 MA 587 BP 177A EP 177A PN 1 PG 1 WC Hematology SC Hematology GA 111GS UT WOS:000242440000588 ER PT J AU Mora-Jensen, H Rizzatti, EG Wiestner, A AF Mora-Jensen, Helena Rizzatti, Edgar G. Wiestner, Adrian TI Resistance to bortezomib develops slowly in MCL cells, extends to the class of proteasome inhibitors, and is associated with decreased proliferation of the resistant cells. SO BLOOD LA English DT Meeting Abstract CT 48th Annual Meeting of the American-Society-of-Hematology CY DEC 09-12, 2006 CL Orlando, FL SP Amer Soc Hematol C1 NIH, NHLBI, Hematol Branch, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2006 VL 108 IS 11 MA 4397 BP 177B EP 177B PN 2 PG 1 WC Hematology SC Hematology GA 111GW UT WOS:000242440401081 ER PT J AU Shami, PJ Eddington, JK Udupi, V Kosak, KM Saavedra, JE Keefer, LK AF Shami, Paul J. Eddington, Jordan K. Udupi, Vidya Kosak, Ken M. Saavedra, Joseph E. Keefer, Larry K. TI Synergy studies between the nitric oxide (NO) donor JS-K and other anti-leukemic agents. SO BLOOD LA English DT Meeting Abstract CT 48th Annual Meeting of the American-Society-of-Hematology CY DEC 09-12, 2006 CL Orlando, FL SP Amer Soc Hematol C1 Univ Utah, Huntsman Canc Inst, Salt Lake City, UT USA. SAIC, Frederick, MD USA. NCI, NIH, Comparat Carcinogenesis Lab, Frederick, MD 21701 USA. RI Keefer, Larry/N-3247-2014 OI Keefer, Larry/0000-0001-7489-9555 NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2006 VL 108 IS 11 MA 4396 BP 177B EP 177B PN 2 PG 1 WC Hematology SC Hematology GA 111GW UT WOS:000242440401080 ER PT J AU Shenoy, AG Solomon, SR Pichon, S Cadoz, M Nancy, H Barrett, AJ AF Shenoy, Aarthi G. Solomon, Scott R. Pichon, Sylvie Cadoz, Michel Nancy, Hensel Barrett, A. John TI Protecting stem cell transplant recipients against CMV reactivation by vaccinating their donors with a canarypox pp65 vaccine (ALVAC). SO BLOOD LA English DT Meeting Abstract CT 48th Annual Meeting of the American-Society-of-Hematology CY DEC 09-12, 2006 CL Orlando, FL SP Amer Soc Hematol C1 NIH, NHLBI, Bethesda, MD 20892 USA. Clin Dept, Sanofi Pasteur, Marcy Letoile, France. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2006 VL 108 IS 11 MA 590 BP 178A EP 178A PN 1 PG 1 WC Hematology SC Hematology GA 111GS UT WOS:000242440000591 ER PT J AU Peranteau, WH Gu, YC Volk, S Tuschong, LM Bauer, TR Badillo, A Kaye, A Johnson, MP Hickstein, DD Flake, AW AF Peranteau, William H. Gu, Yuchen Volk, Susan Tuschong, Laura M. Bauer, Thomas R. Badillo, Andrea Kaye, Adam Johnson, Mark P. Hickstein, Dennis D. Flake, Alan W. TI In utero hematopoietic cell transplantation using haploidentical parental donors reverses the lethal phenotype in dogs with canine leukocyte adhesion deficiency. SO BLOOD LA English DT Meeting Abstract CT 48th Annual Meeting of the American-Society-of-Hematology CY DEC 09-12, 2006 CL Orlando, FL SP Amer Soc Hematol C1 Childrens Hosp Philadelphia, Ctr Fetal Res, Philadelphia, PA 19104 USA. Natl Canc Inst, Expt Transplantat & Immunol, Bethesda, MD USA. NR 0 TC 1 Z9 1 U1 0 U2 1 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2006 VL 108 IS 11 MA 624 BP 188A EP 188A PG 1 WC Hematology SC Hematology GA 111GS UT WOS:000242440000625 ER PT J AU Zhao, L Cannons, JL Anderson, S Kirby, MR Xu, L Castilla, L Schwartzberg, PL Bosselut, R Liu, PP AF Zhao, Ling Cannons, Jennifer L. Anderson, Stacie Kirby, Martha R. Xu, Liping Castilla, Lucio Schwartzberg, Pamela L. Bosselut, Remy Liu, P. Paul TI CBFB is required for early T cell development in the thymus. SO BLOOD LA English DT Meeting Abstract CT 48th Annual Meeting of the American-Society-of-Hematology CY DEC 09-12, 2006 CL Orlando, FL SP Amer Soc Hematol C1 NHGRI, Genet Mol Biol Branch, Bethesda, MD 20892 USA. NIH, NHGRI, Genet Dis Res Branch, Bethesda, MD 20892 USA. Univ Massachusetts, Sch Med, Program Gen Funct & Express, Worcester, MA USA. NIH, NCI, Lab Immune Cell Biol, Bethesda, MD 20892 USA. RI Liu, Paul/A-7976-2012 OI Liu, Paul/0000-0002-6779-025X NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2006 VL 108 IS 11 MA 648 BP 195A EP 195A PN 1 PG 1 WC Hematology SC Hematology GA 111GS UT WOS:000242440000649 ER PT J AU Chen, Z Balduinui, A Conti, MA Adelstein, RS Shivdasani, RA AF Chen, Zhao Balduinui, Alessandra Conti, Mary Anne Adelstein, Robert S. Shivdasani, Ramesh A. TI Loss of non-muscle myosin heavy chain IIA function does not restrict megakaryocyte maturation or spontaneous platelet release and likely affects non-cell-autonomous aspects of thrombopoiesis. SO BLOOD LA English DT Meeting Abstract CT 48th Annual Meeting of the American-Society-of-Hematology CY DEC 09-12, 2006 CL Orlando, FL SP Amer Soc Hematol C1 Dana Farber Canc Inst, Boston, MA 02115 USA. Univ Pavia, I-27100 Pavia, Italy. NHLBI, Natl Inst Hlth, Mol Cardiol Lab, Bethesda, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2006 VL 108 IS 11 MA 701 BP 210A EP 210A PN 1 PG 1 WC Hematology SC Hematology GA 111GS UT WOS:000242440000702 ER PT J AU Melenhorst, JJ Lu, J Sosa, E Hensel, NF Barrett, AJ AF Melenhorst, J. Joseph Lu, Jun Sosa, Edgardo Hensel, Nancy F. Barrett, A. John TI Immunomagnetic depletion of CD25-expressing T cells from donor blood removes a mixed population of regulatory and effector T cells - Implications for graft engineering. SO BLOOD LA English DT Meeting Abstract CT 48th Annual Meeting of the American-Society-of-Hematology CY DEC 09-12, 2006 CL Orlando, FL SP Amer Soc Hematol C1 NIH, NHLBI, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2006 VL 108 IS 11 MA 724 BP 217A EP 218A PN 1 PG 2 WC Hematology SC Hematology GA 111GS UT WOS:000242440000725 ER PT J AU Mielke, S Nunes, R Rezvani, K Fellowes, VS Fan, Y Solomon, SR Scotto, C Read, EJ Barrett, AJ AF Mielke, Stephan Nunes, Raquel Rezvani, Katayoun Fellowes, Vicki S. Fan, Yong Solomon, Scott R. Scotto, Christian Read, Elizabeth J. Barrett, A. John TI High efficiency clinical scale selective depletion of alloreacting T cells using expanded T lymphocytes as antigen-presenting cells and a TH9402-based photodepletion technique in HLA-mismatched and matched donor-recipient pairs. SO BLOOD LA English DT Meeting Abstract CT 48th Annual Meeting of the American-Society-of-Hematology CY DEC 09-12, 2006 CL Orlando, FL SP Amer Soc Hematol C1 NHLBI, NIH, Stem Cell Allotransplant Sect, Hematol Branch, Bethesda, MD USA. Natl Inst Hlth, Ctr Clin, Dept Transfus Med, Cell Proc Sect, Bethesda, MD USA. Celmed Biosci Inc, St Laurent, PQ, Canada. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2006 VL 108 IS 11 MA 721 BP 217A EP 217A PG 1 WC Hematology SC Hematology GA 111GS UT WOS:000242440000722 ER PT J AU Branford, S Cross, NCP Hochhaus, A Radich, J Saglio, G Kim, DW Fletcher, L Wang, YL Higgins, M Kovalenko, S Shih, LY Tang, JL Ma, E Wong, M Cortes, J Jones, D Lynch, K Goldman, JM Hughes, T AF Branford, Susan Cross, Nicholas C. P. Hochhaus, Andreas Radich, Jerald Saglio, Giuseppe Kim, D. W. Fletcher, Linda Wang, Y. L. Higgins, Melinda Kovalenko, Serge Shih, Lee-Yung Tang, J. L. Ma, Edmond Wong, Michael Cortes, Jorge Jones, Dan Lynch, Kevin Goldman, John M. Hughes, Timothy TI First results from a collaborative initiative to develop an international scale for the measurement of BCR-ABL by RQ-PCR based on deriving laboratory-specific conversion factors. SO BLOOD LA English DT Meeting Abstract CT 48th Annual Meeting of the American-Society-of-Hematology CY DEC 09-12, 2006 CL Orlando, FL SP Amer Soc Hematol C1 IMVS, Adelaide, SA, Australia. Univ Southampton, Southampton, Hants, England. Univ Heidelberg, Heidelberg, Germany. Fred Hutchinson Canc Res Ctr, Seattle, WA USA. Univ Turin, Turin, Italy. Cornell Univ, Weill Med Coll, Ithaca, NY 14853 USA. Royal Perth Hosp, Perth, WA, Australia. Peter MacCallum Canc Inst, Melbourne, Vic, Australia. Natl Taiwan Univ Hosp, Taipei, Taiwan. Hong Kong Sanatorium & Hosp, Hong Kong, Peoples R China. Tuen Mun Hosp, Tuen Mun, Hong Kong, Peoples R China. MD Anderson Canc Ctr, Houston, TX USA. NHLBI, Bethesda, MD USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2006 VL 108 IS 11 MA 737 BP 221A EP 221A PN 1 PG 1 WC Hematology SC Hematology GA 111GS UT WOS:000242440000738 ER PT J AU Blum, W Klisovic, RB Kefauver, C Johnson, A Phelps, M Dalton, JT Lucas, D Huynh, LN Liu, S Grever, MR Colevas, AD Marcucci, G Byrd, JC AF Blum, William Klisovic, Rebecca B. Kefauver, Cheryl Johnson, Amy Phelps, Mitch Dalton, James T. Lucas, David Huynh, Le Nguyen Liu, Shujun Grever, Michael R. Colevas, A. D. Marcucci, Guido Byrd, John C. TI Updated results of a phase I study of flavopiridol in acute leukemias using a novel, pharmacolkinetically derived schedule: Clinical activity including hyperacute tumor lysis syndrome (TLS), pharmacokinetics (PIC), and pharmacodynamics (PD). SO BLOOD LA English DT Meeting Abstract CT 48th Annual Meeting of the American-Society-of-Hematology CY DEC 09-12, 2006 CL Orlando, FL SP Amer Soc Hematol C1 Ohio State Univ, Columbus, OH 43210 USA. Natl Canc Inst, CTEP, Rockville, MD USA. RI Klisovic, Rebecca/E-3401-2011; Phelps, Mitch/H-3941-2013; Blum, William/E-2769-2011 OI Phelps, Mitch/0000-0002-1615-5280; NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2006 VL 108 IS 11 MA 4578 BP 224B EP 224B PN 2 PG 1 WC Hematology SC Hematology GA 111GW UT WOS:000242440401262 ER PT J AU Hsu, LL Champion, HC Campbell-Lee, SA Bivalacqua, TJ Manci, EA Diwan, BA Schimel, DM Cochard, AE Wang, X Schechter, AN Noguchi, CT Gladwin, MT AF Hsu, Lewis L. Champion, Hunter C. Campbell-Lee, Sally A. Bivalacqua, Trinity J. Manci, Elizabeth A. Diwan, Bhalchandra A. Schimel, Daniel M. Cochard, Audrey E. Wang, Xunde Schechter, Alan N. Noguchi, Constance Tom Gladwin, Mark T. TI Hemolysis in sickle cell mice causes pulmonary hypertension due to global impairment in nitric oxide bioavailability. SO BLOOD LA English DT Meeting Abstract CT 48th Annual Meeting of the American-Society-of-Hematology CY DEC 09-12, 2006 CL Orlando, FL SP Amer Soc Hematol C1 Drexel Univ, Coll Med, St Christophers Hosp Children, Marian Anderson Sickle Cell Ctr, Philadelphia, PA 19104 USA. NIH, Critical Care Med Clin Ctr, Bethesda, MD 20892 USA. Johns Hopkins Univ, Baltimore, MD USA. Univ S Alabama, Sickle Cell Pathol Unit, Mobile, AL 36688 USA. SAIC Frederick Inc, Frederick, MD USA. NCI, Basic Res Program, Frederick, MD 21701 USA. Natl Inst Neurol Disorders & Stroke, Charles River Labs & Mouse Imaging Facil, Bethesda, MD USA. NIDDK, Mol Med Branch, Bethesda, MD USA. NHLBI, Vasc Branch, Bethesda, MD 20892 USA. RI Hsu, Lewis/A-3360-2008 NR 0 TC 0 Z9 0 U1 0 U2 1 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2006 VL 108 IS 11 MA 785 BP 235A EP 235A PN 1 PG 1 WC Hematology SC Hematology GA 111GS UT WOS:000242440001045 ER PT J AU Sebastiani, P Nolan, VG Baldwin, CT Abad-Grau, MM Wang, L Adewoye, AH McMahon, LC Farrer, LA Taylor, JG Kato, GJ Gladwin, MT Steinberg, MH AF Sebastiani, Paola Nolan, Vikki G. Baldwin, Clinton T. Abad-Grau, Maria M. Wang, Ling Adewoye, Adeboye H. McMahon, Lillian C. Farrer, Lindsay A. Taylor, James G. Kato, Gregory J. Gladwin, Mark T. Steinberg, Martin H. TI Severity of sickle cell disease: Modeling interrelationships among hemolysis, pulmonary hypertension and risk of death. SO BLOOD LA English DT Meeting Abstract CT 48th Annual Meeting of the American-Society-of-Hematology CY DEC 09-12, 2006 CL Orlando, FL SP Amer Soc Hematol C1 Boston Univ, Sch Publ Hlth, Boston, MA 02215 USA. Boston Univ, Sch Med, Boston, MA 02118 USA. Univ Granada, Granada, Spain. NHLBI, Vasc Med Branch, Bethesda, MD 20892 USA. RI Abad Grau, Maria del Mar/B-2172-2012; Kato, Gregory/I-7615-2014 OI Abad Grau, Maria del Mar/0000-0001-8470-9719; Kato, Gregory/0000-0003-4465-3217 NR 0 TC 0 Z9 0 U1 0 U2 1 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2006 VL 108 IS 11 MA 786 BP 235A EP 236A PN 1 PG 2 WC Hematology SC Hematology GA 111GS UT WOS:000242440001046 ER PT J AU Taylor, JG Nolan, VG Kato, GJ Gladwin, M Steinberg, MH AF Taylor, James G. Nolan, Vikki G. Kato, Gregory J. Gladwin, Mark Steinberg, Martin H. TI The hyperhemolysis phenotype in sickle cell anemia: Increased risk of leg ulcers, priapism, pulmonary hypertension and death with decreased risk of vasoocclusive events. SO BLOOD LA English DT Meeting Abstract CT 48th Annual Meeting of the American-Society-of-Hematology CY DEC 09-12, 2006 CL Orlando, FL SP Amer Soc Hematol C1 NIH, NHLBI, Vasc Med Branch, Bethesda, MD 20892 USA. Boston Univ, Sch Med, Dept Med, Boston, MA 02118 USA. NIH, Bethesda, MD 20892 USA. RI Kato, Gregory/I-7615-2014 OI Kato, Gregory/0000-0003-4465-3217 NR 0 TC 2 Z9 2 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2006 VL 108 IS 11 MA 787 BP 236A EP 236A PN 1 PG 1 WC Hematology SC Hematology GA 111GS UT WOS:000242440001047 ER PT J AU Cozen, W Eric, EA Cerhan, JR Linet, M Bernstein, L Colt, JS Davis, SS Severson, RK Martinez-Maza, O Hartge, P AF Cozen, Wendy Eric, Engels A. Cerhan, James R. Linet, Martha Bernstein, Leslie Colt, Joanne S. Davis, Scott S. Severson, Richard K. Martinez-Maza, Otoniel Hartge, Patricia TI Childhood crowding, atopy and risk of non-Hodgkin lymphoma. SO BLOOD LA English DT Meeting Abstract CT 48th Annual Meeting of the American-Society-of-Hematology CY DEC 09-12, 2006 CL Orlando, FL SP Amer Soc Hematol C1 Univ So California, Keck Sch Med, Los Angeles, CA USA. Natl Canc Inst, Div Canc Epidemiol & Genet, Dept Hlth & Human Serv, Bethesda, MD USA. Mayo Clin, Dept Hlth Sci Res, Rochester, MN USA. Fred Hutchinson Canc Ctr, Dept Hlth Sci Res, Seattle, WA USA. Karmanos Canc Ins, Dept Family Med, Detroit, MI USA. Univ Calif Los Angeles, David Geffen Sch Med, Immunol & Mol Genet, Los Angeles, CA USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2006 VL 108 IS 11 MA 4648 BP 243B EP 243B PN 2 PG 1 WC Hematology SC Hematology GA 111GW UT WOS:000242440401332 ER PT J AU Geyer, SM Morton, LM Habermann, TM Allmer, C Davis, S Cozen, W Severson, IK Lynch, CF Wang, S Maurer, MJ Hartge, P Cerhan, JR AF Geyer, Susan M. Morton, Lindsay M. Habermann, Thomas M. Allmer, Cristine Davis, Scott Cozen, Wendy Severson, Iiichard K. Lynch, Charles F. Wang, Sophia Maurer, Matthew J. Hartge, Patricia Cerhan, James R. TI Smoking, obesity and overall survival in non-Hodgkin lymphoma (NHL): A population-based study. SO BLOOD LA English DT Meeting Abstract CT 48th Annual Meeting of the American-Society-of-Hematology CY DEC 09-12, 2006 CL Orlando, FL SP Amer Soc Hematol C1 Mayo Clin, Coll Med, Rochester, MN USA. Natl Canc Inst, Rockville, MD USA. Fred Hutchinson Canc Res Ctr, Seattle, WA 98104 USA. Univ So California, Los Angeles, CA USA. Wayne State Univ, Detroit, MI USA. Univ Iowa, Iowa City, IA USA. RI Geyer, Susan/E-3112-2011 NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2006 VL 108 IS 11 MA 4649 BP 243B EP 243B PN 2 PG 1 WC Hematology SC Hematology GA 111GW UT WOS:000242440401333 ER PT J AU Roberts, RA Rimsza, LM Staudt, L Rosenwald, A Chan, WC Dave, S Gascoyne, RD Connors, JM Smeland, EB Muller-Hermelink, HK Campo, E Jaffe, ES Wilson, W Tan, BK Fisher, RI Grogan, TM Miller, TP AF Roberts, Robin A. Rimsza, Lisa M. Staudt, Louis Rosenwald, Andreas Chan, Wing-Chung Dave, Sandeep Gascoyne, Randy D. Connors, Joseph M. Smeland, Erlend B. Muller-Hermelink, H. K. Campo, Elias Jaffe, Elaine S. Wilson, Wyndham Tan, Bruce K. Fisher, Richard I. Grogan, Thomas M. Miller, Thomas P. TI Gene expression differences between low and high stage diffuse large B cell lymphoma (DLBCL). SO BLOOD LA English DT Meeting Abstract CT 48th Annual Meeting of the American-Society-of-Hematology CY DEC 09-12, 2006 CL Orlando, FL SP Amer Soc Hematol C1 Univ Arizona, Tucson, AZ USA. Arizona Canc Ctr, Tucson, AZ USA. Univ Wurzburg, Wurzburg, Germany. Univ Nebraska, Omaha, NE 68182 USA. NCI, Metab Branch, Bethesda, MD 20892 USA. Univ Rochester, James P Wilmot Canc Ctr, Rochester, NY USA. BC Canc Agcy, Vancouver, BC, Canada. Norwegian Radium Hosp, Oslo, Norway. Univ Barcelona, Barcelona, Spain. NCI, Bethesda, MD 20892 USA. NR 0 TC 2 Z9 2 U1 0 U2 1 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2006 VL 108 IS 11 MA 809 BP 243A EP 243A PG 1 WC Hematology SC Hematology GA 111GS UT WOS:000242440001069 ER PT J AU Young, KH Leory, K Moller, MB Sanchez-Beato, M Colleoni, GWB Kerbauy, FR Koduru, PPK Haioun, C Gaulard, P Piris, MA Campo, E Delabie, J Gascoyne, RD Rosenwald, A Ott, G Huang, J Braziel, RM Jaffe, ES Staudt, LM Wilson, WH Kanehira, K Rehrauer, WM Eickhoff, JC Kahl, BS Malter, JS Chan, WC Wisenburger, DD Greiner, TC AF Young, Ken H. Leory, Karen Moller, Michael B. Sanchez-Beato, Margarita Colleoni, Gisele W. B. Kerbauy, Fabio R. Koduru, Prasad P. K. Haioun, Corinne Gaulard, Philippe Piris, Miguel A. Campo, Elias Delabie, Jan Gascoyne, Randy D. Rosenwald, Andreas Ott, German Huang, James Braziel, Rita M. Jaffe, Elaine S. Staudt, Louis M. Wilson, Wyndham H. Kanehira, Kazunori Rehrauer, William M. Eickhoff, Jens C. Kahl, Brad S. Malter, James S. Chan, Wing-Chung Wisenburger, Dennis D. Greiner, Timothy C. TI Structural profiles of p53 gene mutations predict clinical outcome in diffuse large B-cell lymphoma: An International Collaborative study. SO BLOOD LA English DT Meeting Abstract CT 48th Annual Meeting of the American-Society-of-Hematology CY DEC 09-12, 2006 CL Orlando, FL SP Amer Soc Hematol C1 Univ Wisconsin, Sch Med, Dept Pathol & Lab Med, Madison, WI USA. Univ Wisconsin, Dept Hematol, Madison, WI USA. Univ Wisconsin, Dept Bioinformat, Madison, WI USA. Hop Henri Mondor, Paris, France. Odense Univ Hosp, DK-5000 Odense, Denmark. CNIO, Spanish Natl Canc Inst, Madrid, Spain. Univ Fed Sao Paulo, Sao Paulo, Brazil. N Shore Univ Hosp, New York, NY USA. Univ Barcelona, E-08007 Barcelona, Spain. Norwegian Radium Hosp, Oslo, Norway. Univ Wurzburg, D-97070 Wurzburg, Germany. Oregon Hlth Sci Univ, Portland, OR 97201 USA. Natl Canc Inst, Bethesda, MD USA. Univ Nebraska Med Ctr, Omaha, NE USA. RI Moller, Michael/G-8340-2016 OI Moller, Michael/0000-0003-2041-3630 NR 0 TC 0 Z9 0 U1 1 U2 1 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2006 VL 108 IS 11 MA 811 BP 243A EP 244A PN 1 PG 2 WC Hematology SC Hematology GA 111GS UT WOS:000242440001071 ER PT J AU Cerhan, JR Wang, S Maurer, MJ Ansell, SM Geyer, SM Cozen, W Morton, LM Davis, S Severson, RK Rothman, N Lynch, CF Chanock, S Habermann, TM Hartge, P AF Cerhan, James R. Wang, Sophia Maurer, Matthew J. Ansell, Stephen M. Geyer, Susan M. Cozen, Wendy Morton, Lindsay M. Davis, Scott Severson, Richard K. Rothman, Nathaniel Lynch, Charles F. Chanock, Stephen Habermann, Thomas M. Hartge, Patricia TI Cytokine gene polymorphisms and overall survival in follicular lymphoma: Results from a large population-based study. SO BLOOD LA English DT Meeting Abstract CT 48th Annual Meeting of the American-Society-of-Hematology CY DEC 09-12, 2006 CL Orlando, FL SP Amer Soc Hematol C1 Mayo Clin Coll Med, Rochester, MN USA. Natl Canc Inst, Rockville, MD USA. Univ So Calif, Los Angeles, CA USA. Fred Hutchinson Canc Res Ctr, Seattle, WA 98104 USA. Wayne State Univ, Detroit, MI 48202 USA. Univ Iowa, Iowa City, IA 52242 USA. RI Geyer, Susan/E-3112-2011 NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2006 VL 108 IS 11 MA 820 BP 246A EP 246A PN 1 PG 1 WC Hematology SC Hematology GA 111GS UT WOS:000242440001080 ER PT J AU Rizzatti, EG Mora-Jensen, H Lai, R Daibata, M White, T Dunleavy, K Wilson, W Wiestner, A AF Rizzatti, Edgar G. Mora-Jensen, Helena Lai, Raymond Daibata, Masanori White, Therese Dunleavy, Kieron Wilson, Wyndham Wiestner, Adrian TI Bortezomib induces an antioxidant and ER-stress response gene expression signature in mantle cell lymphoma: Implications for response prediction and optimized chemotherapy regimens. SO BLOOD LA English DT Meeting Abstract CT 48th Annual Meeting of the American-Society-of-Hematology CY DEC 09-12, 2006 CL Orlando, FL SP Amer Soc Hematol C1 NHLBI, Hematol Branch, Bethesda, MD 20892 USA. NCI, Ctr Canc Res, Bethesda, MD 20892 USA. Univ Alberta, Dept Lab Med & Pathol, Edmonton, AB, Canada. Kochi Med Sch, Dept Hematol & Respirat Med, Kochi, Japan. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2006 VL 108 IS 11 MA 830 BP 249A EP 249A PN 1 PG 1 WC Hematology SC Hematology GA 111GS UT WOS:000242440001090 ER PT J AU Sloand, EM Rezvani, K Yong, A Douek, D Kurlander, R Price, D Barrett, J Young, NS AF Sloand, Elaine M. Rezvani, Katayoun Yong, Agnes Douek, Daniel Kurlander, Roger Price, David Barrett, John Young, Neal S. TI Cytotoxic CD8 T cell immune responses to Wilms tumor protein (WT-1) characterizes immunosuppression-responsive myelodysplasia (MDS). SO BLOOD LA English DT Meeting Abstract CT 48th Annual Meeting of the American-Society-of-Hematology CY DEC 09-12, 2006 CL Orlando, FL SP Amer Soc Hematol C1 NIH, Hematol Branch, Bethesda, MD 20892 USA. NIH, Vaccine Res Ctr, Bethesda, MD 20892 USA. RI Price, David/C-7876-2013 OI Price, David/0000-0001-9416-2737 NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2006 VL 108 IS 11 MA 849 BP 255A EP 255A PG 1 WC Hematology SC Hematology GA 111GS UT WOS:000242440001109 ER PT J AU Adams, GB Alley, IR Chabner, KT Chung, UI Marsters, ES Weinstein, LS Kronenberg, HM Scadden, DT AF Adams, Gregor B. Alley, Ian R. Chabner, Karissa T. Chung, Ung-il Marsters, Emily S. Weinstein, Lee S. Kronenberg, Henry M. Scadden, David T. TI Hematopoietic stem cell engraftment in bone marrow is dependent upon G(s)alpha. SO BLOOD LA English DT Meeting Abstract CT 48th Annual Meeting of the American-Society-of-Hematology CY DEC 09-12, 2006 CL Orlando, FL SP Amer Soc Hematol C1 Massachusetts Gen Hosp, Ctr Regenerat Med, Boston, MA 02114 USA. Massachusetts Gen Hosp, Endocrine Unit, Boston, MA 02114 USA. Tokyo Univ Hosp, Div Tissue Engn, Tokyo 113, Japan. NIDDK, Bethesda, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2006 VL 108 IS 11 MA 857 BP 257A EP 257A PN 1 PG 1 WC Hematology SC Hematology GA 111GS UT WOS:000242440001117 ER PT J AU Nemeth, M Yang, YZ Bodine, D AF Nemeth, Michael Yang, Yingzi Bodine, David TI Canonical and non-canonical Wnt signaling regulate the balance between HSC self-renewal and differentiation. SO BLOOD LA English DT Meeting Abstract CT 48th Annual Meeting of the American-Society-of-Hematology CY DEC 09-12, 2006 CL Orlando, FL SP Amer Soc Hematol C1 NIH, NHGRI, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2006 VL 108 IS 11 MA 862 BP 258A EP 259A PN 1 PG 2 WC Hematology SC Hematology GA 111GS UT WOS:000242440001122 ER PT J AU Melenhorst, JJ Scheinberg, P Ambrozak, DR Hensel, NF Douek, DC Price, DA Barrett, AJ AF Melenhorst, J. Joseph Scheinberg, Phillip Ambrozak, David R. Hensel, Nancy F. Douek, Daniel C. Price, David A. Barrett, A. John TI Acquisition of FOXP3 expression by human effector CD4+T cells is a natural consequence of antigen recognition. SO BLOOD LA English DT Meeting Abstract CT 48th Annual Meeting of the American-Society-of-Hematology CY DEC 09-12, 2006 CL Orlando, FL SP Amer Soc Hematol C1 NIH, Hematol Natl Heart Lung & Blood Inst, Bethesda, MD 20892 USA. NIH, NIAID, Vaccine Res Ctr, Immunol Lab,Human Immunol Sect, Bethesda, MD 20892 USA. RI Price, David/C-7876-2013 OI Price, David/0000-0001-9416-2737 NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2006 VL 108 IS 11 MA 870 BP 261A EP 261A PN 1 PG 1 WC Hematology SC Hematology GA 111GS UT WOS:000242440001130 ER PT J AU Sportes, C Krumlauf, M Babb, R Foruraghi, L Daub, J Avila, D Chow, C Zhang, H Chua, K Fry, T Memon, S Hakim, F Fleisher, T Brown, M Engel, J Buffet, R Morre, M Gress, R Mackall, C AF Sportes, Claude Krumlauf, Michael Babb, Rebecca Foruraghi, Ladan Daub, Janine Avila, Daniele Chow, Catherine Zhang, Hua Chua, Kevin Fry, Terry Memon, Sarfraz Hakim, Frances Fleisher, Thomas Brown, Margaret Engel, Julie Buffet, Renaud Morre, Michel Gress, Ronald Mackall, Crystal TI IL7 administration in humans results in preferential expansion of naive and memory CD4+ & CD8+T cells with a relative decrease in regulatory T-cells (T-regs). SO BLOOD LA English DT Meeting Abstract CT 48th Annual Meeting of the American-Society-of-Hematology CY DEC 09-12, 2006 CL Orlando, FL SP Amer Soc Hematol C1 Natl Canc Inst, Expt Transplantat & Immunol Branch, Bethesda, MD USA. Natl Canc Inst, Pediat Branch, Bethesda, MD USA. NIH, Ctr Clin, Bethesda, MD 20892 USA. Cytheris Inc, Rockville, MD USA. RI Memon, Sarfraz/E-1198-2013 NR 0 TC 0 Z9 0 U1 0 U2 1 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2006 VL 108 IS 11 MA 871 BP 261A EP 261A PN 1 PG 1 WC Hematology SC Hematology GA 111GS UT WOS:000242440001131 ER PT J AU Lundqvist, A Greeneltch, K Berg, M Srivastava, S Harashima, N Yokoyarna, H Smith, A Abrams, S Childs, R AF Lundqvist, Andreas Greeneltch, Krist Berg, Maria Srivastava, Shivani Harashima, Nanae Yokoyarna, Hisayuki Smith, Aleah Abrams, Scott Childs, Richard TI In vitro and in vivo sensitization of malignant cells to autologous natural killer cell cytotoxicity following exposure to bortezomib. SO BLOOD LA English DT Meeting Abstract CT 48th Annual Meeting of the American-Society-of-Hematology CY DEC 09-12, 2006 CL Orlando, FL SP Amer Soc Hematol C1 NIH, NHLBI, Hematol Branch, Bethesda, MD 20892 USA. NIH, NCI, Tumor Immunol & Biol Lab, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2006 VL 108 IS 11 MA 925 BP 277A EP 277A PG 1 WC Hematology SC Hematology GA 111GS UT WOS:000242440001185 ER PT J AU Zhou, JX Lee, CH Qi, CF Maghashfar, Z Zhao, M Morse, HC AF Zhou, Jeff X. Lee, Chang-Hoon Qi, Chen-Feng Maghashfar, Zohreh Zhao, Ming Morse, Herbert C. TI Transcriptional activation of Mdm2 in germinal-center B cells is induced by IRF8. SO BLOOD LA English DT Meeting Abstract CT 48th Annual Meeting of the American-Society-of-Hematology CY DEC 09-12, 2006 CL Orlando, FL SP Amer Soc Hematol C1 NIH, NIAID, Immunopathol Lab, Rockville, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2006 VL 108 IS 11 MA 932 BP 278A EP 278A PN 1 PG 1 WC Hematology SC Hematology GA 111GS UT WOS:000242440001192 ER PT J AU Bolan, C Ronquillo, J Yau, YY Wesley, R Cecco, S Alvandi, F Reynolds, J Byrne, P Matthews, C Cantilena, C Collins, M Rehak, N Leitman, S AF Bolan, Charles Ronquillo, Jeremiah Yau, Yu Ying Wesley, Robert Cecco, Stacey Alvandi, Firoozeh Reynolds, James Byrne, Phyllis Matthews, Cynthia Cantilena, Cathy Collins, Michael Rehak, Nadja Leitman, Susan TI Citrate effects and bone mineral density (BMD) in serial long-term apheresis donors. SO BLOOD LA English DT Meeting Abstract CT 48th Annual Meeting of the American-Society-of-Hematology CY DEC 09-12, 2006 CL Orlando, FL SP Amer Soc Hematol C1 Ctr Clin, Bethesda, MD USA. Lab Med, Bethesda, MD USA. NIH, NIDCR, Bethesda, MD USA. NR 0 TC 1 Z9 1 U1 0 U2 1 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2006 VL 108 IS 11 MA 953 BP 284A EP 285A PN 1 PG 2 WC Hematology SC Hematology GA 111GS UT WOS:000242440001213 ER PT J AU Rizzatti, FG Stroncek, D Sibmooh, N Schechter, AN AF Rizzatti, Fabiola G. Stroncek, David Sibmooh, Nathawut Schechter, Alan N. TI Effect of storage on levels of nitric oxide derivatives in blood components. SO BLOOD LA English DT Meeting Abstract CT 48th Annual Meeting of the American-Society-of-Hematology CY DEC 09-12, 2006 CL Orlando, FL SP Amer Soc Hematol C1 Natl Inst Hlth, NIDDK, Mol Med Branch, Bethesda, MD USA. Ctr Clin, NIH, Dept Transfus Med, Immunogenet Sect, Bethesda, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2006 VL 108 IS 11 MA 950 BP 284A EP 284A PN 1 PG 1 WC Hematology SC Hematology GA 111GS UT WOS:000242440001210 ER PT J AU Young, NS Antonioli, E Rotoli, B Schrezenmeier, H Schubert, J Urbano-Ispizua, A Coyle, L de Castro, C Fu, CL Maciejewski, JP Mojcik, CF Rother, RP Hillmen, P AF Young, Neal S. Antonioli, Elisabetta Rotoli, Bruno Schrezenmeier, Hubert Schubert, Joerg Urbano-Ispizua, Alvaro Coyle, Luke de Castro, Carlos Fu, Chieh-Lin Maciejewski, Jaroslaw P. Mojcik, Christopher F. Rother, Russell P. Hillmen, Peter TI Safety and efficacy of the terminal complement inhibitor eculizumab in patients with paroxysmal nocturnal hemoglobinuria: Interim shepherd phase III clinical study. SO BLOOD LA English DT Meeting Abstract CT 48th Annual Meeting of the American-Society-of-Hematology CY DEC 09-12, 2006 CL Orlando, FL SP Amer Soc Hematol C1 NIH, NHLBI, Bethesda, MD USA. Azienda Ospedaliera Univ Careggi, Florence, Italy. Univ Studi Napoli, Naples, Italy. Inst Klin Transfusionmed & Immungenet Helmholtzst, Helmholtzstr, Germany. Univ Saarland, Sch Med, D-6650 Homburg, Germany. Clin Hosp Prov, Barcelona, Spain. Royal N Shore Hosp, St Leonards, NSW 2065, Australia. Duke Univ, Med Ctr, Durham, NC USA. Cleveland Clin Florida, Weston, FL USA. Cleveland Clin Fdn, Cleveland, OH 44195 USA. Alexion Pharmaceut Inc, Chester, CT USA. Leeds Gen Infirm, Leeds, W Yorkshire, England. NR 0 TC 4 Z9 4 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2006 VL 108 IS 11 MA 971 BP 290A EP 290A PN 1 PG 1 WC Hematology SC Hematology GA 111GS UT WOS:000242440001231 ER PT J AU Hill, A Reid, SA Rother, RP Gladwin, MT Collinson, PO Gaze, DC Lowe, A Guthrie, A Sivananthan, MU Hillmen, P AF Hill, Anita Reid, Scott A. Rother, Russell P. Gladwin, Mark T. Collinson, Paul O. Gaze, David C. Lowe, Angela Guthrie, Ashley Sivananthan, Mohan U. Hillmen, Peter TI High definition contrast-enhanced MR imaging in paroxysmal nocturnal hemoglobinuria (PNH) suggests a high frequency of subelinical thrombosis. SO BLOOD LA English DT Meeting Abstract CT 48th Annual Meeting of the American-Society-of-Hematology CY DEC 09-12, 2006 CL Orlando, FL SP Amer Soc Hematol C1 Leeds Gen Infirm, Dept Haematol, Leeds, W Yorkshire, England. Univ Leeds, Leeds, W Yorkshire, England. Alexion Pharmaceut Inc, Dept Res, Chester, CT USA. Nuffield Hosp, Dept Radiol, Leeds, W Yorkshire, England. St George Hosp, Dept Chem Pathol, London, England. NIH, NHLBI, Vasc Therapeut Sect, Bethesda, MD USA. NR 0 TC 2 Z9 2 U1 0 U2 1 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2006 VL 108 IS 11 MA 979 BP 292A EP 292A PN 1 PG 1 WC Hematology SC Hematology GA 111GS UT WOS:000242440001239 ER PT J AU Regal, JA Calado, RT Shenoy, A Lansdorp, PM Young, NS AF Regal, Joshua A. Calado, Rodrigo T. Shenoy, Aarthi Lansdorp, Peter M. Young, Neal S. TI A large mennonite family with a novel K570N TERT gene mutation: Association with a clinical spectrum of Bone Marrow Failure, acute myeloid leukemia, and acute liver failure. SO BLOOD LA English DT Meeting Abstract CT 48th Annual Meeting of the American-Society-of-Hematology CY DEC 09-12, 2006 CL Orlando, FL SP Amer Soc Hematol C1 NIH, NHLBI, Hematol Branch, Bethesda, MD 20892 USA. Univ British Columbia, Dept Med, Vancouver, BC V5Z 1M9, Canada. RI Calado, Rodrigo/G-2619-2011 NR 0 TC 1 Z9 1 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2006 VL 108 IS 11 MA 992 BP 296A EP 296A PN 1 PG 1 WC Hematology SC Hematology GA 111GS UT WOS:000242440001252 ER PT J AU Al-Rahawan, MM Alter, BP Bryant, BJ Elghetany, MT AF Al-Rahawan, Mohamad M. Alter, Blanche P. Bryant, Barbara J. Elghetany, M. Tarek TI Predictive markers of myelodysplastic syndrome in the bone marrow of patients with Fanconi Anemia. SO BLOOD LA English DT Meeting Abstract CT 48th Annual Meeting of the American-Society-of-Hematology CY DEC 09-12, 2006 CL Orlando, FL SP Amer Soc Hematol C1 Natl Canc Inst, Div Canc Epidemiol & Genet, Clin Genet Branch, Rockville, MD USA. Childrens Natl Med Ctr, Washington, DC 20010 USA. Natl Inst Hlth, Dept Transfus Med, Bethesda, MD USA. Univ Texas, Med Branch, Dept Pathol, Galveston, TX 77550 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2006 VL 108 IS 11 MA 994 BP 297A EP 297A PN 1 PG 1 WC Hematology SC Hematology GA 111GS UT WOS:000242440001254 ER PT J AU Giri, N Khaghani, S Alter, BP AF Giri, Neelam Khaghani, Sara Alter, Blanche P. TI Immunoglobulin and lymphocyte subset abnormalities in patients with Fanconi Anemia and dyskeratosis congenita. SO BLOOD LA English DT Meeting Abstract CT 48th Annual Meeting of the American-Society-of-Hematology CY DEC 09-12, 2006 CL Orlando, FL SP Amer Soc Hematol C1 NIH, Natl Canc Inst, Div Canc Epidemiol & Genet, Clin Genet Branch, Rockville, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2006 VL 108 IS 11 MA 996 BP 297A EP 297A PG 1 WC Hematology SC Hematology GA 111GS UT WOS:000242440001256 ER PT J AU Rosenberg, PS Alter, BP Ebell, W AF Rosenberg, Philip S. Alter, Blanche P. Ebell, Wolfram TI Cancer risks in Fanconi Anemia: Experience of the German Fanconi Anemia (GEFA) SO BLOOD LA English DT Meeting Abstract CT 48th Annual Meeting of the American-Society-of-Hematology CY DEC 09-12, 2006 CL Orlando, FL SP Amer Soc Hematol C1 Natl Canc Inst, Div Canc Epidemiol & Genet, Biostatistics Branch, Bethesda, MD USA. Natl Canc Inst, Div Canc Epidemiol & Genet, Clin Genet Branch, Bethesda, MD USA. Humboldt Univ, Childrens Hosp, Charite Hosp, Campus Virchow Klinikum, Berlin, Germany. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2006 VL 108 IS 11 MA 995 BP 297A EP 297A PN 1 PG 1 WC Hematology SC Hematology GA 111GS UT WOS:000242440001255 ER PT J AU Solomou, EE Gibellini, F Chanock, SJ Malide, D Berg, M Visconte, V Luppi, M Childs, R Green, S Young, NS AF Solomou, Elena E. Gibellini, Federica Chanock, Stephen J. Malide, Daniela Berg, Maria Visconte, Valeria Luppi, Mario Childs, Richard Green, Spencer Young, Neal S. TI Perforin gene mutations in patients with acquired aplastic anemia. SO BLOOD LA English DT Meeting Abstract CT 48th Annual Meeting of the American-Society-of-Hematology CY DEC 09-12, 2006 CL Orlando, FL SP Amer Soc Hematol C1 NIH, NHLBI, Hematol Branch, Bethesda, MD 20892 USA. NIH, NCI, Pediat Oncol Branch, Bethesda, MD 20892 USA. Univ Modena, I-41100 Modena, Italy. NR 0 TC 1 Z9 1 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2006 VL 108 IS 11 MA 998 BP 298A EP 298A PN 1 PG 1 WC Hematology SC Hematology GA 111GS UT WOS:000242440001258 ER PT J AU Batra, R Herndon, TM Ascensao, J Schechter, GP AF Batra, Reema Herndon, Thomas M. Ascensao, Joao Schechter, Geraldine P. TI Ribavirin-induced dysplasia. SO BLOOD LA English DT Meeting Abstract CT 48th Annual Meeting of the American-Society-of-Hematology CY DEC 09-12, 2006 CL Orlando, FL SP Amer Soc Hematol C1 Vet Affairs Med Ctr, Dept Hematol, Washington, DC 20422 USA. NHLBI, NIH, Dept Hematol, Bethesda, MD 20892 USA. NR 2 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2006 VL 108 IS 11 MA 4861 BP 300B EP 301B PN 2 PG 2 WC Hematology SC Hematology GA 111GW UT WOS:000242440401544 ER PT J AU Bussel, JB Patel, V Dunbar, C Lemery, S Tibbs, K Watts, M Magilavy, D AF Bussel, James B. Patel, Vivek Dunbar, Cynthia Lemery, Stephen Tibbs, Krista Watts, Michael Magilavy, Daniel TI GMA161 treatment of refractory ITP: Efficacy of Fc gamma-RIII blockade. SO BLOOD LA English DT Meeting Abstract CT 48th Annual Meeting of the American-Society-of-Hematology CY DEC 09-12, 2006 CL Orlando, FL SP Amer Soc Hematol C1 Weill Cornell Med Coll, Hematol Branch, New York, NY 20892 USA. NHLBI, Bethesda, MD USA. Genzyme Corp, Cambridge, MA USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2006 VL 108 IS 11 MA 1074 BP 320A EP 320A PG 1 WC Hematology SC Hematology GA 111GS UT WOS:000242440001333 ER PT J AU Nurden, AT Nurden, P Bermejo, E Washington, AV McVicar, DW AF Nurden, Alan T. Nurden, Paquita Bermejo, Emilse Washington, Anthony V. McVicar, Daniel W. TI Heterogeneity in the gray platelet syndrome: Variable expression of the TREM family member, TLT-1, in platelets of patients of two unrelated families. SO BLOOD LA English DT Meeting Abstract CT 48th Annual Meeting of the American-Society-of-Hematology CY DEC 09-12, 2006 CL Orlando, FL SP Amer Soc Hematol C1 Hop Xavier Arzonan, Plate Forme Technol Innovation biomed, Pessac, France. Univ Buenos Aires, Fac Med, Dept Bioquimica Humana, Buenos Aires, DF, Argentina. NCI Frederick, Frederick, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2006 VL 108 IS 11 MA 1101 BP 328A EP 328A PN 1 PG 1 WC Hematology SC Hematology GA 111GS UT WOS:000242440001360 ER PT J AU Lee, E Xu, XL Munson, P Cooper, R Raghavachari, N White, T Marti, GE Wilson, WH Wiestner, A AF Lee, Elinor Xu, Xiuli Munson, Peter Cooper, Ronald Raghavachari, Nalini White, Therese Marti, Gerald E. Wilson, Wyndham H. Wiestner, Adrian TI Rituximab induces an interferon gene expression signature in patients with CLL. SO BLOOD LA English DT Meeting Abstract CT 48th Annual Meeting of the American-Society-of-Hematology CY DEC 09-12, 2006 CL Orlando, FL SP Amer Soc Hematol C1 NIH, NHLBI, Hematol Branch, Bethesda, MD USA. NIH, NHLBI, Bethesda, MD USA. NIH, NCI, Ctr Canc Res, Bethesda, MD USA. US FDA, Ctr Biol Evaluat & Res, Bethesda, MD USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2006 VL 108 IS 11 MA 4988 BP 335B EP 335B PN 2 PG 1 WC Hematology SC Hematology GA 111GW UT WOS:000242440402107 ER PT J AU Visconte, V Solomou, EE Keyvanfar, K Green, S Selleri, C Young, NS AF Visconte, Valeria Solomou, Elena E. Keyvanfar, Keyvan Green, Spencer Selleri, Carmine Young, Neal S. TI Increased expression of the signaling lymphocyte-activation molecule (mSLAM) in patients with paroxysmal nocturnal hemoglobinuria (PNH). SO BLOOD LA English DT Meeting Abstract CT 48th Annual Meeting of the American-Society-of-Hematology CY DEC 09-12, 2006 CL Orlando, FL SP Amer Soc Hematol C1 NHLBI, NIH, Hematol Branch, Bethesda, MD USA. Univ Naples Federico II, Dept Biochem & Med Biotechnol, Naples, Italy. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2006 VL 108 IS 11 MA 1139 BP 337A EP 338A PN 1 PG 2 WC Hematology SC Hematology GA 111GS UT WOS:000242440001398 ER PT J AU Wu, T Kim, HJ Sellers, SE Meade, KE Agricola, BA Metzger, ME Kato, I Donahue, RE Dunbar, CE Tisdale, JF AF Wu, Tong Kim, Hyeoung Joon Sellers, Stephanie E. Meade, Kristin E. Agricola, Brian A. Metzger, Mark E. Kato, Ikunoshin Donahue, Robert E. Dunbar, Cynthia E. Tisdale, John F. TI Prolonged high-level detection of retrovirally marked hematopoietic cells in nonhuman primates after transduction of CD34+progenitors using clinically feasible methods. SO BLOOD LA English DT Meeting Abstract CT 48th Annual Meeting of the American-Society-of-Hematology CY DEC 09-12, 2006 CL Orlando, FL SP Amer Soc Hematol C1 NHLBI, Hematol Branch, Bethesda, MD USA. NIDDK, Natl Inst Hlth, Molecular & Clin Hematol, Bethesda, MD USA. Takara Shuzo Co Ltd, Biotechnol Res Labs, Shiga, Japan. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2006 VL 108 IS 11 MA 1137 BP 337A EP 337A PN 1 PG 1 WC Hematology SC Hematology GA 111GS UT WOS:000242440001396 ER PT J AU Landgren, O Fears, TR Turesson, I Bjorkholm, M Kristinsson, SY Gridley, G Caporaso, NE AF Landgren, Ola Fears, Thomas R. Turesson, Ingemar Bjorkholm, Magnus Kristinsson, Sigurdur Y. Gridley, Gloria Caporaso, Neil E. TI Patterns of venous thromboembolism (VTE) following monoclonal gammopathy of undetermined significance (MGUS) and multiple myeloma (MM) among 4 million US veterans. SO BLOOD LA English DT Meeting Abstract CT 48th Annual Meeting of the American-Society-of-Hematology CY DEC 09-12, 2006 CL Orlando, FL SP Amer Soc Hematol C1 NIH, Natl Canc Inst, Bethesda, MD 20892 USA. Lund Univ, Dept Med, Malmo, Sweden. Karolinska Inst, Hematol Ctr, Stockholm, Sweden. RI Kristinsson, Sigurdur /M-2910-2015 OI Kristinsson, Sigurdur /0000-0002-4964-7476 NR 0 TC 0 Z9 0 U1 0 U2 1 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2006 VL 108 IS 11 MA 4998 BP 338B EP 338B PN 2 PG 1 WC Hematology SC Hematology GA 111GW UT WOS:000242440402117 ER PT J AU Solomon, EE Visconte, V Gibellini, F Young, NS AF Solomon, Elena E. Visconte, Valeria Gibellini, Federica Young, Neal S. TI SAP (SH2D1A), the immunomodulator deficient in X-linked lymphoproliferative syndrome (XLP), is profoundly recreased in aplastic anemia: An immunologic link between constitutional and acquired bone marrow failure. SO BLOOD LA English DT Meeting Abstract CT 48th Annual Meeting of the American-Society-of-Hematology CY DEC 09-12, 2006 CL Orlando, FL SP Amer Soc Hematol C1 NHLBI, NIH, Hematol Branch, Bethesda, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2006 VL 108 IS 11 MA 1141 BP 338A EP 338A PN 1 PG 1 WC Hematology SC Hematology GA 111GS UT WOS:000242440001400 ER PT J AU Aerbajinai, W Zhu, JQ Gao, P Chin, K Rodgers, GP AF Aerbajinai, Wulin Zhu, Jianqiong Gao, Peter Chin, Kyung Rodgers, Griffin P. TI Thalidomide induces gamma-globin gene expression in adult primary erythroid cells through increased intracellular reactive oxygen species mediated activation of p38 MAPK signal pathway. SO BLOOD LA English DT Meeting Abstract CT 48th Annual Meeting of the American-Society-of-Hematology CY DEC 09-12, 2006 CL Orlando, FL SP Amer Soc Hematol C1 NIDDK, Natl Inst Hlth, Mol & Clin Hematol Branch, Bethesda, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2006 VL 108 IS 11 MA 1192 BP 351A EP 351A PN 1 PG 1 WC Hematology SC Hematology GA 111GS UT WOS:000242440001451 ER PT J AU Rogers, HM Yu, XB Noguchi, CT AF Rogers, Heather M. Yu, Xiaobing Noguchi, Constance Tom TI SCL/TAL1 regulates erythropoietin receptor expression. SO BLOOD LA English DT Meeting Abstract CT 48th Annual Meeting of the American-Society-of-Hematology CY DEC 09-12, 2006 CL Orlando, FL SP Amer Soc Hematol C1 Johns Hopkins Univ, Inst Cell Engn, Baltimore, MD USA. NIDDK, Natl Inst Hlth, Bethesda, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2006 VL 108 IS 11 MA 1195 BP 352A EP 352A PN 1 PG 1 WC Hematology SC Hematology GA 111GS UT WOS:000242440001454 ER PT J AU Kato, GJ Zeneng, W Taylor, JG Machado, RF Blackwelder, WC Gladwin, MT Hazen, SL AF Kato, Gregory J. Zeneng, Wang Taylor, James G. Machado, Roberto F. Blackwelder, William C. Gladwin, Mark T. Hazen, Stanley L. TI Arginine metabolite profiling in sickle cell disease: Abnormal levels and correlations with pulmonary hypertension, desaturation, hemolysis and organ dysfunction. SO BLOOD LA English DT Meeting Abstract CT 48th Annual Meeting of the American-Society-of-Hematology CY DEC 09-12, 2006 CL Orlando, FL SP Amer Soc Hematol C1 Natl Inst Hlth, NHLBI, Vasc Med Branch, Bethesda, MD USA. NIH, Ctr Clin, Dept Crit Care Med, Bethesda, MD 20892 USA. RI Kato, Gregory/I-7615-2014 OI Kato, Gregory/0000-0003-4465-3217 NR 0 TC 0 Z9 0 U1 0 U2 1 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2006 VL 108 IS 11 MA 1205 BP 355A EP 355A PN 1 PG 1 WC Hematology SC Hematology GA 111GS UT WOS:000242440001464 ER PT J AU Taylor, JG Ackah, D Cobb, C Castro, O Kato, GJ Chanock, SJ Gladwin, M AF Taylor, James G. Ackah, Diana Cobb, Crystal Castro, Oswaldo Kato, Gregory J. Chanock, Stephen Jacob Gladwin, Mark TI Mutations and polymorphisms influencing hemolysis in hemoglobin genes and risk of pulmonary hypertension in sickle cell disease: Effect of hemoglobin SC. SO BLOOD LA English DT Meeting Abstract CT 48th Annual Meeting of the American-Society-of-Hematology CY DEC 09-12, 2006 CL Orlando, FL SP Amer Soc Hematol C1 NIH, Bethesda, MD 20892 USA. NHLBI, Bethesda, MD 20892 USA. Howard Univ, Ctr Sick Cell Dis, Washington, DC 20059 USA. NIH NCI, Sec Genom Variat, Gaithersburg, MD USA. RI Kato, Gregory/I-7615-2014 OI Kato, Gregory/0000-0003-4465-3217 NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2006 VL 108 IS 11 MA 1206 BP 355A EP 355A PN 1 PG 1 WC Hematology SC Hematology GA 111GS UT WOS:000242440001465 ER PT J AU Morris, CR Suh, J Vichinsky, EP Klings, ES Steinberg, MH Shigenaga, M Ames, BN Gladwin, MT Kato, GJ AF Morris, Claudia R. Suh, Jung Vichinsky, Elliott P. Klings, Elizabeth S. Steinberg, Martin H. Shigenaga, Mark Ames, Bruce N. Gladwin, Mark T. Kato, Gregory J. TI Oral arginine increases erythrocyte glutathione levels in sickle cell disease: Implications for pulmonary hypertension. SO BLOOD LA English DT Meeting Abstract CT 48th Annual Meeting of the American-Society-of-Hematology CY DEC 09-12, 2006 CL Orlando, FL SP Amer Soc Hematol C1 Childrens Hosp, Cent Res, Dept Emergency Med Hematol Oncol, Oakland, CA 94609 USA. Boston Univ, Sch Med, Dept Med, Boston, MA 02118 USA. NIH, Bethesda, MD USA. RI Kato, Gregory/I-7615-2014 OI Kato, Gregory/0000-0003-4465-3217 NR 0 TC 0 Z9 0 U1 0 U2 2 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 2021 L ST NW, SUITE 900, WASHINGTON, DC 20036 USA SN 0006-4971 EI 1528-0020 J9 BLOOD JI Blood PD NOV 16 PY 2006 VL 108 IS 11 MA 1208 BP 356A EP 356A PN 1 PG 1 WC Hematology SC Hematology GA 111GS UT WOS:000242440001467 ER PT J AU Morris, CR Suh, J Vichinsky, EP Klings, ES Steinberg, MH Shigenaga, M Ames, BN Gladwin, MT Kato, GJ AF Morris, Claudia R. Suh, Jung Vichinsky, Elliott P. Klings, Elizabeth S. Steinberg, Martin H. Shigenaga, Mark Ames, Bruce N. Gladwin, Mark T. Kato, Gregory J. TI Oral arginine increases erythrocyte glutathione levels in sickle cell disease: Implications for pulmonary hypertension. SO BLOOD LA English DT Meeting Abstract CT 48th Annual Meeting of the American-Society-of-Hematology CY DEC 09-12, 2006 CL Orlando, FL SP Amer Soc Hematol C1 Wake Forest Univ, Winston Salem, NC 27109 USA. Natl Heart & Lung Inst, Clin Ctr, Bethesda, MD USA. Wake Forest Univ, Winston Salem, NC 27109 USA. RI Kato, Gregory/I-7615-2014 OI Kato, Gregory/0000-0003-4465-3217 NR 0 TC 0 Z9 0 U1 0 U2 2 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 2021 L ST NW, SUITE 900, WASHINGTON, DC 20036 USA SN 0006-4971 EI 1528-0020 J9 BLOOD JI Blood PD NOV 16 PY 2006 VL 108 IS 11 MA 1208 BP 356A EP 356A PN 1 PG 1 WC Hematology SC Hematology GA 111GS UT WOS:000242440001468 ER PT J AU Asakura, T Yang, JS Chen, QK Evans, G Abdulmalik, O AF Asakura, Toshio Yang, Jisheng Chen, Qiukan Evans, Greg Abdulmalik, Osheiza TI New approach for finding novel antisickling agents at the NIHNHLBI sickle cell disease reference laboratory. SO BLOOD LA English DT Meeting Abstract CT 48th Annual Meeting of the American-Society-of-Hematology CY DEC 09-12, 2006 CL Orlando, FL SP Amer Soc Hematol C1 Childrens Hosp Philadelphia, Philadelphia, PA 19104 USA. NIH, NHLBI, Sickle Cell Dis Res Grp, Bethesda, MD USA. NR 0 TC 0 Z9 0 U1 1 U2 1 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2006 VL 108 IS 11 MA 1219 BP 359A EP 359A PN 1 PG 1 WC Hematology SC Hematology GA 111GS UT WOS:000242440001478 ER PT J AU Villagra, JD Nichols, JT Gladwin, MT Kato, GJ AF Villagra, Jose D. Nichols, James T. Gladwin, Mark T. Kato, Gregory J. TI Platelets from patients with sickle cell disease and pulmonary arterial hypertension are hypersensitive to agonist-induced activation. SO BLOOD LA English DT Meeting Abstract CT 48th Annual Meeting of the American-Society-of-Hematology CY DEC 09-12, 2006 CL Orlando, FL SP Amer Soc Hematol C1 NHLBI, NIH, Vasc Med Branch, Bethesda, MD USA. Ctr Clin, NIH, Dept Crit Care Med, Bethesda, MD USA. Childrens Natl Med Ctr, Childrens Res Inst, Div Hematol & Oncol, Washington, DC 20010 USA. RI Kato, Gregory/I-7615-2014 OI Kato, Gregory/0000-0003-4465-3217 NR 0 TC 0 Z9 0 U1 0 U2 1 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2006 VL 108 IS 11 MA 1239 BP 364A EP 365A PG 2 WC Hematology SC Hematology GA 111GS UT WOS:000242440001498 ER PT J AU Konkle, BA Melendez-Morales, L Preiss, L Zhang, MD Mathew, P Eyster, ME Goedert, JJ AF Konkle, Barbara A. Melendez-Morales, Lehida Preiss, Liliana Zhang, Mingdong Mathew, Prasad Eyster, M. Elaine Goedert, James J. TI Correlates of spontaneous clearance of hepatitis C virus among HIV-infected persons with hemophilia. SO BLOOD LA English DT Meeting Abstract CT 48th Annual Meeting of the American-Society-of-Hematology CY DEC 09-12, 2006 CL Orlando, FL SP Amer Soc Hematol C1 Univ Penn, Philadelphia, PA 19104 USA. NIH, Natl Canc Inst, Viral Epidemiol Branch, Rockville, MD USA. Res Triangle Inst, Rockville, MD USA. Univ New Mexico, Albuquerque, NM 87131 USA. Penn State Univ, Coll Med, Hershey, PA USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2006 VL 108 IS 11 MA 1265 BP 371A EP 372A PN 1 PG 2 WC Hematology SC Hematology GA 111GS UT WOS:000242440001524 ER PT J AU Faulhaber, M Patel, KV Bandinelli, S Longo, DL Ferrucci, L Guralnik, JM AF Faulhaber, Marion Patel, Kushang V. Bandinelli, Stefania Longo, Dan L. Ferrucci, Luigi Guralnik, Jack M. TI Association of erythropoietin and inflammation with the incidence of anemia in older persons. SO BLOOD LA English DT Meeting Abstract CT 48th Annual Meeting of the American-Society-of-Hematology CY DEC 09-12, 2006 CL Orlando, FL SP Amer Soc Hematol C1 Nat Inst Aging, Lab Epidemiol Demograpy & Biometry, Bethesda, MD USA. Azienda Sanitaria Firenze, Florence, Italy. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2006 VL 108 IS 11 MA 1292 BP 378A EP 379A PG 2 WC Hematology SC Hematology GA 111GS UT WOS:000242440001551 ER PT J AU Rezvani, K Agnes, Y Eniafe, RB Mielke, S Savani, BN Price, DA Gostick, E Douek, DC Goldman, JM Barrett, AJ AF Rezvani, Katayoun Agnes, Yong Eniafe, Rhoda B. Mielke, Stephan Savani, Bipin N. Price, David A. Gostick, Emma Douek, Daniel C. Goldman, John M. Barrett, A. John TI PR1-specific T cell responses in the first months following T-cell depleted allogeneic stem cell transplantation occur in both myeloid and non-myeloid malignancies but are only associated with a GVL effect in myeloid leukemias. SO BLOOD LA English DT Meeting Abstract CT 48th Annual Meeting of the American-Society-of-Hematology CY DEC 09-12, 2006 CL Orlando, FL SP Amer Soc Hematol C1 NIH, NHLBI, Bethesda, MD 20892 USA. NIH, VRC, Bethesda, MD 20892 USA. Univ Oxford, Nuffield Med Ctr, Oxford, England. RI Price, David/C-7876-2013 OI Price, David/0000-0001-9416-2737 NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2006 VL 108 IS 11 MA 5195 BP 389B EP 390B PG 2 WC Hematology SC Hematology GA 111GW UT WOS:000242440402313 ER PT J AU Sood, R Rivera, L Chahal, J Burnetti, A English, M Bodine, D Liu, P AF Sood, Raman Rivera, Linda Chahal, Jagman Burnetti, Anthony English, Milton Bodine, David Liu, Paul TI Generation of zebrafish lines with new gata1 mutations and their characterization with a novel in vitro colony-forming assay. SO BLOOD LA English DT Meeting Abstract CT 48th Annual Meeting of the American-Society-of-Hematology CY DEC 09-12, 2006 CL Orlando, FL SP Amer Soc Hematol C1 NIH, NHGRI, GMBB, Bethesda, MD 20892 USA. RI Liu, Paul/A-7976-2012 OI Liu, Paul/0000-0002-6779-025X NR 0 TC 0 Z9 0 U1 0 U2 1 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2006 VL 108 IS 11 MA 1336 BP 390A EP 391A PN 1 PG 2 WC Hematology SC Hematology GA 111GS UT WOS:000242440001595 ER PT J AU Boni, A Muranski, P Wrzesinski, C Kaiser, A Paulos, C Palmer, D Gattinoni, L Restifo, NP AF Boni, Andrea Muranski, Pawel Wrzesinski, Claudia Kaiser, Andrew Paulos, Chrystal Palmer, Douglas Gattinoni, Luca Restifo, Nicholas P. TI Partly MHC matched allogeneic tumor specific T cells mediate tumor regression without inducing GVHD in immunosuppressed host. SO BLOOD LA English DT Meeting Abstract CT 48th Annual Meeting of the American-Society-of-Hematology CY DEC 09-12, 2006 CL Orlando, FL SP Amer Soc Hematol C1 NIH, Natl Canc Inst, Surg Branch, Bethesda, MD 20892 USA. RI Restifo, Nicholas/A-5713-2008; Muranski, Pawel/E-5572-2010 NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2006 VL 108 IS 11 MA 5210 BP 393B EP 393B PN 2 PG 1 WC Hematology SC Hematology GA 111GW UT WOS:000242440402328 ER PT J AU Hystad, ME Bo, TH Rian, E Myklebust, JH Sivertsen, E Forfang, L Chiorazzi, M Rosenwald, A Jonassen, I Staudt, LM Smeland, EB AF Hystad, Marit E. Bo, Trond H. Rian, Edith Myklebust, June H. Sivertsen, Einar Forfang, Lise Chiorazzi, Michael Rosenwald, Andreas Jonassen, Inge Staudt, Louis M. Smeland, Erlend B. TI Characterization of early human B cell development by gene expression profiling. SO BLOOD LA English DT Meeting Abstract CT 48th Annual Meeting of the American-Society-of-Hematology CY DEC 09-12, 2006 CL Orlando, FL SP Amer Soc Hematol C1 Norwegian Radium Hosp, Dept Immunol, Oslo, Norway. Univ Bergen, Computat Biol Unit, Bergen, Norway. Natl Canc Inst, Bethesda, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 2 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2006 VL 108 IS 11 MA 1352 BP 395A EP 395A PN 1 PG 1 WC Hematology SC Hematology GA 111GS UT WOS:000242440001611 ER PT J AU Dohse, M Robey, RW Brendel, C Bates, S Neubauer, A Scharenberg, C AF Dohse, Marius Robey, Robert W. Brendel, Cornelia Bates, Susan Neubauer, Andreas Scharenberg, Christian TI Efflux of the tyrosine kinase inhibitors imatinib and nilotinib (AMN107) is mediated by ABCB1 (MDR1)-Type P-glycoprotein. SO BLOOD LA English DT Meeting Abstract CT 48th Annual Meeting of the American-Society-of-Hematology CY DEC 09-12, 2006 CL Orlando, FL SP Amer Soc Hematol C1 Univ Marburg, Dept Hematol & Oncol & Immunol, Marburg, Germany. Univ Marburg, Dept Anat & Cell Biol, D-3550 Marburg, Germany. NCI, Natl Inst Hlth, Ctr Canc Res, Bethesda, MD 20892 USA. Dept Hematol, Dept Internal Med, Div Internal Med, Skovde, Sweden. NR 0 TC 2 Z9 2 U1 0 U2 2 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2006 VL 108 IS 11 MA 1367 BP 399A EP 399A PN 1 PG 1 WC Hematology SC Hematology GA 111GS UT WOS:000242440001626 ER PT J AU Slape, C Hartung, H Lin, YW Bies, J Wolff, L Aplan, PD AF Slape, Christopher Hartung, Helge Lin, Yingwei Bies, Juraj Wolff, Linda Aplan, Peter D. TI Retroviral insertion tagging identifies Mn1 as a specific collaborator of NUP98-HOXD13 in a murine model of leukemogenesis. SO BLOOD LA English DT Meeting Abstract CT 48th Annual Meeting of the American-Society-of-Hematology CY DEC 09-12, 2006 CL Orlando, FL SP Amer Soc Hematol C1 NIH, NCI, Ctr Canc Res, Genet Branch, Bethesda, MD 20892 USA. NIH, NCI, Ctr Canc Res, Leukemogenesis Sect, Bethesda, MD 20892 USA. RI Slape, Christopher/H-8586-2016; Aplan, Peter/K-9064-2016 OI Slape, Christopher/0000-0002-8407-3092; NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2006 VL 108 IS 11 MA 1409 BP 410A EP 410A PN 1 PG 1 WC Hematology SC Hematology GA 111GS UT WOS:000242440001668 ER PT J AU Bergerson, RJS Collier, LS Cox, T Hudson, WA Allaei, R Wolff, L Kersey, JH Adams, DJ Largaespada, DA AF Bergerson, Rachel J. S. Collier, Lara S. Cox, Tony Hudson, Wendy A. Allaei, Raha Wolff, Linda Kersey, John H. Adams, David J. Largaespada, David A. TI A screen for Mll-AF9 cooperating mutations in leukemogenesis using MLV-based mutagenesis. SO BLOOD LA English DT Meeting Abstract CT 48th Annual Meeting of the American-Society-of-Hematology CY DEC 09-12, 2006 CL Orlando, FL SP Amer Soc Hematol C1 Univ Minnesota, Ctr Canc, Minneapolis, MN USA. Wellcome Trust Sanger Inst, Hinxton, England. NCI, Ctr Canc Res, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2006 VL 108 IS 11 MA 1417 BP 412A EP 412A PN 1 PG 1 WC Hematology SC Hematology GA 111GS UT WOS:000242440001676 ER PT J AU Metais, JY Wieser, R Dunbar, CE AF Metais, Jean-Yves Wieser, Rotraud Dunbar, Cynthia E. TI MDS1-EVI1 and EVI1 overexpression results in changes in the behavior of murine hematopoietic cells. SO BLOOD LA English DT Meeting Abstract CT 48th Annual Meeting of the American-Society-of-Hematology CY DEC 09-12, 2006 CL Orlando, FL SP Amer Soc Hematol C1 NIH, NHLBI, Hematol Branch, Bethesda, MD 20892 USA. Med Univ Wien, KIMCL, Abt Humangenet, Vienna, Austria. NR 0 TC 0 Z9 0 U1 0 U2 1 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2006 VL 108 IS 11 MA 1452 BP 420A EP 420A PN 1 PG 1 WC Hematology SC Hematology GA 111GS UT WOS:000242440001711 ER PT J AU Sloand, EM More, K Shah, S Pfannes, L Ellison, F Chen, J Home, M Young, NS AF Sloand, Elaine M. More, Kenneth Shah, Simant Pfannes, Loretta Ellison, Felicia Chen, Jichun Home, McDonald Young, Neal S. TI Soluble urokinase plasminogen activator receptor is increased in patients with paroxysmal nocturnal hemoglobinuria (PNH) and thrombosis and inhibits plasmin generation in vitro and promotes thrombosis in the mouse model. SO BLOOD LA English DT Meeting Abstract CT 48th Annual Meeting of the American-Society-of-Hematology CY DEC 09-12, 2006 CL Orlando, FL SP Amer Soc Hematol C1 NHLBI, Hematol Branch, Bethesda, MD 20892 USA. Bethesda Nav Hosp, Div Hematol Oncol, Bethesda, MD USA. NIH, Ctr Clin, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2006 VL 108 IS 11 MA 1460 BP 422A EP 422A PN 1 PG 1 WC Hematology SC Hematology GA 111GS UT WOS:000242440001719 ER PT J AU Hardy, NM Odom, J Snow, K Dean, R Pavletic, S Sportes, C Gress, R Fowler, DH Bishop, MR AF Hardy, Nancy M. Odom, Jeanne Snow, Kelly Dean, Robert Pavletic, Steven Sportes, Claude Gress, Ronald Fowler, Daniel H. Bishop, Michael R. TI Safety and efficacy of cytotoxic chemotherapy after allogeneic hematopoietic stem cell transplantation for relapsed hematologic malignancy. SO BLOOD LA English DT Meeting Abstract CT 48th Annual Meeting of the American-Society-of-Hematology CY DEC 09-12, 2006 CL Orlando, FL SP Amer Soc Hematol C1 NIH, NCI, Bethesda, MD 20892 USA. NIH, Ctr Clin, Dept Transfus Med, Bethesda, MD 20892 USA. Univ Penn, Abramson Family Canc Res Inst, Philadelphia, PA 19104 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2006 VL 108 IS 11 MA 5333 BP 425B EP 426B PG 2 WC Hematology SC Hematology GA 111GW UT WOS:000242440402450 ER PT J AU Mitchell, S Jacobsohn, D Thormann, K Cowen, E Fall-Dickson, J Turner, M Schubert, M Baird, K Bolanos-Meade, J Boyd, K Gerber, L Guadagnini, JP Higman, M Imanguli, M Lawley, L Li, L Pracbenko, O Reeve, B Smith, J Vogelsang, G Pavletic, S AF Mitchell, S. Jacobsohn, D. Thormann, K. Cowen, E. Fall-Dickson, J. Turner, M. Schubert, M. Baird, K. Bolanos-Meade, J. Boyd, K. Gerber, L. Guadagnini, J. P. Higman, M. Imanguli, M. Lawley, L. Li, L. Pracbenko, O. Reeve, B. Smith, J. Vogelsang, G. Pavletic, S. TI Feasibility and reproducibility of the NIH consensus criteria to evaluate response in chronic graft versus host disease (cGvHD). SO BLOOD LA English DT Meeting Abstract CT 48th Annual Meeting of the American-Society-of-Hematology CY DEC 09-12, 2006 CL Orlando, FL SP Amer Soc Hematol C1 Natl Canc Inst, cGVHD Study Grp, Bethesda, MD USA. Childrens Mem Hosp, Chicago, IL 60614 USA. Seattle Canc Care Alliance, Seattle, WA USA. Johns Hopkins Univ, Baltimore, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2006 VL 108 IS 11 MA 5344 BP 428B EP 429B PN 2 PG 2 WC Hematology SC Hematology GA 111GW UT WOS:000242440402461 ER PT J AU Valance Washington, A Giomarelli, B Chisholm, MM Quigley, L McMahon, JB Mori, T McVicar, DW AF Valance Washington, A. Giomarelli, Barbara Chisholm, Maia M. Quigley, Laura McMahon, James B. Mori, Toshiyuki McVicar, Daniel W. TI Inhibition of thrombin-induced platelet aggregation using human single chain fv antibodies specific for TREM-like transcript-1. SO BLOOD LA English DT Meeting Abstract CT 48th Annual Meeting of the American-Society-of-Hematology CY DEC 09-12, 2006 CL Orlando, FL SP Amer Soc Hematol C1 Univ Ctr Caribe, Sch Med, Dept Anat & Cell Biol, Bayamon, PR USA. Natl Canc Inst, Mol Targets Dev Program, Frederick, MD USA. Natl Canc Inst, Expt Immunol Lab, Frederick, MD USA. Takeda Pharmaceut Co Ltd, Biochem Res Lab, Osaka, Japan. NR 0 TC 0 Z9 0 U1 0 U2 2 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2006 VL 108 IS 11 MA 1533 BP 441A EP 441A PN 1 PG 1 WC Hematology SC Hematology GA 111GS UT WOS:000242440002049 ER PT J AU Raghavachari, N Xu, XL Villagra, J Kato, G Munson, PJ Morris, S Gladwin, MT AF Raghavachari, Nalini Xu, Xiuli Villagra, Jose Kato, Greg Munson, Peter J. Morris, Sidney Gladwin, Mark T. TI Amplified expression profiling of platelet transcriptome reveals global activation of arginine metabolic pathways in patients with sickle cell disease. SO BLOOD LA English DT Meeting Abstract CT 48th Annual Meeting of the American-Society-of-Hematology CY DEC 09-12, 2006 CL Orlando, FL SP Amer Soc Hematol C1 NIH, Bethesda, MD 20892 USA. NIH, Bethesda, MD 20892 USA. Ctr Informat Technol, NIH, Bethesda, MD USA. Univ Pittsburgh, Sch Med, Dept Mol Genet & Biochem, Pittsburgh, PA 15261 USA. RI Kato, Gregory/I-7615-2014 OI Kato, Gregory/0000-0003-4465-3217 NR 0 TC 0 Z9 0 U1 0 U2 1 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 2021 L ST NW, SUITE 900, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2006 VL 108 IS 11 MA 1536 BP 442A EP 442A PN 1 PG 1 WC Hematology SC Hematology GA 111GS UT WOS:000242440002052 ER PT J AU McLaren, GD McLaren, CE Adams, PC Barton, JC Reboussin, DM Gordeuk, VR Acton, RT Harris, EL Speechley, M Sholinsky, P Dawkins, FW Snively, BM Vogt, T Eckfeldt, JH AF McLaren, Gordon D. McLaren, Christine E. Adams, Paul C. Barton, James C. Reboussin, David M. Gordeuk, Victor R. Acton, Ronald T. Harris, Emily L. Speechley, Mark Sholinsky, Phyliss Dawkins, Fitzroy W. Snively, Beverly M. Vogt, Thomas Eckfeldt, John H. TI Symptoms and signs of hemochromatosis in HFE C282Y homozygotes identified by screening in primary care. SO BLOOD LA English DT Meeting Abstract CT 48th Annual Meeting of the American-Society-of-Hematology CY DEC 09-12, 2006 CL Orlando, FL SP Amer Soc Hematol C1 Dept Vet Affairs Long Beach Healthcare Syst, Long Beach, CA 20059 USA. Univ Calif Irvine, Irvine, CA USA. London Hlth Sci Ctr, London, ON, Canada. So Iron Disorders Ctr, Birmingham, AL USA. Wake Forest Univ, Sch Med, Winston Salem, NC 20892 USA. Howard Univ, Washington, DC USA. Univ Alabama, Birmingham, AL USA. Kaiser Permanente Ctr Hlth Res, Portland, OR USA. Univ Western Ontario, London, ON, Canada. NIH, NHLBI, DHHS, Bethesda, MD USA. Kaiser Permanente Ctr Hlth Res, Honolulu, HI USA. Univ Minnesota, Minneapolis, MN USA. NR 0 TC 2 Z9 2 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2006 VL 108 IS 11 MA 1545 BP 444A EP 444A PN 1 PG 1 WC Hematology SC Hematology GA 111GS UT WOS:000242440002061 ER PT J AU Shiva, S Huang, Z MacArthur, PH Ringwood, LA Gladwin, MT AF Shiva, Sruti Huang, Zhi MacArthur, Peter H. Ringwood, Loma A. Gladwin, Mark T. TI Myoglobin is a nitrite reductase that generates NO and regulates mitochondrial respiration. SO BLOOD LA English DT Meeting Abstract CT 48th Annual Meeting of the American-Society-of-Hematology CY DEC 09-12, 2006 CL Orlando, FL SP Amer Soc Hematol C1 NHLBI, NIH, Vasc Med Branch, Bethesda, MD 20892 USA. NIH, Dept Crit Care Med, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2006 VL 108 IS 11 MA 1561 BP 448A EP 448A PN 1 PG 1 WC Hematology SC Hematology GA 111GS UT WOS:000242440002077 ER PT J AU Basu, S Huang, JM Huang, Z Jeffers, A Jiang, A He, XJ Azarov, I Seibert, R Patel, RP Hogg, N King, B Gladwin, MT Kim-Shapiro, D AF Basu, Swati Huang, Jinming Huang, Zhi Jeffers, Anne Jiang, Alice He, Xiaojun Azarov, Ivan Seibert, Ryan Patel, Rakesh P. Hogg, Neil King, Bruce Gladwin, Mark T. Kim-Shapiro, Daniel TI Formation ofNitroso compounds in the reaction of nitrite and hemoglobin. SO BLOOD LA English DT Meeting Abstract CT 48th Annual Meeting of the American-Society-of-Hematology CY DEC 09-12, 2006 CL Orlando, FL SP Amer Soc Hematol C1 Wake Forest Univ, Winston Salem, NC 27109 USA. Wake Forest Univ, Winston Salem, NC 27109 USA. NIH, Bethesda, MD 20892 USA. Univ Alabama, Birmingham, AL USA. Med Coll Wisconsin, Milwaukee, WI 53226 USA. NR 0 TC 0 Z9 0 U1 0 U2 2 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 2021 L ST NW, SUITE 900, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2006 VL 108 IS 11 MA 1565 BP 449A EP 449A PN 1 PG 1 WC Hematology SC Hematology GA 111GS UT WOS:000242440002081 ER PT J AU Gantt, NM Walker, B Lee, YT Jiang, Y Staker, P Oneal, PA Bhanu, NAV Meltzer, PS Miller, JL AF Gantt, Nicole M. Walker, Bob Lee, Y. Terry Jiang, Yuan Staker, Pamela Oneal, Patricia A. Bhanu, Natarajan V. Meltzer, Paul S. Miller, Jeffery L. TI Genomic composition of Howell-Jolly Bodies. SO BLOOD LA English DT Meeting Abstract CT 48th Annual Meeting of the American-Society-of-Hematology CY DEC 09-12, 2006 CL Orlando, FL SP Amer Soc Hematol C1 NIH, Nat Inst Diabet Digest & Kidney Dis, Mol Med Branch, Bethesda, MD 20892 USA. NIH, NHGRI, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2006 VL 108 IS 11 MA 1570 BP 450A EP 450A PN 1 PG 1 WC Hematology SC Hematology GA 111GS UT WOS:000242440002086 ER PT J AU Sibmooh, N Piknova, B Schechter, AN AF Sibmooh, Nathawut Piknova, Barbera Schechter, Alan N. TI Ascorbic acid catalyzes nitric oxide production from nitrite ions. SO BLOOD LA English DT Meeting Abstract CT 48th Annual Meeting of the American-Society-of-Hematology CY DEC 09-12, 2006 CL Orlando, FL SP Amer Soc Hematol C1 NIH, Inst Nat Diabet & Digest & Kidney Dis, Mol Med Branch, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2006 VL 108 IS 11 MA 1574 BP 451A EP 451A PN 1 PG 1 WC Hematology SC Hematology GA 111GS UT WOS:000242440002090 ER PT J AU Hai, M Bauer, TR Tuschong, LM Gu, Y Sokolic, RA Hickstein, DD AF Hai, Mehreen Bauer, Thomas R. Tuschong, Laura M. Gu, Yuchen Sokolic, Robert A. Hickstein, Dennis D. TI Polyclonality of retroviral insertion sites following successful retroviral mediated gene transfer of CD18 in canine leukocyte adhesion deficiency. SO BLOOD LA English DT Meeting Abstract CT 48th Annual Meeting of the American-Society-of-Hematology CY DEC 09-12, 2006 CL Orlando, FL SP Amer Soc Hematol C1 Natl Canc Inst, Natl Inst Hlth, Experimental Transplant & Immunol Branch, Bethesda, MD USA. RI Sokolic, Robert/I-6072-2012 NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2006 VL 108 IS 11 MA 5479 BP 466B EP 466B PN 2 PG 1 WC Hematology SC Hematology GA 111GW UT WOS:000242440402596 ER PT J AU Sachs, U Andrei-Selmer, C Maniar, A Paddock, C Newman, P Chavakis, T Santoso, S AF Sachs, Ulrich Andrei-Selmer, Cornelia Maniar, Amudhan Paddock, Cathy Newman, Peter Chavakis, Triantafyllos Santoso, Sentot TI The neutrophil specific CD177 is a novel counter-recep tor for endothelial PECAM-1. SO BLOOD LA English DT Meeting Abstract CT 48th Annual Meeting of the American-Society-of-Hematology CY DEC 09-12, 2006 CL Orlando, FL SP Amer Soc Hematol C1 Univ Giessen, Inst Clin Immunol & Transfus Med, D-6300 Giessen, Germany. Blood Ctr Wisconsin, Blood Res Inst, Milwaukee, WI USA. NIH, Expt Immunol Branch, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2006 VL 108 IS 11 MA 1635 BP 467A EP 467A PN 1 PG 1 WC Hematology SC Hematology GA 111GS UT WOS:000242440002151 ER PT J AU Ravin, SSTD Naumann, N Friend, J Ulrick, J Hilligoss, D Kwateema, N Malech, HL AF Ravin, Suk See Ting-De Naumann, Nora Friend, Julia Ulrick, Jean Hilligoss, Dianne Kwateema, Nana Malech, Harry L. TI Autoimmune disease in chronic granulomatous disease (CGD): A diverse spectrum. SO BLOOD LA English DT Meeting Abstract CT 48th Annual Meeting of the American-Society-of-Hematology CY DEC 09-12, 2006 CL Orlando, FL SP Amer Soc Hematol C1 NIH, NIAID, Host Def Lab, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2006 VL 108 IS 11 MA 1642 BP 468A EP 469A PN 1 PG 2 WC Hematology SC Hematology GA 111GS UT WOS:000242440002158 ER PT J AU Logdberg, LE Akerstrom, B Hair, GA Allhorn, M Vikulina, T Kirshenbaum, AS Sundstrom, JB AF Logdberg, Lennart E. Akerstrom, Bo Hair, Gregory A. Allhorn, Maria Vikulina, Tatyana Kirshenbaum, Arnold S. Sundstrom, J. Bruce TI Do lipocalins play a role in mast cell physiology? SO BLOOD LA English DT Meeting Abstract CT 48th Annual Meeting of the American-Society-of-Hematology CY DEC 09-12, 2006 CL Orlando, FL SP Amer Soc Hematol C1 Emory Univ, Sch Med, Atlanta, GA 30322 USA. Lund Univ, Lund, Sweden. NIH, NIAID, Lab Allerg Dis, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2006 VL 108 IS 11 MA 1645 BP 469A EP 469A PN 1 PG 1 WC Hematology SC Hematology GA 111GS UT WOS:000242440002161 ER PT J AU Mariotti, J Foley, J Wong, E Behbahani, B Fowler, DH Sportes, C AF Mariotti, Jacopo Foley, Jason Wong, Elaine Behbahani, Babak Fowler, Daniel H. Sportes, Claude TI Ex vivo rapamycin generates Th2 cells with enhanced mitochondrial function and reduced apoptosis via intrinsic and extrinsic pathways. SO BLOOD LA English DT Meeting Abstract CT 48th Annual Meeting of the American-Society-of-Hematology CY DEC 09-12, 2006 CL Orlando, FL SP Amer Soc Hematol C1 NCI, NIH, ETIB, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2006 VL 108 IS 11 MA 1736 BP 493A EP 493A PN 1 PG 1 WC Hematology SC Hematology GA 111GS UT WOS:000242440002254 ER PT J AU Zhang, XF Wang, JF Maor, YS Kunos, G Groopman, JE AF Zhang, Xuefeng Wang, Jian Feng Maor, Yehoshua Kunos, George Groopman, Jerome E. TI Endogenous cannabinoid-like arachidonoyl serine protects against LPS-induced endothelial apoptosis. SO BLOOD LA English DT Meeting Abstract CT 48th Annual Meeting of the American-Society-of-Hematology CY DEC 09-12, 2006 CL Orlando, FL SP Amer Soc Hematol C1 Harvard Univ, Sch Med, BIDMC, Div Expt Med, Boston, MA USA. Harvard Univ, Sch Med, BIDMC, Dept Surg, Boston, MA USA. Hebrew Univ Jerusalem, Dept Med Chem & Nat Prod, Jerusalem, Israel. NIH, NIAAA, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 1 U2 1 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2006 VL 108 IS 11 MA 1808 BP 513A EP 513A PN 1 PG 1 WC Hematology SC Hematology GA 111GS UT WOS:000242440002326 ER PT J AU Taylor, JG Idelman, G Tongbai, R Chen, RA Haggerty, CM Chanock, SJ Gardner, K AF Taylor, James G. Idelman, Gila Tongbai, Ron Chen, Renee A. Haggerty, Cynthia M. Chanock, Stephen Jacob Gardner, Kevin TI Rare VCAM1 promoter haplotypes prevalent in African Americans are hyperinducible. SO BLOOD LA English DT Meeting Abstract CT 48th Annual Meeting of the American-Society-of-Hematology CY DEC 09-12, 2006 CL Orlando, FL SP Amer Soc Hematol C1 NIH, NHLBI, Vasc Med Branch, Bethesda, MD 20892 USA. NIH, NCI, POB, Sect Genom Variat, Bethesda, MD 20892 USA. NIH, NCI, Lab Receptor Biol and Gene Express, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2006 VL 108 IS 11 MA 1813 BP 514A EP 514A PN 1 PG 1 WC Hematology SC Hematology GA 111GS UT WOS:000242440002331 ER PT J AU Gelderman-Fuhrmann, MP Schiffmann, R Simak, J AF Gelderman-Fuhrmann, Monique P. Schiffmann, Raphael Simak, Jan TI Elevated counts of circulating endothelial microparticles in pediatric Fabry patients decreased after enzyme replacement therapy. SO BLOOD LA English DT Meeting Abstract CT 48th Annual Meeting of the American-Society-of-Hematology CY DEC 09-12, 2006 CL Orlando, FL SP Amer Soc Hematol C1 US FDA, CBER, LCH, Rockville, MD 20857 USA. NIH, NINDS, DMNB, Bethesda, MD 20892 USA. RI Simak, Jan/C-1153-2011 NR 0 TC 0 Z9 0 U1 0 U2 2 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2006 VL 108 IS 11 MA 1818 BP 515A EP 515A PG 1 WC Hematology SC Hematology GA 111GS UT WOS:000242440002336 ER PT J AU DeAngelo, DJ Silverman, LB Couban, S Dahlberg, S Amrein, PC Seftel, MD Turner, AR Wadleigh, M Sirulnik, LA Galinsky, I Sallan, SE Stone, RM AF DeAngelo, Daniel J. Silverman, Lewis B. Couban, Stephen Dahlberg, Suzanne Amrein, Philip C. Seftel, Matthew D. Turner, A. Robert Wadleigh, Martha Sirulnik, L. Andres Galinsky, Ilene Sallan, Stephen E. Stone, Richard M. TI A multicenter phase II study using a dose intensified pediatric regimen in adults with untreated acute lymphoblastic leukemia. SO BLOOD LA English DT Meeting Abstract CT 48th Annual Meeting of the American-Society-of-Hematology CY DEC 09-12, 2006 CL Orlando, FL SP Amer Soc Hematol C1 Dana Farber Canc Inst, Boston, MA 02115 USA. NCI, Clin Trials Grp, Kingston, ON, Canada. Massachusetts Gen Hosp, Boston, MA 02114 USA. Canc Care Manitoba, Winnipeg, MB, Canada. Cross Canc Inst, Edmonton, AB, Canada. NR 0 TC 5 Z9 5 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2006 VL 108 IS 11 MA 1858 BP 526A EP 526A PN 1 PG 1 WC Hematology SC Hematology GA 111GS UT WOS:000242440002376 ER PT J AU Akar, U Ozpolat, B Colburn, N Lopez-Berestein, G AF Akar, Ugur Ozpolat, Bulent Colburn, Nancy Lopez-Berestein, Gabriel TI p38 MAPK signaling mediates retinoic acid-induced expression of a novel tumor suppressor protein programmed cell death 4 (PDCD4) in acute promyelocytic leukemia cells. SO BLOOD LA English DT Meeting Abstract CT 48th Annual Meeting of the American-Society-of-Hematology CY DEC 09-12, 2006 CL Orlando, FL SP Amer Soc Hematol C1 Univ Texas, MD Anderson Canc Ctr, Houston, TX 77030 USA. NCI, Gene Regulat Sect, Frederick, TX USA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2006 VL 108 IS 11 MA 1942 BP 549A EP 549A PN 1 PG 1 WC Hematology SC Hematology GA 111GS UT WOS:000242440002460 ER PT J AU Kirschbaum, M Stein, AS Tuscano, J Zain, JM Popplewell, L O'Donnell, MR Karanes, C Krishnan, A Wright, JJ Pulone, B Rincon, A Frankel, P Forman, SJ Edward, N AF Kirschbaum, Mark Stein, Anthony Seliwyn Tuscano, Joseph Zain, Jasmine M. Popplewell, Leslie O'Donnell, Margaret R. Karanes, Chatchada Krishnan, Amrita Wright, John J. Pulone, Bernadette Rincon, Amalia Frankel, Paul Forman, Stephen J. Edward, Newman TI A phase I study of the farnesyltransferase inhibitor tipifarnib in a week-on week-off dose schedule in acute myelogenous leukemia. SO BLOOD LA English DT Meeting Abstract CT 48th Annual Meeting of the American-Society-of-Hematology CY DEC 09-12, 2006 CL Orlando, FL SP Amer Soc Hematol C1 City Hope Natl Med Ctr, HCT, Duarte, CA 91010 USA. Univ Calif Davis, Sacramento, CA 95817 USA. NCI, CTEP, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2006 VL 108 IS 11 MA 1948 BP 551A EP 551A PN 1 PG 1 WC Hematology SC Hematology GA 111GS UT WOS:000242440002466 ER PT J AU Alvarez, RH Kantarijan, H Garcia-Manero, G Estrov, Z Ravandi-Kashani, F Verstovsek, S Giles, F O'Brien, S Koller, CA Faderl, S Thomas, D Wright, JJ Cortes, J AF Alvarez, Ricardo H. Kantarijan, Hagop Garcia-Manero, Guillermo Estrov, Zeev Ravandi-Kashani, Farhad Verstovsek, Srdan Giles, Francis O'Brien, Susan Koller, Charles Asa Faderl, Stefan Thomas, Deborah Wright, John J. Cortes, Jorge TI Farnesyl transferase inhibitor (Tipifarnib, zarnestra; z) in combination with standard chemotherapy with idarubicin (Ida) and cytarabime (ara-C) for patients (pts) with newly diagnosed acute myeloid leukemia (AML) or high-risk myelodysplastic syndrome (MDS). SO BLOOD LA English DT Meeting Abstract CT 48th Annual Meeting of the American-Society-of-Hematology CY DEC 09-12, 2006 CL Orlando, FL SP Amer Soc Hematol C1 Univ Texas, MD Anderson Canc Ctr, Houston, TX 77030 USA. NCI, CTEP, Bethesda, MD USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2006 VL 108 IS 11 MA 1999 BP 565A EP 566A PN 1 PG 2 WC Hematology SC Hematology GA 111GS UT WOS:000242440002519 ER PT J AU Habermann, TM Wang, S Maurer, MJ Morton, LM Lynch, CF Ansell, SM Hartge, P Severson, RK Rothman, N Davis, S Geyer, SM Cozen, W Chanock, S Cerhan, JR AF Habermann, Thomas M. Wang, Sophia Maurer, Matthew J. Morton, Lindsay M. Lynch, Charles F. Ansell, Stephen M. Hartge, Patricia Severson, Richard K. Rothman, Nathaniel Davis, Scott Geyer, Susan M. Cozen, Wendy Chanock, Stephen Cerhan, James R. TI Germline single nucleotide polymorphisms (SNPs) in IL1A, IL6, IL10, and IFNGR2 in combination with clinical with demographic factors predict overall survival in diffuse large B-cell lymphoma (DLBCL). SO BLOOD LA English DT Meeting Abstract CT 48th Annual Meeting of the American-Society-of-Hematology CY DEC 09-12, 2006 CL Orlando, FL SP Amer Soc Hematol C1 Mayo Clin, Coll Med, Rochester, MN USA. Natl Canc Inst, Rockville, MD USA. Univ So Calif, Los Angeles, CA USA. Fred Hutchinson Canc Res Ctr, Seattle, WA 98104 USA. Wayne State Univ, Detroit, MI USA. Univ Iowa, Iowa City, IA USA. RI Geyer, Susan/E-3112-2011 NR 0 TC 0 Z9 0 U1 0 U2 1 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2006 VL 108 IS 11 MA 2028 BP 574A EP 574A PN 1 PG 1 WC Hematology SC Hematology GA 111GS UT WOS:000242440002548 ER PT J AU Sloand, EM Calado, R Shah, S Pfannes, L Blancato, J Young, N AF Sloand, Elaine M. Calado, Rodrigo Shah, Simant Pfannes, Loretta Blancato, Jan Young, Neal TI Telomere shortening and genomic instability: Primary cells from patients with telomere repair complex mutations are susceptible to end-to-end chromosome fusion and aneuploidy. SO BLOOD LA English DT Meeting Abstract CT 48th Annual Meeting of the American-Society-of-Hematology CY DEC 09-12, 2006 CL Orlando, FL SP Amer Soc Hematol C1 NHLBI, Hematol Branch, Bethesda, MD 20892 USA. Georgetown Univ, Washington, DC USA. RI Calado, Rodrigo/G-2619-2011 NR 0 TC 1 Z9 1 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2006 VL 108 IS 11 MA 2079 BP 589A EP 589A PN 1 PG 1 WC Hematology SC Hematology GA 111GS UT WOS:000242440002599 ER PT J AU Johnson, AJ Wagner, AJ Smith, LL Lucas, DM De Lay, MD Allison, JM Ivy, SP Lin, TS Byrd, JC AF Johnson, Amy J. Wagner, Amy J. Smith, Lisa L. Lucas, David M. De Lay, Michael D. Allison, Jamie M. Ivy, S. Percy Lin, Thomas S. Byrd, John C. TI The geldanalmycin derivative DMAG demonstrates improved cytotoxicity and down-modulation of Hsp90 client proteins relative to 17-AAG in chronic lymphocytic leukemia (CLL) cells: Justification for clinical trials in CLL. SO BLOOD LA English DT Meeting Abstract CT 48th Annual Meeting of the American-Society-of-Hematology CY DEC 09-12, 2006 CL Orlando, FL SP Amer Soc Hematol C1 Ohio State Univ, Ctr Comprehens Canc, Columbus, OH 43210 USA. Natl Canc Inst, Canc Therapy Evaluat Program, Rockville, MD USA. RI Johnson, Amy/A-5662-2009 NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2006 VL 108 IS 11 MA 2101 BP 596A EP 596A PN 1 PG 1 WC Hematology SC Hematology GA 111GS UT WOS:000242440002622 ER PT J AU Yong, ASM Keyvanfar, K Eniafe, R Savani, BN Sloand, EM Goldman, JM Barrett, AJ AF Yong, Agnes S. M. Keyvanfar, Keyvan Eniafe, Rhoda Savani, Bipin N. Sloand, Elaine M. Goldman, John M. Barrett, A. John TI Hematopoietic stem cells and primitive progenitors express leukemia associated antigens that may be targets for graft-versus-leukemia effect or for vaccine-based immunotherapy in chronic myeloid leukemia. SO BLOOD LA English DT Meeting Abstract CT 48th Annual Meeting of the American-Society-of-Hematology CY DEC 09-12, 2006 CL Orlando, FL SP Amer Soc Hematol C1 NIH, NHLBI, Hematol Branch, Bethesda, MD 20892 USA. NR 0 TC 1 Z9 1 U1 0 U2 1 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2006 VL 108 IS 11 MA 2125 BP 602A EP 603A PN 1 PG 2 WC Hematology SC Hematology GA 111GS UT WOS:000242440002646 ER PT J AU Kaeda, J Hochhaus, A Radich, J Branford, S So, C Gathmann, I Wehrle, E Goldman, J Hughes, T AF Kaeda, Jaspal Hochhaus, Andreas Radich, Jerald Branford, Susan So, Charlene Gathmann, Insa Wehrle, Elisabeth Goldman, John Hughes, Timothy CA IRIS Study Grp TI Patients with chronic phase CML in the IRIS study who receive imatinib mesylate (IM) 2nd line after prior IFN/Ara-C have sustained complete cytogenetic and major molecular response rates similar to 1st line IM patients. SO BLOOD LA English DT Meeting Abstract CT 48th Annual Meeting of the American-Society-of-Hematology CY DEC 09-12, 2006 CL Orlando, FL SP Amer Soc Hematol C1 Univ London Imperial Coll Sci & Technol, London, England. Univ Heidelberg, Mannheim, Germany. IVMS, Adelaide, SA, Australia. Novartis, Basel, Switzerland. NHLBI, Bethesda, MD USA. NR 0 TC 1 Z9 1 U1 0 U2 1 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2006 VL 108 IS 11 MA 2139 BP 607A EP 607A PN 1 PG 1 WC Hematology SC Hematology GA 111GS UT WOS:000242440002660 ER PT J AU Aue, G Du, Y Dunbar, CE Jenkins, NA Copeland, NG AF Aue, Georg Du, Yang Dunbar, Cynthia E. Jenkins, Nancy A. Copeland, Neal G. TI PU.1 is a downstream target of SOX4 in myeloid cells. SO BLOOD LA English DT Meeting Abstract CT 48th Annual Meeting of the American-Society-of-Hematology CY DEC 09-12, 2006 CL Orlando, FL SP Amer Soc Hematol C1 NIH, NCI, Mouse Canc Genet Porgram, Frederick, MD USA. NIH, NHLBI, Hematol Branch, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2006 VL 108 IS 11 MA 2217 BP 628A EP 629A PN 1 PG 2 WC Hematology SC Hematology GA 111GS UT WOS:000242440003008 ER PT J AU Resar, L Dhara, S Sumter, TF Mukherjee, M Turkson, J Jove, R Elbahloul, O Aplan, P Lin, YW Bhattacharya, R AF Resar, Linda Dhara, Surajit Sumter, Takita Felder Mukherjee, Mita Turkson, James Jove, Rich Elbahloul, Ossama Aplan, Peter Lin, Ying-Wei Bhattacharya, Raka TI STAT3: A direct HMGA1 gene target important in lymphoid malignancy. SO BLOOD LA English DT Meeting Abstract CT 48th Annual Meeting of the American-Society-of-Hematology CY DEC 09-12, 2006 CL Orlando, FL SP Amer Soc Hematol C1 Johns Hopkins Univ, Sch Med, Baltimore, MD USA. Moffitt Canc Ctr, Res Inst, Molecular Oncol Program, Tampa, FL USA. NIH, NCI, Genet Branch, Bethesda, MD 20892 USA. RI Aplan, Peter/K-9064-2016 NR 0 TC 0 Z9 0 U1 0 U2 1 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2006 VL 108 IS 11 MA 2222 BP 630A EP 630A PN 1 PG 1 WC Hematology SC Hematology GA 111GS UT WOS:000242440003013 ER PT J AU Sulis, ML Palomero, T Real, PJ Barnes, KC Aplan, P Copeland, N Utpal, D Gounari, F Grosveld, G Kappes, DJ Kee, B Kelliher, M Lenz, J Richardson, C Ferrando, A Ferrando, A AF Sulis, Maria Luisa Palomero, Teresa Real, Pedro J. Barnes, Kelly C. Aplan, Peter Copeland, Neal Utpal, Dave Gounari, Fotini Grosveld, Gerald Kappes, Dietmar J. Kee, Barbara Kelliher, Michelle Lenz, Jack Richardson, Christine Ferrando, Adolfo Ferrando, Adolfo TI Identification of oncogenic pathways of T-Acute lymphoblastic leukemia (T-ALL) through gene expression profiling of mouse tumor models. SO BLOOD LA English DT Meeting Abstract CT 48th Annual Meeting of the American-Society-of-Hematology CY DEC 09-12, 2006 CL Orlando, FL SP Amer Soc Hematol C1 Columbia Univ, Inst Canc Genet, New York, NY USA. NIH, NCI, Genet Branch, Bethesda, MD 20892 USA. NCI, Dept Mol Genet, Frederick, MD 21701 USA. Vanderbilt Univ, Div Hematol Oncol, Nashville, TN USA. Tufts Univ New England Med Ctr, Mol Oncol Res Inst, Boston, MA USA. St Jude Childrens Res Hosp, Dept Genet, Memphis, TN 38105 USA. Fox Chase Canc Ctr, Div Basic Sci, Philadelphia, PA 19111 USA. Univ Chicago, Dept Pathol, Chicago, IL 60637 USA. Univ Massachusetts, Dept Canc Biol, Worcester, MA 01605 USA. Albert Einstein Coll Med, Dept Mol Genet, Bronx, NY, England. RI Aplan, Peter/K-9064-2016 NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2006 VL 108 IS 11 MA 2234 BP 633A EP 633A PN 1 PG 1 WC Hematology SC Hematology GA 111GS UT WOS:000242440003025 ER PT J AU Solomou, EE Rezvani, K Mielke, S Malide, D Visconte, V Keyvanfar, K Bruno, TC John Barrett, A Young, NS AF Solomou, Elena E. Rezvani, Katayoun Mielke, Stephan Malide, Daniela Visconte, Valeria Keyvanfar, Keyvan Bruno, Tullia C. John Barrett, A. Young, Neal S. TI FOXP3-Positive regulatory T-Cells in acquired aplastic anemia. SO BLOOD LA English DT Meeting Abstract CT 48th Annual Meeting of the American-Society-of-Hematology CY DEC 09-12, 2006 CL Orlando, FL SP Amer Soc Hematol C1 NIH, NHLBI, Hematol Branch, Bethesda, MD 20892 USA. NIH, NHLBI, Light Microscopy Core Facil, Bethesda, MD 20892 USA. NR 0 TC 3 Z9 3 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2006 VL 108 IS 11 MA 2248 BP 636A EP 637A PN 1 PG 2 WC Hematology SC Hematology GA 111GS UT WOS:000242440003039 ER PT J AU Shin, DM Shaffer, DJ Roopenian, DC Morse, H AF Shin, Dong-Mi Shaffer, Daniel J. Roopenian, Derry C. Morse, Herbert TI Mouse B cell lineage neoplasms: Comparative analyses of gene expression using high throughput real time RT-PCR and oligonucleotide microarrays. SO BLOOD LA English DT Meeting Abstract CT 48th Annual Meeting of the American-Society-of-Hematology CY DEC 09-12, 2006 CL Orlando, FL SP Amer Soc Hematol C1 NIH, NIAID, Immunopathol Lab, Rockville, MD USA. Jackson Lab, Bar Harbor, ME 04609 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2006 VL 108 IS 11 MA 2253 BP 638A EP 638A PN 1 PG 1 WC Hematology SC Hematology GA 111GS UT WOS:000242440003044 ER PT J AU Domingo-Domenech, E Benavente, Y Gonzalez-Barca, E Montalban, C Guma, J Wang, SS Whitby, D Fernandez De Sevilla, A Rothman, N de Sanjose, S AF Domingo-Domenech, Eva Benavente, Yolanda Gonzalez-Barca, Eva Montalban, Carlos Guma, Josep Wang, Sophia S. Whitby, Denise Fernandez de Sevilla, Alberto Rothman, Nathaniel de Sanjose, Silvia TI Impact of IL-10 polymorphisms in survival of lymphoid neoplasms. SO BLOOD LA English DT Meeting Abstract CT 48th Annual Meeting of the American-Society-of-Hematology CY DEC 09-12, 2006 CL Orlando, FL SP Amer Soc Hematol C1 Hosp Llobregat, Inst Catala Oncol, Barcelona, Spain. Hosp Llobregat, Inst Catala Oncol, Barcelona, Spain. Hosp Ramon & Cajal, E-28034 Madrid, Spain. Hosp Sant Joan, Tarragona, Spain. Natl Canc Inst, Div Canc Epidemiol & Genet, Bethlehem, WA USA. RI de Sanjose Llongueras, Silvia/H-6339-2014; Benavente, Yolanda/H-9810-2014 NR 0 TC 0 Z9 0 U1 0 U2 1 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 2021 L ST NW, SUITE 900, WASHINGTON, DC 20036 USA SN 0006-4971 EI 1528-0020 J9 BLOOD JI Blood PD NOV 16 PY 2006 VL 108 IS 11 MA 2382 BP 675A EP 675A PN 1 PG 1 WC Hematology SC Hematology GA 111GS UT WOS:000242440003173 ER PT J AU Thompson, CA Wang, S Maurer, MJ Habermann, TM Severson, RK Rothman, N Lynch, CF Davis, S Morton, LM Cozen, W Hartge, P Geyer, SM Chanock, S Cerhan, JR AF Thompson, Carrie A. Wang, Sophia Maurer, Matthew J. Habermann, Thomas M. Severson, Richard K. Rothman, Nathaniel Lynch, Charles F. Davis, Scott Morton, Lindsay M. Cozen, Wendy Hartge, Patricia Geyer, Susan M. Chanock, Stephen Cerhan, James R. TI Host immunogenetic single nucleotide polymorphisms (SNPs) predict overall survival in small lymphocytic lymphoma. SO BLOOD LA English DT Meeting Abstract CT 48th Annual Meeting of the American-Society-of-Hematology CY DEC 09-12, 2006 CL Orlando, FL SP Amer Soc Hematol C1 Mayo Clin, Coll Med, Rochester, MN USA. Natl Canc Inst, Rockville, MD USA. Fred Hutchinson Canc Res Ctr, Seattle, WA 98104 USA. Univ So Calif, Los Angeles, CA USA. Univ Iowa, Iowa City, IA USA. Wayne State Univ, Detroit, MI USA. RI Geyer, Susan/E-3112-2011 NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2006 VL 108 IS 11 MA 2396 BP 678A EP 678A PN 1 PG 1 WC Hematology SC Hematology GA 111GS UT WOS:000242440003187 ER PT J AU Pickarz, RL Frye, R Turner, M Wright, J Allen, S Kirschbaum, MH Zain, J Prince, M Hutchins, L Showe, LC Figg, WD Fojo, T Bates, SE AF Pickarz, Richard L. Frye, Robin Turner, Maria Wright, John Allen, Steven Kirschbaum, Mark H. Zain, Jasmine Prince, Miles Hutchins, Laura Showe, Louise C. Figg, William D. Fojo, Tito Bates, Susan E. CA All Collaborators TI Phase II trial of romidepsin, FK228, in cutaneous and peripheral T-cell lymphoma: Clinical activity and molecular markers. SO BLOOD LA English DT Meeting Abstract CT 48th Annual Meeting of the American-Society-of-Hematology CY DEC 09-12, 2006 CL Orlando, FL SP Amer Soc Hematol C1 NCI, Canc Res Ctr, Bethesda, MD 20892 USA. NCI, CTEP, Bethesda, MD 20892 USA. N Shore Univ Hosp, Manhasset, NY USA. Peter MacCallum Canc Ctr, Melbourne, Vic, Australia. Univ Arkansas, Little Rock, AR 72204 USA. Wistar Inst Anat & Biol, Philadelphia, PA 19104 USA. RI Figg Sr, William/M-2411-2016 NR 0 TC 0 Z9 0 U1 0 U2 1 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2006 VL 108 IS 11 MA 2469 BP 699A EP 699A PN 1 PG 1 WC Hematology SC Hematology GA 111GS UT WOS:000242440003259 ER PT J AU Smith, SM Pro, B Smith, S Stiff, P Lester, E Modi, S van Besien, K AF Smith, Sonali M. Pro, Barbara Smith, Scott Stiff, Patrick Lester, Eric Modi, Sanjiv van Besien, Koen TI Molecular inhibition of mTOR with temsirolimus (TORISEL (TM), CCI-779) is a promising strategy in relapsed NHL: The University of Chicago phase II consortium. SO BLOOD LA English DT Meeting Abstract CT 48th Annual Meeting of the American-Society-of-Hematology CY DEC 09-12, 2006 CL Orlando, FL SP Amer Soc Hematol C1 Univ Chicago, Hematol Oncol Sect, Chicago, IL 60637 USA. Univ Texas, MD Anderson Canc Ctr, Houston, TX 77030 USA. Loyola Univ, Med Ctr, Maywood, IL 60153 USA. Oncol Care Associates, St Joseph, MI USA. NCI, CTEP, Rockville, MD USA. Joliet Oncol Hematol Associates Ltd, Joliet, IL USA. RI van Besien, Koen/G-4221-2012 OI van Besien, Koen/0000-0002-8164-6211 NR 0 TC 5 Z9 5 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2006 VL 108 IS 11 MA 2483 BP 703A EP 704A PN 1 PG 2 WC Hematology SC Hematology GA 111GS UT WOS:000242440003273 ER PT J AU Kitada, S Jia, L Coward, LC Gorman, GS Noker, P Pellecchia, M Reed, JC AF Kitada, Shinichi Jia, Lee Coward, Lori C. Gorman, Greg S. Noker, Patricia Pellecchia, Maurizio Reed, John C. TI Bcl-2 antagonist ApoGossypol (NSC736630) displays single-agent activity in bcl-2 transgenic mice and has superior efficacy and pharmacology with less toxicity compared to gossypol (NSC19048). SO BLOOD LA English DT Meeting Abstract CT 48th Annual Meeting of the American-Society-of-Hematology CY DEC 09-12, 2006 CL Orlando, FL SP Amer Soc Hematol C1 Burnham Inst Med Res, Apoptosis Program, La Jolla, CA USA. NIH, NCI, DCTD, Dev Therapeut Program, Rockville, MD USA. So Res Inst, Birmingham, AL USA. NR 0 TC 0 Z9 0 U1 0 U2 2 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2006 VL 108 IS 11 MA 2487 BP 704A EP 705A PN 1 PG 2 WC Hematology SC Hematology GA 111GS UT WOS:000242440003277 ER PT J AU Dowdell, KC Pesnicak, L Hoffman, V Steadman, K Ruddel, M Straus, SE AF Dowdell, Kennichi C. Pesnicak, Lesley Hoffman, Victoria Steadman, Kenneth Ruddel, Mark Straus, Stephen E. TI Valproic acid (VPA), a historic deacetylase (HDAC) inhibitor, diminishes lymphoproliferation in the fas deficient MRL/lpr-/- murine model of autoimmune lymphoproliferative syndrome (ALPS). SO BLOOD LA English DT Meeting Abstract CT 48th Annual Meeting of the American-Society-of-Hematology CY DEC 09-12, 2006 CL Orlando, FL SP Amer Soc Hematol C1 NIH, NIAID, LCID, Bethesda, MD 20892 USA. NIH, NIAID, DVR, Bethesda, MD 20892 USA. NIH, NCI, MOB, Bethesda, MD 20892 USA. NIH, CC, DLM, Bethesda, MD 20892 USA. RI Steadman, Kenneth/J-3883-2013 NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2006 VL 108 IS 11 MA 2497 BP 707A EP 707A PN 1 PG 1 WC Hematology SC Hematology GA 111GS UT WOS:000242440003287 ER PT J AU Klion, AD Rothenberg, ME Murray, JJ Singh, A Simon, HU AF Klion, Amy D. Rothenberg, Marc E. Murray, John J. Singh, Anish Simon, Hans-Uwe TI Safety and tolerability of anti-IL-5 monoclonal antibody (Mepolizumab) therapy in patients with HES: A multicenter, randomized, double-blind, placebo-controlled trial. SO BLOOD LA English DT Meeting Abstract CT 48th Annual Meeting of the American-Society-of-Hematology CY DEC 09-12, 2006 CL Orlando, FL SP Amer Soc Hematol C1 NIH, Parasit Dis Lab, Bethesda, MD 20892 USA. Childrens Hosp, Med Ctr, Dept Pediat, Cincinnati, OH 45229 USA. Vanderbilt Univ, Dept Med, Nashville, TN USA. Sir Charles Gairdner Hosp, Perth, WA, Australia. Univ Bern, Dept Pharmacol, Bern, Switzerland. NR 0 TC 1 Z9 2 U1 0 U2 2 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2006 VL 108 IS 11 MA 2694 BP 762A EP 762A PN 1 PG 1 WC Hematology SC Hematology GA 111GS UT WOS:000242440003484 ER PT J AU Dunleavy, K Pittaluga, S Janik, J Grant, N Shovlin, M Little, R Yarchoan, R Steinberg, S Jaffe, ES Wilson, WH AF Dunleavy, Kieron Pittaluga, Stefania Janik, John Grant, Nicole Shovlin, Margaret Little, Richard Yarchoan, Robert Steinberg, Seth Jaffe, Elaine S. Wilson, Wyndham H. TI Novel treatment of Burkitt lymphoma with dose-adjusted EPOCHR-rituximab: Preliminary results showing excellent outcome. SO BLOOD LA English DT Meeting Abstract CT 48th Annual Meeting of the American-Society-of-Hematology CY DEC 09-12, 2006 CL Orlando, FL SP Amer Soc Hematol C1 Ctr Canc Res, Natl Canc Inst, Bethesda, MD USA. RI Jaffe, Elaine/G-8984-2014 OI Jaffe, Elaine/0000-0003-4632-0301 NR 0 TC 1 Z9 1 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2006 VL 108 IS 11 MA 2736 BP 774A EP 774A PG 1 WC Hematology SC Hematology GA 111GS UT WOS:000242440003525 ER PT J AU Wayne, AS Little, R Grant, N Steinberg, S Jaffe, ES Pittaluga, S Yarchoan, R Carrasquillo, J Janik, J Wilson, WH AF Wayne, Alan S. Little, Richard Grant, Nicole Steinberg, Seth Jaffe, Elaine S. Pittaluga, Stefania Yarchoan, Robert Carrasquillo, Jorge Janik, John Wilson, Wyndham H. TI Abbreviated treatment with EPOCH-Rituximab and HAART suspension is highly effective in AIDS-related lymphoma (AR-L). SO BLOOD LA English DT Meeting Abstract CT 48th Annual Meeting of the American-Society-of-Hematology CY DEC 09-12, 2006 CL Orlando, FL SP Amer Soc Hematol C1 Ctr Canc Res, Natl Canc Inst, Bethesda, MD USA. RI Carrasquillo, Jorge/E-7120-2010 NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2006 VL 108 IS 11 MA 2740 BP 775A EP 775A PG 1 WC Hematology SC Hematology GA 111GS UT WOS:000242440003529 ER PT J AU Hirt, C Schueler, F Kiefer, T Haas, A Niederwieser, D Neser, S Assmann, M Dachselt, K Leithaeuser, M Rabkin, CS Herold, M Dolken, G AF Hirt, Carsten Schueler, Frank Kiefer, Thomas Haas, Antje Niederwieser, Dietger Neser, Sabine Assmann, Michael Dachselt, Klaus Leithaeuser, Matte Rabkin, Charles S. Herold, Michael Dolken, Gottfried TI Prognostic significance of quantitative t(14;18) PCR monitoring in advanced stage follicular lymphoma patients. SO BLOOD LA English DT Meeting Abstract CT 48th Annual Meeting of the American-Society-of-Hematology CY DEC 09-12, 2006 CL Orlando, FL SP Amer Soc Hematol C1 Univ Greifswald, Med Ctr, Greifswald, Germany. Klinikum Ernst Von Bergmann, Potsdam, Germany. Univ Leipzig, D-7010 Leipzig, Germany. Klin Chemnitz, Chemnitz, Germany. Krankenhaus Riesa, Riesa, Germany. Suedharzkrankenhaus Nordhausen, Nordhausen, Germany. Univ Rostock, Rostock, Germany. DCEG, Natl Canc Inst, Bethesda, MD USA. Helios Klin Erfurt, Erfurt, Germany. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2006 VL 108 IS 11 MA 2757 BP 780A EP 780A PN 1 PG 1 WC Hematology SC Hematology GA 111GS UT WOS:000242440003546 ER PT J AU Lin, TS Phelps, M Dalton, JT Fischer, B Blum, KA Moran, ME McEldowney, MB Broering, S Colevas, D Byrd, JC Grever, MR AF Lin, Thomas S. Phelps, Mitch Dalton, James T. Fischer, Beth Blum, Kristie A. Moran, Mollie E. McEldowney, Michelle B. Broering, Sara Colevas, Dimitrios Byrd, John C. Grever, Michael R. TI Flavopiridol can be safely dose escalated in relapsed CLL patients: Achievement of target C-max results in improved clinical activity. SO BLOOD LA English DT Meeting Abstract CT 48th Annual Meeting of the American-Society-of-Hematology CY DEC 09-12, 2006 CL Orlando, FL SP Amer Soc Hematol C1 Ohio State Univ, Div Hematol & Oncol, Columbus, OH 43210 USA. Ohio State Univ, Coll Pharm, Columbus, OH 43210 USA. Natl Canc Inst, Canc Therapy Evaluat Program, Rockville, MD USA. RI Phelps, Mitch/H-3941-2013; Blum, Kristie/E-2768-2011 OI Phelps, Mitch/0000-0002-1615-5280; NR 0 TC 3 Z9 3 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2006 VL 108 IS 11 MA 2845 BP 805A EP 806A PN 1 PG 2 WC Hematology SC Hematology GA 111GS UT WOS:000242440003634 ER PT J AU Hardy, NM Hakim, F Steinberg, S Krumlauf, M Babb, R Odom, J Fowler, D Gress, R Bishop, MR AF Hardy, Nancy M. Hakim, Frances Steinberg, Seth Krumlauf, Michael Babb, Rebecca Odom, Jeanne Fowler, Daniel Gress, Ronald Bishop, Michael R. TI Ex-vivo reduction of allograft T cell dose does not prevent acute graft-vs-host disease after reduced-intensity hematopoietic stem cell transplantation. SO BLOOD LA English DT Meeting Abstract CT 48th Annual Meeting of the American-Society-of-Hematology CY DEC 09-12, 2006 CL Orlando, FL SP Amer Soc Hematol C1 NIH, NIC CCR, Experiment Tranplantat & Immunol Branch, Bethesda, MD USA. NIH, NIC CCR, Biostat & Data Manage Sect, Bethesda, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2006 VL 108 IS 11 MA 2871 BP 813A EP 813A PG 1 WC Hematology SC Hematology GA 111GS UT WOS:000242440003660 ER PT J AU Boyiadzis, M Hakim, FT Memon, SA Dean, R Fowler, D Gress, RE Bishop, MR AF Boyiadzis, Michael Hakim, Frances T. Memon, Sarfraz A. Dean, Robert Fowler, Daniel Gress, Ronald E. Bishop, Michael R. TI Early reconstitution of natural killer cells following non-myeloablative hematopoietic stem cell transplantation predicts the development of acute graft-versus-host disease. SO BLOOD LA English DT Meeting Abstract CT 48th Annual Meeting of the American-Society-of-Hematology CY DEC 09-12, 2006 CL Orlando, FL SP Amer Soc Hematol C1 Natl Canc Inst, Experiment Transplantat & Immunol Branch, Bethesda, MD USA. RI Memon, Sarfraz/E-1198-2013 NR 0 TC 0 Z9 0 U1 0 U2 1 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2006 VL 108 IS 11 MA 2882 BP 816A EP 816A PG 1 WC Hematology SC Hematology GA 111GS UT WOS:000242440003671 ER PT J AU Srivastava, S Savani, BN Geller, N Carvallo, C Srinivasan, R Takahashi, Y Lundqvist, A Kurlander, R Goodwin, R Barrett, AJ Fleisher, T Childs, RW AF Srivastava, Shivani Savani, Bipin N. Geller, N. Carvallo, C. Srinivasan, Ramaprasad Takahashi, Y. Lundqvist, A. Kurlander, R. Goodwin, R. Barrett, A. John Fleisher, T. Childs, Richard W. TI Pre-transplant T-cell lymphopenia accelerates early donor T-cell and myeloid chimerism but is not required for full donor lymphohematopoietic engraftment or to prevent graft rejection following nonmyeloabladve hematopoietic cell transplantation (NST). SO BLOOD LA English DT Meeting Abstract CT 48th Annual Meeting of the American-Society-of-Hematology CY DEC 09-12, 2006 CL Orlando, FL SP Amer Soc Hematol C1 Natl Inst Hlth, NHLBI, Hematol Branch, Bethesda, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2006 VL 108 IS 11 MA 2981 BP 845A EP 845A PN 1 PG 1 WC Hematology SC Hematology GA 111GS UT WOS:000242440004029 ER PT J AU Hsieh, MM Kang, EM Link, B Berg, M Childs, RW Kurlander, R Powell, J Rodgers, GP Tisdale, JF AF Hsieh, Matthew M. Kang, Elizabeth M. Link, Beth Berg, Maria Childs, Richard W. Kurlander, Roger Powell, Jonathan Rodgers, Griffin P. Tisdale, John F. TI Novel allogeneic transplant conditioning regimen designed for tolerance induction in patients with severe sickle cell disease. SO BLOOD LA English DT Meeting Abstract CT 48th Annual Meeting of the American-Society-of-Hematology CY DEC 09-12, 2006 CL Orlando, FL SP Amer Soc Hematol C1 NIH, NIDDK, MCHB, Bethesda, MD 20892 USA. NIAID, LHD, Bethesda, MD USA. NHLBI, HB, Bethesda, MD USA. NIH, DLM, CC, Bethesda, MD USA. Johns Hopkins Sch Med, Baltimore, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2006 VL 108 IS 11 MA 2994 BP 849A EP 849A PN 1 PG 1 WC Hematology SC Hematology GA 111GS UT WOS:000242440004042 ER PT J AU Savani, BN Mielke, S Rezvani, K Yong, A Hensel, N Read, EJ Childs, R Barrett, AJ AF Savani, Bipin N. Mielke, Stephan Rezvani, Katayoun Yong, Agnes Hensel, Nancy Read, Elizabeth J. Childs, Richard Barrett, A. John TI Total lymphocyte and natural killer (NK) cell count day 30 post transplant strongly predict transplant outcome after T cell depleted allogeneic stem cell transplantation. SO BLOOD LA English DT Meeting Abstract CT 48th Annual Meeting of the American-Society-of-Hematology CY DEC 09-12, 2006 CL Orlando, FL SP Amer Soc Hematol C1 Natl Inst Hlth, NHLBI, Hematol Branch, Bethesda, MD USA. Natl Inst Hlth, Ctr Clin, Dept Transfus Med, Cell Processing Sect, Bethesda, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2006 VL 108 IS 11 MA 2993 BP 849A EP 849A PG 1 WC Hematology SC Hematology GA 111GS UT WOS:000242440004041 ER PT J AU Murphy, WJ Welniak, LA Li, MH Sayers, TJ Panoskaltsis-Mortari, A Blazar, BR Sun, K AF Murphy, William J. Welniak, Lisbeth A. Li, Minghui Sayers, Thomas J. Panoskaltsis-Mortari, Angela Blazar, Bruce R. Sun, Kai TI Removal of donor CD4+T cells markedly promotes graft-versus-tumor (GVT) effects and inhibits GVHD-dependent toxicity associated with prolonged bortezomib administration after allogeneic BMT. SO BLOOD LA English DT Meeting Abstract CT 48th Annual Meeting of the American-Society-of-Hematology CY DEC 09-12, 2006 CL Orlando, FL SP Amer Soc Hematol C1 Univ Nevada, Reno, NV 89557 USA. Natl Canc Inst, Expt Immunol Lab, Frederick, MD USA. Univ Minnesota, Ctr Canc, Dept Pediat, Minneapolis, MN USA. RI Sayers, Thomas/G-4859-2015 NR 0 TC 0 Z9 0 U1 0 U2 1 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2006 VL 108 IS 11 MA 3160 BP 902A EP 902A PN 1 PG 1 WC Hematology SC Hematology GA 111GS UT WOS:000242440004208 ER PT J AU Kawai, T Choi, U Liu, PC Malech, HL AF Kawai, Toshinao Choi, Uimook Liu, Po-Ching Malech, Harry L. TI Enhanced engraftment of human CD34+stem cells in NOD/SCID mice by diprotin a occurs by inhibition of recipient CD26/Dipeptidyl Peptidase-IV (DPP-IV). SO BLOOD LA English DT Meeting Abstract CT 48th Annual Meeting of the American-Society-of-Hematology CY DEC 09-12, 2006 CL Orlando, FL SP Amer Soc Hematol C1 NIAID, Natl Inst Hlth, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2006 VL 108 IS 11 MA 3178 BP 907A EP 907A PN 1 PG 1 WC Hematology SC Hematology GA 111GS UT WOS:000242440004226 ER PT J AU Li, NN Zhang, CY Lin, CL McCulloch, B Wright, J Kirschbaum, M Forman, S Zeng, DF AF Li, Nainong Zhang, Chunyan Lin, Chia-Lei McCulloch, Bill Wright, John Kirschbaum, Mark Forman, Stephen Zeng, Defu TI A radiation-free immune and epigenetics based conditioning regimen for allogeneic HCT: Combination of anti-CD3 and romidepsin. SO BLOOD LA English DT Meeting Abstract CT 48th Annual Meeting of the American-Society-of-Hematology CY DEC 09-12, 2006 CL Orlando, FL SP Amer Soc Hematol C1 City Hope Natl Med Ctr, Beckman Res Inst, Div Hematol, Duarte, CA 91010 USA. CTEP, Natl Canc Inst, Rockville, MD USA. Gloucester Pharmaceut, Cambridge, MA USA. Fujian Med Univ Union Hosp, Dept Hematol, Fujian, Peoples R China. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2006 VL 108 IS 11 MA 3204 BP 914A EP 914A PN 1 PG 1 WC Hematology SC Hematology GA 111GS UT WOS:000242440004252 ER PT J AU Lundqvist, A McCoy, P Samsel, L Smith, A Srivastava, S Harashima, N Yokoyama, H Berg, M Childs, R AF Lundqvist, Andreas McCoy, Philip Samsel, Leigh Smith, Aleah Srivastava, Shivani Harashima, Nanae Yokoyama, Hisayuki Berg, Maria Childs, Richard TI Adoptive infusion of alloreactive donor NK cells reduces GVHD, mediates anti-tumor effects and prolongs survival in recipients of MHC-Matched hematopoietic cell transplantation. SO BLOOD LA English DT Meeting Abstract CT 48th Annual Meeting of the American-Society-of-Hematology CY DEC 09-12, 2006 CL Orlando, FL SP Amer Soc Hematol C1 NIH, NHLBI, Hematol Branch, Bethesda, MD 20892 USA. NIH, NHLBI, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2006 VL 108 IS 11 MA 3233 BP 923A EP 923A PG 1 WC Hematology SC Hematology GA 111GS UT WOS:000242440004281 ER PT J AU Ryu, BY Gray, JT Bodine, DM Nienhuis, AW AF Ryu, Byoung Y. Gray, John T. Bodine, David M. Nienhuis, Arthur W. TI The effect of a chromatin insulator (5'cHS4) on enhanced expression of the LMO2 proto-oncogene by an oncoretroviral long terminal repeat. SO BLOOD LA English DT Meeting Abstract CT 48th Annual Meeting of the American-Society-of-Hematology CY DEC 09-12, 2006 CL Orlando, FL SP Amer Soc Hematol C1 St Jude Childrens Res Hosp, Memphis, TN 38105 USA. NHGRI, Genet & Mol Biol Branch, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2006 VL 108 IS 11 MA 3253 BP 928A EP 928A PN 1 PG 1 WC Hematology SC Hematology GA 111GS UT WOS:000242440004301 ER PT J AU Neschadim, A Sato, T Fowler, DH Lavie, A Medin, JA AF Neschadim, Anton Sato, Takeya Fowler, Daniel H. Lavie, Arnon Medin, Jeffrey A. TI Development of improved lentiviral 'suicide' gene therapy for the management of GvHD and GvL/GvT responses in allogeneic BMT. SO BLOOD LA English DT Meeting Abstract CT 48th Annual Meeting of the American-Society-of-Hematology CY DEC 09-12, 2006 CL Orlando, FL SP Amer Soc Hematol C1 UHN, OCI, Div Stem Cell & Dev Biol, Toronto, ON, Canada. NCI, NIH, Ctr Canc Res, Bethesda, MD 20892 USA. Univ Illinois, Chicago, IL 60607 USA. Univ Toronto, Toronto, ON, Canada. Univ Toronto, Inst Med Sci, Toronto, ON, Canada. RI Lavie, Arnon/H-4927-2012 NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2006 VL 108 IS 11 MA 3256 BP 929A EP 929A PN 1 PG 1 WC Hematology SC Hematology GA 111GS UT WOS:000242440004304 ER PT J AU Harrow, FJ Frazar, TF Seidel, NE Gallagher, PG Bodine, DM AF Harrow, Faith J. Frazar, Tiffany F. Seidel, Nancy E. Gallagher, Patrick G. Bodine, David M. TI Lentivirus vectors containing a band 3/gamma-globin gene flanked by distinct insulator elements are resistant to gene silencing in primary mouse erythroid cells. SO BLOOD LA English DT Meeting Abstract CT 48th Annual Meeting of the American-Society-of-Hematology CY DEC 09-12, 2006 CL Orlando, FL SP Amer Soc Hematol C1 NHGRI, Hematopoiesis Sect, Bethesda, MD USA. Childrens Hosp, Boston, MA 02115 USA. Yale Univ, New Haven, CT USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2006 VL 108 IS 11 MA 3260 BP 930A EP 930A PN 1 PG 1 WC Hematology SC Hematology GA 111GS UT WOS:000242440004308 ER PT J AU Kim, YJ Hussein, NL Hematti, P Hong, BK Calmels, B Donahue, RE Hanawa, H Nienhuis, AW Dunbar, CE AF Kim, Yoo-Jin Hussein, Nadia L. Hematti, Peiman Hong, Bum-Kee Calmels, Boris Donahue, Robert E. Hanawa, Hideki Nienhuis, Arthur W. Dunbar, Cynthia E. TI Long-term polyclonal and stable gene transfer into rhesus repopulating hematopoietic stem cells using a simian immunodeficiency virus-based lentiviral vector system. SO BLOOD LA English DT Meeting Abstract CT 48th Annual Meeting of the American-Society-of-Hematology CY DEC 09-12, 2006 CL Orlando, FL SP Amer Soc Hematol C1 NHLBI, Natl Inst Hlth, Hematol Branch, Bethesda, MD 20892 USA. St Jude Childrens Res Hosp, Dept Hematol Oncol, Memphis, TN 38105 USA. RI calmels, boris/R-2538-2016 NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2006 VL 108 IS 11 MA 3259 BP 930A EP 930A PN 1 PG 1 WC Hematology SC Hematology GA 111GS UT WOS:000242440004307 ER PT J AU Laflamme, K Elnitski, L Owen, AN Gallagher, PG Bodine, DM AF Laflamme, Karina Elnitski, Laura Owen, Ashley N. Gallagher, Patrick G. Bodine, David M. TI Identification of a novel core promoter element that enhances transcription: Application to ankyrin promoters for globin gene therapy. SO BLOOD LA English DT Meeting Abstract CT 48th Annual Meeting of the American-Society-of-Hematology CY DEC 09-12, 2006 CL Orlando, FL SP Amer Soc Hematol C1 NHGRI, Hematopoiesis Sect, Bethesda, MD USA. NHGRI, Genome Technol Branch, Rockville, MD USA. Yale Univ, New Haven, CT USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2006 VL 108 IS 11 MA 3261 BP 931A EP 931A PN 1 PG 1 WC Hematology SC Hematology GA 111GS UT WOS:000242440004309 ER PT J AU Larochelle, A Choi, U Naumann, N Clevenger, JR Malech, HL Dunbar, CE AF Larochelle, Andre Choi, Uimook Naumann, Nora Clevenger, Josh R. Malech, Harry L. Dunbar, Cynthia E. TI Methylguanine methyltransferase-based in vivo selection results in only transient improvement in long-term marking after autologous transplantation of transduced hematopoietic stem cells in rhesus macaques. SO BLOOD LA English DT Meeting Abstract CT 48th Annual Meeting of the American-Society-of-Hematology CY DEC 09-12, 2006 CL Orlando, FL SP Amer Soc Hematol C1 NHLBI, Natl Inst Hlth, Bethesda, MD USA. NIAID, Natl Inst Hlth, Bethesda, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2006 VL 108 IS 11 MA 3272 BP 934A EP 934A PN 1 PG 1 WC Hematology SC Hematology GA 111GS UT WOS:000242440004320 ER PT J AU Moayeri, M De Ravin, SS Kennedy, DR Naumann, N Ikeda, Y Felsburg, PJ Malech, HL AF Moayeri, Morvarid De Ravin, Suk See Kennedy, Douglas R. Naumann, Nora Ikeda, Yasuhiro Felsburg, Peter J. Malech, Harry L. TI Improvement of canine XSCID by in vivo gene therapy using RD114/TR-pseudotyped SIV lentiviral vectors. SO BLOOD LA English DT Meeting Abstract CT 48th Annual Meeting of the American-Society-of-Hematology CY DEC 09-12, 2006 CL Orlando, FL SP Amer Soc Hematol C1 NIH, NIAID, Host Def Lab, Bethesda, MD 20892 USA. Univ Penn, Sch Vet Med, Philadelphia, PA 19104 USA. Mayo Clin, Coll Med, Program Mol Med, Rochester, MN USA. NR 0 TC 1 Z9 1 U1 1 U2 1 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2006 VL 108 IS 11 MA 3275 BP 935A EP 935A PN 1 PG 1 WC Hematology SC Hematology GA 111GS UT WOS:000242440004323 ER PT J AU Naumann, N De Ravin, SS Choi, U Moayeri, M Ikeda, Y Malech, HL AF Naumann, Nora De Ravin, Suk See Choi, Uimook Moayeri, Morvarid Ikeda, Yasuhiro Malech, Harry L. TI Correction of human X-linked chronic granulomatous disease (X-CGD) following transduction of X-CGD CD34+cells with a modified RD114-pseudotyped simian immunodeficiency virus lentiviral vector in a NOD/SCID mouse xenograft model. SO BLOOD LA English DT Meeting Abstract CT 48th Annual Meeting of the American-Society-of-Hematology CY DEC 09-12, 2006 CL Orlando, FL SP Amer Soc Hematol C1 NIH, NIAID, Host Def Lab, Bethesda, MD 20892 USA. Mayo Clin, Coll Med, Program Mol Med, Rochester, MN USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2006 VL 108 IS 11 MA 3278 BP 936A EP 936A PN 1 PG 1 WC Hematology SC Hematology GA 111GS UT WOS:000242440004326 ER PT J AU Werner, EM Treadwell, M Hassell, K Keller, S Levine, R AF Werner, Ellen M. Treadwell, Marsha Hassell, Kathryn Keller, San Levine, Roger TI Sickle cell disease health-related quality of life questionnaire project. SO BLOOD LA English DT Meeting Abstract CT 48th Annual Meeting of the American-Society-of-Hematology CY DEC 09-12, 2006 CL Orlando, FL SP Amer Soc Hematol C1 NHLBI, NIH, Blood Dis Program, Bethesda, MD 20892 USA. Childrens Hosp, Res Ctr, No CA Sickle Cell Ctr, Oakland, CA 94609 USA. Amer Inst Res, Chapel Hill, NC USA. NR 0 TC 3 Z9 3 U1 1 U2 3 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2006 VL 108 IS 11 MA 3339 BP 953A EP 953A PN 1 PG 1 WC Hematology SC Hematology GA 111GS UT WOS:000242440004387 ER PT J AU Qiang, YW Chen, Y Brown, N Ojha, RP Rudikoff, S Barlogie, B Shaughnessy, JD AF Qiang, Ya-Wei Chen, Yu Brown, Nathan Ojha, Rohit P. Rudikoff, Stuart Barlogie, Bart Shaughnessy, John D., Jr. TI Toward defining the functional relevance of Wnt signaling in osteoclasts in multiple myeloma. SO BLOOD LA English DT Meeting Abstract CT 48th Annual Meeting of the American-Society-of-Hematology CY DEC 09-12, 2006 CL Orlando, FL SP Amer Soc Hematol C1 Univ Arkansas Med Sci, Myeloma Inst Res & Therapy, Little Rock, AR 72205 USA. NIH, Natl Canc Inst, Mol & Cellular Biol Lab, Bethesda, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2006 VL 108 IS 11 MA 3422 BP 977A EP 977A PN 1 PG 1 WC Hematology SC Hematology GA 111GS UT WOS:000242440004471 ER PT J AU Qiang, YW Chen, Y Stephens, O Rubin, J Rudikoff, S Barlogie, B Shaughnessy, JD AF Qiang, Ya-Wei Chen, Yu Stephens, Owen Rubin, Jeff Rudikoff, Stuart Barlogie, Bart Shaughnessy, John D., Jr. TI On the molecular mechanism of DKK1 inhibition of osteoblast differentiation in multiple myeloma. SO BLOOD LA English DT Meeting Abstract CT 48th Annual Meeting of the American-Society-of-Hematology CY DEC 09-12, 2006 CL Orlando, FL SP Amer Soc Hematol C1 Univ Arkansas Med Sci, Mye Inst Res & Therapy, Little Rock, AR 72205 USA. Natl Canc Inst, NIH, Cellular & Mol Biol Lab, Bethesda, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2006 VL 108 IS 11 MA 3429 BP 979A EP 979A PN 1 PG 1 WC Hematology SC Hematology GA 111GS UT WOS:000242440004478 ER PT J AU Kiziltepe, T Hideshima, T Raje, N Ishitsuka, K Ocio, EM Catley, L Li, CQ Trudel, L Yasui, H Shirashi, N Tai, YT Chauhan, D Mitsiades, C Saavedra, JE Wogan, GN Keefer, LK Shami, PJ Anderson, KC AF Kiziltepe, Tanyel Hideshima, Teru Raje, Noopur Ishitsuka, Kenji Ocio, Enrique M. Catley, Laurence Li, Chun-Qi Trudel, Laura Yasui, Hiroshi Shirashi, Norihiko Tai, Yu-Tzu Chauhan, Dharminder Mitsiades, Constantine Saavedra, Joseph E. Wogan, Gerald N. Keefer, Larry K. Shami, Paul J. Anderson, Kenneth C. TI JS-K, a GST-activated nitric oxide, generator, induces DNA-double strand breaks and inhibits growth and survival of multiple myeloma cells in vitro and in vivo. SO BLOOD LA English DT Meeting Abstract CT 48th Annual Meeting of the American-Society-of-Hematology CY DEC 09-12, 2006 CL Orlando, FL SP Amer Soc Hematol C1 Harvard Med Sch, Jerome Lipper Multiple Myeloma Ctr, Dana Farber Canc Inst, Boston, MA USA. MIT, Biol Engn Div, Cambridge, MA 02139 USA. SAIC, Frederick, MD USA. NIH, NCI, Lab Comparat Carcinogenesis, Frederick, MD USA. Univ Utah, Salt Lake City Vet Adm Med Ctr, Div Med Oncol, Salt Lake City, UT USA. RI Catley, Laurence/E-5313-2013; Keefer, Larry/N-3247-2014 OI Keefer, Larry/0000-0001-7489-9555 NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2006 VL 108 IS 11 MA 3453 BP 985A EP 985A PN 1 PG 1 WC Hematology SC Hematology GA 111GS UT WOS:000242440004502 ER PT J AU Maric, I Robyn, J Fu, W Stoddard, J Metcalfe, DD Noel, P AF Maric, Irina Robyn, Jamie Fu, Weiming Stoddard, Jennifer Metcalfe, Dean D. Noel, Pierre TI Detection of c-kit mutation in peripheral blood vs. bone marrow aspirates in patients with systemic mastocytosis: Comparison study of pathological and clinical laboratory findings in patients with and without detectable c-kit mutation in the peripheral blood. SO BLOOD LA English DT Meeting Abstract CT 48th Annual Meeting of the American-Society-of-Hematology CY DEC 09-12, 2006 CL Orlando, FL SP Amer Soc Hematol C1 NIH, CC, Dept Lab Med, Bethesda, MD 20892 USA. NIH, NIAID, Allerg Dis Res Lab, Bethesda, MD 20892 USA. NR 0 TC 1 Z9 1 U1 0 U2 1 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2006 VL 108 IS 11 MA 3596 BP 1027A EP 1027A PN 1 PG 1 WC Hematology SC Hematology GA 111GS UT WOS:000242440004645 ER PT J AU Lee, YN Noel, P Shahlaee, A Carter, M Kapur, R Wayne, A Metcalfe, DD Takemoto, C AF Lee, Youl-Nam Noel, Pierre Shahlaee, Amir Carter, Melody Kapur, Reuben Wayne, Alan Metcalfe, Dean D. Takemoto, Clifford TI Kit signaling regulates mitf expression in mastocytosis. SO BLOOD LA English DT Meeting Abstract CT 48th Annual Meeting of the American-Society-of-Hematology CY DEC 09-12, 2006 CL Orlando, FL SP Amer Soc Hematol C1 Johns Hopkins Univ, Baltimore, MD USA. NIH, Dept Lab Med, Bethesda, MD 20892 USA. Univ Florida, Gainesville, FL USA. NIH, NIAID, Allerg Dis Res Lab, Bethesda, MD 20892 USA. Indiana Univ, Sch Med, Indianapolis, IN 46204 USA. NIH, Pediat Oncol Branch, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2006 VL 108 IS 11 MA 3601 BP 1028A EP 1029A PN 1 PG 2 WC Hematology SC Hematology GA 111GS UT WOS:000242440004650 ER PT J AU Tawab, A Fan, Y Mai, T Read, EJ Kurlander, RJ AF Tawab, Abdul Fan, Yong Mai, Thao Read, Elizabeth J. Kurlander, Roger J. TI Prolonging the incubation of monocytes with GM-CSF and IL-4 for more than 3 days during the generation of dendritic cells (DCS) in vitro markedly diminishes IL-12 and increases IL-10 production when DCS are subsequently matured. SO BLOOD LA English DT Meeting Abstract CT 48th Annual Meeting of the American-Society-of-Hematology CY DEC 09-12, 2006 CL Orlando, FL SP Amer Soc Hematol C1 NIH, Ctr Clin, Dept Lab Med, Bethesda, MD 20892 USA. NIH, Ctr Clin, Dept Transfus Med, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2006 VL 108 IS 11 MA 3653 BP 1043A EP 1044A PN 1 PG 2 WC Hematology SC Hematology GA 111GS UT WOS:000242440004702 ER PT J AU Rezvani, K Yong, A Mielke, S Savani, BN Price, DA Gostick, E Douek, DC Barrett, AJ AF Rezvani, Katayoun Yong, Agnes Mielke, Stephan Savani, Bipin N. Price, David A. Gostick, Emma Douek, Daniel C. Barrett, A. John TI WT1-specific CD8+ T lymphocytes may participate in the elimination of acute lymphoblastic leukemia following allogeneic stem cell transplantation. SO BLOOD LA English DT Meeting Abstract CT 48th Annual Meeting of the American-Society-of-Hematology CY DEC 09-12, 2006 CL Orlando, FL SP Amer Soc Hematol C1 NHLBI, NIH, Bethesda, MD 20892 USA. Vaccine Res Ctr, NIH, Bethesda, MD USA. Nuffield Dept Med, Oxford, England. RI Price, David/C-7876-2013 OI Price, David/0000-0001-9416-2737 NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2006 VL 108 IS 11 MA 3679 BP 1051A EP 1051A PG 1 WC Hematology SC Hematology GA 111GS UT WOS:000242440004728 ER PT J AU Muranski, P Boni, A Paulos, CM Irvine, KR Antony, PA Restifo, NP AF Muranski, Pawel Boni, Andrea Paulos, Crystal M. Irvine, Kari R. Antony, Paul A. Restifo, Nicholas P. TI Treatment of established B16 murine melanoma tumors with Tyrp-1 specific CD4(+) lymphocytes. SO BLOOD LA English DT Meeting Abstract CT 48th Annual Meeting of the American-Society-of-Hematology CY DEC 09-12, 2006 CL Orlando, FL SP Amer Soc Hematol C1 NIH, Natl Canc Inst, Bethesda, MD 20892 USA. RI Restifo, Nicholas/A-5713-2008; Muranski, Pawel/E-5572-2010 NR 0 TC 0 Z9 0 U1 0 U2 2 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2006 VL 108 IS 11 MA 3688 BP 1054A EP 1054A PN 1 PG 1 WC Hematology SC Hematology GA 111GS UT WOS:000242440004737 ER PT J AU Mossoba, ME Walia, JS Rasaiah, VL Fowler, DH Medin, JA AF Mossoba, Miriam E. Walia, Jagdeep S. Rasaiah, Vanessa L. Fowler, Daniel H. Medin, Jeffrey A. TI Overcoming self-tolerance: Long-term protection against specific erbB2-expressing prostate tumors using low doses of lentivirus-transduced DCs. SO BLOOD LA English DT Meeting Abstract CT 48th Annual Meeting of the American-Society-of-Hematology CY DEC 09-12, 2006 CL Orlando, FL SP Amer Soc Hematol C1 Univ Toronto, Dept Biomed Phys, Toronto, ON, Canada. Univ Hlth Network, Div Stem Cell & Dev Biol, Toronto, ON, Canada. NIH, Ctr Canc Res, Rockville, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2006 VL 108 IS 11 MA 3696 BP 1056A EP 1056A PN 1 PG 1 WC Hematology SC Hematology GA 111GS UT WOS:000242440004745 ER PT J AU Yong, ASM Rezvani, K Savani, BN Eniafe, R Mielke, S Goldman, JM Barrett, AJ AF Yong, Agnes S. M. Rezvani, Katayoun Savani, Bipin N. Eniafe, Rhoda Mielke, Stephan Goldman, John M. Barrett, A. John TI Cytotoxic T lymphocyte responses to PR1 peptide in chronic myeloid leukemia patients inversely correlate with proteinase 3 and elastase expression but donor PR1 responses determine survival after stem cell transplantation. SO BLOOD LA English DT Meeting Abstract CT 48th Annual Meeting of the American-Society-of-Hematology CY DEC 09-12, 2006 CL Orlando, FL SP Amer Soc Hematol C1 NIH, NHLBI, Hematol Branch, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2006 VL 108 IS 11 MA 3697 BP 1056A EP 1056A PG 1 WC Hematology SC Hematology GA 111GS UT WOS:000242440004746 ER PT J AU Hewitt, RE Melenhorst, JJ Price, DA Gostick, E Hensel, NF Mccoy, JP Barrett, AJ AF Hewitt, Rachel E. Melenhorst, J. Joseph Price, David A. Gostick, Emina Hensel, Nancy F. Mccoy, J. P. Barrett, A. John TI Widening the applicability of human neutrophil elastase and proteinase 3 peptide vaccines by elucidating immunogenic non-HLA-A2 MHC class I restricted epitopes. SO BLOOD LA English DT Meeting Abstract CT 48th Annual Meeting of the American-Society-of-Hematology CY DEC 09-12, 2006 CL Orlando, FL SP Amer Soc Hematol C1 NIH, NHLBI, Bethesda, MD 20892 USA. Univ Oxford, Nuffield Dept Med, Oxford, England. NIH, NHLBI, Flow Cytometry Core Facil, Bethesda, MD 20892 USA. RI Price, David/C-7876-2013 OI Price, David/0000-0001-9416-2737 NR 0 TC 1 Z9 1 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 16 PY 2006 VL 108 IS 11 MA 3708 BP 1059A EP 1059A PN 1 PG 1 WC Hematology SC Hematology GA 111GS UT WOS:000242440004757 ER PT J AU Andreani, A Burnelli, S Granaiola, M Leoni, A Locatelli, A Morigi, R Rambaldi, M Varoli, L Kunkel, MW AF Andreani, Aldo Burnelli, Silvia Granaiola, Massimiliano Leoni, Alberto Locatelli, Alessandra Morigi, Rita Rambaldi, Mirella Varoli, Lucilla Kunkel, Mark W. TI Antitumor activity of substituted E-3-(3,4,5-trimethoxybenzylidene)-1,3-dihydroindol-2-ones SO JOURNAL OF MEDICINAL CHEMISTRY LA English DT Article ID MULTIPLE MECHANISMS; CARDIOTONIC ACTIVITY; CANCER CELLS; 2-INDOLINONES AB The design and synthesis of anticancer E-3-( 3,4,5-trimethoxybenzylidene)-1,3-dihydroindol-2-ones is reported. Strong COMPARE correlations among the cell line responses suggest that these compounds may be acting similarly through a combination of different mechanisms of action. The 5-methoxy derivative ( 2h) was the most active compound with a mean pGI(50) of 6.34, and it is now under review by Biological Evaluation Committee of the National Cancer Institute for possible further studies. C1 Univ Bologna, Dipartimento Sci Farmaceut, I-40126 Bologna, Italy. NCI, Dev Therapeut Program, Informat Technol Branch, Div Canc Treatment & Diag, Bethesda, MD 20892 USA. RP Andreani, A (reprint author), Univ Bologna, Dipartimento Sci Farmaceut, Via Belmeloro 6, I-40126 Bologna, Italy. EM aldo.andreani@unibo.it OI LEONI, ALBERTO/0000-0001-8528-8207 NR 15 TC 42 Z9 42 U1 0 U2 3 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA SN 0022-2623 J9 J MED CHEM JI J. Med. Chem. PD NOV 16 PY 2006 VL 49 IS 23 BP 6922 EP 6924 DI 10.1021/jm0607808 PG 3 WC Chemistry, Medicinal SC Pharmacology & Pharmacy GA 103NP UT WOS:000241894000034 PM 17154522 ER PT J AU Coward, L Gorman, G Noker, P Kerstner-Wood, C Pellecchia, A Reed, JC Jia, L AF Coward, L. Gorman, G. Noker, P. Kerstner-Wood, C. Pellecchia, A. Reed, J. C. Jia, L. TI Quantitative determination of apogossypol, a pro-apoptotic analog of gossypol, in mouse plasma using LC/MS/MS SO JOURNAL OF PHARMACEUTICAL AND BIOMEDICAL ANALYSIS LA English DT Article DE apogossypol; gossypol; LC/MS/MS; quantitative analysis ID PERFORMANCE LIQUID-CHROMATOGRAPHY; ENANTIOMERS; BINDING AB A simple and selective liquid chromatography/tandem mass spectrometry (LC/MS/MS) method based on internal standard quantitation using apigenin as the internal standard has been developed and validated for the analysis of the gossypol analog apogossypol, a pro-apoptotic compound, in mouse plasma. The methodology involves protein precipitation of plasma samples followed by LC/MS/MS analysis. Ascorbic acid was added to the spiking solutions and plasma samples to stabilize the easily oxidized compound. Separation of apogossypol and the internal standard from the plasma matrix was achieved using a C 18 column with a gradient elution profile consisting of 5 mM ammonium acetate and methanol. The validated range of the method extended from 10 to 2000 ng/mL with accuracies of 85-115% and precision of < 15%. The average recovery of apogossypol at three concentrations (50, 200 and 1000 ng/mL) assayed in triplicate using this methodology was determined to be 90.8 +/- 12.9%. Recovery for the internal standard (apigenin) at a concentration of 500 ng/mL was found to be 99.9 +/- 6.41%. Apogossypol concentrations of 50 ng/mL and above were found to be stable in extracted plasma for 24 h when stored at 25 degrees C. This method has been applied to the determination of apogossypol concentrations in plasma collected from mice given an IV dose of apogossypol. (c) 2006 Elsevier B.V. All rights reserved. C1 So Res Inst, Birmingham, AL 35205 USA. Burnham Inst, La Jolla, CA 92037 USA. NCI, Dev Therapeut Program, NIH, Rockville, MD 20852 USA. RP Coward, L (reprint author), So Res Inst, 2000 9th Ave S, Birmingham, AL 35205 USA. EM coward@sri.org FU NCI NIH HHS [N01-CM-52203] NR 12 TC 13 Z9 15 U1 1 U2 11 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND SN 0731-7085 J9 J PHARMACEUT BIOMED JI J. Pharm. Biomed. Anal. PD NOV 16 PY 2006 VL 42 IS 5 BP 581 EP 586 DI 10.1016/j.jpba.2006.05.020 PG 6 WC Chemistry, Analytical; Pharmacology & Pharmacy SC Chemistry; Pharmacology & Pharmacy GA 114FI UT WOS:000242651700008 PM 16859853 ER PT J AU Chandrashekar, J Hoon, MA Ryba, NJP Zuker, CS AF Chandrashekar, Jayaram Hoon, Mark A. Ryba, Nicholas J. P. Zuker, Charles S. TI The receptors and cells for mammalian taste SO NATURE LA English DT Review ID GATED CATION CHANNEL; BITTER-TASTE; SWEET TASTE; UMAMI TASTE; SOUR TASTE; SACCHARIN PREFERENCE; AMINO-ACIDS; TRANSIENT RECEPTOR; POSITIONAL CLONING; K+ CHANNELS AB The emerging picture of taste coding at the periphery is one of elegant simplicity. Contrary to what was generally believed, it is now clear that distinct cell types expressing unique receptors are tuned to detect each of the five basic tastes: sweet, sour, bitter, salty and umami. Importantly, receptor cells for each taste quality function as dedicated sensors wired to elicit stereotypic responses. C1 Univ Calif San Diego, Howard Hughes Med Inst, La Jolla, CA 92093 USA. Univ Calif San Diego, Dept Neurobiol, La Jolla, CA 92093 USA. Univ Calif San Diego, Dept Neurosci, La Jolla, CA 92093 USA. Natl Inst Dent & Craniofacial Res, NIH, Bethesda, MD 20892 USA. RP Ryba, NJP (reprint author), Univ Calif San Diego, Howard Hughes Med Inst, La Jolla, CA 92093 USA. EM nick.ryba@nih.gov; czuker@ucsd.edu RI Marion-Poll, Frederic/D-8882-2011 OI Marion-Poll, Frederic/0000-0001-6824-0180 FU Intramural NIH HHS NR 100 TC 619 Z9 648 U1 68 U2 258 PU NATURE PUBLISHING GROUP PI LONDON PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND SN 0028-0836 J9 NATURE JI Nature PD NOV 16 PY 2006 VL 444 IS 7117 BP 288 EP 294 DI 10.1038/nature05401 PG 7 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA 105GL UT WOS:000242018300034 PM 17108952 ER PT J AU Baur, JA Pearson, KJ Price, NL Jamieson, HA Lerin, C Kalra, A Prabhu, VV Allard, JS Lopez-Lluch, G Lewis, K Pistell, PJ Poosala, S Becker, KG Boss, O Gwinn, D Wang, MY Ramaswamy, S Fishbein, KW Spencer, RG Lakatta, EG Le Couteur, D Shaw, RJ Navas, P Puigserver, P Ingram, DK de Cabo, R Sinclair, DA AF Baur, Joseph A. Pearson, Kevin J. Price, Nathan L. Jamieson, Hamish A. Lerin, Carles Kalra, Avash Prabhu, Vinayakumar V. Allard, Joanne S. Lopez-Lluch, Guillermo Lewis, Kaitlyn Pistell, Paul J. Poosala, Suresh Becker, Kevin G. Boss, Olivier Gwinn, Dana Wang, Mingyi Ramaswamy, Sharan Fishbein, Kenneth W. Spencer, Richard G. Lakatta, Edward G. Le Couteur, David Shaw, Reuben J. Navas, Placido Puigserver, Pere Ingram, Donald K. de Cabo, Rafael Sinclair, David A. TI Resveratrol improves health and survival of mice on a high-calorie diet SO NATURE LA English DT Article ID ACTIVATED PROTEIN-KINASE; REPLICATIVE LIFE-SPAN; GENE SET ENRICHMENT; MITOCHONDRIAL BIOGENESIS; SACCHAROMYCES-CEREVISIAE; CAENORHABDITIS-ELEGANS; RESTRICTION MIMETICS; COACTIVATOR PGC-1; DEFICIENT MICE; C-ELEGANS AB Resveratrol ( 3,5,4'- trihydroxystilbene) extends the lifespan of diverse species including Saccharomyces cerevisiae, Caenorhabditis elegans and Drosophila melanogaster. In these organisms, lifespan extension is dependent on Sir2, a conserved deacetylase proposed to underlie the beneficial effects of caloric restriction. Here we show that resveratrol shifts the physiology of middle- aged mice on a high- calorie diet towards that of mice on a standard diet and significantly increases their survival. Resveratrol produces changes associated with longer lifespan, including increased insulin sensitivity, reduced insulin- like growth factor- 1 ( IGF- I) levels, increased AMP- activated protein kinase ( AMPK) and peroxisome proliferator- activated receptor-gamma coactivator 1 alpha ( PGC- 1 alpha) activity, increased mitochondrial number, and improved motor function. Parametric analysis of gene set enrichment revealed that resveratrol opposed the effects of the high- calorie diet in 144 out of 153 significantly altered pathways. These data show that improving general health in mammals using small molecules is an attainable goal, and point to new approaches for treating obesity- related disorders and diseases of ageing. C1 Harvard Univ, Sch Med, Dept Pathol, Paul F Glenn Labs Biol Mech Aging, Boston, MA 02115 USA. NIA, Lab Expt Gerontol, NIH, Baltimore, MD 21224 USA. NIA, Gene Express & Genom Unit, NIH, Baltimore, MD 21224 USA. NIA, Res Resources Branch, NIH, Baltimore, MD 21224 USA. NIA, Cardiovasc Sci Lab, NIH, Baltimore, MD 21224 USA. NIA, Clin Invest Lab, Res Resources Branch, Gerontol Res Ctr,NIH, Baltimore, MD 21224 USA. Univ Sydney, ANZAC Res Inst, Concord, NSW 2139, Australia. Univ Sydney, Ctr Educ, Concord, NSW 2139, Australia. Johns Hopkins Univ, Sch Med, Dept Cell Biol, Baltimore, MD 21205 USA. Univ Pablo Olavide, CSIC, Ctr andaluz Biol Desarrollo, Seville 41013, Spain. Sirtris Pharmaceut Inc, Cambridge, MA 02139 USA. Salk Inst Biol Studies, Mol & Cell Biol Lab, La Jolla, CA 92037 USA. Louisiana State Univ, Pennington Biomed Res Ctr, Nutr Neurosci & Aging Lab, Baton Rouge, LA 70808 USA. RP de Cabo, R (reprint author), Harvard Univ, Sch Med, Dept Pathol, Paul F Glenn Labs Biol Mech Aging, 77 Ave Louis Pasteur, Boston, MA 02115 USA. EM deCaboRa@grc.nia.nih.gov; david_sinclair@hms.harvard.edu RI de Cabo, Rafael/E-7996-2010; Baur, Joseph/D-8163-2011; Lopez-Lluch, Guillermo/N-4742-2014; de Cabo, Rafael/J-5230-2016; OI Lopez-Lluch, Guillermo/0000-0001-9830-8502; de Cabo, Rafael/0000-0002-3354-2442; Baur, Joseph/0000-0001-8262-6549; Becker, Kevin/0000-0002-6794-6656; Sinclair, David/0000-0002-9936-436X; , rafael/0000-0003-2830-5693; Fishbein, Kenneth/0000-0002-6353-4603 FU NIA NIH HHS [R01 AG028730, P01 AG027916, R01 AG019719, R01 AG019972, R37 AG028730]; NIGMS NIH HHS [R01 GM068072] NR 44 TC 2309 Z9 2418 U1 48 U2 436 PU NATURE PUBLISHING GROUP PI LONDON PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND SN 0028-0836 J9 NATURE JI Nature PD NOV 16 PY 2006 VL 444 IS 7117 BP 337 EP 342 DI 10.1038/nature05354 PG 6 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA 105GL UT WOS:000242018300041 PM 17086191 ER PT J AU Sommer, MA Wurtz, RH AF Sommer, Marc A. Wurtz, Robert H. TI Influence of the thalamus on spatial visual processing in frontal cortex SO NATURE LA English DT Article ID BRAIN-STEM TELLS; EYE FIELD; COROLLARY DISCHARGE; SUPERIOR COLLICULUS; SIGNALS SENT; MONKEY; MOVEMENTS; REPRESENTATION; SACCADES; PATHWAY AB Each of our movements activates our own sensory receptors, and therefore keeping track of self- movement is a necessary part of analysing sensory input. One way in which the brain keeps track of self- movement is by monitoring an internal copy, or corollary discharge, of motor commands(1 - 13). This concept could explain why we perceive a stable visual world despite our frequent quick, or saccadic, eye movements: corollary discharge about each saccade would permit the visual system to ignore saccade- induced visual changes(6 - 9). The critical missing link has been the connection between corollary discharge and visual processing. Here we show that such a link is formed by a corollary discharge from the thalamus that targets the frontal cortex. In the thalamus, neurons in the mediodorsal nucleus relay a corollary discharge of saccades from the midbrain superior colliculus to the cortical frontal eye field(10 - 12). In the frontal eye field, neurons use corollary discharge to shift their visual receptive fields spatially before saccades(14,15). We tested the hypothesis that these two components - a pathway for corollary discharge and neurons with shifting receptive fields - form a circuit in which the corollary discharge drives the shift. First we showed that the known spatial and temporal properties of the corollary discharge predict the dynamic changes in spatial visual processing of cortical neurons when saccades are made. Then we moved from this correlation to causation by isolating single cortical neurons and showing that their spatial visual processing is impaired when corollary discharge from the thalamus is interrupted. Thus the visual processing of frontal neurons is spatiotemporally matched with, and functionally dependent on, corollary discharge input from the thalamus. These experiments establish the first link between corollary discharge and visual processing, delineate a brain circuit that is well suited for mediating visual stability, and provide a framework for studying corollary discharge in other sensory systems. C1 Univ Pittsburgh, Dept Neurosci, Pittsburgh, PA 15260 USA. Univ Pittsburgh, Ctr Neural Basis Cognit, Pittsburgh, PA 15260 USA. Univ Pittsburgh, Ctr Neurosci, Pittsburgh, PA 15260 USA. NEI, Sensorimotor Res Lab, NIH, Bethesda, MD 20892 USA. RP Sommer, MA (reprint author), Univ Pittsburgh, Dept Neurosci, Pittsburgh, PA 15260 USA. EM sommer@bns.pitt.edu FU Intramural NIH HHS NR 23 TC 239 Z9 240 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 NOV 16 PY 2006 VL 444 IS 7117 BP 374 EP 377 DI 10.1038/nature05279 PG 4 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA 105GL UT WOS:000242018300050 PM 17093408 ER PT J AU Tang, C Iwahara, J Clore, GM AF Tang, Chun Iwahara, Junji Clore, G. Marius TI Visualization of transient encounter complexes in protein-protein association SO NATURE LA English DT Article ID PARAMAGNETIC RELAXATION ENHANCEMENT; PHOSPHORYL TRANSFER COMPLEX; NMR STRUCTURES; BINDING; DNA; BARSTAR; BARNASE; SYSTEM; DOMAIN; HPR AB Kinetic data on a number of protein - protein associations have provided evidence for the initial formation of a pre- equilibrium encounter complex that subsequently relaxes to the final stereospecific complex (1). Site- directed mutagenesis(2 - 4) and brownian dynamics simulations(5 - 7) have suggested that the rate of association can be modulated by perturbations in charge distribution outside the direct interaction surfaces. Furthermore, rate enhancement through non- specific binding may occur by either a reduction in dimensionality(8) or the presence of a short- range, non- specific attractive potential(9). Here, using paramagnetic relaxation enhancement, we directly demonstrate the existence and visualize the distribution of an ensemble of transient, non- specific encounter complexes under equilibrium conditions for a relatively weak protein - protein complex between the amino- terminal domain of enzyme I and the phosphocarrier protein HPr. Neither the stereospecific complex(10) alone nor any single alternative conformation can account fully for the intermolecular paramagnetic relaxation enhancement data. Restrained rigid- body simulated annealing refinement against the paramagnetic relaxation enhancement data enables us to obtain an atomic probability distribution map of the non- specific encounter complex ensemble that qualitatively correlates with the electrostatic surface potentials on the interacting proteins. Qualitatively similar results are presented for two other protein - protein complexes. C1 NIDDKD, Chem Phys Lab, NIH, Bethesda, MD 20892 USA. RP Clore, GM (reprint author), NIDDKD, Chem Phys Lab, NIH, Bldg 2, Bethesda, MD 20892 USA. EM mariusc@intra.niddk.nih.gov RI Clore, G. Marius/A-3511-2008; OI Clore, G. Marius/0000-0003-3809-1027; Iwahara, Junji/0000-0003-4732-2173 FU Intramural NIH HHS NR 28 TC 254 Z9 263 U1 5 U2 58 PU NATURE PUBLISHING GROUP PI LONDON PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND SN 0028-0836 J9 NATURE JI Nature PD NOV 16 PY 2006 VL 444 IS 7117 BP 383 EP 386 DI 10.1038/nature05201 PG 4 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA 105GL UT WOS:000242018300052 PM 17051159 ER PT J AU Liu, J Sempos, CT Donahue, RP Dorn, J Trevisan, M Grundy, SM AF Liu, Jian Sempos, Christopher T. Donahue, Richard P. Dorn, Joan Trevisan, Maurizio Grundy, Scott M. TI Non-high-density lipoprotein and very-low-density lipoprotein cholesterol and their risk predictive values in coronary heart disease SO AMERICAN JOURNAL OF CARDIOLOGY LA English DT Article ID NON-HDL CHOLESTEROL; CARDIOVASCULAR-DISEASE; ARTERY-DISEASE; APOLIPOPROTEIN-B; LDL-CHOLESTEROL; MEN; MORTALITY; EVENTS; PLASMA; THERAPY AB To determine if non-high-density lipoprotein (HDL) cholesterol is a more useful predictor of coronary heart disease (CHD) risk than low-density lipoprotein (LDL) cholesterol and if very-low-density lipoprotein (VLDL) cholesterol is an independent predictor of CHD risk, data from the Framingham Heart Study (2,693 men, 3,101 women) were used for this analysis. All subjects were aged >= 30 years and free of CHD at baseline, and incident CHD was the end point (618 men, 372 women). Cox proportional-hazards models were used to assess the risk for CHD (relative risks and 95% confidence intervals) on the basis of the joint distribution of LDL cholesterol and non-HDL cholesterol (in milligrams per deciliter), as well as LDL cholesterol, non-HDL cholesterol, and VLDL cholesterol as continuous variables. After multivariate adjustment, within non-HDL cholesterol level, no association was found between LDL cholesterol and the risk for CHD, whereas within LDL cholesterol levels, a strong positive and graded association between non-HDL cholesterol and risk for CHD was observed. When the analysis was repeated within triglyceride levels (< 200 vs 2:200 mg/dl), the risk pattern did not change significantly. Also, VLDL cholesterol was found to be a significant predictor of CHD risk after adjusting for LDL cholesterol at triglyceride levels of < 200 or < 200 mg/dI. In conclusion, these results suggest that nonHDL cholesterol level is a stronger predictor of CHD risk than LDL cholesterol; that is, VLDL cholesterol may play a critical role in the development of CHD. (c) 2006 Elsevier Inc. All rights reserved. C1 Brock Univ, St Catharines, ON L2S 3A1, Canada. NIH, Bethesda, MD 20892 USA. Univ Buffalo, Buffalo, NY USA. Univ Texas, SW Med Ctr, Dallas, TX USA. RP Liu, J (reprint author), Brock Univ, St Catharines, ON L2S 3A1, Canada. EM jliu@brocku.ca NR 26 TC 138 Z9 145 U1 0 U2 5 PU EXCERPTA MEDICA INC-ELSEVIER SCIENCE INC PI BRIDGEWATER PA 685 ROUTE 202-206, BRIDGEWATER, NJ 08807 USA SN 0002-9149 J9 AM J CARDIOL JI Am. J. Cardiol. PD NOV 15 PY 2006 VL 98 IS 10 BP 1363 EP 1368 DI 10.1016/j.amjcard.2006.06.032 PG 6 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA 133ZM UT WOS:000244052400013 PM 17134630 ER PT J AU Murabito, JM Guo, CY Fox, CS D'Agostino, RB AF Murabito, Joanne M. Guo, Chao-Yu Fox, Caroline S. D'Agostino, Ralph B. TI Heritability of the ankle-brachial index - The Framingham Offspring study SO AMERICAN JOURNAL OF EPIDEMIOLOGY LA English DT Article DE blood pressure; genetic predisposition to disease; peripheral vascular diseases ID PERIPHERAL ARTERIAL-DISEASE; CORONARY-HEART-DISEASE; BLOOD-PRESSURE INDEX; GENOME-WIDE LINKAGE; INTIMA-MEDIA THICKNESS; CARDIOVASCULAR HEALTH; RISK-FACTORS; ARM INDEX; ENVIRONMENTAL CONTRIBUTIONS; ELDERLY WOMEN AB The ankle-brachial blood pressure index (ABI) is a widely utilized measure for detecting peripheral arterial disease. Genetic contributions to variation in ABI are largely unknown. The authors sought to estimate ABI heritability in a community-based sample. From 1995 to 1998, ABI was measured in 1,097 men and 1,189 women (mean age = 57 years; range, 29-85 years) from 999 families in the Framingham Offspring cohort. Correlation coefficients for sibling pairs were calculated using the family correlations (FCOR) procedure in S.A.G.E. (Case Western Reserve University, Cleveland, Ohio). The heritability of ABI was estimated using variance-components methods in SOLAR (Southwest Foundation for Biomedical Research, San Antonio, Texas). Analyses were performed on normalized crude ABI and on normalized residuals from multiple linear regression analyses in SAS (SAS Institute, Inc., Cary, North Carolina) that adjusted for age, sex, smoking, diabetes, hypertension, ratio of total cholesterol to high density lipoprotein cholesterol, log triglyceride level, and body mass index. The mean ABI was 1.1 (range, 0.4-1.4). The age- and sex-adjusted and multivariable-adjusted sibling-pair correlation coefficients for normalized ABI were 0.15 and 0.11, respectively, resulting in heritability estimates of 0.30 and 0.22. Crude, age- and sex-adjusted, and multivariable-adjusted heritabilities for normalized ABI estimated using variance-components analysis were 0.27 (standard error, 0.06), 0.30 (standard error, 0.06), and 0.21 (standard error, 0.06), respectively (all p values < 0.0001). A modest proportion of the variability in ABI is explained by genetic factors. C1 NHLBI, Framingham Heart Study, Framingham, MA 01702 USA. Boston Univ, Sch Med, Sect Gen Internal Med, Boston, MA 02215 USA. Boston Univ, Stat & Consulting Unit, Boston, MA 02215 USA. NHLBI, Bethesda, MD 20892 USA. Brigham & Womens Hosp, Dept Endocrinol Diabet & Hypertens, Boston, MA 02115 USA. Harvard Univ, Sch Med, Boston, MA 02115 USA. RP Murabito, JM (reprint author), NHLBI, Framingham Heart Study, 5 Thurber St, Framingham, MA 01702 USA. EM murabito@bu.edu OI Murabito, Joanne/0000-0002-0192-7516 FU NHLBI NIH HHS [N01-HC-25195] NR 53 TC 43 Z9 44 U1 0 U2 0 PU OXFORD UNIV PRESS INC PI CARY PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA SN 0002-9262 J9 AM J EPIDEMIOL JI Am. J. Epidemiol. PD NOV 15 PY 2006 VL 164 IS 10 BP 963 EP 968 DI 10.1093/aje/kwj295 PG 6 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA 104LC UT WOS:000241958900006 PM 16928729 ER PT J AU Toydemir, RM Chen, H Proud, VK Martin, R van Bokhoven, H Hamel, BCJ Tuerlings, JH Stratakis, CA Jorde, LB Bamshad, MJ AF Toydemir, Reha M. Chen, Harold Proud, Virginia K. Martin, Rick van Bokhoven, Hans Hamel, Ben C. J. Tuerlings, Joep H. Stratakis, Constantine A. Jorde, Lynn B. Bamshad, Michael J. TI Trismus-pseudocamptodactyly syndrome is caused by recurrent mutation of MYH8 SO AMERICAN JOURNAL OF MEDICAL GENETICS PART A LA English DT Article DE distal arthrogryposis; trismus-pseudocamptoclactyly; Dutch-Kentucky syndrome; Hecht-Beals syndrome; myosin heavy chain; Carney complex ID HECHT-BEALS-SYNDROME; MYOSIN HEAVY-CHAIN; MASSETERIC FIBROUS BANDS; PSEUDOCAMPYLODACTYLY SYNDROME; DISTAL ARTHROGRYPOSES; DUTCH-KENTUCKY; CARNEY COMPLEX; MANAGEMENT; MOUTH; SECONDARY AB Tristmus-pseudocamptodactyly syndrome (TPS) is a rare autosomal dominant distal arthrogryposis (DA) character ized by an inability to open the mouth fully (trismus) and an unusual camptoclactyly of the fingers that is apparent only upon dorsiflexion of the wrist (i.e., pseudocamptodactyly). TPS is also known as Dutch-Kentucky syndrome because a Dutch founder Mutation is presumed to be the origin of TPS cases in the Southeast US, including Kentucky. To date only a single mutation, p.R674Q, in MYH8 has been reported to cause TPS. Several individuals with this mutation also had a so-called "variant" of Carney complex, suggesting that the pathogenesis of TPS and Carney complex might be shared. We screened MYH8 in four TPS pedigrees, including the original Dutch family in which TPS was reported. All four TPS families shared the p.R674Q substitution. However, haplotype analysis revealed that this mutation has arisen independently in North American and European TPS pedigrees. None of the individuals with TPS studied had features of Carney complex, and p.R674Q was not found in 49 independent cases of Carney complex that were screened. Our findings show that distal arthrogryposis syndromes share a similar pathogenesis and are, in general, caused by disruption of the contractile complex of muscle. (c) 2006 Wiley-Liss, Inc. C1 Univ Washington, Sch Med, Dept Pediat, Div Genet & Dev Med, Seattle, WA 98195 USA. Univ Washington, Dept Genome Sci, Seattle, WA 98195 USA. Univ Utah, Dept Human Genet, Salt Lake City, UT USA. Louisiana State Univ, Hlth Sci Ctr, Dept Pediat, Div Perinatal Genet, Shreveport, LA 71105 USA. Eastern Virginia Med Sch, Childrens Hosp Kings Daughters, Dept Pediat, Div Med Genet, Norfolk, VA 23501 USA. Washington Univ, Sch Med, Dept Pediat, St Louis, MO 63110 USA. Radboud Univ Nijmegen, Med Ctr, Dept Human Genet, Nijmegen, Netherlands. NICHHD, Sect Endocrinol & Genet, Dev Endocrinol Branch, NIH, Bethesda, MD 20892 USA. Childrens Hosp & Reg Med Ctr, Seattle, WA USA. RP Bamshad, MJ (reprint author), Univ Washington, Sch Med, Dept Pediat, Div Genet & Dev Med, 1959 NE Pacific St,HSB RR349, Seattle, WA 98195 USA. EM mbamshad@u.washington.edu RI van Bokhoven, Hans/D-8764-2012; Bokhoven, J.H.L.M./H-8015-2014 FU Intramural NIH HHS; NICHD NIH HHS [R01-HD048895] NR 39 TC 32 Z9 32 U1 0 U2 5 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 1552-4825 J9 AM J MED GENET A JI Am. J. Med. Genet. A PD NOV 15 PY 2006 VL 140A IS 22 BP 2387 EP 2393 DI 10.1002/ajmg.a.31495 PG 7 WC Genetics & Heredity SC Genetics & Heredity GA 101MZ UT WOS:000241746200001 PM 17041932 ER PT J AU O'Neill, SM Peters, JA Vogel, VG Feingold, E Rubinstein, WS AF O'Neill, Suzanne M. Peters, June A. Vogel, Victor G. Feingold, Eleanor Rubinstein, Wendy S. TI Referral to cancer genetic counseling: Are there stages of readiness? SO AMERICAN JOURNAL OF MEDICAL GENETICS PART C-SEMINARS IN MEDICAL GENETICS LA English DT Article DE cancer genetic counseling; stages of change; transtheoretical model; referral; adherence; genetic testing; breast cancer; oncology; psychology; risk assessment ID HEREDITARY BREAST-CANCER; FAMILY-HISTORY; DECISION-MAKING; TRANSTHEORETICAL MODEL; BREAST/OVARIAN CANCER; WOMENS DECISIONS; HEALTH BEHAVIOR; RISK-ASSESSMENT; BRCA1; SUSCEPTIBILITY AB As genetic awareness spreads among healthcare providers and the general public, and evidence mounts to show the efficacy of cancer control methods, referrals to cancer genetic counseling services for risk assessment are becoming more common. However, few studies have examined referral patterns to genetics and even less is known about referral uptake to clinical cancer genetic counseling. We investigated outcome of genetics referral in 43 affected women attending a breast cancer treatment program who were referred based on having BRCA mutation carrier risks > 10%. Within 6 months, of the 36 women we were able to recontact, 13 (36%) came to an appointment at the cancer genetic counseling clinic (Acceptors), 10 (27%) said they intended to come in the future (Intenders), and 13 (36%) said they would not consider genetic counseling (Decliners). Referral uptake was framed by elements of the Transtheoretical model (TTM) to determine if decisional balance scores (DBSs), a summary of an individual's "Pro" and "Con" opinions related to genetic testing, correlated with their decision to follow through. Mean DBS's were strongly negative for the Decliner group (-7.4), weakly negative for the Intender group (-1.1), and positive for the Acceptor group (5.4). The difference in the DBS along the continuum was due more to the mean "Con" score decreasing, rather than the mean "Pro" score increasing. Theoretical frameworks are needed to study adherence to referral for cancer genetic counseling. Stage-based theories may have a role to play. (c) 2006 Wiley-Liss, Inc. C1 Northwestern Univ, Healthcare Ctr Med Genet, Evanston, IL 60201 USA. Northwestern Univ, Feinberg Sch Med, Evanston, IL 60201 USA. Natl Canc Inst, Canc Genet Branch, Div Canc Epidemiol & Genet, Dept Hlth & Human Serv,NIH, Bethesda, MD 20892 USA. Univ Pittsburgh, Magee Womens Hosp, Breast Canc Prevent Program, Pittsburgh, PA 15260 USA. Univ Pittsburgh, Grad Sch Publ Hlth, Dept Human Genet, Pittsburgh, PA 15260 USA. RP O'Neill, SM (reprint author), Northwestern Univ, Healthcare Ctr Med Genet, 1000 Cent St,Suite 620, Evanston, IL 60201 USA. EM soneill@enh.org OI Feingold, Eleanor/0000-0003-2898-6484 NR 53 TC 31 Z9 31 U1 1 U2 3 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 1552-4868 J9 AM J MED GENET C JI Am. J. Med. Genet. C PD NOV 15 PY 2006 VL 142C IS 4 BP 221 EP 231 DI 10.1002/ajmg.c.30109 PG 11 WC Genetics & Heredity SC Genetics & Heredity GA 102ZD UT WOS:000241851500003 PM 17068804 ER PT J AU Lipinski, SE Lipinski, MJ Biesecker, LG Biesecker, BB AF Lipinski, Shawn E. Lipinski, Michael J. Biesecker, Leslie G. Biesecker, Barbara B. TI Uncertainty and perceived personal control among parents of children with rare chromosome conditions: The role of genetic counseling SO AMERICAN JOURNAL OF MEDICAL GENETICS PART C-SEMINARS IN MEDICAL GENETICS LA English DT Article DE uncertainty; perceived personal control; adaptation; genetic counseling; rare chromosomal disorders ID MOTHERS; STRESS AB Little is known about the impact of genetic counseling on parental uncertainty or perceived control regarding the prognosis of a child with a chromosomal disorder. By exploring the parents' concerns and needs surrounding the child's diagnosis, a genetic provider can help to facilitate effective coping. This study tested the association of measures of parental uncertainty and perceived control with the perceived helpfulness of the genetic counselor. A survey was distributed to 875 members of the Chromosome Deletion Outreach (CDO) support group. We hypothesized that parents' perceptions about the helpfulness of the genetic counselor would modify the relationship between perceived uncertainty, perceived control, and coping. Among the 363 respondents, there was a significant negative correlation of the perceived helpfulness of seeing a genetic counselor with the levels of uncertainty (rs = -0.20, P-value < 0.001). Lower perceived helpfulness of the genetic counselor, along with less perceived personal control, less benefit of a diagnosis, and lower parental age were significant predictors of the highest perceptions of uncertainty. The Transactional Model of Stress and Coping was used as a framework for interpreting the relationships between parental uncertainty, perceived control, and outcome variables. There was a significant positive correlation between parents' perceived personal control and their reports of helpfulness of the genetic counselor (rs = 0.20, P-value < 0.0006). Genetic counseling can be enhanced for parents faced with rare disorders by using interventions focused on reducing feelings of uncertainty and enhancing feelings of control. (c) 2006 Wiley-Liss, Inc. C1 Univ Virginia, Dept Pediat, Div Genet, Lyosomal Storage Dis Treatment Program, Charlottesville, VA 22908 USA. Univ Virginia Hlth Syst, Charlottesville, VA USA. Univ Wisconsin, Madison, WI 53706 USA. Univ Michigan, Ann Arbor, MI 48109 USA. NHGRI, Genet Dis Res Branch, NIH, Bethesda, MD 20892 USA. NHGRI, Phys Sci Dev Program, NIH, Bethesda, MD 20892 USA. NHGRI, Genet Serv Unit, Social & Behav Res Branch, NIH, Bethesda, MD 20892 USA. RP Lipinski, SE (reprint author), Univ Virginia, Dept Pediat, Div Genet, Lyosomal Storage Dis Treatment Program, POB 800386, Charlottesville, VA 22908 USA. EM slipinski@virginia.edu FU Intramural NIH HHS NR 31 TC 29 Z9 29 U1 2 U2 8 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 1552-4868 J9 AM J MED GENET C JI Am. J. Med. Genet. C PD NOV 15 PY 2006 VL 142C IS 4 BP 232 EP 240 DI 10.1002/ajmg.c.30107 PG 9 WC Genetics & Heredity SC Genetics & Heredity GA 102ZD UT WOS:000241851500004 PM 17068805 ER PT J AU O'Neill, SC Demarco, T Peshkin, BN Rogers, S Rispoli, J Brown, K Valdimarsdottir, H Schwartz, MD AF O'Neill, Suzanne C. Demarco, Tiffani Peshkin, Beth N. Rogers, Sarah Rispoli, Jessica Brown, Karen Valdimarsdottir, Heiddis Schwartz, Marc D. TI Tolerance for uncertainty and perceived risk among women receiving uninformative BRCA1/2 test results SO AMERICAN JOURNAL OF MEDICAL GENETICS PART C-SEMINARS IN MEDICAL GENETICS LA English DT Article DE BRCA1/2; distress; uncertainty ID FAMILIAL BREAST-CANCER; OVARIAN-CANCER; PROPHYLACTIC OOPHORECTOMY; PSYCHOLOGICAL DISTRESS; HUNTINGTONS-DISEASE; AFRICAN-AMERICAN; DECISION-MAKING; DUTCH PROGRAM; IMPACT; MUTATIONS AB Women who receive uninformative BRCA1/2 genetic test results face ongoing uncertainty about their future cancer risks. This article prospectively examined the influence of intolerance for uncertainty and perceived breast cancer risk on psychological distress following the receipt of uninformative BRCA1/2 test results. Sixty-four women who received uninformative BRCA1/2 mutation test results completed measures of Intolerance for Uncertainty, perceived breast cancer risk, and measures of cancer-related, genetic testing, and general distress. Cancer-related (Delta R-2 = 0.18, P <= 0.001), general (Delta R-2 = 0.04, P <= 0.05), and genetic testing distress (Delta R-2 = 0. 12, P <= 0.01) were associated with intolerance for uncertainty at 1 month post-disclosure. The interaction of intolerance for uncertainty and breast cancer perceived risk predicted cancer-related (Delta R-2 = 0.10, P < 0.001) and genetic testing distress (Delta R-2 = 0.09, P < 0.01) at 6 months post-disclosure. Distress was highest among patients with highest perceived risk and intolerance for uncertainty, suggesting that those who have difficulty coping with their ambiguous risk are at risk for long-term distress. The clinical and research implications of these results are discussed. (c) 2006 Wiley-Liss, Inc. C1 NHGRI, Social & Behav Res Branch, NIH, Bethesda, MD 20892 USA. Georgetown Univ, Dept Oncol, Div Canc Control, Lombardi Comprehens Canc Ctr, Washington, DC 20057 USA. Baltimore Washington Med Ctr, Glen Burnie, MD USA. CUNY Mt Sinai Sch Med, Dept Human Genet, New York, NY 10029 USA. CUNY Mt Sinai Sch Med, Dept Oncol Sci, New York, NY 10029 USA. RP O'Neill, SC (reprint author), NHGRI, Social & Behav Res Branch, NIH, 10 Ctr Dr,Bldg 2,Room 5E14, Bethesda, MD 20892 USA. EM oneills@mail.nih.gov FU NCI NIH HHS [R01 CA 82346, 2R25 CA 57726] NR 51 TC 30 Z9 30 U1 0 U2 7 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 1552-4868 J9 AM J MED GENET C JI Am. J. Med. Genet. C PD NOV 15 PY 2006 VL 142C IS 4 BP 251 EP 259 DI 10.1002/ajmg.c.30104 PG 9 WC Genetics & Heredity SC Genetics & Heredity GA 102ZD UT WOS:000241851500006 PM 17024668 ER PT J AU Sutton, EJ Rosapep, L Ball, K Truitt, M Biesecker, B Guidotti, R Mclean, D AF Sutton, Erica J. Rosapep, Lauren Ball, Karen Truitt, Megan Biesecker, Barbara Guidotti, Rick Mclean, Diane TI Through the viewfinder: Positive exposure a year later SO AMERICAN JOURNAL OF MEDICAL GENETICS PART C-SEMINARS IN MEDICAL GENETICS LA English DT Article DE positive exposure; photography; craniofacial conditions; self-esteem; stigma ID CRANIOFACIAL ANOMALIES; SELF; PREADOLESCENTS; ADJUSTMENT AB Positive Exposure, a non-profit organization founded and directed by former fashion photographer Rick Guidotti and co-directed by psychiatrist Dr. Diane McLean, uses photography and video interviews to explore the lived experiences of people affected with genetic conditions. Positive Exposure challenges pervasive social biases and stereotypes about genetic variation and strives to broaden and enrich societal perceptions of human beauty and spirit. Presented here are the open-ended personal reflections completed by four individuals with craniofacial differences recruited from a support group, Inner Faces. These four case studies aim to relay the professional photo-shoot experiences of people who maybe challenged by the stigma associated with craniofacial differences. Questions addressed issues of perceived self-esteem, stigma, hopefulness, and photography experiences. These personal reflections were gathered 1 year following participation in a Positive Exposure photo-shoot. Participants described the ways in which the photo-shoot has been a lasting and life-promoting experience. In addition, these individuals emphasize the integral and enduring role the photographer, Rick Guidotti, played in their personal awakening. Positive Exposure provided these individuals with renewed identification of both inner and outer sources of beauty. These four case studies suggest that Positive Exposure may serve as a sustainable intervention to bolster self-esteem and self-image. Published 2006 Wiley-Liss, Inc. C1 Univ Toronto, New Womens Coll Hosp, Toronto, ON M4X 1K9, Canada. Univ Toronto, Dept Publ Hlth Sci, Toronto, ON M4X 1K9, Canada. Univ Toronto, Joint Ctr Bioeth, Toronto, ON M4X 1K9, Canada. Sturge Weber Fdn, Mt Freedom, NJ USA. NHGRI, Genet Serv Unit, Social & Behav Res Branch, NIH, Bethesda, MD 20892 USA. Columbia Univ Hosp, New York, NY USA. JHU, NHGRI, Genet Counseling Program, Bethesda, MD USA. RP Biesecker, B (reprint author), NHGRI, NIH, 10 Ctr Dr 10-10C 101, Bethesda, MD 20892 USA. EM barbarab@mail.nih.gov FU Intramural NIH HHS NR 17 TC 3 Z9 3 U1 0 U2 3 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 1552-4868 J9 AM J MED GENET C JI Am. J. Med. Genet. C PD NOV 15 PY 2006 VL 142C IS 4 BP 260 EP 268 DI 10.1002/ajmg.c.30113 PG 9 WC Genetics & Heredity SC Genetics & Heredity GA 102ZD UT WOS:000241851500007 PM 17068811 ER PT J AU Cruceanu, M Stephen, AG Beuning, PJ Gorelick, RJ Fisher, RJ Williams, MC AF Cruceanu, Margareta Stephen, Andrew G. Beuning, Penny J. Gorelick, Robert J. Fisher, Robert J. Williams, Mark C. TI Single DNA molecule stretching measures the activity of chemicals that target the HIV-1 nucleocapsid protein SO ANALYTICAL BIOCHEMISTRY LA English DT Article DE HIV-1NC antagonists; nucleic acid chaperone activity; force-induced melting; helix-coil transition; transition width ID NUCLEIC-ACID-CHAPERONE; ZINC-FINGER STRUCTURES; REVERSE TRANSCRIPTION; STRAND TRANSFER; IN-VITRO; BINDING; RNA; NCP7; REPLICATION; RECOGNITION AB We develop a biophysical method for investigating chemical compounds that target the nucleic acid chaperone activity of HIV-1 nucleocapsid protein (NCp7). We used an optical tweezers instrument to stretch single ?,-DNA molecules through the helix-coil transition in the presence of NCp7 and various chemical compounds. The change in the helix-coil transition width induced by wild-type NCp7 and its zinc fingi.r variants correlates with in vitro nucleic acid chaperone activity measurements and in vivo assays. The compound-NC interaction measured here reduces NCpTs capability to alter the transition width. Purified compounds from the NO Diversity set, 119889, 119911, and 119913 reduce the chaperone activity of 5 nM NC in aqueous solution at 10, 25, and 100 nM concentrations respectively. Similarly,, gallein reduced the activity of 4 nM NC at 100 nM concentration. Further analysis allows us to dissect the impact of each compound on both sequence-specific and non-sequence-specific DNA binding of NC, two of the main components of NC's nucleic acid chaperone activity. These results suggest that DNA stretching experiments can be used to screen chemical compounds targeting NC proteins and to further explore the mechanisms by which these compounds interact with NC and alter its nucleic acid chaperone activity. (c) 2006 Elsevier Inc. All rights reserved. C1 Northeastern Univ, Dept Phys, Boston, MA 02115 USA. NCI, SAIC Frederick, Prot Chem Lab, Ft Detrick, MD 21702 USA. Northeastern Univ, Dept Chem & Biol Chem, Boston, MA 02115 USA. SAIC Frederick, AIDS Vaccine Program, Ft Detrick, MD 21702 USA. Northeastern Univ, Ctr Interdisciplinary Res Complex Syst, Boston, MA 02115 USA. RP Williams, MC (reprint author), Northeastern Univ, Dept Phys, Boston, MA 02115 USA. EM mark@neu.edu RI Fisher, Robert/B-1431-2009; OI Williams, Mark C./0000-0003-3219-376X FU NCI NIH HHS [N01-CO-12400, N01CO12400]; NIGMS NIH HHS [GM 072462, R01 GM072462] NR 43 TC 26 Z9 27 U1 0 U2 4 PU ACADEMIC PRESS INC ELSEVIER SCIENCE PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA SN 0003-2697 J9 ANAL BIOCHEM JI Anal. Biochem. PD NOV 15 PY 2006 VL 358 IS 2 BP 159 EP 170 DI 10.1016/j.ab.2006.08.037 PG 12 WC Biochemical Research Methods; Biochemistry & Molecular Biology; Chemistry, Analytical SC Biochemistry & Molecular Biology; Chemistry GA 100PM UT WOS:000241681000001 PM 17034752 ER PT J AU Hama, Y Urano, Y Koyama, Y Bernardo, M Choyke, PL Kobayashi, H AF Hama, Yukihiro Urano, Yasuteru Koyama, Yoshinori Bernardo, Marcelino Choyke, Peter L. Kobayashi, Hisataka TI A comparison of the emission efficiency of four common green fluorescence dyes after internalization into cancer cells SO BIOCONJUGATE CHEMISTRY LA English DT Article ID IN-VIVO; RECEPTOR; BINDING AB In vivo optical imaging to enhance the detection of cancer during endoscopy or surgery requires a targeted fluorescent probe with high emission efficiency and high signal-to-background ratio. One strategy to accurately detect cancers is to have the fluorophore internalize within the cancer cells permitting nonbound fluorophores to be washed away or absorbed. The choice of fluorophores for this task must be carefully considered. For depth of penetration, near-infrared probes are ordinarily preferred but suffer from relatively low quantum efficiency. Although green fluorescent protein has been widely used to image tumors on internal organs in mice, green fluorescent probes are better suited for imaging the superficial tissues because of the short penetration distance of green light in tissue and the highly efficient production of signal. While the fluorescence properties of green fluorophores are well-known in vitro, less attention has been paid to their fluorescence once they are internalized within cells. In this study, the emission efficiency after cellular internalization of four common green fluorophores conjugated to avidin ( Av-fluorescein, Av-Oregon green, Av-BODIPY-FL, and Av-rhodamine green) were compared after each conjugate was incubated with SHIN3 ovarian cancer cells. Using the lectin binding receptor system, the avidin-fluorophore conjugates were endocytosed, and their fluorescence was evaluated with fluorescence microscopy and flow cytometry. While fluorescein demonstrated the highest signal outside the cell, among the four fluorophores, internalized Av-rhodamine green emitted the most light from SHIN3 ovarian cancer cells both in vitro and in vivo. The internalized Av-rhodamine green complex appeared to localize to the endoplasmic vesicles. Thus, among the four common green fluorescent dyes, rhodamine green is the brightest green fluorescence probe after cellular internalization. This information could have implications for the design of tumor-targeted fluorescent probes that rely on cellular internalization for cancer detection. C1 NCI, Mol Imaging Program, Ctr Canc Res, NIH, Bethesda, MD 20892 USA. Univ Tokyo, Grad Sch Pharmaceut Sci, Tokyo 1130033, Japan. Sci Applicat Int Corp, Res Technol Program, Ft Detrick, MD 21702 USA. RP Kobayashi, H (reprint author), NCI, Mol Imaging Program, Ctr Canc Res, NIH, Bethesda, MD 20892 USA. EM Kobayash@mail.nih.gov RI Urano, Yasuteru/H-1380-2012 FU Intramural NIH HHS [Z01 BC010657-03, Z99 CA999999]; NCI NIH HHS [N01-CO-12400, N01CO12400] NR 17 TC 36 Z9 36 U1 1 U2 9 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA SN 1043-1802 J9 BIOCONJUGATE CHEM JI Bioconjugate Chem. PD NOV 15 PY 2006 VL 17 IS 6 BP 1426 EP 1431 DI 10.1021/bc0601626 PG 6 WC Biochemical Research Methods; Biochemistry & Molecular Biology; Chemistry, Multidisciplinary; Chemistry, Organic SC Biochemistry & Molecular Biology; Chemistry GA 105HL UT WOS:000242020900009 PM 17105220 ER PT J AU Shiotani, K Li, TY Miyazaki, A Tsuda, Y Bryant, SD Ambo, A Sasaki, Y Lazarus, LH Okada, Y AF Shiotani, Kimitaka Li, Tingyou Miyazaki, Anna Tsuda, Yuko Bryant, Sharon D. Ambo, Akihiro Sasaki, Yusuke Lazarus, Lawrence H. Okada, Yoshio TI Synthesis of 3,6-bis[H-Tyr/H-Dmt-NH(CH2)(m,n)]-2(1H)pyrazinone derivatives: Function of alkyl chain length on opioid activity SO BIOORGANIC & MEDICINAL CHEMISTRY LETTERS LA English DT Article DE 2 ',6 '-dimethyl-L-tyrosine; pyrazinone; mu-selective opioid; ligand ID AMPHIBIAN SKIN; HIGH-AFFINITY; ENDOGENOUS AGONIST; MEDIATED ANALGESIA; RECEPTOR AGONISTS; PEPTIDES; POTENT; DERMORPHIN; SELECTIVITY; IDENTIFICATION AB Dimeric opioid analogues linked to a pyrazinone platform, 3-[Tyr/Dmt-NH(CH2)(m)]-6-[Tyr/Dmt-NH(CH2)(n)]-2(1H)-pyrazinone (m, n = 3 or 4), were synthesized. The Tyr-containing compound (m = 4, n = 3) exhibited mu-receptor affinity (K-i mu; 7.58 nM) comparable to that of morphine, while the Dmt derivatives exhibited considerably higher affinity (K-i mu; 0.021-0.051 nM) with corresponding agonism (IC50 = 1.79-4.93 nM). Interestingly one compound (m = 4, n = 3) revealed modest delta-opioid agonism; the converse analogue (m = 3, n = 4), however, was inactive in MVD assay. (c) 2006 Elsevier Ltd. All rights reserved. C1 Kobe Gakuin Univ, Grad Sch Food & Med Sci, Nishi Ku, Kobe, Hyogo 6512180, Japan. Kobe Gakuin Univ, Fac Pharmaceut Sci, Nishi Ku, Kobe, Hyogo 6512180, Japan. NIEHS, Med Chem Grp, Lab Pharmacol & Chem, Res Triangle Pk, NC 27709 USA. Tohoku Pharmaceut Univ, Dept Biochem, Aoba Ku, Sendai, Miyagi 9818558, Japan. RP Okada, Y (reprint author), Kobe Gakuin Univ, Grad Sch Food & Med Sci, Nishi Ku, Kobe, Hyogo 6512180, Japan. EM okada@pharm.kobegakuin.ac.jp FU Intramural NIH HHS [Z99 ES999999, Z01 ES100472-06, Z01 ES090053-20] NR 26 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 0960-894X J9 BIOORG MED CHEM LETT JI Bioorg. Med. Chem. Lett. PD NOV 15 PY 2006 VL 16 IS 22 BP 5793 EP 5796 DI 10.1016/j.bmcl.2006.08.079 PG 4 WC Chemistry, Medicinal; Chemistry, Organic SC Pharmacology & Pharmacy; Chemistry GA 102YT UT WOS:000241850400016 PM 16949282 ER PT J AU Bauer, TR Hai, MR Tuschong, LM Burkholder, TH Gu, YC Sokolic, RA Ferguson, C Dunbar, CE Hickstein, DD AF Bauer, Thomas R., Jr. Hai, Mehreen Tuschong, Laura M. Burkholder, Tanya H. Gu, Yu-chen Sokolic, Robert A. Ferguson, Cole Dunbar, Cynthia E. Hickstein, Dennis D. TI Correction of the disease phenotype in canine leukocyte adhesion deficiency using ex vivo hematopoietic stem cefl gene therapy SO BLOOD LA English DT Article; Proceedings Paper CT 47th Annual Meeting of the American-Society-of-Hematology CY DEC 10-13, 2005 CL Atlanta, GA SP Amer Soc Hematol ID APE LEUKEMIA-VIRUS; CHRONIC GRANULOMATOUS-DISEASE; BONE-MARROW-TRANSPLANTATION; TOTAL-BODY IRRADIATION; REPOPULATING CELLS; RETROVIRAL VECTORS; PACKAGING CELLS; DOGS; TRANSDUCTION; FIBRINOGEN AB Canine leukocyte adhesion deficiency (CLAD) represents the canine counterpart of the human disease leukocyte adhesion deficiency (LAD). Defects in the leukocyte integrin CD18 adhesion molecule in both CLAD and LAD lead to recurrent, life-threatening bacterial infections. We evaluated ex vivo retroviral-mediated gene therapy in CLAD using 2 nonmyeloablative conditioning regimens-200 cGy total body irradiation (TBI) or 10 mg/kg busulfan-with or without posttransplantation immunosuppression. In 6 of 11 treated CLAD dogs, therapeutic levels of CD18(+) leukocytes were achieved. Conditioning with either TBI or busulfan allowed long-term engraftment, and immunosuppression was not required for efficacy. The percentage of CD18+ leukocytes in the peripheral blood progressively increased over 6 to 8 months after infusion to levels ranging from 1.26% to 8.37% at 1-year follow-up in the 6 dogs. These levels resulted in reversal or moderation of the severe CLAD phenotype. Linear amplification-mediated polymerase chain reaction assays indicated polyclonality of insertion sites. These results describe ex vivo hematopoietic stem cell gene transfer in a disease-specific, large animal model using 2 clinically applicable conditioning regimens, and they provide support for the use of nonmyeloablative conditioning regimens in preclinical protocols of retroviral-mediated gene transfer for nonmalignant hematopoietic diseases such as LAD. C1 NCI, Expt Transplantat & Immunol Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA. NIH, Off Res Serv, Div Vet Resources, Bethesda, MD 20892 USA. NHLBI, Hematol Branch, Mol Hematopoiesis Branch, Bethesda, MD 20892 USA. RP Bauer, TR (reprint author), NCI, Expt Transplantat & Immunol Branch, Ctr Canc Res, NIH, 10 Ctr Dr,MSC1203,Bldg 10 CRC,Rm 3-3264, Bethesda, MD 20892 USA. EM bauert@mail.nih.gov RI Sokolic, Robert/I-6072-2012 FU Intramural NIH HHS NR 39 TC 24 Z9 29 U1 1 U2 2 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 15 PY 2006 VL 108 IS 10 BP 3313 EP 3320 DI 10.1182/blood-2006-03-006908 PG 8 WC Hematology SC Hematology GA 103VM UT WOS:000241915000019 PM 16868255 ER PT J AU Fann, M Godlove, JM Catalfamo, M Wood, WH Chrest, FJ Chun, N Granger, L Wersto, R Madara, K Becker, K Henkart, PA Weng, NP AF Fann, Monchou Godlove, Jason M. Catalfamo, Marta Wood, William H., III Chrest, Francis J. Chun, Nicholas Granger, Larry Wersto, Robert Madara, Karen Becker, Kevin Henkart, Pierre A. Weng, Nan-ping TI Histone acetylation is associated with differential gene expression in the rapid and robust memory CD8+ T-cell response SO BLOOD LA English DT Article ID DEACETYLASE INHIBITOR TRICHOSTATIN; IN-VIVO; EFFECTOR; CHROMATIN; CODE; PHENOTYPE; CD4(+); POTENT; IL-15; NAIVE AB To understand the molecular basis for the rapid and robust memory T-cell responses, we examined gene expression and chromatin modification by histone H3 lysine 9 (H3K9) acetylation in resting and activated human naive and memory CD8(+) T cells. We found that, although overall gene expression patterns were similar, a number of genes are differentially expressed in either memory or naive cells in their resting and activated states. To further elucidate the basis for differential gene expression, we assessed the role of histone H3K9 acetylation in differential gene expression. Strikingly, higher H3K9 acetylation levels were detected in resting memory cells, prior to their activation, for those genes that were differentially expressed following activation, indicating that hyperacetylation of histone H3K9 may play a role in selective and rapid gene expression of memory CD8+ T cells. Consistent with this model, we showed that inducing high levels of H3K9 acetylation resulted in an increased expression in naive cells of those genes that are normally expressed differentially in memory cells. Together, these findings suggest that differential gene expression mediated at least in part by histone H3K9 hyperacetylation may be responsible for the rapid and robust memory CD8(+) T-cell response. C1 NIA, Immunol Lab, NIH, Baltimore, MD 21224 USA. NIA, Flow Cytometry Lab, NIH, Baltimore, MD 21224 USA. NIA, Gene Express & Genom Unit, NIH, Baltimore, MD 21224 USA. NIA, Apheresis Unit, NIH, Baltimore, MD 21224 USA. NCI, Expt Immunol Branch, NIH, Bethesda, MD 20892 USA. RP Weng, NP (reprint author), 5600 Nathan Shock Dr, Baltimore, MD 21224 USA. EM wengn@mail.nih.gov OI Becker, Kevin/0000-0002-6794-6656 FU Intramural NIH HHS; NIDA NIH HHS [R90 DA023426] NR 26 TC 37 Z9 39 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 15 PY 2006 VL 108 IS 10 BP 3363 EP 3370 DI 10.1182/blood-2006-02-005520 PG 8 WC Hematology SC Hematology GA 103VM UT WOS:000241915000026 PM 16868257 ER PT J AU Kashkar, H Seeger, JM Hombach, A Deggerich, A Yazdanpanah, B Utermohlen, O Heimlich, G Abken, H Kronke, M AF Kashkar, Hamid Seeger, Jens-Michael Hombach, Andreas Deggerich, Anke Yazdanpanah, Benjamin Utermoehlen, Olaf Heimlich, Gerd Abken, Hinrich Kroenke, Martin TI XIAP targeting sensitizes Hodgkin lymphoma cells for cytolytic T-cell attack SO BLOOD LA English DT Article ID INDUCED APOPTOSIS REQUIRES; CYTOCHROME-C RELEASE; B-INDUCED APOPTOSIS; GRANZYME-B; CASPASE ACTIVATION; CD95-MEDIATED APOPTOSIS; MEDIATED CYTOTOXICITY; MITOCHONDRIAL RELEASE; DEATH RECEPTOR; INHIBITION AB The immunosurveil lance of Hodgkin lymphoma (HL) by cytotoxic T lymphocytes (CTLs) is insufficient, and the clinical experience with adoptive transfer of CTLs is limited. We have previously reported that defects in mitochondrial apoptotic pathways and elevated XIAP expression confer resistance to different apoptotic stimuli in HL cells. Here, we aimed to develop molecular strategies to overcome the resistance of HIL cells against CTL-mediated killing via granzyme B (grzB). In HIL cells, grzB-induced mitochondrial release of proapoptotic Smac is blocked, which results in complete abrogation of cytotoxicity mediated by CTLs. Cytosolic expression of recombinant mature Smac enhanced caspase activity induced by grzB and restored the apoptotic response of HIL cells. Similarly, down-regulation of XIAP by RNA interference markedly enhanced the susceptibility of HL cells for CTL-mediated cytotoxicity. XIAP gene knockdown sensitized HIL cells for killing by antigen-specific CTLs redirected by grafting with a chimeric antiCD30scFv-CD3zeta immunoreceptor. The results suggest that XIAP targeting by Smac agonists or XIAP-siRNA can be used as a synergistic strategy for cellular immunotherapy of Hodgkin lymphoma. C1 Univ Cologne, Inst Med Microbiol Immunol & Hyg, Ctr Mol Med, D-50935 Cologne, Germany. Univ Cologne, Clin Internal Med 1, D-50935 Cologne, Germany. Natl Inst Environm Hlth Sci, Lab Signal Transduct, NIH, Res Triangle Pk, NC USA. RP Kashkar, H (reprint author), Univ Cologne, Inst Med Microbiol Immunol & Hyg, Ctr Mol Med, Goldenfesstr 19-21, D-50935 Cologne, Germany. EM h.kashkar@uni-koeln.de NR 40 TC 36 Z9 36 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD NOV 15 PY 2006 VL 108 IS 10 BP 3434 EP 3440 DI 10.1182/blood-2006-05-021675 PG 7 WC Hematology SC Hematology GA 103VM UT WOS:000241915000035 PM 16868249 ER PT J AU Becker, D Mihm, MC Hewitt, SM Sondak, VK Fountain, JW Thurin, M AF Becker, Dorothea Mihm, Martin C. Hewitt, Stephen M. Sondak, Vernon K. Fountain, Jane W. Thurin, Magdalena TI Markers and tissue resources for melanoma: Meeting report SO CANCER RESEARCH LA English DT Editorial Material ID CUTANEOUS MALIGNANT-MELANOMA; SUBCELLULAR-LOCALIZATION; METASTATIC MELANOMA; GENE-EXPRESSION; CELL ADHESION; LYMPH-NODES; T-CELLS; PROGRESSION; MICROARRAYS; PROGNOSIS AB The Markers and Tissue Resources for Melanoma meeting convened by the Cancer Diagnosis Program, Division of Cancer Treatment and Diagnosis, Specialized Programs of Research Excellence at the Organ Systems Branch of the National Cancer Institute (NCI), and the Melanoma Research Foundation was held in Gaithersburg, MD on October 2005. The meeting reviewed the current status of biomarkers for early- and advanced-stage melanoma and addressed some of the challenges scientists and clinicians face as they unravel the biology of melanoma and try to apply these findings to patient care. Specifically, the participants focused on molecular changes associated with melanoma progression, potential diagnostic and prognostic markers emerging from molecular profiling studies, and new treatment targets for current and future clinical trials. They also highlighted the ongoing challenges about translational research in melanoma, including availability of tissue resources, and summarized the status of nevus and melanoma tissue microarrays, recently developed as a collaborative project between the melanoma research community and the NCI. The meeting report is intended to provide a perspective on emerging scientific approaches in translational research that can enhance the progress in discovery and validation of markers for melanoma. C1 NCI, Canc Diag Program, Organ Syst Branch, Rockville, MD 20852 USA. NCI, Ctr Canc Res, Rockville, MD 20852 USA. NCI, Div Canc Treatment & Diag, Rockville, MD 20852 USA. Univ S Florida, Tampa, FL USA. Harvard Univ, Sch Med, Boston, MA 02115 USA. Univ Pittsburgh, Pittsburgh, PA USA. RP Thurin, M (reprint author), NCI, Canc Diag Program, Organ Syst Branch, Execut Plaza N,6130 Execut Blvd,Room 6044, Rockville, MD 20852 USA. EM thurinm@mail.nih.gov OI Hewitt, Stephen/0000-0001-8283-1788 NR 43 TC 21 Z9 22 U1 0 U2 0 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 NOV 15 PY 2006 VL 66 IS 22 BP 10652 EP 10657 DI 10.1158/0008-5472.CAN-06-0921 PG 6 WC Oncology SC Oncology GA 108UJ UT WOS:000242264400004 PM 17108101 ER PT J AU Kirshner, J Jobling, MF Pajares, MJ Ravani, SA Glick, AB Lavin, MJ Koslov, S Shiloh, Y Barcellos-Hoff, MH AF Kirshner, Julia Jobling, Michael F. Pajares, Maria Jose Ravani, Shraddha A. Glick, Adam B. Lavin, Martin J. Koslov, Sergei Shiloh, Yosef Barcellos-Hoff, Mary Helen TI Inhibition of transforming growth factor-beta 1 signaling attenuates ataxia telanglectasia mutated activity in response to genotoxic stress SO CANCER RESEARCH LA English DT Article ID GROWTH-FACTOR-BETA; DOUBLE-STRAND BREAKS; CELL-CYCLE CHECKPOINTS; DNA-DAMAGE; TGF-BETA; MAMMARY-GLAND; IONIZING-RADIATION; GENE-EXPRESSION; IN-VITRO; ATM AB Ionizing radiation causes DNA damage that elicits a cellular program of damage control coordinated by the kinase activity of ataxia telangiectasia mutated protein (ATM). Transforming growth factor beta (TGF beta)-1, which is activated by radiation, is a potent and pleiotropic mediator of physiologic and pathologic processes. Here we show that TGF beta inhibition impedes the canonical cellular DNA damage stress response. Irradiated Tgf beta 1 nail murine epithelial cells or human epithelial cells treated with a small-molecule inhibitor of TGF beta type I receptor kinase exhibit decreased phosphorylation of Chk2, Rad17, and p53; reduced gamma H2AX radiation-induced foci; and increased radiosensitivity compared with TGF beta competent cells. We determined that loss of TGF beta signaling in epithelial cells truncated ATM autophosphorylation and significantly reduced its kinase activity, without affecting protein abundance. Addition of TGF beta restored functional ATM and downstream DNA damage responses. These data reveal a heretofore undetected critical link between the microenvironment and ATM, which directs epithelial cell stress responses, cell fate, and tissue integrity. Thus, Tgf beta 1, in addition to its role in homoeostatic growth control, plays a complex role in regulating responses to genotoxic stress, the failure of which would contribute to the development of cancer; conversely, inhibiting TGF beta may be used to advantage in cancer therapy. C1 Lawrence Berkeley Natl Lab, Div Life Sci, Berkeley, CA 94720 USA. NCI, Lab Cellular Carcinogenesis & Tumor Promot, Bethesda, MD USA. Royal Brisbane Hosp, Queensland Inst Med Res, Herston, Qld, Australia. Tel Aviv Univ, Dept Human Genet, Sackler Sch Med, Ramat Aviv, Israel. RP Barcellos-Hoff, MH (reprint author), Lawrence Berkeley Natl Lab, Div Life Sci, Bldg 977,1 Cyclotron Rd, Berkeley, CA 94720 USA. EM mhbarcellos-hoff@lbl.gov RI Lavin, Martin/F-5961-2014; Kozlov, Sergei/M-2067-2014 OI Lavin, Martin/0000-0002-5940-4769; Kozlov, Sergei/0000-0001-6183-7339 NR 48 TC 81 Z9 87 U1 0 U2 1 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 NOV 15 PY 2006 VL 66 IS 22 BP 10861 EP + DI 10.1158/0008-5472.CAN-06-2565 PG 10 WC Oncology SC Oncology GA 108UJ UT WOS:000242264400029 PM 17090522 ER PT J AU Subleski, JJ Hall, VL Back, TC Ortaldo, JR Wiltrout, RH AF Subleski, Jeff J. Hall, Veronica L. Back, Timothy C. Ortaldo, John R. Wiltrout, Robert H. TI Enhanced antitumor response by divergent modulation of natural killer and natural killer T cells in the liver SO CANCER RESEARCH LA English DT Article ID INTERFERON-GAMMA PRODUCTION; IFN-GAMMA; NKT CELLS; IN-VIVO; GENE-EXPRESSION; CANCER; IL-12; INTERLEUKIN-18; ACTIVATION; THERAPY AB The use of interleukin-18 (IL-18) together with IL-12 induced high levels of IFN-gamma in tumor-bearing mice and regression of liver tumors that was abolished in IFN-gamma((-/-)) mice. Natural killer (NK) and NKT cells were the major producers of IFN-gamma in the livers of mice treated with IL-18 and/or IL-12. Liver NK cells were significantly increased by treatment with IL-18/ IL-12, whereas the degree of liver NKT cell TCR detection was diminished by this treatment. Reduction of NK cells with anti-asGM1 decreased the antitumor activity of IL-18/IL-12 therapy and revealed NK cells to be an important component for tumor regression in the liver. In contrast, the antitumor effects of both IL-18 and IL-12 were further increased in CD1d((-/-)) mice, which lack NKT cells. Our data, therefore, show that the antitumor activity induced in mice by IL-18/IL-12 is NK and IFN-gamma dependent and is able to overcome an endogenous immunosuppressive effect of NKT cells in the liver microenvironment. These results suggest that immunotherapeutic approaches that enhance NK cell function while eliminating or altering NKT cells could be effective in the treatment of cancer in the liver. C1 Natl Canc Inst, Expt Immunol Lab, Canc Res Ctr, Frederick Canc Res & Dev Ctr, Ft Detrick, MD 21702 USA. Natl Canc Inst, Intramural Res Support Program, Canc Res Ctr, Frederick Canc Res & Dev Ctr, Ft Detrick, MD 21702 USA. RP Wiltrout, RH (reprint author), Natl Canc Inst, Expt Immunol Lab, Canc Res Ctr, Frederick Canc Res & Dev Ctr, 560-31-93, Ft Detrick, MD 21702 USA. EM wiltrour@mail.nih.gov FU Intramural NIH HHS NR 45 TC 57 Z9 59 U1 0 U2 2 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA SN 0008-5472 J9 CANCER RES JI Cancer Res. PD NOV 15 PY 2006 VL 66 IS 22 BP 11005 EP 11012 DI 10.1158/0008-5472.CAN-06-0811 PG 8 WC Oncology SC Oncology GA 108UJ UT WOS:000242264400046 PM 17108139 ER PT J AU Garcia-Pineres, AJ Hildesheim, A Herrero, R Trivett, M Williams, M Atmetlla, I Ramirez, M Villegas, M Schiffman, M Rodriguez, AC Burk, RD Hildesheim, M Freer, E Bonilla, J Bratti, C Berzofsky, JA Pinto, LA AF Garcia-Pineres, Alfonso J. Hildesheim, Allan Herrero, Rolando Trivett, Matthew Williams, Marcus Atmetlla, Ivannia Ramirez, Margarita Villegas, Maricela Schiffman, Mark Rodriguez, Ana Cecilia Burk, Robert D. Hildesheim, Mariana Freer, Enrique Bonilla, Jose Bratti, Concepcion Berzofsky, Jay A. Pinto, Ligia A. TI Persistent human papillomavirus infection is associated with a generalized decrease in immune responsiveness in older women SO CANCER RESEARCH LA English DT Article ID CERVICAL INTRAEPITHELIAL NEOPLASIA; DIFFERENTIAL T-HELPER; HPV DNA DETECTION; REFERENCE RANGES; LYMPHOCYTE SUBSETS; COSTA-RICA; REFERENCE VALUES; NATURAL-HISTORY; HEALTHY-ADULTS; FLOW-CYTOMETRY AB The development of cervical cancer and its precursors are linked to persistent infection with oncogenic types of human papillomavirus (HPV). Host immune responses seem to be determinants of risk for this disease. However, little is known about the immunologic determinants of HPV persistence. Here, we examined the association between lymphoproliferative responses to antigens/mitogens and persistent HPV infection in women older than 45 years. Women included in this study were participants in a 10,000-woman population-based cohort study of cervical neoplasia in Costa Rica. Women older than 45 years and HPV DNA positive at a screening visit were selected as cases (n = 283). We selected a comparably sized control group of HPV DNA-negative women, matched to cases on age and time since enrollment (n = 261). At an additional clinical visit, women were cytologically and virologically rescreened, and cervical and blood specimens were collected. Proliferative responses to phytohemagglutinin (PHA), influenza virus (Flu), and HPV16 virus-like particle (VLP) were lower among women with persistent HPV infection [median counts per minute (cpm): 72,849 for PHA, 1,241 for Flu, and 727 for VLP] than for the control group (median cpm: 107,049 for PHA, 2,111 for Flu, and 2,068 for VLP). The decreases were most profound in women with long-term persistence and were only observed for the oldest age group ( >= 65 years). Our results indicate that an impairment in host immunologic responses is associated to persistent HPV infection. The fact that effects were evident for all studied stimuli is suggestive of a generalized effect. C1 Sci Applicat Int Corp Frederick Inc, HPV Immunol Lab, Natl Canc Inst Frederick, Frederick, MD 21702 USA. NCI, Div Canc Epidemiol & Genet, NIH, Bethesda, MD 20892 USA. NCI, Vaccine Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA. Med Res Solut, Bethesda, MD USA. Univ Costa Rica, Proyecto Epidemiol Guanacaste, San Jose, Costa Rica. Univ Costa Rica, Ctr Investigac Estruct Microscop, San Jose, Costa Rica. Univ Costa Rica, Ctr Investigac Biol Celular & Mol, San Jose, Costa Rica. Albert Einstein Coll Med, Bronx, NY 10467 USA. RP Pinto, LA (reprint author), Sci Applicat Int Corp Frederick Inc, HPV Immunol Lab, Natl Canc Inst Frederick, Bldg 469,Room 120, Frederick, MD 21702 USA. EM lpinto@ncifcrf.gov FU NCI NIH HHS [N01-CO-12400, N01-CP-21081, N01-CP-33061, N01-CP-40542, N01-CP-50535, N01-CP-81023, N02-CP-31003, U01-CA78527] NR 45 TC 55 Z9 55 U1 1 U2 2 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA SN 0008-5472 J9 CANCER RES JI Cancer Res. PD NOV 15 PY 2006 VL 66 IS 22 BP 11070 EP 11076 DI 10.1158/0008-5472.CAN-06-2034 PG 7 WC Oncology SC Oncology GA 108UJ UT WOS:000242264400054 PM 17108147 ER PT J AU Modarres, R Hui, TP Zheng, G AF Modarres, Reza Hui, Terrence P. Zheng, Gang TI Resampling methods for ranked set samples SO COMPUTATIONAL STATISTICS & DATA ANALYSIS LA English DT Article DE RSS; nonparametric bootstrap; exact bootstrap; L-estimator; ranked set sampling ID BOOTSTRAP AB When measuring units are expensive or time consuming, while ranking them can be done easily, it is known that ranked set sampling (RSS) is preferred to simple random sampling (SRS). Available results for RSS are developed under specific parametric assumptions or are asymptotic in nature, with few results available for finite size samples when the underlying distribution of the observed data is unknown. We investigate the use of resampling techniques to draw inferences on population characteristics. To obtain standard error and confidence interval estimates we discuss and compare three methods of resampling a given ranked set sample. Chen et al. (2004. Ranked Set Sampling: Theory and Applications. Springer, New York) suggest a natural method to obtain bootstrap samples from each row of a RSS. We prove that this method is consistent for a location estimator. We propose two other methods that are designed to obtain more stratified resamples from the given sample. Algorithms are provided for these methods. We recommend a method that obtains a bootstrap RSS from the observations. We prove several properties of this method, including consistency for a location parameter. We define two types of L-estimators for RSS and obtain expressions for their exact moments. We discuss an application to obtain confidence intervals for the Winsorized mean of a RSS. (c) 2005 Elsevier B.V. All rights reserved. C1 George Washington Univ, Dept Stat, Washington, DC 20052 USA. NHLBI, Off Biostat Res, Bethesda, MD 20892 USA. RP Modarres, R (reprint author), George Washington Univ, Dept Stat, Washington, DC 20052 USA. EM reza@gwu.edu NR 16 TC 8 Z9 8 U1 3 U2 6 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0167-9473 J9 COMPUT STAT DATA AN JI Comput. Stat. Data Anal. PD NOV 15 PY 2006 VL 51 IS 2 BP 1039 EP 1050 DI 10.1016/j.csda.2005.10.010 PG 12 WC Computer Science, Interdisciplinary Applications; Statistics & Probability SC Computer Science; Mathematics GA 111VU UT WOS:000242484200045 ER PT J AU Wang, LL Abbasi, F Gaigalas, AK Vogt, RF Marti, GE AF Wang, Lili Abbasi, Fatima Gaigalas, Adolfas K. Vogt, Robert F. Marti, Gerald E. TI Comparison of fluorescein and phycoerythrin conjugates for quantifying CD20 expression on normal and leukemic B-cells SO CYTOMETRY PART B-CLINICAL CYTOMETRY LA English DT Article DE CD20; CD4; QuantiBRITE (TM) PE quantification kits; ABC value; MESF value; RM (TM) 8640; B-cell chronic lymphocytic leukemia ID CHRONIC LYMPHOCYTIC-LEUKEMIA; PERIPHERAL-BLOOD; FLOW-CYTOMETRY; MESF VALUES; INTENSITY; ANTIGEN; SUBSETS; DENSITY AB Background: Numerous methods for quantitative fluorescence calibration (QFC) have been developed to quantify receptor expression on lymphocytes as potential disease biomarkers. CD20 expression in B-cell chronic lymphocytic leukemia (B-CLL) is one of the best examples of such a biomarker, but results from the use of different QFC methods vary considerably. Methods: We measured CD20 expression on normal and B-CLL B-cells, using FITC and PE conjugates from the same monoclonal antibody (Mab). As a biological control and calibrator, we also measured CD4 expression on T-cells with FITC and PE Mab. Calibration curves were constructed using the CLSI (formerly NCCLS) consensus guidelines for QFC. Calibration with QuantiBRITE (TM) PE-labeled microspheres and the use of unimolar PE conjugates provided direct measurement of antibody bound per cell (ABC) for CD4 and CD20. Calibration for FITC conjugates was based on molecules of equivalent soluble fluorochrome (MESF), as determined by NIST RM 8640 microsphere standards. These MESF values were then converted to ABC, using the CD4 T-cell as a biologic calibrator, to normalize FITC and PE results for CD20 expression. Results: On normal B cells, the mean ABC value for unimolar CD20-PE conjugate was 143,500 (CV +/- 19.1%). The mean ABC value for B-CLL B-cells stained with the same conjugate was 21,700 (CV +/- 42.0%). Using the CD4 T-cell as a biologic calibrator for FITC conjugate, the mean ABC value for CD20FITC on normal B-cells was 199,300. CD20-FITC staining an B-CLL cells was generally too weak for accurate quantification. On normal T-cells, the mean ABC value for CD4 unimolar PE conjugate was (36,800 +/- 10.4)%, and it did not differ significantly in CLL samples. Conclusion: The expression of CD20 on normal and B-CLL lymphocytes can he quantified in ABC units using unimolar CD20-PE conjugates. In addition, CD4 expression on T-cells can be used as a biological calibrator to quantify CD20-FITC ABC, with reasonable agreement between the two conjugates with different fluorochromes. Issues regarding the accuracy of MESF microsphere calibrators and effective F/P ratios for FITC conjugates will require additional laboratory studies. (c) 2006 International Society for Analytical Cytology. C1 Natl Inst Stand & Technol, Biochem Sci Div, Gaithersburg, MD 20899 USA. US FDA, Ctr Biol Evaluat & Res, NIH, Gaithersburg, MD 20899 USA. CDC, Div Sci Lab, Atlanta, GA 30341 USA. RP Wang, LL (reprint author), Natl Inst Stand & Technol, Biochem Sci Div, 100 Bur Dr,Stop 8312, Gaithersburg, MD 20899 USA. EM lili.wang@nist.gov; gemarti@helix.nih.gov NR 17 TC 20 Z9 21 U1 0 U2 0 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 1552-4949 J9 CYTOM PART B-CLIN CY JI Cytom. Part B-Clin. Cytom. PD NOV 15 PY 2006 VL 70B IS 6 BP 410 EP 415 DI 10.1002/cyto.b.20140 PG 6 WC Medical Laboratory Technology; Pathology SC Medical Laboratory Technology; Pathology GA 099UY UT WOS:000241623100004 PM 16967494 ER PT J AU Noguchi, K Vassilev, A Ghosh, S Yates, JL DePamphilis, ML AF Noguchi, Kohji Vassilev, Alex Ghosh, Soma Yates, John L. DePamphilis, Melvin L. TI The BAH domain facilitates the ability of human Orc1 protein to activate replication origins in vivo SO EMBO JOURNAL LA English DT Article DE cell cycle; DNA replication; Epstein-Barr virus; origin recognition complex; oriP ID EPSTEIN-BARR-VIRUS; RECOGNITION COMPLEX PROTEIN-1; DNA-REPLICATION; CELL-CYCLE; SACCHAROMYCES-CEREVISIAE; CHROMATIN ASSOCIATION; METAZOAN CHROMOSOMES; STRUCTURAL BASIS; LATENT ORIGIN; INITIATION AB Selection of initiation sites for DNA replication in eukaryotes is determined by the interaction between the origin recognition complex (ORC) and genomic DNA. In mammalian cells, this interaction appears to be regulated by Orc1, the only ORC subunit that contains a bromo-adjacent homology (BAH) domain. Since BAH domains mediate protein-protein interactions, the human Orc1 BAH domain was mutated, and the mutant proteins expressed in human cells to determine their affects on ORC function. The BAH domain was not required for nuclear localization of Orc1, association of Orc1 with other ORC subunits, or selective degradation of Orc1 during S-phase. It did, however, facilitate reassociation of Orc1 with chromosomes during the M to G1-phase transition, and it was required for binding Orc1 to the Epstein-Barr virus oriP and stimulating oriP-dependent plasmid DNA replication. Moreover, the BAH domain affected Orc1's ability to promote binding of Orc2 to chromatin as cells exit mitosis. Thus, the BAH domain in human Orc1 facilitates its ability to activate replication origins in vivo by promoting association of ORC with chromatin. C1 NICHHD, NIH, Bethesda, MD 20892 USA. Roswell Pk Canc Inst, Dept Canc Genet, Buffalo, NY 14263 USA. RP DePamphilis, ML (reprint author), NICHHD, NIH, Bldg 6-3A15,9000 Rockville Pike, Bethesda, MD 20892 USA. EM depamphm@mail.nih.gov NR 57 TC 51 Z9 52 U1 0 U2 1 PU NATURE PUBLISHING GROUP PI NEW YORK PA 75 VARICK STREET, 9TH FLOOR, NEW YORK, NY 10013-1917 USA SN 0261-4189 J9 EMBO J JI Embo J. PD NOV 15 PY 2006 VL 25 IS 22 BP 5372 EP 5382 DI 10.1038/sj.emboj.7601396 PG 11 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA 108BM UT WOS:000242215000013 PM 17066079 ER PT J AU Liebe, B Petukhova, G Barchi, M Bellani, M Braselmann, H Nakano, T Pandita, TK Jasin, M Fornace, A Meistrich, ML Baarends, WM Schimenti, J de Lange, T Keeney, S Camerini-Otero, RD Scherthan, H AF Liebe, B. Petukhova, G. Barchi, M. Bellani, M. Braselmann, H. Nakano, T. Pandita, T. K. Jasin, M. Fornace, A. Meistrich, M. L. Baarends, W. M. Schimenti, J. de Lange, T. Keeney, S. Camerini-Otero, R. D. Scherthan, H. TI Mutations that affect meiosis in male mice influence the dynamics of the mid-preleptotene and bouquet stages SO EXPERIMENTAL CELL RESEARCH LA English DT Review DE ATM; bouquet; DSB; meiosis; mouse; recombination; telomere; spermatogenesis ID DOUBLE-STRAND BREAKS; MEIOTIC CHROMOSOME SYNAPSIS; KINASE CATALYTIC SUBUNIT; SPHINGOMYELINASE-DEFICIENT MICE; DNA-DAMAGE; SACCHAROMYCES-CEREVISIAE; ATAXIA-TELANGIECTASIA; PRIMARY SPERMATOCYTES; GENOMIC INSTABILITY; MOUSE SPERMATOCYTES AB Meiosis pairs and segregates homologous chromosomes and thereby forms haploid germ cells to compensate the genome doubling at fertilization. Homologue pairing in many eukaryotic species depends on formation of DNA double strand breaks (DSBs) during early prophase I when telomeres begin to cluster at the nuclear periphery (bouquet stage). By fluorescence in situ hybridization criteria, we observe that mid-preleptotene and bouquet stage frequencies are altered in male mice deficient for proteins required for recombination, ubiquitin conjugation and telomere length control. The generally low frequencies of mid-preleptotene spermatocytes were significantly increased in male mice lacking recombination proteins SPO11, ME11, MLH1, KU80, ubiquitin conjugating enzyme HR6B, and in mice with only one copy of the telomere length regulator Terf1. The bouquet stage was significantly enriched in Atm(-/-), Spoil(-/-), meil(mJcs/m1Jcs), Mlh1(-/-), Terf1(+/-) and Hr6b(-/-) spermatogenesis, but not in mice lacking recombination proteins DMC1 and HOP2, the non-homologous end-joining DNA repair factor KU80 and the ATM downstream effector GADD45a. Mice defective in spermiogenesis (Tnp1(-/-), Gmcl1(-/-), Asm(-/-)) showed wild-type mid-preleptotene and bouquet frequencies. A low frequency of bouquet spermatocytes in Spoil-'-Atm-'- spermatogenesis suggests that DSBs contribute to the Atm(-/-)-correlated bouquet stage exit defect. insignificant changes of bouquet frequencies in mice with defects in early stages of DSB repair (Dmc1(-/-), Hop2(-/-)) suggest that there is an ATM-specific influence on bouquet stage duration. Altogether, it appears that several pathways influence telomere dynamics in mammalian meiosis. (c) 2006 Elsevier Inc. All rights reserved. C1 Max Planck Inst Mol Genet, D-14195 Berlin, Germany. NIDDK, Genet & Biochem Branch, NIH, Bethesda, MD 20892 USA. Mem Sloan Kettering Canc Ctr, Program Mol Biol, New York, NY 10021 USA. GSF Forschungszentrum Umwelt & Gesundheit GmbH, Inst Mol Strahlenbiol Biostat, D-80937 Munich, Germany. Osaka Univ, Res Inst Microbial Dis, Dept Mol Cell Biol, Osaka 5650871, Japan. Washington Univ, Sch Med, Dept Radiat Oncol, St Louis, MO 63108 USA. NCI, Gene Resp Sect, Ctr Canc Res, Bethesda, MD 20892 USA. Univ Texas, MD Anderson Canc Ctr, Houston, TX 77030 USA. Erasmus MC, Dept Reprod & Dev, NL-3000 CA Rotterdam, Netherlands. Cornell Univ, Coll Vet Med, Dept Biomed Sci, Ctr Vertebrate Genom, Ithaca, NY 14853 USA. Rockefeller Univ, Lab Cell Biol & Genet, New York, NY 10021 USA. Bundeswehr Inst Radiobiol, D-80937 Munich, Germany. RP Scherthan, H (reprint author), Max Planck Inst Mol Genet, Ihnestr 73, D-14195 Berlin, Germany. EM scherth@web.de RI Fornace, Albert/A-7407-2008; de Lange, Titia de Lange/B-8263-2011; OI Fornace, Albert/0000-0001-9695-085X; Barchi, Marco/0000-0003-1104-6234; Keeney, Scott/0000-0002-1283-6417 FU NCI NIH HHS [CA10445]; NINDS NIH HHS [NS34746] NR 101 TC 36 Z9 37 U1 1 U2 4 PU ELSEVIER INC PI SAN DIEGO PA 525 B STREET, STE 1900, SAN DIEGO, CA 92101-4495 USA SN 0014-4827 J9 EXP CELL RES JI Exp. Cell Res. PD NOV 15 PY 2006 VL 312 IS 19 BP 3768 EP 3781 DI 10.1016/j.yexcr.2006.07.019 PG 14 WC Oncology; Cell Biology SC Oncology; Cell Biology GA 102DC UT WOS:000241790000006 PM 17010969 ER PT J AU Jeffers, A Gladwin, MT Kim-Shapiro, DB AF Jeffers, Anne Gladwin, Mark T. Kim-Shapiro, Daniel B. TI Computation of plasma hemoglobin nitric oxide scavenging in hemolytic anemias SO FREE RADICAL BIOLOGY AND MEDICINE LA English DT Article DE red blood cell; sickle cell disease; vasodilation ID SICKLE-CELL-DISEASE; CROSS-LINKED HEMOGLOBIN; SOLUBLE GUANYLATE-CYCLASE; RED-BLOOD-CELLS; PULMONARY-HYPERTENSION; ERYTHROCYTE CONSUMPTION; MATHEMATICAL-MODELS; RELAXING FACTOR; DIFFUSION; SUBSTITUTES AB Intravascular hemoglobin limits the amount of endothelial-derived nitric oxide (NO) available for vasodilation. Cell-free hemoglobin scavenges NO more efficiently than red blood cell-encapsulated hemoglobin. Hemolysis has recently been suggested to contribute to endothelial dysfunction based on a mechanism of NO scavenging by cell-free hemoglobin. Although experimental evidence for this phenomenon has been presented, support from a theoretical approach has, until now, been missing. Indeed, due to the low amounts of cell-free hemoglobin present in these pathological conditions, the role of cell-free hemoglobin scavenging of NO in disease has been questioned. In this study, we model the effects of cell-free hemoglobin on NO bioavailability, focusing on conditions that closely mimic those under known pathological conditions. We find that as little as 1 mu M cell-free intraluminal hemoglobin (heme concentration) can significantly reduce NO bioavailability. In addition, extravasation of hemoglobin out of the lumen has an even greater effect. We also find that low hematocrit associated with anemia increases NO bioavailability but also leads to increased susceptibility to NO scavenging by cell-free hemoglobin. These results support the paradigm that cell-free hemoglobin released into plasma during intravascular hemolysis in human disease contributes to the experimentally observed reduction in NO bioavailability and endothelial dysfunction. (c) 2006 Elsevier Inc. All rights reserved. C1 Wake Forest Univ, Dept Phys, Winston Salem, NC 27157 USA. Wake Forest Univ, Sch Med, Dept Biomed Engn, Winston Salem, NC 27157 USA. NIH, Vasc Med Branch, Natl Heart Lung & Blood Inst, Bethesda, MD 20892 USA. NIH, Crit Care Med Dept, Ctr Clin, Bethesda, MD 20892 USA. RP Kim-Shapiro, DB (reprint author), Wake Forest Univ, Dept Phys, Winston Salem, NC 27157 USA. EM shapiro@wfu.edu FU NHLBI NIH HHS [R29 HL058091, HL58091, K02 HL078706, R37 HL058091, R01 HL058091] NR 74 TC 53 Z9 54 U1 0 U2 2 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 NOV 15 PY 2006 VL 41 IS 10 BP 1557 EP 1565 DI 10.1016/j.freeradbiomed.2006.08.017 PG 9 WC Biochemistry & Molecular Biology; Endocrinology & Metabolism SC Biochemistry & Molecular Biology; Endocrinology & Metabolism GA 098ZT UT WOS:000241563000006 PM 17045924 ER PT J AU Katori, T Donzelli, S Tocchetti, CG Miranda, KM Cormaci, G Thomas, DD Ketner, EA Lee, MJ Maneardi, D Wink, DA Kass, DA Paolocci, N AF Katori, Tatsuo Donzelli, Sonia Tocchetti, Carlo G. Miranda, Katrina M. Cormaci, Gianfrancesco Thomas, Douglas D. Ketner, Elizabeth A. Lee, Myung Jae Maneardi, Daniele Wink, David A. Kass, David A. Paolocci, Nazareno TI Peroxynitrite and myocardial contractility: In vivo versus in vitro effects SO FREE RADICAL BIOLOGY AND MEDICINE LA English DT Article DE peroxynitrite; adrenergic (ant)agonists; contractile function; heart failure; nitric oxide; isolated myocytes; nitroxyl (HNO); Angeli's salt ID PERFUSED RAT-HEART; OXIDE DONOR SIN-1; NITRIC-OXIDE; NITROXYL ANION; ISCHEMIA-REPERFUSION; TYROSINE NITRATION; CARDIAC INOTROPY; SEPTIC SHOCK; SUPEROXIDE; FAILURE AB Generation of peroxynitrite (ONOO-) as a result of altered redox balance has been shown to affect cardiac function; however, inconsistencies in the data exist, particularly for myocardial contractility. The hypothesis that the cardiac impact of ONOO- formation depends on its site of generation, intravascular or intramyocardial, was examined. Cardiac contractility was assessed by pressure-volume analysis to delineate vascular versus cardiac changes on direct infusion of ONOO- into the right atria of conscious dogs both with normal cardiac function and in heart failure. Additionally, ONOO- was administered to isolated murine cardiomyocytes to mimic in situ cardiac generation. When infused in vivo, ONOO had little impact on inotropy but led to systemic arterial dilation, likely as a result of rapid decomposition to NO2- and NO3-. In contrast, infused ONOO- was long lived enough to abolish beta-adrenergic (dobutamine)-stimulated contractility/relaxation, most likely through catecholamine oxidation to aminochrome. When administered to isolated murine cardiomyocytes, ONOO- induced a rapid reduction in sarcomere shortening and whole cell calcium transients, although neither decomposed ONOO- or NaNO2 had any effect. Thus, systemic generation of ONOO- is unlikely to have primary cardiac effects, but may modulate cardiac contractile reserve, via blunted beta-adrenergic stimulation, and vascular tone, as a result of generation of NO2- and NO3. However, myocyte generation of ONOO- may impair contractile function by directly altering Ca2+ handling. These data demonstrate that the site of generation within the cardiovascular system largely dictates the ability of ONOO- to directly or indirectly modulate cardiac pump function. (c) 2006 Elsevier Inc. All rights reserved. C1 Johns Hopkins Med Inst, Dept Med, Div Cardiol, Baltimore, MD 21205 USA. NCI, Radiat Biol Branch, Bethesda, MD 20892 USA. Univ Arizona, Dept Chem, Tucson, AZ 85721 USA. RP Paolocci, N (reprint author), Johns Hopkins Med Inst, Dept Med, Div Cardiol, 935 Ross,720 Rutland Ave, Baltimore, MD 21205 USA. EM npaoloc1@jhmi.edu RI Miranda, Katrina/B-7823-2009; OI tocchetti, carlo gabriele/0000-0001-5983-688X; MANCARDI, Daniele/0000-0003-3809-6047; Paolocci, Nazareno/0000-0001-7011-997X FU NHLBI NIH HHS [P50-HL52307, HL-47511, HL075265] NR 58 TC 37 Z9 37 U1 1 U2 8 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 NOV 15 PY 2006 VL 41 IS 10 BP 1606 EP 1618 DI 10.1016/j.freeradbiomed.2006.08.023 PG 13 WC Biochemistry & Molecular Biology; Endocrinology & Metabolism SC Biochemistry & Molecular Biology; Endocrinology & Metabolism GA 098ZT UT WOS:000241563000010 PM 17045928 ER PT J AU Hirano, T Jiao, XN Chen, Z Van Waes, C Gu, XX AF Hirano, Takashi Jiao, Xinan Chen, Zhong Van Waes, Carter Gu, Xin-Xing TI Kinetics of mouse antibody and lymphocyte responses during intranasal vaccination with a lipooligosaccharide-based conjugate vaccine SO IMMUNOLOGY LETTERS LA English DT Article DE intranasal immunization; nasal-associated lymphoid tissue; lipooligosaccharide conjugate vaccine ID NONTYPABLE HAEMOPHILUS-INFLUENZAE; PROTECTIVE IMMUNITY; DETOXIFIED LIPOOLIGOSACCHARIDE; STREPTOCOCCUS-PNEUMONIAE; PNEUMOCOCCAL INFECTIONS; MORAXELLA-CATARRHALIS; MUCOSAL IMMUNIZATION; CHOLERA-TOXIN; IGA RESPONSES; OTITIS-MEDIA AB We investigated the kinetics of humoral immunity and its related cellular immune responses to intranasal (IN) immunization with a detoxified lipooligosaccharide (dLOS)-tetanus toxoid (TT) conjugate against nontypeable Haemophilus influenzae (NTHi) in mice. IN vaccination with dLOS-TT elicited high titers of LOS-specific IgA in nasal washes and IgG in sera during a course of 4 inoculations while high titers of TT-specific IgA and IgG were found in sera. A significant increase of LOS-specific IgA antibody forming cells (AFCs) was observed in nasopharyngealassociated lymphoid tissue (NALT) and nasal passages. However, TT induced broad responses with higher numbers of IgA and IgG AFCs found in NALT and nasal passages, less but significant IgA AFCs in cervical lymphoid nodes (CLN), spleen, and lungs. Phenotypic analysis revealed a significant rise of total B220+ B-lymphocytes in NALT and CLN, particularly a rise in IgA+/IgM+ cells in the NALT after the immunization. The latter result was complied with a significant rise of IL-4 but not IFN-gamma positive CD4+ T-lymphocytes in NALT. Analysis of IgG antibody subclasses showed that an IgGI response to both LOS and TT epitopes dominated in serum when compared to IgG2a. These kinetic antibody patterns and cellular responses may provide useful information regarding to effective mucosal vaccines against NTHi infections. (c) 2006 Elsevier B.V. All rights reserved. C1 Natl Inst Deafness & Commun Disorders, Vaccine Res Sect, Rockville, MD USA. Natl Inst Deafness & Communicat Disorders, Tumor Biol Sect, Head & Neck Surg Branch, Bethesda, MD USA. Oita Univ, Dept Otolaryngol, Oita 87011, Japan. RP Gu, XX (reprint author), 5 Res Court,Room 2A31, Rockville, MD 20850 USA. EM guxx@nidcd.nih.gov FU Intramural NIH HHS NR 38 TC 9 Z9 10 U1 0 U2 3 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0165-2478 J9 IMMUNOL LETT JI Immunol. Lett. PD NOV 15 PY 2006 VL 107 IS 2 BP 131 EP 139 DI 10.1016/j.imlet.2006.08.005 PG 9 WC Immunology SC Immunology GA 118RF UT WOS:000242958700008 PM 17030407 ER PT J AU Linet, MS Taggart, T Severson, RK Cerhan, JR Cozen, W Hartge, P Colt, J AF Linet, Martha S. Taggart, Theresa Severson, Richard K. Cerhan, James R. Cozen, Wendy Hartge, Patricia Colt, Joanne TI Cellular telephones and non-Hodgkin lymphoma SO INTERNATIONAL JOURNAL OF CANCER LA English DT Article DE lymphoma; non-Hodgkin; hand-held cellular telephone; radiofrequency/microwave radiation; case-control study; epidemiology ID RAT-BRAIN CELLS; PERIPHERAL-BLOOD LYMPHOCYTES; E-MU-PIM1 TRANSGENIC MICE; AMATEUR RADIO OPERATORS; LONG-TERM; ELECTROMAGNETIC-RADIATION; RADIOFREQUENCY RADIATION; MICROWAVE-RADIATION; UNITED-STATES; STRAND BREAKS AB Dramatic increase in hand-held cellular telephone use since the 1980s and excess risk of lymphoproliferative malignancies associated with radio-frequency radiation (RFR) exposures in epidemiological and experimental studies motivated assessment of cellular telephones within a comprehensive US case-control investigation of non-Hodgkin lymphoma (NHL). A questionnaire ascertained cellular telephone use in 551 NHL cases and 462 frequency-matched population controls. Compared to persons who had never used cellular telephones, risks were not increased among individuals whose lifetime use was fewer than 10 (odds ratio (OR) = 0.9, 95% confidence intervals (CI): 0.6, 1.3), 10-100 (OR = 1.0, 95 % CI: 0.7, 1.5) or more than 100 times (e.g., regular users, OR = 0.9, 95% Cl: 0.6, 1.4). Among regular users compared to those who had never used hand-held cellular telephones, risks of NHL were not significantly associated with minutes per week, duration, cumulative lifetime or year of first use, although NHL was non-significantly higher in men who used cellular telephones for more than 8 years. Little evidence linked use of cellular telephones with total, diffuse large B-cell lymphoma or follicular NHL. These findings must be interpreted in the context of less than 5% of the population reporting duration of use of 6 or more years or lifetime cumulative use of 200 or more hours. (c) 2006 Wiley-Liss, Inc. C1 NCI, Radiat Epidemiol Branch, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA. Univ Washington, Fred Hutchinson Canc Res Ctr, Div Publ Hlth Sci, Seattle, WA 98195 USA. Wayne State Univ, Karmanos Canc Inst, Epidemiol Sect, Detroit, MI 48202 USA. Univ Iowa, Coll Med, Dept Prevent Med & Environm Hlth, Iowa City, IA 52242 USA. Mayo Clin, Coll Med, Dept Hlth Sci Res, Rochester, MN USA. Univ So Calif, Keck Sch Med, Dept Prevent Med, Los Angeles, CA 90089 USA. RP Linet, MS (reprint author), NCI, Radiat Epidemiol Branch, Div Canc Epidemiol & Genet, 6120 Execut Blvd,EPS Room 7048, Bethesda, MD 20892 USA. EM linetm@mail.nih.gov OI Cerhan, James/0000-0002-7482-178X FU NCI NIH HHS [N01-PC-65064, N01-PC-67008, N01-PC-67009, N01-PC-67010, N02-PC-71105] NR 59 TC 10 Z9 12 U1 1 U2 1 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 0020-7136 J9 INT J CANCER JI Int. J. Cancer PD NOV 15 PY 2006 VL 119 IS 10 BP 2382 EP 2388 DI 10.1002/ijc.22151 PG 7 WC Oncology SC Oncology GA 094EM UT WOS:000241222300019 PM 16894556 ER PT J AU Cantwell, MM Lacey, JV Schairer, C Schatzkin, A Michaud, DS AF Cantwell, Marie M. Lacey, James V., Jr. Schairer, Catherine Schatzkin, Arthur Michaud, Dominique S. TI Reproductive factors, exogenous hormone use and bladder cancer risk in a prospective study SO INTERNATIONAL JOURNAL OF CANCER LA English DT Article DE bladder cancer; hormone therapy; reproductive factors; estrogen; parity; age at menarche; menopause ID PROGESTIN REPLACEMENT THERAPY; BREAST-CANCER; MENOPAUSAL ESTROGEN; FOLLOW-UP; WOMEN; SMOKING; COHORT; PARITY; HISTORIES; MORTALITY AB Sex is a consistent predictor of bladder cancer: men experience 2-4-fold higher age-adjusted rates than women in the U.S. and Europe. The objective of this study was to examine whether hormone-related factors are associated with bladder cancer in women. We examined parity, age at menarche, age at first birth, age at menopause, oral contraceptive use and menopausal hormone therapy (HT) use and bladder cancer risk in the Breast Cancer Detection Demonstration Project Follow-Up Study. Endpoint and exposure information was collected on 54,308 women, using annual telephone interviews (1980-86) and 3 mailed, self-administered questionnaires (1987-98). During an average follow-up time of 15.3 years, 167 cases of bladder cancer were identified. Univariate and adjusted rate ratios (RRs) were estimated using Poisson regression. Parity, age at menarche, age at first birth, age at menopause, and oral contraceptive use were not associated with bladder cancer risk. The majority of menopausal women who took HT used estrogen therapy (ET). Postmenopausal women with less than 4 years, 4-9 years, 10-19 years and 20 or more years of ET use had RRs of 1.55 (95 % CI = 0.96-2.51), 1.00 (95 % CI = 0.49-2.04), 1.23 (95% CI = 0.62-2.43) and 0.57 (95% CI = 0.14-2.34), respectively, compared with nonusers (p = 0.50). Findings from this study are not consistent with the hypothesis that hormone-related factors in women are associated with bladder cancer. (c) 2006 Wiley-Liss, Inc. C1 NCI, Nutrit Epidemiol Branch, Div Canc Epidemiol & Genet, NIH, Bethesda, MD 20892 USA. NCI, Canc Prevent Fellowship Program, NIH, Bethesda, MD 20892 USA. NCI, Hormonal & Reprod Epidemiol Branch, Div Canc Epidemiol & Genet, NIH, Bethesda, MD 20892 USA. NCI, Biostat Branch, Div Canc Epidemiol & Genet, NIH, Bethesda, MD 20892 USA. RP Cantwell, MM (reprint author), Queens Univ Belfast, Ctr Clin & Populat Sci, Royal Grp Hosp, Mulhouse Bldg,Grosvenor Rd, Belfast BT12 6BJ, Antrim, North Ireland. EM m.cantwell@qub.ac.uk RI Michaud, Dominique/I-5231-2014 NR 32 TC 44 Z9 44 U1 0 U2 1 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 0020-7136 J9 INT J CANCER JI Int. J. Cancer PD NOV 15 PY 2006 VL 119 IS 10 BP 2398 EP 2401 DI 10.1002/ijc.22175 PG 4 WC Oncology SC Oncology GA 094EM UT WOS:000241222300021 PM 16894568 ER PT J AU Adly, L Hill, D Sherman, ME Sturgeon, SR Fears, T Mies, C Ziegler, RG Hoover, RN Schairer, C AF Adly, Laila Hill, Deirdre Sherman, Mark E. Sturgeon, Susan R. Fears, Thomas Mies, Carolyn Ziegler, Regina G. Hoover, Robert N. Schairer, Catherine TI Serum concentrations of estrogens, sex hormone-binding globulin, and androgens and risk of breast cancer in postmenopausal women SO INTERNATIONAL JOURNAL OF CANCER LA English DT Article DE breast cancer; estrogens; androgens; androstenediol ID DEHYDROEPIANDROSTERONE-SULFATE; STEROID-HORMONES; ESTRADIOL; PLASMA; TESTOSTERONE; REPRODUCIBILITY; RELIABILITY; SHBG AB We assessed the relationship between serum concentrations of estrogens, androgens, and sex hormone-binding globulin and risk of breast cancer among postmenopausal women. Study participants provided serum prior to breast biopsy or mastectomy in 3 hospitals in Grand Rapids, Michigan between 1977 and 1987. A total of 179 subjects with localized breast cancer were compared to 152 subjects with nonproliferative breast changes that have not been associated with elevated breast cancer risk. Increasing serum concentrations of estrone and estrone sulfate were associated with increases in breast cancer risk; the odds ratios (ORs) in the fourth quartiles compared to the first were 2.3 (95% confidence interval (CI) 1.1-4.6) for both (p-trend = 0.02 and 0.03, respectively). Estradiol and bioavailable estradiol concentrations were associated with nonstatistically significant increases in risk. Androstenediol levels were associated with risk (p-trend = 0.01); the OR in the fourth compared to the first quartile was 2.2 (95% CI 1.0-4.6). Testosterone, dehydroepiandrosterone and androstenedione levels were not associated with increased risk. Sex hormone-binding globulin was associated with a nonsignificant decrease in risk. Associations with estrone and estrone sulfate persisted after adjustment for androstenediol (ORs for fourth compared to first quartiles were 2.0 (95% CI 0.9-4.5) and 2.2 (95% CI 1.0-4.6), respectively (p-trend = 0.16 for both). The association with androstenediol was attenuated after adjustment for estrone (OR for fourth compared to first quartile was 1.6 (95% CI 0.7-3.6); p-trend = 0.13). Higher serum concentrations of estrogens were associated with increased breast cancer risk in postmenopausal women. Androgen levels were not independently associated with substantially increased risk. (c) 2006 Wiley-Liss, Inc. C1 George Washington Univ, Dept Epidemiol & Biostat, Sch publ Hlth & Hlth Serv, Washington, DC USA. Univ New Mexico, Div Epidemiol, Albuquerque, NM 87131 USA. Univ Massachusetts, Sch Publ Hlth, Dept Publ Hlth, Amherst, MA 01003 USA. Univ Penn, Dept Pathol, Philadelphia, PA 19104 USA. RP Schairer, C (reprint author), NCI, EPS, Div Canc Epidemiol & Genet, 6120 Execut Blvd,Room 8020-MSC 7234, Rockville, MD 20852 USA. EM schairec@exchange.nih.gov RI Perez , Claudio Alejandro/F-8310-2010 OI Perez , Claudio Alejandro/0000-0001-9688-184X FU Intramural NIH HHS NR 33 TC 30 Z9 30 U1 0 U2 3 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 0020-7136 J9 INT J CANCER JI Int. J. Cancer PD NOV 15 PY 2006 VL 119 IS 10 BP 2402 EP 2407 DI 10.1002/ijc.22203 PG 6 WC Oncology SC Oncology GA 094EM UT WOS:000241222300022 PM 16894564 ER PT J AU Rajaraman, P Sigurdson, AJ Doody, MM Freedman, DM Hauptmann, M Ron, E Alexander, BH Linet, MS AF Rajaraman, Preetha Sigurdson, Alice J. Doody, Michele M. Freedman, D. Michal Hauptmann, Michael Ron, Elaine Alexander, Bruce H. Linet, Martha S. TI Lung cancer risk among US radiologic technologists, 1983-1998 SO INTERNATIONAL JOURNAL OF CANCER LA English DT Article DE lung cancer; cohort; occupation; radiation; risk factors; radiologic technologist ID ATOMIC-BOMB SURVIVORS; BRITISH RADIOLOGISTS; IONIZING-RADIATION; UNITED-STATES; MORTALITY; EXPOSURE; FOLLOW; HEALTH AB While exposure to moderate to high-dose ionizing radiation is an established risk factor for lung cancer, the relationship between lung cancer and chronic low dose radiation remains uncertain. We examined lung cancer risk among 71,894 US radiologic technologists who were certified during 1926-1982, responded to a baseline questionnaire (1983-1989), and were free of cancer other than non-melanoma skin cancer at baseline. Study participants were followed until completion of a second questionnaire (19941998), death, or August 31, 1998. We identified 287 lung cancer cases: 66 incident cases and 221 decedents. Exposure to radiation was inferred based on work history information provided in the baseline questionnaire. Relative risks (RRs) and 95% confidence intervals (CIs) were calculated using Cox proportional hazard models adjusted for age, race/ethnicity and smoking. Smoking-adjusted lung cancer risk was not related to working as a radiologic technologist in early years when radiation exposures were likely highest (RR = 0.9; 95% CI, 0.5-1.8 for year first worked before 1940 compared to year first worked >= 1960), nor was risk related to the year first worked after 1940 or the number of years worked in any decade. While lung cancer risk was increased in radiologic technologists who held patients for X-rays, or who allowed others to take numerous practice X-rays on them, the trend was not statistically significant in either case. Although we adjusted for smoking, the possibility of residual confounding exists. Overall, we find very limited evidence that chronic low-to-moderate dose occupational exposure increased lung cancer risk in the US Radiologic Technologist cohort. (c) 2006 Wiley-Liss, Inc. C1 NCI, Radiat Oncol Branch, Div Canc Epidemiol & Genet, DHHS,NIH, Bethesda, MD 20892 USA. NCI, Biostat Branch, Div Canc Epidemiol & Genet, DHHS,NIH, Bethesda, MD 20892 USA. Univ Minnesota, Sch Publ Hlth, Div Environm Hlth Sci, Minneapolis, MN USA. RP Rajaraman, P (reprint author), NCI, Radiat Oncol Branch, Div Canc Epidemiol & Genet, DHHS,NIH, 6120 Execut Blvd,EPS 7085,MSC 7238, Bethesda, MD 20892 USA. EM rajarama@mail.nih.gov FU NCI NIH HHS [N02-CP-81121, N02-CP-81005, N01-CP-15673, N01-CP-51016] NR 26 TC 8 Z9 9 U1 2 U2 8 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 NOV 15 PY 2006 VL 119 IS 10 BP 2481 EP 2486 DI 10.1002/ijc.22148 PG 6 WC Oncology SC Oncology GA 094EM UT WOS:000241222300034 PM 16858679 ER PT J AU Deerfield, D Davis, CH Wymore, T Stafford, DW Pedersen, LG AF Deerfield, David, II Davis, Charles H. Wymore, Troy Stafford, Darrel W. Pedersen, Lee G. TI Quantum chemical study of the mechanism of action of vitamin K epoxide reductase (VKOR) SO INTERNATIONAL JOURNAL OF QUANTUM CHEMISTRY LA English DT Article; Proceedings Paper CT 5th Congress of the International-Society-for-Theoretical-Chemical-Physics CY JUL 20-26, 2005 CL New Orleans, LA SP Int Soc Theoret Chem Phys DE vitamin K; VKOR; reductase; mechanisms; intermediates ID STRENGTH AMPLIFICATION MECHANISM; DISEASE AB Possible model, but simplistic, mechanisms for the action of vitamin K epoxide reductase (VKOR) are investigated with quantum mechanical methods (B3LYP/6-311G**). The geometries of proposed model intermediates in the mechanisms are energy optimized. Finally, the energetics of the proposed (pseudo-enzymatic) pathways are compared. We find that the several pathways are all energetically feasible. These results will be useful for designing quantum mechanical/molecular mechanical method (QM/MM) studies of the enzymatic pathway once three-dimensional structural data are determined and available for VKOR. (C) 2006 Wiley Periodicals, Inc. C1 NIEHS, Struct Biol Lab, Res Triangle Pk, NC 27709 USA. Univ N Carolina, Dept Chem, Chapel Hill, NC 27599 USA. Pittsburgh Supercomp Ctr, Biomed Grp, Pittsburgh, PA 15213 USA. Univ N Carolina, Dept Biochem & Biophys, Chapel Hill, NC 27599 USA. Univ N Carolina, Dept Biol, Chapel Hill, NC 27599 USA. RP Pedersen, LG (reprint author), NIEHS, Struct Biol Lab, POB 12233, Res Triangle Pk, NC 27709 USA. EM lee_pedersen@unc.edu RI Pedersen, Lee/E-3405-2013 OI Pedersen, Lee/0000-0003-1262-9861 NR 24 TC 13 Z9 14 U1 0 U2 3 PU JOHN WILEY & SONS INC PI HOBOKEN PA 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 0020-7608 J9 INT J QUANTUM CHEM JI Int. J. Quantum Chem. PD NOV 15 PY 2006 VL 106 IS 14 BP 2944 EP 2952 DI 10.1002/qua.21119 PG 9 WC Chemistry, Physical; Mathematics, Interdisciplinary Applications; Physics, Atomic, Molecular & Chemical SC Chemistry; Mathematics; Physics GA 094ZB UT WOS:000241276800015 ER PT J AU Lin, P Yang, WT Pedersen, LC Negishi, M Pedersen, LG AF Lin, Ping Yang, Weitao Pedersen, Lars C. Negishi, Masa Pedersen, Lee G. TI Searching for the minimum energy path in the sulfuryl transfer reaction catalyzed by human estrogen sulfotransferase: Role of enzyme dynamics SO INTERNATIONAL JOURNAL OF QUANTUM CHEMISTRY LA English DT Article; Proceedings Paper CT 5th Congress of the International-Society-for-Theoretical-Chemical-Physics CY JUL 20-26, 2005 CL New Orleans, LA SP Int Soc Theoret Chem Phys DE mechanism of sulfotransferases; QM/MM; estrogen sulfotransferase ID 3'-PHOSPHOADENOSINE 5'-PHOSPHOSULFATE PAPS; SINGLE TRANSITION-STATE; CYTOSOLIC SULFOTRANSFERASES; CRYSTAL-STRUCTURE; MECHANICAL METHODS; MOLECULAR-BIOLOGY; SULFATE ESTERS; RESP MODEL; HYDROLYSIS; NITROPHENYL AB The enzymatic transfer of a sulfuryl group from the ubiquitous biological source of sulfate X-phosphoadenosine 5'-phosphosulfate (PAPS) to estrogen is investigated by the pseudo-bond quantum mechanical/molecular mechanical method (QM/MM) method. Calculations of the reaction path are performed starting with models based on two crystal structures, which differ in information about the cofactor and substrates. In addition, a subsequent relaxation of the enzyme was performed with the found transition state frozen, followed by redetermination of the path. An activation barrier of 22 kcal/mol is estimated. The reaction mechanism features a proton transfer from the estrogen to a catalytic histidine followed by the rate determining SO, transfer. The mechanism found is largely dissociative. (C) 2006 Wiley Periodicals, Inc. C1 Univ N Carolina, Dept Chem, Chapel Hill, NC 27599 USA. Duke Univ, Dept Chem, Durham, NC 27708 USA. NIEHS, Struct Biol Lab, Res Triangle Pk, NC 27709 USA. RP Pedersen, LG (reprint author), Univ N Carolina, Dept Chem, CB 3290, Chapel Hill, NC 27599 USA. EM lee_pedersen@unc.edu RI Yang, Weitao/C-1109-2008; Pedersen, Lee/E-3405-2013; Lin, Ping/C-7115-2008 OI Pedersen, Lee/0000-0003-1262-9861; Lin, Ping/0000-0003-1200-4423 NR 49 TC 13 Z9 13 U1 0 U2 4 PU WILEY-BLACKWELL PI HOBOKEN PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA SN 0020-7608 EI 1097-461X J9 INT J QUANTUM CHEM JI Int. J. Quantum Chem. PD NOV 15 PY 2006 VL 106 IS 14 BP 2981 EP 2998 DI 10.1002/qua.21123 PG 18 WC Chemistry, Physical; Mathematics, Interdisciplinary Applications; Physics, Atomic, Molecular & Chemical SC Chemistry; Mathematics; Physics GA 094ZB UT WOS:000241276800019 ER PT J AU Yoon, HY Miura, K Cuthbert, EJ Davis, KK Ahvazi, B Casanova, JE Randazzo, PA AF Yoon, Hye-Young Miura, Koichi Cuthbert, E. Jebb Davis, Kathryn Kay Ahvazi, Bijan Casanova, James E. Randazzo, Paul A. TI ARAP2 effects on the actin cytoskeleton are dependent on Arf6-specific GTPase-activating-protein activity and binding to RhoA-GTP SO JOURNAL OF CELL SCIENCE LA English DT Article DE actin; Rho; Arf; GTPase-activating protein ID ADP-RIBOSYLATION FACTOR; ARF-GAP ASAP1; FOCAL ADHESIONS; CELL-MIGRATION; STRESS FIBERS; MEMBRANE; KINASE; REORGANIZATION; COMPLEX; RHOGAP AB ARAP2 is a protein that contains both ArfGAP and RhoGAP domains. We found that it is a phosphatidylinositol ( 3,4,5)-trisphosphate-dependent Arf6 GAP that binds RhoA-GTP but lacks RhoGAP activity. In agreement with the hypothesis that ARAP2 mediates effects of RhoA, endogenous ARAP2 associated with focal adhesions (FAs) and reduction of ARAP2 expression, by RNAi, resulted in fewer FAs and actin stress fibers (SFs). In cells with reduced levels of endogenous ARAP2, FAs and SFs could be restored with wild-type recombinant ARAP2 but not mutants lacking ArfGAP or Rho-binding activity. Constitutively active Arf6 also caused a loss of SFs. The Rho effector ROK alpha was ineffective in restoring FAs. Conversely, overexpression of ARAP2 did not restore SFs in cells treated with a ROK inhibitor but induced punctate accumulations of paxillin. We conclude that ARAP2 is an Arf6GAP that functions downstream of RhoA to regulate focal adhesion dynamics. C1 NCI, Cellular Oncol Lab, Ctr Canc Res, US Dept HHS, Bethesda, MD 20892 USA. Univ Virginia, Sch Med, Dept Microbiol, Charlottesville, VA 22908 USA. NIAMSD, Off Sci & Technol, Xray Crystallog Facil, NIH, Bethesda, MD 20892 USA. RP Randazzo, PA (reprint author), NCI, Cellular Oncol Lab, Ctr Canc Res, US Dept HHS, Bldg 37, Bethesda, MD 20892 USA. EM randazzo@helix.nih.gov FU Intramural NIH HHS; NIGMS NIH HHS [GM 662510] NR 69 TC 43 Z9 43 U1 0 U2 7 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 NOV 15 PY 2006 VL 119 IS 22 BP 4650 EP 4666 DI 10.1242/jcs.03237 PG 17 WC Cell Biology SC Cell Biology GA 103NK UT WOS:000241893400009 PM 17077126 ER PT J AU Deane, JA Bolland, S AF Deane, Jonathan A. Bolland, Silvia TI Nucleic acid-sensing TLRs as modifiers of autoimmunity SO JOURNAL OF IMMUNOLOGY LA English DT Review ID TOLL-LIKE RECEPTORS; SYSTEMIC-LUPUS-ERYTHEMATOSUS; PLASMACYTOID DENDRITIC CELLS; INTERFERON-ALPHA INDUCTION; COPY NUMBER POLYMORPHISM; IFN-GAMMA PRODUCTION; ACTIVATE B-CELLS; MURINE LUPUS; DIFFERENTIAL ROLES; IMMUNE-SYSTEM AB The immune system requires precise regulation of activating and inhibitory signals so that it can mount effective responses against pathogens while ensuring tolerance to self-components. Some of the most potent activation signals are triggered by innate immune molecules, particularly those in the TLR family. Recent studies have shown that engagement of TLRs plays a significant role in both innate and adaptive immunity. This review focuses on the ways that TLR function might contribute to the etiology of lupus-like syndromes in the context of an autoimmune-prone environment. By considering the sources, localization, and expression of both nucleic acids and the molecules that bind them, we discuss several ways that innate immunity can play a role in the development of systemic autoimmunity. C1 NIAID, Immunogenet Lab, Rockville, MD 20852 USA. RP Bolland, S (reprint author), NIAID, Immunogenet Lab, 12441 Parklawn Dr,Room 217, Rockville, MD 20852 USA. EM sbolland@nih.gov FU Intramural NIH HHS NR 77 TC 42 Z9 44 U1 0 U2 0 PU AMER ASSOC IMMUNOLOGISTS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA SN 0022-1767 J9 J IMMUNOL JI J. Immunol. PD NOV 15 PY 2006 VL 177 IS 10 BP 6573 EP 6578 PG 6 WC Immunology SC Immunology GA 105DN UT WOS:000242009700001 PM 17082566 ER PT J AU Erman, B Alag, AS Dahle, O van Laethem, F Sarafova, SD Guinter, TI Sharrow, SO Grinberg, A Love, PE Singer, A AF Erman, Batu Alag, Amala S. Dahle, Oyvind van Laethem, Francois Sarafova, Sophia D. Guinter, Terry I. Sharrow, Susan O. Grinberg, Alexander Love, Paul E. Singer, Alfred TI Coreceptor signal strength regulates positive selection but does not determine CD4/CD8 lineage choice in a physiologic in vivo model SO JOURNAL OF IMMUNOLOGY LA English DT Article ID T-CELL DEVELOPMENT; TRANSGENIC MICE; CD8 LINEAGE; THYMOCYTE DEVELOPMENT; NEGATIVE SELECTION; ANTIGEN RECEPTOR; TYROSINE KINASE; GENE-EXPRESSION; COMMITMENT; DIFFERENTIATION AB TCR signals drive thymocyte development, but it remains controversial what impact, if any, the intensity of those signals have on T cell differentiation in the thymus. In this study, we assess the impact of CD8 coreceptor signal strength on positive selection and CD4/CD8 lineage choice using novel gene knockin mice in which the endogenous CD8 alpha gene has been re-engineered to encode the stronger signaling cytoplasmic tail of CD4, with the re-engineered CD8 alpha gene referred to as CD8.4. We found that stronger signaling CD8.4 coreceptors specifically improved the efficiency of CD8-dependent positive selection and quantitatively increased the number of MHC class I (MHC-I)-specific thymocytes signaled to differentiate into CD8(+) T cells, even for thymocytes expressing a single, transgenic TCR. Importantly, however, stronger signaling CD8.4 coreceptors did not alter the CD8 lineage choice of any MHC-I-specific thymocytes, even MHC-I-specific thymocytes expressing the high-affinity F5 transgenic TCR. This study documents in a physiologic in vivo model that coreceptor signal strength alters TCR-signaling thresholds for positive selection and so is a major determinant of the CD4:CD8 ratio, but it does not influence CD4/CD8 lineage choice. C1 NCI, Expt Immunol Branch, Bethesda, MD 20892 USA. Sabanci Univ, Biol Sci & Bioengn Program, Fac Engn & Nat Sci, Istanbul, Turkey. NICHHD, Lab Mammalian Genes & Dev, Bethesda, MD 20892 USA. RP Singer, A (reprint author), NCI, Expt Immunol Branch, Bldg 10 Room 4B36, Bethesda, MD 20892 USA. EM singera@nih.gov FU Intramural NIH HHS NR 50 TC 13 Z9 14 U1 0 U2 0 PU AMER ASSOC IMMUNOLOGISTS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA SN 0022-1767 J9 J IMMUNOL JI J. Immunol. PD NOV 15 PY 2006 VL 177 IS 10 BP 6613 EP 6625 PG 13 WC Immunology SC Immunology GA 105DN UT WOS:000242009700008 PM 17082573 ER PT J AU Ito, D Albers, A Zhao, YX Visus, C Appella, E Whiteside, TL DeLeo, AB AF Ito, Daisuke Albers, Andreas Zhao, Yong Xiang Visus, Carmen Appella, Ettore Whiteside, Theresa L. DeLeo, Albert B. TI The wild-type sequence (wt) p53(25-35) peptide induces HLA-DR7 and HLA-DR11-restricted CD4(+) Th cells capable of enhancing the ex vivo expansion and function of anti-wt p53(264-272) peptide CD8(+) T cells SO JOURNAL OF IMMUNOLOGY LA English DT Article ID DENDRITIC CELLS; BREAST-CANCER; TUMOR-ANTIGEN; P53; EPITOPE; IMMUNITY; LYMPHOCYTES; VACCINATION; ANTIBODIES; RESPONSES AB Tumor peptide-based vaccines are more effective when they include tumor-specific Th cell-defined as well as CTL-defined peptides. Presently, two overlapping wild-type sequences (wt) p53 helper peptides, p53(108-122) and p53(110-124), have been identified as HLA-DR1- and/or HILA-DR4-restricted epitopes. These HLA-DR alleles are expressed by similar to 35% of subjects with cancer. To identify Th cell-defined wt p53 peptides suitable for use on the remaining subject population, a dendritic cell (DC)-based coculture system was developed. CD4(+) T cells isolated from PBMC obtained from HLA-DR4(-) normal donors were stimulated ex vivo with autologous DC transfected with wt p53 or mutant p53 cDNA. Reactivity of T cells was tested in ELISPOT IFN-gamma assays against DC pulsed individually with a panel of algorithm-predicted, multiple HLA-DR-binding wt p53 peptides. The wt p53(25-35) peptide was identified as capable of inducing and being recognized by CD4(+) T cells in association, at a minimum, with IILA-DR7 and -DR11 molecules, each of which is expressed by similar to 15% of the population. In addition, the presence of anti-p5315-35 CD4(+) Th cells was shown to enhance the in vitro generation/expansion of HLA-A2-restricted, anti-wt p53(264-272), CD8(+) T cells, which from one donor were initially "nonresponsive" to the wt p53(264-272) peptide. The wt p53(25-23), peptide has attributes of a naturally presented Th cell-defined peptide, which could be incorporated into antitumor vaccines applicable to a broader population of subjects for whom a wt p53 helper peptide is presently unavailable, as well as used for monitoring anti-p53 Th cell activity in cancer subjects receiving p53-based immunotherapy. C1 Univ Pittsburgh, Inst Canc, Hillman Canc Ctr, Div Basic Res, Pittsburgh, PA 15213 USA. Univ Pittsburgh, Sch Med, Dept Pathol, Pittsburgh, PA 15213 USA. Univ Pittsburgh, Sch Med, Dept Pathol Otolaryngol, Pittsburgh, PA 15213 USA. NCI, Bethesda, MD 20839 USA. RP DeLeo, AB (reprint author), Univ Pittsburgh, Inst Canc, Hillman Canc Ctr, Div Basic Res, Res Pavil,5117 Ctr Ave, Pittsburgh, PA 15213 USA. EM deleo@imap.pitt.edu FU NCI NIH HHS [P50 CA97190]; NIDCR NIH HHS [P01 DE12321] NR 29 TC 12 Z9 12 U1 0 U2 0 PU AMER ASSOC IMMUNOLOGISTS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA SN 0022-1767 J9 J IMMUNOL JI J. Immunol. PD NOV 15 PY 2006 VL 177 IS 10 BP 6795 EP 6803 PG 9 WC Immunology SC Immunology GA 105DN UT WOS:000242009700028 PM 17082593 ER PT J AU Adriani, M Garbi, C Amodio, G Russo, I Giovannini, M Amorosi, S Matrecano, E Cosentini, E Candotti, F Pignata, C AF Adriani, Marsilio Garbi, Corrado Amodio, Giada Russo, Ilaria Giovannini, Marica Amorosi, Stefania Matrecano, Eliana Cosentini, Elena Candotti, Fabio Pignata, Claudio TI Functional interaction of common gamma-chain and, growth hormone receptor signaling apparatus SO JOURNAL OF IMMUNOLOGY LA English DT Article ID SEVERE COMBINED IMMUNODEFICIENCY; TYROSINE PHOSPHORYLATION; FACTOR-I; GH RECEPTOR; NUCLEAR TRANSLOCATION; STAT PROTEINS; ACTIVATION; CELLS; PROLACTIN; BINDING AB We previously reported on an X-linked SCID (X-SCID) patient, who also had peripheral growth hormone (GH) hyporesponsiveness and abnormalities of the protein phosphorylation events following GH receptor (GHR) stimulation. In the present study, we examined a potential role of common cytokine receptor gamma-chain (gamma(c)) in GHR signaling using EBV-transformed lymphocytes from healthy subjects and gamma(c)-negative X-SCID patients. We demonstrated that the proliferative response to GH stimulation of the B cell lines of gamma(c)-negative patients was impaired despite a comparable cellular expression of GHR molecules to controls. In patients, after GH stimulation, no phosphorylation of STAT5 was observed. In addition, the molecule localization through confocal microscopy revealed that in B cell lines of patients no nuclear translocation of STAT5b following GH stimulation occurred differently from controls. Biochemical analysis of the nuclear extracts of gamma(c)-negative cell lines provided further evidence that the amount of STAT5b and its phosphorylated form did not increase following GH stimulation. In patients, cells reconstituted with wild-type T. abnormal biochemical and functional events were restored resulting in nuclear translocation of STAT5. Confocal experiments revealed that GHR and gamma(c) were colocalized on the cell membrane. Our study demonstrates the existence of a previously unappreciated relationship between GHR-signaling pathway and y(c), which is required for the activation of STAT5b in B cell lines. These data also confirm that growth failure in X-SCID is primarily related to the genetic alteration of the IL2RG gene. C1 Univ Naples Federico II, Dept Pediat, Immunol Unit, I-80131 Naples, Italy. Univ Naples Federico II, Dept Cellular & Mol Biol & Pathol, I-80131 Naples, Italy. Univ Naples Federico II, Immunohematol Unit, I-80131 Naples, Italy. NHGRI, Genet & Mol Biol Branch, NIH, Bethesda, MD 20892 USA. RP Pignata, C (reprint author), Univ Naples Federico II, Dept Pediat, Immunol Unit, Via S Pansini 5, I-80131 Naples, Italy. EM pignata@unina.it RI Adriani, Marsilio/F-2553-2013; Pignata, Claudio/O-2466-2013; Amodio, Giada/J-8788-2016 OI Pignata, Claudio/0000-0003-1568-9843; Amodio, Giada/0000-0002-2457-387X NR 43 TC 17 Z9 17 U1 0 U2 1 PU AMER ASSOC IMMUNOLOGISTS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA SN 0022-1767 J9 J IMMUNOL JI J. Immunol. PD NOV 15 PY 2006 VL 177 IS 10 BP 6889 EP 6895 PG 7 WC Immunology SC Immunology GA 105DN UT WOS:000242009700038 PM 17082603 ER PT J AU Fujimoto, C Yu, CR Shi, GP Vistica, BP Wawrousek, EF Klinman, DM Chan, CC Egwuagu, CE Gery, I AF Fujimoto, Chiaki Yu, Cheng-Rong Shi, Guangpu Vistica, Barbara P. Wawrousek, Eric F. Klinman, Dennis M. Chan, Chi-Chao Egwuagu, Charles E. Gery, Igal TI Pertussis toxin is superior to TLR ligands in enhancing pathogenic autolimmunity, targeted at a neo-self antigen, by triggering robust expansion of Th1 cells and their cytokine production SO JOURNAL OF IMMUNOLOGY LA English DT Article ID EXPERIMENTAL ALLERGIC ENCEPHALOMYELITIS; EXPERIMENTAL AUTOIMMUNE UVEORETINITIS; ACTIVATED PROTEIN-KINASE; CENTRAL-NERVOUS-SYSTEM; T-CELLS; DENDRITIC CELLS; OCULAR INFLAMMATION; EFFECTOR FUNCTIONS; ADJUVANT ACTION; IN-VIVO AB Microbial products are assumed to play a major role in triggering pathogenic autoimmunity. Recently accumulated data have shown that these products stimulate the immune system by interacting with TLRs, expressed on APCs. To examine the capacity of various TLR ligands to trigger pathogenic autoimmunity, we used a system in which naive CD4 cells, specific against hen egg lysozyme (HEL), are injected into recipient mice expressing HEL in their eyes. Only when stimulated, the naive cells acquire pathogenic capacity and induce ocular inflammation. Seven TLR ligands were tested in this system: lipoteichoic acid/peptidoglycan, zymosan, poly (I:C), LPS, pertussis toxin (PTX), flagellin, and CpG oligodeoxynucleotide. Treatment of recipient mice with HEL alone stimulated proliferation of the transferred cells, but no disease, whereas ocular inflammation did develop in recipient mice coinjected with HEL and any one of the seven TLR ligands. Inflammation induced by PTX surpassed by its severity those induced by all other tested TLR ligands and was accompanied by a dramatic increase in number of the transferred cells that acquired features of effector Th1 lymphocytes. Ocular inflammation and number of transferred cells in recipients injected with PTX and HEL were substantially reduced by treatment with Abs against IFN-gamma or IL-12, thus indicating the role of these cytokines in the PTX effect. Overall, our observations demonstrate that various TLR ligands are capable of triggering pathogenic autoimmunity and that PTX surpasses other microbial products in this activity, by stimulating excessive proliferation and polarization toward Th1 of naive T cells. C1 NEI, Immunol Lab, NIH, Bethesda, MD 20892 USA. NEI, Mol & Dev Biol Lab, NIH, Bethesda, MD 20892 USA. Ctr Biol Evaluat & Res Food & Drug Adm, Bethesda, MD 20892 USA. RP Gery, I (reprint author), NEI, Immunol Lab, NIH, Bldg 10,Room 10N208, Bethesda, MD 20892 USA. EM geryi@nei.nih.gov RI Wawrousek, Eric/A-4547-2008 FU Intramural NIH HHS NR 48 TC 27 Z9 27 U1 0 U2 1 PU AMER ASSOC IMMUNOLOGISTS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA SN 0022-1767 J9 J IMMUNOL JI J. Immunol. PD NOV 15 PY 2006 VL 177 IS 10 BP 6896 EP 6903 PG 8 WC Immunology SC Immunology GA 105DN UT WOS:000242009700039 PM 17082604 ER PT J AU Leon, F Contractor, N Fuss, I Marth, T Lahey, E Iwaki, S La Sala, A Hoffmann, V Strober, W Kelsall, BL AF Leon, Francisco Contractor, Nikhat Fuss, Ivan Marth, Thomas Lahey, Edward Iwaki, Shoko la Sala, Andrea Hoffmann, Victoria Strober, Warren Kelsall, Brian L. TI Antibodies to complement receptor 3 treat established inflammation in murine models of colitis and a novel model of psoriasiform dermatitis SO JOURNAL OF IMMUNOLOGY LA English DT Article ID REGULATORY T-CELLS; MYELOMONOCYTIC CELLS; ADHESION RECEPTORS; CROHNS-DISEASE; INTERLEUKIN-12; IL-12; MICE; SKIN; RECRUITMENT; EXPRESSION AB Prior studies indicated the ability of Abs to complement receptor 3 (CR3, CD11b/CD18) to suppress the production of IL-12 from immune cells. Therefore, we tested the ability of an anti-CR3 Ab (clone M1/70) to treat established IL-12-dependent Th1-mediated inflammation in murine models. Systemic administration of anti-CR3 significantly ameliorated established intestinal inflammation following the intrarectal administration of trinitrobenzene sulfonic acid (TNBS-colitis), as well as colitis and skin inflammation in C57BL/10 RAG-2(-/-) mice reconstituted with CD4(+)CD45RB(high) T cells. The hyperproliferative skin inflammation in this novel murine model demonstrated many characteristics of human psoriasis, and was prevented by the adoptive transfer of CD45RB(low) cells. In vitro and in vivo studies suggest that anti-CR3 treatment may act, at least in part, by directly inhibiting IL-12 production by APCs. Administration of anti-CR3 may be a useful therapeutic approach to consider for the treatment of inflammatory bowel disease and psoriasis in humans. C1 Natl Inst Allergy & Infect Dis, NIH, Lab Mol Immunol, Bethesda, MD 20892 USA. Natl Inst Allergy & Infect Dis, NIH, Host Def Lab, Bethesda, MD 20892 USA. Natl Inst Allergy & Infect Dis, NIH, Lab Allerg Dis, Bethesda, MD 20892 USA. NIH, Off Res Serv, Div Vet Resources, Off Director, Bethesda, MD 20892 USA. RP Kelsall, BL (reprint author), 10-11N113,10 Ctr Dr, Bethesda, MD 20892 USA. EM kelsall@nih.gov RI la Sala, Andrea/A-3228-2009 OI la Sala, Andrea/0000-0003-1268-6516 NR 44 TC 28 Z9 29 U1 0 U2 1 PU AMER ASSOC IMMUNOLOGISTS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA SN 0022-1767 J9 J IMMUNOL JI J. Immunol. PD NOV 15 PY 2006 VL 177 IS 10 BP 6974 EP 6982 PG 9 WC Immunology SC Immunology GA 105DN UT WOS:000242009700047 PM 17082612 ER PT J AU Feng, CG Kaviratne, M Rothfuchs, AG Cheever, A Hieny, S Young, HA Wynn, TA Sher, A AF Feng, Carl G. Kaviratne, Mallika Rothfuchs, Antonio Gigliotti Cheever, Allen Hieny, Sara Young, Howard A. Wynn, Thomas A. Sher, Alan TI NK cell-derived IFN-gamma differentially regulates innate resistance and neutrophil response in T cell-deficient hosts infected with Mycobacterium tuberculosis SO JOURNAL OF IMMUNOLOGY LA English DT Article ID NATURAL-KILLER-CELLS; TUMOR-NECROSIS-FACTOR; INTERFERON-GAMMA; GRANULOMA-FORMATION; IN-VIVO; INTRACELLULAR BACTERIUM; ALTERNATIVE ACTIVATION; MACROPHAGE ACTIVATION; CHEMOKINE PRODUCTION; EFFECTOR FUNCTION AB Although it is known that IFN-gamma-secreting T cells are critical for control of Mycobacterium tuberculosis infection, the contribution of IFN-gamma produced by NK cells to host resistance to the pathogen is less well understood. By using T cell-deficient RAG(-/-) mice, we showed that M. tuberculosis stimulates NK cell-dependent IFN-gamma production in naive splenic cultures and in lungs of infected animals. More importantly, common cytokine receptor gamma-chain(-/-)RAG(-/-) animals deficient in NK cells, p40(-/-)RAG(-/-), or anti-IFN-gamma mAb-treated RAG(-/-) mice displayed significantly increased susceptibility to M. tuberculosis infection compared with untreated NK-sufficient RAG(-/-) controls. Studies comparing IL-12 p40- and p35-deficient RAG(-/-) mice indicated that IL-12 plays a more critical role in the induction of IFN-gamma-mediated antimycobacterial effector functions than IL-23 or other p40-containing IL-12 family members. The increased susceptibility of IL-12-deficient or anti-IFN-gamma mAb-treated RAG(-/-) mice was associated not only with elevated bacterial loads, but also with the development of granulocyte-enriched foci in lungs. This tissue response correlated with increased expression of the granulocyte chemotactic chemokines KC and MIP-2 in NK as well as other leukocyte populations. Interestingly, depletion of granulocytes further increased bacterial burdens and exacerbated pulmonary pathology in these animals, revealing a compensatory function for neutrophils in the absence of IFN-gamma. The above observations indicate that NK cell-derived IFN-gamma differentially regulates T-independent resistance and granulocyte function in M. tuberculosis infection and suggest that this response could serve as an important barrier in AIDS patients or other individuals with compromised CD4(+) T cell function. C1 NIAID, Parasit Dis Lab, Immunobiol Sect, NIH, Bethesda, MD 20892 USA. NIAID, Parasit Dis Lab, Immunopathogenesis, NIH, Bethesda, MD 20892 USA. Biomed Res Inst, Rockville, MD 20852 USA. NCI, Canc Res Ctr, Expt Immunol Lab, Frederick, MD 21701 USA. RP Feng, CG (reprint author), NIAID, Parasit Dis Lab, Immunobiol Sect, NIH, Room 6148,Bldg 50,50 South Dr, Bethesda, MD 20892 USA. EM cfeng@niaid.nih.gov RI Young, Howard/A-6350-2008; Wynn, Thomas/C-2797-2011; Rothfuchs, Antonio/F-5981-2013 OI Young, Howard/0000-0002-3118-5111; Rothfuchs, Antonio/0000-0001-6001-7240 NR 54 TC 108 Z9 110 U1 0 U2 13 PU AMER ASSOC IMMUNOLOGISTS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA SN 0022-1767 J9 J IMMUNOL JI J. Immunol. PD NOV 15 PY 2006 VL 177 IS 10 BP 7086 EP 7093 PG 8 WC Immunology SC Immunology GA 105DN UT WOS:000242009700060 PM 17082625 ER PT J AU Yin, HH Davis, MI Ronesi, JA Lovinger, DM AF Yin, Henry H. Davis, Margaret I. Ronesi, Jennifer A. Lovinger, David M. TI The role of protein synthesis in striatal long-term depression SO JOURNAL OF NEUROSCIENCE LA English DT Article DE long-term depression; protein synthesis; cycloheximide; translation; striatum; endocannabinoid; plasticity ID SYNAPTIC DEPRESSION; ENDOCANNABINOID RELEASE; DORSOLATERAL STRIATUM; PLASTICITY; FACILITATION; TRANSPORT; AXONS; TRANSLATION; GLUTAMATE; SYNAPSES AB Long-term depression (LTD) at the corticostriatal synapse is postsynaptically induced but presynaptically expressed, the depression being a result of retrograde endocannabinoid signaling that activates presynaptic cannabinoid CB1 receptors and reduces the probability of glutamate release. To study the role of protein synthesis in striatal LTD, we used a striatum-only preparation in which the presynaptic cell body is cut off, leaving intact only its axons, whose terminals synapse on medium spiny neurons. LTD (duration > 150 min) was induced in this preparation, thus providing evidence that transcription in the presynaptic cell nucleus is not necessary for this form of plasticity. The maintenance of striatal LTD, however, was blocked by bath application of protein translation inhibitors but not by the same inhibitors loaded into the postsynaptic cell. These results suggest that local translation is critical for the expression of striatal LTD, distinguishing this form of mammalian synaptic plasticity from other forms that require postsynaptic protein synthesis. Possible roles of axonal or glial translation in striatal LTD are considered. C1 NIAAA, Sect Synapt Pharmacol, Lab Integrat Neurosci, NIH, Bethesda, MD 20892 USA. RP Lovinger, DM (reprint author), NIAAA, Sect Synapt Pharmacol, Lab Integrat Neurosci, NIH, 5625 Fishers Lane,TS-13, Bethesda, MD 20892 USA. EM lovindav@willco.niaaa.nih.gov RI Davis, Margaret/F-4165-2010; yu, yan/C-2322-2012; OI Davis, Margaret/0000-0002-0489-8351 FU Intramural NIH HHS NR 39 TC 47 Z9 48 U1 1 U2 4 PU SOC NEUROSCIENCE PI WASHINGTON PA 11 DUPONT CIRCLE, NW, STE 500, WASHINGTON, DC 20036 USA SN 0270-6474 J9 J NEUROSCI JI J. Neurosci. PD NOV 15 PY 2006 VL 26 IS 46 BP 11811 EP 11820 DI 10.1523/JNEUROSCI.3196-06.2006 PG 10 WC Neurosciences SC Neurosciences & Neurology GA 110OA UT WOS:000242387000002 PM 17108154 ER PT J AU Senatorov, V Malyukova, I Fariss, R Wawrousek, EF Swaminathan, S Sharan, SK Tomarev, S AF Senatorov, Vladimir Malyukova, Irina Fariss, Robert Wawrousek, Eric F. Swaminathan, Srividya Sharan, Shyam K. Tomarev, Stanislav TI Expression of mutated mouse myocilin induces open-angle glaucoma in transgenic mice SO JOURNAL OF NEUROSCIENCE LA English DT Article DE glaucoma; myocilin; transgenic mice; trabecular meshwork; retina; retinal ganglion cells ID TRABECULAR MESHWORK CELLS; RETINAL GANGLION-CELLS; SEQUENCE TAG ANALYSIS; INTRAOCULAR-PRESSURE; AQUEOUS-HUMOR; NON-SECRETION; DBA/2J MICE; GENE; ACCUMULATION; MUTATIONS AB We developed a genetic mouse model of open-angle glaucoma by expression of mutated mouse myocilin (Myoc) in transgenic (Tg) mice. The Tyr423His point mutation, corresponding to the severe glaucoma-causing Tyr437His mutation in the human MYOC gene, was introduced into bacterial artificial chromosome DNA encoding the full-length mouse Myoc gene and long flanking regions. Both wildtype (Wt) and Tg animals expressed Myoc in tissues of the irido-corneal angle and the sclera. Expression of mutated Myoc induced the accumulation of Myoc in cell cytoplasm and prevented its secretion into the extracellular space. The levels of ATPase-1 were reduced in the irido-corneal angle of Tg mice compared with Wt animals. Tg mice demonstrated a moderate elevation of intraocular pressure, the loss of similar to 20% of the retinal ganglion cells (RGCs) in the peripheral retina, and axonal degeneration in the optic nerve. RGC depletion was associated with the shrinkage of their nuclei and DNA fragmentation in the peripheral retina. Pathological changes observed in the eyes of Tg mice are similar to those observed in glaucoma patients. C1 NEI, Sect Mol Mech Glaucoma, Mol & Dev Biol Lab, NIH, Bethesda, MD 20892 USA. NEI, Biol Imaging Core, NIH, Bethesda, MD 20892 USA. NCI, Mouse Canc Genet Program, Frederick, MD 21702 USA. RP Tomarev, S (reprint author), NEI, Sect Mol Mech Glaucoma, Mol & Dev Biol Lab, NIH, Bethesda, MD 20892 USA. EM tomarevs@nei.nih RI Wawrousek, Eric/A-4547-2008 NR 39 TC 62 Z9 65 U1 0 U2 5 PU SOC NEUROSCIENCE PI WASHINGTON PA 11 DUPONT CIRCLE, NW, STE 500, WASHINGTON, DC 20036 USA SN 0270-6474 J9 J NEUROSCI JI J. Neurosci. PD NOV 15 PY 2006 VL 26 IS 46 BP 11903 EP 11914 DI 10.1523/JNEUROSCI.3020-06.2006 PG 12 WC Neurosciences SC Neurosciences & Neurology GA 110OA UT WOS:000242387000012 PM 17108164 ER PT J AU Geng, T Seitz, PK Thomas, ML Xu, B Soman, KV Kurosky, A Luxon, BA Cunningham, KA AF Geng, Tao Seitz, Patricia K. Thomas, Mary L. Xu, Bo Soman, Kizhake V. Kurosky, Alexander Luxon, Bruce A. Cunningham, Kathryn A. TI Use of surface enhanced laser desorption/ionization-time of flight mass spectrometry (SELDI-TOF MS) to study protein expression in a rat model of cocaine withdrawal SO JOURNAL OF NEUROSCIENCE METHODS LA English DT Article DE brain; cocaine; proteomics; mass spectrometry; SELDI; SELDI-TOF ID VENTRAL TEGMENTAL AREA; BEHAVIORAL SENSITIZATION; GEL-ELECTROPHORESIS; TYROSINE-HYDROXYLASE; CEREBROSPINAL-FLUID; ALZHEIMERS-DISEASE; PROTEOMIC ANALYSIS; NUCLEUS-ACCUMBENS; SEEKING BEHAVIOR; CENTRAL AMYGDALA AB Surface enhanced laser desorption/ionization-time of flight mass spectrometry (SELDI-TOF MS) is an analytical technology for proteomic analysis that combines chromatography and mass spectrometry. At present, this technology is most commonly being exploited for the simultaneous measurement of numerous proteins in serum, but has also been utilized in organ tissue, although rarely in the brain. We applied SELDI-TOF MS technology to study protein expression in the brain of rats withdrawn from repeated cocaine exposure. Our goals were to optimize sample preparation and ProteinChip (R) Array protocols for brain tissue, to verify the reproducibility of SELDI-TOF mass spectra and to determine whether SELDI-TOF MS detects differentially expressed proteins in cocaine-versus saline-treated rats. Consequently, we have developed an optimal protocol and generated a reproducible spectral pattern with six dominant peaks in all test samples. We have detected two smaller peaks (m/z: 5179, 5030) that were significantly increased (P < 0.05) in cocaine-treated rats compared to saline-treated rats. In summary, the application of SELDI-TOF MS to the study of protein expression in a rat model of cocaine withdrawal is feasible and has the potential to generate new hypotheses. (c) 2006 Elsevier B.V. All rights reserved. C1 Univ Texas, Med Branch, Dept Pharmacol & Toxicol, Addict Res Ctr, Galveston, TX 77555 USA. Univ Texas, NHLBI, Prote Ctr, Dept Biochem & Mol Biol,Med Branch, Galveston, TX 77555 USA. Univ Texas, Med Branch, Dept Biochem & Mol Biol, Bioinformat Program, Galveston, TX 77555 USA. RP Seitz, PK (reprint author), Univ Texas, Med Branch, Dept Pharmacol & Toxicol, Addict Res Ctr, 301 Univ Blvd, Galveston, TX 77555 USA. EM pseitz@utmb.edu RI Soman, Kizhake/C-2028-2012; Luxon, Bruce/C-9140-2012; Cunningham, Kathryn/O-2718-2013 FU NIDA NIH HHS [DA000260, DA006511, DA016905, DA020087] NR 65 TC 9 Z9 10 U1 0 U2 3 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 NOV 15 PY 2006 VL 158 IS 1 BP 1 EP 12 DI 10.1016/j.jneumeth.2006.04.025 PG 12 WC Biochemical Research Methods; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA 104BT UT WOS:000241931600001 PM 16766040 ER PT J AU Bix, G Castello, R Burrows, M Zoeller, JJ Weech, M Iozzo, RA Cardi, C Thakur, ML Barker, CA Camphausen, K Iozzo, RV AF Bix, Gregory Castello, Remedios Burrows, Michelle Zoeller, Jason J. Weech, Michelle Iozzo, Rex A. Cardi, Christopher Thakur, Mathew L. Barker, Christopher A. Camphausen, Kevin Iozzo, Renato V. TI Endorepellin in vivo: Targeting the tumor vasculature and retarding cancer growth and metabolism SO JOURNAL OF THE NATIONAL CANCER INSTITUTE LA English DT Article ID INFRARED-LABELED ENDOSTATIN; BASEMENT-MEMBRANES; ENDOTHELIAL-CELLS; ALPHA(2)BETA(1) INTEGRINS; ANTIANGIOGENIC ACTIVITY; ANGIOGENESIS INHIBITOR; PERLECAN; PROTEIN; MICE; PROTEOGLYCANS AB Background. The antiangiogenic approach to controlling cancer requires a better understanding of angiogenesis and the discovery of new compounds that modulate this key biological process. Here we investigated the role of endorepellin, an angiostatic protein fragment that is derived from the C-terminus of perlecan, a heparan sulfate proteoglyean, in controlling tumor angiogenesis in vivo. Methods: We administered human recombinant endorepellin systemically to mice bearing orthotopic squamous carcinoma xenografts or syngeneic Lewis lung carcinoma tumors. We monitored tumor growth, angiogenesis, metabolism, hypoxia, and mitotic index by using quantitative immunohistochemistry and positron emission tomography scan imaging. In addition, we determined the localization of injected endorepellin using near-infrared labeling and immunohistochemistry of frozen tumor sections. Finally, we isolated tumor-derived endothelial cells and tested whether endorepellin could interact with these cells and disrupt in vitro capillary morphogenesis. All statistical tests were two-sided. Results: Endorepellin specifically targeted the tumor vasculature as determined by immunohistochemical analysis and accumulated in the tumor perivascular zones where it persisted for several days as discrete deposits. This led to inhibition of tumor angiogenesis (as measured by decreased CD31-positive cells, mean control = 1902 CD31-positive pixels, mean endorepellin treated = 343.9, difference between means = 1558, 95% confidence interval [CI] = 1296 to 1820, P <.001), enhanced tumor hypoxia, and a statistically significant decrease in tumor metabolism and mitotic index (as measured by decreased Ki67-positive cells, mean control Ki67 pixels = 5970, mean endorepellin-treated Ki67 pixels = 3644, difference between means = 2326, 95% CI = 1904 to 2749, P <.001) compared to untreated controls. Endorepellin was actively internalized by tumor-derived endothelial cells causing a redistribution of alpha 2 beta 1 integrin such that both proteins colocalized to punctate deposits in the perivascular region. Endorepellin treatment inhibited in vitro capillary morphogenesis of both normal and tumor-derived endothelia. Conclusions: Our results provide support for the hypothesis that endorepellin is an effective antitumor vasculature agent that could be used as a therapeutic modality to combat cancer. C1 Thomas Jefferson Univ, Dept Pathol Anat & Cell Biol, Kimmel Canc Ctr, Philadelphia, PA 19107 USA. Thomas Jefferson Univ, Cellular Biol & Signaling Program, Kimmel Canc Ctr, Philadelphia, PA 19107 USA. Thomas Jefferson Univ, Dept Radiat, Radiopharmaceut Res Ctr, Philadelphia, PA 19107 USA. Natl Canc Inst, Imaging & Mol Therapeut Sect, Radiat Oncol Branch, Bethesda, MD USA. RP Iozzo, RV (reprint author), Thomas Jefferson Univ, Dept Pathol Anat & Cell Biol, Kimmel Canc Ctr, Rm 249 JAH, Philadelphia, PA 19107 USA. EM iozzo@mail.jci.tju.edu RI Barker, Christopher/I-9477-2012; OI Iozzo, Renato/0000-0002-5908-5112 FU NCI NIH HHS [R01 CA39481, R01 CA47282, T32 CA09678]; NIAAA NIH HHS [T32 AA07463] NR 55 TC 68 Z9 71 U1 0 U2 8 PU OXFORD UNIV PRESS INC PI CARY PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA SN 0027-8874 J9 J NATL CANCER I JI J. Natl. Cancer Inst. PD NOV 15 PY 2006 VL 98 IS 22 BP 1634 EP 1646 DI 10.1093/jnci/djj441 PG 13 WC Oncology SC Oncology GA 110LF UT WOS:000242379700010 PM 17105986 ER PT J AU Gilmour, PS Schladweiler, MC Nyska, A McGee, JK Thomas, R Jaskot, RH Schmid, J Kodavanti, UP AF Gilmour, Peter S. Schladweiler, Mette C. Nyska, Abraham McGee, John K. Thomas, Ronald Jaskot, Richard H. Schmid, Judy Kodavanti, Urmila P. TI Systemic imbalance of essential metals and cardiac gene expression in rats following acute pulmonary zinc exposure SO JOURNAL OF TOXICOLOGY AND ENVIRONMENTAL HEALTH-PART A-CURRENT ISSUES LA English DT Article ID PARTICULATE AIR-POLLUTION; LONG-TERM EXPOSURE; COPPER DEFICIENCY; EPITHELIAL-CELLS; DIETARY ZINC; FUME FEVER; PARTICLES; HEART; LUNG; METALLOTHIONEIN AB It was recently demonstrated that particulate matter (PM) containing water-soluble zinc produces cardiac injury following pulmonary exposure. To investigate whether pulmonary zinc exposure produces systemic metal imbalance and direct cardiac effects, male Wistar Kyoto (WKY) rats (12-14 wk age) were intratracheally (IT) instilled with saline or 2 mu mol/kg zinc sulfate. Temporal analysis was performed for systemic levels of essential metals (zinc, copper, and selenium), and induction of zinc transporter-2 (ZT-2) and metallothionein-1 (MT-1) mRNA in the lung, heart, and liver. Additionally, cardiac gene expression profile was evaluated using Affymetrix GeneChips (rat 230A) arrays to identify zinc-specific effects. Pulmonary zinc instillation produced an increase in plasma zinc to similar to 20% at 1 and 4 h postexposure with concomitant decline in the lung levels. At 24 and 48 h postexposure, zinc levels rose significantly (similar to 35%) in the liver. At these time points, plasma and liver levels of copper and selenium also increased significantly, suggesting systemic disturbance in essential metals. Zinc exposure was associated with marked induction of MT-1 and ZT-2 mRNA in lung, heart, and liver, suggesting systemic metal sequestration response. Given the functional role of zinc in hundreds of proteins, the gene expression profiles demonstrated changes that are expected based on its physiological role. Zinc exposure produced an increase in expression of kinases and inhibition of expression of phosphatases; up- or downregulation of genes involved in mitochondrial function; changes in calcium regulatory proteins suggestive of elevated intracellular free calcium and increases in sulfotransferases; upregulation of potassium channel genes; and changes in free radical-sensitive proteins. Some of these expression changes are reflective of a direct effect of zinc on myocardium following pulmonary exposure, which may result in impaired mitochondrial respiration, stimulated cell signaling, altered Ca2+ homeostasis, and increased transcription of sulfotransferases. Cardiotoxicity may be an outcome of acute zinc toxicosis and occupational exposures to metal fumes containing soluble zinc. Imbalance of systemic metal homeostasis as a result of pulmonary zinc exposure may underlie the cause of extrapulmonary effects. C1 US EPA, Pulm Toxicol Branch, Expt Toxicol Div, Natl Hlth & Environm Effects Res Lab,ORD, Res Triangle Pk, NC 27709 USA. Univ N Carolina, Sch Med, Ctr Environm Med Asthma & Lung Biol, Chapel Hill, NC 27515 USA. Natl Inst Environm Hlth Sci, Lab Expt Pathol, Res Triangle Pk, NC USA. US EPA, Reprod Toxicol Div, Natl Hlth & Environm Effects Res Lab, ORD, Res Triangle Pk, NC 27709 USA. RP Kodavanti, UP (reprint author), US EPA, Pulm Toxicol Branch, Expt Toxicol Div, Natl Hlth & Environm Effects Res Lab,ORD, MD B143-01, Res Triangle Pk, NC 27709 USA. EM kodavanti.urmila@epa.gov NR 65 TC 20 Z9 21 U1 0 U2 5 PU TAYLOR & FRANCIS INC PI PHILADELPHIA PA 325 CHESTNUT ST, SUITE 800, PHILADELPHIA, PA 19106 USA SN 1528-7394 J9 J TOXICOL ENV HEAL A JI J. Toxicol. Env. Health Part A PD NOV 15 PY 2006 VL 69 IS 22 BP 2011 EP 2032 DI 10.1080/15287390600746173 PG 22 WC Environmental Sciences; Public, Environmental & Occupational Health; Toxicology SC Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology GA 100DP UT WOS:000241648000003 PM 17074742 ER PT J AU Austein, T Kerstan, H Aue, G Schnieder, I von Bloh, J Badge, S AF Austein, Thorsten Kerstan, Holger Aue, Georg Schnieder, Inga von Bloh, Julia Badge, Stephanie TI First manifestation of multiple myeloma as lethal streptococcal sepsis SO MEDIZINISCHE KLINIK LA German DT Article DE multiple myeloma; Streptococcus pneumoniae; sepsis ID BACTEREMIA; MORTALITY AB Background: The multiple myeloma has the highest incidence among tumors of the bone and the bone marrow. Due to its rather mild and uncharacteristic clinical onset, first diagnosis of multiple myeloma is often delayed. Case Report: The case of a 60-year-old female patient is reported who had been admitted to the authors' hospital in a state of severe septicemia. The patient's medical history had been unremarkable, apart from osteoporotic complaints. Smears of both peripheral blood as well as bone marrow samples showed a massive streptococcal infestation as demonstrated by light microscopy. In addition, plasma cells were the dominant cell type in these samples allowing the diagnosis of a yet unknown full-blown multiple myeloma. Conclusion: The case suggests that in the event of indistinct bone ache, a routine serum electrophoresis is advisable to minimize the risk of missing an underlying multiple myeloma. C1 St Bernhard Hosp, Med Klin, D-26919 Brake, Germany. NHLBI, NIH, Hematol Branch, Bethesda, MD 20892 USA. RP Austein, T (reprint author), St Bernhard Hosp, Med Klin, Claussenstr 3, D-26919 Brake, Germany. EM dr.austein@sbhospital.de NR 10 TC 0 Z9 0 U1 1 U2 3 PU URBAN & VOGEL PI MUNICH PA NEUMARKTER STRASSE 43, D-81673 MUNICH, GERMANY SN 0723-5003 J9 MED KLIN JI Med. Klin. PD NOV 15 PY 2006 VL 101 IS 11 BP 905 EP 907 DI 10.1007/s00063-006-1113-x PG 3 WC Medicine, General & Internal SC General & Internal Medicine GA 110KN UT WOS:000242377900008 PM 17235478 ER PT J AU Yu, YK Zhang, YC Laureti, P Moret, L AF Yu, Yi-Kuo Zhang, Yi-Cheng Laureti, Paolo Moret, Lionel TI Decoding information from noisy, redundant, and intentionally distorted sources SO PHYSICA A-STATISTICAL MECHANICS AND ITS APPLICATIONS LA English DT Article DE reputation systems; information filtering AB Advances in information technology reduce barriers to information propagation, but at the same time they also induce the information overload problem. For the making of various decisions.. mere digestion of the relevant information has become a daunting task due to the massive amount of information available. This information, such as that generated by evaluation systems developed by various web sites, is in general useful but may be noisy and may also contain biased entries. In this study, we establish a framework to systematically tackle the challenging problem of information decoding in the presence of massive and redundant data. When applied to a voting system, our method simultaneously ranks the raters and the ratees using only the evaluation data, consisting of an array of scores each of which represents the rating of a ratee by a rater. Not only is our approach effective in decoding information, it is also shown to be robust against various hypothetical types of noise as well as intentional abuses. (c) 2006 Elsevier B.V. All rights reserved. C1 Univ Fribourg, Dept Phys, CH-1700 Fribourg, Switzerland. Natl Lib Med, Natl Ctr Biotechnol Informat, NIH, Bethesda, MD 20894 USA. RP Moret, L (reprint author), Univ Fribourg, Dept Phys, CH-1700 Fribourg, Switzerland. EM lionel.moret@unifr.ch NR 10 TC 20 Z9 21 U1 0 U2 3 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-4371 J9 PHYSICA A JI Physica A PD NOV 15 PY 2006 VL 371 IS 2 BP 732 EP 744 DI 10.1016/j.physa.2006.04.057 PG 13 WC Physics, Multidisciplinary SC Physics GA 093WC UT WOS:000241200000053 ER PT J AU Chen, Y Samal, B Hamelink, CR Xiang, CC Chen, Y Chen, M Vaudry, D Brownstein, MJ Hallenbeck, JM Eiden, LE AF Chen, Yun Samal, Babru Hamelink, Carol R. Xiang, Charlie C. Chen, Yong Chen, Mei Vaudry, David Brownstein, Michael J. Hallenbeck, John M. Eiden, Lee E. TI Neuroprotection by endogenous and exogenous PACAP following stroke SO REGULATORY PEPTIDES LA English DT Article; Proceedings Paper CT Workshop on Signalling Mechanisms of VIP, PACAP and Related Peptides - Contribution of Genomics, Proteomics and Bioinformatics CY SEP, 2005 CL Rouen, FRANCE DE pituitary adenylate cyclase activating polypeptide; PACAP; PACAP-deficient mouse; middle cerebral artery occlusion; MCAO; neurological severity score; NSS; cerebral ischerma; infarct volume; cDNA microarray; PACAP responsive gene; neuroprotection; neurotrauma ID CYCLASE-ACTIVATING POLYPEPTIDE; FOCAL CEREBRAL-ISCHEMIA; TRAUMATIC BRAIN-INJURY; VASOACTIVE-INTESTINAL-PEPTIDE; HIPPOCAMPAL GENE-EXPRESSION; CEREBELLAR GRANULE CELLS; MICROARRAY ANALYSIS; LIGAND/RECEPTOR SYSTEM; PROENKEPHALIN GENE; GENOMIC RESPONSE AB We investigated the effects of PACAP treatment, and endogenous PACAP deficiency, on infarct volume, neurological function, and the cerebrocortical transcriptional response in a mouse model of stroke, middle cerebral artery occlusion (MCAO). PACAP-38 administered i.v. or i.e. v. 1 h after MCAO significantly reduced infarct volume, and ameliorated functional motor deficits measured 24 h later in wild-type mice. Infarct volumes and neurological deficits (walking faults) were both greater in PACAP-deficient than in wild-type mice, but treatment with PACAP reduced lesion volume and neurological deficits in PACAP-deficient mice to the same level of improvement as in wild-type mice. A 35,546-clone mouse cDNA microarray was used to investigate cortical transcriptional changes associated with cerebral ischemia in wild-type and PACAP-deficient mice, and with PACAP treatment after MCAO in wild-type mice. 229 known (named) transcripts were increased (228) or decreased (1) in abundance at least 50% following cerebral ischemia, in wild-type mice. 49 transcripts were significantly up-regulated only at 1 h post-MCAO (acute response transcripts), 142 were up-regulated only at 24 h post-MCAO (delayed response transcripts) and 37 transcripts were upregulated at both times (sustained response transcripts). More than half of these are transcripts not previously reported to be altered in ischemia. A larger percentage of genes up-regulated at 24 hr than at 1 hr required endogenous PACAP, suggesting a more prominent role for PACAP in later response to injury than in the initial response. This is consistent with a neuroprotective role for PACAP in late response to injury, i.e., even when administered 1 hr or more after MCAO. Putative injury effector transcripts regulated by PACAP include beta-actin, rnidline 2, and metallothionein 1. Potential neuroprotective transcripts include several demonstrated to be PACAP-regulated in other contexts. Prominent among these were transcripts encoding the PACAP-regulated gene ler3, and the neuropeptides enkephalin, substance P (tachykinin 1), and neurotensin. (c) 2006 Elsevier B.V. All rights reserved. C1 NIH, Mol Neurosci Sect, Lab Cellular & Mol Regulat, Bethesda, MD 20892 USA. NIMH, Genet Lab, NIH, Bethesda, MD 20892 USA. NINDS, Stroke Branch, NIH, Bethesda, MD 20892 USA. RP Eiden, LE (reprint author), NIH, Mol Neurosci Sect, Lab Cellular & Mol Regulat, Bldg 10, Bethesda, MD 20892 USA. EM eidenl@mail.nih.gov RI Samal, Babru/C-5563-2008; OI Eiden, Lee/0000-0001-7524-944X; Vaudry, David/0000-0003-3567-7452 FU Intramural NIH HHS [Z01 MH002386-21, Z01 MH002386-22] NR 78 TC 68 Z9 69 U1 2 U2 8 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0167-0115 J9 REGUL PEPTIDES JI Regul. Pept. PD NOV 15 PY 2006 VL 137 IS 1-2 BP 4 EP 19 DI 10.1016/j.regpep.2006.06.016 PG 16 WC Endocrinology & Metabolism; Physiology SC Endocrinology & Metabolism; Physiology GA 117OD UT WOS:000242881700002 PM 17027094 ER PT J AU Freidlin, B Korn, EL AF Freidlin, Boris Korn, Edward L. TI Letter to the editor - Testing treatment effects in the presence of competing risks by Boris Freidlin and Edward L. Korn, Statistics in Medicine 2005 ; 24 : 1703-1712 - Authors' reply SO STATISTICS IN MEDICINE LA English DT Letter C1 NCI, Div Canc Treatment & Diagnosis, Biometr Res Branch, Bethesda, MD 20892 USA. RP Freidlin, B (reprint author), NCI, Div Canc Treatment & Diagnosis, Biometr Res Branch, Bethesda, MD 20892 USA. EM freidlinb@ctep.nci.nih.gov NR 3 TC 0 Z9 0 U1 0 U2 0 PU JOHN WILEY & SONS LTD PI CHICHESTER PA THE ATRIUM, SOUTHERN GATE, CHICHESTER PO19 8SQ, W SUSSEX, ENGLAND SN 0277-6715 J9 STAT MED JI Stat. Med. PD NOV 15 PY 2006 VL 25 IS 21 BP 3761 EP 3763 DI 10.1002/sim.2610 PG 3 WC Mathematical & Computational Biology; Public, Environmental & Occupational Health; Medical Informatics; Medicine, Research & Experimental; Statistics & Probability SC Mathematical & Computational Biology; Public, Environmental & Occupational Health; Medical Informatics; Research & Experimental Medicine; Mathematics GA 097XQ UT WOS:000241483500011 ER PT J AU Margaryan, A Moaddel, R Aldrich, JR Tsuruda, JM Chen, AM Leal, WS Wainer, IW AF Margaryan, Armenak Moaddel, Ruin Aldrich, Jeffrey R. Tsuruda, Jennifer M. Chen, Angela M. Leal, Walter S. Wainer, Irving W. TI Synthesis of an immobilized Bombyx mori pheromone-binding protein liquid chromatography stationary phase SO TALANTA LA English DT Article; Proceedings Paper CT 1st Workshop of the European-Union CY OCT 20-21, 2005 CL Dubrovnik, CROATIA SP European Union DE affinity chromatography; screening; conformational mobility; odorant binding protein ID DROSOPHILA; ANTENNA; MOTH; PH AB The pheromone-binding protein from the silkworm moth, Bombyx mori (BmorPBP) has been covalently bonded to a liquid chromatographic stationary phase. The resulting column was evaluated using radiolabeled bombykol and the immobilized protein retained its ability to bind this ligand. The data also demonstrate that the BmorPBP column was able to distinguish between four compounds, and rank them in their relative order of affinity for the protein from highest to lowest: bombykol > bombykal > 1-hexadecanol > (ZE)-5,7-dodecadien-1-ol, and that the immobilized BmorPBP retained its pH-dependent conformational mobility. The results of this study demonstrate that pheromone-binding protein from the silkworm moth, Bombyx mori and an odorant binding protein (OBP) obtained from the female mosquito Culex quinquefasciatoes have been immobilized on a silica support with retention of ligand-binding activity. The data indicate that proteins from non-mammalian organisms can be used to create liquid chromatography affinity columns. (c) 2006 Elsevier B.V. All rights reserved. C1 NIA, Gerontol Res Ctr, NIH, Baltimore, MD 21224 USA. USDA ARS, Chem Affecting Insect Behav Lab, Beltsville, MD 20705 USA. Univ Calif Davis, Dept Entomol, Davis, CA 95616 USA. RP Wainer, IW (reprint author), NIA, Gerontol Res Ctr, NIH, Baltimore, MD 21224 USA. EM Wainerir@grc.nia.nih.gov OI Leal, Walter/0000-0002-6800-1240 NR 13 TC 3 Z9 4 U1 2 U2 10 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0039-9140 J9 TALANTA JI Talanta PD NOV 15 PY 2006 VL 70 IS 4 BP 752 EP 755 DI 10.1016/j.talanta.2006.01.046 PG 4 WC Chemistry, Analytical SC Chemistry GA 097XC UT WOS:000241481800010 PM 18970835 ER PT J AU Peng, R Voltan, R Cristillo, AD Alvord, WG Davis-Warren, A Zhou, QF Murthy, KK Robert-Guroff, M AF Peng, Ro Voltan, Rebecca Cristillo, Anthony D. Alvord, W. Gregory Davis-Warren, Alberta Zhou, Qifeng Murthy, Krishna K. Robert-Guroff, Marjorie TI Replicating Ad-recombinants encoding non-myristoylated rather than wild-type HIV Nef elicit enhanced cellular immunity SO AIDS LA English DT Article DE vaccine; cellular immunity; CD4; primate; animal models ID SIMIAN IMMUNODEFICIENCY VIRUS; COMPLEX CLASS-I; CD8 T-CELLS; DOWN-REGULATION; SURFACE EXPRESSION; SIV NEF; THERAPEUTIC VACCINATION; CD8-T-CELL MEMORY; RHESUS MACAQUES; CD4-T-CELL HELP AB Objective: To determine if immunization with non-myrisloylated nef would elicit enhanced cellular immune responses resulting from improved presentation of Nef pepticles by MHC-I on the cell surface, and enhanced T-cell help. Design: The myristoylation site of HIV and SIV Nef is required for several Nef functions that modulate the immune response in an infected host, including downregulation of MHC-I, MHC-II, and CD4, and increased expression of the invariant chain on the cell surface. We constructed replication-competent Ad5- and Ad7-HIV recombinants encoding wild-type nef (nef(WT)) or a nef mutant (nef(NM)) lacking 19 amino-terminal amino acids, including the myristoylation site, and sequentially immunized chimpanzees mucosally, Methods: Peripheral blood lymphocytes were evaluated over the immunization course for Nef-specific cellular immune responses by interferon (IFN)-gamma ELISPOT and T-cell proliferation assays. Nef-specific CD4 and CD8 memory T cells that produced intracellular IFN-gamma, interleukin-2, and tumor necrosis factor (TNF)-alpha were assessed by flow cytometry. Results: In comparison to immunization with Ad-HIVnef(WT), Ad-HIVnef(NM) elicited statistically significant increases in numbers of IFN-gamma-secreting cells after the Ad7-HIVnefNm immunization and increased T-cell proliferative responses following both Ad5- and Ad7-HIVnefNm immunizations. Nef-specific CD4 and CD8 memory T-cell populations secreting TNF-alpha were also significantly increased in the Ad-HIVnefNM immunization group. Conclusions: The results support the hypothesis that immunization with Ad-recombinants encoding HIVnef(NM) rather than HIVnef(WT) elicits enhanced cellular immunity resulting from improved antigen presentation and greater T-cell help. C1 NCI, Vaccine Branch, Ctr Canc Res, Bethesda, MD 20892 USA. Adv Biosci Labs Inc, Kensington, MD USA. NCI, SW Fdn Biomed Res, Frederick, MD 21701 USA. RP Robert-Guroff, M (reprint author), NCI, NIH, 41 Medlars Dr,Bldg 41,Room D804, Bethesda, MD 20892 USA. EM guroffm@mail.nih.gov NR 50 TC 0 Z9 0 U1 0 U2 3 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0269-9370 J9 AIDS JI Aids PD NOV 14 PY 2006 VL 20 IS 17 BP 2149 EP 2157 PG 9 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA 114PA UT WOS:000242676900003 ER PT J AU Vionnet, J Kempner, ES Vann, WF AF Vionnet, Justine Kempner, Ellis S. Vann, Willie F. TI Functional molecular mass of Escherichia coli K92 polysialyltransferase as determined by radiation target analysis SO BIOCHEMISTRY LA English DT Article ID POLYSIALIC ACID; INACTIVATION ANALYSIS; K1; PROTEIN; WEIGHT AB The polysialyltransferase of Escherichia coli K92 catalyzes the transfer of sialic acid from CMP-sialic acid to a growing chain of polysialic acid at the nonreducing end. The enzyme encoded by the neuS gene is membrane-associated and has been suggested to be organized within a complex of several proteins encoded by the K92 gene cluster. Attempts to prepare a soluble active NeuS enzyme have been unsuccessful. Recent results suggest that de novo synthesis of polysialic acid requires coexpression of four genes from the cluster: neuS, neuE, kpsC, and kpsS. However, elongation of preexisting polysialic acid chains only requires expression of neuS. The molecular organization of the catalytic unit of bacterial polysialyltransferases has not been described. We used radiation inactivation to measure the size of the minimum functional unit catalyzing the polysialyltransferase chain extension and de novo reactions. Membranes harboring NeuS in the presence and absence of other products of the K92 gene cluster were exposed to high-energy electrons. The rate of loss of polysialyltransferase activity reveals the mass of the molecules essential for catalytic activity. We observed that the transfer of neuNAc from CMP-neuNAc to a polysialic acid acceptor is catalyzed by a complex with a target size larger than that of monomeric NeuS. The target size of the unit catalyzing the extension of existing polysialic acid chains does not differ significantly from the size of the unit catalyzing transfer of sialic acid to the endogenous acceptor. Parallel samples of membranes containing NeuS and a green fluorescent protein (GFP) chimera were compared by target analysis. The target size of this structural unit was estimated by analysis of the rate of decay of the GFP-NeuS chimera band migrating in the immunoblots. The target size of the structural unit is larger than expected for a monomer. The results of these experiments show that while the target size of the catalytic activity for K92 polysialyltransferase is larger than a monomer of NeuS, a large complex is not required for catalysis. C1 US FDA, Lab Bacterial Polysaccharides, Ctr Biol Evaluat & Res, Bethesda, MD 20892 USA. NIAMSD, Off Sci & Technol, NIH, Bethesda, MD 20892 USA. RP Vann, WF (reprint author), US FDA, Lab Bacterial Polysaccharides, Ctr Biol Evaluat & Res, Bldg 29,Room 103,8800 Rockville Pike, Bethesda, MD 20892 USA. EM wvann@helix.nih.gov NR 18 TC 7 Z9 7 U1 0 U2 0 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA SN 0006-2960 J9 BIOCHEMISTRY-US JI Biochemistry PD NOV 14 PY 2006 VL 45 IS 45 BP 13511 EP 13516 DI 10.1021/bi061486k PG 6 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA 102JZ UT WOS:000241808300011 PM 17087504 ER PT J AU Chakrabarti, S Lanczycki, CJ Panchenko, AR Przytycka, TM Thiessen, PA Bryant, SH AF Chakrabarti, Saikat Lanczycki, Christopher J. Panchenko, Anna R. Przytycka, Teresa M. Thiessen, Paul A. Bryant, Stephen H. TI State of the art: refinement of multiple sequence alignments SO BMC BIOINFORMATICS LA English DT Article ID PROTEIN SEQUENCES; DATABASE; ACCURACY; IMPROVEMENT; STRATEGIES; ALGORITHM; QUALITY; MAFFT AB Background: Accurate multiple sequence alignments of proteins are very important in computational biology today. Despite the numerous efforts made in this field, all alignment strategies have certain shortcomings resulting in alignments that are not always correct. Refinement of existing alignment can prove to be an intelligent choice considering the increasing importance of high quality alignments in large scale high-throughput analysis. Results: We provide an extensive comparison of the performance of the alignment refinement algorithms. The accuracy and efficiency of the refinement programs are compared using the 3D structure-based alignments in the BAliBASE benchmark database as well as manually curated high quality alignments from Conserved Domain Database (CDD). Conclusion: Comparison of performance for refined alignments revealed that despite the absence of dramatic improvements, our refinement method, REFINER, which uses conserved regions as constraints performs better in improving the alignments generated by different alignment algorithms. In most cases REFINER produces a higher-scoring, modestly improved alignment that does not deteriorate the well-conserved regions of the original alignment. C1 Natl Lib Med, Natl Ctr Biotechnol Informat, NIH, Bethesda, MD 20894 USA. RP Chakrabarti, S (reprint author), Natl Lib Med, Natl Ctr Biotechnol Informat, NIH, Bethesda, MD 20894 USA. EM chakraba@ncbi.nlm.nih.gov; lanczyck@ncbi.nlm.nih.gov; panch@ncbi.nlm.nih.gov; przytyck@ncbi.nlm.nih.gov; thiessen@ncbi.nlm.nih.gov; bryant@ncbi.nlm.nih.gov FU Intramural NIH HHS NR 30 TC 6 Z9 6 U1 0 U2 2 PU BIOMED CENTRAL LTD PI LONDON PA MIDDLESEX HOUSE, 34-42 CLEVELAND ST, LONDON W1T 4LB, ENGLAND SN 1471-2105 J9 BMC BIOINFORMATICS JI BMC Bioinformatics PD NOV 14 PY 2006 VL 7 AR 499 DI 10.1186/1471-2105-7-499 PG 10 WC Biochemical Research Methods; Biotechnology & Applied Microbiology; Mathematical & Computational Biology SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Mathematical & Computational Biology GA 107RK UT WOS:000242188500001 PM 17105653 ER PT J AU Borlaug, BA Melenovsky, V Russell, SD Kessler, K Pacak, K Becker, LC Kass, DA AF Borlaug, Barry A. Melenovsky, Vojtech Russell, Stuart D. Kessler, Kristy Pacak, Karel Becker, Lewis C. Kass, David A. TI Impaired chronotropic and vasodilator reserves limit exercise capacity in patients with heart failure and a preserved ejection fraction SO CIRCULATION LA English DT Article DE diastole; exercise; heart failure; heart rate; hemodynamics; nervous system, autonomic ID LEFT-VENTRICULAR HYPERTROPHY; CORONARY-ARTERY DISEASE; DIASTOLIC DYSFUNCTION; BLOOD-POOL; PERFORMANCE; VOLUME; CARDIOMYOPATHY; SENSITIVITY; COMMUNITY; AGE AB Background - Nearly half of patients with heart failure have a preserved ejection fraction (HFpEF). Symptoms of exercise intolerance and dyspnea are most often attributed to diastolic dysfunction; however, impaired systolic and/or arterial vasodilator reserve under stress could also play an important role. Methods and Results - Patients with HFpEF (n = 17) and control subjects without heart failure (n = 19) generally matched for age, gender, hypertension, diabetes mellitus, obesity, and the presence of left ventricular hypertrophy underwent maximal-effort upright cycle ergometry with radionuclide ventriculography to determine rest and exercise cardiovascular function. Resting cardiovascular function was similar between the 2 groups. Both had limited exercise capacity, but this was more profoundly reduced in HFpEF patients (exercise duration 180 +/- 71 versus 455 +/- 184 seconds; peak oxygen consumption 9.0 +/- 3.4 versus 14.4 +/- 3.4 mL (.) kg(-1) (.) min(-1); both P < 0.001). At matched low-level workload, HFpEF subjects displayed approximate to 40% less of an increase in heart rate and cardiac output and less systemic vasodilation (all P < 0.05) despite a similar rise in end-diastolic volume, stroke volume, and contractility. Heart rate recovery after exercise was also significantly delayed in HFpEF patients. Exercise capacity correlated with the change in cardiac output, heart rate, and vascular resistance but not end-diastolic volume or stroke volume. Lung blood volume and plasma norepinephrine levels rose similarly with exercise in both groups. Conclusions - HFpEF patients have reduced chronotropic, vasodilator, and cardiac output reserve during exercise compared with matched subjects with hypertensive cardiac hypertrophy. These limitations cannot be ascribed to diastolic abnormalities per se and may provide novel therapeutic targets for interventions to improve exercise capacity in this disorder. C1 Johns Hopkins Med Inst, Dept Med, Div Cardiol, Baltimore, MD 21205 USA. NICHHD, Reprod Biol & Med Branch, NIH, Bethesda, MD 20892 USA. RP Kass, DA (reprint author), Johns Hopkins Med Inst, Dept Med, Div Cardiol, Ross 835,720 Rutland Ave, Baltimore, MD 21205 USA. EM dkass@jhmi.edu OI Melenovsky, Vojtech/0000-0001-8921-7078 FU NHLBI NIH HHS [T32-HL07227]; NIA NIH HHS [R01-AG18324] NR 45 TC 265 Z9 276 U1 1 U2 10 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0009-7322 J9 CIRCULATION JI Circulation PD NOV 14 PY 2006 VL 114 IS 20 BP 2138 EP 2147 DI 10.1161/CIRCULATIONAHA.106.632745 PG 10 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 124XQ UT WOS:000243406200011 PM 17088459 ER PT J AU Marple, AF Antman, EM Hand, MM AF Marple, Amy F. Antman, Elliott M. Hand, Mary M. TI Modern treatment for heart attacks - Opening blocked arteries quickly SO CIRCULATION LA English DT Editorial Material C1 Brigham & Womens Hosp, Dept Med, Boston, MA 02115 USA. Agcy Healthcare Res & Qual, Off Extramural Res Educ & Prior Populat, Rockville, MD USA. RP Hand, MM (reprint author), NHLBI, Hlth Informat Ctr, POB 30105, Bethesda, MD 20824 USA. NR 4 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0009-7322 J9 CIRCULATION JI Circulation PD NOV 14 PY 2006 VL 114 IS 20 BP E578 EP E580 DI 10.1161/CIRCULATIONAHA.106.648279 PG 3 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 124XQ UT WOS:000243406200018 PM 17101859 ER PT J AU Cisneros, GA Piquemal, JP Darden, TA AF Cisneros, G. Andres Piquemal, Jean-Philip Darden, Thomas A. TI Generalization of the Gaussian electrostatic model: Extension to arbitrary angular momentum, distributed multipoles, and speedup with reciprocal space methods SO JOURNAL OF CHEMICAL PHYSICS LA English DT Article ID INTERMOLECULAR INTERACTION ENERGY; MOLECULAR-DYNAMICS SIMULATIONS; DENSITY-FUNCTIONAL METHODS; BIOMOLECULAR SIMULATION; CHARGE-DISTRIBUTION; OVERLAP-MODEL; BASIS-SETS; POTENTIALS; MECHANICS; EFFICIENT AB The simulation of biological systems by means of current empirical force fields presents shortcomings due to their lack of accuracy, especially in the description of the nonbonded terms. We have previously introduced a force field based on density fitting termed the Gaussian electrostatic model-0 (GEM-0) J.-P. Piquemal [J. Chem. Phys. 124, 104101 (2006)] that improves the description of the nonbonded interactions. GEM-0 relies on density fitting methodology to reproduce each contribution of the constrained space orbital variation (CSOV) energy decomposition scheme, by expanding the electronic density of the molecule in s-type Gaussian functions centered at specific sites. In the present contribution we extend the Coulomb and exchange components of the force field to auxiliary basis sets of arbitrary angular momentum. Since the basis functions with higher angular momentum have directionality, a reference molecular frame (local frame) formalism is employed for the rotation of the fitted expansion coefficients. In all cases the intermolecular interaction energies are calculated by means of Hermite Gaussian functions using the McMurchie-Davidson [J. Comput. Phys. 26, 218 (1978)] recursion to calculate all the required integrals. Furthermore, the use of Hermite Gaussian functions allows a point multipole decomposition determination at each expansion site. Additionally, the issue of computational speed is investigated by reciprocal space based formalisms which include the particle mesh Ewald (PME) and fast Fourier-Poisson (FFP) methods. Frozen-core (Coulomb and exchange-repulsion) intermolecular interaction results for ten stationary points on the water dimer potential-energy surface, as well as a one-dimensional surface scan for the canonical water dimer, formamide, stacked benzene, and benzene water dimers, are presented. All results show reasonable agreement with the corresponding CSOV calculated reference contributions, around 0.1 and 0.15 kcal/mol error for Coulomb and exchange, respectively. Timing results for single Coulomb energy-force calculations for (H2O)(n), n=64, 128, 256, 512, and 1024, in periodic boundary conditions with PME and FFP at two different rms force tolerances are also presented. For the small and intermediate auxiliaries, PME shows faster times than FFP at both accuracies and the advantage of PME widens at higher accuracy, while for the largest auxiliary, the opposite occurs. C1 NIEHS, Struct Biol Lab, Res Triangle Pk, NC 27709 USA. Univ Paris 06, Chim Theor Lab, F-75252 Paris, France. RP Cisneros, GA (reprint author), NIEHS, Struct Biol Lab, Res Triangle Pk, NC 27709 USA. EM cisnero1@niehs.nih.gov RI Cisneros, Gerardo/B-3128-2010; Piquemal, Jean-Philip/B-9901-2009 OI Piquemal, Jean-Philip/0000-0001-6615-9426 FU Intramural NIH HHS [NIH0011757912, Z01 ES090601-11] NR 73 TC 60 Z9 61 U1 0 U2 14 PU AMER INST PHYSICS PI MELVILLE PA CIRCULATION & FULFILLMENT DIV, 2 HUNTINGTON QUADRANGLE, STE 1 N O 1, MELVILLE, NY 11747-4501 USA SN 0021-9606 J9 J CHEM PHYS JI J. Chem. Phys. PD NOV 14 PY 2006 VL 125 IS 18 AR 184101 DI 10.1063/1.2363374 PG 16 WC Chemistry, Physical; Physics, Atomic, Molecular & Chemical SC Chemistry; Physics GA 105AT UT WOS:000242002400004 PM 17115732 ER PT J AU McLellan, JS Yao, SQ Zheng, XY Geisbrecht, BV Ghirlando, R Beachy, PA Leahy, DJ AF McLellan, Jason S. Yao, Shenqin Zheng, Xiaoyan Geisbrecht, Brian V. Ghirlando, Rodolfo Beachy, Philip A. Leahy, Daniel J. TI Structure of a heparin-dependent complex of hedgehog and Ihog SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE signaling; heparan sulfate proteoglycan ID SONIC HEDGEHOG; CRYSTAL-STRUCTURE; CELL-SURFACE; SULFATE PROTEOGLYCANS; LIPID MODIFICATIONS; PROTEIN SIGNALS; III DOMAIN; TOUT-VELU; IN-VIVO; DROSOPHILA AB Hedgehog (Hh) signaling molecules mediate key tissue-patterning events during animal development, and inappropriate activation of Hh signaling in adults has been associated with human cancers. Recently, a conserved family of type I integral membrane proteins required for normal response to the Hh signal was discovered. One member of this family, Ihog (interference hedgehog), functions upstream or at the level of Patched (Ptc), but how Ihog participates in Hh signaling remains unclear. Here, we show that heparin binding induces Ihog dimerization and is required to mediate high-affinity interactions between Ihog and Hh. We also present crystal structures of a Hh-binding fragment of Ihog, both alone and complexed with Hh. Heparin is not well ordered in these structures, but a basic cleft in the first Mill domain of Ihog (IhogFn1) is shown by mutagenesis to mediate heparin binding. These results establish that Hh directly binds Ihog and provide the first demonstration of a specific role for heparin in Hh responsiveness. C1 Johns Hopkins Univ, Sch Med, Dept Biophys & Biophys Chem, Baltimore, MD 21205 USA. Johns Hopkins Univ, Sch Med, Dept Mol Biol & Genet, Baltimore, MD 21205 USA. Johns Hopkins Univ, Sch Med, Howard Hughes Med Inst, Baltimore, MD 21205 USA. NIDDKD, NIH, Mol Biol Lab, Bethesda, MD 20892 USA. RP Leahy, DJ (reprint author), Johns Hopkins Univ, Sch Med, Dept Biophys & Biophys Chem, 725 N Wolfe St, Baltimore, MD 21205 USA. EM dleahy@jhmi.edu RI Ghirlando, Rodolfo/A-8880-2009; McLellan, Jason/A-6874-2010 FU Intramural NIH HHS NR 37 TC 54 Z9 56 U1 0 U2 0 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD NOV 14 PY 2006 VL 103 IS 46 BP 17208 EP 17213 DI 10.1073/pnas.0606738103 PG 6 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA 108OP UT WOS:000242249400028 PM 17077139 ER PT J AU Batra, VK Shock, DD Prasad, R Beard, WA Hou, EW Pedersen, LC Sayer, JM Yagi, H Kumar, S Jerina, DM Wilson, SH AF Batra, Vinod K. Shock, David D. Prasad, Rajendra Beard, William A. Hou, Esther W. Pedersen, Lars C. Sayer, Jane M. Yagi, Haruhiko Kumar, Subodh Jerina, Donald M. Wilson, Samuel H. TI Structure of DNA polymerase beta with a benzo[c]phenanthrene diol epoxide-adducted template exhibits inutagenic features SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE DNA adduct; DNA repair; fidelity; mutagenesis ID NUCLEOTIDE EXCISION-REPAIR; POLYCYCLIC AROMATIC-HYDROCARBONS; BENZOPHENANTHRENE 3,4-DIOL 1,2-EPOXIDES; DAMAGE RECOGNITION; MAMMALIAN-CELLS; IN-VITRO; DEOXYGUANOSINE ADDUCTS; CRYSTAL-STRUCTURE; ESCHERICHIA-COLI; NEWBORN MICE AB We have determined the crystal structure of the human base excision repair enzyme DNA polymerase beta (Pol beta) in complex with a 1-nt gapped DNA substrate containing a template N-2-guanine adduct of the tumorigenic (-)-benzo[c]phenanthrene 4R,3S-diol 2S,1R-epoxide in the gap. Nucleotide insertion opposite this adduct favors incorrect purine nucleotides over the correct dCMP and hence can be mutagenic. The structure reveals that the phenanthrene ring system is stacked with the base pair immediately 3' to the modified guanine, thereby occluding the normal binding site for the correct incoming nucleoside triphosphate. The modified guanine base is displaced downstream and prevents the polymerase from achieving the catalytically competent closed conformation. The incoming nucleotide binding pocket is distorted, and the adducted cleoxyguanosine is in a syn conformation, exposing its Hoogsteen edge, which can hydrogen-bond with dATP or dGTP. In a reconstituted base excision repair system, repair of a deaminated cytosine (i.e., uracil) opposite the adducted guanine was dramatically decreased at the Pol 13 insertion step, but not blocked. The efficiency of gap-filling dCMP insertion opposite the adduct was diminished by > 6 orders of magnitude compared with an unadducted templating guanine. In contrast, significant misinsertion of purine nucleotides (but not dTMP) opposite the adducted guanine was observed. Pol beta also misinserts a purine nucleotide opposite the adduct with ungapped DNA and exhibits limited bypass DNA synthesis. These results indicate that Pol P-dependent base excision repair of uracil opposite, or replication through, this bulky DNA adduct can be mutagenic. C1 NIEHS, Struct Biol Lab, NIH, Dept Hlth & Human Serv, Res Triangle Pk, NC 27709 USA. NIDDKD, NIH, Lab Bioorgan Chem, Dept Hlth & Human Serv, Bethesda, MD 20892 USA. SUNY Coll Buffalo, Environm Toxicol & Chem Lab, Great Lakes Ctr, Buffalo, NY 14222 USA. RP Wilson, SH (reprint author), NIEHS, Struct Biol Lab, NIH, Dept Hlth & Human Serv, Res Triangle Pk, NC 27709 USA. EM wilson5@niehs.nih.gov FU Intramural NIH HHS; NCI NIH HHS [1U19CA105010, U19 CA105010] NR 56 TC 22 Z9 22 U1 0 U2 3 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD NOV 14 PY 2006 VL 103 IS 46 BP 17231 EP 17236 DI 10.1073/pnas.0605069103 PG 6 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA 108OP UT WOS:000242249400032 PM 17079493 ER PT J AU Levine, BL Humeau, LM Boyer, J MacGregor, RR Rebello, T Lu, XB Binder, GK Slepushkin, V Lemiale, F Mascola, JR Bushman, FD Dropulic, B June, CH AF Levine, Bruce L. Humeau, Laurent M. Boyer, Jean MacGregor, Rob-Roy Rebello, Tessio Lu, Xiaobin Binder, Gwendolyn K. Slepushkin, Vladimir Lemiale, Franck Mascola, John R. Bushman, Frederic D. Dropulic, Boro June, Carl H. TI Gene transfer in humans using a conditionally replicating lentiviral vector SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE clinical trials; HIV; immunotherapy; gene therapy ID IMMUNODEFICIENCY-VIRUS TYPE-1; T-CELL PROLIFERATION; HIV-1 REPLICATION; HUMAN GENOME; THERAPY; TRANSCRIPTION; TRANSDUCTION; INTEGRATION; INFECTION; PRODUCTS AB We report findings from a clinical evaluation of lentiviral vectors in a phase I open-label nonrandomized clinical trial for HIM This trial evaluated the safety of a conditionally replicating HIV-1-derived vector expressing an antisense gene against the HIV envelope. Five subjects with chronic HIV infection who had failed to respond to at least two antiviral regimens were enrolled. A single i.v. infusion of gene-modified autologous CD4 T cells was well tolerated in all patients. Viral loads were stable, and one subject exhibited a sustained decrease in viral load. CD4 counts remained steady or increased in four subjects, and sustained gene transfer was observed. Self-limiting mobilization of the vector was observed in four of five patients. There is no evidence for insertional mutagenesis after 21-36 months of observation. immune function improved in four subjects. Lentiviral vectors appear promising for gene transfer to humans. C1 Univ Penn, Ctr Canc, Abramson Family Canc Res Inst, Dept Pathol & Lab Med, Philadelphia, PA 19104 USA. Univ Penn, Ctr Canc, Abramson Family Canc Res Inst, Dept Med, Philadelphia, PA 19104 USA. Univ Penn, Ctr Canc, Abramson Family Canc Res Inst, Dept Microbiol, Philadelphia, PA 19104 USA. VIRxSYS Corp, Gaithersburg, MD 20877 USA. NIH, Vaccine Res Ctr, Bethesda, MD 20892 USA. RP June, CH (reprint author), Univ Penn, Ctr Canc, Abramson Family Canc Res Inst, Dept Pathol & Lab Med, Philadelphia, PA 19104 USA. EM cjune@mail.med.upenn.edu RI Levine, Bruce/D-1688-2009; OI Bushman, Frederic/0000-0003-4740-4056 FU NIAID NIH HHS [2R44AI051908, R44 AI051908, U19 AI066290, U19 AI066290-010001, U19-AI066290] NR 23 TC 297 Z9 325 U1 1 U2 20 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD NOV 14 PY 2006 VL 103 IS 46 BP 17372 EP 17377 DI 10.1073/pnas.0608138103 PG 6 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA 108OP UT WOS:000242249400056 PM 17090675 ER PT J AU Wilke, M Logothetis, NK Leopoldt, DA AF Wilke, Melanie Logothetis, Nikos K. Leopoldt, David A. TI Local field potential reflects perceptual suppression in monkey visual cortex SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE attention; perception; rivalry; V1; consciousness ID LATERAL GENICULATE-NUCLEUS; BINOCULAR-RIVALRY; INTEROCULAR RIVALRY; MASKING; METACONTRAST; RESPONSES; PRIMATE; SIGNALS; FMRI; TIME AB Neurophysiological and functional imaging experiments remain in apparent disagreement on the role played by the earliest stages of the visual cortex in supporting a visual percept. Here, we report electrophysiological findings that shed light on this issue. We monitored neural activity in the visual cortex of monkeys as they reported their perception of a high-contrast visual stimulus that was induced to vanish completely from perception on a subset of trials. We found that the spiking of neurons in cortical areas V1 and V2 was uncorrelated with the perceptual visibility of the target, whereas that in area V4 showed significant perception-related changes. In contrast, power changes in the lower frequency bands (particularly 9-30 Hz) of the local field potential (LFP), collected on the same trials, showed consistent and sustained perceptual modulation in all three areas. In addition, for the gamma frequency range (30-50 Hz), the responses during perceptual suppression of the target were correlated significantly with the responses to its physical removal in all areas, although the modulation magnitude was considerably higher in area V4 than in V1 and V2. These results, taken together, suggest that low-frequency LFP power in early cortical processing is more closely related to the representation of stimulus visibility than is spiking or higher frequency LFP activity. C1 NIMH, Unit Cognit Neurophysiol & Imaging, Neuropsychol Lab, NIH, Bethesda, MD 20892 USA. Max Planck Inst Biol Cybernet, D-72076 Tubingen, Germany. RP Leopoldt, DA (reprint author), NIMH, Unit Cognit Neurophysiol & Imaging, Neuropsychol Lab, NIH, Bldg 49,Room B2J 45,MSC 4400,49 Convent Dr, Bethesda, MD 20892 USA. EM leopoldd@mail.nih.gov OI Leopold, David/0000-0002-1345-6360 NR 35 TC 116 Z9 117 U1 3 U2 10 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD NOV 14 PY 2006 VL 103 IS 46 BP 17507 EP 17512 DI 10.1073/pnas.0604673103 PG 6 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA 108OP UT WOS:000242249400079 PM 17088545 ER PT J AU Barzilay, JI Davis, BR Cutler, JA Pressel, SL Whelton, PK Basile, J Margolis, KL Ong, ST Sadler, LS Summerson, J AF Barzilay, Joshua I. Davis, Barry R. Cutler, Jeffrey A. Pressel, Sara L. Whelton, Paul K. Basile, Jan Margolis, Karen L. Ong, Stephen T. Sadler, Laurie S. Summerson, John CA ALLHAT Collaborative Res Grp TI Fasting glucose levels and incident diabetes mellitus in older nondiabetic adults randomized to receive 3 different classes of antihypertensive treatment - A report from the Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial (ALLHAT) SO ARCHIVES OF INTERNAL MEDICINE LA English DT Article ID ISOLATED SYSTOLIC HYPERTENSION; CARDIOVASCULAR EVENTS; THIAZIDE DIURETICS; THERAPY; RISK; OUTCOMES; INTOLERANCE; POTASSIUM; REDUCTION; INHIBITOR AB Background: Elevated blood glucose levels are reported with thiazide-type diuretic treatment of hypertension. The significance of this finding is uncertain. Our objectives were to compare the effect of first-step antihypertensive drug therapy with thiazide-type diuretic, calcium-channel blocker, or angiotensin-converting enzyme inhibitor on fasting glucose (FG) levels and to determine cardiovascular and renal disease risks associated with elevated FG levels and incident diabetes mellitus (DM) in 3 treatment groups. Methods: We performed post hoc subgroup analyses from the Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial (ALLHAT) among nondiabetic participants who were randomized to receive treatment with chlorthalidone (n= 8419), amlodipine (n= 4958), or lisinopril ( n= 5034) and observed for a mean of 4.9 years. Results: Mean FG levels increased during follow-up in all treatment groups. At year 2, those randomized to the chlorthalidone group had the greatest increase ( + 8.5 mg/dL [0.47 mmol/L] vs + 5.5 mg/dL [0.31 mmol/L] for amlodipine and + 3.5 mg/dL [0.19 mmol/L] for lisinopril). The odds ratios for developing DM with lisinopril (0.55 [95% confidence interval, 0.43-0.70]) or amlodipine (0.73 [ 95% confidence interval, 0.58-0.91]) vs chlorthalidone at 2 years were significantly lower than 1.0 (P <. 01). There was no significant association of FG level change at 2 years with subsequent coronary heart disease, stroke, cardiovascular disease, total mortality, or endstage renal disease. There was no significant association of incident DM at 2 years with clinical outcomes, except for coronary heart disease ( risk ratio, 1.64; P=. 006), but the risk ratio was lower and nonsignificant in the chlorthalidone group ( risk ratio, 1.46; P=. 14). Conclusions: Fasting glucose levels increase in older adults with hypertension regardless of treatment type. For those taking chlorthalidone vs other medications, the risk of developing FG levels higher than 125 mg/dL (6.9 mmol/L) is modestly greater, but there is no conclusive or consistent evidence that this diuretic-associated increase in DM risk increases the risk of clinical events. C1 Univ Texas, Sch Publ Hlth, Coordinating Ctr Clin Trials, Houston, TX 77030 USA. Emory Univ, Sch Med, Kaiser Permanente, Atlanta, GA 30322 USA. Emory Univ, Sch Med, Div Endocrinol, Atlanta, GA 30322 USA. NHLBI, Div Epidemiol & Clin Applicat, Bethesda, MD 20892 USA. Tulane Univ, Hlth Sci Ctr, New Orleans, LA 70118 USA. Med Univ S Carolina, Ralph H Johnson Vet Affairs Med Ctr, Charleston, SC 29425 USA. Hennepin Cty Med Ctr, Div Clin Epidemiol, Minneapolis, MN 55415 USA. Ong Med Ctr, Oxon Hill, MD USA. St Vincent Char Hosp & Hlth Ctr, Lipid Res Ctr, Cleveland, OH USA. Wake Forest Univ, Sch Med, Dept Publ Hlth Sci, Winston Salem, NC 27109 USA. RP Davis, BR (reprint author), Univ Texas, Sch Publ Hlth, Coordinating Ctr Clin Trials, 1200 Herman Pressler St,Suite E801, Houston, TX 77030 USA. EM barry.r.davis@uth.tmc.edu FU NHLBI NIH HHS [N01-HC-35130] NR 30 TC 147 Z9 153 U1 1 U2 3 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610-0946 USA SN 0003-9926 J9 ARCH INTERN MED JI Arch. Intern. Med. PD NOV 13 PY 2006 VL 166 IS 20 BP 2191 EP 2201 DI 10.1001/archinte.166.20.2191 PG 11 WC Medicine, General & Internal SC General & Internal Medicine GA 104VF UT WOS:000241987500005 PM 17101936 ER PT J AU Muller, M Klein, I Kopacsi, S Remaley, AT Rajnavolgyi, E Sarkadi, B Varadi, A AF Muller, Marianna Klein, Izabella Kopacsi, Szilard Remaley, Alan T. Rajnavolgyi, Eva Sarkadi, Balazs Varadi, Andras TI Co-expression of human ABCG5 and ABCG8 in insect cells generates an androstan stimulated membrane ATPase activity SO FEBS LETTERS LA English DT Article DE sitosterolemia; steroid hormones; ATP binding cassette transporters ID CANCER RESISTANCE PROTEIN; DIETARY-CHOLESTEROL; IN-VITRO; EXPRESSION; TRANSPORT; HORMONES; GENE AB Mutations in the ATP-binding cassette (ABC) proteins ABCG5 or ABCG8 cause sitosterolemia, a condition with increased accumulation of plant sterols. Upon high level expression of the ABCG5 and ABCG8 proteins in baculovirus-Sf9 cell expression system we found a distinct, vanadate sensitive ATPase activity in isolated membrane preparations only when the two proteins were co-expressed. This ATPase activity was significantly stimulated by the addition of certain androgen hormones and analogs, and was effectively inhibited by progesterone. Our results provide a new aspect of biochemical and functional characterization of the ABCG5/ABCG8 proteins and their possible involvement in steroid hormone transport or regulation. (c) 2006 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved. C1 Hungarian Acad Sci, Inst Enzymol, H-1113 Budapest, Hungary. Hungarian Acad Sci, Membrane Res Grp, Natl Med Ctr, Inst Haematol & Immunol, H-1113 Budapest, Hungary. NHLBI, NIH, Bethesda, MD 20892 USA. Univ Debrecen, Inst Immunol, Med & Hlth Sci Ctr, Debrecen, Hungary. RP Varadi, A (reprint author), Hungarian Acad Sci, Inst Enzymol, H-1113 Budapest, Hungary. EM varadi@enzim.hu RI Varadi, Andras/A-2055-2012; Sarkadi, Balazs/I-5024-2013; Rajnavolgyi, Eva/D-4384-2013 NR 20 TC 6 Z9 6 U1 0 U2 2 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0014-5793 J9 FEBS LETT JI FEBS Lett. PD NOV 13 PY 2006 VL 580 IS 26 BP 6139 EP 6144 DI 10.1016/j.febslet.2006.10.012 PG 6 WC Biochemistry & Molecular Biology; Biophysics; Cell Biology SC Biochemistry & Molecular Biology; Biophysics; Cell Biology GA 108II UT WOS:000242233100017 PM 17055487 ER PT J AU Malley, JD AF Malley, James D. TI The collapse of Bell determinism SO PHYSICS LETTERS A LA English DT Article AB The simplified Bell-Kochen-Specker hidden-variable conditions (BKS) require an assignment of 0 or I to every vector on a state space H such that the assignment respects orthogonality. We show that the pair of conditions {BKS, dim H >= 3} are not merely inconsistent, but in fact imply dim H = 1. (c) 2006 Elsevier B.V. All rights reserved. C1 NIH, Ctr Informat Technol, Bethesda, MD 20892 USA. RP Malley, JD (reprint author), NIH, Ctr Informat Technol, Bldg 10, Bethesda, MD 20892 USA. EM jmalley@mail.nih.gov OI Malley, James/0000-0002-9895-7454 NR 2 TC 5 Z9 5 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0375-9601 J9 PHYS LETT A JI Phys. Lett. A PD NOV 13 PY 2006 VL 359 IS 2 BP 122 EP 125 DI 10.1016/j.physleta.2006.06.022 PG 4 WC Physics, Multidisciplinary SC Physics GA 106ZQ UT WOS:000242140900009 ER PT J AU Tahiri-Alaoui, A Sim, VL Caughey, B James, W AF Tahiri-Alaoui, Abdessamad Sim, Valerie L. Caughey, Byron James, William TI Molecular heterosis of prion protein beta-oligomers - A potential mechanism of human resistance to disease SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID CREUTZFELDT-JAKOB-DISEASE; SOLUBLE OLIGOMERS; IN-VITRO; RECOMBINANT; POLYMORPHISM; CONVERSION; GENE; PRP; STABILITY; SUSCEPTIBILITY AB The gene encoding prion protein is polymorphic in human populations, with over 40% of native Europeans, for example, being heterozygous for the Met-129 and Val-129 alleles. The polymorphism affects both the incidence and the clinical presentation of a range of prion diseases, with heterozygotes generally showing the highest levels of resistance. It has been suggested that an earlier epidemic of prion diseases exerted balancing selection on the two alleles, and we have previously demonstrated that the two encoded proteins have potentially compensating tendencies to form amyloid and soluble beta-oligomers, respectively, in vitro. More strikingly, here we demonstrate that mixed oligomers, composed of both allelic forms, show an extreme sluggishness in converting to amyloid in comparison with oligomers homogenous for either allele. It may be that this example of molecular heterosis in vitro provides the basis for maintenance of the polymorphism in the population and that beta-oligomers represent a form of PrP sequestered from pathogenic amyloid formation in vivo. C1 Univ Oxford, Sir William Dunn Sch Pathol, Oxford OX1 3RE, England. NIAID, Rocky Mt Lab, Persistent Viral Dis Lab, NIH, Hamilton, MT 59840 USA. RP James, W (reprint author), Univ Oxford, Sir William Dunn Sch Pathol, S Pk Rd, Oxford OX1 3RE, England. EM abdou.tahiri-alaoui@bbsrc.ac.uk; William.james@path.ox.ac.uk RI Sim, Valerie/C-4137-2013 OI Sim, Valerie/0000-0002-0088-8666 FU Intramural NIH HHS NR 41 TC 15 Z9 15 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 NOV 10 PY 2006 VL 281 IS 45 BP 34171 EP 34178 DI 10.1074/jbc.M606606200 PG 8 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA 101UZ UT WOS:000241767600037 PM 16980300 ER PT J AU Sztalryd, C Bell, M Lu, XY Mertz, P Hickenbottom, S Chang, BHJ Chan, L Kimmel, AR Londos, C AF Sztalryd, Carole Bell, Ming Lu, Xinyue Mertz, Pamela Hickenbottom, Sabrina Chang, Benny H. -J. Chan, Lawrence Kimmel, Alan R. Londos, Constantine TI Functional compensation for adipose differentiation-related protein (ADFP) by Tip47 in an ADFP null embryonic cell line SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID LIPID GLOBULE-MEMBRANE; ENDOPLASMIC-RETICULUM; METABOLIC SYNDROME; DROPLETS; PERILIPIN; ADIPOCYTES; MECHANISMS; RESISTANCE; CONVERSION; LIPOLYSIS AB Ectopic accumulation of lipid droplets in non-adipose tissues correlates with the degree of insulin resistance in these tissues. Emerging evidence indicates that lipid droplets are specialized organelles that participate in lipid metabolism and intracellular trafficking. These properties are thought to derive from the lipid droplet-associated PAT protein family (perilipin, ADFP, and Tip47). The functions of the ubiquitously distributed adipose differentiation-related protein (ADFP) and Tip47 remain unknown. To evaluate the roles of ADFP and Tip47 in lipid biogenesis and metabolism, ADFP null and wild type (wt) clonal cell lines were established from ADFP null and wt mice, respectively. In ADFP null cells, Tip47 was identified as the sole lipid droplet-associated protein from the PAT family by mass spectroscopy, which was further confirmed by immunoblotting and immunocytochemistry. Following incubation with oleic acid, ADFP null cells were able to form lipid droplets to the same extent as wt cells. No statistical differences between the two cell types were observed in NEFA uptake or lipolysis. Small interference RNAs (siRNAs) against Tip47 were found to down-regulate protein levels for Tip47 by 85%. ADFP null cells treated with Tip47 siRNA retained the ability to form lipid droplets but to a lesser extent and shunted the utilization of exogenously added NEFA from triglycerides to phospholipids. These data support the hypothesis that Tip47 plays an important role in lipid metabolism. Tip47 and ADFP in peripheral tissues may play a critical role in regulating the formation and turnover, and hence metabolic consequences, of ectopic fat. C1 Univ Maryland, Sch Med, Geriatr Res Educ & Clin Ctr, Baltimore Vet Affairs Hlth Care Ctr,Dept Med, Baltimore, MD 21201 USA. NIDDK, Cellular & Dev Biol Lab, NIH, Bethesda, MD 20892 USA. Baylor Coll Med, Dept Mol & Cellular Biol, Houston, TX 77030 USA. Baylor Coll Med, Dept Med, Houston, TX 77030 USA. RP Sztalryd, C (reprint author), Vet Affairs Med Ctr, GRECC Geriatr, 10 N Greene St, Baltimore, MD 21201 USA. EM csztalry@grecc.umaryland.edu FU Intramural NIH HHS; NHLBI NIH HHS [HL51586]; NIDDK NIH HHS [DK56338] NR 39 TC 79 Z9 84 U1 1 U2 6 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD NOV 10 PY 2006 VL 281 IS 45 BP 34341 EP 34348 DI 10.1074/jbc.M602497200 PG 8 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA 101UZ UT WOS:000241767600054 PM 16968708 ER PT J AU Bird, JG Sharma, S Roshwalb, SC Hoskins, JR Wickner, S AF Bird, Jeremy G. Sharma, Suveena Roshwalb, Sara C. Hoskins, Joel R. Wickner, Sue TI Functional analysis of CbpA, a DnaJ homolog and nucleoid-associated DNA-binding protein SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID ESCHERICHIA-COLI DNAJ; HEAT-SHOCK PROTEINS; J-DOMAIN; THERMUS-THERMOPHILUS; MOLECULAR CHAPERONES; CRYSTAL-STRUCTURE; HSP40; HSP70; REPLICATION; REPA AB DnaK/Hsp70 proteins are universally conserved ATP-dependent molecular chaperones that help proteins adopt and maintain their native conformations. DnaJ/Hsp40 and GrpE are co-chaperones that assist DnaK. CbpA is an Escherichia coli DnaJ homolog. It acts as a multicopy suppressor for dnaJ mutations and functions in vitro in combination with DnaK and GrpE in protein remodeling reactions. CbpA binds nonspecifically to DNA with preference for curved DNA and is a nucleoid-associated protein. The DNA binding and co-chaperone activities of CbpA are modulated by CbpM, a small protein that binds specifically to CbpA. To identify the regions of CbpA involved in the interaction of CbpA with CbpM and those involved in DNA binding, we constructed and characterized deletion and substitution mutants of CbpA. We discovered that CbpA interacted with CbpM through its N-terminal J-domain. We found that the region C-terminal to the J-domain was required for DNA binding. Moreover, we found that the CbpM interaction, DNA binding, and co-chaperone activities were separable; some mutants were proficient in some functions and defective in others. C1 NCI, Mol Biol Lab, NIH, Bethesda, MD 20892 USA. RP Wickner, S (reprint author), NCI, Mol Biol Lab, NIH, Bldg 37,Rm 5144,37 Convent Dr MSC37-4264, Bethesda, MD 20892 USA. EM wickners@mail.nih.gov FU Intramural NIH HHS NR 32 TC 17 Z9 17 U1 0 U2 4 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD NOV 10 PY 2006 VL 281 IS 45 BP 34349 EP 34356 DI 10.1074/jbc.M603365200 PG 8 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA 101UZ UT WOS:000241767600055 PM 16973605 ER PT J AU Unoki, M Shen, JC Zheng, ZM Harris, CC AF Unoki, Motoko Shen, Jiang Cheng Zheng, Zhi-Ming Harris, Curtis C. TI Novel splice variants of ING4 and their possible roles in the regulation of cell growth and motility SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID GTPASE-ACTIVATING PROTEIN; TUMOR-SUPPRESSOR GENE; MESSENGER-RNA; PHD FINGER; BINDING; EXPRESSION; CANCER; P53; DIVERSITY; CYTOPLASM AB The ING4 gene is a candidate tumor suppressor gene that functions in cell proliferation, contact inhibition, and angiogenesis. We identified three novel splice variants of ING4 with differing activities in controlling cell proliferation, cell spreading, and cell migration. ING4_v1 (the longest splice variant), originally identified as ING4, encodes an intact nuclear localization signal (NLS), whereas the other three splice variants (ING4_v2, ING4_v3, and ING4_v4) lack the full NLS, resulting in increased cytoplasmic localization of these proteins. We found that one of the three ING4 variants, ING4_v2, is expressed at the same level as the original ING4 (ING4_v1), suggesting that ING4 variants may have significant biological functions. Growth suppressive effects of the variants that have a partial NLS (ING4_v2 and ING4_v4) were attenuated by a weaker effect of the variants on p21(WAF1) promoter activation. ING4_v4 lost cell spreading and migration suppressive effects; on the other hand, ING4_v2 retained a cell migration suppressive effect but lost a cell spreading suppressive effect. Therefore, ING4_v2, which localized primarily into cytoplasm, might have an important role in the regulation of cell migration. We also found that ING4_v4 played dominant-negative roles in the induction of p21(WAF1) promoter activation and in the suppression of cell motility by ING4_v1. In addition, ING4 variants had different binding affinities to two cytoplasmic proteins, protein-tyrosine phosphatase, receptor type, f polypeptide (PTPRF), interacting protein (liprin), alpha 1, and G3BP2a. Understanding the functions of the four splice variants may aid in defining their roles in human carcinogenesis. C1 NCI, Human Carcinogenesis Lab, CCR, NIH, Bethesda, MD 20892 USA. NCI, HIV & AIDS Malignancy Branch, CCR, NIH, Bethesda, MD 20892 USA. RP Harris, CC (reprint author), NCI, Human Carcinogenesis Lab, CCR, NIH, 37 Convent Dr,Bldg 37,Rm 3068, Bethesda, MD 20892 USA. EM Curtis_Harris@nih.gov FU Intramural NIH HHS NR 34 TC 66 Z9 76 U1 0 U2 0 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD NOV 10 PY 2006 VL 281 IS 45 BP 34677 EP 34686 DI 10.1074/jbc.M606296200 PG 10 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA 101UZ UT WOS:000241767600086 PM 16973615 ER PT J AU Shibusawa, Y Yamakawa, Y Noji, R Yanagida, A Shindo, H Ito, Y AF Shibusawa, Yoichi Yamakawa, Yutaka Noji, Ryoko Yanagida, Akio Shindo, Heisaburo Ito, Yoichiro TI Three-phase solvent systems for comprehensive separation of a wide variety of compounds by high-speed counter-current chromatography SO JOURNAL OF CHROMATOGRAPHY A LA English DT Article DE three-phase solvent systems; high-speed counter-current chromatography; comprehensive separation; hydrophobicity ID LIQUID PARTITION CHROMATOGRAPHY; COIL PLANET CENTRIFUGE; SOLID SUPPORT AB Three-phase solvent systems were efficiently utilized for high-speed counter-current chromatography (HSCCC) to separate multiple components with a wide range of hydrophobicity. The compositions of three-phase systems were optimized according to their physical parameters such as volume ratio, viscosity and specific gravity of upper (UP), middle (MP) and lower (LP) phases. The three-phase systems composed of n-hexane-methyl acetate-acetonitrile-water (4:4:3:4, v/v/v/v) was selected for HSCCC separation of a mixture of 15 standard compounds with a wide range in hydrophobicity from beta-carotene to tryptophan. The separation was initiated by filling the column with a mixture of MP and LP both as a stationary phase followed by elution with UP to separate the hydrophobic compounds. Then the mobile phase was switched to MP to elute the moderately hydrophobic compounds, and finally the polar compounds still retained in the column were fractionated by eluting the column with LP. The system successfully resolved all 15 compounds in one-step operation in 70 min. (c) 2006 Elsevier B.V. All rights reserved. C1 Tokyo Univ Pharm & Life Sci, Div Struct Biol & Analyt Sci, Hachioji, Tokyo 1920392, Japan. NHLBI, Lab Bopphys Chem, NIH, Bethesda, MD 20892 USA. RP Shibusawa, Y (reprint author), Tokyo Univ Pharm & Life Sci, Div Struct Biol & Analyt Sci, 1432-1 Horinouchi, Hachioji, Tokyo 1920392, Japan. EM sibusawa@ps.toyaku.ac.jp NR 12 TC 20 Z9 21 U1 3 U2 17 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0021-9673 J9 J CHROMATOGR A JI J. Chromatogr. A PD NOV 10 PY 2006 VL 1133 IS 1-2 BP 119 EP 125 DI 10.1016/j.chroma.2006.08.004 PG 7 WC Biochemical Research Methods; Chemistry, Analytical SC Biochemistry & Molecular Biology; Chemistry GA 101WV UT WOS:000241772800015 PM 16920128 ER PT J AU Rowland, JH Hewitt, M Ganz, PA AF Rowland, Julia H. Hewitt, Maria Ganz, Patricia A. TI Cancer survivorship: A new challenge in delivering quality cancer care SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Editorial Material ID PEDIATRIC CANCER C1 NCI, Div Canc Control & Populat Sci, Bethesda, MD 20892 USA. NCI, Off Canc Survivorship, Bethesda, MD 20892 USA. Univ Calif Los Angeles, Jonsson Comprehens Canc Ctr, Los Angeles, CA 90024 USA. RP Rowland, JH (reprint author), NCI, Div Canc Control & Populat Sci, Bethesda, MD 20892 USA. NR 32 TC 103 Z9 104 U1 0 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 NOV 10 PY 2006 VL 24 IS 32 BP 5101 EP 5104 DI 10.1200/JCO.2006.09.2700 PG 4 WC Oncology SC Oncology GA 109AM UT WOS:000242280300001 PM 17093270 ER PT J AU Gulley, JL Parnes, HL Wright, J Dahut, WL AF Gulley, James L. Parnes, Howard L. Wright, John Dahut, William L. TI Early treatment gets the benefit SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Letter ID PROSTATE-CANCER C1 NCI, Tumor Immunol & Biol Lab, Bethesda, MD 20892 USA. Natl Canc Inst, Med Oncol Branch, Ctr Canc Res, Bethesda, MD USA. Natl Canc Inst, Canc Therapy Evaluat Program, Bethesda, MD USA. RP Gulley, JL (reprint author), NCI, Tumor Immunol & Biol Lab, Bldg 10, Bethesda, MD 20892 USA. RI Gulley, James/K-4139-2016 OI Gulley, James/0000-0002-6569-2912 NR 5 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 NOV 10 PY 2006 VL 24 IS 32 BP 5172 EP 5173 DI 10.1200/JCO.2006.07.9053 PG 2 WC Oncology SC Oncology GA 109AM UT WOS:000242280300015 PM 17093283 ER PT J AU Joffe, S Miller, FG AF Joffe, Steven Miller, Franklin G. TI Dynamic and modern: Bringing the ethics of phase I trials up to date - Reply SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Letter C1 Dana Farber Canc Inst, Dept Pediat Oncol, 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 NR 1 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 NOV 10 PY 2006 VL 24 IS 32 BP 5179 EP 5180 DI 10.1200/JCO.2006.09.1827 PG 2 WC Oncology SC Oncology GA 109AM UT WOS:000242280300026 ER PT J AU Cruceanu, M Gorelick, RJ Musier-Forsyth, K Rouzina, I Williams, MC AF Cruceanu, Margareta Gorelick, Robert J. Musier-Forsyth, Karin Rouzina, Ioulia Williams, Mark C. TI Rapid kinetics of protein-nucleic acid interaction is a major component of HIV-1 nucleocapsid protein's nucleic acid chaperone function SO JOURNAL OF MOLECULAR BIOLOGY LA English DT Article DE nucleocapsid protein; nucleic acid chaperone; single molecule; DNA stretching; DNA melting; DNA cooperativity ID IMMUNODEFICIENCY-VIRUS TYPE-1; T4 GENE-32 PROTEIN; MOLECULE FORCE SPECTROSCOPY; ZINC-FINGER STRUCTURES; MINUS-STRAND TRANSFER; ASSEMBLY IN-VITRO; REVERSE TRANSCRIPTION; SINGLE DNA; OVERSTRETCHING TRANSITION; COMPLEMENTARY SEQUENCE AB The nucleic acid chaperone activity of the human immunodeficiency virus type-1 (HIV-1) nucleocapsid protein (NC) plays an important role in the retroviral life cycle, in part, by facilitating numerous nucleic acid rearrangements throughout the reverse transcription process. Recent studies have identified duplex destabilization and nucleic acid aggregation as the two major components of NC's chaperone activity. In order to better understand the contribution of the functional domains of NC to these two activities, we used optical tweezers to stretch single lambda DNA molecules through the helix-coil transition in the presence of wild-type or mutant HIV-1 NC. Protein-induced duplex destabilization was measured directly as an average decrease of the force-induced melting free energy, while NC's ability to facilitate strand annealing was determined by the amount of hysteresis in the DNA stretch-relax cycle. By studying zinc-free variants of full-length and truncated NC, the relative contributions of NC's zinc fingers and N-terminal basic domain to the two major components of chaperone activity were elucidated. In addition, examination of NC variants containing mutations affecting one or both zinc finger motifs showed that effective strand annealing activity is correlated with NC's ability to rapidly bind and dissociate from nucleic acids. NC variants with slow on/off rates are inefficient in strand annealing, even though they may still be capable of high affinity nucleic acid binding, duplex destabilization, and/or nucleic acid aggregation. Taken together, these observations establish the rapid kinetics of protein-nucleic acid interaction as another major component of NC's chaperone function. (c) 2006 Elsevier Ltd. All rights reserved. C1 Univ Minnesota, Dept Chem, Minneapolis, MN 55455 USA. Univ Minnesota, Inst Mol Virol, Minneapolis, MN 55455 USA. Northeastern Univ, Dept Phys, Dana Res Ctr 111, Boston, MA 02115 USA. NCI Frederick, AIDS Vaccine Program, SAIC Frederick Inc, Frederick, MD 21702 USA. Northeastern Univ, Ctr Interdisciplinary Res Complex Syst, Dana Res Ctr 111, Boston, MA 02115 USA. RP Rouzina, I (reprint author), Univ Minnesota, Dept Chem, 207 Pleasant St,SE, Minneapolis, MN 55455 USA. EM rouzi002@umn.edu; mark@neu.edu OI Williams, Mark C./0000-0003-3219-376X FU NCI NIH HHS [N01-CO-12400]; NIGMS NIH HHS [GM065056, GM072462] NR 65 TC 63 Z9 64 U1 0 U2 6 PU ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD PI LONDON PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND SN 0022-2836 J9 J MOL BIOL JI J. Mol. Biol. PD NOV 10 PY 2006 VL 363 IS 5 BP 867 EP 877 DI 10.1016/j.jmb.2006.08.070 PG 11 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA 101RC UT WOS:000241757100001 PM 16997322 ER PT J AU Baxter, K Lee, J Minakhin, L Severinov, K Hinton, DM AF Baxter, Kimberly Lee, Jennifer Minakhin, Leonid Severinov, Konstantin Hinton, Deborah M. TI Mutational analysis of sigma(70) region 4 needed for appropriation by the bacteriophage T4 transcription factors AsiA and MotA SO JOURNAL OF MOLECULAR BIOLOGY LA English DT Article DE transcription; sigma(70); AsiA; MotA; polymerase ID COLI RNA-POLYMERASE; PROTEIN-PROTEIN INTERACTIONS; ESCHERICHIA-COLI; ACTIVATOR MOTA; PROMOTER RECOGNITION; T4 ASIA; SIGMA-70 SUBUNIT; COACTIVATOR ASIA; STRUCTURAL BASIS; IN-VIVO AB Transcriptional activation of bacteriophage T4 middle promoters requires sigma(70)-containing Escherichia coli RNA polymerase, the T4 activator MotA, and the T4 co-activator AsiA. T4 middle promoters contain the sigma(70)-10 DNA element. However, these promoters lack the sigma(70)-35 element, having instead a MotA box centered at -30, which is bound by MotA. Previous work has indicated that AsLk and MotA interact with region 4 of sigma(70), the C-terminal portion that normally contacts -35 DNA and the beta-flap structure in core. AsiA binding prevents the sigma(70)/beta-flap and sigma(70)/-35 DNA interactions, inhibiting transcription from promoters that require a -35 element. To test the importance of residues within a region 4 for MotA and AsiA function, we investigated how sigma(70) region 4 mutants interact with AsiA, MotA, and the beta-flap and function in transcription assays in vitro. We find that alanine substitutions at residues 584-588 (region 4.2) do not impair the interaction of region 4 with the beta-flap or MotA, but they eliminate the interaction with AsiA and prevent AsiA inhibition and MotA/AsiA activation. In contrast, alanine substitutions at 551-552, 554-555 (region 4.1) eliminate the region 4/beta-flap interaction, significantly impair the AsiA/sigma(70) interaction, and eliminate AsiA inhibition. However, the 4.1 mutant sigma(70) is Still fully competent for activation if both MotA and AsiA are present. A previous NMR structure shows AsiA binding to sigma(70) region 4, dramatically distorting regions 4.1 and 4.2 and indirectly changing the conformation of the MotA interaction site at the sigma(70) C terminus. Our analyses provide biochemical relevance for the a 70 residues identified in the structure, indicate that the interaction of AsiA with sigma(70) region 4.2 is crucial for activation, and support the idea that AsiA binding facilitates an interaction between MotA and the far C terminus of sigma(70) .Published by Elsevier Ltd. C1 NIDDK, Gene Express & Regulat Sect, Mol & Cellular Biol Lab, NIH, Bethesda, MD 20892 USA. Rutgers State Univ, Waksman Inst Microbiol, Dept Genet, Piscataway, NJ 08855 USA. RP Hinton, DM (reprint author), NIDDK, Gene Express & Regulat Sect, Mol & Cellular Biol Lab, NIH, Bethesda, MD 20892 USA. EM dhinton@helix.nih.gov RI Severinov, Konstantin/C-8545-2016 FU Intramural NIH HHS; NIGMS NIH HHS [R01 GM059295, R01 GM59295] NR 66 TC 20 Z9 21 U1 1 U2 3 PU ACADEMIC PRESS LTD ELSEVIER SCIENCE LTD PI LONDON PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND SN 0022-2836 J9 J MOL BIOL JI J. Mol. Biol. PD NOV 10 PY 2006 VL 363 IS 5 BP 931 EP 944 DI 10.1016/j.jmb.2006.08.074 PG 14 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA 101RC UT WOS:000241757100006 PM 16996538 ER PT J AU Lewis, AM Varghese, S Xu, H Alexander, HR AF Lewis, Anne M. Varghese, Sheelu Xu, Hui Alexander, H. Richard TI Interleukin-1 and cancer progression: the emerging role of interleukin-1 receptor antagonist as a novel therapeutic agent in cancer treatment SO JOURNAL OF TRANSLATIONAL MEDICINE LA English DT Review ID ENDOTHELIAL GROWTH-FACTOR; TUMOR-HOST INTERACTIONS; IL-1 RECEPTOR; INFLAMMATORY CYTOKINES; HUMAN KERATINOCYTES; ACCESSORY PROTEIN; CONVERTING-ENZYME; MULTIPLE-MYELOMA; GENE-EXPRESSION; MICE DEFICIENT AB The tumor microenvironment consists of tumor, immune, stromal, and inflammatory cells which produce cytokines, growth factors, and adhesion molecules that promote tumor progression and metastasis. Of particular interest in this setting is interleukin-1 (IL-1), a pleiotropic cytokine with numerous roles in both physiological and pathological states. It is known to be up regulated in many tumor types and has been implicated as a factor in tumor progression via the expression of metastatic and angiogenic genes and growth factors. A number of studies have reported that high IL-1 concentrations within the tumor microenvironment are associated with a more virulent tumor phenotype. Solid tumors in which IL-1 has been shown to be up regulated include breast, colon, lung, head and neck cancers, and melanomas, and patients with IL-1 producing tumors have generally bad prognoses. The exact mechanisms by which IL-1 promotes tumor growth remain unclear, though the protein is believed to act via induction of pro-metastatic genes such as matrix metalloproteinases and through the stimulation of adjacent cells to produce angiogenic proteins and growth factors such as VEGF, IL-8, IL-6, TNF alpha, and TGF beta. The IL-1 receptor antagonist (IL-1ra) is a naturally occurring inhibitor to IL-1 and acts by binding to the IL-1 receptor without activating it. The protein has been shown to decrease tumor growth, angiogenesis, and metastases in murine xenograft models. Our focus in this review is to summarize the known data on the role of IL-1 in tumor progression and metastasis and the use of IL-1 inhibition as a novel therapeutic approach in the treatment of solid organ malignancies. C1 NCI, Surg Metab Sect, Surg Branch, Ctr Canc Res, Bethesda, MD 20892 USA. NIH, Howard Hughes Med Inst, Res Scholars Program, Chevy Chase, MD USA. Univ Maryland, Med Ctr, Dept Surg, Baltimore, MD 21201 USA. Univ Maryland, Med Ctr, Greenebaum Canc Ctr, Baltimore, MD 21201 USA. RP Alexander, HR (reprint author), NCI, Surg Metab Sect, Surg Branch, Ctr Canc Res, Bethesda, MD 20892 USA. EM anne-lewis@uiowa.edu; Varghess@mail.nih.gov; hxu@mail.nih.gov; HRAlexander@smail.umaryland.edu NR 47 TC 143 Z9 152 U1 2 U2 11 PU BIOMED CENTRAL LTD PI LONDON PA MIDDLESEX HOUSE, 34-42 CLEVELAND ST, LONDON W1T 4LB, ENGLAND SN 1479-5876 J9 J TRANSL MED JI J. Transl. Med. PD NOV 10 PY 2006 VL 4 AR 48 DI 10.1186/1479-5876-4-48 PG 12 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA 113JR UT WOS:000242594700002 PM 17096856 ER PT J AU Sodergren, E Weinstock, GM Davidson, EH Cameron, RA Gibbs, RA Weinstock, GM Angerer, RC Angerer, LM Arnone, MI Burgess, DR Burke, RD Cameron, RA Coffman, JA Davidson, EH Dean, M Elphick, MR Ettensohn, CA Foltz, KR Hamdoun, A Hynes, RO Klein, WH Marzluff, W McClay, DR Morris, RL Mushegian, A Rast, JP Sodergren, E Smith, LC Thorndyke, MC Vacquier, VD Weinstock, GM Wessel, GM Wray, G Zhang, L Sodergren, E Weinstock, GM Angerer, RC Angerer, LM Cameron, RA Davidson, EH Elsik, CG Ermolaeva, O Hlavina, W Hofmann, G Kitts, P Landrum, MJ Mackey, AJ Maglott, D Panopoulou, G Poustka, AJ Pruitt, K Sapojnikov, V Song, XZ Souvorov, A Solovyev, V Wei, Z Whittaker, CA Worley, K Zhang, L Sodergren, E Weinstock, GM Durbin, KJ Gibbs, RA Shen, YF Song, XZ Worley, K Zhang, L Wray, G Fedrigo, O Garfield, D Haygood, R Primus, A Satija, R Severson, T Zhang, L Sodergren, E Weinstock, GM Gonzalez-Garay, ML Jackson, AR Milosavljevic, A Song, XZ Tong, M Worley, K Ettensohn, CA Cameron, RA Killian, CE Landrum, MJ Livingston, BT Wilt, FH Coffman, JA Marzluff, W Mushegian, A Adams, N Belle, R Carbonneau, S Cheung, R Cormier, P Cosson, B Croce, J Fernandez-Guerra, A Geneviere, AM Goel, M Kelkar, H Morales, J Mulner-Lorillon, O Robertson, AJ Hamdoun, A Goldstone, JV Adams, N Cole, B Dean, M Epel, D Gold, B Hahn, ME Howard-Ashby, M Scally, M Stegeman, JJ Morris, RL Allgood, EL Cool, J Judkins, KM McCafferty, SS Musante, AM Obar, RA Rawson, AP Rossetti, BJ Burgess, DR Allgood, EL Cool, J Gibbons, IR Hoffman, MP Judkins, KM Leone, A McCafferty, SS Morris, RL Musante, AM Obar, RA Rawson, AP Rossetti, BJ Wessel, GM Davidson, EH Cameron, RA Istrail, S Materna, SC Samanta, MP Stolc, V Tongprasit, W Tu, Q Angerer, RC Angerer, LM Wei, Z Hynes, RO Bergeron, KF Brandhorst, BP Burke, RD Whittaker, CA Whittle, J Cameron, RA Berney, K Bottjer, DJ Calestani, C Davidson, EH Peterson, K Chow, E Yuan, QA Elhaik, E Elsik, CG Graur, D Reese, JT Bosdet, I Heesun, S Marra, MA Schein, J Dean, M Hamdoun, A Rast, JP Smith, LC Anderson, MK Berney, K Brockton, V Buckley, KM Cameron, RA Cohen, AH Fugmann, SD Hibino, T Loza-Coll, M Majeske, AJ Messier, C Nair, SV Pancer, Z Terwilliger, DP Burke, RD Elphick, MR Klein, WH Thorndyke, MC Agca, C Angerer, LM Arboleda, E Arnone, MI Brandhorst, BP Chen, NS Churcher, AM Hallbook, F Humphrey, GW Hynes, RO Idris, MM Kiyama, T Liang, SG Mellott, D Mu, XQ Murray, G Olinski, RP Raible, F Rowe, M Taylor, JS Tessmar-Raible, K Wang, D Wilson, KH Yaguchi, S Foltz, KR Vacquier, VD Wessel, GM Gaasterland, T Galindo, BE Gunaratne, HJ Howard-Ashby, M Humphrey, GW Juliano, C Kinukawa, M Moy, GW Neill, AT Nomura, M Raisch, M Reade, A Roux, MM Song, JL Su, YH Townley, IK Voronina, E Wong, JL Arnone, MI Thorndyke, MC Amore, G Angerer, LM Arboleda, E Branno, M Brown, ER Cavalieri, V Duboc, V Duloquin, L Elphick, MR Flytzanis, C Gache, C Geneviere, AM Idris, MM Lapraz, F Lepage, T Locascio, A Martinez, P Matassi, G Matranga, V McClay, DR Morales, J Poustka, AJ Raible, F Range, R Rizzo, F Rottinger, E Rowe, M Tessmar-Raible, K Sodergren, E Weinstock, GM Wilson, K McClay, DR Angerer, LM Arnone, MI Beane, W Bradham, C Byrum, C Croce, J Duboc, V Duloquin, L Gache, C Geneviere, AM Glenn, T Hibino, T Hussain, S Lapraz, F Lepage, T Livingston, BT Loza, M Manning, G Miranda, E Range, R Rizzo, F Rottinger, E Thomason, R Walton, K Wei, Z Wessel, GM Wikramanayke, A Wilson, KH Whittaker, C Wu, SY Xu, RH Davidson, EH Arnone, MI Branno, M Brown, CT Cameron, RA Chen, LL Gray, RF Howard-Ashby, M Istrail, S Lee, PY Locascio, A Martinez, P Materna, SC Nam, J Oliveri, P Rizzo, F Smith, J Muzny, D Sodergren, E Gibbs, RA Weinstock, GM Bell, S Chacko, J Cree, A Curry, S Davis, C Dinh, H Dugan-Rocha, S Fowler, J Gill, R Hamilton, C Hernandez, J Hines, S Hume, J Jackson, L Jolivet, A Kovar, C Lee, S Lewis, L Miner, G Morgan, M Nazareth, LV Okwuonu, G Parker, D Pu, LL Shen, YF Thom, R Wright, R AF Sodergren, Erica Weinstock, George M. Davidson, Eric H. Cameron, R. Andrew Gibbs, Richard A. Weinstock, George M. Angerer, Robert C. Angerer, Lynne M. Arnone, Maria Ina Burgess, David R. Burke, Robert D. Cameron, R. Andrew Coffman, James A. Davidson, Eric H. Dean, Michael Elphick, Maurice R. Ettensohn, Charles A. Foltz, Kathy R. Hamdoun, Amro Hynes, Richard O. Klein, William H. Marzluff, William McClay, David R. Morris, Robert L. Mushegian, Arcady Rast, Jonathan P. Sodergren, Erica Smith, L. Courtney Thorndyke, Michael C. Vacquier, Victor D. Weinstock, George M. Wessel, Gary M. Wray, Greg Zhang, Lan Sodergren, Erica Weinstock, George M. Angerer, Robert C. Angerer, Lynne M. Cameron, R. Andrew Davidson, Eric H. Elsik, Christine G. Ermolaeva, Olga Hlavina, Wratko Hofmann, Gretchen Kitts, Paul Landrum, Melissa J. Mackey, Aaron J. Maglott, Donna Panopoulou, Georgia Poustka, Albert J. Pruitt, Kim Sapojnikov, Victor Song, Xingzhi Souvorov, Alexandre Solovyev, Victor Wei, Zheng Whittaker, Charles A. Worley, Kim Zhang, Lan Sodergren, Erica Weinstock, George M. Durbin, K. James Gibbs, Richard A. Shen, Yufeng Song, Xingzhi Worley, Kim Zhang, Lan Wray, Greg Fedrigo, Olivier Garfield, David Haygood, Ralph Primus, Alexander Satija, Rahul Severson, Tonya Zhang, Lan Sodergren, Erica Weinstock, George M. Gonzalez-Garay, Manuel L. Jackson, Andrew R. Milosavljevic, Aleksandar Song, Xingzhi Tong, Mark Worley, Kim Ettensohn, Charles A. Cameron, R. Andrew Killian, Christopher E. Landrum, Melissa J. Livingston, Brian T. Wilt, Fred H. Coffman, James A. Marzluff, William Mushegian, Arcady Adams, Nikki Belle, Robert Carbonneau, Seth Cheung, Rocky Cormier, Patrick Cosson, Bertrand Croce, Jenifer Fernandez-Guerra, Antonio Geneviere, Anne-Marie Goel, Manisha Kelkar, Hemant Morales, Julia Mulner-Lorillon, Odile Robertson, Anthony J. Hamdoun, Amro Goldstone, Jared V. Adams, Nikki Cole, Bryan Dean, Michael Epel, David Gold, Bert Hahn, Mark E. Howard-Ashby, Meredith Scally, Mark Stegeman, John J. Morris, Robert L. Allgood, Erin L. Cool, Jonah Judkins, Kyle M. McCafferty, Shawn S. Musante, Ashlan M. Obar, Robert A. Rawson, Amanda P. Rossetti, Blair J. Burgess, David R. Allgood, Erin L. Cool, Jonah Gibbons, Ian R. Hoffman, Matthew P. Judkins, Kyle M. Leone, Andrew McCafferty, Shawn S. Morris, Robert L. Musante, Ashlan M. Obar, Robert A. Rawson, Amanda P. Rossetti, Blair J. Wessel, Gary M. Davidson, Eric H. Cameron, R. Andrew Istrail, Sorin Materna, Stefan C. Samanta, Manoj P. Stolc, Viktor Tongprasit, Waraporn Tu, Qiang Angerer, Robert C. Angerer, Lynne M. Wei, Zheng Hynes, Richard O. Bergeron, Karl-Frederik Brandhorst, Bruce P. Burke, Robert D. Whittaker, Charles A. Whittle, James Cameron, R. Andrew Berney, Kevin Bottjer, David J. Calestani, Cristina Davidson, Eric H. Peterson, Kevin Chow, Elly Yuan, Qiu Autumn Elhaik, Eran Elsik, Christine G. Graur, Dan Reese, Justin T. Bosdet, Ian Heesun, Shin Marra, Marco A. Schein, Jacqueline Dean, Michael Hamdoun, Amro Rast, Jonathan P. Smith, L. Courtney Anderson, Michele K. Berney, Kevin Brockton, Virginia Buckley, Katherine M. Cameron, R. Andrew Cohen, Avis H. Fugmann, Sebastian D. Hibino, Taku Loza-Coll, Mariano Majeske, Audrey J. Messier, Cynthia Nair, Sham V. Pancer, Zeev Terwilliger, David P. Burke, Robert D. Elphick, Maurice R. Klein, William H. Thorndyke, Michael C. Agca, Cavit Angerer, Lynne M. Arboleda, Enrique Arnone, Maria Ina Brandhorst, Bruce P. Chen, Nansheng Churcher, Allison M. Hallboeoek, F. Humphrey, Glen W. Hynes, Richard O. Idris, Mohammed M. Kiyama, Takae Liang, Shuguang Mellott, Dan Mu, Xiuqian Murray, Greg Olinski, Robert P. Raible, Florian Rowe, Matthew Taylor, John S. Tessmar-Raible, Kristin Wang, D. Wilson, Karen H. Yaguchi, Shunsuke Foltz, Kathy R. Vacquier, Victor D. Wessel, Gary M. Gaasterland, Terry Galindo, Blanca E. Gunaratne, Herath J. Howard-Ashby, Meredith Humphrey, Glen W. Juliano, Celina Kinukawa, Masashi Moy, Gary W. Neill, Anna T. Nomura, Mamoru Raisch, Michael Reade, Anna Roux, Michelle M. Song, Jia L. Su, Yi-Hsien Townley, Ian K. Voronina, Ekaterina Wong, Julian L. Arnone, Maria Ina Thorndyke, Michael C. Amore, Gabriele Angerer, Lynne M. Arboleda, Enrique Branno, Margherita Brown, Euan R. Cavalieri, Vincenzo Duboc, Veronique Duloquin, Louise Elphick, Maurice R. Flytzanis, Constantin Gache, Christian Geneviere, Anne-Marie Idris, Mohammed M. Lapraz, Francois Lepage, Thierry Locascio, Annamaria Martinez, Pedro Matassi, Giorgio Matranga, Valeria McClay, David R. Morales, Julia Poustka, Albert J. Raible, Florian Range, Ryan Rizzo, Francesca Roettinger, Eric Rowe, Matthew Tessmar-Raible, Kristin Sodergren, Erica Weinstock, George M. Wilson, Karen McClay, David R. Angerer, Lynne M. Arnone, Maria Ina Beane, Wendy Bradham, Cynthia Byrum, Christine Croce, Jenifer Duboc, Veronique Duloquin, Louise Gache, Christian Geneviere, Anne-Marie Glenn, Tom Hibino, Taku Hussain, Sofia Lapraz, Francois Lepage, Thierry Livingston, Brian T. Loza, Mariano Manning, Gerard Miranda, Esther Range, Ryan Rizzo, Francesca Roettinger, Eric Thomason, Rebecca Walton, Katherine Wei, Zheng Wessel, Gary M. Wikramanayke, Athula Wilson, Karen H. Whittaker, Charles Wu, Shu-Yu Xu, Ronghui Davidson, Eric H. Arnone, Maria Ina Branno, Margherita Brown, C. Titus Cameron, R. Andrew Chen, Lili Gray, Rachel F. Howard-Ashby, Meredith Istrail, Sorin Lee, Pei Yun Locascio, Annamaria Martinez, Pedro Materna, Stefan C. Nam, Jongmin Oliveri, Paola Rizzo, Francesca Smith, Joel Muzny, Donna Sodergren, Erica Gibbs, Richard A. Weinstock, George M. Bell, Stephanie Chacko, Joseph Cree, Andrew Curry, Stacey Davis, Clay Dinh, Huyen Dugan-Rocha, Shannon Fowler, Jerry Gill, Rachel Hamilton, Cerrissa Hernandez, Judith Hines, Sandra Hume, Jennifer Jackson, LaRonda Jolivet, Angela Kovar, Christie Lee, Sandra Lewis, Lora Miner, George Morgan, Margaret Nazareth, Lynne V. Okwuonu, Geoffrey Parker, David Pu, Ling-Ling Shen, Yufeng Thom, Rachel Wright, Rita CA Sea Urchin Genome Sequencing Consortium TI Research article - The genome of the sea urchin Strongylocentrotus purpuratus SO SCIENCE LA English DT Article ID ARYL-HYDROCARBON RECEPTOR; IMMUNE-SYSTEM; EVOLUTION; VERTEBRATE; COMPLEMENT; INSIGHTS; DUPLICATION; CELOMOCYTES; SEQUENCE; CHORDATE C1 Baylor Coll Med, Human Genome Sequencing Ctr, Houston, TX 77030 USA. Baylor Coll Med, Dept Mol & Human Genet, Houston, TX 77030 USA. CALTECH, Div Biol, Pasadena, CA 91125 USA. Natl Inst Dent & Craniofacial Res, NIH, Bethesda, MD 20892 USA. Stn Zool A Dohrn, I-70121 Bari, Italy. Boston Coll, Dept Biol, Chestnut Hill, MA 02467 USA. Univ Victoria, Dept Biochem & Microbiol, Victoria, BC V8W 3N5, Canada. Mt Desert Isl Biol Lab, Salsbury Cove, ME 04672 USA. NCI, Human Genet Sect, Lab Genom Divers, Frederick, MD 21702 USA. Queen Mary Univ London, Sch Biol & Chem Sci, London E1 4NS, England. Carnegie Mellon Univ, Dept Biol Sci, Pittsburgh, PA 15213 USA. Univ Calif Santa Barbara, Dept Mol Cellular & Dev Biol, Santa Barbara, CA 93106 USA. Univ Calif Santa Barbara, Inst Marine Sci, Santa Barbara, CA 93106 USA. Stanford Univ, Hopkins Marine Stn, Pacific Grove, CA 93950 USA. MIT, Howard Hughes Med Inst, Ctr Canc Res, Cambridge, MA 02139 USA. Univ Texas, MD Anderson Canc Ctr, Dept Biochem & Mol Biol, Houston, TX 77030 USA. Univ N Carolina, Dept Mol Biol & Biotechnol, Chapel Hill, NC 27599 USA. Duke Univ, Dept Biol, Durham, NC 27708 USA. Wheaton Coll, Dept Biol, Norton, MA 02766 USA. Stowers Inst Med Res, Kansas City, MO 64110 USA. Univ Kansas, Med Ctr, Dept Microbiol, Kansas City, KS 66160 USA. Univ Toronto, Sunnybrook Res Inst, Toronto, ON M4N 3M5, Canada. Univ Toronto, Dept Med Biophys, Toronto, ON M4N 3M5, Canada. Univ Toronto, Dept Immunol, Toronto, ON M4N 3M5, Canada. George Washington Univ, Dept Biol Sci, Washington, DC 20052 USA. Royal Swedish Acad Sci, Kristineberg Marine Res Stn, S-45034 Fiskebackskil, Sweden. Univ Calif San Diego, Scripps Inst Oceanog, La Jolla, CA 92093 USA. Brown Univ, Dept Mol & Cellular Biol & Biochem, Providence, RI 02912 USA. Duke Univ, Dept Biol, Durham, NC 27708 USA. Duke Univ, Inst Genome Sci & Policy, Durham, NC 27708 USA. Texas A&M Univ, Dept Anim Sci, College Stn, TX 77843 USA. Natl Ctr Biotechnol Informat, Natl Lib Med, NIH, Bethesda, MD 20894 USA. Univ Calif Santa Barbara, Dept Ecol Evolut & Marine Biol, Santa Barbara, CA 93106 USA. Natl Ctr Biotechnol Informat, NIH, Bethesda, MD 20892 USA. Univ Penn, Penn Genom Inst, Philadelphia, PA 19104 USA. Max Planck Inst Mol Genet, Evolut & Dev Grp, D-14195 Berlin, Germany. Royal Holloway Univ London, Egham TW20 0EX, Surrey, England. MIT, Ctr Canc Res, Cambridge, MA 02139 USA. Univ Calif Berkeley, Dept Mol & Cell Biol, Berkeley, CA 94720 USA. Univ S Florida, Dept Biol, Tampa, FL 33618 USA. Univ Paris 06, UMR 7150, Equipe Cycle Cellulaire & Dev, Stn Biol Roscoff, F-29682 Roscoff, France. CNRS, UMR 7150, Stn Biol Roscoff, F-29682 Roscoff, France. Univ Paris 06, UMR7628, F-66650 Banyuls sur Mer, France. Univ N Carolina, Ctr Bioinformat, Chapel Hill, NC 27599 USA. Woods Hole Oceanog Inst, Dept Biol, Woods Hole, MA 02543 USA. Tethys Res LLC, Bangor, ME 04401 USA. Univ Calif Berkeley, Dept Mol Cellular & Dev Biol, Berkeley, CA 94720 USA. Brown Univ, Ctr Computat Mol Biol, Providence, RI 02912 USA. Brown Univ, Dept Comp Sci, Providence, RI 02912 USA. NASA, Ames Res Ctr, Genome Res Facil, Moffett Field, CA 94035 USA. Systemix Inst, Cupertino, CA 95014 USA. Simon Fraser Univ, Dept Biochem & Mol Biol, Burnaby, BC V5A 1S6, Canada. MIT, Ctr Canc Res, Dept Biol, Cambridge, MA 02139 USA. Univ So Calif, Dept Earth Sci, Los Angeles, CA 90089 USA. Univ Cent Florida, Dept Biol, Orlando, FL 32816 USA. Dartmouth Coll, Dept Biol Sci, Hanover, NH 03755 USA. CALTECH, Beckman Inst, Ctr Computat Regulatory Genom, Pasadena, CA 91125 USA. Univ Houston, Dept Biol & Biochem, Houston, TX 77204 USA. British Columbia Canc Agcy, Genome Sci Ctr, Vancouver, BC V5Z 4E6, Canada. Univ Maryland, Dept Biol, College Pk, MD 20742 USA. Univ Maryland, Syst Res Inst, College Pk, MD 20742 USA. NIA, Cellular & Mol Biol Lab, NIH, Baltimore, MD 21224 USA. Macquarie Univ, Sch Biol Sci, Sydney, NSW 2109, Australia. UMBI, Ctr Marine Biotechnol, Baltimore, MD 21202 USA. Louisiana State Univ, Hlth Sci Ctr, Dept Cell Biol & Anat, New Orleans, LA 70112 USA. Univ Victoria, Dept Biol, Victoria, BC V8W 2Y2, Canada. Uppsala Univ, Dept Neurosci, Uppsala, Sweden. NICHD, Lab Cellular & Mol Biophys, NIH, Bethesda, MD 20892 USA. European Mol Biol Lab, Dev Unit, D-69117 Heidelberg, Germany. European Mol Biol Lab, Computat Unit, D-69117 Heidelberg, Germany. Univ Nacl Autonoma Mexico, Inst Biotechnol, Cuernavaca 62250, Morelos, Mexico. Univ Palermo, Dept Cellular & Dev Biol Alberto Monroy, I-90146 Palermo, Italy. CNRS, UMR 7009, Dev Biol Lab, F-06230 Villefranche Sur Mer, France. Univ Paris 06, Observ Oceanol, F-06230 Villefranche Sur Mer, France. Univ Patras, Dept Biol, Patras, Greece. Baylor Coll Med, Dept Mol & Cellular Biol, Houston, TX 77030 USA. Univ Barcelona, Dept Genet, E-08028 Barcelona, Spain. Inst Catalana Recerca & Estudis Avancats, Barcelona, Spain. Inst Jacques Monod, CNR, UMR 7592, F-75005 Paris, France. CNR, Ist Biomed & Immunol Mol Alberto Monroy, I-90146 Palermo, Italy. Salk Inst Biol Studies, Razavi Newman Ctr Bioinformat, San Diego, CA 92186 USA. Univ Hawaii Manoa, Dept Zool, Honolulu, HI 96822 USA. RP Weinstock, GM (reprint author), Baylor Coll Med, Human Genome Sequencing Ctr, 1 Baylor Plaza, Houston, TX 77030 USA. EM gwstock@bcm.tmc.edu RI Marra, Marco/B-5987-2008; Matassi, Giorgio/G-6301-2014; Su, Yi-Hsien/F-2910-2014; Rizzo, Francesca/K-3057-2016; Mu, Xiuqian/I-9146-2014; Elsik, Christine/C-4120-2017; Brandhorst, Bruce/A-3157-2008; Tu, Qiang/B-4667-2008; Peterson, Kevin/A-2188-2009; Tessmar-Raible, Kristin/F-9642-2011; Brown, Euan/A-5558-2008; Raible, Florian/G-6019-2011; Chen, Nansheng/E-6450-2012; Dean, Michael/G-8172-2012; Geneviere, Anne-Marie/A-3942-2013; 拓, 日比野/D-8115-2013; Churcher, Allison/M-6169-2013; Tang, Macy/B-9798-2014; Locascio, Annamaria/E-8714-2015; Martinez, Pedro/O-5025-2014 OI Matassi, Giorgio/0000-0003-4923-226X; Rizzo, Francesca/0000-0003-1783-5015; Mu, Xiuqian/0000-0002-8003-7529; Elsik, Christine/0000-0002-4248-7713; Smith, Joel/0000-0003-0311-7055; Tu, Qiang/0000-0002-7579-8315; Brown, Euan/0000-0002-5995-834X; Dean, Michael/0000-0003-2234-0631; Churcher, Allison/0000-0003-1902-3002; Locascio, Annamaria/0000-0001-6956-2157; Martinez, Pedro/0000-0003-3956-7541 NR 50 TC 559 Z9 581 U1 5 U2 104 PU AMER ASSOC ADVANCEMENT SCIENCE PI WASHINGTON PA 1200 NEW YORK AVE, NW, WASHINGTON, DC 20005 USA SN 0036-8075 J9 SCIENCE JI Science PD NOV 10 PY 2006 VL 314 IS 5801 BP 941 EP 952 DI 10.1126/science.1133609 PG 12 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA 103OG UT WOS:000241896000039 ER PT J AU Viboud, C Tam, T Fleming, D Handel, A Miller, MA Simonsen, L AF Viboud, Cecile Tam, Theresa Fleming, Douglas Handel, Andreas Miller, Mark A. Simonsen, Lone TI Transmissibility and mortality impact of epidemic and pandemic influenza, with emphasis on the unusually deadly 1951 epidemic SO VACCINE LA English DT Article; Proceedings Paper CT 2nd European Influenza Conference CY SEP 11-14, 2005 CL St Julians, MALTA DE influenza; epidemic; pandemic; mortality; transmissibility; reproduction number; Canada; England and Wales ID A VIRUS; EVOLUTION AB There are important gaps in our current understanding of the influenza virus behavior. In particular, it remains unclear why some interpandemic seasons are associated with unusually high mortality impact, sometimes comparable to that of pandernics. Here we compare the epidemiological patterns of the unusually deadly 1951 influenza epidemic (A/H1N1) in England and Wales and Canada with those of surrounding epidemic and pandemic seasons, in terms of overall mortality impact and transmissibility. Based on the statistical and mathematical analysis of vital statistics and morbidity epidemic curves in these two countries, we show that the 1951 epidemic was associated with both higher mortality impact and higher transmissibility than the 1957 and 1968 pandernics. Surprisingly in Liverpool, considered the 'epicenter' of the severe 1951 epidemic, the mortality impact and transmissibility even surpassed the 1918 pandemic. Published by Elsevier Ltd. C1 NIH, Div Int Epidemiol & Populat Studies, Fogarty Int Ctr, Bethesda, MD 20892 USA. Ctr Infect Dis Populat & Control, Publ Hlth Agcy, Ottawa, ON, Canada. Royal Coll Gen Practitioners, Birmingham Res Unit, Birmingham, W Midlands, England. Emory Univ, Dept Biol, Atlanta, GA 30322 USA. NIAID, NIH, Bethesda, MD 20892 USA. RP Viboud, C (reprint author), NIH, Div Int Epidemiol & Populat Studies, Fogarty Int Ctr, 16 Ctr Dr, Bethesda, MD 20892 USA. EM viboudc@mail.nih.gov RI Handel, Andreas/F-6056-2012; OI Handel, Andreas/0000-0002-4622-1146; Simonsen, Lone/0000-0003-1535-8526 NR 28 TC 76 Z9 78 U1 0 U2 3 PU ELSEVIER SCI LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND SN 0264-410X J9 VACCINE JI Vaccine PD NOV 10 PY 2006 VL 24 IS 44-46 BP 6701 EP 6707 DI 10.1016/j.vaccine.2006.05.067 PG 7 WC Immunology; Medicine, Research & Experimental SC Immunology; Research & Experimental Medicine GA 111IG UT WOS:000242444000033 PM 16806596 ER PT J AU Finkel, T AF Finkel, Toren TI Cell biology - A clean energy programme SO NATURE LA English DT Editorial Material ID METABOLISM; COACTIVATORS; REGULATORS; MICE C1 NHLBI, Cardiol Branch, NIH, Bethesda, MD 20892 USA. RP Finkel, T (reprint author), NHLBI, Cardiol Branch, NIH, 10-CRC 5-3330,10 Ctr Dr, Bethesda, MD 20892 USA. EM finkelt@nih.gov NR 10 TC 18 Z9 18 U1 0 U2 3 PU NATURE PUBLISHING GROUP PI LONDON PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND SN 0028-0836 J9 NATURE JI Nature PD NOV 9 PY 2006 VL 444 IS 7116 BP 151 EP 152 DI 10.1038/444151a PG 2 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA 103DZ UT WOS:000241867200022 PM 17093435 ER PT J AU Luan, HJ Peabody, NC Vinson, CR White, BH AF Luan, Haojiang Peabody, Nathan C. Vinson, Charles R. White, Benjamin H. TI Refined spatial manipulation of neuronal function by combinatorial restriction of transgene expression SO NEURON LA English DT Article ID NEURAL CIRCUITRY; GENE-EXPRESSION; NERVOUS-SYSTEM; DROSOPHILA; PROTEIN; GAL4; SPECIFICITY; ACTIVATION; NETWORK; FUSION AB Selective genetic manipulation of neuronal function in vivo requires techniques for targeting gene expression to specific cells. Existing systems accomplish this using the promoters of endogenous genes to drive expression of transgenes directly in cells of interest or, in "binary" systems, to drive expression of a transcription factor or recombinase that subsequently activates the expression of other transgenes. All such techniques are constrained by the limited specificity of the available promoters. We introduce here a combinatorial system in which the DNA-binding (DBD) and transcription-activation (AD) domains of a transcription factor are independently targeted using two different promoters. The domains heterodimerize to become transcriptionally competent and thus drive transgene expression only at the intersection of the expression patterns of the two promoters. We use this system to dissect a neuronal network in Drosophila by selectively targeting expression of the cell death gene reaper to subsets of neurons within the network. C1 NIMH, Mol Biol Lab, Bethesda, MD 20892 USA. NCI, Lab Metab, NIH, Bethesda, MD 20892 USA. RP White, BH (reprint author), NIMH, Mol Biol Lab, 9000 Rockville Pike, Bethesda, MD 20892 USA. EM benjaminwhite@mail.nih.gov RI Marion-Poll, Frederic/D-8882-2011 OI Marion-Poll, Frederic/0000-0001-6824-0180 FU Intramural NIH HHS; NIMH NIH HHS [Z01 MH002800-03] NR 37 TC 112 Z9 115 U1 5 U2 15 PU CELL PRESS PI CAMBRIDGE PA 1100 MASSACHUSETTS AVE, CAMBRIDGE, MA 02138 USA SN 0896-6273 J9 NEURON JI Neuron PD NOV 9 PY 2006 VL 52 IS 3 BP 425 EP 436 DI 10.1016/j.neuron.2006.08.028 PG 12 WC Neurosciences SC Neurosciences & Neurology GA 108WK UT WOS:000242269700006 PM 17088209 ER PT J AU Chowdhury, S Shepherd, JD Okuno, H Lyford, G Petralia, RS Plath, N Kuhl, D Huganir, RL Worley, PF AF Chowdhury, Shoaib Shepherd, Jason D. Okuno, Hiroyuki Lyford, Gregory Petralia, Ronald S. Plath, Niels Kuhl, Dietmar Huganir, Richard L. Worley, Paul F. TI Arc/Arg3.1 interacts with the endocytic machinery to regulate AMPA receptor trafficking SO NEURON LA English DT Article ID LONG-TERM POTENTIATION; IMMEDIATE-EARLY GENE; CLATHRIN-MEDIATED ENDOCYTOSIS; SYNAPTIC VESICLE ENDOCYTOSIS; METABOTROPIC GLUTAMATE RECEPTORS; DOMAIN-CONTAINING PROTEIN; SH3 DOMAIN; DEPENDENT ENDOCYTOSIS; HIPPOCAMPAL-NEURONS; CULTURED NEURONS AB Arc/Arg3.1 is an immediate-early gene whose mRNA is rapidly transcribed and targeted to dendrites of neurons as they engage in information processing and storage. Moreover, Arc/Arg3.1 is known to be required for durable forms of synaptic plasticity and learning. Despite these intriguing links to plasticity, Arc/Arg3.1's molecular function remains enigmatic. Here, we demonstrate that Arc/Arg3.1 protein interacts with dynamin and specific isoforms of endophilin to enhance receptor endocytosis. Arc/Arg3.1 selectively modulates trafficking of AMPA-type glutamate receptors (AMPARs) in neurons by accelerating endocytosis and reducing surface expression. The Arc/Arg3.1-endocytosis pathway appears to regulate basal AMPAR levels since Arc/Arg3.1 KO neurons exhibit markedly reduced endocytosis and increased steady-state surface levels. These findings reveal a novel molecular pathway that is regulated by Arc/Arg3.1 and likely contributes to late-phase synaptic plasticity and memory consolidation. C1 Johns Hopkins Univ, Sch Med, Dept Neurosci, Baltimore, MD 21205 USA. Johns Hopkins Univ, Sch Med, Cellular & Mol Med Grad Program, Baltimore, MD 21205 USA. Johns Hopkins Univ, Sch Med, Howard Hughes Med Inst, Baltimore, MD 21205 USA. Johns Hopkins Univ, Sch Med, Dept Neurol, Baltimore, MD 21205 USA. Natl Inst Deafness & Other Commun Disorders, Neurochem Lab, NIH, Bethesda, MD 20892 USA. Free Univ Berlin, Dept Biol Chem Pharm, D-14195 Berlin, Germany. RP Worley, PF (reprint author), Johns Hopkins Univ, Sch Med, Dept Neurosci, Baltimore, MD 21205 USA. EM pworley@jhmi.edu RI Kuhl, Dietmar/A-4689-2009; OI Kuhl, Dietmar/0000-0002-4772-6701; Shepherd, Jason/0000-0001-7384-8289 FU Intramural NIH HHS; NIMH NIH HHS [P50 MH068830, R01 MH053608] NR 78 TC 325 Z9 344 U1 1 U2 32 PU CELL PRESS PI CAMBRIDGE PA 1100 MASSACHUSETTS AVE, CAMBRIDGE, MA 02138 USA SN 0896-6273 J9 NEURON JI Neuron PD NOV 9 PY 2006 VL 52 IS 3 BP 445 EP 459 DI 10.1016/j.neuron.2006.08.033 PG 15 WC Neurosciences SC Neurosciences & Neurology GA 108WK UT WOS:000242269700008 PM 17088211 ER PT J AU Pelkey, KA Topolnik, L Lacaille, JC McBain, CJ AF Pelkey, Kenneth A. Topolnik, Lisa Lacaille, Jean-Claude McBain, Chris J. TI Compartmentalized Ca2+ channel regulation at divergent mossy-fiber release sites underlies target cell-dependent plasticity SO NEURON LA English DT Article ID METABOTROPIC GLUTAMATE-RECEPTOR; LONG-TERM POTENTIATION; SINGLE NERVE-TERMINALS; FEEDFORWARD INHIBITION; RAT HIPPOCAMPUS; TRANSMITTER RELEASE; PYRAMIDAL CELLS; SYNAPTIC TRANSMISSION; PRESYNAPTIC CALCIUM; NEUROTRANSMITTER RELEASE AB Hippocampal mossy fibers (MFs) innervate CA3 targets via anatomically distinct presynaptic elements: MF boutons (MFBs) innervate pyramidal cells (PYRs), whereas filopodial extensions (Fils) of MFBs innervate st. lucidum interneurons (SLINs). Surprisingly, the same high-frequency stimulation (HFS) protocol induces presynaptically expressed LTP and LTD at PYR and SLIN inputs, respectively. This differential distribution of plasticity indicates that neighboring, functionally divergent presynaptic elements along the same axon serve as autonomous computational elements capable of modifying release independently. Indeed we report that HFS persistently depresses voltage-gated calcium channel (VGCC) function in Fil terminals, leaving MFB VGCCs unchanged despite similar contributions of N- and P/Q-type VGCCs to transmission at each terminal. Selective Fil VGCC depression results from HFS-induced mGluR7 activation leading to persistent P/Q-type VGCC inhibition. Thus, mGluR7 localization to MF-SLIN terminals and not MFBs allows for MF-SLIN LTD expression via depressed presynaptic VGCC function, whereas MF-PYR plasticity proceeds independently of VGCC alterations. C1 NICHHD, Lab Cellular & Synapt Neurophysiol, NIH, Bethesda, MD 20892 USA. Univ Montreal, Dept Physiol, Ctr Rech Sci Neurol, Montreal, PQ H3C 3J7, Canada. RP Pelkey, KA (reprint author), NICHHD, Lab Cellular & Synapt Neurophysiol, NIH, Bldg 35, Bethesda, MD 20892 USA. EM pelkeyk2@mail.nih.gov FU Intramural NIH HHS NR 67 TC 74 Z9 75 U1 0 U2 2 PU CELL PRESS PI CAMBRIDGE PA 1100 MASSACHUSETTS AVE, CAMBRIDGE, MA 02138 USA SN 0896-6273 J9 NEURON JI Neuron PD NOV 9 PY 2006 VL 52 IS 3 BP 497 EP 510 DI 10.1016/j.neuron.2006.08.032 PG 14 WC Neurosciences SC Neurosciences & Neurology GA 108WK UT WOS:000242269700012 PM 17088215 ER PT J AU McCulloch, SD Kunkel, TA AF McCulloch, Scott D. Kunkel, Thomas A. TI Multiple solutions to inefficient lesion bypass by T7 DNA polyrnerase SO DNA REPAIR LA English DT Article DE DNA damage; DNA synthesis fidelity; DNA polymerase; replication errors; translesion synthesis ID SYN THYMINE DIMER; ERROR-PRONE; CIS-SYN; A-RULE; REPLICATION FIDELITY; POLYMERASE-ETA; TRANSLESION SYNTHESIS; CRYSTAL-STRUCTURE; STRUCTURAL BASIS; ABASIC LESION AB We hypothesize that enzymatic switching during translesion synthesis (TLS) to relieve stalled replication forks occurs during transitions from preferential to disfavored use of damaged primer-templates, and that the polymerase or T-exonuclease used for each successive nucleotide incorporated is the one whose properties result in the highest efficiency and the highest fidelity of bypass. Testing this hypothesis requires quantitative determination of the relative lesion bypass ability of both TLS polymerases and major replicative polymerases. As a model of the latter, here we measure the efficiency and fidelity of cis-syn TT dimer and abasic site bypass using the structurally well-characterized T7 DNA polymerase. No bypass of either lesion occurred during a single round of synthesis, and the exonuclease activity of wild-type T7 DNA polymerase was critical in preventing TLS. When repetitive cycling of the exonuclease-deficient enzyme was allowed, limited bypass did occur but hundreds to thousands of cycles were required to achieve even a single bypass event. Analysis of TLS fidelity indicated that these rare bypass events involved rearrangements of the template and primer strands, insertions opposite the lesion, and combinations of these events, with the choice among these strongly depending on the sequence context of the lesion. Moreover, the presence of a lesion affected the fidelity of copying adjacent undamaged template bases, even when lesion bypass itself was correct. The results also indicate that a TT dimer presents a different type of block to the polymerase than an abasic site, even though both lesions are extremely potent blocks to processive synthesis. The approaches used here to quantify the efficiency and fidelity of TLS can be applied to other polymerase-lesion combinations, to provide guidance as to which of many possible polymerases is most likely to bypass various lesions in biological contexts. (c) 2006 Elsevier B.V. All rights reserved. C1 Natl Inst Environm Hlth Sci, Genet Mol Lab, NIH, DHHS, Res Triangle Pk, NC 27709 USA. Natl Inst Environm Hlth Sci, Struct Biol Lab, NIH, DHHS, Res Triangle Pk, NC 27709 USA. RP Kunkel, TA (reprint author), Natl Inst Environm Hlth Sci, Genet Mol Lab, NIH, DHHS, Res Triangle Pk, NC 27709 USA. EM kunkel@niehs.nih.gov FU Intramural NIH HHS [Z01 ES065070-17, Z01 ES065089-11] NR 51 TC 12 Z9 12 U1 0 U2 1 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 1568-7864 EI 1568-7856 J9 DNA REPAIR JI DNA Repair PD NOV 8 PY 2006 VL 5 IS 11 BP 1373 EP 1383 DI 10.1016/j.dnarep.2006.06.003 PG 11 WC Genetics & Heredity; Toxicology SC Genetics & Heredity; Toxicology GA 105TR UT WOS:000242055700008 PM 16876489 ER PT J AU Du, CW Yu, M Volkow, ND Koretsky, AP Fowler, JS Benveniste, H AF Du, Congwu Yu, Mei Volkow, Nora D. Koretsky, Alan P. Fowler, Joanna S. Benveniste, Helene TI Cocaine increases the intracellular calcium concentration in brain independently of its cerebrovascular effects SO JOURNAL OF NEUROSCIENCE LA English DT Article DE cocaine; cerebrovascular; calcium; blood volume; oxygenation; neurotoxicity ID CEREBRAL-BLOOD-FLOW; POSITRON EMISSION TOMOGRAPHY; PERFUSED MOUSE HEART; IN-VIVO; RAT-BRAIN; COMPARATIVE NEUROTOXICITY; HEMODYNAMIC-RESPONSES; FLUORESCENCE; ISCHEMIA; NEURONS AB Cocaine abuse increases the risk of life-threatening neurological complications such as strokes and seizures. Although the vasoconstricting properties of cocaine underlie its cerebrovascular effects, the mechanisms underlying its neurotoxicity remain incompletely understood. Here, we use optical techniques to measure cerebral blood volume, hemoglobin oxygenation (S(t)O(2)), and intracellular calcium ([Ca(2+)](i)) to test the hypothesis that cocaine increases [Ca(2+)](i) in the brain. The effects of cocaine were compared with those of methylphenidate, which has similar catecholaminergic effects as cocaine ( except for serotonin increases) but no local anesthetic properties, and of lidocaine, which has similar local anesthetic effects as cocaine but is devoid of catecholaminergic actions. To control for the hemodynamic effects of cocaine, we assessed the effects of cocaine in animals in which normal blood pressure was maintained by infusion of phenylephrine, and we also measured the effects of transient hypotension ( mimicking that induced by cocaine). We show that cocaine induced significant increases (similar to 10-15%) in [Ca(2+)](i) that were independent of its hemodynamic effects and of the anesthetic used (isofluorance or alpha-chloralose). Lidocaine but not methylphenidate also induced significant [Ca(2+)](i) increases (similar to 10-13%). This indicates that cocaine at a dose within the range used by drug users significantly increases the [Ca(2+)](i) in the brain and its local anesthetic, but neither its catecholaminergic nor its hemodynamic actions, underlies this effect. Cocaine-induced [Ca(2+)](i) increases are likely to accentuate the neurotoxic effects from cocaine-induced vasoconstriction and to facilitate the occurrence of seizures from the catecholaminergic effects of cocaine. These findings support the use of calcium channel blockers as a strategy to minimize the neurotoxic effects of cocaine. C1 Brookhaven Natl Lab, Dept Med, Upton, NY 11973 USA. Brookhaven Natl Lab, Dept Chem, Upton, NY 11973 USA. NIAAA, Bethesda, MD 20892 USA. NINDS, Lab Funct & Mol Imaging, NIH, Bethesda, MD 20892 USA. SUNY Stony Brook, Dept Anesthesiol, Stony Brook, NY 11794 USA. RP Benveniste, H (reprint author), Brookhaven Natl Lab, Dept Med, Upton, NY 11973 USA. EM congwu@bnl.gov; Benveniste@bnl.gov RI Koretsky, Alan/C-7940-2015 OI Koretsky, Alan/0000-0002-8085-4756 FU Intramural NIH HHS [Z01 NS002989-08] NR 70 TC 34 Z9 34 U1 2 U2 5 PU SOC NEUROSCIENCE PI WASHINGTON PA 11 DUPONT CIRCLE, NW, STE 500, WASHINGTON, DC 20036 USA SN 0270-6474 J9 J NEUROSCI JI J. Neurosci. PD NOV 8 PY 2006 VL 26 IS 45 BP 11522 EP 11531 DI 10.1523/JNEUROSCI.3612-06.2006 PG 10 WC Neurosciences SC Neurosciences & Neurology GA 103NE UT WOS:000241892700003 PM 17093073 ER PT J AU Banke, TG McBain, CJ AF Banke, Tue G. McBain, Chris J. TI GABAergic input onto CA3 hippocampal interneurons remains shunting throughout development SO JOURNAL OF NEUROSCIENCE LA English DT Article DE GABA; synaptic inhibition; hippocampus; interneurons; development; CA3 ID INTRACELLULAR CHLORIDE; SYNAPTIC INHIBITION; RAT HIPPOCAMPUS; FEEDFORWARD INHIBITION; COTRANSPORTER KCC2; GABA RESPONSES; NEURONS; EXPRESSION; SYNAPSES; NETWORK AB In hippocampus, the net flow of excitability is controlled by inhibitory input provided by the many populations of local circuit inhibitory interneurons. In principal cells, GABA(A) receptor-mediated synaptic input undergoes a highly coordinated shift from depolarizing early in life to a more conventional hyperpolarizing inhibition on maturation. This switch in inhibitory input polarity is controlled by the developmental regulation of two chloride cotransporters ( NKCC1 and KCC2) that results in a net shift from high to low intracellular Cl-. Whether inhibitory input onto inhibitory interneurons demonstrates a similar developmental shift in intracellular Cl- is unexplored. Using the gramicidin perforated-patch configuration, we recorded from CA3 hippocampal stratum lucidum interneurons and pyramidal cells to monitor inhibitory input across a broad developmental range. GABAA receptor-mediated synaptic input onto stratum lucidum inhibitory interneurons was shunting in nature across the entire developmental age range tested, as resting membrane potential and the IPSC reversal potential remained within a few millivolts ( 1 - 4mV) between postnatal day 5 ( P5) and P31. Furthermore, sensitivity to block of the two chloride cotransporters KCC2 and NKCC1 did not differ across the same age range, suggesting that their relative expression is fixed across development. In contrast, pyramidal cell synaptic inhibition demonstrated the well described switch from depolarizing to hyperpolarizing over the same age range. Thus, in contrast to principal cells, inhibitory synaptic input onto CA3 interneurons remains shunting throughout development. C1 NICHHD, Lab Cellular & Synapt Neurophysiol, NIH, Bethesda, MD 20892 USA. RP McBain, CJ (reprint author), NICHHD, Lab Cellular & Synapt Neurophysiol, NIH, Bldg 35,Room 3C903, Bethesda, MD 20892 USA. EM mcbainc@mail.nih.gov OI Banke, Tue/0000-0001-8417-4400 FU Intramural NIH HHS NR 33 TC 88 Z9 88 U1 0 U2 4 PU SOC NEUROSCIENCE PI WASHINGTON PA 11 DUPONT CIRCLE, NW, STE 500, WASHINGTON, DC 20036 USA SN 0270-6474 J9 J NEUROSCI JI J. Neurosci. PD NOV 8 PY 2006 VL 26 IS 45 BP 11720 EP 11725 DI 10.1523/JNEUROSCI.2887-06.2006 PG 6 WC Neurosciences SC Neurosciences & Neurology GA 103NE UT WOS:000241892700023 PM 17093093 ER PT J AU Lai, C Xie, CS McCormack, SG Chiang, HC Michalak, MK Lin, X Chandran, J Shim, H Shimoji, M Cookson, MR Huganir, RL Rothstein, JD Price, DL Wong, PC Martin, LJ Zhu, JJ Cai, HB AF Lai, Chen Xie, Chengsong McCormack, Stefanie G. Chiang, Hsueh-Cheng Michalak, Marta K. Lin, Xian Chandran, Jayanth Shim, Hoon Shimoji, Mika Cookson, Mark R. Huganir, Richard L. Rothstein, Jeffrey D. Price, Donald L. Wong, Philip C. Martin, Lee J. Zhu, J. Julius Cai, Huaibin TI Amyotrophic lateral sclerosis 2-deficiency leads to neuronal degeneration in amyotrophic lateral sclerosis through altered AMPA receptor trafficking SO JOURNAL OF NEUROSCIENCE LA English DT Article DE ALS2; knock-out mouse; motor neuron; GRIP1; AMPA receptor; excitotoxicity ID NUCLEOTIDE EXCHANGE FACTOR; NEOCORTICAL PYRAMIDAL NEURONS; DOMAIN-CONTAINING PROTEIN; LONG-TERM POTENTIATION; SYNAPTIC PLASTICITY; IN-VIVO; ENDOSOME TRAFFICKING; ALS2-DEFICIENT MICE; MISSENSE MUTATION; ALS2 GENE AB Amyotrophic lateral sclerosis ( ALS), the most common adult-onset motor neuron disease is caused by a selective loss of motor neurons. One form of juvenile onset autosomal recessive ALS ( ALS2) has been linked to the loss of function of the ALS2 gene. The pathogenic mechanism of ALS2-deficiency, however, remains unclear. To further understand the function of alsin that is encoded by the full-length ALS2 gene, we screened proteins interacting with alsin. Here, we report that alsin interacted with glutamate receptor interacting protein 1 ( GRIP1) both in vitro and in vivo, and colocalized with GRIP1 in neurons. In support of the physiological interaction between alsin and GRIP1, the subcellular distribution of GRIP1 was altered in ALS2(-/-) spinal motor neurons, which correlates with a significant reduction of AMPA-type glutamate receptor subunit 2 ( GluR2) at the synaptic/cell surface of ALS2(-/-) neurons. The decrease of calcium-impermeable GluR2-containing AMPA receptors at the cell/synaptic surface rendered ALS2(-/-) neurons more susceptible to glutamate receptor-mediated neurotoxicity. Our findings reveal a novel function of alsin in AMPA receptor trafficking and provide a novel pathogenic link between ALS2-deficiency and motor neuron degeneration, suggesting a protective role of alsin in maintaining the survival of motor neurons. C1 NIA, Sect Transgenesis, Neurogenet Lab, NIH, Bethesda, MD 20892 USA. Univ Virginia, Sch Med, Dept Pharmacol, Charlottesville, VA 22908 USA. Univ Virginia, Sch Med, Grad Program Neurosci, Charlottesville, VA 22908 USA. Johns Hopkins Univ, Sch Med, Dept Pathol, Baltimore, MD 21205 USA. Johns Hopkins Univ, Sch Med, Dept Neurosci, Baltimore, MD 21205 USA. Johns Hopkins Univ, Sch Med, Dept Neurol, Baltimore, MD 21205 USA. Johns Hopkins Univ, Sch Med, Howard Hughes Med Inst, Baltimore, MD 21205 USA. Tech Univ Lodz, Biotechnol Grad Program, PL-90924 Lodz, Poland. RP Cai, HB (reprint author), NIA, Sect Transgenesis, Neurogenet Lab, NIH, Bldg 35,Room 1A116,35 Convent Dr, Bethesda, MD 20892 USA. EM caih@mail.nih.gov RI rothstein, jeffrey/C-9470-2013; Cai, Huaibin/H-3359-2013 OI Cai, Huaibin/0000-0002-8596-6108 FU Intramural NIH HHS [Z01 AG000959-04, Z99 AG999999]; NINDS NIH HHS [R01 NS053570, NS053570, NS34100, NS40014, NS52098, R01 NS034100, R01 NS040014, R01 NS052098] NR 48 TC 50 Z9 51 U1 0 U2 5 PU SOC NEUROSCIENCE PI WASHINGTON PA 11 DUPONT CIRCLE, NW, STE 500, WASHINGTON, DC 20036 USA SN 0270-6474 J9 J NEUROSCI JI J. Neurosci. PD NOV 8 PY 2006 VL 26 IS 45 BP 11798 EP 11806 DI 10.1523/JNEUROSCI.2084-06.2006 PG 9 WC Neurosciences SC Neurosciences & Neurology GA 103NE UT WOS:000241892700030 PM 17093100 ER PT J AU Yamaguchi, H Durell, SR Feng, HQ Bai, YW Anderson, CW Appella, E AF Yamaguchi, Hiroshi Durell, Stewart R. Feng, Hanqiao Bai, Yawen Anderson, Carl W. Appella, Ettore TI Development of a substrate-based cyclic phosphopeptide inhibitor of protein phosphatase 2C delta, Wip1 SO BIOCHEMISTRY LA English DT Article ID PROTEIN-TYROSINE-PHOSPHATASE; UV-RADIATION; PPM1D; P38; P53; KINASE; PHOSPHORYLATION; AMPLIFICATION; ACTIVATION; TUMORIGENESIS AB The wild-type p53-induced phosphatase, Wip1 ( PP2C delta or PPM1D) is a member of the protein phosphatase 2C (PP2C) family and functions as a negative regulator of the p38 MAP kinase-p53 signaling pathway. PPM1D is amplified or Wip1 is overexpressed in several human cancers, and it acts as a weak oncogene. Although inhibition of Wip1 may have therapeutic value, no specific inhibitors are available. In this study, we designed phosphopeptide inhibitors for Wip1 on the basis of its optimal substrate sequence. We found that phosphoserine-containing diphosphorylated peptides with the sequence pSXpY inhibited Wip1 phosphatase activity, whereas phosphothreonine-containing peptides with the sequence pTXpY were physiological substrates. Moreover, the X residue in the pSXpY sequence modulated inhibitor activity, and beta-branched amino acid- substituted (Ile or Val) phosphopeptides showed high inhibitory potencies. A thioether cyclic phosphopeptide c(MpSIpYVA) had a K-i < 1.0 mu M. Two serine/threonine phosphatases, PP2C alpha and PP2A, were not significantly inhibited by the cyclic phosphopeptide with a nonhydrolyzable phosphoserine mimetic. A homology model of Wip1 bound to a cyclic phosphopeptide and site-directed mutagenesis helped to identify residues important for Wip1 inhibitor selectivity among the PP2C family. These results provide the first proof of concept of a specific inhibitor of the catalytic site of Wip1 and should be useful for developing potential anti-cancer drugs. C1 NCI, Cell Biol Lab, NIH, Bethesda, MD 20892 USA. NCI, Biochem Lab, NIH, Bethesda, MD 20892 USA. Brookhaven Natl Lab, Dept Biol, Upton, NY 11973 USA. RP Appella, E (reprint author), NCI, Cell Biol Lab, NIH, Bethesda, MD 20892 USA. EM appellae@pop.nci.nih.gov FU Intramural NIH HHS NR 40 TC 39 Z9 40 U1 1 U2 7 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA SN 0006-2960 J9 BIOCHEMISTRY-US JI Biochemistry PD NOV 7 PY 2006 VL 45 IS 44 BP 13193 EP 13202 DI 10.1021/bi061356b PG 10 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA 100LJ UT WOS:000241670300007 PM 17073441 ER PT J AU Hayer-Hartl, M Minton, AP AF Hayer-Hartl, Manajit Minton, Allen P. TI A simple semiempirical model for the effect of molecular confinement upon the rate of protein folding SO BIOCHEMISTRY LA English DT Article ID SIMULATIONS; STABILITY; CAGE AB A simple two-state model for the dependence of the rate of folding of a polypeptide confined within a spherical cavity upon the size of the cavity relative to that of the polypeptide is presented. A general prediction of the model is that decreasing the size of the cavity will increase the rate of refolding until the cavity becomes only slightly larger than the native state of the protein, at which point a further decrease in cavity size decreases the rate of refolding. The model qualitatively accounts for the behavior of several previously published simulations of folding within a cavity, as well as recently reported experimental measurements of the relative rate of refolding of each of five proteins encapsulated within wild-type and mutant GroEL-GroES complexes that have been engineered to provide internal cavities with similar surface composition and varying volume. C1 NIDDKD, Lab Biochem & Genet, NIH, US Dept HHS, Bethesda, MD 20892 USA. Max Planck Inst Biochem, Dept Cellular Biochem, D-82152 Martinsried, Germany. RP Minton, AP (reprint author), NIDDKD, Lab Biochem & Genet, NIH, US Dept HHS, Bldg 8,Room 226, Bethesda, MD 20892 USA. EM minton@helix.nih.gov OI Minton, Allen/0000-0001-8459-1247 NR 16 TC 30 Z9 30 U1 2 U2 10 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA SN 0006-2960 J9 BIOCHEMISTRY-US JI Biochemistry PD NOV 7 PY 2006 VL 45 IS 44 BP 13356 EP 13360 DI 10.1021/bi061597j PG 5 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA 100LJ UT WOS:000241670300022 PM 17073456 ER PT J AU Liu, SL Li, YH Shi, GY Chen, YH Huang, CW Hong, JS Wu, HL AF Liu, Shu-Lin Li, Yi-Heng Shi, Guey-Yueh Chen, Yung-Huan Huang, Chia-Wei Hong, Jau-Shyong Wu, Hua-Lin TI A novel inhibitory effect of naloxone on macrophage activation and atherosclerosis formation in mice SO JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY LA English DT Article ID LOW-DENSITY-LIPOPROTEIN; DEFICIENT MICE; NADPH-OXIDASE; THERAPEUTIC INTERVENTION; SUPEROXIDE GENERATION; DOPAMINERGIC-NEURONS; NEOINTIMA FORMATION; OXIDATIVE STRESS; ENDOTOXIC-SHOCK; CAROTID-ARTERY AB OBJECTIVES We investigated whether naloxone could reduce macrophage activation and influence atherosclerotic lesion formation in mice. BACKGROUND Macrophages play an important role in the inflammatory process in atherosclerosis. Naloxone could inhibit activation of microglia, the resident macrophage in the nervous system. METHODS The anti-inflammatory effect of naloxone was evaluated by stimulating the macrophage cell culture and FVB mice with lipopolysaccharide or oxidized low-density lipoprotein with and without naloxone pretreatment. Apolipoprotein-E (apoE)-deficient mice received naloxone injection for 10 weeks, and the severity of aortic atherosclerosis was measured. The left common carotid arteries of C57BL/6 mice were ligated near the carotid bifurcation. The mice then received naloxone injection for 4 weeks after ligation, and the severity of neointima formation was evaluated. RESULTS Naloxone pretreatment significantly suppressed the production of tumor necrosis factor-alpha (TNF-alpha), interleukin-6, monocyte chemoattractant protein-1, and superoxide in macrophages after stimulation. In FVB mice, naloxone reduced the TNF-alpha level in circulation, inflammatory cell infiltration in lungs, and superoxide production in aorta. Naloxone injection significantly decreased the severity of aortic atherosclerosis in the apoE-deficient mice and carotid neointima formation in the C57BL/6 mice after ligation. CONCLUSIONS Naloxone, with its novel anti-inflammatory effect, significantly reduces atherosclerosis and neointima formation in mice. C1 Natl Cheng Kung Univ, Coll Med, Dept Biochem & Mol Biol, Tainan 701, Taiwan. Natl Cheng Kung Univ, Coll Med, Inst Basic Med Sci, Tainan 701, Taiwan. Natl Cheng Kung Univ, Coll Med, Cardiovasc Res Ctr, Tainan 701, Taiwan. Natl Cheng Kung Univ, Coll Med, Dept Internal Med, Tainan 701, Taiwan. Natl Inst Environm Hlth Sci, Neuropharmacol Sect, Lab Pharmacol & Chem, Res Triangle Pk, NC USA. RP Wu, HL (reprint author), Natl Cheng Kung Univ, Coll Med, Dept Biochem & Mol Biol, Tainan 701, Taiwan. EM halnwu@mail.ncku.edu.tw NR 33 TC 14 Z9 14 U1 0 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 NOV 7 PY 2006 VL 48 IS 9 BP 1871 EP 1879 DI 10.1016/j.jacc.2006.07.036 PG 9 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA 102IO UT WOS:000241804400024 PM 17084265 ER PT J AU Ono, T Kasamatsu, A Oka, S Moss, J AF Ono, Tohru Kasamatsu, Atsushi Oka, Shunya Moss, Joel TI The 39-kDa poly(ADP-ribose) glycohydrolase ARH3 hydrolyzes O-acetyl-ADP-ribose, a product of the Sir2 family of acetyl-histone deacetylases SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE ADP-ribosylhydrolase; ADP-ribosyltransferase; sirtuin; ADP-ribose ID RIBOSYLARGININE HYDROLASES; SIR2-LIKE PROTEINS; NAD; IDENTIFICATION; RIBOSYLTRANSFERASES; ERYTHROCYTES; METABOLISM; SUBSTRATE; RESIDUES; ISOFORMS AB The silent information regulator 2 (Sir2) family of NAD-dependent N-acetyl-protein deacetylases participates in the regulation of gene silencing, chromatin structure, and longevity. In the Sir2-catalyzed reaction, the acetyl moiety of N-acetyl-histone is transferred to the ADP-ribose of NAD, yielding O-acetyl-ADP-ribose and nicotinamide. We hypothesized that, if O-acetyl-ADP-ribose were an important signaling molecule, a specific hydrolase would cleave the (O-acetyl)-(ADP-ribose) linkage. We report here that the poly(ADP-ribose) glycohydrolase ARH3 hydrolyzed O-acetyl-ADP-ribose to produce ADP-ribose in a time- and Mg2+-dependent reaction and thus could participate in two signaling pathways. This O-acetyl-ADP-ribose hydrolase belongs to a family of three structurally related 39-kDa ADP-ribose-binding proteins (ARH1-ARH3). ARH1 was reported to hydrolyze ADP-ribosylarginine, whereas ARH3 degraded poly(ADP-ribose). ARH3-catalyzed generation of ADP-ribose from O-acetyl-ADP-ribose was significantly faster than from poly(ADP-ribose). Like the degradation of poly(ADP-ribose) by ARH3, hydrolysis of O-acetyl-ADP-ribose was abolished by replacement of the vicinal aspartates at positions 77 and 78 of ARH3 with asparagine. The rate of O-acetyl-ADP-ribose hydrolysis by recombinant ARH3 was 250-fold that observed with ARH1; ARH2 and poly(ADP-ribose) glycohydrolase were inactive. All data support the conclusion that the Sir2 reaction product O-acetylADP-ribose is degraded by ARH3. C1 NHLBI, Pulm Crit Care Med Branch, NIH, Bethesda, MD 20892 USA. RP Moss, J (reprint author), NHLBI, Pulm Crit Care Med Branch, NIH, Bldg 10,Room 6D05, Bethesda, MD 20892 USA. EM mossj@nhlbi.nih.gov FU Intramural NIH HHS NR 27 TC 48 Z9 49 U1 0 U2 0 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD NOV 7 PY 2006 VL 103 IS 45 BP 16687 EP 16691 DI 10.1073/pnas.0607911103 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA 104PB UT WOS:000241969500014 PM 17075046 ER PT J AU Vishnyakova, TG Kurlander, R Bocharov, AV Baranova, IN Chen, ZG Abu-Asab, MS Tsokos, M Malide, D Basso, F Remaley, A Csako, G Eggerman, TL Patterson, AP AF Vishnyakova, Tatyana G. Kurlander, Roger Bocharov, Alexander V. Baranova, Irina N. Chen, Zhigang Abu-Asab, Mones S. Tsokos, Maria Malide, Daniela Basso, Federica Remaley, Alan Csako, Gyorgy Eggerman, Thomas L. Patterson, Amy P. TI CLA-1 and its splicing variant CLA-2 mediate bacterial adhesion and cytosolic bacterial invasion in mammalian cells SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE bacterial adhesion; internalization; phagocytes; cytosolic invasion; high-density lipoprotein receptor ID RECEPTOR CLASS-B; HIGH-DENSITY-LIPOPROTEIN; SERUM-AMYLOID-A; SCAVENGER RECEPTOR; BINDING; HDL; LIPOPOLYSACCHARIDE; RECOGNITION; TRANSPORT; PEPTIDES AB CD36 and LIMPII analog 1, CLA-1, and its splicing variant, CLA-2 (SR-BI and SR-BII in rodents), are human high density lipoprotein receptors with an identical extracellular domain which binds a spectrum of ligands including bacterial cell wall components. In this study, CLA-1- and CLA-2-stably transfected HeLa and HEK293 cells demonstrated several-fold increases in the uptake of various bacteria over mock-transfected cells. All bacteria tested, including both Gram-negatives (Escherichia coli K12, K1 and Salmonella typhimurium) and Gram-positives (Staphylococcus aureus and Listeria monocytogenes), demonstrated various degrees of lower uptake in control cells. This result is consistent with the presence of high-density lipoprotein-receptor-independent bacterial uptake that is enhanced by CLA-1/CLA-2 overexpression. Bacterial lipopolysaccharides, lipoteichoic acid, and synthetic amphipathic helical peptides (L-37pA and D-37pA) competed with E. coli K12 for CLA-1 and CLA-2 binding. Transmission electron microscopy and confocal microscopy revealed cytosolic accumulation of bacteria in CLA-1/CLA-2-overexpressing HeLa cells. The antibiotic protection assay confirmed that E. coli K12 was able to survive and replicate intracellularly in CLA-1- and CLA-2-overexpressing HeLa, but both L-37pA and D-37pA prevented E. coli K12 invasion. Peritoneal macrophages isolated from SR-BI/BII-knockout mice demonstrated a 30% decrease in bacterial uptake when compared with macrophages from normal mice. Knockout macrophages were also characterized by decreased bacterial cytosolic invasion, ubiquitination, and proteasome mobilization while retaining bacterial lysosomal accumulation. These results indicate that, by facilitating bacterial adhesion and cytosolic invasion, CLA-1 and CLA-2 may play an important role in infection and sepsis. C1 NIH, Ctr Clin, Dept Lab Med, Bethesda, MD 20892 USA. NHLBI, Light Microscopy Core Facil, NIH, Bethesda, MD 20892 USA. NCI, NIH, Bethesda, MD 20892 USA. NIDDKD, NIH, Div Diabet Endocrinol & Metab Dis, Bethesda, MD 20892 USA. RP Bocharov, AV (reprint author), NIH, Ctr Clin, Dept Lab Med, Bldg 9,Room 1N128,8800 Rockville Pl, Bethesda, MD 20892 USA. EM abocharov@mail.cc.nih.gov OI Abu-Asab, Mones/0000-0002-4047-1232 NR 24 TC 39 Z9 41 U1 0 U2 6 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD NOV 7 PY 2006 VL 103 IS 45 BP 16888 EP 16893 DI 10.1073/pnas.0602126103 PG 6 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA 104PB UT WOS:000241969500048 PM 17071747 ER PT J AU Kamada, K Igarashi, T Martin, MA Khamsri, B Hatcho, K Yamashita, T Fujita, M Uchiyama, T Adachi, A AF Kamada, Kazuya Igarashi, Tatsuhiko Martin, Malcolm A. Khamsri, Boonruang Hatcho, Kazuki Yamashita, Tomoki Fujita, Mikako Uchiyama, Tsuneo Adachi, Akio TI Generation of HIV-1 derivatives that productively infect macaque monkey lymphoid cells SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE APOBEC3; host range; monkey model; TRIM5 alpha; cyclophilin A ID HUMAN-IMMUNODEFICIENCY-VIRUS; RHESUS-MONKEYS; CYCLOPHILIN-A; VIF PROTEIN; NEUTRALIZING ANTIBODIES; ENZYME APOBEC3G; TRIM5-ALPHA; GENE; REGION; AIDS AB The narrow host range of human immunodeficiency virus type 1 (HIV-1) is caused in part by innate cellular factors such as apolipoprotein B mRNA-editing enzyme-catalytic polypeptide-like 3G (APOBEC3G) and TRIM5 alpha, which restrict virus replication in monkey cells. Variant HIV-1 molecular clones containing both a 21-nucleotide simian immunodeficiency virus (SIV) Gag CA element, corresponding to the HIV-1 cyclophilin A-binding site, and the entire SIV vif gene were constructed. Long-term passage in a cynomolgus monkey lymphoid cell line resulted in the acquisition of two nonsynonymous changes in env, which conferred improved replication properties. A proviral molecular clone, derived from infected cells and designated NL-DT5R, was used to generate virus stocks capable of establishing spreading infections in the cynomolgus monkey T cell line and CD8-depleted peripheral blood mononuclear cells from five of five pig-tailed macaques and one of three rhesus monkeys. NL-DT5R, which genetically is > 93% HIV-1, provides the opportunity, not possible with currently available SIV/HIV chimeric viruses, to analyze the function of multiple HIV-1 genes in a broad range of nonhuman primate species. C1 NIAID, Mol Microbiol Lab, NIH, Bethesda, MD 20892 USA. Univ Tokushima, Grad Sch, Inst Hlth Biosci, Dept Virol, Tokushima 7708503, Japan. RP Martin, MA (reprint author), NIAID, Mol Microbiol Lab, NIH, Bldg 4,Room 315, Bethesda, MD 20892 USA. EM mmartin@niaid.nih.gov; adachi@basic.med.tokushima-u.ac.jp FU Intramural NIH HHS NR 38 TC 75 Z9 81 U1 0 U2 1 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD NOV 7 PY 2006 VL 103 IS 45 BP 16959 EP 16964 DI 10.1073/pnas.0608289103 PG 6 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA 104PB UT WOS:000241969500060 PM 17065315 ER PT J AU Tiwari, S Zhang, YW Hellert, J Abernethy, DR Soldatov, NM AF Tiwari, Swasti Zhang, Yuwei Hellert, Jennifer Abernethy, Darrell R. Soldatov, Nikolai M. TI Atherosclerosis-related molecular alteration of the human Ca(V)1.2 calcium channel alpha(1C) subunit SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE alternative splicing; cell proliferation; vascular smooth muscle cells ID SMOOTH-MUSCLE-CELLS; CA2+ CHANNEL; SUBUNIT GENE; FUNCTIONAL EXPRESSION; ALPHA(1) SUBUNIT; INHIBITION; DIHYDROPYRIDINES; DIFFERENTIATION; DETERMINANTS; LOCALIZATION AB Atherosclerosis is an inflammatory process characterized by proliferation and dedifferentiation of vascular smooth muscle cells (VSMC). Ca(v)1.2 calcium channels may have a role in atherosclerosis because they are essential for Ca2+-signal transduction in VSMC. The pore-forming Ca(v)1.2 alpha 1 subunit of the channel is subject to alternative splicing. Here, we investigated whether the Cav1.2a1 splice variants are affected by atherosclerosis. VSMC were isolated by laser-capture microdissection from frozen sections of adjacent regions of arteries affected and not affected by atherosclerosis. In VSMC from nonatherosclerotic regions, RT-PCR analysis revealed an extended repertoire of Cav1.2a1 transcripts characterized by the presence of exons 21 and 41A. In VSMC affected by atherosclerosis, expression of the Ca(v)1.2 alpha 1 transcript was reduced and the Ca(v)1.2a1 splice variants were replaced with the unique exon-22 isoform lacking exon 41A. Molecular remodeling of the Cav1.2a1 subunits associated with atherosclerosis caused changes in electrophysiological properties of the channels, including the kinetics and voltage-dependence of inactivation, recovery from inactivation, and rundown of the Ca2+ current. Consistent with the pathophysiological state of VSMC in atherosclerosis, cell culture data pointed to a potentially important association of the exon-22 isoform of Ca(v)1.2 alpha 1 with proliferation of VSMC. Our findings are consistent with a hypothesis that localized changes in cytokine expression generated by inflammation in atherosclerosis affect alternative splicing of the Ca(v)1.2 alpha 1 gene in the human artery that causes molecular and electrophysiological remodeling of Ca(v)1.2 calcium channels and possibly affects VSMC proliferation. C1 NIA, NIH, Baltimore, MD 21224 USA. Johns Hopkins Bayview Med Ctr, Div Vasc Surg, Baltimore, MD 21224 USA. RP Soldatov, NM (reprint author), NIA, NIH, 5600 Nathan Shock Dr, Baltimore, MD 21224 USA. EM soldatovn@grc.nia.nih.gov FU Intramural NIH HHS NR 38 TC 36 Z9 42 U1 1 U2 1 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD NOV 7 PY 2006 VL 103 IS 45 BP 17024 EP 17029 DI 10.1073/pnas.0606539103 PG 6 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA 104PB UT WOS:000241969500071 PM 17071743 ER PT J AU Duran, I Kortmansky, J Singh, D Hirte, H Kocha, W Goss, G Le, L Oza, A Nicklee, T Ho, J Birle, D Pond, GR Arboine, D Dancey, J Aviel-Ronen, S Tsao, MS Hedley, D Siu, LL AF Duran, I. Kortmansky, J. Singh, D. Hirte, H. Kocha, W. Goss, G. Le, L. Oza, A. Nicklee, T. Ho, J. Birle, D. Pond, G. R. Arboine, D. Dancey, J. Aviel-Ronen, S. Tsao, M-S Hedley, D. Siu, L. L. TI A phase II clinical and pharmacodynamic study of temsirolimus in advanced neuroendocrine carcinomas SO BRITISH JOURNAL OF CANCER LA English DT Article; Proceedings Paper CT AACR/NCI/EORTC International Conference on Molecular Targets and Cancer Therapeutics CY NOV 14-18, 2005 CL Philadelphia, PA SP AACR, NCI, EORTC, AMGEN, AstraZeneca, Britol-Myers Squibb Co, Pfizer, Sanofi Aventis, Bayer Hlth Car Pharmaceut, Lilly, Genentech, GSK GlaxoSmithKline, Johnson &Johnson, MERCK, NOVARTIS ONCOL, Centocor, OSI Oncol, Schering-Plough, BTG, Servier, RADPHARM, Cvitkovic & Associes DE mTOR; neuroendocrine carcinoma; phase II; pS6; temsirolimus ID ISLET-CELL-CARCINOMA; DOXORUBICIN THERAPY; ONCOLOGY-GROUP; MTOR; STREPTOZOCIN; TUMORS; CCI-779; FLUOROURACIL; INHIBITOR; KINASE AB Standard cytotoxic treatments for neuroendocrine tumours have been associated with limited activity and remarkable toxicity. A phase II study was designed to evaluate the efficacy, safety and pharmacodynamics of temsirolimus in patients with advanced neuroendocrine carcinoma (NEC). Thirty-seven patients with advanced progressive NEC received intravenous weekly doses of 25 mg of temsirolimus. Patients were evaluated for tumour response, time to progression (TTP), overall survival (OS) and adverse events (AE). Twenty-two archival specimens, as well as 13 paired tumour biopsies obtained pretreatment and after 2 weeks of temsirolimus were assessed for potential predictive and correlative markers. The intent-to-treat response rate was 5.6% (95% CI 0.6-18.7%), median TTP 6 months and 1-year OS rate 71.5%. The most frequent drug-related AE of all grades as percentage of patients were: fatigue (78%), hyperglycaemia (69%) and rash/desquamation (64%). Temsirolimus effectively inhibited the phosphorylation of S6 (P=0.02). Higher baseline levels of pmTOR (phosphorylated mammalian target of rapamycin) (P=0.01) predicted for a better response. Increases in pAKT (P=0.041) and decreases in pmTOR (P=0.048) after treatment were associated with an increased TTP. Temsirolimus appears to have little activity and does not warrant further single-agent evaluation in advanced NEC. Pharmacodynamic analysis revealed effective mTOR pathway downregulation. C1 Princess Margaret Hosp, Dept Med Oncol & Hematol, Toronto, ON M5G 2M9, Canada. Mem Sloan Kettering Canc Ctr, New York, NY 10021 USA. Univ Chicago, Chicago, IL 60637 USA. NCI, Bethesda, MD 20892 USA. RP Siu, LL (reprint author), Princess Margaret Hosp, Dept Med Oncol & Hematol, 2 Consortium,610 Univ Ave,Suite 5-718, Toronto, ON M5G 2M9, Canada. EM lillian.siu@uhn.on.ca FU NCI NIH HHS [N01-CM-17107, N01-CO-124001] NR 29 TC 203 Z9 210 U1 0 U2 5 PU NATURE PUBLISHING GROUP PI LONDON PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND SN 0007-0920 J9 BRIT J CANCER JI Br. J. Cancer PD NOV 6 PY 2006 VL 95 IS 9 BP 1148 EP 1154 DI 10.1038/sj.bjc.6603419 PG 7 WC Oncology SC Oncology GA 101PC UT WOS:000241751700005 PM 17031397 ER PT J AU Garcia-Closas, M Brinton, LA Anderson, WF Sherman, ME AF Garcia-Closas, M. Brinton, L. A. Anderson, W. F. Sherman, M. E. TI Reply: Study design and statistics in epidemiology of breast cancer SO BRITISH JOURNAL OF CANCER LA English DT Letter C1 NCI, Div Canc Epidemiol & Genet, NIH, Rockville, MD 20852 USA. RP Garcia-Closas, M (reprint author), NCI, Div Canc Epidemiol & Genet, NIH, 6120 Exective Blvd Execut Pl S,Room 7076,MSC 7234, Rockville, MD 20852 USA. EM montse@nih.gov RI Garcia-Closas, Montserrat /F-3871-2015; Brinton, Louise/G-7486-2015 OI Garcia-Closas, Montserrat /0000-0003-1033-2650; Brinton, Louise/0000-0003-3853-8562 NR 5 TC 0 Z9 0 U1 0 U2 0 PU NATURE PUBLISHING GROUP PI LONDON PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND SN 0007-0920 J9 BRIT J CANCER JI Br. J. Cancer PD NOV 6 PY 2006 VL 95 IS 9 BP 1302 EP 1303 DI 10.1038/sj.bjc.6603371 PG 2 WC Oncology SC Oncology GA 101PC UT WOS:000241751700031 ER PT J AU Varnai, P Thyagarajan, B Rohacs, T Balla, T AF Varnai, Peter Thyagarajan, Baskaran Rohacs, Tibor Balla, Tamas TI Rapidly inducible changes in phosphatidylinositol 4,5-bisphosphate levels influence multiple regulatory functions of the lipid in intact living cells SO JOURNAL OF CELL BIOLOGY LA English DT Article ID INOSITOL-POLYPHOSPHATE 5-PHOSPHATASE; ION CHANNELS; MEMBRANE; RECEPTOR; DOMAIN; ACTIVATION; BINDING; TRPM8; 1,4,5-TRISPHOSPHATE; PI(4,5)P-2 AB Rapamycin (rapa)-induced heterodimerization of the FRB domain of the mammalian target of rapa and FKBP12 was used to translocate a phosphoinositide 5-phosphatase (5-ptase) enzyme to the plasma membrane (PM) to evoke rapid changes in phosphatidylinositol 4,5-bisphosphate (PtdIns(4,5) P-2) levels. Rapa-induced PM recruitment of a truncated type IV 5-ptase containing only the 5-ptase domain fused to FKBP12 rapidly decreased PM PtdIns(4,5) P-2 as monitored by the PLC delta 1PH-GFP fusion construct. This decrease was paralleled by rapid termination of the ATP-induced Ca2+ signal and the prompt inactivation of menthol-activated transient receptor potential melastatin 8 (TRPM8) channels. Depletion of PM PtdIns(4,5) P-2 was associated with a complete blockade of transferrin uptake and inhibition of epidermal growth factor internalization. None of these changes were observed upon rapa-induced translocation of an mRFP-FKBP12 fusion protein that was used as a control. These data demonstrate that rapid inducible depletion of PM PtdIns(4,5) P-2 is a powerful tool to study the multiple regulatory roles of this phospholipid and to study differential sensitivities of various processes to PtdIns(4,5) P-2 depletion. C1 NICHHD, Endocrinol & Reprod Res Branch, NIH, Bethesda, MD 20892 USA. Semmelweis Univ, Sch Med, Dept Physiol, H-1085 Budapest, Hungary. Univ Med & Dent New Jersey, New Jersey Med Sch, Dept Pharmacol & Physiol, Newark, NJ 07103 USA. RP Balla, T (reprint author), NICHHD, Endocrinol & Reprod Res Branch, NIH, Bethesda, MD 20892 USA. EM ballat@mail.nih.gov OI Balla, Tamas/0000-0002-9077-3335 FU Intramural NIH HHS NR 28 TC 203 Z9 208 U1 1 U2 5 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 1114 FIRST AVE, 4TH FL, NEW YORK, NY 10021 USA SN 0021-9525 J9 J CELL BIOL JI J. Cell Biol. PD NOV 6 PY 2006 VL 175 IS 3 BP 377 EP 382 DI 10.1083/jcb.200607116 PG 6 WC Cell Biology SC Cell Biology GA 108BB UT WOS:000242213800002 PM 17088424 ER PT J AU Zaretsky, JZ Barnea, I Aylon, Y Gorivodsky, M Wreschner, DH Keydar, I AF Zaretsky, Joseph Z. Barnea, Itay Aylon, Yael Gorivodsky, Marat Wreschner, Daniel H. Keydar, Iafa TI MUCI gene overexpressed in breast cancer: structure and transcriptional activity of the MUC1 promoter and role of estrogen receptor alpha (ER alpha) in regulation of the MUC1 gene expression SO MOLECULAR CANCER LA English DT Article ID RESPONSE ELEMENTS; EPITHELIAL MUCIN; CARCINOMA-CELLS; PROTEIN; DNA; PROGESTERONE; TAMOXIFEN; ESTRADIOL; ANTIGEN; BINDING AB Background: The MUC1 gene encodes a mucin glycoprotein(s) which is basally expressed in most epithelial cells. In breast adenocarcinoma and a variety of epithelial tumors its transcription is dramatically upregulated. Of particular relevance to breast cancer, steroid hormones also stimulate the expression of the MUC1 gene. The MUC1 gene directs expression of several protein isoforms, which participate in many crucial cell processes. Although the MUC1 gene plays a critical role in cell physiology and pathology, little is known about its promoter organization and transcriptional regulation. The goal of this study was to provide insight into the structure and transcriptional activity of the MUC1 promoter. Results: Using TRANSFAC and TSSG soft-ware programs the transcription factor binding sites of the MUC1 promoter were analyzed and a map of transcription cis-elements was constructed. The effect of different MUC1 promoter regions on MUC1 gene expression was monitored. Different regions of the MUC1 promoter were analyzed for their ability to control expression of specific MUC1 isoforms. Differences in the expression of human MUC1 gene transfected into mouse cells (heterologous artificial system) compared to human cells ( homologous natural system) were observed. The role of estrogen on MUC1 isoform expression in human breast cancer cells, MCF-7 and T47D, was also analyzed. It was shown for the first time that synthesis of MUC1/SEC is dependent on estrogen whereas expression of MUC1/TM did not demonstrate such dependence. Moreover, the estrogen receptor alpha, ER alpha, could bind in vitro estrogen responsive cis-elements, EREs, that are present in the MUC1 promoter. The potential roles of different regions of the MUC1 promoter and ER in regulation of MUC1 gene expression are discussed. Conclusion: Analysis of the structure and transcriptional activity of the MUC1 promoter performed in this study helps to better understand the mechanisms controlling transcription of the MUC1 gene. The role of different regions of the MUC1 promoter in expression of the MUC1 isoforms and possible function of ER alpha in this process has been established. The data obtained in this study may help in development of molecular modalities for controlled regulation of the MUC1 gene thus contributing to progress in breast cancer gene therapy. C1 Tel Aviv Univ, Fac Life Sci, Dept Cell Res & Immunol, IL-69978 Tel Aviv, Israel. Weizmann Inst Sci, Dept Mol & Cell Biol, IL-76100 Rehovot, Israel. NICHD, Lab Mammalian Genes & Dev, Sect Transgene Regulat, NIH, Bethesda, MD 20892 USA. RP Zaretsky, JZ (reprint author), Tel Aviv Univ, Fac Life Sci, Dept Cell Res & Immunol, IL-69978 Tel Aviv, Israel. EM josephz@post.tau.ac.il; barneait@post.tau.ac.il; yael.aylon@weimann.ac.il; gorivodm@mail.nih.gov; danielhw@post.tau.ac.il; keydari@post.tau.ac.il NR 65 TC 36 Z9 39 U1 0 U2 5 PU BIOMED CENTRAL LTD PI LONDON PA MIDDLESEX HOUSE, 34-42 CLEVELAND ST, LONDON W1T 4LB, ENGLAND SN 1476-4598 J9 MOL CANCER JI Mol. Cancer PD NOV 5 PY 2006 VL 5 AR 57 DI 10.1186/1476-4598-5-57 PG 14 WC Biochemistry & Molecular Biology; Oncology SC Biochemistry & Molecular Biology; Oncology GA 113KL UT WOS:000242596700001 PM 17083744 ER PT J AU Hummel, FC Voller, B Celnik, P Floel, A Giraux, P Gerloff, C Cohen, LG AF Hummel, Friedhelm C. Voller, Bernhard Celnik, Pablo Floel, Agnes Giraux, Pascal Gerloff, Christian Cohen, Leonardo G. TI Effects of brain polarization on reaction times and pinch force in chronic stroke SO BMC NEUROSCIENCE LA English DT Article ID TRANSCRANIAL MAGNETIC STIMULATION; NONINVASIVE CORTICAL STIMULATION; FINGER-TAPPING SEQUENCES; MOTOR CORTEX; COPENHAGEN STROKE; SKILL ACQUISITION; ISCHEMIC-STROKE; HAND AREA; GRIP; RELIABILITY AB Background: Previous studies showed that anodal transcranial DC stimulation (tDCS) applied to the primary motor cortex of the affected hemisphere (MI (affected) (hemisphere)) after subcortical stroke transiently improves performance of complex tasks that mimic activities of daily living (ADL). It is not known if relatively simpler motor tasks are similarly affected. Here we tested the effects of tDCS on pinch force (PF) and simple reaction time (RT) tasks in patients with chronic stroke in a double-blind cross-over Sham-controlled experimental design. Results: Anodal tDCS shortened reaction times and improved pinch force in the paretic hand relative to Sham stimulation, an effect present in patients with higher impairment. Conclusion: tDCS of MI (affected) (hemisphere) can modulate performance of motor tasks simpler than those previously studied, a finding that could potentially benefit patients with relatively higher impairment levels. C1 Natl Inst Neurol Disorders & Stroke, Human Cortical Physiol Sect, Bethesda, MD 20892 USA. Natl Inst Neurol Disorders & Stroke, Stroke Neurorehabil Clin, Bethesda, MD 20892 USA. Univ Hamburg Eppendorf, Med Ctr, Dept Neurol, Brain Imaging & Neurostimulat Lab, D-20246 Hamburg, Germany. RP Cohen, LG (reprint author), Natl Inst Neurol Disorders & Stroke, Human Cortical Physiol Sect, Bethesda, MD 20892 USA. EM f.hummel@uke.uni-hamburg.de; bernhard.voller@meduniwien.ac.at; CelnikP@ninds.nih.gov; floeel@uni-muenster.de; pascal.giraux@univ-st-etienne.fr; gerloff@uke.uni-hamburg.de; cohenl@ninds.nih.gov RI Floel, Agnes/A-9426-2017; OI Voller, Bernhard/0000-0001-5809-874X FU Intramural NIH HHS; NICHD NIH HHS [5K12HD001097, K12 HD001097] NR 51 TC 105 Z9 112 U1 0 U2 8 PU BIOMED CENTRAL LTD PI LONDON PA MIDDLESEX HOUSE, 34-42 CLEVELAND ST, LONDON W1T 4LB, ENGLAND SN 1471-2202 J9 BMC NEUROSCI JI BMC Neurosci. PD NOV 3 PY 2006 VL 7 AR 73 DI 10.1186/1471-2202-7-73 PG 10 WC Neurosciences SC Neurosciences & Neurology GA 107HL UT WOS:000242161200001 PM 17083730 ER PT J AU Netzel-Arnett, S Currie, BM Szabo, R Lin, CY Chen, LM Chai, KX Antalis, TM Bugge, TH List, K AF Netzel-Arnett, Sarah Currie, Brooke M. Szabo, Roman Lin, Chen-Yong Chen, Li-Mei Chai, Karl X. Antalis, Toni M. Bugge, Thomas H. List, Karin TI Evidence for a matriptase-prostasin proteolytic cascade regulating terminal epidermal differentiation SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID SERINE-PROTEASE; BARRIER FUNCTION; OVARIAN-CANCER; NETHERTON-SYNDROME; CELLULAR-LOCALIZATION; EPITHELIAL-CELLS; STRATUM-CORNEUM; MESSENGER-RNA; BREAST-CANCER; IN-VIVO AB Recent gene ablation studies in mice have shown that matriptase, a type II transmembrane serine protease, and prostasin, a glycosylphosphatidylinositol-anchored membrane serine protease, are both required for processing of the epidermis-specific polyprotein, profilaggrin, stratum corneum formation, and acquisition of epidermal barrier function. Here we present evidence that matriptase acts upstream of prostasin in a zymogen activation cascade that regulates terminal epidermal differentiation and is required for prostasin zymogen activation. Enzymatic gene trapping of matriptase combined with prostasin immunohistochemistry revealed that matriptase was co-localized with prostasin in transitional layer cells of the epidermis and that the developmental onset of expression of the two membrane proteases was coordinated and correlated with acquisition of epidermal barrier function. Purified soluble matriptase efficiently converted soluble prostasin zymogen to an active two-chain form that formed SDS-stable complexes with the serpin protease nexin-1. Whereas two forms of prostasin with molecular weights corresponding to the prostasin zymogen and active prostasin were present in wild type epidermis, prostasin was exclusively found in the zymogen form in matriptase-deficient epidermis. These data suggest that matriptase, an autoactivating protease, acts upstream from prostasin to initiate a zymogen cascade that is essential for epidermal differentiation. C1 NIDCR, Proteases & Tissue Remodeling Unit, NIH, Bethesda, MD 20892 USA. Univ Maryland, Sch Med, Ctr Vasc & Inflammatory Dis, Washington, DC 20201 USA. Univ Maryland, Sch Med, Dept Physiol, Washington, DC 20201 USA. Georgetown Univ, Med Ctr, Lombardi Canc Ctr, Washington, DC 20007 USA. Univ Cent Florida, Dept Mol Biol & Microbiol, Orlando, FL 32816 USA. RP Bugge, TH (reprint author), NIDCR, Proteases & Tissue Remodeling Unit, NIH, 30 Convent Dr,Rm 211, Bethesda, MD 20892 USA. EM thomas.bugge@nih.gov FU Intramural NIH HHS; NCI NIH HHS [R01 CA098369, CA098369, R01-CA-096851, R01-CA-104944]; NHLBI NIH HHS [HL07698, R01 HL084387]; NICHD NIH HHS [HD40241] NR 43 TC 124 Z9 125 U1 0 U2 3 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD NOV 3 PY 2006 VL 281 IS 44 BP 32941 EP 32945 DI 10.1074/jbc.C600208200 PG 5 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA 099UJ UT WOS:000241621400002 PM 16980306 ER PT J AU Joyce, CW Wagner, EM Basso, F Amar, MJ Freeman, LA Shamburek, RD Knapper, CL Syed, J Wu, J Vaisman, BL Fruchart-Najib, J Billings, EM Paigen, B Remaley, AT Santamarina-Fojo, S Brewer, HB AF Joyce, Charles W. Wagner, Elke M. Basso, Federica Amar, Marcelo J. Freeman, Lita A. Shamburek, Robert D. Knapper, Catherine L. Syed, Jafri Wu, Justina Vaisman, Boris L. Fruchart-Najib, Jamila Billings, Eric M. Paigen, Beverly Remaley, Alan T. Santamarina-Fojo, Silvia Brewer, H. Bryan, Jr. TI ABCA1 overexpression in the liver of LDLr-KO mice leads to accumulation of pro-atherogenic lipoproteins and enhanced atherosclerosis SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID HIGH-DENSITY-LIPOPROTEIN; CASSETTE TRANSPORTER 1; REVERSE CHOLESTEROL TRANSPORT; PLASMA RATIO METHOD; TANGIER-DISEASE; TRANSGENIC MICE; AORTIC ATHEROSCLEROSIS; HEPATIC ABCA1; KNOCKOUT MICE; IN-VIVO AB The identification of ABCA1 as a key transporter responsible for cellular lipid efflux has led to considerable interest in defining its role in cholesterol metabolism and atherosclerosis. In this study, the effect of overexpressing ABCA1 in the liver of LDLr-KO mice was investigated. Compared with LDLr-KO mice, ABCA1-Tg x LDLr-KO (ABCA1-Tg) mice had significantly increased plasma cholesterol levels, mostly because of a 2.8-fold increase in cholesterol associated with a large pool of apoB-lipoproteins. ApoB synthesis was unchanged but the catabolism of I-125-apoB-VLDL and -LDL were significantly delayed, accounting for the 1.35-fold increase in plasma apoB levels in ABCA1-Tg mice. We also found rapid in vivo transfer of free cholesterol from HDL to apoB-lipoproteins in ABCA1-Tg mice, associated with a significant 2.7-fold increase in the LCAT-derived cholesteryl linoleate content found primarily in apoB-lipoproteins. ABCA1-Tg mice had 1.4-fold increased hepatic cholesterol concentrations, leading to a compensatory 71% decrease in de novo hepatic cholesterol synthesis, as well as enhanced biliary cholesterol, and bile acid secretion. CAV-1, CYP2b10, and ABCG1 were significantly induced in ABCA1-overexpressing livers; however, no differences were observed in the hepatic expression of CYP7 alpha 1, CYP27 alpha 1, or ABCG5/G8 between ABCA1-Tg and control mice. As expected from the pro-atherogenic plasma lipid profile, aortic atherosclerosis was increased 10-fold in ABCA1-Tg mice. In summary, hepatic overexpression of ABCA1 in LDLr-KO mice leads to: 1) expansion of the pro-atherogenic apoB-lipoprotein cholesterol pool size via enhanced transfer of HDL-cholesterol to apoB-lipoproteins and delayed catabolism of cholesterol-enriched apoB-lipoproteins; 2) increased cholesterol concentration in the liver, resulting in up-regulated hepatobiliary sterol secretion; and 3) significantly enhanced aortic atherosclerotic lesions. C1 NHLBI, NIH, Mol Dis Sect, Bethesda, MD 20892 USA. NHLBI, NIH, Bioinformat Core Facil, Bethesda, MD 20892 USA. Inst Pasteur, Dept Atherosclerose, F-59019 Lille, France. Cardiovasc Res Inst, Washington, DC 20010 USA. RP Wagner, EM (reprint author), NHLBI, NIH, Mol Dis Sect, Bldg 10,Rm 7N105, Bethesda, MD 20892 USA. EM ewagner@mail.nih.gov NR 65 TC 44 Z9 47 U1 1 U2 6 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD NOV 3 PY 2006 VL 281 IS 44 BP 33053 EP 33065 DI 10.1074/jbc.M604526200 PG 13 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA 099UJ UT WOS:000241621400014 PM 16928680 ER PT J AU Soubias, O Teague, WE Gawrisch, K AF Soubias, Olivier Teague, Walter E. Gawrisch, Klaus TI Evidence for specificity in lipid-rhodopsin interactions SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID PROTEIN-COUPLED RECEPTOR; SEGMENT DISK MEMBRANES; SARCOPLASMIC-RETICULUM; RECOMBINANT MEMBRANES; CANNABINOID RECEPTOR; ANGSTROM RESOLUTION; PHOSPHOLIPIDS; BOVINE; NMR; BACTERIORHODOPSIN AB The interaction of bovine rhodopsin with poly- and monounsaturated lipids was studied by (1)H MAS NMR with magnetization transfer from rhodopsin to lipid. Experiments were conducted on bovine rod outer segment (ROS) disks and on recombinant membranes containing lipids with polyunsaturated, docosahexaenoyl (DHA) chains. Poly- and monounsaturated lipids interact specifically with different sites on the rhodopsin surface. Rates of magnetization transfer from protein to DHA are lipid headgroup-dependent and increased in the sequence PC < PS < PE. Boundary lipids are in fast exchange with the lipid matrix on a time scale of milliseconds or shorter. All rhodopsin photointermediates transferred magnetization preferentially to DHA-containing lipids, but highest rates were observed for Meta-III rhodopsin. The experiments show clearly that the surface of rhodopsin has sites for specific interaction with lipids. Current theories of lipid-protein interaction do not account for such surface heterogeneity. C1 NIAAA, NMR Sect, Lab Membrane Biochem & Biophys, NIH, Bethesda, MD 20892 USA. RP Gawrisch, K (reprint author), NIAAA, NMR Sect, Lab Membrane Biochem & Biophys, NIH, 5625 Fishers Lane, Bethesda, MD 20892 USA. EM gawrisch@helix.nih.gov FU Intramural NIH HHS NR 47 TC 57 Z9 58 U1 0 U2 11 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD NOV 3 PY 2006 VL 281 IS 44 BP 33233 EP 33241 DI 10.1074/jbc.M603059200 PG 9 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA 099UJ UT WOS:000241621400032 PM 16959786 ER PT J AU Morrison, AR Moss, J Stevens, LA Evans, JE Farrell, C Merithew, E Lambright, DG Greiner, DL Mordes, JP Rossini, AA Bortell, R AF Morrison, Alan R. Moss, Joel Stevens, Linda A. Evans, James E. Farrell, Caitlin Merithew, Eric Lambright, David G. Greiner, Dale L. Mordes, John P. Rossini, Aldo A. Bortell, Rita TI ART2, a T cell surface mono-ADP-ribosyltransferase, generates extracellular poly(ADP-ribose) SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID POLY(ADENOSINE DIPHOSPHATE RIBOSE); NICOTINAMIDE ADENINE-DINUCLEOTIDE; CRYSTAL-STRUCTURE; NAD GLYCOHYDROLASE; IN-VITRO; RAT; RIBOSYLATION; RT6; POLYMERASE; ACTIVATION AB NAD functions in multiple aspects of cellular metabolism and signaling through enzymes that covalently transfer ADP-ribose from NAD to acceptor proteins, thereby altering their function. NAD is a substrate for two enzyme families, mono-ADP-ribosyltransferases (mARTs) and poly(ADP-ribose) polymerases (PARPs), that covalently transfer an ADP-ribose monomer or polymer, respectively, to acceptor proteins. ART2, a mART, is a phenotypic marker of immunoregulatory cells found on the surface of T lymphocytes, including intestinal intraepithelial lymphocytes (IELs). We have shown that the auto-ADP-ribosylation of the ART2.2 allelic protein is multimeric. Our backbone structural alignment of ART2 (two alleles of the rat art2 gene have been reported, for simplicity, the ART2.2 protein investigated in this study will be referred to as ART2) and PARP suggested that multimeric auto-ADP-ribosylation of ART2 may represent an ADP-ribose polymer, rather than multiple sites of mono-ADP-ribosylation. To investigate this, we used highly purified recombinant ART2 and demonstrated that ART2 catalyzes the formation of an ADP-ribose polymer by sequencing gel and by HPLC and MS/MS mass spectrometry identification of PR-AMP, a breakdown product specific to poly(ADP-ribose). Furthermore, we identified the site of ADP-ribose polymer attachment on ART2 as Arg-185, an arginine in a crucial loop of its catalytic core. We found that endogenous ART2 on IELs undergoes multimeric auto-ADP-ribosylation more efficiently than ART2 on peripheral T cells, suggesting that these distinct lymphocyte populations differ in their ART2 surface topology. Furthermore, ART2.2 IELs are more resistant to NAD-induced cell death than ART2.1 IELs that do not have multimeric auto-ADP-ribosylation activity. The data suggest that capability of polymerizing ADP-ribose may not be unique to PARPs and that poly(ADP-ribosylation), an established nuclear activity, may occur extracellularly and modulate cell function. C1 Univ Massachusetts, Sch Med, Dept Med, Worcester, MA 01605 USA. Univ Massachusetts, Sch Med, Dept Mol Pharmacol & Biochem, Worcester, MA 01605 USA. NHLBI, Pulm & Crit Care Med Branch, NIH, Bethesda, MD 20892 USA. RP Bortell, R (reprint author), Diabet Div, Suite 218,373 Plantat St, Worcester, MA 01605 USA. EM rita.bortell@umassmed.edu FU Intramural NIH HHS; NIDDK NIH HHS [DK25306, DK32520, DK36024, DK49106] NR 37 TC 15 Z9 16 U1 0 U2 4 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD NOV 3 PY 2006 VL 281 IS 44 BP 33363 EP 33372 DI 10.1074/jbc.M607259200 PG 10 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA 099UJ UT WOS:000241621400046 PM 16931513 ER PT J AU Pu, YM Peach, ML Garfield, SH Wincovitch, S Marquez, VE Blumberg, PM AF Pu, Yongmei Peach, Megan L. Garfield, Susan H. Wincovitch, Stephen Marquez, Victor E. Blumberg, Peter M. TI Effects on ligand interaction and membrane translocation of the positively charged arginine residues situated along the C1 domain binding cleft in the atypical protein kinase C isoforms SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID PHORBOL 12-MYRISTATE 13-ACETATE; PKC-IOTA; NUCLEAR IMPORT; LUNG-CANCER; ESTER; DELTA; ZETA; INHIBITION; ALPHA; DIFFERENTIATION AB The C1 domain zinc finger structure is highly conserved among the protein kinase C (PKC) superfamily members. As the interaction site for the second messenger sn-1,2-diacylglycerol (DAG) and for the phorbol esters, the C1 domain has been an important target for developing selective ligands for different PKC isoforms. However, the C1 domains of the atypical PKC members are DAG/phorbol ester-insensitive. Compared with the DAG/phorbol ester-sensitive C1 domains, the rim of the binding cleft of the atypical PKC C1 domains possesses four additional positively charged arginine residues ( at positions 7, 10, 11, and 20). In this study, we showed that mutation to arginines of the four corresponding sites in the C1b domain of PKC delta abolished its high potency for phorbol 12,13-dibutyrate in vitro, with only marginal remaining activity for phorbol 12-myristate 13-acetate in vivo. We also demonstrated both in vitro and in vivo that the loss of potency to ligands was cumulative with the introduction of the arginine residues along the rim of the binding cavity rather than the consequence of loss of a single, specific residue. Computer modeling reveals that these arginine residues reduce access of ligands to the binding cleft and change the electrostatic profile of the C1 domain surface, whereas the basic structure of the binding cleft is still maintained. Finally, mutation of the four arginine residues of the atypical PKC C1 domains to the corresponding residues in the delta C1b domain conferred response to phorbol ester. We speculate that the arginine residues of the C1 domain of atypical PKCs may provide an opportunity for the design of ligands selective for the atypical PKCs. C1 NCI, Cellular Carcinogenesis & Tumor Promot Lab, NIH, Bethesda, MD 20892 USA. NCI, Expt Carcinogenesis Lab, Ctr Canc Res, NIH, Bethesda, MD 20892 USA. NCI, Basic Res Program, SAIC Frederick Inc, Frederick, MD 21702 USA. NCI, Med Chem Lab, Ctr Canc Res, Frederick, MD 21702 USA. RP Blumberg, PM (reprint author), NCI, Cellular Carcinogenesis & Tumor Promot Lab, NIH, Bldg 37,Rm 4048,37 Convent Dr,MSC 4255, Bethesda, MD 20892 USA. EM blumberp@dc37a.nci.nih.gov FU Intramural NIH HHS; NCI NIH HHS [N01-CO-12400] NR 50 TC 28 Z9 28 U1 0 U2 5 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD NOV 3 PY 2006 VL 281 IS 44 BP 33773 EP 33788 DI 10.1074/jbc.M606560200 PG 16 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA 099UJ UT WOS:000241621400084 PM 16950780 ER PT J AU Stockwin, LH Blonder, J Bumke, MA Lucas, DA Chan, KC Conrads, TP Issaq, HJ Veenstra, TD Newton, DL Rybak, SM AF Stockwin, Luke H. Blonder, Josip Bumke, Maja A. Lucas, David A. Chan, King C. Conrads, Thomas P. Issaq, Haleem J. Veenstra, Timothy D. Newton, Dianne L. Rybak, Susanna M. TI Proteomic analysis of plasma membrane from hypoxia-adapted malignant melanoma SO JOURNAL OF PROTEOME RESEARCH LA English DT Article DE quantitative proteomics; O-16/O-18 stable isotope labeling; plasma membrane; malignant melanoma; hypoxia ID MASS-SPECTROMETRY; CELL-PROLIFERATION; ADHESION MOLECULE; TUMOR OXYGENATION; AMINOPEPTIDASE-N; ANALYSIS REVEALS; GENE-EXPRESSION; YEAST PROTEOME; SOLID TUMORS; GROWTH AB Hypoxic conditions often persist within poorly vascularized tumors. At the cellular level constitutive activation of transcriptional regulators of the hypoxic response leads to the emergence of clones with aggressive phenotypes. The primary interface between the cell and the hypoxic environment is the plasma membrane. A detailed investigation of this organelle is expected to yield further targets for therapeutic perturbation of the response to hypoxia. In the present study, quantitative proteomic analysis of plasma membrane from hypoxia-adapted murine B16F10 melanoma was performed using differential O-16/O-18 stable isotopic labeling and multidimensional liquid chromatography-tandem mass spectrometry. The analysis resulted in the identification of 24,853 tryptic peptides, providing quantitative information for 2,433 proteins. For a subset of plasma membrane and secreted proteins, quantitative RT-PCR was used to gain further insight into the genomic regulatory events underlying the response to hypoxia. Consistent increases at the proteomic and transcriptomic levels were observed for aminopeptidase N (CD13), carbonic anhydrase IX, potassium-transporting ATPase, matrix metalloproteinase 9, and stromal cell derived factor I ( SDF-1). Antibody-based analysis of a panel of human melanoma cell lines confirmed that CD13 and SDF-1 were consistently upregulated during hypoxia. This study provides the basis for the discovery of novel hypoxia-induced membrane proteins. C1 SAIC Frederick Inc, Drug Mech Grp, Frederick, MD USA. SAIC Frederick Inc, Lab Prote & Analyt Technol, Frederick, MD USA. NCI, Dev Therapeut Program, Div Canc Treatment & Diagnosis, Frederick, MD 21702 USA. RP Stockwin, LH (reprint author), SAIC Frederick Inc, Drug Mech Grp, Frederick, MD USA. EM Stockwin@ncifcrf.gov FU NCI NIH HHS [N01-CO-12400] NR 63 TC 40 Z9 43 U1 1 U2 3 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA SN 1535-3893 J9 J PROTEOME RES JI J. Proteome Res. PD NOV 3 PY 2006 VL 5 IS 11 BP 2996 EP 3007 DI 10.1021/pr0601739 PG 12 WC Biochemical Research Methods SC Biochemistry & Molecular Biology GA 101QL UT WOS:000241755400013 PM 17081051 ER PT J AU Agnati, LF Ferre, S Genedani, S Leo, G Guidolin, D Filaferro, M Carriba, P Casado, V Lluis, C Franco, R Woods, AS Fuxe, K AF Agnati, Luigi F. Ferre, Sergi Genedani, Susanna Leo, Giuseppina Guidolin, Diego Filaferro, Monica Carriba, Paulina Casado, Vicent Lluis, Carme Franco, Rafael Woods, Amina S. Fuxe, Kjell TI Allosteric modulation of dopamine D-2 receptors by homocysteine SO JOURNAL OF PROTEOME RESEARCH LA English DT Article DE homocysteine; dopamine D-2 receptor; allosteric modulation; mass spectrometry; Parkinson's disease ID ADENOSINE A(2A) RECEPTORS; PARKINSONS-DISEASE; INTEGRATIVE MECHANISM; PLASMA HOMOCYSTEINE; ALZHEIMERS-DISEASE; D-2 RECEPTORS; CELLS; GLUTAMATE; LEVODOPA; HYPERHOMOCYSTEINAEMIA AB It has been suggested that L-DOPA-induced hyperhomocysteinemia can increase the risk of stroke, heart disease, and dementia and is an additional pathogenetic factor involved in the progression of Parkinson's disease. In Chinese hamster ovary (CHO) cells stably cotransfected with adenosine A(2A) and dopamine D-2 receptors, homocysteine selectively decreased the ability of D-2 receptor stimulation to internalize adenosine A(2A)-dopamine D-2 receptor complexes. Radioligand-binding experiments in the same cell line demonstrated that homocysteine acts as an allosteric D-2 receptor antagonist, by selectively reducing the affinity of D-2 receptors for agonists but not for antagonists. Mass spectrometric analysis showed that, by means of an arginine (Arg)-thiol electrostatic interaction, homocysteine forms noncovalent complexes with the two Arg-rich epitopes of the third intracellular loop of the D-2 receptor, one of them involved in A(2A)-D-2 receptor heteromerization. However, homocysteine was unable to prevent or disrupt A(2A)-D-2 receptor heteromerization, as demonstrated with Fluorescence Resonance Energy Transfer (FRET) experiments in stably cotransfected HEK cells. The present results could have implications for Parkinson's disease. C1 Univ Modena, Dept Biomed Sci, Sect Phisiol, I-41100 Modena, Italy. NIDA, Behav Neurosci Branch, IRP, NIH,DHHS, Baltimore, MD 21224 USA. Univ Barcelona, Dept Biochem & Mol Biol, E-08028 Barcelona, Spain. Karolinska Inst, Dept Neurosci, S-17177 Stockholm, Sweden. RP Agnati, LF (reprint author), Univ Modena, Dept Biomed Sci, Sect Phisiol, Via Campi 287, I-41100 Modena, Italy. EM luigiagnati@tin.it RI Ferre, Sergi/K-6115-2014; Franco, Rafael/C-3694-2015; Genedani, Susanna/K-4370-2016; Casado, Vicent/K-1660-2014; OI Ferre, Sergi/0000-0002-1747-1779; Franco, Rafael/0000-0003-2549-4919; Genedani, Susanna/0000-0003-1526-153X; Casado, Vicent/0000-0002-1764-3825; Guidolin, Diego/0000-0003-2133-3552 FU Intramural NIH HHS NR 44 TC 30 Z9 30 U1 0 U2 0 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA SN 1535-3893 J9 J PROTEOME RES JI J. Proteome Res. PD NOV 3 PY 2006 VL 5 IS 11 BP 3077 EP 3083 DI 10.1021/pr0601382 PG 7 WC Biochemical Research Methods SC Biochemistry & Molecular Biology GA 101QL UT WOS:000241755400021 PM 17081059 ER PT J AU Chi, A Valencia, JC Hu, ZZ Watabe, H Yamaguchi, H Mangini, NJ Huang, HZ Canfield, VA Cheng, KC Yang, F Abe, R Yamagishi, S Shabanowitz, J Hearing, VJ Wu, C Appella, E Hunt, DF AF Chi, An Valencia, Julio C. Hu, Zhang-Zhi Watabe, Hidenori Yamaguchi, Hiroshi Mangini, Nancy J. Huang, Hongzhan Canfield, Victor A. Cheng, Keith C. Yang, Feng Abe, Riichiro Yamagishi, Shoichi Shabanowitz, Jeffrey Hearing, Vincent J. Wu, Cathy Appella, Ettore Hunt, Donald F. TI Proteomic and bioinformatic characterization of the biogenesis and function of melanosomes SO JOURNAL OF PROTEOME RESEARCH LA English DT Article DE proteomics; organelles; lysosome related; biogenesis ID OCULOCUTANEOUS ALBINISM TYPE-1; TANDEM MASS-SPECTROMETRY; MYOSIN VA; ORGANELLE PROTEOMICS; HUMAN MELANOCYTES; SEPIA-EUMELANIN; IN-VIVO; TYROSINASE; PROTEINS; IDENTIFICATION AB Melanin, which is responsible for virtually all visible skin, hair, and eye pigmentation in humans, is synthesized, deposited, and distributed in subcellular organelles termed melanosomes. A comprehensive determination of the protein composition of this organelle has been obstructed by the melanin present. Here, we report a novel method of removing melanin that includes in-solution digestion and immobilized metal affinity chromatography ( IMAC). Together with in-gel digestion, this method has allowed us to characterize melanosome proteomes at various developmental stages by tandem mass spectrometry. Comparative profiling and functional characterization of the melanosome proteomes identified similar to 1500 proteins in melanosomes of all stages, with similar to 600 in any given stage. These proteins include 16 homologous to mouse coat color genes and many associated with human pigmentary diseases. Approximately 100 proteins shared by melanosomes from pigmented and nonpigmented melanocytes define the essential melanosome proteome. Proteins validated by confirming their intracellular localization include PEDF (pigment-epithelium derived factor) and SLC24A5 (sodium/potassium/calcium exchanger 5, NCKX5). The sharing of proteins between melanosomes and other lysosome-related organelles suggests a common evolutionary origin. This work represents a model for the study of the biogenesis of lysosome-related organelles. C1 NIH, Cell Biol Lab, Bethesda, MD 20892 USA. Univ Virginia, Dept Chem, Charlottesville, VA 22904 USA. Georgetown Univ, Med Ctr, Washington, DC 20007 USA. Indiana Univ, Sch Med NW, Gary, IN 46408 USA. Penn State Univ, Coll Med, Dept Pharmacol, Hershey, PA 17033 USA. Penn State Univ, Coll Med, Jake Gittlen Canc Res Fdn, Hershey, PA 17033 USA. Hokkaido Univ, Grad Sch, Dept Dermatol, Sapporo, Hokkaido, Japan. Kurume Univ, Sch Med, Kurume, Fukuoka 830, Japan. Univ Virginia, Dept Pathol, Charlottesville, VA 22908 USA. RP Appella, E (reprint author), NIH, Cell Biol Lab, Bldg 37,Room 2140, Bethesda, MD 20892 USA. EM appellae@nih.gov; dfh@virginia.edu RI Crozier, Laura/A-4821-2010; Cheng, Keith/B-6506-2011; Abe, Riichiro/A-5450-2012; Hunt, Donald/I-6936-2012 OI Hunt, Donald/0000-0003-2815-6368 FU NCRR NIH HHS [RR01744]; NHGRI NIH HHS [U01-HG02712]; NICHD NIH HHS [HD40179]; NIGMS NIH HHS [GM 37537] NR 49 TC 106 Z9 194 U1 1 U2 13 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA SN 1535-3893 J9 J PROTEOME RES JI J. Proteome Res. PD NOV 3 PY 2006 VL 5 IS 11 BP 3135 EP 3144 DI 10.1021/pr060363j PG 10 WC Biochemical Research Methods SC Biochemistry & Molecular Biology GA 101QL UT WOS:000241755400027 PM 17081065 ER PT J AU Butt, RH Lee, MWY Pirshahid, SA Backlund, PS Wood, S Coorssen, JR AF Butt, R. Hussain Lee, Maggie W. Y. Pirshahid, S. Ahmadi Backlund, Peter S. Wood, Stephen Coorssen, Jens R. TI An initial proteomic analysis of human preterm labor: Placental membranes SO JOURNAL OF PROTEOME RESEARCH LA English DT Article DE premature birth; obstetrics; 2D-PAGE; LC-MS/MS; child and maternal health; annexin 4 ID AMINO-ACID SEQUENCE; ANNEXIN-IV; PREMATURE RUPTURE; ENDOTHELIAL-CELLS; MASS-SPECTROMETRY; FETAL FIBRONECTIN; FIBROUS PROTEINS; AMNIOTIC-FLUID; BOVINE AORTA; GLYOXALASE-I AB Human preterm labor (PL) is the single most significant problem in modern Obstetrics and Gynecology, affecting similar to 10% of pregnancies worldwide, constituting the leading cause of perinatal mortality and morbidity, and contributing significantly to chronic childhood disease. Currently, our molecular understanding of PL remains staggeringly inadequate to reliably diagnose or rationally intervene in PL events; several molecular alterations have been implicated in PL, but these have proven of limited value as diagnostic/prognostic markers. The majority of PL events remain spontaneous and unpredictable: critical care emergencies. Here, we apply functional proteomics to dissect molecular mechanisms of human PL. Human placental tissue was collected in clearly differentiated cases of preterm and term labor. Highly refined two-dimensional gel electrophoresis (2DE) was used for protein separation, coupled with automated differential gel image analysis to compare the resulting proteomic maps. For this initial study, only the most important protein differences were selected for further analysis, that is, proteins that were unique to one sample, and absent from the other, with 100% reproducibility across the sample population. In total, 11 such proteins were identified by tandem mass spectrometry, falling into three distinct functional classes: structural/cytoskeletal components, ER lumenal proteins with enzymatic or chaperone functions, and proteins with anticoagulant properties. These expression changes form the groundwork for further molecular investigation of this devastating medical condition. This approach therefore holds the potential not only to define the underlying molecular components, but also to identify novel diagnostic tools and targets for rational drug intervention. C1 Univ Calgary, Fac Med, Dept Physiol & Biophys, Hotchkiss Brain Inst, Calgary, AB T2N 4N1, Canada. Univ Calgary, Fac Med, Dept Biochem & Mol Biol, Hotchkiss Brain Inst, Calgary, AB T2N 4N1, Canada. Univ Calgary, Fac Med, Dept Obstet & Gynecol, Hotchkiss Brain Inst, Calgary, AB T2N 4N1, Canada. Univ Calgary, Fac Med, Dept Cell Biol & Anat, Hotchkiss Brain Inst, Calgary, AB T2N 4N1, Canada. NIHCD, NIH, Bethesda, MD 20892 USA. RP Coorssen, JR (reprint author), Room 174 Heritage Med Res Bldg,3330 Hosp Dr NW, Calgary, AB T2N 4N1, Canada. EM jcoorsse@ucalgary.ca NR 65 TC 30 Z9 31 U1 0 U2 1 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA SN 1535-3893 J9 J PROTEOME RES JI J. Proteome Res. PD NOV 3 PY 2006 VL 5 IS 11 BP 3161 EP 3172 DI 10.1021/pr060282n PG 12 WC Biochemical Research Methods SC Biochemistry & Molecular Biology GA 101QL UT WOS:000241755400030 PM 17081068 ER PT J AU Kang, YH Park, JE Yu, LR Soung, NK Yun, SM Bang, JK Seong, YS Yu, HT Garfield, S Veenstra, TD Lee, KS AF Kang, Young H. Park, Jung-Eun Yu, Li-Rong Soung, Nak-Kyun Yun, Sang-Moon Bang, Jeong K. Seong, Yeon-Sun Yu, Hongtao Garfield, Susan Veenstra, Timothy D. Lee, Kyung S. TI Self-regulated Plk1 recruitment to kinetochores by the Plk1-PBIP1 interaction is critical for proper chromosome segregation SO MOLECULAR CELL LA English DT Article ID POLO-BOX DOMAIN; SPINDLE-CHECKPOINT PROTEINS; KINASE; CELLS; POLO-LIKE-KINASE-1; ASSOCIATION; EXPRESSION; TENSION; COMPLEX; MLF1IP AB The polo-box domain (PBD) of mammalian polo-like kinase 1 (Plk1) is essential in targeting its catalytic activity to specific subcellular structures critical for mitosis. The mechanism underlying Plk1 recruitment to the kinetochores and the role of Plk1 at this site remain elusive. Here, we demonstrate that a PBD-binding protein, PBIP1, is crucial for recruiting Plk1 to the interphase and mitotic kinetochores. Unprecedentedly, Plk1 phosphorylated PBIP1 at T78, creating a self-tethering site that specifically interacted with the PBD of Plk1, but not Plk2 or Plk3. Later in mitosis, Plk1 also induced PBIP1 degradation in a T78-dependent manner, thereby enabling itself to interact with other components critical for proper kinetochore functions. Absence of the p-T78-dependent Plk1 localization induced a chromosome congression defect and compromised the spindle checkpoint, ultimately leading to aneuploidy. Thus, Plk1 self-regulates the Plk1-PBIP1 interaction to timely localize to the kinetochores and promote proper chromosome segregation. C1 NCI, Lab Metab, Ctr Canc Res, Bethesda, MD 20892 USA. NCI, Cell Biol Lab, Ctr Canc Res, Bethesda, MD 20892 USA. NCI, Expt Carcinogenesis Lab, Ctr Canc Res, Bethesda, MD 20892 USA. NCI, Lab Proteom & Analyt Technol, Frederick, MD 21702 USA. Dankook Univ, Coll Med, Dept Biochem, Chunan 330714, South Korea. Univ Texas, SW Med Ctr, Dept Pharmacol, Dallas, TX 75390 USA. RP Lee, KS (reprint author), NCI, Lab Metab, Ctr Canc Res, Bethesda, MD 20892 USA. EM kyunglee@mail.nih.gov FU Intramural NIH HHS; NCI NIH HHS [R01 CA115884, R01 CA75638] NR 21 TC 146 Z9 151 U1 1 U2 7 PU CELL PRESS PI CAMBRIDGE PA 1100 MASSACHUSETTS AVE, CAMBRIDGE, MA 02138 USA SN 1097-2765 J9 MOL CELL JI Mol. Cell PD NOV 3 PY 2006 VL 24 IS 3 BP 409 EP 422 DI 10.1016/j.molcel.2006.10.016 PG 14 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA 103EW UT WOS:000241869500008 PM 17081991 ER PT J AU Freed, EO Mouland, AJ AF Freed, Eric O. Mouland, Andrew J. TI The cell biology of HIV-I and other retroviruses SO RETROVIROLOGY LA English DT Review ID IMMUNODEFICIENCY-VIRUS TYPE-1; ROUS-SARCOMA-VIRUS; 5' RNA TERMINUS; PLASMA-MEMBRANE; CYCLOPHILIN-A; MESSENGER-RNA; GENOMIC RNAS; ESCRT-III; GAG; INTEGRATION AB In recognition of the growing influence of cell biology in retrovirus research, we recently organized a Summer conference sponsored by the American Society for Cell Biology (ASCB) on the Cell Biology of HIV-1 and other Retroviruses (July20-23, 2006, Emory University, Atlanta, Georgia). The meeting brought together a number of leading investigators interested in the interplay between cell biology and retrovirology with an emphasis on presentation of new and unpublished data. The conference was arranged from early to late events in the virus replication cycle, with sessions on viral fusion, entry, and transmission; post-entry restrictions to retroviral infection; nuclear import and integration; gene expression/regulation of retroviral Gag and genomic RNA; and assembly/release. In this review, we will attempt to touch briefly on some of the highlights of the conference, and will emphasize themes and trends that emerged at the meeting. Meeting report: The conference began with a keynote address from W. Sundquist on the biochemistry of HIV-1 budding. This presentation will be described in the section on Assembly and Release of Retroviruses. C1 McGill Univ, HIV1 RNA Trafficking Lab, Lady Davis Inst Med Res, Sir Mortimer B Davis Jewish Gen Hosp,Dept Med, Montreal, PQ H3T 1E2, Canada. NCI, Virus Cell Interact Sect, HIV Drug Resistance Program, Frederick, MD 21702 USA. McGill Univ, HIV1 RNA Trafficking Lab, Lady Davis Inst Med Res,Dept Microbiol, Sir Mortimer B Davis Jewish Gen Hosp, Montreal, PQ H3T 1E2, Canada. McGill Univ, HIV1 RNA Trafficking Lab, Lady Davis Inst Med Res,Dept Immunol, Sir Mortimer B Davis Jewish Gen Hosp, Montreal, PQ H3T 1E2, Canada. RP Freed, EO (reprint author), McGill Univ, HIV1 RNA Trafficking Lab, Lady Davis Inst Med Res, Sir Mortimer B Davis Jewish Gen Hosp,Dept Med, Montreal, PQ H3T 1E2, Canada. EM efreed@nih.gov; andrew.mouland@McGill.ca FU Intramural NIH HHS NR 64 TC 37 Z9 40 U1 0 U2 12 PU BIOMED CENTRAL LTD PI LONDON PA MIDDLESEX HOUSE, 34-42 CLEVELAND ST, LONDON W1T 4LB, ENGLAND SN 1742-4690 J9 RETROVIROLOGY JI Retrovirology PD NOV 3 PY 2006 VL 3 AR 77 DI 10.1186/1742-4690-3-77 PG 10 WC Virology SC Virology GA 114CX UT WOS:000242645400001 PM 17083721 ER PT J AU Newman, AH Cha, JH Cao, JJ Kopajtic, T Katz, JL Parnas, ML Vaughan, R Lever, JR AF Newman, Amy Hauck Cha, Joo Hwan Cao, Jianjing Kopajtic, Theresa Katz, Jonathan L. Parnas, M. Laura Vaughan, Roxanne Lever, John R. TI Design and synthesis of a novel photoaffinity ligand for the dopamine and serotonin transporters based on 2 beta-carbomethoxy-3 beta-biphenyltropane SO JOURNAL OF MEDICINAL CHEMISTRY LA English DT Article ID UPTAKE INHIBITORS COCAINE; IRREVERSIBLE LIGANDS; BINDING-SITE; AFFINITY; ANALOGS; RECOGNITION; BENZTROPINE; MAZINDOL AB Tropane-based photoaffinity ligands covalently bind to discrete points of attachment on the dopamine transporter (DAT). To further explore structure-activity relations, a ligand in which the photoactivated group was extended from the 3-position of the tropane ring was synthesized from cocaine via a Stille or Suzuki coupling strategy. 3-(4'-Azido-3'-iodo-biphenyl-4-yl)-8-methyl-8-aza-bicyclo[3.2.1] octane-2-carboxylic acid methyl ester (11; K-i = 15.1 +/- 2.2 nM) demonstrated high binding affinity for the DAT. Moreover, this compound showed moderate binding affinity for the serotonin transporter (SERT, K-i = 109 +/- 14 nM), suggesting the potential utility of [I-125] 11 in both DAT and SERT protein structure studies. C1 NIDA, Med Chem Sect, NIH, Dept Hlth & Human Serv, Baltimore, MD 21224 USA. NIDA, Psychobiol Sect, NIH, Dept Hlth & Human Serv, Baltimore, MD USA. Univ Missouri, Columbia, MO USA. Univ N Dakota, Sch Med, Grand Forks, ND 58201 USA. Dept Radiol, Columbia, MO USA. Dept Med Pharmacol, Columbia, MO USA. Dept Physiol, Columbia, MO USA. Harry S Truman Mem Vet Hosp, Columbia, MO USA. RP Newman, AH (reprint author), NIDA, Med Chem Sect, NIH, Dept Hlth & Human Serv, POB 5180, Baltimore, MD 21224 USA. EM anewman@intra.nida.nih.gov FU NIDA NIH HHS [DA 15175] NR 21 TC 11 Z9 11 U1 0 U2 2 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA SN 0022-2623 J9 J MED CHEM JI J. Med. Chem. PD NOV 2 PY 2006 VL 49 IS 22 BP 6621 EP 6625 DI 10.1021/jm0603973 PG 5 WC Chemistry, Medicinal SC Pharmacology & Pharmacy GA 098WM UT WOS:000241553700021 PM 17064081 ER PT J AU Small, A AF Small, Alex TI Brief: goodbye to a quirky perspective on science SO NATURE LA English DT Letter C1 NICHHD, Lab Integrat & Med Biophys, Bethesda, MD 20892 USA. RP Small, A (reprint author), NICHHD, Lab Integrat & Med Biophys, Bethesda, MD 20892 USA. NR 1 TC 0 Z9 0 U1 0 U2 0 PU NATURE PUBLISHING GROUP PI LONDON PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND SN 0028-0836 J9 NATURE JI Nature PD NOV 2 PY 2006 VL 444 IS 7115 BP 31 EP 31 DI 10.1038/444031d PG 1 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA 100WS UT WOS:000241701500024 ER PT J AU He, LM Wu, XS Mohan, R Wu, LG AF He, Liming Wu, Xin-Sheng Mohan, Raja Wu, Ling-Gang TI Two modes of fusion pore opening revealed by cell-attached recordings at a synapse SO NATURE LA English DT Article ID FROG NEUROMUSCULAR JUNCTION; KISS-AND-RUN; TRANSMITTER RELEASE; SECRETORY VESICLE; NERVE-TERMINALS; TRAPEZOID BODY; CAPACITANCE; SINGLE; MEMBRANE; ENDOCYTOSIS AB Fusion of a vesicle with the cell membrane opens a pore that releases transmitter to the extracellular space(1-3). The pore can either dilate fully so that the vesicle collapses completely, or close rapidly to generate 'kiss-and-run' fusion(1,2,4-7). The size of the pore determines the release rate(2). At synapses, the size of the fusion pore is unclear, 'kiss-and-run' remains controversial(8-15), and the ability of 'kiss-and-run' fusion to generate rapid synaptic currents(16,17) is questionable(18). Here, by recording fusion pore kinetics during single vesicle fusion, we found both full collapse and 'kiss-and-run' fusion at calyx-type synapses. For full collapse, the initial fusion pore conductance (G(p)) was usually > 375 pS and increased rapidly at >= 299 pS ms(-1). 'Kiss-and-run' fusion was seen as a brief capacitance flicker (< 2 s) with G(p) > 288 pS for most flickers, but within 15 - 288 pS for the remaining flickers. Large G(p) (> 288 pS) might discharge transmitter rapidly and thereby cause rapid synaptic currents, whereas small Gp might generate slow and small synaptic currents. These results show that 'kiss-and-run' fusion occurs at synapses and that it can generate rapid postsynaptic currents, and suggest that various fusion pore sizes help to control the kinetics and amplitude of synaptic currents. C1 NINDS, Bethesda, MD 20892 USA. RP Wu, LG (reprint author), NINDS, 35 Convent Dr,Bldg 35,Room 2B-1012, Bethesda, MD 20892 USA. EM wul@ninds.nih.gov FU Intramural NIH HHS NR 30 TC 107 Z9 115 U1 2 U2 10 PU NATURE PUBLISHING GROUP PI LONDON PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND SN 0028-0836 J9 NATURE JI Nature PD NOV 2 PY 2006 VL 444 IS 7115 BP 102 EP 105 DI 10.1038/nature05250 PG 4 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA 100WS UT WOS:000241701500054 PM 17065984 ER PT J AU Jedrzejczak, R Dauter, M Dauter, Z Olszewski, M Dlugolecka, A Kur, J AF Jedrzejczak, Robert Dauter, Miroslawa Dauter, Zbigniew Olszewski, Marcin Dlugolecka, Anna Kur, Jozef TI Structure of the single-stranded DNA-binding protein SSB from Thermus aquaticus SO ACTA CRYSTALLOGRAPHICA SECTION D-BIOLOGICAL CRYSTALLOGRAPHY LA English DT Article ID ESCHERICHIA-COLI SSB; X-RAY-DIFFRACTION; CRYSTAL-STRUCTURE; DEINOCOCCUS-RADIODURANS; REFINEMENT; DOMAIN; THERMOPHILUS; VARIABILITY; RESOLUTION; SSDNA AB The crystal structure of the single-stranded DNA-binding protein from Thermus aquaticus has been solved and refined at 1.85 angstrom resolution. Two monomers, each encompassing two oligonucleotide/oligosaccharide-binding (OB) domains and a number of flexible beta-hairpin loops, form an oligomer of approximate D-2 symmetry typical of bacterial SSBs. Comparison with other SSB structures confirms considerable variability in the mode of oligomerization and aggregation of SSB oligomers. C1 NCI, Synchrotron Radiat Res Sect, MCL, Argonne Natl Lab, Argonne, IL 60439 USA. Argonne Natl Lab, Basic Res Program, SAIC Frederick, Argonne, IL 60439 USA. Gdansk Univ Technol, Fac Chem, Dept Microbiol, PL-80952 Gdansk, Poland. RP Dauter, Z (reprint author), NCI, Synchrotron Radiat Res Sect, MCL, Argonne Natl Lab, Argonne, IL 60439 USA. EM dauter@anl.gov; kur@chem.pg.gda.pl FU NCI NIH HHS [N01-CO-12400] NR 19 TC 14 Z9 15 U1 1 U2 2 PU BLACKWELL PUBLISHING PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DQ, OXON, ENGLAND SN 0907-4449 J9 ACTA CRYSTALLOGR D JI Acta Crystallogr. Sect. D-Biol. Crystallogr. PD NOV PY 2006 VL 62 BP 1407 EP 1412 DI 10.1107/S0907444906036031 PN 11 PG 6 WC Biochemical Research Methods; Biochemistry & Molecular Biology; Biophysics; Crystallography SC Biochemistry & Molecular Biology; Biophysics; Crystallography GA 096ML UT WOS:000241381100017 PM 17057346 ER PT J AU Porta, J Kolar, C Kozmin, SG Pavlov, YI Borgstahl, GEO AF Porta, Jason Kolar, Carol Kozmin, Stanislav G. Pavlov, Youri I. Borgstahl, Gloria E. O. TI Structure of the orthorhombic form of human inosine triphosphate pyrophosphatase SO ACTA CRYSTALLOGRAPHICA SECTION F-STRUCTURAL BIOLOGY AND CRYSTALLIZATION COMMUNICATIONS LA English DT Article ID ESCHERICHIA-COLI; METHANOCOCCUS-JANNASCHII; PROTEIN; IDENTIFICATION; 6-N-HYDROXYLAMINOPURINE; FRAGMENTATION; VALIDATION; YEAST; GENE AB The structure of human inosine triphosphate pyrophosphohydrolase (ITPA) has been determined using diffraction data to 1.6 angstrom resolution. ITPA contributes to the accurate replication of DNA by cleansing cellular dNTP pools of mutagenic nucleotide purine analogs such as dITP or dXTP. A similar high-resolution unpublished structure has been deposited in the Protein Data Bank from a monoclinic and pseudo-merohedrally twinned crystal. Here, cocrystallization of ITPA with a molar ratio of XTP appears to have improved the crystals by eliminating twinning and resulted in an orthorhombic space group. However, there was no evidence for bound XTP in the structure. Comparison with substrate-bound NTPase from a thermophilic organism predicts the movement of residues within helix alpha 1, the loop before alpha 6 and helix alpha 7 to cap off the active site when substrate is bound. C1 Univ Nebraska, Med Ctr, Eppley Inst Res Canc & Allied Dis, Omaha, NE 68198 USA. Natl Inst Environm Hlth Sci, Genet Mol Lab, Res Triangle Pk, NC 27709 USA. St Petersburg State Univ, Dept Genet, St Petersburg 199034, Russia. RP Borgstahl, GEO (reprint author), Univ Nebraska, Med Ctr, Eppley Inst Res Canc & Allied Dis, 600 S 42nd St, Omaha, NE 68198 USA. EM gborgstahl@unmc.edu RI Kozmin, Stanislav/J-6849-2012 OI Kozmin, Stanislav/0000-0002-4128-4447 NR 29 TC 10 Z9 12 U1 0 U2 2 PU BLACKWELL PUBLISHING PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DQ, OXON, ENGLAND SN 1744-3091 J9 ACTA CRYSTALLOGR F JI Acta Crystallogr. F-Struct. Biol. Cryst. Commun. PD NOV PY 2006 VL 62 BP 1076 EP 1081 DI 10.1107/S1744309106041790 PN 11 PG 6 WC Biochemical Research Methods; Biochemistry & Molecular Biology; Biophysics; Crystallography SC Biochemistry & Molecular Biology; Biophysics; Crystallography GA 100PT UT WOS:000241681700006 PM 17077483 ER PT J AU Woodard, GE Zhao, J Rosado, JA AF Woodard, G. E. Zhao, J. Rosado, J. A. TI Different effect of ATP on ANP receptor guanylyl cyclase in spontaneously hypertensive and normotensive rats SO ACTA PHYSIOLOGICA LA English DT Article DE ANP(1-28); ATP; renal glomeruli; ATP gamma S; spontaneously hypertensive rats; WKY ID NATRIURETIC-PEPTIDE RECEPTOR; REGULATED MODULE ARM; ADENINE-NUCLEOTIDES; SIGNAL-TRANSDUCTION; CGMP PRODUCTION; LUNG MEMBRANES; ACTIVATION; DOMAIN; DESENSITIZATION; BINDING AB Aim: Natriuretic peptide receptor A (NPR-A) is the main physiological receptor for atrial natriuretic peptide (ANP). Maximal activation of NPR-A guanylyl cyclase (GC) requires ANP binding and ATP interaction with a putative cytoplasmic site. This study investigates the regulatory effect of ATP on GC-coupled NPR-A activity in Wistar Kyoto (WKY) and spontaneously hypertensive rats (SHR). Methods: Cyclic GMP production and competitive inhibition of [I-125] ANP(1-28) binding were performed in solubilized glomerular and papillary renal membranes. Results: Here, we report that incubation of renal glomerular and papillary membranes with ATP induced a concentration-dependent increase in basal and ANP(1-28)-stimulated GC activity that was significantly greater in SHR than in age- matched WKY. ATP gamma S was more effective than ATP and induced a greater stimulation of cGMP production in SHR than in WKY. In contrast, in solubilized membranes ATP exerted an inhibitory role on basal and ANP(1-28)-induced GC activity, suggesting that an accessory protein is required for ATP-induced GC activation. ATP increases NPR-A affinity for ANP(1-28) and decreased B-max in crude and solubilized membranes. Kinetic analysis of GC-coupled NPR-A revealed that ATP reduced the Km and increased the V-max, an effect that was greater in SHR. Conclusion: Our observations indicate that ATP exerts a greater net effect on NPR-A in SHR than in WKY, which might explain the greater rate of cGMP production observed in SHR compared to WKY. C1 NIDDK, NIH, Bethesda, MD 20892 USA. Addenbrookes Hosp, Dept Med, Cambridge CB2 2QQ, England. Univ Extremadura, Dept Physiol, Caceres, Spain. RP Woodard, GE (reprint author), NIDDK, NIH, 10 Ctr Dr,MSC 1752, Bethesda, MD 20892 USA. EM geoffreyw@intra.niddk.nih.gov RI Woodard, Geoffrey/A-8608-2009; rosado, juan/H-3488-2015 OI rosado, juan/0000-0002-9749-2325 NR 44 TC 3 Z9 3 U1 0 U2 0 PU BLACKWELL PUBLISHING PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DQ, OXON, ENGLAND SN 1748-1708 J9 ACTA PHYSIOL JI Acta Physiol. PD NOV-DEC PY 2006 VL 188 IS 3-4 BP 195 EP 206 DI 10.1111/j.1748-1716.2006.01628.x PG 12 WC Physiology SC Physiology GA 096XM UT WOS:000241410100005 PM 17054659 ER PT J AU Mlambo, G Mutambu, SL Mduluza, T Soko, W Mbedzi, J Chivenga, J Lanar, DE Singh, S Carucci, D Gemperli, A Kumar, N AF Mlambo, Godfree Mutambu, Susan L. Mduluza, Takafira Soko, White Mbedzi, Joel Chivenga, James Lanar, David E. Singh, Sanjay Carucci, Daniel Gemperli, Armin Kumar, Nirbhay TI Antibody responses to Plasmodium falciparum vaccine candidate antigens in three areas distinct with respect to altitude SO ACTA TROPICA LA English DT Article DE P. falciparum; antibody responses; malaria vaccine; transmission; Zimbabwe ID MEROZOITE SURFACE PROTEIN-1; APICAL MEMBRANE ANTIGEN-1; NEW-GUINEAN CHILDREN; BLOOD-STAGE VACCINE; INHIBITORY ANTIBODIES; MALARIA TRANSMISSION; CLINICAL MALARIA; IN-VITRO; PROTECTION; IMMUNOGENICITY AB Antibody levels against malaria antigens were measured among patients presenting with uncomplicated malaria at health centers from three locations in Zimbabwe (Bindura, Chiredzi and Kariba) that are distinct with regard to altitude and climatic conditions. Antibody levels were determined by ELISA using the antigens, apical membrane antigen 1 (AMA-1), erythrocyte binding antigen 175 (EBA-175), circumsporozoite surface protein (CSP), merozoite surface protein 1 (MSP-1) and Pfg27. For all the antigens tested, IgG and IgM levels were higher for Bindura (altitude 1100 m) compared to Kariba (< 600 m, altitude) and Chiredzi (similar to 600 m, altitude) with the exception of IgG and IgM to AMA-1 and EBA-175 which were similar between Chiredzi and Bindura. Plasma samples were further analyzed for their functional activity by testing their ability to inhibit the growth of Plasmodium falciparum in culture. Our results, determined by microscopy and verified by the LDH assay revealed that plasma from the three locations had similar inhibitory activity against the growth of P falciparum in vitro. Our data revealed that highest growth inhibition correlated with the highest levels of MSP-1 antibody values. (c) 2006 Published by Elsevier B.V.. C1 Johns Hopkins Univ, Bloomberg Sch Publ Hlth, Dept Mol Microbiol & Immunol, Malaria Res Inst, Baltimore, MD 21205 USA. Natl Inst Hlth Res, Harare, Zimbabwe. Univ Zimbabwe, Dept Biochem, Harare, Zimbabwe. Walter Reed Army Inst Res, Silver Spring, MD 20910 USA. NIAD, Malaria Vaccine Dev Unit, NIH, Bethesda, MD USA. USN, Med Res Ctr, Malaria Program, Silver Spring, MD 20910 USA. RP Kumar, N (reprint author), Johns Hopkins Univ, Bloomberg Sch Publ Hlth, Dept Mol Microbiol & Immunol, Malaria Res Inst, 615 N Wolfe St, Baltimore, MD 21205 USA. EM nkumar@jhsph.edu RI Lanar, David/B-3560-2011 FU FIC NIH HHS [TW001587]; NCRR NIH HHS [RR00052] NR 42 TC 13 Z9 13 U1 0 U2 1 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0001-706X J9 ACTA TROP JI Acta Trop. PD NOV PY 2006 VL 100 IS 1-2 BP 70 EP 78 DI 10.1016/j.actatropica.2006.09.012 PG 9 WC Parasitology; Tropical Medicine SC Parasitology; Tropical Medicine GA 126GR UT WOS:000243501200009 PM 17113021 ER PT J AU Goldstein, RB Olfson, M Martens, EG Wolk, SI AF Goldstein, Rise B. Olfson, Mark Martens, Elaine Goff Wolk, Susan I. TI Subjective unmet need for mental health services in depressed children grown up SO ADMINISTRATION AND POLICY IN MENTAL HEALTH AND MENTAL HEALTH SERVICES RESEARCH LA English DT Article DE depressive disorder; substance-related disorders; mental health services; utilization; unmet need ID INITIAL TREATMENT CONTACT; PSYCHIATRIC-DISORDERS; SOCIAL-CONSEQUENCES; 1ST ONSET; INTERPERSONAL RELATIONSHIPS; UNITED-STATES; CARE USE; ADOLESCENTS; EPISODE; ANXIETY AB Background Limited attention has been devoted to characterizing unmet need for treatment among individuals with mental disorders. A longitudinal follow-up of depressed, anxious, and psychiatrically normal children into adulthood provided an opportunity to examine factors associated with subjective unmet need. Methods Respondents (n = 208) comprise a sub-sample of a cohort ascertained between 1977 and 1985 consisting of three subgroups: one with major depressive disorder (MDD), one with anxiety disorders but no MDD, and controls with no psychiatric disorder up to ascertainment. Psychiatric status was reassessed in adulthood using the SADS-LA by interviewers blind to childhood diagnoses. Best-estimate diagnoses describing participants' lifetime clinical course were formulated by senior clinicians. Participants who completed SADS-LA interviews about themselves were invited to complete an additional interview about experiences with health care, including subjective unmet need for and barriers to mental health treatment. Results About 37% of respondents reported lifetime histories of subjective unmet need for mental health services. Unmet need was associated with female gender and lifetime mood and substance dependence disorders. The most commonly cited barriers included attitudes toward treatment, not knowing where to obtain it, and financial concerns. Conclusions Subjective unmet need was common in this sample. Approaches to reducing it might include public health initiatives to foster more favorable attitudes toward treatment, increase knowledge of where to obtain it, and lower financial barriers. C1 NIAAA, Lab Epidemiol & Biometry, Div Intramural Clin & Biol Res, Bethesda, MD 20892 USA. Columbia Univ, Coll Phys & Surg, Dept Psychiat, Div Clin Genet Epidemiol, New York, NY USA. New York State Psychiat Inst & Hosp, Div Clin Genet Epidemiol, New York, NY 10032 USA. Univ Connecticut, Ctr Hlth, Dept Neurosci, Farmington, CT USA. RP Goldstein, RB (reprint author), NIAAA, Lab Epidemiol & Biometry, Div Intramural Clin & Biol Res, 5635 Fishers Ln,Rm 3068,MS 9304, Bethesda, MD 20892 USA. EM goldster@mail.nih.gov OI Goldstein, Rise/0000-0002-9603-9473 FU NIMH NIH HHS [R01 MH50666] NR 39 TC 8 Z9 8 U1 2 U2 3 PU SPRINGER PI NEW YORK PA 233 SPRING STREET, NEW YORK, NY 10013 USA SN 0894-587X J9 ADM POLICY MENT HLTH JI Adm. Policy. Ment. Health PD NOV PY 2006 VL 33 IS 6 BP 666 EP 673 DI 10.1007/s10488-006-0082-y PG 8 WC Health Policy & Services; Public, Environmental & Occupational Health SC Health Care Sciences & Services; Public, Environmental & Occupational Health GA 111NI UT WOS:000242458800007 PM 16823630 ER PT J AU Coppin, AK Shumway-Cook, A Saczynski, JS Patel, KV Ble, A Ferrucci, L Guralnik, JM AF Coppin, Antonia K. Shumway-Cook, Anne Saczynski, Jane S. Patel, Kushang V. Ble, Alessandro Ferrucci, Luigi Guralnik, Jack M. TI Association of executive function and performance of dual-task physical tests among older adults: analyses from the InChianti study SO AGE AND AGEING LA English DT Article DE executive function; older adults; physical performance; dual tasks; mobility; elderly ID WALKING; ABILITY; DECLINE; COSTS; YOUNG; GAIT; AGE AB Background: previous studies have reported an association between cognitive function and physical performance, particularly among older adults. Objective: to examine the association between executive function and performance difference on complex versus usual walking tasks in a sample of non-demented older adults. Design: population-based epidemiological study of older people residing in the Chianti area (Tuscany, Italy). Participants: 737 community-dwelling individuals aged 65 years and older. Methods: gait speed (m/s) was measured during the performance of complex walking tasks (walking/talking, walking/picking-up an object, walking/carrying a large package, walking over obstacles, walking with a weighted vest) and reference walking tasks (7 m usual pace, 7 m fast pace and 60 m fast pace). Executive function was assessed using the Trail Making Test (TMT). Other measures included Mini-Mental State Examination (MMSE), sociodemographic characteristics and selected physiological impairments. Results: gait speed for the selected reference and complex walk tasks was consistently lower among participants with poor executive function. Per cent decline in gait speed compared with the reference task differed by executive function for certain tasks (e. g. walking/obstacles: 30 versus 24% decline in low versus high executive function respectively, P = 0.0006) but not for others. Conclusions: poor executive function is associated with measures of gait, including specific challenges. Overall, the results showed that the cost associated with the addition of a challenge to the basic walking task differs by executive function and the nature of the task. Further research is needed to determine whether improvement in executive function abilities translates to better performance on selected complex walking tasks. C1 NIA, Lab Epidemiol Demog & Biometry, NIH, Bethesda, MD 20892 USA. Univ Washington, Dept Rehabil Med, Seattle, WA 98195 USA. NIA, Longitudinal Studies Sect, Clin Res Branch, NIH, Bethesda, MD USA. RP Coppin, AK (reprint author), NIA, Lab Epidemiol Demog & Biometry, NIH, Bethesda, MD 20892 USA. EM coppina@mail.nih.gov FU Intramural NIH HHS [Z99 AG999999]; NIMHD NIH HHS [R01 MD009164] NR 31 TC 106 Z9 113 U1 3 U2 16 PU OXFORD UNIV PRESS PI OXFORD PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND SN 0002-0729 J9 AGE AGEING JI Age Ageing PD NOV PY 2006 VL 35 IS 6 BP 619 EP 624 DI 10.1093/ageing/afl107 PG 6 WC Geriatrics & Gerontology SC Geriatrics & Gerontology GA 097FN UT WOS:000241432500014 PM 17047008 ER PT J AU Wu, L Kottilil, S Lempicki, R Yang, J McLaughlin, M Hu, ZH Koratich, C Reitano, KN Rehm, CA Masur, H Wood, B Kleiner, DE Polis, MA AF Wu, Lynne Kottilil, Shyam Lempicki, Richard Yang, Jun McLaughlin, Mary Hu, Zonghui Koratich, Chad Reitano, Kristin N. Rehm, Catherine A. Masur, Henry Wood, Brad Kleiner, David E. Polis, Michael A. TI Hepatic histologic response (HR) to combination therapy among HCV/HIV-coinfected individuals: Interferon induces HR independent of sustained virologic response (SVR) SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Article ID HUMAN-IMMUNODEFICIENCY-VIRUS; ALPHA-2A PLUS RIBAVIRIN; HIV-INFECTED PATIENTS; C VIRUS; LIVER FIBROSIS; PEGYLATED INTERFERON-ALPHA-2B; CONTROLLED-TRIAL; METALLOTHIONEIN; PROGRESSION; MICE AB Most HIV/HCV-coinfected patients fail to achieve a sustained virologic response (SVR) to peginterferon-ribavirin therapy. We examined the hepatic histologic response (HR), defined as an improvement in hepatic inflammation scores of two points or more, to combination therapy among HIV/HCV-coinfected subjects. An open label prospective trial treated 32 HIV/HCV-coinfected patients with peginterferon alpha-2b and ribavirin for 48 weeks. Liver biopsies, scored by a single pathologist using the Histology Activity Index (HAI, range 0 - 18) and Ishak fibrosis scores ( range 0 - 6), were performed before and after treatment. Gene expression profiles of PBMCs were performed using Affymetrix U133A gene chips. A total of 87% of SVR subjects and 88% of nonresponders (NR) had an HR, but no significant change in the liver fibrosis scores was observed ( p > 0.05). For genotype 1 patients, a baseline fibrosis score <= 2 was related to a higher likelihood of SVR than those with a score > 2 ( p = 0.012). Combination therapy for HCV among HIV-coinfected subjects resulted in a modest SVR rate. Persons with mild liver disease had a better SVR rate, suggesting early treatment may be beneficial. Combination therapy resulted in an HR for most of the patients, however, further follow-up of these patients will determine the durability of such an HR. C1 NIAID, LIR, Immunopathogenesis Sect, NIH,DHHS,Lab Immunoregulat, Bethesda, MD 20892 USA. NCI, SAIC, Frederick, MD 21701 USA. NIAID, Biostat Res Branch, NIH, DHHS, Bethesda, MD 20892 USA. NIH, Dept Crit Care Med, CC, DHHS, Bethesda, MD 20892 USA. NIH, Dept Diagnost Radiol, DHHS, CC, Bethesda, MD 20892 USA. NCI, NIH, DHHS, Bethesda, MD 20892 USA. RP Kottilil, S (reprint author), NIAID, LIR, Immunopathogenesis Sect, NIH,DHHS,Lab Immunoregulat, Bldg 10 Rm 11N204,9000 Rockville Pike, Bethesda, MD 20892 USA. EM Skottilil@niaid.nih.gov RI Lempicki, Richard/E-1844-2012; OI Lempicki, Richard/0000-0002-7059-409X; Polis, Michael/0000-0002-9151-2268; Kleiner, David/0000-0003-3442-4453 FU Intramural NIH HHS NR 26 TC 4 Z9 4 U1 0 U2 0 PU MARY ANN LIEBERT INC PI NEW ROCHELLE PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD NOV PY 2006 VL 22 IS 11 BP 1091 EP 1098 DI 10.1089/aid.2006.22.1091 PG 8 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA 115YW UT WOS:000242770700005 PM 17147494 ER PT J AU Gomez-Carrillo, M Pampuro, S Duran, A Losso, M Harris, DR Read, JS Duarte, G De Souza, R Soto-Ramirez, L Salomon, H AF Gomez-Carrillo, Manuel Pampuro, Sandra Duran, Adriana Losso, Marcelo Harris, D. Robert Read, Jennifer S. Duarte, Geraldo De Souza, Ricardo Soto-Ramirez, Luis Salomon, Horacio CA NISDI Perinatal Study Grp TI Analysis of HIV type 1 diversity in pregnant women from four Latin American and Caribbean countries SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Article ID MOLECULAR EPIDEMIOLOGY; GENETIC DIVERSITY; SOUTH-AMERICA; TRANSMISSION; ARGENTINA; VARIANTS; SUBTYPE; STRAINS; SPREAD AB Worldwide, the distribution of HIV-1 subtypes and intersubtype recombinants is not homogeneous. In Latin America and the Caribbean, HIV-1 subtype B predominates. However, in the south of Brazil and in countries of the Southern cone ( Argentina, Chile, Paraguay, and Uruguay) there is a different distribution of viral subtypes and intersubtype recombinants. The aim of this work was to analyze HIV-1 diversity in a cohort of pregnant women ( with primarily heterosexual acquisition of the infection) who were diagnosed with HIV-1 infection during their current pregnancy and who received ARVs during pregnancy for perinatal transmission prophylaxis. Analysis of 121 partial pol sequences from subjects enrolled in Argentina, Brazil, the Bahamas, and Mexico was performed by phylogenetic and recombinant characterization. Different prevalences of subtype B were observed (100% for specimens from Mexico and the Bahamas, 61% for Brazil, and 30% for Argentina). Subtypes C and F were found, along with BC, BF, FC, and CBF recombinants in specimens from Brazilians. A high prevalence of BF recombinants was found (70%) in specimens from Argentina. The different patterns of HIV-1 subtypes and intersubtype recombinants in South America ( Argentina and Brazil) compared to those in Central and North America should be considered in the design of future HIV-1 vaccine trials. C1 Univ Buenos Aires, Fac Med, Dept Microbiol, Sch Med,Ctr Nacl Referencia SIDA, RA-1121 Buenos Aires, DF, Argentina. Hosp Gen Agudos Jose Maria Ramos Mejia, Buenos Aires, DF, Argentina. Westat Corp, Rockville, MD USA. NICHD, Pediat Adolescent & Maternal AIDS Branch, CRMC, NICHD,NIH, Bethesda, MD USA. Univ Sao Paulo, BR-14049 Ribeirao Preto, Brazil. Univ Caxias Sul, Caxias Do Sul, Brazil. Inst Nacl Nutr Salvador Zubiran, Dept Infect Dis, Mexico City 14000, DF, Mexico. RP Salomon, H (reprint author), Univ Buenos Aires, Fac Med, Dept Microbiol, Sch Med,Ctr Nacl Referencia SIDA, Paraguay 2155 Piso 11, RA-1121 Buenos Aires, DF, Argentina. EM hsalomon@fmed.uba.ar RI Mussi-Pinhata, Marisa/G-6568-2012; Duarte, Geraldo/J-7906-2012 FU NICHD NIH HHS [N01-HD-3-3345] NR 17 TC 22 Z9 22 U1 0 U2 0 PU MARY ANN LIEBERT INC PI NEW ROCHELLE PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD NOV PY 2006 VL 22 IS 11 BP 1186 EP 1191 DI 10.1089/aid.2006.22.1186 PG 6 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA 115YW UT WOS:000242770700020 PM 17147509 ER PT J AU Russell, M Fleg, JL Galloway, J Henderson, JA Howard, WJ Lee, ET Poolaw, B Ratner, RE Roman, MJ Silverman, A Stylianou, M Weir, MR Wilson, C Yeh, F Zhu, JH Howard, BV AF Russell, Marie Fleg, Jerome L. Galloway, James Henderson, Jeffrey A. Howard, Wm. James Lee, Elisa T. Poolaw, Bryce Ratner, Robert E. Roman, Mary J. Silverman, Angela Stylianou, Mario Weir, Matthew R. Wilson, Charlton Yeh, Fawn Zhu, Jianhui Howard, Barbara V. TI Examination of lower targets for low-density lipoprotein cholesterol and blood pressure in diabetes - the Stop Atherosclerosis in Native Diabetics Study (SANDS) SO AMERICAN HEART JOURNAL LA English DT Article ID CORONARY-HEART-DISEASE; INTIMA-MEDIA THICKNESS; TREATMENT PANEL-III; CARDIOVASCULAR-DISEASE; CLINICAL-TRIALS; RISK-FACTORS; DOPPLER-ECHOCARDIOGRAPHY; OLDER-ADULTS; RECOMMENDATIONS; VALIDATION AB Diabetes incidence is increasing rapidly in the United States. Diabetes increases the risk for cardiovascular disease, the major cause of death in diabetic individuals. The conventional cardiovascular risk factors of hyperlipidemia and hypertension worsen diabetic vascular disease. Treatment targets for low-density lipoprotein cholesterol (LDL-C) and blood pressure in diabetic individuals are being debated. The SANDS is a randomized, open-label, 3-year trial to examine the effects of aggressive LDL-C (goal < 70 mg/dL) and blood pressure (BP) (goal < 115/75 mm Hg) reduction versus the standard goal's of < 100 mg/dL for LDL-C and < 130/85 mm Hg for BP. Five hundred forty-nine American-Indian men and women > 40 years old with type 2 diabetes were randomized to I of 2 groups. Lipids and BP are managed using Food and Drug Administration-approved medications in an algorithmic approach. The presence and progression of atherosclerosis are evaluated by carotid ultrasonography; echocardiography assesses cardiac function. The primary end point is the composite outcome of change in carotid artery intimal medial thickness and fatal/nonfatal cardiovascular events. These outcomes are combined by using a ranked analysis for carotid thickness and assigning a "worst rank" for a cardiovascular event. Secondary end points include carotid plaque score, left ventricular, geometry and function, serum C-reactive protein, and safety measures. Unique aspects of the study design and analysis plan involve the use of a composite outcome and changes during the trial of LDL-C treatment goals for participants with baseline or incident cardiovascular disease in the conventional group because of changes in the standard of care. Study results will further understanding of the effects of aggressive risk factor reduction on atherosclerosis burden and cardiac function in diabetic individuals in US populations and will help determine optimal LDL-C and BP treatment goals for diabetic patients. C1 Phoenix Indian Med Ctr, Phoenix, AZ USA. Natl Heart Lung & Blood Inst, Bethesda, MD USA. Native Amer Cardiol Program, Flagstaff, AZ USA. Black Hills Ctr Amer Indian Hlth, Rapid City, SD USA. Washington Hosp Ctr, Washington, DC 20010 USA. Univ Oklahoma, Hlth Sci Ctr, Oklahoma City, OK USA. Lawton Indian Hosp, Lawton, OK USA. MedStar Res Inst, Washington, DC USA. Cornell Univ, Weill Med Coll, New York, NY USA. Univ Maryland, Sch Med, Baltimore, MD 21201 USA. RP Howard, BV (reprint author), 6495 New Hampshire Ave,Suite 201, Adelphi, MD 20783 USA. EM barbara.v.howard@medstar.net FU NHLBI NIH HHS [U01 HL067031, 1 U01 HL67031-01A1] NR 53 TC 20 Z9 21 U1 0 U2 1 PU MOSBY, INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 USA SN 0002-8703 J9 AM HEART J JI Am. Heart J. PD NOV PY 2006 VL 152 IS 5 BP 867 EP 875 DI 10.1016/j.ahj.2006.05.021 PG 9 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA 101MV UT WOS:000241745800012 PM 17070147 ER PT J AU Ahmed, A Perry, GJ Fleg, JL Love, TE Goff, DC Kitzman, DW AF Ahmed, Ali Perry, Gilbert J. Fleg, Jerome L. Love, Thomas E. Goff, David C., Jr. Kitzman, Dalane W. TI Outcomes in ambulatory chronic systolic and diastolic heart failure: A propensity score analysis SO AMERICAN HEART JOURNAL LA English DT Article ID VENTRICULAR EJECTION FRACTION; OLDER-ADULTS; DIG TRIAL; MORTALITY; PROGNOSIS; DIGOXIN; HOSPITALIZATION; DYSFUNCTION; MORBIDITY; ASSOCIATION AB Background Prior studies demonstrating significant difference in outcomes in systolic and diastolic heart failure (HF) are often limited to hospitalized acute HF patients, and may be confounded by residual bias. In this analysis, we examined long-term mortality and hospitalization in a propensity score matched cohort of ambulatory chronic systolic and diastolic HF patients. Methods Of the 7788 patients in the Digitalis Investigation Group trial, 6800 had systolic HF (ejection fraction <= 45%) and 988 had diastolic HF (ejection fraction > 45%). We restricted our analysis to 7617 patients without valvular heart disease: 916 diastolic HF and 6701 systolic HF. Propensity scores for diastolic HF, calculated for each patient by a non-parsimonious multivariable logistic regression model, were used to match 697 diastolic HF with 2091 systolic HF patients. Matched Cox regression models were used to estimate hazard ratios (HR) and 95% confidence intervals (CI) for outcomes in diastolic (versus systolic) HF. Results During a median 38-month follow-up, compared with 32% mortality in systolic HF, 23% of diastolic HF patients died (HR=0.70; 95% CI=0.59-0.84; P <.0001). Respective HR (95%CI) for cardiovascular and HF mortality were 0.60 (0.48-0.74; P <.0001) and 0.56 (0.39-0.79; P=.001). All-cause hospitalizations occured in 64% of systolic and 67% of diastolic HF patients (HR=0.99; 95% CI=0.87-1.11; P=.801). Respective HR (95%CI) for cardiovascular and HF hospitalizations were 0.84 (0.73-0.96; P=.011) and 0.63 (0.51-0.77; P <.0001). Conclusions Despite lower mortality and cardiovascular morbidity, diastolic HF patients had similar overall hospitalizations as in systolic HF. Ejection fraction should be assessed in all HF patients to guide therapy, with special attention to non-cardiovascular morbidity in diastolic HF. C1 Univ Alabama, Birmingham, AL 35294 USA. VA Med Ctr, Birmingham, AL USA. NHLBI, Bethesda, MD 20892 USA. Case Western Reserve Univ, Cleveland, OH 44106 USA. Wake Forest Univ, Winston Salem, NC 27109 USA. RP Ahmed, A (reprint author), Univ Alabama, 1530 3rd Ave S,CH-19,Ste 219, Birmingham, AL 35294 USA. EM aahmed@uab.edu RI Ahmed, Ali/A-2934-2008 OI Ahmed, Ali/0000-0002-6832-6424 FU NHLBI NIH HHS [P50 HL077100, R01 HL085561, R01 HL085561-01, 1-R01-HL085561-01]; NIA NIH HHS [R37 AG018915, K23 AG019211-03, 1-K23-AG19211-04, K23 AG019211-04, K23 AG019211, R01 AG018915] NR 48 TC 42 Z9 45 U1 0 U2 1 PU MOSBY, INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 USA SN 0002-8703 J9 AM HEART J JI Am. Heart J. PD NOV PY 2006 VL 152 IS 5 BP 956 EP 966 DI 10.1016/j.ahj.2006.06.020 PG 11 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA 101MV UT WOS:000241745800032 PM 17070167 ER PT J AU Ravitsky, V Wilfond, BS AF Ravitsky, Vardit Wilfond, Benjamin S. TI Disclosing individual genetic results to research participants SO AMERICAN JOURNAL OF BIOETHICS LA English DT Article DE clinical utility; clinical validity; disclosure; research results; genetic research ID CORONARY HEART-DISEASE; CLINICAL-RESEARCH; BREAST-CANCER; ALZHEIMERS-DISEASE; POPULATION; PRIVACY; CONSENT; TRIAL AB Investigators and institutional review boards should integrate plans about the appropriate disclosure of individual genetic results when designing research studies. The ethical principles of beneficence, respect, reciprocity, and justice provide justification for routinely offering certain results to research participants. We propose a result-evaluation approach that assesses the expected information and the context of the study in order to decide whether results should be offered. According to this approach, the analytic validity and the clinical utility of a specific result determine whether it should be offered routinely. Different results may therefore require different decisions even within the same study. We argue that the threshold of clinical utility for disclosing a result in a research study should be lower than the threshold used for clinical use of the same result. The personal meaning of a result provides additional criteria for evaluation. Finally, the context of the study allows for a more nuanced analysis by addressing the investigators' capabilities for appropriate disclosure, participants' alternative access to the result, and their relationship with the investigators. This analysis shows that the same result may require different decisions in different contexts. C1 [Ravitsky, Vardit] NIH, Bethesda, MD USA. [Ravitsky, Vardit] Univ Penn, Philadelphia, PA 19104 USA. [Wilfond, Benjamin S.] NHGRI, Social & Behva Res Branch, NIH, Bethesda, MD 20892 USA. [Wilfond, Benjamin S.] NIH, Clin Ctr, Dept Clin Bioeth, Bethesda, MD USA. [Wilfond, Benjamin S.] Univ Washington, Seattle, WA 98195 USA. RP Ravitsky, V (reprint author), NIH, Bethesda, MD USA. FU Intramural NIH HHS NR 32 TC 174 Z9 174 U1 1 U2 14 PU ROUTLEDGE JOURNALS, TAYLOR & FRANCIS LTD PI ABINGDON PA 4 PARK SQUARE, MILTON PARK, ABINGDON OX14 4RN, OXFORDSHIRE, ENGLAND SN 1526-5161 J9 AM J BIOETHICS JI Am. J. Bioeth. PD NOV-DEC PY 2006 VL 6 IS 6 BP 8 EP 17 DI 10.1080/16265160600934772 PG 10 WC Ethics; Medical Ethics; Social Issues; Social Sciences, Biomedical SC Social Sciences - Other Topics; Medical Ethics; Social Issues; Biomedical Social Sciences GA 102ER UT WOS:000241794300003 PM 17085395 ER PT J AU Wade, CH Kalfoglou, AL AF Wade, Christopher H. Kalfoglou, Andrea L. TI When do genetic researchers have a duty to recontact study participants? SO AMERICAN JOURNAL OF BIOETHICS LA English DT Editorial Material ID LEGAL C1 NHGRI, Social & Behav Res Branch, Bethesda, MD USA. RP Wade, CH (reprint author), NHGRI, Social & Behav Res Branch, Bethesda, MD USA. NR 4 TC 12 Z9 12 U1 1 U2 3 PU ROUTLEDGE JOURNALS, TAYLOR & FRANCIS LTD PI ABINGDON PA 4 PARK SQUARE, MILTON PARK, ABINGDON OX14 4RN, OXFORDSHIRE, ENGLAND SN 1526-5161 J9 AM J BIOETHICS JI Am. J. Bioeth. PD NOV-DEC PY 2006 VL 6 IS 6 BP 26 EP 27 DI 10.1080/15265160600935746 PG 2 WC Ethics; Medical Ethics; Social Issues; Social Sciences, Biomedical SC Social Sciences - Other Topics; Medical Ethics; Social Issues; Biomedical Social Sciences GA 102ER UT WOS:000241794300008 PM 17085400 ER PT J AU Manolio, TA AF Manolio, Teri A. TI Taking our obligations to research participants seriously: Disclosing individual results of genetic research SO AMERICAN JOURNAL OF BIOETHICS LA English DT Editorial Material C1 NHGRI, NIH, Bethesda, MD USA. RP Manolio, TA (reprint author), NHGRI, NIH, Bethesda, MD USA. NR 9 TC 17 Z9 17 U1 0 U2 1 PU ROUTLEDGE JOURNALS, TAYLOR & FRANCIS LTD PI ABINGDON PA 4 PARK SQUARE, MILTON PARK, ABINGDON OX14 4RN, OXFORDSHIRE, ENGLAND SN 1526-5161 J9 AM J BIOETHICS JI Am. J. Bioeth. PD NOV-DEC PY 2006 VL 6 IS 6 BP 32 EP 34 DI 10.1080/15265160600935953 PG 4 WC Ethics; Medical Ethics; Social Issues; Social Sciences, Biomedical SC Social Sciences - Other Topics; Medical Ethics; Social Issues; Biomedical Social Sciences GA 102ER UT WOS:000241794300011 PM 17085403 ER PT J AU Facio, FM AF Facio, Flavia M. TI One size does not fit all SO AMERICAN JOURNAL OF BIOETHICS LA English DT Editorial Material ID DISEASE; IMPACT C1 NHGRI, NIH, Bethesda, MD USA. RP Facio, FM (reprint author), NHGRI, NIH, Bethesda, MD USA. NR 8 TC 6 Z9 6 U1 0 U2 0 PU ROUTLEDGE JOURNALS, TAYLOR & FRANCIS LTD PI ABINGDON PA 4 PARK SQUARE, MILTON PARK, ABINGDON OX14 4RN, OXFORDSHIRE, ENGLAND SN 1526-5161 J9 AM J BIOETHICS JI Am. J. Bioeth. PD NOV-DEC PY 2006 VL 6 IS 6 BP 40 EP 42 DI 10.1080/15265160600938351 PG 4 WC Ethics; Medical Ethics; Social Issues; Social Sciences, Biomedical SC Social Sciences - Other Topics; Medical Ethics; Social Issues; Biomedical Social Sciences GA 102ER UT WOS:000241794300015 PM 17085407 ER PT J AU Ravitsky, V Wilfond, BS AF Ravitsky, Vardit Wilfond, Benjamin S. TI Response to open peer commentaries on "Disclosing individual genetic results to research participants": Defining clinical utility and revisiting the role of relationships SO AMERICAN JOURNAL OF BIOETHICS LA English DT Letter C1 NIH, Bethesda, MD 20892 USA. Univ Penn, Philadelphia, PA 19104 USA. Univ Washington, Seattle, WA 98195 USA. RP Ravitsky, V (reprint author), NIH, Bldg 10, Bethesda, MD 20892 USA. NR 17 TC 2 Z9 2 U1 0 U2 0 PU ROUTLEDGE JOURNALS, TAYLOR & FRANCIS LTD PI ABINGDON PA 4 PARK SQUARE, MILTON PARK, ABINGDON OX14 4RN, OXFORDSHIRE, ENGLAND SN 1526-5161 J9 AM J BIOETHICS JI Am. J. Bioeth. PD NOV-DEC PY 2006 VL 6 IS 6 BP W10 EP W12 DI 10.1080/15265160601021272 PG 3 WC Ethics; Medical Ethics; Social Issues; Social Sciences, Biomedical SC Social Sciences - Other Topics; Medical Ethics; Social Issues; Biomedical Social Sciences GA 102ER UT WOS:000241794300031 ER PT J AU Flood, A Peters, U Jenkins, DJA Chatterjee, N Subar, AF Church, TR Bresalier, R Weissfeld, JL Hayes, RB Schatzkin, A AF Flood, Andrew Peters, Ulrike Jenkins, David J. A. Chatterjee, Nilanjan Subar, Amy F. Church, Timothy R. Bresalier, Robert Weissfeld, Joel L. Hayes, Richard B. Schatzkin, Arthur CA Protate Lung Colorectal Ovarian TI Carbohydrate, glycemic index, and glycemic load and colorectal adenomas in the Prostate, Lung, Colorectal, and Ovarian Screening Study SO AMERICAN JOURNAL OF CLINICAL NUTRITION LA English DT Article DE colorectal adenoma; glycemic index; glycemic load; carbohydrate; insulin resistance; fiber ID NATIONAL-CANCER-INSTITUTE; DENSITY-LIPOPROTEIN CHOLESTEROL; FOOD FREQUENCY QUESTIONNAIRES; DIABETES-MELLITUS; INSULIN-RESISTANCE; DIETARY FIBER; COLON-CANCER; US ADULTS; PLASMA-GLUCOSE; WOMENS HEALTH AB Background: It is possible that high-glycemic-load diets, through their hyperinsulinemic effects, can increase the risk of colorectal cancer. Objective: We analyzed data from a cancer screening study to determine whether persons with high-glycemic-load diets would be at an increased risk of distal adenomas. Design: We included subjects with no prior adenoma or cancer from the Prostate, Lung, Colorectal, and Ovarian screening trial and whose results from flexible sigmoidoscopy exams indicated either no lesions (n = 34 817) or >= 1 distal adenoma (n = 3696). We used a 137-item food-frequency questionnaire to assess usual dietary intake over the preceding 12 mo. Using logistic regression analysis, we calculated, separately for men and women, prevalence odds ratios (ORs) and 95% CIs of sigmoidoscopy-detected, distal adenomas for quintiles of energy-adjusted dietary carbohydrate, glycemic index, and glycemic load. Results: ORs decreased with increasing intakes of carbohydrate for both the men and the women in unadjusted models, but these associations were attenuated in multivariate-adjusted models. Among the men, the association remained significant after adjustment (OR: 0.71; 95% CI 0.60, 0.84; P for trend < 0.0001), but in the women it did not (OR: 0.89; 95% CI: 0.73, 1.10; P for trend = 0.30). The results for glycemic index showed no associations in either men or women. Results for glycemic load closely mirrored those for carbohydrate. Conclusion: Despite expectations that increasing glycemic load and glycemic index would increase the risk of adenoma, we observed no association in women and even an inverse association in men. C1 Univ Minnesota, Div Epidemiol, Minneapolis, MN 55454 USA. NCI, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA. Fred Hutchinson Canc Res Ctr, Seattle, WA 98104 USA. Univ Washington, Seattle, WA 98195 USA. Univ Toronto, Toronto, ON, Canada. Henry Ford Hosp, Div Canc Control & Populat Sci, Detroit, MI 48202 USA. Univ Pittsburgh, Pittsburgh, PA USA. RP Flood, A (reprint author), Univ Minnesota, Div Epidemiol, 1300 S 2nd St,Suite 300, Minneapolis, MN 55454 USA. EM flood@epi.umn.edu RI Jenkins, David/A-1992-2009; OI Church, Timothy R./0000-0003-3292-5035 FU NCI NIH HHS [K07-CA108910-01A1] NR 46 TC 31 Z9 31 U1 1 U2 5 PU AMER SOC CLINICAL NUTRITION PI BETHESDA PA 9650 ROCKVILLE PIKE, SUBSCRIPTIONS, RM L-3300, BETHESDA, MD 20814-3998 USA SN 0002-9165 J9 AM J CLIN NUTR JI Am. J. Clin. Nutr. PD NOV PY 2006 VL 84 IS 5 BP 1184 EP 1192 PG 9 WC Nutrition & Dietetics SC Nutrition & Dietetics GA 104DZ UT WOS:000241937700032 PM 17093173 ER PT J AU Wright, ME Lawson, KA Weinstein, SJ Pietinen, P Taylor, PR Virtamo, J Albanes, D AF Wright, Margaret E. Lawson, Karla A. Weinstein, Stephanie J. Pietinen, Pirjo Taylor, Philip R. Virtamo, Jartno Albanes, Demetrius TI Higher baseline serum concentrations of vitamin E are associated with lower total and cause-specific mortality in the Alpha-Tocopherol, Beta-Carotene Cancer Prevention Study SO AMERICAN JOURNAL OF CLINICAL NUTRITION LA English DT Article DE antioxidants; alpha-tocopherol; cancer; cardiovascular disease; cohort study; mortality; smokers ID LIFE-STYLE FACTORS; GAMMA-TOCOPHEROL; FOLLOW-UP; CONTROLLED-TRIAL; CARDIOVASCULAR-DISEASE; ANTIOXIDANT VITAMINS; ELDERLY POPULATION; E SUPPLEMENTATION; MALE SMOKERS; ALL-CAUSE AB Background: A meta-analysis of 19 trials suggested a small increase in the risk of all-cause mortality with high-dose vitamin E supplementation. Little is known, however, about the relation between mortality and circulating concentrations of vitamin E resulting from dietary intake, low-dose supplementation, or both. Objective: We examined whether baseline serum a-tocopherol concentrations are associated with total and cause-specific mortality. Design: A prospective cohort study of 29 092 Finnish male smokers aged 50-69 y who participated in the Alpha-Tocopherol, Beta-Carotene Cancer Prevention (ATBC) Study was carried out. Fasting serum a-tocopherol was measured at baseline by using HPLC. Only 10% of participants reported vitamin E supplement use at baseline, and thus serum concentrations of vitamin E mainly reflected dietary intake and other host factors. Risks of total and cause-specific mortality were estimated by using proportional hazards models. Results: During up to 19 y of follow-up, 13 380 deaths (including 4518 and 5776 due to cancer and cardiovascular disease, respectively) were identified. Men in the higher quintiles of serum a-tocopherol had significantly lower risks of total and cause-specific mortality than did those in the lowest quintile [relative risk (RR) = 0.82 (95% CI: 0.78, 0.86) for total mortality and 0.79 (0.72, 0.86), 0.81 (0.75, 0.88), and 0.70 (0.63, 0.79) for deaths due to cancer, cardiovascular disease, and other causes, respectively; P for trend for all < 0.0001]. Cubic regression spline analysis of continuous serum a-tocopherol values indicated greater risk reductions with increasing concentrations up to approximate to 13-14 mg/L, after which no further benefit was noted. Conclusion: Higher circulating concentrations of a-tocopherol within the normal range are associated with significantly lower total and cause-specific mortality in older male smokers. C1 NCI, Div Canc Epidemiol & Genet, NIH, Bethesda, MD 20892 USA. NCI, Nutr Epidemiol Branch, NIH, Bethesda, MD 20892 USA. NCI, Genet Epidemiol Branch, NIH, Bethesda, MD 20892 USA. NCI, Canc Prevent Fellowhip Program, Div Canc Prevent, NIH, Bethesda, MD 20892 USA. Natl Publ Hlth Inst, Dept Hlth Promot & Chron Dis Prevent, Helsinki, Finland. RP Wright, ME (reprint author), NCI, Div Canc Epidemiol & Genet, NIH, 6120 Execut Blvd,EPS 3048, Bethesda, MD 20892 USA. EM wrighmar@mail.nih.gov RI Albanes, Demetrius/B-9749-2015 FU Intramural NIH HHS NR 49 TC 69 Z9 70 U1 3 U2 6 PU AMER SOC CLINICAL NUTRITION PI BETHESDA PA 9650 ROCKVILLE PIKE, SUBSCRIPTIONS, RM L-3300, BETHESDA, MD 20814-3998 USA SN 0002-9165 J9 AM J CLIN NUTR JI Am. J. Clin. Nutr. PD NOV PY 2006 VL 84 IS 5 BP 1200 EP 1207 PG 8 WC Nutrition & Dietetics SC Nutrition & Dietetics GA 104DZ UT WOS:000241937700034 PM 17093175 ER PT J AU Kant, AK Graubard, BI AF Kant, Ashima K. Graubard, Barry I. TI Secular trends in patterns of self-reported food consumption of adult Americans: NHANES 1971-1975 to NHANES 1999-2002 SO AMERICAN JOURNAL OF CLINICAL NUTRITION LA English DT Article DE secular trends; National Health and Nutrition Examination Surveys; NHANES; eating frequency; snack intake; breakfast intake; energy density; evening eating; portion size; energy intake; obesity; body mass index ID NUTRITION EXAMINATION SURVEY; 3RD NATIONAL-HEALTH; ENERGY-INTAKE; DIETARY-INTAKE; UNITED-STATES; NUTRIENT INTAKE; PORTION SIZES; WEIGHT CHANGE; US CHILDREN; BODY-WEIGHT AB Background: The contributors to trends in increasing prevalence of obesity in the US population are poorly understood. Objective: We examined secular trends in food consumption behaviors to understand their possible contribution to increasing energy intakes and adiposity in the American population. Design: We used dietary data from 4 consecutive National Health and Nutrition Examination Surveys (NHANES) to examine trends (1971-2002) in frequency of eating episodes, meal and snack consumption, quantity of food consumed, and the energy density of foods reported by adult Americans (n = 39 094). Logistic and linear regression methods were used to adjust for multiple covariates and survey design. Results: The reported number of all eating episodes increased slightly in women from 4.90 in 1971-1975 to 5.04 in 1999-2002 (P for trend = 0.002). The amount (in g) of foods and beverages consumed, the energy density of foods, and energy intake per eating episode increased, but the mention of breakfast declined in both sexes (P for trend < 0.0001). The observed trends in mention of a snack (in men) and percentage of energy from evening food intake (in women) were downward. The amount (in g) of foods and their energy density were independent positive correlates of obesity in combined data from all surveys (P for trend < 0.0001). Conclusions: Our results do not support large increases in eating frequency, snacking, or evening eating by the American population from 1971 to 2002. The quantity of foods and their energy density increased beginning in NHANES III (1988-1994) with trajectories roughly parallel to the rates of prevalence of obesity in the US population. However, we urge cautious interpretation of these results because of concurrent changes in dietary methods during this period. C1 CUNY Queens Coll, Dept Family Nutr & Exercise Sci, Flushing, NY 11367 USA. NCI, Div Canc Epidemiol & Genet, Biostat Branch, NIH, Bethesda, MD 20892 USA. RP Kant, AK (reprint author), CUNY Queens Coll, Dept Family Nutr & Exercise Sci, Remsen Hall,Room 306E, Flushing, NY 11367 USA. EM ashima.kant@qc.cuny.edu FU Intramural NIH HHS; NIDDK NIH HHS [R21 DK069413, DK069413] NR 43 TC 131 Z9 132 U1 3 U2 26 PU AMER SOC CLINICAL NUTRITION PI BETHESDA PA 9650 ROCKVILLE PIKE, SUBSCRIPTIONS, RM L-3300, BETHESDA, MD 20814-3998 USA SN 0002-9165 J9 AM J CLIN NUTR JI Am. J. Clin. Nutr. PD NOV PY 2006 VL 84 IS 5 BP 1215 EP 1223 PG 9 WC Nutrition & Dietetics SC Nutrition & Dietetics GA 104DZ UT WOS:000241937700036 PM 17093177 ER PT J AU Green, D Cushman, M Dermond, N Johnson, EA Castro, C Arnett, D Hill, J Manolio, TA AF Green, David Cushman, Mary Dermond, Norma Johnson, Eric A. Castro, Cecilia Arnett, Donna Hill, Joel Manolio, Teri A. TI Obtaining informed consent for genetic studies - The Multiethnic Study of Atherosclerosis SO AMERICAN JOURNAL OF EPIDEMIOLOGY LA English DT Article DE DNA; genetics; informed consent ID CLINICAL-TRIALS; POPULATION; PARTICIPATION; COHORT AB Studies of DNA may yield important information about atherosclerosis. To determine how often study participants' consent to examine DNA is denied and the factors associated with that denial, information was collected on participants in the US Multiethnic Study of Atherosclerosis (MESA) during 2000-2004. Permission was sought for preparation of DNA, transformation of cells into cell lines, evaluation of genes related to heart and other health conditions, and access to DNA by private companies. Of the 5,494 participants at entry, 897 (16.3%) refused consent for some items and 247 (4.5%) completely denied consent. At a second examination 18 months later, 819 (15.0%) partially refused and 229 (4.2%) completely denied consent. Age among men (odds ratio per 10 years = 0.68, 95% confidence interval: 0.54, 0.85; p = 0.004), ethnicity (odds ratio for African American = 2.34, 95% confidence interval: 1.66, 3.32; p < 0.001), and field center (p < 0.001) were associated with complete denial. For those giving partial consent, the most common item refused was access to DNA by private companies (baseline: 99%; second examination: 90%); younger age, male gender, and African-American ethnicity were associated with refusal. The authors concluded that a small percentage of participants in epidemiologic studies refuse consent for DNA studies, and the majority are concerned about sharing their DNA data with industry. C1 Northwestern Univ, Feinberg Sch Med, Dept Med, Chicago, IL 60611 USA. Univ Vermont, Dept Med, Colchester, VT USA. Univ Vermont, Dept Pathol, Colchester, VT USA. Univ Washington, Dept Biostat, Seattle, WA 98195 USA. Columbia Univ Coll Phys & Surg, Dept Med, New York, NY 10032 USA. Univ Alabama, Dept Epidemiol, Birmingham, AL 35294 USA. Johns Hopkins Univ, Bloomberg Sch Publ Hlth, Dept Epidemiol, Baltimore, MD USA. Natl Heart & Lung Inst, Div Epidemiol & Clin Applicat, NIH, Bethesda, MD USA. RP Green, D (reprint author), 676 N St Clair St,Suite 850, Chicago, IL 60611 USA. EM d-green@northwestern.edu FU NHLBI NIH HHS [N01-HC-95159, N01-HC-95165, N01-HC-95169] NR 20 TC 13 Z9 13 U1 0 U2 1 PU OXFORD UNIV PRESS INC PI CARY PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA SN 0002-9262 J9 AM J EPIDEMIOL JI Am. J. Epidemiol. PD NOV 1 PY 2006 VL 164 IS 9 BP 845 EP 851 DI 10.1093/aje/kwj286 PG 7 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA 097FI UT WOS:000241432000005 PM 16928727 ER PT J AU Kannel, WB AF Kannel, William B. TI Cardiovascular disease preventive measures for the older patient: An epidemiologic perspective SO AMERICAN JOURNAL OF GERIATRIC CARDIOLOGY LA English DT Editorial Material ID CORONARY-HEART-DISEASE; UNRECOGNIZED MYOCARDIAL-INFARCTION; ISOLATED SYSTOLIC HYPERTENSION; BLOOD-PRESSURE; METABOLIC SYNDROME; DIABETES-MELLITUS; CHOLESTEROL; RISK; PROGRESSION; POPULATION C1 Boston Univ, Sch Med Framington Heart Study, NHLBI, Framingham, MA 01702 USA. RP Kannel, WB (reprint author), Boston Univ, Sch Med Framington Heart Study, NHLBI, 73 Mt Wayte Ave, Framingham, MA 01702 USA. EM billkannel@yahoo.com FU NHLBI NIH HHS [N01 HC 25195] NR 40 TC 3 Z9 3 U1 0 U2 0 PU LE JACQ LTD PI DARIEN PA 3 PARKLANDS DRIVE, DARIEN, CT 06820 USA SN 1076-7460 J9 AM J GERIATR CARDIOL JI Am. J. Geriatr. Cardiol. PD NOV-DEC PY 2006 VL 15 IS 6 BP 382 EP 388 DI 10.1111/j.1076-7460.2006.04397.x PG 7 WC Cardiac & Cardiovascular Systems; Geriatrics & Gerontology SC Cardiovascular System & Cardiology; Geriatrics & Gerontology GA 104BS UT WOS:000241931500011 PM 17086034 ER PT J AU Martin, BK Frangakis, CE Rosenberg, PR Mintzer, JE Katz, IR Porsteinsson, AP Schneider, LS Rabins, PV Munro, CA Meinert, CL Niederehe, G Lyketsos, CG AF Martin, Barbara K. Frangakis, Constantine E. Rosenberg, Paul R. Mintzer, Jacobo E. Katz, Ira R. Porsteinsson, Anton P. Schneider, Lon S. Rabins, Peter V. Munro, Cynthia A. Meinert, Curtis L. Niederehe, George Lyketsos, Constantine G. TI Design of depression in Alzheimer's disease study-2 SO AMERICAN JOURNAL OF GERIATRIC PSYCHIATRY LA English DT Article DE Alzheimer disease; depression; randomized; controlled trial; clinical trial; selective serotonin reuptake inhibitors; sertraline ID PROVISIONAL DIAGNOSTIC-CRITERIA; LONG-TERM-CARE; DOUBLE-BLIND; BEHAVIORAL DISTURBANCES; CONTROLLED TRIAL; CLINICAL-TRIAL; CACHE COUNTY; DEMENTIA; PLACEBO; PREVALENCE AB Objective: Research on the efficacy of antidepressant therapy for depressive symptoms in Alzheimer disease has been hampered by lack of systematic diagnosis, small sample sizes, and short-term follow up. To address these issues, the authors present the design of the Depression in Alzheimer's Disease Study-2 (DIADS-2), a randomized, placebo-controlled multicenter trial to evaluate the efficacy and safety of the selective serotonin reuptake inhibitor sertraline for the treatment of depression in people with Alzheimer disease. Methods: The authors present and discuss the following important aspects of the design: the inclusion of structured psychosocial therapy for the caregivers of all participants; the measurement not only of patient mood outcomes, but also of global and functional outcomes for patients and mood and burden outcomes for caregivers; the ongoing rating of multiple diagnostic criteria to allow nosologic study of depression in Alzheimer disease; the evaluation of both short-term efficacy and longer-term outcomes; the follow up of all patients regardless of whether they complete study treatment; and the unmasking of treatment assignment at the conclusion of each patient's treatment phase. Conclusions: The authors believe these design elements are important features to be included in trials of depression and other neuropsychiatric disturbances in Alzheimer disease. C1 Johns Hopkins Bloomberg Sch Publ Hlth, Baltimore, MD USA. Johns Hopkins Sch Med, Baltimore, MD USA. Med Univ S Carolina, Charleston, SC 29425 USA. Univ Penn, Sch Med, Philadelphia, PA 19104 USA. Univ Rochester, Sch Med, Rochester, NY USA. Univ So Calif, Keck Sch Med, Los Angeles, CA USA. NIMH, Bethesda, MD 20892 USA. RP Martin, BK (reprint author), John Hopkins Ctr Clin Trials, 615 N Wolfe St,Suite W5010, Baltimore, MD 21205 USA. EM bmartin@jhsph.edu FU NIMH NIH HHS [1U01MH066175, 1U01MH066177, 1U01MH068014, 1U01MH066136, 1U01MH066174, 1U01MH066176] NR 42 TC 22 Z9 22 U1 1 U2 1 PU AMER PSYCHIATRIC PUBLISHING, INC PI ARLINGTON PA 1000 WILSON BOULEVARD, STE 1825, ARLINGTON, VA 22209-3901 USA SN 1064-7481 J9 AM J GERIAT PSYCHIAT JI Am. J. Geriatr. Psychiatr. PD NOV PY 2006 VL 14 IS 11 BP 920 EP 930 DI 10.1097/01.JGP.0000240977.71305.ee PG 11 WC Geriatrics & Gerontology; Gerontology; Psychiatry SC Geriatrics & Gerontology; Psychiatry GA 104WY UT WOS:000241992500004 PM 17068314 ER PT J AU Simons-Morton, B AF Simons-Morton, Bruce TI Possible selves and proximal goals for the academy SO AMERICAN JOURNAL OF HEALTH BEHAVIOR LA English DT Editorial Material C1 NICHHD, Prevent Res Branch, Div Stat Epidemiol & Prevent Res, Bethesda, MD 20892 USA. RP Simons-Morton, B (reprint author), NICHHD, Prevent Res Branch, Div Stat Epidemiol & Prevent Res, 6100 Execut Blvd 7B13M, Bethesda, MD 20892 USA. EM mortonb@mail.nih.gov OI Simons-Morton, Bruce/0000-0003-1099-6617 NR 0 TC 0 Z9 0 U1 0 U2 2 PU PNG PUBLICATIONS PI STAR CITY PA PO BOX 4593, STAR CITY, WV 26504-4593 USA SN 1087-3244 J9 AM J HEALTH BEHAV JI Am. J. Health Behav. PD NOV-DEC PY 2006 VL 30 IS 6 BP 598 EP 601 PG 4 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA 104ZJ UT WOS:000241998800006 PM 17096617 ER PT J AU Hemachandra, AH Klebanoff, MA AF Hemachandra, Anusha H. Klebanoff, Mark A. TI Use of serial ultrasound to identify periods of fetal growth restriction in relation to neonatal anthropometry SO AMERICAN JOURNAL OF HUMAN BIOLOGY LA English DT Article ID CORONARY HEART-DISEASE; BIRTH-WEIGHT; BREAST-CANCER; DUTCH FAMINE; PRENATAL EXPOSURE; WOMEN; RISK; AGE; INFANCY; OBESITY AB The developmental origins of the health and disease hypothesis suggests that fetal growth restriction (FGR) is a risk factor for several chronic diseases of adulthood. However, most supporting studies use birth weight as a proxy measure of FGR. To examine the relationship between birth weight and FGR, the present study used serial prenatal ultrasound to identify periods of FGR during gestation, and related these periods to birth size and shape. The data in this study included serial prenatal ultrasounds performed on 1,349 high-risk Scandinavian women enrolled in the National Institute of Child Health and Human Development Study of Successive Small for Gestational Age Births. Fetal growth velocity between ultrasounds was used to identify periods of isolated FGR, and these were studied in relation to anthropometry at birth. FGR was identified in 184 subjects. A control group of 384 subjects without FGR was also identified. Infants with first-trimester FGR (n = 20) had the highest birth weight, ponderal index, and subscapular skinfold thickness. Infants with second-trimester FGR (n = 37) had the highest arm fat percentage. Infants with early third-trimester FGR (n = 55) had the lowest mean birth weight and ponderal index. When infant gender, gestational age, maternal body mass index, and smoking were controlled, birth weight was predicted only by third-trimester FGR (not first- or second-trimester FGR), and arm fat percent was predicted only by second-trimester FGR. These results suggest that birth weight is not a valid indicator of FGR occurring before the third trimester. Body composition may be a more sensitive marker of early FGR. C1 NICHD, NIH, DESPR, Div Epidemiol Stat & Prevent Res,Dept Hlth & Huma, Bethesda, MD 20892 USA. Johns Hopkins Univ, Sch Med, Div Neonatol, Baltimore, MD 21287 USA. RP Hemachandra, AH (reprint author), NICHD, NIH, DESPR, Div Epidemiol Stat & Prevent Res,Dept Hlth & Huma, Bldg 6100,Room 7B07, Bethesda, MD 20892 USA. EM hemachaa@mail.nih.gov FU Intramural NIH HHS NR 26 TC 24 Z9 24 U1 0 U2 4 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 1042-0533 J9 AM J HUM BIOL JI Am. J. Hum. Biol. PD NOV-DEC PY 2006 VL 18 IS 6 BP 791 EP 797 DI 10.1002/ajhb.20552 PG 7 WC Anthropology; Biology SC Anthropology; Life Sciences & Biomedicine - Other Topics GA 098TC UT WOS:000241544700007 PM 17039476 ER PT J AU Psaty, BM Arnold, AM Olson, J Saad, MF Shea, S Post, W Burke, GL AF Psaty, Bruce M. Arnold, Alice M. Olson, Jean Saad, Mohammed F. Shea, Steven Post, Wendy Burke, Gregory L. TI Association between levels of blood pressure and measures of subclinical disease - Multi-ethnic study of atherosclerosis SO AMERICAN JOURNAL OF HYPERTENSION LA English DT Article DE hypertension; subclinical disease; cardiovascular disease; observational study ID LEFT-VENTRICULAR HYPERTROPHY; CORONARY-ARTERY CALCIUM; RISK-FACTORS; CARDIOVASCULAR-DISEASE; ESSENTIAL-HYPERTENSION; COMPUTED-TOMOGRAPHY; MAGNETIC-RESONANCE; HEART-DISEASE; CALCIFICATION; ADULTS AB Background: High blood pressure (BP) is associated with the presence and severity of subclinical disease. Less is known about associations between normal levels of BP and various measures of subclinical disease. Methods: The Multi-Ethnic Study of Atheroclerosis (MESA) enrolled 6814 participants free of clinical cardiovascular disease (38% white, 28% African American, 22% Hispanic, and 12% Asian). The baseline examination included standardized measures of BP, common carotid intimal-medial thickness determined by ultrasonography, coronary artery calcium by computed tomography, and left ventricular mass by magnetic resonance imaging. Participants with treated hypertension (n = 2173) were excluded. Statistical methods included analysis of variance, linear regression, and chi(2) tests. Results: Among the 4640 participants, BP was strongly related to age and African American ethnicity. Carotid intimal-medial thickness was directly associated with systolic BP (SBP) and inversely associated with diastolic BP (DBP, P <.001 for both). For SBP in men, for instance, the adjusted regression coefficient was 0.058 mm per 1 SD (21 mm Hg; 95% CI, 0.045 to 0.070), and for SBP in women it was 0.043 (95% CI, 0.033 to 0.052). Left ventricular mass was directly related to SBP and DBP. The proportion with non-zero calcium scores increased with SBP but decreased with DBP. Conclusions: The range of BP examined in this study fell largely within the normal or prehypertension stage. In cross-sectional analysis of data from a population-based study, these untreated levels of BP were associated with a variety of measures of subclinical cardiovascular disease. C1 Univ Washington, Cardiovasc Hlth Res Unit, Seattle, WA 98101 USA. Univ Washington, Dept Med, Seattle, WA 98195 USA. Univ Washington, Dept Epidemiol, Seattle, WA 98195 USA. Univ Washington, Dept Hlth Serv, Seattle, WA 98195 USA. Univ Washington, Dept Biostat, Seattle, WA 98195 USA. NHLBI, Epidemiol & Biometry Program, Div Epidemiol & Clin Applicat, Bethesda, MD 20892 USA. Stony Brook Med Sch, Dept Prevent Med, Stony Brook, NY USA. Columbia Univ, Dept Med, New York, NY USA. Columbia Univ, Dept Epidemiol, New York, NY USA. Johns Hopkins Univ, Dept Med, Baltimore, MD USA. Johns Hopkins Univ, Dept Epidemiol, Baltimore, MD USA. Wake Forest Univ, Sch Med, Dept Publ Hlth Sci, Winston Salem, NC 27109 USA. RP Psaty, BM (reprint author), Univ Washington, Cardiovasc Hlth Res Unit, 1730 Minor Ave,Suite 1360, Seattle, WA 98101 USA. EM psaty@u.washington.edu FU NHLBI NIH HHS [N01-HC-95169, N01-HC-95165, N01-HC-95164, N01-HC-95162, N01-HC-95160, N01-HC-95163, N01-HC-95161, HL43201, N01-HC-95159, HL74745]; NIA NIH HHS [AG09556] NR 30 TC 19 Z9 20 U1 0 U2 1 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0895-7061 J9 AM J HYPERTENS JI Am. J. Hypertens. PD NOV PY 2006 VL 19 IS 11 BP 1110 EP 1117 DI 10.1016/j.amjhyper.2006.04.002 PG 8 WC Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 107AF UT WOS:000242142400005 PM 17070420 ER PT J AU Anderson, DE Metter, EJ Hougaku, H Najjar, SS AF Anderson, David E. Metter, E. Jeffrey Hougaku, Hidetaka Najjar, Samer S. TI Suppressed anger is associated with increased carotid arterial stiffness in older adults SO AMERICAN JOURNAL OF HYPERTENSION LA English DT Article DE age; anger; arterial stiffness; blood pressure; carotid artery ID INTIMA-MEDIA THICKNESS; BLOOD-PRESSURE; TRAIT ANGER; CARDIOVASCULAR-DISEASE; ESSENTIAL-HYPERTENSION; AORTIC STIFFNESS; ATHEROSCLEROSIS; WOMEN; MEN; PROGRESSION AB Background: Anger and hostility have been implicated in the pathogenesis of heart disease, but the extent to which the large conduit arteries play an intermediate role in this relationship remains to be clarified. The present study investigated associations of anger frequency and expression style with carotid artery intima-media thickness (IMT) and stiffness in healthy adults older than 50 years. Methods: Two hundred participants (95 men) in the Baltimore Longitudinal Study of Aging completed the Spielberger Anger Expression Inventory, which assesses anger frequency (trait anger), anger expression (angerout), and anger suppression (anger-in). The carotid artery IMT was assessed by ultrasonography. Carotid stiffness was determined from the log of systolic over diastolic blood pressure (BP) as a function of carotid distensibility. Results: In univariate correlational analysis, a significant positive association of anger-in with stiffness was observed (P <.01), together with a less significant association of anger-in with carotid artery IMT (P <.05). Neither anger-out nor trait anger was significantly associated with carotid artery IMT or stiffness. Moreover, none of the anger measures was significantly associated with resting BP in this normotensive sample. As expected, carotid artery IMT, stiffness, and systolic BP were all positively associated. In multivariate analysis, anger-in remained a determinant of stiffness independent of BP, and a marginally significant determinant of carotid artery IMT. Conclusions: This is the first known finding that high anger-in is a significant independent determinant of carotid artery stiffness. These results suggest that high anger-in can potentiate the effects of age on stiffening of the central arteries. C1 NIA, Cardiovasc Sci Lab, Baltimore, MD 21224 USA. NIA, Clin Res Branch, Baltimore, MD 21224 USA. Osaka Univ, Grad Sch Med, Osaka, Japan. RP Anderson, DE (reprint author), Gerontol Res Ctr, Cardiovasc Sci Lab, 5600 Nathan Shock Dr, Baltimore, MD 21224 USA. EM AndersoD@GRC.NIA.NIH.GOV NR 33 TC 12 Z9 15 U1 0 U2 4 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0895-7061 J9 AM J HYPERTENS JI Am. J. Hypertens. PD NOV PY 2006 VL 19 IS 11 BP 1129 EP 1134 DI 10.1016/j.amjhyper.2006.04.018 PG 6 WC Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 107AF UT WOS:000242142400008 PM 17070423 ER PT J AU Khan, A Hyde, RK Dutra, A Mohide, P Liu, P AF Khan, Aneal Hyde, R. Katherine Dutra, Amalia Mohide, Patrick Liu, Paul TI Core binding factor beta (CBFB) haploinsufficiency due to an interstitial deletion at 16q21q22 resulting in delayed cranial ossification, cleft palate, congenital heart anomalies, and feeding difficulties but favorable outcome SO AMERICAN JOURNAL OF MEDICAL GENETICS PART A LA English DT Article DE CBFB; core binding factor; deletion; 16q21; cranial suture diastasis ID LONG ARM; SKELETAL DEVELOPMENT; PARTIAL MONOSOMY; CHROMOSOME 16; RUNX3; EXPRESSION; GENE; MATURATION; MUTATIONS; PHENOTYPE AB The core binding factor beta gene (CBFB), essential to bone rnorphogenesis, is located at 16q22.1. Homozygous deficiency of CBFB leads to ossification defects in mice. CBFB forms a heterodimer with RUNX2 (CBFA1) during embryonic bone development. RUNX2 mutations lead to cleidocranial dysplasia in humans. We describe an infant boy with an interstitial deletion of 16q21q22, delayed skull ossification, cleft palate, and heart anomalies who had a difficult course in infancy but eventually improved and is healthy. He was found to have CBFB haploinsufficiency, but did not have mutations in RUNX2. We suggest that 16q21q22 deletion be considered when there are antenatal or postnatal findings of enlarged cranial sutures with or without cleft palate. The finding of CBFB haploinsufficiency in our case and the similarity of cranial ossification defects with a mouse model of CBFB deletion suggest a role for CBFB in cranial bone development in humans. (c) 2006 Wiley-Liss, Inc. C1 McMaster Univ, MaMaster Childrens Hosp, Dept Pediat, Hamilton, ON L8N 3Z5, Canada. NHGRI, Genet & Mol Biol Branch, NIH, Bethesda, MD 20892 USA. McMaster Univ, Med Ctr, Dept Obstet & Gynecol, Hamilton, ON, Canada. RP Khan, A (reprint author), McMaster Univ, MaMaster Childrens Hosp, Dept Pediat, Rm 3N18,1200 Main St W, Hamilton, ON L8N 3Z5, Canada. EM anealkhan@mac.com RI Liu, Paul/A-7976-2012 OI Liu, Paul/0000-0002-6779-025X NR 29 TC 14 Z9 15 U1 0 U2 5 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 1552-4825 J9 AM J MED GENET A JI Am. J. Med. Genet. A PD NOV 1 PY 2006 VL 140A IS 21 BP 2349 EP 2354 DI 10.1002/ajmg.a.31479 PG 6 WC Genetics & Heredity SC Genetics & Heredity GA 103SF UT WOS:000241906300013 PM 17022082 ER PT J AU Bagnato, F Butman, JA Gupta, S Calabrese, M Pezawas, L Ohayon, JM Tovar-Moll, F Riva, M Cao, MM Talagala, SL McFarland, HF AF Bagnato, F. Butman, J. A. Gupta, S. Calabrese, M. Pezawas, L. Ohayon, J. M. Tovar-Moll, F. Riva, M. Cao, M. M. Talagala, S. L. McFarland, H. F. TI In vivo detection of cortical plaques by MR imaging in patients with multiple sclerosis SO AMERICAN JOURNAL OF NEURORADIOLOGY LA English DT Article; Proceedings Paper CT 42nd Annual Meeting of the American-Society-of-Neuroradiology CY JUN 05-11, 2004 CL Seattle, WA SP Amer Soc Neuroradiol ID ATTENUATED INVERSION-RECOVERY; APPEARING WHITE-MATTER; CEREBRAL-CORTEX; SPIN-ECHO; BRAIN; LESIONS; DEMYELINATION; REGISTRATION; IMPAIRMENT; PATHOLOGY AB BACKGROUND AND PURPOSE: In vivo detection of cortical lesions in patients with multiple sclerosis (MS) by MR imaging is hampered by several factors. Among them is the low contrast between small cortical lesions and surrounding cortical gray matter offered by present techniques, METHODS: T1-weighted 3D spoiled gradient-recalled-echo (SPGR) volumes and 2D fluid-attenuated inversion recovery (FLAIR) sequences of 22 patients with MS who had 12 monthly brain MR imaging examinations at 1.5T, using a quadrature head coil, were retrospectively analyzed. These serial studies were coregistered and averaged to generate a single high signal-to-noise ratio (SNR) mean image, which was used to identify cortical lesions. The means of 12 FLAIRs and SPGRs from 14 age- and sex-matched healthy volunteers were analyzed as well. RESULTS: No cortical lesions were found on images of healthy subjects. Eighty-six cortical lesions were identified in 13 (59.1%) patients, predominantly in the frontal lobe (73.3%); 23.3% of cortical lesions lay entirely in the cortex, whereas the remaining lesions invaded the white matter underneath. CONCLUSION: Averaging multiple SPGRs created a single high SNR volume, allowing identification of cortical lesions. Because data were obtained monthly for 1 year, the average image does not account for transient lesion activity. However, for cortical lesions that remained stable during this time, the findings are valid in demonstrating the importance of high SNR images for detecting cortical brain abnormalities in MS. C1 NINDS, NIB, NIH, Bethesda, MD 20892 USA. NIH, Dept Diagnost Radiol, Warren G Magnuson Clin Ctr, Bethesda, MD 20892 USA. New York Med Coll, Valhalla, NY 10595 USA. Genes Cognit & Psychosis Program, Bethesda, MD USA. NINDS, NIH, MRI Res Facil, Bethesda, MD 20892 USA. RP Bagnato, F (reprint author), NINDS, NIB, NIH, 10 Ctr Dr,Bldg 10,Room 5B16, Bethesda, MD 20892 USA. EM bagnatof@ninds.nih.gov RI Butman, John/A-2694-2008; OI Pezawas, Lukas/0000-0002-1329-6352; Riva, Marco/0000-0003-4643-6451; Butman, John/0000-0002-1547-9195 FU Intramural NIH HHS NR 32 TC 54 Z9 55 U1 1 U2 2 PU AMER SOC NEURORADIOLOGY PI OAK BROOK PA 2210 MIDWEST RD, OAK BROOK, IL 60521 USA SN 0195-6108 J9 AM J NEURORADIOL JI Am. J. Neuroradiol. PD NOV-DEC PY 2006 VL 27 IS 10 BP 2161 EP 2167 PG 7 WC Clinical Neurology; Neuroimaging; Radiology, Nuclear Medicine & Medical Imaging SC Neurosciences & Neurology; Radiology, Nuclear Medicine & Medical Imaging GA 109CE UT WOS:000242284700033 PM 17110688 ER PT J AU Engel, SM Olshan, AF Siega-Riz, AM Savitz, DA Chanock, SJ AF Engel, Stephanie M. Olshan, Andrew F. Siega-Riz, Anna Maria Savitz, David A. Chanock, Stephen J. TI Polymorphisms in folate metabolizing genes and risk for spontaneous preterm and small-for-gestational age birth SO AMERICAN JOURNAL OF OBSTETRICS AND GYNECOLOGY LA English DT Article DE preterm birth; small for gestational age; intrauterine growth; MTHFR; polymorphism; SHMT1; MTRR; MTR ID NEURAL-TUBE DEFECTS; METHIONINE SYNTHASE REDUCTASE; INTRAUTERINE GROWTH RESTRICTION; SERINE HYDROXYMETHYLTRANSFERASE GENES; METHYLENETETRAHYDROFOLATE REDUCTASE; PLASMA HOMOCYSTEINE; THYMIDYLATE SYNTHASE; COMMON MUTATION; PREGNANCY; THROMBOPHILIA AB Objective: Variants in the folate metabolism pathway affect the accumulation of homocysteine are modified by nutrient levels and have been linked to adverse birth outcomes. Study design: We examined the relationship among MTHFR(677), MTHFR(1298), MTR(2756), MTRR(66), and SHMT1(1420), dietary folate intake, and preterm and small-for-gestational-age (SGA) birth in a nested case-control study of black and white women. Results: White carriers of SHMT1(1420) T or MTRR(66)A had an increased risk of spontaneous preterm birth (odds ratio [OR] = 1.9, 95% CI 1.1-3.1; OR = 2.0, 95% CI 1.1-3.6 respectively). In black women, there appeared to be an interaction between dietary folate intake and the SHMT1 (1420) T variant allele, such that only carriers who also were in the lowest quartile of dietary folate intake had higher risk of spontaneous preterm birth (OR = 2.6, 95% CI 0.8-8.0) and SGA (OR = 2.9, 95% CI 0.9-8.9). Conclusion: Our results suggest the possibility of a direct or indirect role for the SHMT1 (1420) T variant in spontaneous preterm or SGA births. (c) 2006 Mosby, Inc. All rights reserved. C1 Mt Sinai Sch Med, Dept Community & Prevent Med, New York, NY USA. Univ N Carolina, Dept Epidemiol, Carolina Populat Ctr, Chapel Hill, NC USA. Univ N Carolina, Sch Publ Hlth, Dept Nutr, Chapel Hill, NC 27599 USA. NCI, Core Genotyping Facil, Adv Technol Ctr, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA. NCI, Sect Genom Variat, Pediat Oncol Branch, Ctr Canc Res, Bethesda, MD 20892 USA. RP Engel, SM (reprint author), Mt Sinai Sch Med, Dept Community & Prevent Med, New York, NY USA. NR 38 TC 22 Z9 27 U1 1 U2 4 PU MOSBY, INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 USA SN 0002-9378 J9 AM J OBSTET GYNECOL JI Am. J. Obstet. Gynecol. PD NOV PY 2006 VL 195 IS 5 BP 1231 EP 1239 DI 10.1016/j.ajog.2006.07.024 PG 9 WC Obstetrics & Gynecology SC Obstetrics & Gynecology GA 105MZ UT WOS:000242035700007 ER PT J AU Dunn, TA Chen, SL Faith, DA Hicks, JL Platz, EA Chen, YD Ewing, CM Sauvageot, J Isaacs, WB De Marzo, AM Luo, J AF Dunn, Thomas A. Chen, Shenglin Faith, Dennis A. Hicks, Jessica L. Platz, Elizabeth A. Chen, Yidong Ewing, Charles M. Sauvageot, Jurga Isaacs, William B. De Marzo, Angelo M. Luo, Jun TI A novel role of myosin VI in human prostate cancer SO AMERICAN JOURNAL OF PATHOLOGY LA English DT Article ID GENE-EXPRESSION ANALYSIS; BORDER CELL-MIGRATION; UNCONVENTIONAL MYOSIN; MOLECULAR ASPECTS; DROSOPHILA; MOTOR; REVEALS; PROTEIN; TISSUE; OVEREXPRESSION AB Myosin VI is an actin motor that moves to the minus end of the polarized actin filament, a direction opposite to all other characterized myosins. Using expression microarrays, we identified myosin VI as one of the top genes that demonstrated cancer-specific overexpression in clinical prostate specimens. Protein expression of myosin VI was subsequently analyzed in arrayed prostate tissues from 240 patients. Notably, medium-grade prostate cancers demonstrated the most consistent cancer-specific myosin VI protein overexpression, whereas prostate cancers associated with more aggressive histological features continued to overexpress myosin VI but to a lesser extent. Myosin VI protein expression in cell lines positively correlated with the presence of androgen receptor. Small interference RNA-mediated myosin VI knockdown in the LNCaP human prostate cancer cell line resulted in impaired in vitro migration and soft-agar colony formation. Depletion of myosin VI expression was also accompanied by global gene expression changes reflective of attenuated tumorigenic potential, as marked by a nearly 10-fold induction of TXNIP (VDUP1), a tumor suppressor with decreased expression in prostate cancer specimens. These results support that myosin VI is critical in maintaining the malignant properties of the majority of human prostate cancers diagnosed today. C1 Johns Hopkins Univ, Sch Med, Dept Urol, Baltimore, MD 21287 USA. Johns Hopkins Univ, Sch Med, Dept Pathol, Baltimore, MD 21287 USA. Johns Hopkins Bloomberg Sch Publ Hlth, Dept Epidemiol, Baltimore, MD USA. NHGRI, Canc Genet Branch, Bethesda, MD 20892 USA. RP Luo, J (reprint author), Johns Hopkins Univ, Sch Med, Dept Urol, 411 Marburg Bldg,600 N Wolfe St, Baltimore, MD 21287 USA. EM ademarz@jhmi.edu; jluol@jhmi.edu RI Chen, Shenglin/B-4049-2010 FU NCI NIH HHS [P50 CA058236, P50CA58236] NR 43 TC 65 Z9 66 U1 1 U2 4 PU AMER SOC INVESTIGATIVE PATHOLOGY, INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3993 USA SN 0002-9440 J9 AM J PATHOL JI Am. J. Pathol. PD NOV PY 2006 VL 169 IS 5 BP 1843 EP 1854 DI 10.2353/ajpath.2006.060316 PG 12 WC Pathology SC Pathology GA 099OD UT WOS:000241603700030 PM 17071605 ER PT J AU Periwal, V Chow, CC AF Periwal, Vipul Chow, Carson C. TI Patterns in food intake correlate with body mass index SO AMERICAN JOURNAL OF PHYSIOLOGY-ENDOCRINOLOGY AND METABOLISM LA English DT Article DE obesity; overweight; energy density ID AFFECTS ENERGY-INTAKE; WITHIN-SUBJECT VARIATION; AFFECTS SATIETY; WEIGHT CONTROL; LIQUID FOOD; US ADULTS; OBESITY; WOMEN; VOLUME; MEN AB Quantifying eating behavior may give clues to both the physiological and behavioral mechanisms behind weight regulation. We analyzed year-long dietary records of 29 stable-weight subjects. The records showed wide daily variations of food intake. We computed the temporal auto-correlation and skewness of food intake mass, energy, carbohydrate, fat, and protein. We also computed the cross-correlation coefficient between intake mass and intake energy. The mass of the food intake exhibited long-term trends that were positively skewed, with wide variability among individuals. The average duration of the trends (P = 0.003) and the skewness (P = 0.006) of the food intake mass were significantly correlated with mean body mass index (BMI). We also found that the lower the correlation coefficient between the energy content and the mass of food intake, the higher the BMI. Our results imply that humans in neutral energy balance eating ad libitum exhibit a long-term positive bias in the food intake that operates partially through the mass of food eaten to defend against eating too little more vigorously than eating too much. C1 NIDDK, NIH, LBM, Bethesda, MD 20892 USA. RP Chow, CC (reprint author), NIDDK, NIH, LBM, Bldg 12A,Room 4007,MSC 5621, Bethesda, MD 20892 USA. EM carsonc@niddk.nih.gov RI Chow, Carson/A-7970-2009; Periwal, Vipul/I-1728-2012 FU Intramural NIH HHS NR 39 TC 7 Z9 7 U1 0 U2 0 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA SN 0193-1849 J9 AM J PHYSIOL-ENDOC M JI Am. J. Physiol.-Endocrinol. Metab. PD NOV PY 2006 VL 291 IS 5 BP E929 EP E936 DI 10.1152/ajpendo.00122.2006 PG 8 WC Endocrinology & Metabolism; Physiology SC Endocrinology & Metabolism; Physiology GA 092OC UT WOS:000241106200009 PM 16772324 ER PT J AU Gladwin, MT Raat, NJH Shiva, S Dezfulian, C Hogg, N Kim-Shapiro, DB Patel, RP AF Gladwin, Mark T. Raat, Nicolaas J. H. Shiva, Sruti Dezfulian, Cameron Hogg, Neil Kim-Shapiro, Daniel B. Patel, Rakesh P. TI Nitrite as a vascular endocrine nitric oxide reservoir that contributes to hypoxic signaling, cytoprotection, and vasodilation SO AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY LA English DT Review DE hemoglobin; hypoxia; S-nitrosated albumin; cysteine 93 ID RED-BLOOD-CELLS; ISCHEMIA-REPERFUSION INJURY; MYOCARDIAL OXYGEN-CONSUMPTION; GUANYLATE-CYCLASE ACTIVATION; FATTY-ACID TRANSDUCTION; S-NITROSOHEMOGLOBIN; IN-VIVO; PHYSIOLOGICAL CONDITIONS; RELAXING FACTOR; SODIUM-NITRITE AB Accumulating evidence suggests that the simple and ubiquitous anion salt, nitrite (NO2-), is a physiological signaling molecule with potential roles in intravascular endocrine nitric oxide (NO) transport, hypoxic vasodilation, signaling, and cytoprotection after ischemia-reperfusion. Human and animal studies of nitrite treatment and NO gas inhalation provide evidence that nitrite mediates many of the systemic therapeutic effects of NO gas inhalation, including peripheral vasodilation and prevention of ischemia-reperfusion-mediated tissue infarction. With regard to nitrite-dependent hypoxic signaling, biochemical and physiological studies suggest that hemoglobin possesses an allosterically regulated nitrite reductase activity that reduces nitrite to NO along the physiological oxygen gradient, potentially contributing to hypoxic vasodilation. An expanded consideration of nitrite as a hypoxia-dependent intrinsic signaling molecule has opened up a new field of research and therapeutic opportunities for diseases associated with regional hypoxia and vasoconstriction. C1 NHLBI, Vasc Med Branch, Bethesda, MD 20892 USA. NIH, Dept Crit Care Med, Ctr Clin, Bethesda, MD 20892 USA. Johns Hopkins Univ Hosp, Pediat Anesthesia & Crit Care Med Div, Baltimore, MD 21287 USA. Med Coll Wisconsin, Milwaukee, WI 53226 USA. Wake Forest Univ, Dept Phys, Winston Salem, NC 27109 USA. Univ Alabama, Dept Pathol, Birmingham, AL USA. Univ Alabama, Ctr Free Rad Biol, Birmingham, AL USA. RP Gladwin, MT (reprint author), NHLBI, Vasc Med Branch, Bldg 10 CRC,Rm 5-5140,10 Ctr Dr,MSC 1454, Bethesda, MD 20892 USA. EM mgladwin@nih.gov OI Dezfulian, Cameron/0000-0002-4486-0446; Patel, Rakesh/0000-0002-1526-4303 NR 103 TC 171 Z9 174 U1 1 U2 17 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA SN 0363-6135 J9 AM J PHYSIOL-HEART C JI Am. J. Physiol.-Heart Circul. Physiol. PD NOV PY 2006 VL 291 IS 5 BP H2026 EP H2035 DI 10.1152/ajpheart.00407.2006 PG 10 WC Cardiac & Cardiovascular Systems; Physiology; Peripheral Vascular Disease SC Cardiovascular System & Cardiology; Physiology GA 092NB UT WOS:000241102700002 PM 16798825 ER PT J AU Wise, RA AF Wise, Roy A. TI The parsing of food reward SO AMERICAN JOURNAL OF PHYSIOLOGY-REGULATORY INTEGRATIVE AND COMPARATIVE PHYSIOLOGY LA English DT Editorial Material ID WATER TEMPERATURE; MEMORY; REINFORCEMENT; AMPHETAMINE; PREFERENCE; DOPAMINE; SUCROSE; RATS C1 NIDA, Intramural Res Program, NIH, Baltimore, MD 21224 USA. RP Wise, RA (reprint author), NIDA, Intramural Res Program, NIH, Baltimore, MD 21224 USA. EM rwise@mail.nih.gov RI Wise, Roy/A-6465-2012 NR 18 TC 6 Z9 6 U1 0 U2 3 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA SN 0363-6119 J9 AM J PHYSIOL-REG I JI Am. J. Physiol.-Regul. Integr. Comp. Physiol. PD NOV PY 2006 VL 291 IS 5 BP R1234 EP R1235 DI 10.1152/ajpregu.00443.2006 PG 2 WC Physiology SC Physiology GA 092OE UT WOS:000241106400004 PM 17028286 ER PT J AU Jensen, AM Li, CL Praetorius, HA Norregaard, R Frische, S Knepper, MA Nielsen, S Frokiaer, J AF Jensen, Anja M. Li, Chunling Praetorius, Helle A. Norregaard, Rikke Frische, Sebastian Knepper, Mark A. Nielsen, Soren Frokiaer, Jorgen TI Angiotensin II mediates downregulation of aquaporin water channels and key renal sodium transporters in response to urinary tract obstruction SO AMERICAN JOURNAL OF PHYSIOLOGY-RENAL PHYSIOLOGY LA English DT Article DE aquaporins; angiotensin; AT(1)-receptor blockade ID THICK ASCENDING LIMB; MEDULLARY COLLECTING DUCT; BILATERAL URETERAL OBSTRUCTION; LONG-TERM REGULATION; RAT-KIDNEY; ALTERED EXPRESSION; CONCENTRATING DEFECT; TUBULAR REABSORPTION; CL COTRANSPORTER; HENLES LOOP AB The renin-angiotensin system is well known to be involved in the pathophysiological changes in renal function after obstruction of the ureter. Previously, we demonstrated that bilateral ureteral obstruction (BUO) is associated with dramatic changes in the expression of both renal sodium transporters and aquaporin water channels (AQPs). We now examined the effects of the AT1-receptor antagonist candesartan on the dysregulation of AQPs and key renal sodium transporters in rats subjected to 24-h BUO and followed 2 days after release of BUO (BUO-2R). Consistent with previous observations, BUO-2R resulted in a significantly decreased expression of AQP1, -2, and -3 compared with control rats. Concomitantly, the rats developed polyuria and reduced urine osmolality. Moreover, expression of the type 2 Na-phosphate cotransporter (NaPi-2) and type 1 bumetanide-sensitive Na-K-2Cl cotransporter (NKCC2) was markedly reduced, consistent with postobstructive natriuresis. Candesartan treatment from the onset of obstruction attenuated the reduction in GFR (3.1 +/- 0.4 vs. 1.7 +/- 0.3 ml center dot min(-1)center dot kg(-1)) and partially prevented the reduction in the expression of AQP2 (66 +/- 21 vs. 13 +/- 2%, n = 7; P < 0.05), NaPi-2 (84 +/- 6 vs. 57 +/- 10%, n = 7; P < 0.05), and NKCC2 (89 +/- 12 vs. 46% +/- 11, n = 7; P < 0.05). Consistent with this, candesartan treatment attenuated the increase in urine output (58 +/- 4 vs. 97 +/- 5 mu l center dot min(-1)center dot kg(-1), n = 7; P < 0.01) and the reduction in sodium reabsorption (433 +/- 62 vs. 233 +/- 45 mu mol center dot min(-1)center dot kg(-1), n = 7; P < 0.05) normally found in rats subjected to BUO. Moreover, candesartan treatment attenuated induction of cyclooxygenase 2 (COX-2) expression in the inner medulla, suggesting that COX-2 induction in response to obstruction is regulated by ANG II. In conclusion, candesartan prevents dysregulation of AQP2, sodium transporters, and development of polyuria seen in BUO. This strongly supports the view that candesartan protects kidney function in response to urinary tract obstruction. C1 Univ Aarhus, Water & Salt Res Ctr, Aarhus, Denmark. Univ Aarhus, Inst Clin Med, Aarhus, Denmark. Univ Aarhus, Inst Anat, Aarhus, Denmark. NHLBI, NIH, Lab Kidney & Electrolyte Metab, Bethesda, MD 20892 USA. RP Frokiaer, J (reprint author), Aarhus Univ Hosp, Inst Clin Med, Dept Clin Physiol, Water & Salt Res Ctr, Brendstrupgaardsvej, DK-8200 Aarhus N, Denmark. EM JF@KI.AU.DK RI Frische, Sebastian/B-2332-2009 OI Frische, Sebastian/0000-0002-0270-3602 FU Intramural NIH HHS [Z01 HL001285-21, Z99 HL999999] NR 59 TC 32 Z9 33 U1 0 U2 5 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA SN 1931-857X J9 AM J PHYSIOL-RENAL JI Am. J. Physiol.-Renal Physiol. PD NOV PY 2006 VL 291 IS 5 BP F1021 EP F1032 DI 10.1152/ajprenal.00387.2005 PG 12 WC Physiology; Urology & Nephrology SC Physiology; Urology & Nephrology GA 092OD UT WOS:000241106300012 PM 16757730 ER PT J AU Freedman, DM Sigurdson, AJ Rajaraman, P Doody, MM Linet, MS Ron, E AF Freedman, D. Michal Sigurdson, Alice J. Rajaraman, Preetha Doody, Michele M. Linet, Martha S. Ron, Elaine TI The mortality risk of smoking and obesity combined SO AMERICAN JOURNAL OF PREVENTIVE MEDICINE LA English DT Article ID BODY-MASS INDEX; US ADULTS; RADIOLOGIC TECHNOLOGISTS; DISEASE RISK; WEIGHT; PREVALENCE; OVERWEIGHT; ASSOCIATION; COHORT; TRENDS AB Background: Both smoking and obesity have been linked to increased mortality, but evaluating the joint effect has been limited. This nationwide, prospective mortality study of U.S. radiologic technologists was designed to evaluate the combined mortality risks of obesity and smoking. Methods: Mortality risk was investigated in 64,120 women and 18,760 men who completed a baseline questionnaire (1983 to 1989). Body mass index (BMI) (weight adjusted for height, or kilograms divided by meters squared) was calculated from self-reported weight and height at baseline, with five categories: less than 18.5 (underweight), 18.5 to 24.9 (normal), 25.0 to 29.9 (overweight), 30.0 to 34.9 (moderately obese), and 35.0 and higher (very obese). Participants were followed from the questionnaire until the date of death or through 2002, whichever occurred first. The combined association among BMI and smoking and all-cause, cancer, and circulatory disease mortality by gender and attained age (less than 65 years, 65 years and older) was examined using Cox proportional hazards regression analyses (conducted in 2005). Person-years at risk averaged 16 years (women aged less than 65), 6 years (women aged 65 and older), 15 years (men aged less than 65), and 7 years (men aged 65 and older), totaling 1.35 million person-years. Results: In all gender/age groups, both obesity and smoking, particularly current smoking, contributed substantially to all-cause mortality, with 3.5- to 5-fold risks for very obese, current smokers compared to normal weight, never smokers. Current smoking was the predominant risk factor for cancer mortality. Combining obesity with current smoking increased circulatory disease mortality by 6- to 11-fold for people aged less than 65 years, compared to normal weight, never smokers. Obese former smokers (less than 65 years) had notably lower risks. Conclusions: Obese smokers (aged less than 65 years) had strikingly high mortality risks, particularly from circulatory disease mortality. C1 NCI, Div Canc Epidemiol & Genet, Radiat Epidemiol Branch, Bethesda, MD 20892 USA. RP Freedman, DM (reprint author), NCI, Div Canc Epidemiol & Genet, Radiat Epidemiol Branch, Execut Plaza S,Room 7036,6120 Execut Blvd, Bethesda, MD 20892 USA. EM mf101e@nih.gov FU Intramural NIH HHS; NCI NIH HHS [N01-CP-15673, N01-CP-51016, N02-CP-81005, N02-CP-81121] NR 19 TC 53 Z9 53 U1 0 U2 10 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0749-3797 EI 1873-2607 J9 AM J PREV MED JI Am. J. Prev. Med. PD NOV PY 2006 VL 31 IS 5 BP 355 EP 362 DI 10.1016/j.amepre.2006.07.022 PG 8 WC Public, Environmental & Occupational Health; Medicine, General & Internal SC Public, Environmental & Occupational Health; General & Internal Medicine GA 098RX UT WOS:000241541600001 PM 17046405 ER PT J AU Atienza, AA Yaroch, AL Masse, LC Moser, RP Hesse, BW King, AC AF Atienza, Audie A. Yaroch, Amy L. Masse, Louise C. Moser, Richard P. Hesse, Bradford W. King, Abby C. TI Identifying sedentary subgroups - The National Cancer Institute's Health Information National Trends Survey SO AMERICAN JOURNAL OF PREVENTIVE MEDICINE LA English DT Article ID CARDIOVASCULAR-DISEASE RISK; PHYSICAL-ACTIVITY; LOGISTIC-REGRESSION; OBESITY; OVERWEIGHT; ADULTS; WOMEN; PROGRAMS; DESIGN; SAMPLE AB Background: Developing effective interventions for the 24% to 28% of U.S. adults who are sedentary requires a better understanding of the factors related to sedentary lifestyles as well as the communication channels to reach various subgroups. This study identified key sociodemographic and health communication characteristics of various subgroups with high rates of inactivity using signal detection methodology. Methods: The sample from the nationally representative Health Information National Trends Survey 2003 (n = 6369) was randomly split into two samples. Exploratory analyses (conducted 2004 and 2005) were employed on the first sample to identify various subgroups, and the stability of inactivity rates in those subgroups was examined in the second sample. Results: Eight subgroups with varying levels of inactivity were identified. Three subgroups had inactivity levels of 40% or higher, while the lowest subgroup had a level of less than 15%. The highest inactivity subgroup consisted of individuals with at least some college education who were in fair/poor health and who watched 4 or more hours of television per day. The second-highest inactivity subgroup was composed of those without a college education who tended not to use or attend to many communication channels. The third highest inactive subgroup consisted of those without a college education who read the newspaper and were obese. Levels of inactivity in the second independent sample subgroups were not significantly different from those found in the exploratory sample. Conclusions: This study identified empirically based, physically inactive subgroups that differed on sociodemographic and health communication characteristics. This information should be useful in creating future evidence-based, targeted, and tailored intervention strategies. C1 NCI, Div Canc Control & Populat Sci, Behav Res Program, Hlth Promot Res Branch, Bethesda, MD 20892 USA. Stanford Univ, Sch Med, Dept Med,Stanford Prvenet Res Ctr, Div Epidemiol,Dept Hlth Res & Policy, Stanford, CA 94305 USA. RP Atienza, AA (reprint author), NCI, Div Canc Control & Populat Sci, Behav Res Program, Hlth Promot Res Branch, 6130 Execut Blvd,EPN 407AA,MSC 7335, Bethesda, MD 20892 USA. EM atienzaa@mail.nih.gov OI Hesse, Bradford/0000-0003-1142-1161 FU Intramural NIH HHS [Z99 CA999999] NR 31 TC 18 Z9 18 U1 1 U2 2 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0749-3797 J9 AM J PREV MED JI Am. J. Prev. Med. PD NOV PY 2006 VL 31 IS 5 BP 383 EP 390 DI 10.1016/j.ampere.2006.07.024 PG 8 WC Public, Environmental & Occupational Health; Medicine, General & Internal SC Public, Environmental & Occupational Health; General & Internal Medicine GA 098RX UT WOS:000241541600005 PM 17046409 ER PT J AU Rush, AJ Trivedi, MH Wisniewski, SR Nierenberg, AA Stewart, JW Warden, D Niederehe, G Thase, ME Lavori, PW Lebowitz, BD McGrath, PJ Rosenbaum, JF Sackeim, HA Kupfer, DJ Luther, J Fava, M AF Rush, A. John Trivedi, Madhukar H. Wisniewski, Stephen R. Nierenberg, Andrew A. Stewart, Jonathan W. Warden, Diane Niederehe, George Thase, Michael E. Lavori, Philip W. Lebowitz, Barry D. McGrath, Patrick J. Rosenbaum, Jerrold F. Sackeim, Harold A. Kupfer, David J. Luther, James Fava, Maurizio TI Acute and longer-term outcomes in depressed outpatients requiring one or several treatment steps: A STAR*D report SO AMERICAN JOURNAL OF PSYCHIATRY LA English DT Article ID SEQUENCED TREATMENT ALTERNATIVES; TREATMENT-RESISTANT DEPRESSION; MEDICATION ALGORITHM PROJECT; ILLNESS RATING-SCALE; REPORT QIDS-SR; QUICK INVENTORY; PSYCHOMETRIC EVALUATION; CLINICAL GUIDELINES; MAJOR DEPRESSION; DISORDERS AB Objective: This report describes the participants and compares the acute and longer-term treatment outcomes associated with each of four successive steps in the Sequenced Treatment Alternatives to Relieve Depression (STAR*D) trial. Method: A broadly representative adult outpatient sample with nonpsychotic major depressive disorder received one (N = 3,671) to four (N = 123) successive acute treatment steps. Those not achieving remission with or unable to tolerate a treatment step were encouraged to move to the next step. Those with an acceptable benefit, preferably symptom remission, from any particular step could enter a 12-month naturalistic follow-up phase. A score of = 5 on the Quick Inventory of Depressive Symptomatology-Self-Report (QIDS-SR16) (equivalent to = 7 on the 17-item Hamilton Rating Scale for Depression [HRSD17]) defined remission; a QIDS-SR16 total score of = 11 (HRSD17 >= 14) defined relapse. Results: The QIDS-SR16 remission rates were 36.8%, 30.6%, 13.7%, and 13.0% for the first, second, third, and fourth acute treatment steps, respectively. The overall cumulative remission rate was 67%. Overall, those who required more treatment steps had higher relapse rates during the naturalistic follow-up phase. In addition, lower relapse rates were found among participants who were in remission at follow-up entry than for those who were not after the first three treatment steps. Conclusions: When more treatment steps are required, lower acute remission rates (especially in the third and fourth treatment steps) and higher relapse rates during the follow-up phase are to be expected. Studies to identify the best multistep treatment sequences for individual patients and the development of more broadly effective treatments are needed. C1 Univ Texas, SW Med Ctr, Dept Psychiat, Dallas, TX 75390 USA. Univ Pittsburgh, Dept Epidemiol, Pittsburgh, PA 15260 USA. Univ Pittsburgh, Dept Psychiat, Pittsburgh, PA 15260 USA. Massachusetts Gen Hosp, Cln Psychopharmacol Unit, Boston, MA 02114 USA. New York State Psychiat Inst & Hosp, New York, NY 10032 USA. Columbia Univ, Coll Phys & Surg, Dept Psychiat, New York, NY 10027 USA. NIMH, Bethesda, MD 20892 USA. Stanford Univ, VA Cooperat Studies Program, Stanford, CA 94305 USA. Univ Calif San Diego, Sam & Rose Stein Inst Res Aging, La Jolla, CA 92093 USA. RP Rush, AJ (reprint author), Univ Texas, SW Med Ctr, Dept Psychiat, 5323 Harry Hines Blvd, Dallas, TX 75390 USA. EM john.rush@utsouthwestern.edu RI McGrath, Patrick/I-6410-2013; OI McGrath, Patrick/0000-0001-7217-7321; Wisniewski, Stephen/0000-0002-3877-9860; Rush, Augustus/0000-0003-2004-2382 FU NIMH NIH HHS [N01MH90003] NR 59 TC 1335 Z9 1375 U1 20 U2 93 PU AMER PSYCHIATRIC PUBLISHING, INC PI ARLINGTON PA 1000 WILSON BOULEVARD, STE 1825, ARLINGTON, VA 22209-3901 USA SN 0002-953X J9 AM J PSYCHIAT JI Am. J. Psychiat. PD NOV PY 2006 VL 163 IS 11 BP 1905 EP 1917 DI 10.1176/appi.ajp.163.11.1905 PG 13 WC Psychiatry SC Psychiatry GA 100LF UT WOS:000241669900014 PM 17074942 ER PT J AU Winterer, G Musso, F Beckmann, C Mattay, V Egan, MF Jones, DW Callicott, JH Coppola, R Weinberger, DR AF Winterer, Georg Musso, Francesco Beckmann, Christian Mattay, Venkata Egan, Michael F. Jones, Douglas W. Callicott, Joseph H. Coppola, Richard Weinberger, Daniel R. TI Instability of prefrontal signal processing in schizophrenia SO AMERICAN JOURNAL OF PSYCHIATRY LA English DT Article ID CEREBRAL BLOOD-FLOW; INDEPENDENT COMPONENT ANALYSIS; WORKING-MEMORY PERFORMANCE; ANTERIOR CINGULATE CORTEX; TO-NOISE RATIO; PHYSIOLOGICAL DYSFUNCTION; GENETIC RISK; FRONTOTEMPORAL CONNECTIVITY; FRONTAL ACTIVATION; FMRI AB Objective: Prefrontal dysfunction is considered a fundamental characteristic of schizophrenia. Recent electrophysiological evidence points to a major instability of signal processing in prefrontal cortical microcircuits because of reduced phase-synchronization (i.e., an increased stimulusrelated variability [noise] of single-trial responses in the spatial and time domain). The authors used functional magnetic resonance imaging (fMRI) during a visual two-choice reaction task in order to measure, with higher topographic accuracy, signal stability in patients with schizophrenia and its relationship to more traditional measures of activation. Method: Twelve clinically stable inpatients with schizophrenia and 16 matched comparison subjects were evaluated. Event-related blood-oxygen-level-dependent responses were subjected to an analysis of residual noise variance and to independent data dimension independent component analysis in the medial prefrontal cortex. Results: In patients with schizophrenia, the authors found increased residual noise variance of the blood-oxygen-level-dependent response that predicted the level of prefrontal activation in these subjects. In the left hemisphere, residual noise variance strongly correlated with psychotic symptoms. Independent component analysis revealed a "fractionized" and unfocussed pattern of activation in patients. Conclusions: These findings suggest that unstable cortical signal processing underlies classic abnormal cortical activation patterns as well as psychosis in schizophrenia. C1 NIH, Genes Cognit & Psychosis Program, NIMH, Bethesda, MD 20892 USA. Univ Mainz, Dept Psychiat, Lab Mol Neuroimaging & Electrophysiol, D-6500 Mainz, Germany. Oxford Ctr Funct Magnet Resonance Imaging Brain, Oxford, England. RP Weinberger, DR (reprint author), NIH, Genes Cognit & Psychosis Program, NIMH, 10 Ctr Dr,MSC 1379, Bethesda, MD 20892 USA. EM weinberd@intra.nimh.nih.gov RI Beckmann, Christian/E-6374-2012; Callicott, Joseph/C-9102-2009 OI Callicott, Joseph/0000-0003-1298-3334 NR 51 TC 37 Z9 37 U1 0 U2 1 PU AMER PSYCHIATRIC PUBLISHING, INC PI ARLINGTON PA 1000 WILSON BOULEVARD, STE 1825, ARLINGTON, VA 22209-3901 USA SN 0002-953X J9 AM J PSYCHIAT JI Am. J. Psychiat. PD NOV PY 2006 VL 163 IS 11 BP 1960 EP 1968 DI 10.1176/appi.ajp.163.11.1960 PG 9 WC Psychiatry SC Psychiatry GA 100LF UT WOS:000241669900020 PM 17074948 ER PT J AU Tan, HY Sust, S Buckholtz, JW Mattay, VS Meyer-Lindenberg, A Egan, MF Weinberger, DR Callicott, JH AF Tan, Hao-Yang Sust, Steven Buckholtz, Joshua W. Mattay, Venkata S. Meyer-Lindenberg, Andreas Egan, Michael F. Weinberger, Daniel R. Callicott, Joseph H. TI Dysfunctional prefrontal regional specialization and compensation in schizophrenia SO AMERICAN JOURNAL OF PSYCHIATRY LA English DT Article ID CORTICAL PYRAMIDAL NEURONS; DENDRITIC SPINE DENSITY; VERBAL WORKING-MEMORY; PHYSIOLOGICAL DYSFUNCTION; FUNCTIONAL CONNECTIVITY; CORTEX DYSFUNCTION; FMRI; MANIPULATION; MAINTENANCE; INFORMATION AB Objective: It has been suggested that in healthy persons higher-order cognitive processing engaged by incremental working memory load hierarchically employs more dorsal than ventral prefrontal resources in healthy individuals. Given that working memory performance is impaired in schizophrenia, especially at higher executive loads, the authors investigated how this prefrontal functional organization might be altered in disease, independent of performance deficits. Method: Using N-back working memory functional magnetic resonance imaging (fMRI) data, the authors studied 15 patients with schizophrenia and 26 healthy comparison subjects. Subgroups based on median performance accuracy at 2-back were analyzed; high performers included eight schizophrenia patients and 14 comparison subjects, and low performers included seven patients and 12 comparison subjects. Results: High-performing but not low-performing comparison subjects responded to incremental working memory executive load with disproportionately greater dorsal but not ventral prefrontal cortex activation, which also predicted performance accuracy. In the high-and low-performing patient groups, incremental working memory load caused a disproportionate increase in ventral but not dorsal prefrontal cortex activation relative to the respective comparison group, which also correlated with accuracy. Functional connectivity between the ventral prefrontal cortex and posterior parietal cortex was relatively greater in patients, whereas comparison subjects had greater functional connectivity between the dorsal prefrontal cortex and posterior parietal cortex. Conclusions: The hierarchical organization of the prefrontal cortex may be compromised in schizophrenia, resulting in loss of functional specialization and integration at the dorsal prefrontal cortex and in compensatory activation from the ventral prefrontal cortex, which may ultimately affect working memory and executive cognition. C1 NIMH, Unit Funct MRI, Clin Brain Disorders Branch, Intramural Res Program, Bethesda, MD 20892 USA. RP Callicott, JH (reprint author), NIMH, Unit Funct MRI, Clin Brain Disorders Branch, Intramural Res Program, 10 Ctr Dr,Rm 4C-216,MSC 1364, Bethesda, MD 20892 USA. EM callicottj@mail.nih.gov RI Buckholtz, Joshua /E-7299-2010; Callicott, Joseph/C-9102-2009; Meyer-Lindenberg, Andreas/H-1076-2011 OI Buckholtz, Joshua /0000-0002-9418-8686; Callicott, Joseph/0000-0003-1298-3334; Meyer-Lindenberg, Andreas/0000-0001-5619-1123 FU Intramural NIH HHS NR 41 TC 142 Z9 144 U1 2 U2 10 PU AMER PSYCHIATRIC PUBLISHING, INC PI ARLINGTON PA 1000 WILSON BOULEVARD, STE 1825, ARLINGTON, VA 22209-3901 USA SN 0002-953X J9 AM J PSYCHIAT JI Am. J. Psychiat. PD NOV PY 2006 VL 163 IS 11 BP 1969 EP 1977 DI 10.1176/appi.ajp.163.11.1969 PG 9 WC Psychiatry SC Psychiatry GA 100LF UT WOS:000241669900021 PM 17074949 ER PT J AU Mann, JM AF Mann, J. M. TI Health and human rights - If not now, when? SO AMERICAN JOURNAL OF PUBLIC HEALTH LA English DT Editorial Material C1 Natl Lib Med, Hist Med Div, Bethesda, MD 20974 USA. Univ New S Wales, Sch Publ Hlth & Community Med, Sydney, NSW, Australia. Harvard Univ, Sch Publ Hlth, Program Int Hlth & Human Rights, Boston, MA 02115 USA. Univ Rochester, Dept Hist, Rochester, NY 14627 USA. Univ Rochester, Dept Community & Prevent Med, Rochester, NY 14627 USA. RP Mann, JM (reprint author), Natl Lib Med, Hist Med Div, 8600 Rockville Pike, Bethesda, MD 20974 USA. NR 0 TC 4 Z9 4 U1 0 U2 3 PU AMER PUBLIC HEALTH ASSOC INC PI WASHINGTON PA 800 I STREET, NW, WASHINGTON, DC 20001-3710 USA SN 0090-0036 J9 AM J PUBLIC HEALTH JI Am. J. Public Health PD NOV PY 2006 VL 96 IS 11 BP 1940 EP 1943 DI 10.2105/AJPH.2006.098079 PG 4 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA 098RM UT WOS:000241540500013 PM 17062844 ER PT J AU Tarantola, D Gruskin, S Brown, TM Fee, E AF Tarantola, Daniel Gruskin, Sofia Brown, Theodore M. Fee, Elizabeth TI Jonathan Mann - Founder of the Health and Human Rights Movements SO AMERICAN JOURNAL OF PUBLIC HEALTH LA English DT Biographical-Item C1 Natl Lib Med, Hist Med Div, Bethesda, MD 20974 USA. Univ New S Wales, Sch Publ Hlth & Community Med, Sydney, NSW, Australia. Harvard Univ, Sch Publ Hlth, Program Int Hlth & Human Rights, Boston, MA 02115 USA. Univ Rochester, Dept Hist, Rochester, NY 14627 USA. Univ Rochester, Dept Community & Prevent Med, Rochester, NY 14627 USA. RP Tarantola, D (reprint author), Natl Lib Med, Hist Med Div, 8600 Rockville Pike, Bethesda, MD 20974 USA. NR 1 TC 3 Z9 3 U1 0 U2 0 PU AMER PUBLIC HEALTH ASSOC INC PI WASHINGTON PA 800 I STREET, NW, WASHINGTON, DC 20001-3710 USA SN 0090-0036 J9 AM J PUBLIC HEALTH JI Am. J. Public Health PD NOV PY 2006 VL 96 IS 11 BP 1942 EP 1943 DI 10.2105/AJPH.2006.098079 PG 2 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA 098RM UT WOS:000241540500014 PM 17018812 ER PT J AU Grady, C Hampson, LA Wallen, GR Rivera-Goba, MV Carrington, KL Mittleman, BB AF Grady, Christine Hampson, Lindsay A. Wallen, Gwenyth R. Rivera-Goba, Migdalia V. Carrington, Kelli L. Mittleman, Barbara B. TI Exploring the ethics of clinical research in an urban community SO AMERICAN JOURNAL OF PUBLIC HEALTH LA English DT Article ID AFRICAN-AMERICANS; MEDICAL-RESEARCH; PARTICIPATION; WILLINGNESS; STRATEGIES; DISTRUST; TRIALS; RACE AB Objectives. We consulted with representatives of an urban community in Washington, DC, about the ethics of clinical research involving residents of the community with limited access to health care. Methods. A semistructured community consultation was conducted with core members of the Health Partnership Program of the National Institute of Arthritis and Musculoskeletal and Skin Diseases. Three research case examples were discussed; questions and probes (a predetermined question or series of questions used to further investigate or follow-up a response) guided the discussion. Results. The community representatives who took part in the consultation were supportive of research and appreciated the opportunity to be heard. They noted the importance of respecting the circumstances, values, needs, and welfare of research participants; supported widely representative recruitment strategies; and cited the positive benefits of providing care or treatment to participants. Monitoring participants' welfare and ensuring care at a study's end were emphasized. Trust was a central theme; participants suggested several trust-enhancing strategies, including full disclosure of information and the involvement of advocates, physicians, and trusted church members. Conclusions. Several important strategies emerged for conducting ethical research in urban communities whose residents have limited access to health care. C1 Natl Inst Hlth, Dept Clin Bioeth, Bethesda, MD 20892 USA. Natl Inst Hlth, Off Res & Outcomes Management, Dept Nursing, Bethesda, MD 20892 USA. NIAMSD, NIH, Bethesda, MD 20892 USA. RP Grady, C (reprint author), Natl Inst Hlth, Dept Clin Bioeth, Bldg 10,1C118, Bethesda, MD 20892 USA. EM cgrady@nih.gov OI Hampson, Lindsay/0000-0002-0740-7984 NR 23 TC 15 Z9 15 U1 0 U2 2 PU AMER PUBLIC HEALTH ASSOC INC PI WASHINGTON PA 800 I STREET, NW, WASHINGTON, DC 20001-3710 USA SN 0090-0036 J9 AM J PUBLIC HEALTH JI Am. J. Public Health PD NOV PY 2006 VL 96 IS 11 BP 1996 EP 2001 DI 10.2105/AJPH.2005.071233 PG 6 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA 098RM UT WOS:000241540500023 PM 17018826 ER PT J AU Chang, SH Yu, KN Lee, YS An, GH Beck, GR Colburn, NH Lee, KH Cho, MH AF Chang, Seung-Hee Yu, Kyeong Nam Lee, Yeon-Sook An, Gil-Hwan Beck, George R., Jr. Colburn, Nancy H. Lee, Kee-Ho Cho, Myung-Haing TI Elevated inorganic phosphate stimulates Akt-ERK1/2-Mnk1 signaling in human lung cells SO AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY LA English DT Article DE Akt; inorganic phosphate; Mnk1; nontumorigenic human bronchial epithelial cells ID OSTEOBLAST DIFFERENTIATION; DIETARY PHOSPHORUS; EPITHELIAL-CELLS; KINASE-B; PHOSPHORYLATION; HOMEOSTASIS; INHIBITION; SURVIVAL AB Inorganic phosphate (Pi) plays a critical role in diverse cellular functions. Among three classes of sodium/phosphate co-transporters (NPTs), two types have been identified in mammalian lung. The potential importance of Pi as a novel signaling molecule and pulmonary expression of NPTs with poor prognosis of diverse lung diseases including cancer have prompted us to begin to define the pathways by which Pi regulates nontumorigenic human bronchial epithelial cells. Pi activates Akt phosphorylation on Thr308 specifically, and activated signal transmits on the Raf/MEK/ERK signaling. Here, we report that Pi controls cell growth by activating ERK cascades and by facilitating the translocation of Mnk1 from cytosol into nucleus through an Akt-mediated MEK pathway. Sequentially, translocated Mnk1 increases elF4E-BP1 phosphorylation. As a result, Pi stimulates cap-dependent protein translation. Such Akt-mediated signaling of inorganic phosphate may provide critical clues for treatment as well as prevention of diverse lung diseases. C1 Seoul Natl Univ, Coll Vet Med, Toxicol Lab, Seoul 151742, South Korea. Seoul Natl Univ, Coll Human Ecol, Dept Food & Nutr, Seoul 151742, South Korea. Seoul Natl Univ, BK Program Vet Sci 21, Seoul 151742, South Korea. Korea Inst Radiol & Med Sci, Mol Oncol Lab, Seoul, South Korea. Chungnam Natl Univ, Dept Food Sci & Technol, Taejon 305764, South Korea. Emory Univ, Sch Med, Div Endocrinol Metab & Lipids, Atlanta, GA 30322 USA. NCI, Lab Canc Prevent, Frederick, MD 21701 USA. RP Cho, MH (reprint author), Seoul Natl Univ, Coll Vet Med, Toxicol Lab, 56-1,Sillim Dong, Seoul 151742, South Korea. EM mchotox@snu.ac.kr RI CHO, Myung-Haing/B-7362-2014 FU NCI NIH HHS [CA84573] NR 18 TC 31 Z9 32 U1 0 U2 0 PU AMER THORACIC SOC PI NEW YORK PA 1740 BROADWAY, NEW YORK, NY 10019-4374 USA SN 1044-1549 J9 AM J RESP CELL MOL JI Am. J. Respir. Cell Mol. Biol. PD NOV PY 2006 VL 35 IS 5 BP 528 EP 539 DI 10.1165/rcmb.2005-04770C PG 12 WC Biochemistry & Molecular Biology; Cell Biology; Respiratory System SC Biochemistry & Molecular Biology; Cell Biology; Respiratory System GA 102LT UT WOS:000241813300003 PM 16763222 ER PT J AU Sonenshine, DE Valenzuela, J Anderson, JM AF Sonenshine, Daniel E. Valenzuela, Jesus Anderson, Jennifer M. TI Proteins and peptides induced in the midguts of blood-fed ticks contribute to control of microbial infections: New insights from a cDNA library of midgut transcripts in Dermacentor variabilis SO AMERICAN JOURNAL OF TROPICAL MEDICINE AND HYGIENE LA English DT Meeting Abstract C1 Old Dominion Univ, Norfolk, VA USA. Natl Inst Hlth, NIAID, Lab Malaria & Vector Res, Rockville, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC TROP MED & HYGIENE PI MCLEAN PA 8000 WESTPARK DR, STE 130, MCLEAN, VA 22101 USA SN 0002-9637 J9 AM J TROP MED HYG JI Am. J. Trop. Med. Hyg. PD NOV PY 2006 VL 75 IS 5 SU S MA 3 BP 1 EP 1 PG 1 WC Public, Environmental & Occupational Health; Tropical Medicine SC Public, Environmental & Occupational Health; Tropical Medicine GA 109XW UT WOS:000242343900004 ER PT J AU Kelly-Hope, LA Alonso, WJ Thiem, VD Anh, DD Canh, DG Lee, H Smith, DL Miller, MA AF Kelly-Hope, Louise A. Alonso, Wladimir J. Thiem, Vu Dinh Anh, Dang Duc Canh, Do Gia Lee, Hyejon Smith, David L. Miller, Mark A. TI Spatio-temporal distribution and ecological determinants of enteric diseases in Vietnam, 1991-2001 SO AMERICAN JOURNAL OF TROPICAL MEDICINE AND HYGIENE LA English DT Meeting Abstract C1 NIH, Bethesda, MD 20892 USA. Natl Inst Hyg & Epidemiol, Hanoi, Vietnam. Int Vaccine Inst, Seoul, South Korea. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC TROP MED & HYGIENE PI MCLEAN PA 8000 WESTPARK DR, STE 130, MCLEAN, VA 22101 USA SN 0002-9637 J9 AM J TROP MED HYG JI Am. J. Trop. Med. Hyg. PD NOV PY 2006 VL 75 IS 5 SU S MA 43 BP 13 EP 13 PG 1 WC Public, Environmental & Occupational Health; Tropical Medicine SC Public, Environmental & Occupational Health; Tropical Medicine GA 109XW UT WOS:000242343900044 ER PT J AU Konda, KA Leon, SR Lescano, AG Klausner, JD Meza, R Jones, FR Caceres, CF Coates, TJ AF Konda, Kelika A. Leon, Segundo R. Lescano, Andres G. Klausner, Jeffrey D. Meza, Rina Jones, Franca R. Caceres, Carlos F. Coates, Thomas J. TI The epidemiology of syphilis cases in three socially marginalized populations of low-income, urban, coastal Peru SO AMERICAN JOURNAL OF TROPICAL MEDICINE AND HYGIENE LA English DT Meeting Abstract C1 Univ Calif Los Angeles, Los Angeles, CA USA. Univ Peruana Cayetano Heredia, Lima, Peru. USN, Med Res Ctr Detachment, Lima, Peru. Dept Publ Hlth, San Francisco, CA USA. USN, Med Res Ctr, Bethesda, MD 20084 USA. NIMH, Multisite Int Grp, Bethesda, MD 20892 USA. RI Lescano, Andres/B-8479-2008 OI Lescano, Andres/0000-0001-9779-633X NR 0 TC 0 Z9 1 U1 0 U2 0 PU AMER SOC TROP MED & HYGIENE PI MCLEAN PA 8000 WESTPARK DR, STE 130, MCLEAN, VA 22101 USA SN 0002-9637 J9 AM J TROP MED HYG JI Am. J. Trop. Med. Hyg. PD NOV PY 2006 VL 75 IS 5 SU S MA 46 BP 14 EP 14 PG 1 WC Public, Environmental & Occupational Health; Tropical Medicine SC Public, Environmental & Occupational Health; Tropical Medicine GA 109XW UT WOS:000242343900047 ER PT J AU Kaplan, J Easterbrook, JD Watson, J Reeves, W Vanasco, N Purcell, R Kosoy, M Graczyk, T Glass, G Klein, S AF Kaplan, Jenifer Easterbrook, Judy D. Watson, Julie Reeves, Will Vanasco, Norma Purcell, Robert Kosoy, Michael Graczyk, Thaddeus Glass, Gregory Klein, Sabra TI A survey of zoonotic pathogens carried by Norway rats in Baltimore, Maryland, USA SO AMERICAN JOURNAL OF TROPICAL MEDICINE AND HYGIENE LA English DT Meeting Abstract C1 Johns Hopkins Univ, Baltimore, MD USA. Johns Hopkins Bloomberg Sch Publ Hlth, Baltimore, MD USA. Johns Hopkins Univ, Sch Med, Baltimore, MD USA. Ctr Dis Control & Prevent, Atlanta, GA USA. Inst Nacl Enfermdades, Adm Nacl Lab Inst Salud, Santa Fe, Argentina. NIAID, Natl Inst Hlth, Bethesda, MD USA. NR 0 TC 0 Z9 0 U1 2 U2 4 PU AMER SOC TROP MED & HYGIENE PI MCLEAN PA 8000 WESTPARK DR, STE 130, MCLEAN, VA 22101 USA SN 0002-9637 J9 AM J TROP MED HYG JI Am. J. Trop. Med. Hyg. PD NOV PY 2006 VL 75 IS 5 SU S MA 80 BP 24 EP 24 PG 1 WC Public, Environmental & Occupational Health; Tropical Medicine SC Public, Environmental & Occupational Health; Tropical Medicine GA 109XW UT WOS:000242343900081 ER PT J AU Dembele, B Keita, AD Coulibaly, S Diallo, A Traore, AK Traore, SF Nutman, TB Klion, AD Coulibaly, YI AF Dembele, Benoit Keita, Adama D. Coulibaly, Siaka Diallo, Abdallah Traore, Abdel K. Traore, Sekou F. Nutman, Thomas B. Klion, Amy D. Coulibaly, Yaya I. TI Ultrasound assessment of subclinical hydroceles in a community coendemic for Wuchereria bancrofti and Mansonella perstans SO AMERICAN JOURNAL OF TROPICAL MEDICINE AND HYGIENE LA English DT Meeting Abstract C1 Univ Mali, Bamako, Mali. Ctr Dis Control, Bamako, Mali. NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC TROP MED & HYGIENE PI MCLEAN PA 8000 WESTPARK DR, STE 130, MCLEAN, VA 22101 USA SN 0002-9637 J9 AM J TROP MED HYG JI Am. J. Trop. Med. Hyg. PD NOV PY 2006 VL 75 IS 5 SU S MA 125 BP 37 EP 37 PG 1 WC Public, Environmental & Occupational Health; Tropical Medicine SC Public, Environmental & Occupational Health; Tropical Medicine GA 109XW UT WOS:000242343900126 ER PT J AU Konda, KA Sandoval, C Lescano, AG Giron, JM Salazar, X Jones, FR Coates, TJ Caceres, CF AF Konda, Kelika A. Sandoval, Clara Lescano, Andres G. Giron, Jessica M. Salazar, Ximena Jones, Franca R. Coates, Thomas J. Caceres, Carlos F. CA NIMHC HIV STD Prevention Trial Grp TI The characteristics, risk behaviors and STI prevalences among socially marginalized women in low-income urban, coastal Peru SO AMERICAN JOURNAL OF TROPICAL MEDICINE AND HYGIENE LA English DT Meeting Abstract C1 Univ Calif Los Angeles, Los Angeles, CA USA. Univ Peruana Cayetano Heredia, Lima, Peru. USN, Med Res Ctr Detachment, Lima, Peru. USN, Med Res Ctr, Bethesda, MD USA. NIMH, Multisite Int Grp, Bethesda, MD USA. RI Lescano, Andres/B-8479-2008 OI Lescano, Andres/0000-0001-9779-633X NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC TROP MED & HYGIENE PI MCLEAN PA 8000 WESTPARK DR, STE 130, MCLEAN, VA 22101 USA SN 0002-9637 J9 AM J TROP MED HYG JI Am. J. Trop. Med. Hyg. PD NOV PY 2006 VL 75 IS 5 SU S MA 138 BP 41 EP 41 PG 1 WC Public, Environmental & Occupational Health; Tropical Medicine SC Public, Environmental & Occupational Health; Tropical Medicine GA 109XW UT WOS:000242343900139 ER PT J AU Jiang, L Duriseti, S Sun, P Miller, LH AF Jiang, Lubin Duriseti, Sai Sun, Peter Miller, Louis H. TI Molecular basis of Plasmodium falciparum receptor BAEBL for binding to erythrocyte ligand glycophorin C SO AMERICAN JOURNAL OF TROPICAL MEDICINE AND HYGIENE LA English DT Meeting Abstract C1 NIAID, NIH, Rockville, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC TROP MED & HYGIENE PI MCLEAN PA 8000 WESTPARK DR, STE 130, MCLEAN, VA 22101 USA SN 0002-9637 J9 AM J TROP MED HYG JI Am. J. Trop. Med. Hyg. PD NOV PY 2006 VL 75 IS 5 SU S MA 157 BP 47 EP 47 PG 1 WC Public, Environmental & Occupational Health; Tropical Medicine SC Public, Environmental & Occupational Health; Tropical Medicine GA 109XW UT WOS:000242343900158 ER PT J AU Takala, SL Coulibaly, D Thera, MA Dicko, A Smith, DL Guindo, AB Kone, AK Ouattara, A Djimde, A Sehdev, P Lyke, KE Diallo, DA Doumbo, OK Plowe, CV AF Takala, Shannon L. Coulibaly, Drissa Thera, Mahamadou A. Dicko, Alassane Smith, David L. Guindo, Ando B. Kone, Abdoulaye K. Ouattara, Amed Djimde, Abdoulaye Sehdev, Paul Lyke, Kirsten E. Diallo, Dapa A. Doumbo, Ogobara K. Plowe, Christopher V. TI Dynamics of Plasmodium falciparum MSP-1(19) genetic diversity at a malaria vaccine-testing site in Mali SO AMERICAN JOURNAL OF TROPICAL MEDICINE AND HYGIENE LA English DT Meeting Abstract C1 Univ Maryland, Sch Med, Baltimore, MD USA. Univ Bamako, Malaria Res & Training Ctr, Bamako, Mali. Fogarty Int Ctr, Natl Inst Hlth, Bethesda, MD USA. RI Smith, David/L-8850-2013 OI Smith, David/0000-0003-4367-3849 NR 0 TC 0 Z9 0 U1 0 U2 1 PU AMER SOC TROP MED & HYGIENE PI MCLEAN PA 8000 WESTPARK DR, STE 130, MCLEAN, VA 22101 USA SN 0002-9637 J9 AM J TROP MED HYG JI Am. J. Trop. Med. Hyg. PD NOV PY 2006 VL 75 IS 5 SU S MA 200 BP 59 EP 59 PG 1 WC Public, Environmental & Occupational Health; Tropical Medicine SC Public, Environmental & Occupational Health; Tropical Medicine GA 109XW UT WOS:000242343900201 ER PT J AU Rollenhagen, JE Kalsy, A Saksena, R Qadri, F Calderwood, SB Kovac, P Wade, W Ryan, ET AF Rollenhagen, Julianne E. Kalsy, Anuj Saksena, Rina Qadri, Firdausi Calderwood, Stephen B. Kovac, Paul Wade, William Ryan, Edward T. TI Transcutaneous immunization with a neoglycoconjugate containing a Vibrio cholerae hexasaccharide derived from V-cholerae O1 Ogawa lipopolysaccharide bound to a protein carrier SO AMERICAN JOURNAL OF TROPICAL MEDICINE AND HYGIENE LA English DT Meeting Abstract C1 Massachusetts Gen Hosp, Div Infect Dis, Boston, MA USA. NIH, NIDDK, LMC Carbohydrates, Bethesda, MD USA. B Ctr Hlth Populat Studies, Int Ctr Diarrhoel Dis Res, Dhaka, Bangladesh. Dartmouth Med Sch, Hanover, NH USA. NR 0 TC 2 Z9 2 U1 0 U2 0 PU AMER SOC TROP MED & HYGIENE PI MCLEAN PA 8000 WESTPARK DR, STE 130, MCLEAN, VA 22101 USA SN 0002-9637 J9 AM J TROP MED HYG JI Am. J. Trop. Med. Hyg. PD NOV PY 2006 VL 75 IS 5 SU S MA 291 BP 84 EP 85 PG 2 WC Public, Environmental & Occupational Health; Tropical Medicine SC Public, Environmental & Occupational Health; Tropical Medicine GA 109XW UT WOS:000242343900292 ER PT J AU Hayton, K Liu, A Nawaz, F Doll, M Wellems, TE AF Hayton, Karen Liu, Anna Nawaz, Fatima Doll, Michelle Wellems, Thomas E. TI A determinate of species range and virulence in Plasmodium falciparum malaria SO AMERICAN JOURNAL OF TROPICAL MEDICINE AND HYGIENE LA English DT Meeting Abstract C1 NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC TROP MED & HYGIENE PI MCLEAN PA 8000 WESTPARK DR, STE 130, MCLEAN, VA 22101 USA SN 0002-9637 J9 AM J TROP MED HYG JI Am. J. Trop. Med. Hyg. PD NOV PY 2006 VL 75 IS 5 SU S MA 295 BP 86 EP 86 PG 1 WC Public, Environmental & Occupational Health; Tropical Medicine SC Public, Environmental & Occupational Health; Tropical Medicine GA 109XW UT WOS:000242343900296 ER PT J AU Mu, JB Awadalla, P Duan, JH Mcgee, KM Keebler, J Siydel, K McVean, GAT Su, XZ AF Mu, Jianbing Awadalla, Philip Duan, Junhui McGee, Kate M. Keebler, jon Siydel, Karl McVean, Gilean A. T. Su, Xin-zhuan TI Genome-wide variation and identification of vaccine targets in the Plasmodium falciparum genome SO AMERICAN JOURNAL OF TROPICAL MEDICINE AND HYGIENE LA English DT Meeting Abstract C1 Natl Inst Allergy & Infect Dis, Rockville, MD USA. N Carolina State Univ, Dept Genet, Raleigh, NC 27695 USA. Univ Oxford, Dept Stat, Oxford OX1 3TG, England. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC TROP MED & HYGIENE PI MCLEAN PA 8000 WESTPARK DR, STE 130, MCLEAN, VA 22101 USA SN 0002-9637 J9 AM J TROP MED HYG JI Am. J. Trop. Med. Hyg. PD NOV PY 2006 VL 75 IS 5 SU S MA 299 BP 87 EP 87 PG 1 WC Public, Environmental & Occupational Health; Tropical Medicine SC Public, Environmental & Occupational Health; Tropical Medicine GA 109XW UT WOS:000242343900300 ER PT J AU Alonso, WJ Kelly-Hope, LA Viboud, C Hirano, EW Miller, MA AF Alonso, Wladimir J. Kelly-Hope, Louise A. Viboud, Cecile Hirano, Eduardo W. Miller, Mark A. TI Changes in the spatial dynamics of seasonal diarrhea in Mexico in 1979-2001 SO AMERICAN JOURNAL OF TROPICAL MEDICINE AND HYGIENE LA English DT Meeting Abstract C1 NIH, Bethesda, MD 20892 USA. Univ Fed Santa Catarina, Dept Mech Engn, Florianopolis, SC, Brazil. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC TROP MED & HYGIENE PI MCLEAN PA 8000 WESTPARK DR, STE 130, MCLEAN, VA 22101 USA SN 0002-9637 J9 AM J TROP MED HYG JI Am. J. Trop. Med. Hyg. PD NOV PY 2006 VL 75 IS 5 SU S MA 313 BP 91 EP 91 PG 1 WC Public, Environmental & Occupational Health; Tropical Medicine SC Public, Environmental & Occupational Health; Tropical Medicine GA 109XW UT WOS:000242343900314 ER PT J AU Coulibaly, YI Dembele, B Diallo, AA Lipner, EM Fay, M Diallo, DA Sissoko, M Yalcoue, D Doumbo, OK Traore, AK Nutman, TB Traore, SF Klion, AD AF Coulibaly, Yaya I. Dembele, Benoit Diallo, Abdallah A. Lipner, Ettie M. Fay, Michael Diallo, Dapa A. Sissoko, Mady Yalcoue, Daniel Doumbo, Ogobara K. Traore, Abdel K. Nutman, Thomas B. Traore, Sekou F. Klion, Amy D. TI Safety and efficacy of doxycycline therapy with and without single dose albendazole ivermectin for the treatment of Mansonella perstans infection SO AMERICAN JOURNAL OF TROPICAL MEDICINE AND HYGIENE LA English DT Meeting Abstract C1 Univ Mali, Bamako, Mali. NIH, Bethesda, MD 20892 USA. Natl Ctr Dis Control, Bamako, Mali. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC TROP MED & HYGIENE PI MCLEAN PA 8000 WESTPARK DR, STE 130, MCLEAN, VA 22101 USA SN 0002-9637 J9 AM J TROP MED HYG JI Am. J. Trop. Med. Hyg. PD NOV PY 2006 VL 75 IS 5 SU S MA 351 BP 102 EP 102 PG 1 WC Public, Environmental & Occupational Health; Tropical Medicine SC Public, Environmental & Occupational Health; Tropical Medicine GA 109XW UT WOS:000242343900352 ER PT J AU Kirkpatrick, BD Haque, R Duggal, P Mondal, D Larsson, C Sreenivasan, M Peterson, K Lockhart, L Khan, S Petri, WA Akter, J AF Kirkpatrick, Beth D. Haque, Rashidul Duggal, Priya Mondal, Dinesh Larsson, Cathy Sreenivasan, Meera Peterson, Kristine Lockhart, Lauren Khan, Salwa Petri, William A. Akter, Jasmin TI A longitudinal study of Cryptosporidium infection in children in Dhaka: The role of genetic susceptibility to infection SO AMERICAN JOURNAL OF TROPICAL MEDICINE AND HYGIENE LA English DT Meeting Abstract C1 Univ Vermont, Coll Med, Burlington, VT 20892 USA. ICDDR B, Dhaka, Bangladesh. NIH, NGHRI, Bethesda, MD USA. Univ Virginia, Charlottesville, VA USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC TROP MED & HYGIENE PI MCLEAN PA 8000 WESTPARK DR, STE 130, MCLEAN, VA 22101 USA SN 0002-9637 EI 1476-1645 J9 AM J TROP MED HYG JI Am. J. Trop. Med. Hyg. PD NOV PY 2006 VL 75 IS 5 SU S MA 380 BP 111 EP 111 PG 1 WC Public, Environmental & Occupational Health; Tropical Medicine SC Public, Environmental & Occupational Health; Tropical Medicine GA 109XW UT WOS:000242343900381 ER PT J AU Kone, A Beavogui, AH Traore, OB Dara, A Dama, S Mu, JB Toure, O Doumbo, OK Wellems, TE Djimde, AA AF Kone, Aminatou Beavogui, Abdoul H. Traore, Oumar B. Dara, Antoine Dama, Souleymane Mu, Jianbing Toure, Ousmane Doumbo, Ogobara K. Wellems, Thomas E. Djimde, Abdoulaye A. TI PfNHE polymorphism' and clinical quinine resistance in Mali SO AMERICAN JOURNAL OF TROPICAL MEDICINE AND HYGIENE LA English DT Meeting Abstract C1 Univ Bamako, Bamako, Mali. NIH, NIAID, Lab Malaria & Vector Res, Rockville, MD USA. NR 0 TC 0 Z9 0 U1 1 U2 2 PU AMER SOC TROP MED & HYGIENE PI MCLEAN PA 8000 WESTPARK DR, STE 130, MCLEAN, VA 22101 USA SN 0002-9637 J9 AM J TROP MED HYG JI Am. J. Trop. Med. Hyg. PD NOV PY 2006 VL 75 IS 5 SU S MA 379 BP 111 EP 111 PG 1 WC Public, Environmental & Occupational Health; Tropical Medicine SC Public, Environmental & Occupational Health; Tropical Medicine GA 109XW UT WOS:000242343900380 ER PT J AU Fukuda, MM Dass, K Wortmann, G Mitre, E Hochberg, L Lucey, D AF Fukuda, Mark M. Dass, Krisha Wortmann, Glenn Mitre, Ed Hochberg, Lisa Lucey, Daniel TI Mucosal leishmaniasis in a central American immigrant diagnosed with real-time PCR: Case report and review of diagnostic and treatment issues SO AMERICAN JOURNAL OF TROPICAL MEDICINE AND HYGIENE LA English DT Meeting Abstract C1 Armed Forces Res Inst Med Sci, Bangkok 10400, Thailand. Washington Hosp Ctr, Washington, DC 20010 USA. Walter Reed Army Med Ctr, Washington, DC 20307 USA. Natl Inst Hlth, Bethesda, MD USA. Walter Reed Army Inst Res, Silver Spring, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC TROP MED & HYGIENE PI MCLEAN PA 8000 WESTPARK DR, STE 130, MCLEAN, VA 22101 USA SN 0002-9637 J9 AM J TROP MED HYG JI Am. J. Trop. Med. Hyg. PD NOV PY 2006 VL 75 IS 5 SU S MA 416 BP 121 EP 121 PG 1 WC Public, Environmental & Occupational Health; Tropical Medicine SC Public, Environmental & Occupational Health; Tropical Medicine GA 109XW UT WOS:000242343900417 ER PT J AU Talaat, KR VanHook, R Nutman, T AF Talaat, Kawsar R. VanHook, Robert Nutman, Thomas TI Reversible lymphatic dysfunction caused by Gnathostoma spinigerum infection SO AMERICAN JOURNAL OF TROPICAL MEDICINE AND HYGIENE LA English DT Meeting Abstract C1 Natl Inst Allergy & Infect Dis, Bethesda, MD USA. Glesser Clin PA, Winter Haven, FL USA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU AMER SOC TROP MED & HYGIENE PI MCLEAN PA 8000 WESTPARK DR, STE 130, MCLEAN, VA 22101 USA SN 0002-9637 J9 AM J TROP MED HYG JI Am. J. Trop. Med. Hyg. PD NOV PY 2006 VL 75 IS 5 SU S MA 435 BP 127 EP 127 PG 1 WC Public, Environmental & Occupational Health; Tropical Medicine SC Public, Environmental & Occupational Health; Tropical Medicine GA 109XW UT WOS:000242343900436 ER PT J AU Jiang, H Ding, J Furuya, T Mu, J Cooper, RA Su, XZ AF Jiang, Hongying Ding, Jinhui Furuya, Tetsuya Mu, Jianbin Cooper, Roland A. Su, Xin-Zhuan TI Genome-wide gene expression and mechanism of chloroquine resistance in the human malaria parasite Plasmodium falciparum SO AMERICAN JOURNAL OF TROPICAL MEDICINE AND HYGIENE LA English DT Meeting Abstract C1 NIAID, NIH, Rockville, MD USA. NIA, NIH, Rockville, MD USA. Old Dominion Univ, Dept Biol Sci, Norfolk, VA 23529 USA. RI Furuya, Tetsuya/J-5916-2013 NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC TROP MED & HYGIENE PI MCLEAN PA 8000 WESTPARK DR, STE 130, MCLEAN, VA 22101 USA SN 0002-9637 J9 AM J TROP MED HYG JI Am. J. Trop. Med. Hyg. PD NOV PY 2006 VL 75 IS 5 SU S MA 548 BP 159 EP 159 PG 1 WC Public, Environmental & Occupational Health; Tropical Medicine SC Public, Environmental & Occupational Health; Tropical Medicine GA 109XW UT WOS:000242343900549 ER PT J AU Cui, L Miao, J Furuya, T Li, XY Su, XZ Cui, LW AF Cui, Long Miao, Jun Furuya, Tetsuya Li, Xinyi Su, Xin-zhuan Cui, Liwang TI Regulation of gene expression in the malaria parasite Plasmodium falciparum by the histone acetyltransferase PFGCN5 SO AMERICAN JOURNAL OF TROPICAL MEDICINE AND HYGIENE LA English DT Meeting Abstract C1 Penn State Univ, University Pk, PA 16802 USA. Natl Inst Hlth, NIAID, Bethesda, MD USA. RI Miao, Jun/F-5340-2010; Furuya, Tetsuya/J-5916-2013 NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC TROP MED & HYGIENE PI MCLEAN PA 8000 WESTPARK DR, STE 130, MCLEAN, VA 22101 USA SN 0002-9637 J9 AM J TROP MED HYG JI Am. J. Trop. Med. Hyg. PD NOV PY 2006 VL 75 IS 5 SU S MA 571 BP 166 EP 166 PG 1 WC Public, Environmental & Occupational Health; Tropical Medicine SC Public, Environmental & Occupational Health; Tropical Medicine GA 109XW UT WOS:000242343901007 ER PT J AU Dodoo, D Kusi, KA Koram, KA Nkrumah, FK Gyan, BA Rogers, WO Akanmori, BD Raczniak, G Naficy, A Richie, T Sedegah, M AF Dodoo, Daniel Kusi, Kwadwo A. Koram, Kwadwo A. Nkrumah, Francis K. Gyan, Ben A. Rogers, William O. Akanmori, Bartholomew D. Raczniak, Gregory Naficy, Abdullah Richie, Thomas Sedegah, Martha TI Validation of assays relevant to immunogenicity assessment of CSP-DNA vaccine in Ghana SO AMERICAN JOURNAL OF TROPICAL MEDICINE AND HYGIENE LA English DT Meeting Abstract C1 Univ Ghana, Noguchi Mem Inst, Accra, Ghana. Naval Med Res Unit 2, Jakarta, Indonesia. Naval Med Res Unit 3, Cairo, Egypt. NIAID, Bethesda, MD 20892 USA. Naval Med Res Ctr, Silver Spring, MD USA. NR 0 TC 0 Z9 0 U1 1 U2 1 PU AMER SOC TROP MED & HYGIENE PI MCLEAN PA 8000 WESTPARK DR, STE 130, MCLEAN, VA 22101 USA SN 0002-9637 J9 AM J TROP MED HYG JI Am. J. Trop. Med. Hyg. PD NOV PY 2006 VL 75 IS 5 SU S MA 574 BP 167 EP 167 PG 1 WC Public, Environmental & Occupational Health; Tropical Medicine SC Public, Environmental & Occupational Health; Tropical Medicine GA 109XW UT WOS:000242343901010 ER PT J AU Glen, JJ Shimp, RL MacDonald, NJ MacDonald, NJ Nguyen, VD Duggan, P Zhang, YL Zhu, DM Wu, YM Saul, A Narum, DL AF Glen, Jacqueline J. Shimp, Richard L. MacDonald, Nicholas J. MacDonald, Nicholas J. Nguyen, Vu D. Duggan, Peter Zhang, Yanling Zhu, Daming Wu, Yimin Saul, Allan Narum, David L. TI Pilot-scale production of the Plasmodium vivax transmission blocking vaccine candidate Pvs28 SO AMERICAN JOURNAL OF TROPICAL MEDICINE AND HYGIENE LA English DT Meeting Abstract C1 NIH, NIAID, Rockville, MD USA. OI Saul, Allan/0000-0003-0665-4091 NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC TROP MED & HYGIENE PI MCLEAN PA 8000 WESTPARK DR, STE 130, MCLEAN, VA 22101 USA SN 0002-9637 J9 AM J TROP MED HYG JI Am. J. Trop. Med. Hyg. PD NOV PY 2006 VL 75 IS 5 SU S MA 578 BP 168 EP 168 PG 1 WC Public, Environmental & Occupational Health; Tropical Medicine SC Public, Environmental & Occupational Health; Tropical Medicine GA 109XW UT WOS:000242343901013 ER PT J AU Subramanian, RA Peckham, E Lehmann, T Atkinson, P O'Brochta, DA AF Subramanian, Ramanand Arun Peckham, Edward Lehmann, Tovi Atkinson, Peter O'Brochta, David A. TI Evolution of Herves transposable element in Anopheles gambiae in Africa SO AMERICAN JOURNAL OF TROPICAL MEDICINE AND HYGIENE LA English DT Meeting Abstract C1 Univ Maryland, Inst Biotechnol, Rockville, MD USA. NIH, NIAID, Twinbrook, MD USA. Univ Calif Riverside, Riverside, CA 92521 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC TROP MED & HYGIENE PI MCLEAN PA 8000 WESTPARK DR, STE 130, MCLEAN, VA 22101 USA SN 0002-9637 J9 AM J TROP MED HYG JI Am. J. Trop. Med. Hyg. PD NOV PY 2006 VL 75 IS 5 SU S MA 587 BP 170 EP 170 PG 1 WC Public, Environmental & Occupational Health; Tropical Medicine SC Public, Environmental & Occupational Health; Tropical Medicine GA 109XW UT WOS:000242343901022 ER PT J AU Jaramillo-Gutierrez, G Kumar, S Brandt, S Schneider, D Barillas-Mury, C AF Jaramillo-Gutierrez, Giovanna Kumar, Sanjeev Brandt, Stephanie Schneider, David Barillas-Mury, Carolina TI Identifying Anopheles gambiae genes that affect plasmodium oocyst development SO AMERICAN JOURNAL OF TROPICAL MEDICINE AND HYGIENE LA English DT Meeting Abstract C1 NIH, Rockville, MD USA. Stanford Univ, Stanford, CA 94305 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC TROP MED & HYGIENE PI MCLEAN PA 8000 WESTPARK DR, STE 130, MCLEAN, VA 22101 USA SN 0002-9637 J9 AM J TROP MED HYG JI Am. J. Trop. Med. Hyg. PD NOV PY 2006 VL 75 IS 5 SU S MA 596 BP 173 EP 173 PG 1 WC Public, Environmental & Occupational Health; Tropical Medicine SC Public, Environmental & Occupational Health; Tropical Medicine GA 109XW UT WOS:000242343901031 ER PT J AU Gupta, L Kumar, S Barillas-Mury, C AF Gupta, Lalita Kumar, Sanjeev Barillas-Mury, Carolina TI STAT signaling regulates Plasmodium berghei infection in Anopheles gambiae mosquito SO AMERICAN JOURNAL OF TROPICAL MEDICINE AND HYGIENE LA English DT Meeting Abstract C1 Natl Inst Hlth, Rockville, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC TROP MED & HYGIENE PI MCLEAN PA 8000 WESTPARK DR, STE 130, MCLEAN, VA 22101 USA SN 0002-9637 J9 AM J TROP MED HYG JI Am. J. Trop. Med. Hyg. PD NOV PY 2006 VL 75 IS 5 SU S MA 666 BP 192 EP 192 PG 1 WC Public, Environmental & Occupational Health; Tropical Medicine SC Public, Environmental & Occupational Health; Tropical Medicine GA 109XW UT WOS:000242343901101 ER PT J AU Dinglasan, RR Kalume, DE Kanzok, SM Ghosh, A Muratova, O Pandey, A Jacobs-Lorena, M AF Dinglasan, Rhoel R. Kalume, Dario E. Kanzok, Stefan M. Ghosh, Anil Muratova, Olga Pandey, Akhilesh Jacobs-Lorena, Marcelo TI A novel antivector Plasmodium falciparum transmission-blocking antibody reveals heterogeneous ookinete invasion strategies SO AMERICAN JOURNAL OF TROPICAL MEDICINE AND HYGIENE LA English DT Meeting Abstract C1 Johns Hopkins Bloomberg Sch Publ Hlth, Baltimore, MD USA. Johns Hopkins Sch Med, Baltimore, MD USA. NIAID, Natl Inst Hlth, Rockville, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC TROP MED & HYGIENE PI MCLEAN PA 8000 WESTPARK DR, STE 130, MCLEAN, VA 22101 USA SN 0002-9637 J9 AM J TROP MED HYG JI Am. J. Trop. Med. Hyg. PD NOV PY 2006 VL 75 IS 5 SU S MA 667 BP 193 EP 193 PG 1 WC Public, Environmental & Occupational Health; Tropical Medicine SC Public, Environmental & Occupational Health; Tropical Medicine GA 109XW UT WOS:000242343901102 ER PT J AU Martin, KK Jia, XL Cole-Tobian, J Singh, S King, CL AF Martin, Kara K. Jia, Xainli Cole-Tobian, Jennifer Singh, Sanjay King, Christopher L. TI Variant-specific binding of recombinant Plasmodium vivax Duffy binding protein to human erythrocytes SO AMERICAN JOURNAL OF TROPICAL MEDICINE AND HYGIENE LA English DT Meeting Abstract C1 Case Western Reserve Univ, Cleveland, OH 44106 USA. NIAID, Bethesda, MD 20892 USA. Case Western Reserve Univ, Vet Affairs Med Ctr, Shaker Hts, OH USA. NR 0 TC 0 Z9 0 U1 1 U2 1 PU AMER SOC TROP MED & HYGIENE PI MCLEAN PA 8000 WESTPARK DR, STE 130, MCLEAN, VA 22101 USA SN 0002-9637 J9 AM J TROP MED HYG JI Am. J. Trop. Med. Hyg. PD NOV PY 2006 VL 75 IS 5 SU S MA 668 BP 193 EP 193 PG 1 WC Public, Environmental & Occupational Health; Tropical Medicine SC Public, Environmental & Occupational Health; Tropical Medicine GA 109XW UT WOS:000242343901103 ER PT J AU Bennuru, S Nutman, TB AF Bennuru, Sasisekhar Nutman, Thomas B. TI Parasite-derived lymphangiogenic molecules: Putative role in mediating the lymphatic dysfunction seen in filarial lymphedema SO AMERICAN JOURNAL OF TROPICAL MEDICINE AND HYGIENE LA English DT Meeting Abstract C1 Natl Inst Hlth, Bethesda, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC TROP MED & HYGIENE PI MCLEAN PA 8000 WESTPARK DR, STE 130, MCLEAN, VA 22101 USA SN 0002-9637 J9 AM J TROP MED HYG JI Am. J. Trop. Med. Hyg. PD NOV PY 2006 VL 75 IS 5 SU S MA 709 BP 204 EP 205 PG 2 WC Public, Environmental & Occupational Health; Tropical Medicine SC Public, Environmental & Occupational Health; Tropical Medicine GA 109XW UT WOS:000242343901144 ER PT J AU Kubofcik, J Klimczak, LJ Nutman, TB AF Kubofcik, Joseph Klimczak, Leszek J. Nutman, Thomas B. TI Distinct host expression signatures induced by closely related filarial parasites SO AMERICAN JOURNAL OF TROPICAL MEDICINE AND HYGIENE LA English DT Meeting Abstract C1 Natl Inst Hlth, Bethesda, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC TROP MED & HYGIENE PI MCLEAN PA 8000 WESTPARK DR, STE 130, MCLEAN, VA 22101 USA SN 0002-9637 J9 AM J TROP MED HYG JI Am. J. Trop. Med. Hyg. PD NOV PY 2006 VL 75 IS 5 SU S MA 707 BP 204 EP 204 PG 1 WC Public, Environmental & Occupational Health; Tropical Medicine SC Public, Environmental & Occupational Health; Tropical Medicine GA 109XW UT WOS:000242343901142 ER PT J AU Diabate, A Dabire, R Ouari, A Millogo, N Lehmann, T AF Diabate, Abdoulaye Dabire, Roch Ouari, Ali Millogo, Niama Lehmann, Tovi TI Analysis of reproductive barriers between the molecular forms of Anopheles gambiae SO AMERICAN JOURNAL OF TROPICAL MEDICINE AND HYGIENE LA English DT Meeting Abstract C1 Natl Inst Hlth, Natl Allergy & Infect Dis, Rockville, MD USA. IRSS Ctr Muraz, Bobo Dioulasso, Burkina Faso. NR 0 TC 0 Z9 0 U1 0 U2 1 PU AMER SOC TROP MED & HYGIENE PI MCLEAN PA 8000 WESTPARK DR, STE 130, MCLEAN, VA 22101 USA SN 0002-9637 J9 AM J TROP MED HYG JI Am. J. Trop. Med. Hyg. PD NOV PY 2006 VL 75 IS 5 SU S MA 724 BP 209 EP 209 PG 1 WC Public, Environmental & Occupational Health; Tropical Medicine SC Public, Environmental & Occupational Health; Tropical Medicine GA 109XW UT WOS:000242343901159 ER PT J AU Sangare, CS Samake, S Sissoko, I Coulibaly, CA Doumbia, S Traore, SF Anderson, JM Valenzuela, JG Lawyer, P Kamhawi, S AF Sangare, Constance Souko Samake, Sibiry Sissoko, Ibrahim Coulibaly, Cheick Amadou Doumbia, Seydou Traore, Sekou F. Anderson, Jennifer M. Valenzuela, Jesus G. Lawyer, Phillip Kamhawi, Shaden TI A longitudinal study of the sand fly population in Baraouli, Mali SO AMERICAN JOURNAL OF TROPICAL MEDICINE AND HYGIENE LA English DT Meeting Abstract C1 Malaria Res & Training Ctr, Bamako, Mali. Natl Inst Allergy & Infect Dis, Lab Malaria & Vector Res, Rockville, MD USA. Natl Inst Allergy & Infect Dis, LPD, Bethesda, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC TROP MED & HYGIENE PI MCLEAN PA 8000 WESTPARK DR, STE 130, MCLEAN, VA 22101 USA SN 0002-9637 J9 AM J TROP MED HYG JI Am. J. Trop. Med. Hyg. PD NOV PY 2006 VL 75 IS 5 SU S MA 741 BP 214 EP 215 PG 2 WC Public, Environmental & Occupational Health; Tropical Medicine SC Public, Environmental & Occupational Health; Tropical Medicine GA 109XW UT WOS:000242343901176 ER PT J AU Ndao, M Camargo, FV Varatharajalu, R MacLean, D Neva, F Brian, W AF Ndao, Momar Camargo, Fabio Vasquez Varatharajalu, Ravi MacLean, Dick Neva, Franklin Brian, Ward TI Immunodiagnosis of strongyloidiasis: Screen with ELISA and confirm with immunoblot using a recombinant antigen SO AMERICAN JOURNAL OF TROPICAL MEDICINE AND HYGIENE LA English DT Meeting Abstract C1 Natl Reference Ctr Parasitol, Montreal, PQ, Canada. NIH, NIAID, Parasit Dis Lab, Bethesda, MD 20892 USA. McGill Univ, Ctr Trop Dis, Montreal, PQ, Canada. McGill Univ, Div Infectious Dis, Montreal, PQ, Canada. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC TROP MED & HYGIENE PI MCLEAN PA 8000 WESTPARK DR, STE 130, MCLEAN, VA 22101 USA SN 0002-9637 J9 AM J TROP MED HYG JI Am. J. Trop. Med. Hyg. PD NOV PY 2006 VL 75 IS 5 SU S MA 824 BP 237 EP 238 PG 2 WC Public, Environmental & Occupational Health; Tropical Medicine SC Public, Environmental & Occupational Health; Tropical Medicine GA 109XW UT WOS:000242343901259 ER PT J AU Schmid, LJ Su, Q Zhu, J Myers, T Kubofcik, J Nutman, TB Klion, AD AF Schmid, Laura J. Su, Qin Zhu, Jack Myers, Tim Kubofcik, Joseph Nutman, Thomas B. Klion, Amy D. TI Temperature-induced differential gene expression patterns in third stage Brugia malayi larvae SO AMERICAN JOURNAL OF TROPICAL MEDICINE AND HYGIENE LA English DT Meeting Abstract C1 NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC TROP MED & HYGIENE PI MCLEAN PA 8000 WESTPARK DR, STE 130, MCLEAN, VA 22101 USA SN 0002-9637 J9 AM J TROP MED HYG JI Am. J. Trop. Med. Hyg. PD NOV PY 2006 VL 75 IS 5 SU S MA 821 BP 237 EP 237 PG 1 WC Public, Environmental & Occupational Health; Tropical Medicine SC Public, Environmental & Occupational Health; Tropical Medicine GA 109XW UT WOS:000242343901256 ER PT J AU Zepeda, O Makobongo, M Hickman, M MacDonald, N Miller, LH Singh, S AF Zepeda, Orlando Makobongo, Morris Hickman, Merrit MacDonald, Nicholas Miller, Louis H. Singh, Sanjay TI Functional characterization of refolded DBL1 < domain of Plasmodium falciparum erthrocyte membrane protein-1 SO AMERICAN JOURNAL OF TROPICAL MEDICINE AND HYGIENE LA English DT Meeting Abstract C1 NIH, NIAID, Malaria Vaccine Dev Branch, Antigen Res Section, Rockville, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC TROP MED & HYGIENE PI MCLEAN PA 8000 WESTPARK DR, STE 130, MCLEAN, VA 22101 USA SN 0002-9637 J9 AM J TROP MED HYG JI Am. J. Trop. Med. Hyg. PD NOV PY 2006 VL 75 IS 5 SU S MA 846 BP 243 EP 244 PG 2 WC Public, Environmental & Occupational Health; Tropical Medicine SC Public, Environmental & Occupational Health; Tropical Medicine GA 109XW UT WOS:000242343901281 ER PT J AU Hume, J Licht, M Simard, F Besansky, N Lehmann, T AF Hume, Jen Licht, Monica Simard, Fred Besansky, Nora Lehmann, Tovi TI Molecular evolution of immune genes in members of the Anopheles gambiae complex SO AMERICAN JOURNAL OF TROPICAL MEDICINE AND HYGIENE LA English DT Meeting Abstract C1 NIAID, Rockville, MD USA. NIH, Rockville, MD USA. Ctr Dis Control & Prevent, Atlanta, GA USA. IRD, Yaounde, Cameroon. Univ Notre Dame, Notre Dame, IN 46556 USA. RI SIMARD, Frederic/J-9489-2016 OI SIMARD, Frederic/0000-0002-2871-5329 NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC TROP MED & HYGIENE PI MCLEAN PA 8000 WESTPARK DR, STE 130, MCLEAN, VA 22101 USA SN 0002-9637 J9 AM J TROP MED HYG JI Am. J. Trop. Med. Hyg. PD NOV PY 2006 VL 75 IS 5 SU S MA 913 BP 263 EP 263 PG 1 WC Public, Environmental & Occupational Health; Tropical Medicine SC Public, Environmental & Occupational Health; Tropical Medicine GA 109XW UT WOS:000242343901348 ER PT J AU Dao, A Yaro, A Adamou, A Traore, S Krzywinski, J Lehmann, T AF Dao, Adama Yaro, Alpha Adamou, Abdoulaye Traore, Sekou Krzywinski, Jaroslaw Lehmann, Tovi TI Does Anopheles gambiae s.l mate indoors? SO AMERICAN JOURNAL OF TROPICAL MEDICINE AND HYGIENE LA English DT Meeting Abstract C1 MRTC, Rockville, MD USA. MRTC, Bamako, Mali. Univ Texas, Arlington, TX 76019 USA. NIH, NIAID, Lab Malaria & Vector Inst, Rockville, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC TROP MED & HYGIENE PI MCLEAN PA 8000 WESTPARK DR, STE 130, MCLEAN, VA 22101 USA SN 0002-9637 J9 AM J TROP MED HYG JI Am. J. Trop. Med. Hyg. PD NOV PY 2006 VL 75 IS 5 SU S MA 926 BP 266 EP 267 PG 2 WC Public, Environmental & Occupational Health; Tropical Medicine SC Public, Environmental & Occupational Health; Tropical Medicine GA 109XW UT WOS:000242343901361 ER PT J AU Lehmann, T DeJong, R Diabate, A Crawford, J Armbruster, P Koebele, C Molina-Cruz, A Kumar, S Dao, A Yaro, A Jaramillo-Guiterrez, G Adamou, A Gupta, L Traore, S Gwadz, R Barillas-Muray, C AF Lehmann, Tovi DeJong, Randy Diabate, Abdoulaye Crawford, Jacob Armbruster, Peter Koebele, Carey Molina-Cruz, Alvaro Kumar, Sanjeev Dao, Adama Yaro, Alpha Jaramillo-Guiterrez, Giovana Adamou, Abdoulaye Gupta, Lalita Traore, Sekou Gwadz, Robert Barillas-Muray, Carolina TI Evaluating trade off between bacterial resistance and life history traits of Anopheles gambiae SO AMERICAN JOURNAL OF TROPICAL MEDICINE AND HYGIENE LA English DT Meeting Abstract C1 NIAID, Rockville, MD USA. Natl Inst Hlth, Rockville, MD USA. Georgetown Univ, Washington, DC USA. MRTC, Bamako, Mali. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC TROP MED & HYGIENE PI MCLEAN PA 8000 WESTPARK DR, STE 130, MCLEAN, VA 22101 USA SN 0002-9637 J9 AM J TROP MED HYG JI Am. J. Trop. Med. Hyg. PD NOV PY 2006 VL 75 IS 5 SU S MA 923 BP 266 EP 266 PG 1 WC Public, Environmental & Occupational Health; Tropical Medicine SC Public, Environmental & Occupational Health; Tropical Medicine GA 109XW UT WOS:000242343901358 ER PT J AU Oakley, MSM AF Oakley, Miranda S. M. TI Molecular factors and biochemical pathways induced by febrile temperature in Plasmodium falciparum parasites SO AMERICAN JOURNAL OF TROPICAL MEDICINE AND HYGIENE LA English DT Meeting Abstract C1 Natl Inst Hlth, Rockville, MD USA. NR 0 TC 1 Z9 1 U1 0 U2 1 PU AMER SOC TROP MED & HYGIENE PI MCLEAN PA 8000 WESTPARK DR, STE 130, MCLEAN, VA 22101 USA SN 0002-9637 J9 AM J TROP MED HYG JI Am. J. Trop. Med. Hyg. PD NOV PY 2006 VL 75 IS 5 SU S MA 974 BP 279 EP 280 PG 2 WC Public, Environmental & Occupational Health; Tropical Medicine SC Public, Environmental & Occupational Health; Tropical Medicine GA 109XW UT WOS:000242343901409 ER PT J AU McArthur, JH Marron, JA Thumar, B Wanionek, KA Lovchik, JM Blaney, JE Murphy, BR Whitehead, SS Durbin, AP AF McArthur, Julie H. Marron, Jennifer A. Thumar, Bhavin Wanionek, Kimberli A. Lovchik, Janece M. Blaney, Joseph E. Murphy, Brian R. Whitehead, Stephen S. Durbin, Anna P. TI The live attenuated dengue serotype 2 vaccine RDEN2 4 Delta 30 is safe and immunogenic in healthy volunteers SO AMERICAN JOURNAL OF TROPICAL MEDICINE AND HYGIENE LA English DT Meeting Abstract C1 Johns Hopkins Univ, Bloomberg Sch Publ Hlth, Baltimore, MD USA. NIH, NIAID, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC TROP MED & HYGIENE PI MCLEAN PA 8000 WESTPARK DR, STE 130, MCLEAN, VA 22101 USA SN 0002-9637 J9 AM J TROP MED HYG JI Am. J. Trop. Med. Hyg. PD NOV PY 2006 VL 75 IS 5 SU S MA 981 BP 281 EP 282 PG 2 WC Public, Environmental & Occupational Health; Tropical Medicine SC Public, Environmental & Occupational Health; Tropical Medicine GA 109XW UT WOS:000242343901416 ER PT J AU Blaney, J Sathe, N Murphy, B Whitehead, S AF Blaney, Joseph Sathe, Neeraj Murphy, Brian Whitehead, Stephen TI Generation of additional live attenuated vaccine candidates for dengue virus serotypes 1 and 3 using reverse genetics SO AMERICAN JOURNAL OF TROPICAL MEDICINE AND HYGIENE LA English DT Meeting Abstract C1 NIH, NIAID, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC TROP MED & HYGIENE PI MCLEAN PA 8000 WESTPARK DR, STE 130, MCLEAN, VA 22101 USA SN 0002-9637 J9 AM J TROP MED HYG JI Am. J. Trop. Med. Hyg. PD NOV PY 2006 VL 75 IS 5 SU S MA 982 BP 282 EP 282 PG 1 WC Public, Environmental & Occupational Health; Tropical Medicine SC Public, Environmental & Occupational Health; Tropical Medicine GA 109XW UT WOS:000242343901417 ER PT J AU Cholera, R Fairhurst, RM Brittain, NJ Arie, T Dvorak, JA Wellems, TE AF Cholera, Rushina Fairhurst, Rick M. Brittain, Nathaniel J. Arie, Takayuki Dvorak, James A. Wellems, Thomas E. TI Impaired cytoadherence of Plasmodium falciparum-infected erythrocytes: Implications for the malaria protective effect of sickle trait SO AMERICAN JOURNAL OF TROPICAL MEDICINE AND HYGIENE LA English DT Meeting Abstract C1 NIH, NIAID, Lab Malaria & Vector Res, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC TROP MED & HYGIENE PI MCLEAN PA 8000 WESTPARK DR, STE 130, MCLEAN, VA 22101 USA SN 0002-9637 J9 AM J TROP MED HYG JI Am. J. Trop. Med. Hyg. PD NOV PY 2006 VL 75 IS 5 SU S MA 996 BP 286 EP 286 PG 1 WC Public, Environmental & Occupational Health; Tropical Medicine SC Public, Environmental & Occupational Health; Tropical Medicine GA 109XW UT WOS:000242343901431 ER PT J AU Ohrt, C Ogutu, B Martin, K Obare, P Adiambo, C Awando, K Prudhomme, W Remich, S Chretien, JP Lucas, C Osoga, J McEvoy, P Odera, JS Lucas, M Nanakorn, A AF Ohrt, Colin Ogutu, Bernhards Martin, Kurt Obare, Peter Adiambo, Christine Awando, Ken Prudhomme, Wendy Remich, Shon Chretien, Jean Paul Lucas, Carmen Osoga, Joseph McEvoy, Peter Odera, James Sande Lucas, Martin Nanakorn, Ampon TI Malaria diagnostics centre for excellence: Microscopy objective testing results and plans for certification SO AMERICAN JOURNAL OF TROPICAL MEDICINE AND HYGIENE LA English DT Meeting Abstract C1 Walter Reed Army Inst Res, Germantown, MD USA. Kenya Govt Med Res Ctr, Kisumu, Kenya. USA, Med Res Unit Kenya, Kisumu, Kenya. Wellcome Trust Res Labs, Kilifi, Kenya. NIH, Fogarty Unit, Bethesda, MD 20892 USA. USA, Med Res Unit, Nairobi, Kenya. Walter Reed Army Inst Res, Silver Spring, MD USA. Naval Med Res Ctr Detachment, Lima, Peru. Armed Forces Inst Pathol, Washington, DC 20306 USA. Ctr Dis Control & Prevent, Kisumu, Kenya. Armed Forces Res Inst Med Sci, Bangkok 10400, Thailand. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC TROP MED & HYGIENE PI MCLEAN PA 8000 WESTPARK DR, STE 130, MCLEAN, VA 22101 USA SN 0002-9637 J9 AM J TROP MED HYG JI Am. J. Trop. Med. Hyg. PD NOV PY 2006 VL 75 IS 5 SU S MA 998 BP 287 EP 287 PG 1 WC Public, Environmental & Occupational Health; Tropical Medicine SC Public, Environmental & Occupational Health; Tropical Medicine GA 109XW UT WOS:000242343901433 ER PT J AU Babu, S Blauvelt, CP Nutman, TB AF Babu, Subash Blauvelt, Carla P. Nutman, Thomas B. TI Filarial parasites induce early activation, cytokine production, and subsequent apoptosis of human NK cells SO AMERICAN JOURNAL OF TROPICAL MEDICINE AND HYGIENE LA English DT Meeting Abstract C1 Natl Inst Hlth, Bethesda, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC TROP MED & HYGIENE PI MCLEAN PA 8000 WESTPARK DR, STE 130, MCLEAN, VA 22101 USA SN 0002-9637 J9 AM J TROP MED HYG JI Am. J. Trop. Med. Hyg. PD NOV PY 2006 VL 75 IS 5 SU S MA 1020 BP 293 EP 294 PG 2 WC Public, Environmental & Occupational Health; Tropical Medicine SC Public, Environmental & Occupational Health; Tropical Medicine GA 109XW UT WOS:000242343901455 ER PT J AU Coullibaly, M Lobo, NF Kern, M Sharakhova, M Hong, Y Grushko, O Sangare, D Fitzpatrick, M Traore, SF Ribeiro, J Collins, FH Besansky, NJ AF Coullibaly, Mamadou Lobo, Neil F. Kern, Marcia Sharakhova, Maria Hong, Young Grushko, Olga Sangare, Djibril Fitzpatrick, Meagan Traore, Sekou F. Ribeiro, Jose Collins, Francis H. Besansky, Nora J. TI Molecular cloning of the 2Rj inversion breakpoints in the Bamako chromosomal form of Anopheles gambiae SO AMERICAN JOURNAL OF TROPICAL MEDICINE AND HYGIENE LA English DT Meeting Abstract C1 Malaria Res & Training Ctr, Bamako, Mali. Univ Notre Dame, Ctr Global Hlth & Infect Dis, South Bend, IN USA. Virginia Tech, Blacksburg, VA USA. Univ Michigan, Ann Arbor, MI 48109 USA. Natl Inst Hlth, Bethesda, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC TROP MED & HYGIENE PI MCLEAN PA 8000 WESTPARK DR, STE 130, MCLEAN, VA 22101 USA SN 0002-9637 J9 AM J TROP MED HYG JI Am. J. Trop. Med. Hyg. PD NOV PY 2006 VL 75 IS 5 SU S MA 1017 BP 293 EP 293 PG 1 WC Public, Environmental & Occupational Health; Tropical Medicine SC Public, Environmental & Occupational Health; Tropical Medicine GA 109XW UT WOS:000242343901452 ER PT J AU Goel, P Kubofcik, J Nutman, TB Semnani, RT AF Goel, Priyanka Kubofcik, Joseph Nutman, Thomas B. Semnani, Roshanak Tolouei TI Live microfilariae of Brugia malayi downregulate the gene expression of TLR3, 4, 5 and 7, and diminish the production of cytokines in response to a TLR3 ligand SO AMERICAN JOURNAL OF TROPICAL MEDICINE AND HYGIENE LA English DT Meeting Abstract C1 NIAID, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC TROP MED & HYGIENE PI MCLEAN PA 8000 WESTPARK DR, STE 130, MCLEAN, VA 22101 USA SN 0002-9637 J9 AM J TROP MED HYG JI Am. J. Trop. Med. Hyg. PD NOV PY 2006 VL 75 IS 5 SU S MA 1019 BP 293 EP 293 PG 1 WC Public, Environmental & Occupational Health; Tropical Medicine SC Public, Environmental & Occupational Health; Tropical Medicine GA 109XW UT WOS:000242343901454 ER PT J AU Munirathinam, G Nutman, TB Lustigman, S Kalyanasundaram, R AF Munirathinam, Gnanasekar Nutman, Thomas B. Lustigman, Sara Kalyanasundaram, Ramaswamy TI Cloning and characterization of a human IL5 receptor binding protein from Brugia malayi SO AMERICAN JOURNAL OF TROPICAL MEDICINE AND HYGIENE LA English DT Meeting Abstract C1 Univ Illinois, Rockford, IL USA. NIAID, Bethesda, MD 20892 USA. New York Blood Ctr, Lindsley F Kimball Res Inst, New York, NY 10021 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC TROP MED & HYGIENE PI MCLEAN PA 8000 WESTPARK DR, STE 130, MCLEAN, VA 22101 USA SN 0002-9637 J9 AM J TROP MED HYG JI Am. J. Trop. Med. Hyg. PD NOV PY 2006 VL 75 IS 5 SU S MA 1022 BP 294 EP 294 PG 1 WC Public, Environmental & Occupational Health; Tropical Medicine SC Public, Environmental & Occupational Health; Tropical Medicine GA 109XW UT WOS:000242343901457 ER PT J AU Semnani, RT Goel, P Kubofcik, J Nutman, TB AF Semnani, Roshanak T. Goel, Priyanka Kubofcik, Joseph Nutman, Thomas B. TI Live microfilariae of Brugia malayi induce apoptosis in human dendritic cells through a TNF- and TRAIL-dependent mechanism and promote the development of regulatory T cells SO AMERICAN JOURNAL OF TROPICAL MEDICINE AND HYGIENE LA English DT Meeting Abstract C1 NIAID, Natl Inst Hlth, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC TROP MED & HYGIENE PI MCLEAN PA 8000 WESTPARK DR, STE 130, MCLEAN, VA 22101 USA SN 0002-9637 J9 AM J TROP MED HYG JI Am. J. Trop. Med. Hyg. PD NOV PY 2006 VL 75 IS 5 SU S MA 1021 BP 294 EP 294 PG 1 WC Public, Environmental & Occupational Health; Tropical Medicine SC Public, Environmental & Occupational Health; Tropical Medicine GA 109XW UT WOS:000242343901456 ER PT J AU Steel, C Klion, AD Nutman, TB AF Steel, Cathy Klion, Amy D. Nutman, Thomas B. TI Patterns of activation to the immunodominant protein SXP1 from Loa loa SO AMERICAN JOURNAL OF TROPICAL MEDICINE AND HYGIENE LA English DT Meeting Abstract C1 Natl Inst Hlth, Bethesda, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC TROP MED & HYGIENE PI MCLEAN PA 8000 WESTPARK DR, STE 130, MCLEAN, VA 22101 USA SN 0002-9637 J9 AM J TROP MED HYG JI Am. J. Trop. Med. Hyg. PD NOV PY 2006 VL 75 IS 5 SU S MA 1023 BP 294 EP 294 PG 1 WC Public, Environmental & Occupational Health; Tropical Medicine SC Public, Environmental & Occupational Health; Tropical Medicine GA 109XW UT WOS:000242343901458 ER PT J AU Toledo, J Soto, J Soto, P Balderama, M Rea, I Gomez, A Soto, J Parra, R Valda, L Guillen, N Anders, G Sindermann, H Engel, J Berman, J AF Toledo, Julia Soto, Jaime Soto, Paula Balderama, Margarita Rea, Ivan Gomez, Ana Soto, Jaime Parra, Rolando Valda, Luis Guillen, Ninoshtka Anders, Gerlind Sindermann, Herbert Engel, Jurgen Berman, Jonathan TI Miltefosine (Impavido (R)) in the treatment of mucocutaneous and cutaneous leishmaniasis in Bolivia SO AMERICAN JOURNAL OF TROPICAL MEDICINE AND HYGIENE LA English DT Meeting Abstract C1 Consorcio Invest Bioclin, Bogota, Colombia. Proyecto OSCAR, Palos Blancos, Bolivia. Hosp Palos Blancos, Palos Blancos, Bolivia. Hosp Clin, La Paz, Bolivia. Zentaris, Frankfurt, Germany. Natl Ctr Complementary Alternative Med, Natl Inst Hlth, Bethesda, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU AMER SOC TROP MED & HYGIENE PI MCLEAN PA 8000 WESTPARK DR, STE 130, MCLEAN, VA 22101 USA SN 0002-9637 J9 AM J TROP MED HYG JI Am. J. Trop. Med. Hyg. PD NOV PY 2006 VL 75 IS 5 SU S MA 1031 BP 297 EP 297 PG 1 WC Public, Environmental & Occupational Health; Tropical Medicine SC Public, Environmental & Occupational Health; Tropical Medicine GA 109XW UT WOS:000242343901466 ER PT J AU Joy, DA Gonzalez-Ceron, L McCutchan, TF Sandoval, MA Nettel, JA Santillan, F Su, XZ AF Joy, Deirdre A. Gonzalez-Ceron, Lilia McCutchan, Thomas F. Sandoval, M. A. Nettel, Jose A. Santillan, Frida Su, Xin-zhuan TI Distinct P-vivax populations in Mexico differentially infect two local vectors SO AMERICAN JOURNAL OF TROPICAL MEDICINE AND HYGIENE LA English DT Meeting Abstract C1 NIH, Rockville, MD USA. Inst Nacl Invest Salud Publ, Ctr Invest Paludismo, Tapachula, Mexico. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC TROP MED & HYGIENE PI MCLEAN PA 8000 WESTPARK DR, STE 130, MCLEAN, VA 22101 USA SN 0002-9637 J9 AM J TROP MED HYG JI Am. J. Trop. Med. Hyg. PD NOV PY 2006 VL 75 IS 5 SU S MA 1076 BP 311 EP 311 PG 1 WC Public, Environmental & Occupational Health; Tropical Medicine SC Public, Environmental & Occupational Health; Tropical Medicine GA 109XW UT WOS:000242343901511 ER PT J AU Sogoba, N Doumbia, S Baber, I Keita, M Maiga, M Mariko, S Konare, S Dolo, G Traore, SF Ribeiro, J AF Sogoba, Nafomon Doumbia, Seydou Baber, Ibrahim Keita, Moussa Maiga, Mahamadou Mariko, Sidiki Konare, Sekou Dolo, Guimoko Traore, Skou F. Ribeiro, Jose TI Dry season malaria transmission in a rural sudan savana of mali SO AMERICAN JOURNAL OF TROPICAL MEDICINE AND HYGIENE LA English DT Meeting Abstract C1 NIAID, Malaria Res & Training Ctr, Lab Malaria & Vector Res, Bamako, Mali. NR 0 TC 0 Z9 0 U1 0 U2 2 PU AMER SOC TROP MED & HYGIENE PI MCLEAN PA 8000 WESTPARK DR, STE 130, MCLEAN, VA 22101 USA SN 0002-9637 J9 AM J TROP MED HYG JI Am. J. Trop. Med. Hyg. PD NOV PY 2006 VL 75 IS 5 SU S MA 1078 BP 311 EP 311 PG 1 WC Public, Environmental & Occupational Health; Tropical Medicine SC Public, Environmental & Occupational Health; Tropical Medicine GA 109XW UT WOS:000242343901513 ER PT J AU Martin, LB Malkin, E Orcutt, AC Muratova, OV Zhou, H Moretz, S Narum, DL Miles, AP Medina, S Mahanty, S Long, CA Miller, LH Saul, A AF Martin, Laura B. Malkin, Elissa Orcutt, Andrew C. Muratova, Olga V. Zhou, Hong Moretz, Samuel Narum, David L. Miles, Aaron P. Medina, Sarimar Mahanty, Siddhartha Long, Carole A. Miller, Louis H. Saul, Allan TI Phase 1 safety and immunogenicity trial of MSP1,2FVO/alhydrogel and MSP1(42)-3D7/alhydrogel bloodstage malaria vaccines in us adults SO AMERICAN JOURNAL OF TROPICAL MEDICINE AND HYGIENE LA English DT Meeting Abstract C1 NIH, NIAID, Malaria Vaccine Dev Branch, Rockville, MD USA. RI Martin, Laura/N-1789-2013; OI Martin, Laura/0000-0002-4431-4381; Saul, Allan/0000-0003-0665-4091 NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC TROP MED & HYGIENE PI MCLEAN PA 8000 WESTPARK DR, STE 130, MCLEAN, VA 22101 USA SN 0002-9637 J9 AM J TROP MED HYG JI Am. J. Trop. Med. Hyg. PD NOV PY 2006 VL 75 IS 5 SU S MA 1098 BP 317 EP 318 PG 2 WC Public, Environmental & Occupational Health; Tropical Medicine SC Public, Environmental & Occupational Health; Tropical Medicine GA 109XW UT WOS:000242343901533 ER PT J AU Dicko, A Sagara, I Ellis, RD Baby, M Diawara, SI Assadou, MH Guindo, O Kamate, B Niambele, MB Sogoba, M Traore, AM Sissoko, M Yalcouye, D Mullen, G Sissoko, MS Thera, MA Dolo, A Long, C Plowe, CV Diallo, DA Miller, LH Saul, AJ Doumbo, OK AF Dicko, Alassane Sagara, Issaka Ellis, Ruth D. Baby, Mounirou Diawara, Sory I. Assadou, Mahamadoun H. Guindo, Ousmane Kamate, Beh Niambele, Mohamed B. Sogoba, Moussa Traore, Abdoulaye M. Sissoko, Mady Yalcouye, Daniel Mullen, Gregory Sissoko, Mahamadou S. Thera, Mahamadou A. Dolo, Amagana Long, Carole Plowe, Christopher V. Diallo, Dapa A. Miller, Louis H. Saul, Allan J. Doumbo, Ogobara K. TI Randomized, controlled, phase 1 study of AMA1-C1/alhydrogelo vaccine for plasmodium falciparum malaria in children in Dontgutbougou, Mali SO AMERICAN JOURNAL OF TROPICAL MEDICINE AND HYGIENE LA English DT Meeting Abstract C1 Univ Bamako, FMP, DEAP, MRTC, Bamako, Mali. NIH, NIAID, MalariaVaacine Devt Branch, Rockville, MD USA. Univ Maryland, Ctr Vaccine Dev, Baltimore, MD 21201 USA. OI Saul, Allan/0000-0003-0665-4091 NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC TROP MED & HYGIENE PI MCLEAN PA 8000 WESTPARK DR, STE 130, MCLEAN, VA 22101 USA SN 0002-9637 J9 AM J TROP MED HYG JI Am. J. Trop. Med. Hyg. PD NOV PY 2006 VL 75 IS 5 SU S MA 1100 BP 318 EP 318 PG 1 WC Public, Environmental & Occupational Health; Tropical Medicine SC Public, Environmental & Occupational Health; Tropical Medicine GA 109XW UT WOS:000242343901535 ER PT J AU Huaman, MC Diouf, A Malkin, E Martin, L Mullen, G Narum, D Miller, L Mahanty, S Long, C AF Huaman, Maria Cecilia Diouf, Ababacar Malkin, Elissa Martin, Laura Mullen, Gregory Narum, David Miller, Louis Mahanty, Siddhartha Long, Carole TI T cell responses in volunteers vaccinated with blood-stage malarial antigens MSP-1 and AMA-1 SO AMERICAN JOURNAL OF TROPICAL MEDICINE AND HYGIENE LA English DT Meeting Abstract C1 Natl Inst Hlth, Rockville, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC TROP MED & HYGIENE PI MCLEAN PA 8000 WESTPARK DR, STE 130, MCLEAN, VA 22101 USA SN 0002-9637 J9 AM J TROP MED HYG JI Am. J. Trop. Med. Hyg. PD NOV PY 2006 VL 75 IS 5 SU S MA 1099 BP 318 EP 318 PG 1 WC Public, Environmental & Occupational Health; Tropical Medicine SC Public, Environmental & Occupational Health; Tropical Medicine GA 109XW UT WOS:000242343901534 ER EF