FN Thomson Reuters Web of Science™
VR 1.0
PT J
AU Jefferson, WN
AF Jefferson, Wendy N.
TI Adult Ovarian Function Can Be Affected by High Levels of Soy
SO JOURNAL OF NUTRITION
LA English
DT Article; Proceedings Paper
CT Workshop on Soy Summit Exploration of the Nutrition and Health Effects
   of Whole Soy
CY SEP 21-22, 2009
CL Columbia Univ, Inst Human Nutr, New York, NY
HO Columbia Univ, Inst Human Nutr
ID ESTROGEN-RECEPTOR-BETA; PREMENOPAUSAL WOMEN; POSTMENOPAUSAL WOMEN;
   JAPANESE WOMEN; PHYTOESTROGENS; FOODS; ISOFLAVONES; INFERTILITY;
   RESPONSES; SOYBEANS
AB Ovarian function in adults is controlled by hormones circulating in the body The primary hormone responsible for cyclicity in animals and humans is estrogen Estrogen is mostly produced in the ovary and enters the circulation where it then signals the brain for a response The parts of the brain that controls reproductive hormones are the hypothalamus and anterior pituitary Estrogen stimulates the hypothalamus to produce gonadotropin releasing hormone which in turn signals the anterior pituitary to produce follicle stimulating hormone and luteinizing hormone These hormones enter the circulation and signal the ovary to ovulate Substances with estrogenic activity can potentially interfere with this signaling if levels of activity are sufficient to cause a response Soy foods contain estrogenic substances called phytoestrogens The predominant phytoestrogens found in soy are genistein and daidzein The female reproductive system is dependent on hormones for proper function and phytoestrogens at very high levels can interfere with this process This paper summarizes the literature on adult soy consumption and its effect on ovarian function J Nutr 140 2322S-2325S 2010
C1 Natl Inst Environm Hlth Sci, Reprod & Dev Toxicol Lab, Res Triangle Pk, NC USA.
RP Jefferson, WN (reprint author), Natl Inst Environm Hlth Sci, Reprod & Dev Toxicol Lab, Res Triangle Pk, NC USA.
NR 31
TC 8
Z9 8
U1 1
U2 9
PU AMER SOC NUTRITIONAL SCIENCE
PI BETHESDA
PA 9650 ROCKVILLE PIKE, RM L-2407A, BETHESDA, MD 20814 USA
SN 0022-3166
J9 J NUTR
JI J. Nutr.
PD DEC
PY 2010
VL 140
IS 12
BP 2322S
EP 2325S
DI 10.3945/jn.110.123802
PG 4
WC Nutrition & Dietetics
SC Nutrition & Dietetics
GA 692AG
UT WOS:000285123300033
PM 20980642
ER

PT J
AU Ballas, SK
   Bauserman, RL
   McCarthy, WF
   Castro, OL
   Smith, WR
   Waclawiw, MA
AF Ballas, Samir K.
   Bauserman, Robert L.
   McCarthy, William F.
   Castro, Oswaldo L.
   Smith, Wally R.
   Waclawiw, Myron A.
CA Investigators Multictr Study Hydro
TI Hydroxyurea and Acute Painful Crises in Sickle Cell Anemia: Effects on
   Hospital Length of Stay and Opioid Utilization During Hospitalization,
   Outpatient Acute Care Contacts, and at Home
SO JOURNAL OF PAIN AND SYMPTOM MANAGEMENT
LA English
DT Article
DE Sickle cell anemia; hydroxyurea; painful crisis; opioid utilization;
   hospitalization
ID ACUTE CHEST SYNDROME; HEALTH-CARE; VASOOCCLUSIVE CRISES; DISEASE;
   ADULTS; MEPERIDINE; FREQUENCY; QUALITY; COST; READMISSION
AB Context. Exploratory findings from the randomized, double-blind, placebo-controlled, multicenter study of hydroxyurea (MSH) in sickle cell anemia (SS). Recurrent acute painful crises may be mild, moderate, or severe in nature and often require treatment at home, in acute care facilities as outpatients, and in the hospital with oral and/or parenteral opioids.
   Objectives. The objectives of this study were to determine the effects of hydroxyurea (HU) on length of stay (LOS) in hospital and opioid utilization during hospitalization, outpatient acute care contacts, and at home.
   Methods. Data from patient diaries, follow-up visit forms, and medical contact forms for the 299 patients enrolled in the MSH were analyzed. Types and dosages of at home, acute care, and in-hospital analgesic usage were explored descriptively.
   Results. At-home analgesics were used on 40% of diary days and 80% of two-week follow-up periods, with oxycodone and codeine the most frequently used. Responders to HU used analgesics on fewer days. During hospitalization, 96% were treated with parenteral opioids, with meperidine the most frequently used; oxycodone was the most commonly used oral medication. The average LOS for responders to HU was about two days less than for other groups, and their cumulative time hospitalized during the trial was significantly less than for nonresponders or placebo groups (P < 0.022). They also had the lowest doses of parenteral opioids during acute care crises (P = 0.015).
   Conclusion. Beneficial effects of HU include shortening the duration of hospitalization because of acute painful episodes and reducing the net amount of opioid utilization. J Pain Symptom Manage 2010;40:870-882. (C) 2010 U.S. Cancer Pain Relief Committee. Published by Elsevier Inc. All rights reserved.
C1 [Ballas, Samir K.] Thomas Jefferson Univ, Jefferson Med Coll, Cardeza Fdn Hematol Res, Dept Med, Philadelphia, PA 19107 USA.
   [Bauserman, Robert L.; McCarthy, William F.] Maryland Med Res Inst, Baltimore, MD USA.
   [Castro, Oswaldo L.] Howard Univ, Washington, DC 20059 USA.
   [Smith, Wally R.] Virginia Commonwealth Univ, Dept Internal Med, Sch Med, Div Qual Hlth Care, Richmond, VA USA.
   [Waclawiw, Myron A.] NHLBI, Bethesda, MD 20892 USA.
RP Ballas, SK (reprint author), Thomas Jefferson Univ, Jefferson Med Coll, Cardeza Fdn Hematol Res, Dept Med, 1015 Walnut St, Philadelphia, PA 19107 USA.
EM samir.ballas@jefferson.edu
FU National Heart, Lung, and Blood Institute [NO1-HB-67129, UO1-HL45696]
FX Funding was provided by the National Heart, Lung, and Blood Institute
   (NO1-HB-67129 and UO1-HL45696). The authors declare no conflicts of
   interest.
NR 51
TC 15
Z9 15
U1 1
U2 8
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0885-3924
J9 J PAIN SYMPTOM MANAG
JI J. Pain Symptom Manage.
PD DEC
PY 2010
VL 40
IS 6
BP 870
EP 882
DI 10.1016/j.jpainsymman.2010.03.020
PG 13
WC Health Care Sciences & Services; Medicine, General & Internal; Clinical
   Neurology
SC Health Care Sciences & Services; General & Internal Medicine;
   Neurosciences & Neurology
GA 704KO
UT WOS:000286052100014
PM 20864308
ER

PT J
AU Abernethy, AP
   Aziz, NM
   Basch, E
   Bull, J
   Cleeland, CS
   Currow, DC
   Fairclough, D
   Hanson, L
   Hauser, J
   Ko, D
   Lloyd, L
   Morrison, RS
   Otis-Green, S
   Pantilat, S
   Portenoy, RK
   Ritchie, C
   Rocker, G
   Wheeler, JL
   Zafar, SY
   Kutner, JS
AF Abernethy, Amy P.
   Aziz, Noreen M.
   Basch, Ethan
   Bull, Janet
   Cleeland, Charles S.
   Currow, David C.
   Fairclough, Diane
   Hanson, Laura
   Hauser, Joshua
   Ko, Danielle
   Lloyd, Linda
   Morrison, R. Sean
   Otis-Green, Shirley
   Pantilat, Steve
   Portenoy, Russell K.
   Ritchie, Christine
   Rocker, Graeme
   Wheeler, Jane L.
   Zafar, S. Yousuf
   Kutner, Jean S.
TI A Strategy To Advance the Evidence Base in Palliative Medicine:
   Formation of a Palliative Care Research Cooperative Group
SO JOURNAL OF PALLIATIVE MEDICINE
LA English
DT Article
ID CONTROLLED-TRIAL; CLINICAL-TRIALS; STATIN THERAPY; CANCER; POPULATION;
   ATORVASTATIN; PREVALENCE; PREVENTION; RISK; PAIN
AB Background: Palliative medicine has made rapid progress in establishing its scientific and clinical legitimacy, yet the evidence base to support clinical practice remains deficient in both the quantity and quality of published studies. Historically, the conduct of research in palliative care populations has been impeded by multiple barriers including health care system fragmentation, small number and size of potential sites for recruitment, vulnerability of the population, perceptions of inappropriateness, ethical concerns, and gate-keeping.
   Methods: A group of experienced investigators with backgrounds in palliative care research convened to consider developing a research cooperative group as a mechanism for generating high-quality evidence on prioritized, clinically relevant topics in palliative care.
   Results: The resulting Palliative Care Research Cooperative (PCRC) agreed on a set of core principles: active, interdisciplinary membership; commitment to shared research purposes; heterogeneity of participating sites; development of research capacity in participating sites; standardization of methodologies, such as consenting and data collection/management; agile response to research requests from government, industry, and investigators; focus on translation; education and training of future palliative care researchers; actionable results that can inform clinical practice and policy. Consensus was achieved on a first collaborative study, a randomized clinical trial of statin discontinuation versus continuation in patients with a prognosis of less than 6 months who are taking statins for primary or secondary prevention. This article describes the formation of the PCRC, highlighting processes and decisions taken to optimize the cooperative group's success.
C1 [Abernethy, Amy P.; Wheeler, Jane L.; Zafar, S. Yousuf] Duke Univ, Med Ctr, Div Med Oncol, Dept Med, Durham, NC 27710 USA.
   [Abernethy, Amy P.] Duke Univ, Med Ctr, Duke Comprehens Canc Ctr, Durham, NC 27710 USA.
   [Aziz, Noreen M.] NINR, Div Extramural Activ, NIH, Bethesda, MD 20892 USA.
   [Basch, Ethan] Mem Sloan Kettering Canc Ctr, Hlth Outcomes Grp, New York, NY 10021 USA.
   [Bull, Janet] Four Seasons, Flat Rock, NC USA.
   [Cleeland, Charles S.] Univ Texas MD Anderson Canc Ctr, Dept Symptom Res, Div Internal Med, Houston, TX 77030 USA.
   [Currow, David C.] Flinders Univ S Australia, Dept Palliat & Support Serv, Div Med, Bedford Pk, SA 5042, Australia.
   [Currow, David C.] Repatriat Gen Hosp, So Adelaide Palliat Serv, Daw Pk, SA, Australia.
   [Fairclough, Diane] Colorado Sch Publ Hlth, Dept Biostat & Informat, Aurora, CO USA.
   [Hanson, Laura] Univ N Carolina, Div Geriatr, Chapel Hill, NC USA.
   [Hauser, Joshua] Northwestern Univ, Palliat Care & Home Hosp Program, Feinberg Sch Med, Chicago, IL 60611 USA.
   [Ko, Danielle] Massachusetts Gen Hosp, Div Gen Internal Med, Boston, MA 02114 USA.
   [Lloyd, Linda] San Diego Hosp, San Diego, CA USA.
   [Lloyd, Linda] Inst Palliat Med, San Diego, CA USA.
   [Morrison, R. Sean] Mt Sinai Sch Med, New York, NY USA.
   [Otis-Green, Shirley] City Hope Natl Med Ctr, Div Nursing Res & Educ, Duarte, CA 91010 USA.
   [Pantilat, Steve] Univ Calif San Francisco, Dept Med, Palliat Care Program, Div Hosp Med, San Francisco, CA 94110 USA.
   [Portenoy, Russell K.] Beth Israel Deaconess Med Ctr, Dept Pain Med & Palliat Care, New York, NY 10003 USA.
   [Ritchie, Christine] Univ Alabama Birmingham, Birmingham Atlanta VA Geriatr Res Educ & Clin Ctr, Birmingham, AL USA.
   [Ritchie, Christine] Univ Alabama Birmingham, Div Gerontol Geriatr & Palliat Care, Birmingham, AL USA.
   [Rocker, Graeme] Dalhousie Univ, Div Respirol, Halifax, NS, Canada.
   [Rocker, Graeme] Dalhousie Univ, Dept Med, Div Palliat Med, Halifax, NS, Canada.
   [Kutner, Jean S.] Univ Colorado, Dept Med, Div Gen Internal Med, Denver Sch Med, Denver, CO USA.
RP Abernethy, AP (reprint author), Duke Univ, Med Ctr, Div Med Oncol, Dept Med, Box 3436, Durham, NC 27710 USA.
EM amy.abernethy@duke.edu
OI Zafar, S. Yousuf/0000-0002-9039-5258; Currow, David/0000-0003-1988-1250;
   Abernethy, Amy/0000-0001-6930-8722
FU Pfizer; Helsinn; Kanglaite; Eisai; Eli Lilly; Biovex; Amgen
FX Amy Abernethy receives research funding from Pfizer, Helsinn, Kanglaite,
   Eisai, Eli Lilly, Biovex, and Amgen, and consulting funding (less than
   $10,000) from Helsinn and Pfizer. Janet Bull is on the speakers bureau
   for MEDI, Pfizer, and Wyeth, and the scientific advisory board for
   Pfizer and MEDI. No competing financial interests are disclosed by Ethan
   Basch, David Currow, Diane Fairclough, Joshua Hauser, Danielle Ko, Jean
   Kutner, Linda Lloyd, Shirley Otis-Green, Steve Pantilat, Christine
   Ritchie, Russell Portenoy, Jane Wheeler, and S. Yousuf Zafar.
NR 39
TC 37
Z9 38
U1 0
U2 8
PU MARY ANN LIEBERT INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 1096-6218
J9 J PALLIAT MED
JI J. Palliat. Med.
PD DEC
PY 2010
VL 13
IS 12
BP 1407
EP 1413
DI 10.1089/jpm.2010.0261
PG 7
WC Health Care Sciences & Services
SC Health Care Sciences & Services
GA 694KC
UT WOS:000285295100004
PM 21105763
ER

PT J
AU Alexander, D
AF Alexander, Duane
TI The Benefits of Having a National Institute of Child Health and Human
   Development
SO JOURNAL OF PEDIATRICS
LA English
DT Editorial Material
C1 [Alexander, Duane] NICHD, Bethesday, MD USA.
   [Alexander, Duane] NIH, John E Fogarty Int Ctr Adv Study Hlth Sci, Bethesday, MD USA.
RP Alexander, D (reprint author), NIH, Fogarty Int Ctr, 31 Ctr Dr MSC 2220, Bethesda, MD 20892 USA.
EM duane.alexander@nih.gov
NR 0
TC 0
Z9 0
U1 0
U2 0
PU MOSBY-ELSEVIER
PI NEW YORK
PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0022-3476
J9 J PEDIATR-US
JI J. Pediatr.
PD DEC
PY 2010
VL 157
IS 6
BP 871
EP 872
DI 10.1016/j.jpeds.2010.08.004
PG 2
WC Pediatrics
SC Pediatrics
GA 681JG
UT WOS:000284307200001
PM 21087698
ER

PT J
AU McCrae, RR
   Scally, M
   Terracciano, A
   Abecasis, GR
   Costa, PT
AF McCrae, Robert R.
   Scally, Matthew
   Terracciano, Antonio
   Abecasis, Goncalo R.
   Costa, Paul T., Jr.
TI An Alternative to the Search for Single Polymorphisms: Toward Molecular
   Personality Scales for the Five-Factor Model
SO JOURNAL OF PERSONALITY AND SOCIAL PSYCHOLOGY
LA English
DT Article
DE genome-wide association study; personality assessment; founder effect;
   five-factor model; NEO-PI-R
ID GENOME-WIDE ASSOCIATION; NOVELTY SEEKING; GENE; 5-HTTLPR; TRAITS;
   METAANALYSIS; NEUROTICISM; ANXIETY; DEPRESSION; IMPUTATION
AB There is growing evidence that personality traits are affected by many genes, all of which have very small effects. As an alternative to the largely unsuccessful search for individual polymorphisms associated with personality traits, the authors identified large sets of potentially related single nucleotide polymorphisms (SNPs) and summed them to form molecular personality scales (MPSs) with from 4 to 2,497 SNPs. Scales were derived from two thirds of a large (N = 3,972) sample of individuals from Sardinia who completed the Revised NEO Personality Inventory (P. T. Costa, Jr., & R. R. McCrae, 1992) and were assessed in a genomewide association scan. When MPSs were correlated with the phenotype in the remaining one third of the sample, very small but significant associations were found for 4 of the 5e personality factors when the longest scales were examined. These data suggest that MPSs for Neuroticism, Openness to Experience, Agreeableness, and Conscientiousness (but not Extraversion) contain genetic information that can be refined in future studies, and the procedures described here should be applicable to other quantitative traits.
C1 [McCrae, Robert R.; Scally, Matthew; Terracciano, Antonio; Costa, Paul T., Jr.] NIA, Lab Personal & Cognit, NIH, US Dept HHS, Baltimore, MD 21224 USA.
   [Abecasis, Goncalo R.] Univ Michigan, Dept Biostat, Ctr Stat Genet, Ann Arbor, MI 48109 USA.
RP Costa, PT (reprint author), Johns Hopkins Bloomberg Sch Publ Hlth, Dept Mental Hlth, Room 852,Hampton House,624 N Broadway, Baltimore, MD 21205 USA.
EM pcosta@jhsph.edu
RI terracciano, antonio/B-1884-2008; Abecasis, Goncalo/B-7840-2010; 
OI Abecasis, Goncalo/0000-0003-1509-1825; Costa, Paul/0000-0003-4375-1712
FU Intramural NIH HHS [ZIA AG000197-04, Z99 AG999999, ZIA AG000196-03, ZIA
   AG000196-04, ZIA AG000197-03]
NR 58
TC 15
Z9 16
U1 0
U2 24
PU AMER PSYCHOLOGICAL ASSOC
PI WASHINGTON
PA 750 FIRST ST NE, WASHINGTON, DC 20002-4242 USA
SN 0022-3514
J9 J PERS SOC PSYCHOL
JI J. Pers. Soc. Psychol.
PD DEC
PY 2010
VL 99
IS 6
BP 1014
EP 1024
DI 10.1037/a0020964
PG 11
WC Psychology, Social
SC Psychology
GA 687YI
UT WOS:000284814000009
PM 21114353
ER

PT J
AU Gorman, GS
   Coward, LU
   Freeman, L
   Noker, PE
   Beattie, CW
   Jia, L
AF Gorman, Greg S.
   Coward, Lori U.
   Freeman, Lea
   Noker, Pat E.
   Beattie, Craig W.
   Jia, Lee
TI A novel and rapid LC/MS/MS assay for bioanalysis of Azurin p28 in serum
   and its pharmacokinetics in mice
SO JOURNAL OF PHARMACEUTICAL AND BIOMEDICAL ANALYSIS
LA English
DT Article
DE Azurin p28; Pharmacokinetics; Cupredoxin bacterial redox protein; Liquid
   chromatography/tandem mass spectrometry
ID SUPPRESSOR PROTEIN P53; BACTERIAL CUPREDOXIN AZURIN; MASS-SPECTROMETRY
   ASSAY; CANCER; INHIBITION; REGRESSION
AB Azurin p28 (NSC745104) is a 28 amino acid peptide fragment that inhibits proliferation of human solid and hematological malignancies in vitro and in vivo by reducing proteasomal degradation of oncogene p53. The present study aimed at developing a novel and fast liquid chromatography/tandem mass spectrometry (LC/MS/MS) method for the bioanalysis of p28 in mouse serum, and determining Azurin p28 stability and pharmacokinetics in mice after full method validation. Both Azurin p28 and its internal standard MP-1 were separated and extracted from serum by using perchloric acid (7%, v/v) without time-consuming reconstitution. Chromatographic separation of Azurin p28 and MP-1 from the serum matrix was achieved using a C18 column with a gradient elution profile consisting of 5 mM ammonium acetate and acetonitrile, both containing formic acid. Mass analysis was conducted using positive ion electrospray ionization (ESI) and multiple reaction monitoring (MRM). It took 7.5 min to analyze one sample. The validated concentration range of the method extended from 100 to 10,000 ng/ml with accuracies of 85-115% and inter-day precision (CV) of <15%. Inter-day accuracy ranged from 96.4% to 103% and CV ranged from 4.61% to 6.90%. The average recovery of Azurin p28 from mouse serum at three concentrations (200, 1000, and 5000 ng/ml) was determined to be 96.4%. Incubation of Azurin p28 at 37 degrees C for 24 h resulted in its degradation 55% in monkey serum, 41% in human serum, and 32-34% in mouse and dog serum. Intravenous administration of Azurin p28 to mice showed its t(1/2 beta) 0.23 h, clearance 1.7 l/kg/h, and volume of distribution at steady state 4.1 l/kg. In conclusion, the novel and fast bioanalytical method was proven to be useful for pharmacokinetic profiling of Azurin p28. Published by Elsevier B.V.
C1 [Jia, Lee] NCI, Dev Therapeut Program, Bethesda, MD 20852 USA.
   [Beattie, Craig W.] CDG Therapeut, Chicago, IL USA.
   [Gorman, Greg S.; Coward, Lori U.; Freeman, Lea; Noker, Pat E.] So Res Inst, Birmingham, AL 35205 USA.
RP Jia, L (reprint author), NCI, Dev Therapeut Program, Bethesda, MD 20852 USA.
EM jiale@mail.nih.gov
FU NCI [N01-CM-52203]
FX This work was supported by NCI contract number N01-CM-52203.
NR 15
TC 8
Z9 8
U1 2
U2 6
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0731-7085
J9 J PHARMACEUT BIOMED
JI J. Pharm. Biomed. Anal.
PD DEC 1
PY 2010
VL 53
IS 4
BP 991
EP 996
DI 10.1016/j.jpba.2010.06.006
PG 6
WC Chemistry, Analytical; Pharmacology & Pharmacy
SC Chemistry; Pharmacology & Pharmacy
GA 643XR
UT WOS:000281334500022
PM 20638810
ER

PT J
AU Ding, Y
   Gao, ZG
   Jacobson, KA
   Suffredini, AF
AF Ding, Yi
   Gao, Zhan-Guo
   Jacobson, Kenneth A.
   Suffredini, Anthony F.
TI Dexamethasone Enhances ATP-Induced Inflammatory Responses in Endothelial
   Cells
SO JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS
LA English
DT Article
ID MESSENGER-RNA EXPRESSION; NUCLEOTIDE RECEPTOR; ADENOSINE-TRIPHOSPHATE;
   SIGNALING MOLECULES; INHIBITION; DISEASE; GAMMA; SHOCK; LINE;
   GLUCOCORTICOIDS
AB The purinergic nucleotide ATP is released from stressed cells and is implicated in vascular inflammation. Glucocorticoids are essential to stress responses and are used therapeutically, yet little information is available that describes the effects of glucocorticoids on ATP-induced inflammation. In a human microvascular endothelial cell line, extracellular ATP-induced interleukin (IL)-6 secretion in a dose-and time-dependent manner. When cells were pretreated with dexamethasone, a prototypic glucocorticoid, ATP-induced IL-6 production was enhanced in a time-and dose-dependent manner. Mifepristone, a glucocorticoid receptor antagonist, blocked these effects. ATP-induced IL-6 release was significantly inhibited by a phospholipase C inhibitor [1-[6-[((17 beta)-3-methoxyestra-1,3,5[10]-trien-17-yl)amino]hexyl]-1H-pyrrole-2,5-dione (U73122)] (63.2 +/- 3%, p < 0.001) and abolished by a p38 mitogen-activated protein kinase inhibitor [4-(4-fluorophenyl)-2-(4-methylsulfinylphenyl)-5-(4-pyridyl)-1H-imidazole (SB 203580)] (88 +/- 1%, p < 0.001). Cells treated with dexamethasone induced mRNA expression of the purinergic P2Y(2) receptor (P2Y(2)R) 1.8- +/- 0.1-fold and, when stimulated with ATP, enhanced Ca2+ release and augmented IL-6 mRNA expression. Silencing of the P2Y(2)R by its small interfering RNA decreased ATP-induced IL-6 production by 81 +/- 1% (p < 0.001). Dexamethasone enhanced the transcription rate of P2Y(2)R mRNA and induced a dose-related increase in the activity of the P2Y(2)R promoter. Furthermore, dexamethasone-enhanced ATP induction of adhesion molecule transcription and augmented the release of IL-8. Dexamethasone leads to an unanticipated enhancement of endothelial inflammatory mediator production by extracellular ATP via a P2Y(2)R-dependent mechanism. These data define a novel positive feedback loop of glucocorticoids and ATP-induced endothelial inflammation.
C1 [Ding, Yi; Suffredini, Anthony F.] NIH, Ctr Clin, Dept Crit Care Med, Bethesda, MD 20892 USA.
   [Gao, Zhan-Guo; Jacobson, Kenneth A.] NIDDKD, Mol Recognit Sect, Bioorgan Chem Lab, NIH, Bethesda, MD 20892 USA.
RP Suffredini, AF (reprint author), NIH, Ctr Clin, Dept Crit Care Med, Bldg 10,Room 2C145,10 Ctr Dr, Bethesda, MD 20892 USA.
EM asuffredini@cc.nih.gov
RI Jacobson, Kenneth/A-1530-2009
OI Jacobson, Kenneth/0000-0001-8104-1493
FU National Institutes of Health Clinical Center; National Institute of
   Diabetes and Digestive and Kidney Diseases
FX This work was supported by the Intramural Research Program of the
   National Institutes of Health Clinical Center and the National Institute
   of Diabetes and Digestive and Kidney Diseases.
NR 44
TC 22
Z9 23
U1 0
U2 5
PU AMER SOC PHARMACOLOGY EXPERIMENTAL THERAPEUTICS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3995 USA
SN 0022-3565
J9 J PHARMACOL EXP THER
JI J. Pharmacol. Exp. Ther.
PD DEC
PY 2010
VL 335
IS 3
BP 693
EP 702
DI 10.1124/jpet.110.171975
PG 10
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA 681JS
UT WOS:000284308800020
PM 20826566
ER

PT J
AU Kopajtic, TA
   Liu, Y
   Surratt, CK
   Donovan, DM
   Newman, AH
   Katz, JL
AF Kopajtic, Theresa A.
   Liu, Yi
   Surratt, Christopher K.
   Donovan, David M.
   Newman, Amy H.
   Katz, Jonathan L.
TI Dopamine Transporter-Dependent and -Independent Striatal Binding of the
   Benztropine Analog JHW 007, a Cocaine Antagonist with Low Abuse
   Liability
SO JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS
LA English
DT Article
ID UPTAKE INHIBITORS COCAINE; GUINEA-PIG; HISTAMINE H1-RECEPTORS;
   RECOGNITION SITES; BRAIN MEMBRANES; RAT; RECEPTORS; IDENTIFICATION;
   CONFORMATION; MAZINDOL
AB The benztropine analog N-(n-butyl)-3 alpha-[bis(4'-fluorophenyl)methoxy]-tropane (JHW 007) displays high affinity for the dopamine transporter (DAT), but unlike typical DAT ligands, has relatively low abuse liability and blocks the effects of cocaine, including its self-administration. To determine sites responsible for the cocaine antagonist effects of JHW 007, its in vitro binding was compared with that of methyl (1R,2S,3S,5S)-3-(4-fluorophenyl)-8-methyl-8-azabicyclo[3.2.1]octane-2-carboxylate (WIN 35428) in rats, mice, and human DAT (hDAT)-transfected cells. A one-site model, with K(d) values of 4.21 (rat) and 8.99 nM (mouse) best fit the [(3)H]WIN 35428 data. [3H] JHW 007 binding best fit a two-site model (rat, 7.40/4400 nM; mouse, 8.18/2750 nM), although a one-site fit was observed with hDAT membranes (43.7 nM). Drugs selective for the norepinephrine and serotonin transporters had relatively low affinity in competition with [(3)H]JHW 007 binding, as did drugs selective for other sites identified previously as potential JHW 007 binding sites. The association of [(3)H]WIN 35428 best fit a one-phase model, whereas the association of [(3)H]JHW 007 best fit a two-phase model in all tissues. Because cocaine antagonist effects of JHW 007 have been observed previously soon after injection, its rapid association observed here may contribute to those effects. Multiple [(3)H]JHW 007 binding sites were obtained in tissue from mice lacking the DAT, suggesting these as yet unidentified sites as potential contributors to the cocaine antagonist effects of JHW 007. Unlike WIN 35428, the binding of JHW 007 was Na(+)-independent. This feature of JHW 007 has been linked to the conformational status of the DAT, which in turn may contribute to the antagonism of cocaine.
C1 [Katz, Jonathan L.] Natl Inst Drug Abuse, Psychobiol Sect, Medicat Discovery Res Branch, Intramural Res Program,NIH, Baltimore, MD 21224 USA.
   [Newman, Amy H.] Natl Inst Drug Abuse, Med Chem Sect, Medicat Discovery Res Branch, Intramural Res Program, Baltimore, MD 21224 USA.
   [Liu, Yi; Surratt, Christopher K.] Duquesne Univ, Mylan Sch Pharm, Pittsburgh, PA 15219 USA.
   [Donovan, David M.] USDA, Anim & Nat Resources Inst, Agr Res Serv, Beltsville, MD 20705 USA.
RP Katz, JL (reprint author), Natl Inst Drug Abuse, Psychobiol Sect, Medicat Discovery Res Branch, Intramural Res Program,NIH, 251 Bayview Blvd,Suite 200, Baltimore, MD 21224 USA.
EM jkatz@intra.nida.nih.gov
OI Katz, Jonathan/0000-0002-1068-1159
NR 41
TC 12
Z9 12
U1 3
U2 5
PU AMER SOC PHARMACOLOGY EXPERIMENTAL THERAPEUTICS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3995 USA
SN 0022-3565
J9 J PHARMACOL EXP THER
JI J. Pharmacol. Exp. Ther.
PD DEC
PY 2010
VL 335
IS 3
BP 703
EP 714
DI 10.1124/jpet.110.171629
PG 12
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA 681JS
UT WOS:000284308800021
PM 20855444
ER

PT J
AU Fantegrossi, WE
   Simoneau, J
   Cohen, MS
   Zimmerman, SM
   Henson, CM
   Rice, KC
   Woods, JH
AF Fantegrossi, W. E.
   Simoneau, J.
   Cohen, M. S.
   Zimmerman, S. M.
   Henson, C. M.
   Rice, K. C.
   Woods, J. H.
TI Interaction of 5-HT2A and 5-HT2C Receptors in
   R(-)-2,5-Dimethoxy-4-iodoamphetamine-Elicited Head Twitch Behavior in
   Mice
SO JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS
LA English
DT Article
ID HALLUCINOGEN-LIKE ACTIONS; RATS; AGONISTS; 5-HYDROXYTRYPTAMINE;
   ANTAGONISTS; DRUGS; SUBTYPES; SUPERSENSITIVITY; PIRENPERONE; MODULATION
AB Drug-elicited head-twitch behavior is a useful model for studying hallucinogen activity at 5-HT2A receptors in the mouse. Chemically diverse compounds active in this assay yield biphasic dose-effect curves, but there is no compelling explanation for the "descending" portion of these functions. A set of experiments was designed to test the hypothesis that the induction of head-twitch behavior is mediated by agonist actions at 5-HT2A receptors, whereas the inhibition of head-twitch behavior observed at higher doses results from competing agonist activity at 5-HT2C receptors. The effects of the phenethylamine hallucinogen R(-)-2,5-dimethoxy-4-iodoamphetamine (DOI) on head-twitch behavior were studied over a range of doses in the mouse, generating a characteristic biphasic dose-response curve. Pretreatment with the selective 5-HT2A antagonist (+)-(2,3-dimethoxyphenyl)-1-[2-(4-fluorophenylethyl)]-4-piperidine-methanol (M100907) shifted only the ascending limb of the DOI dose-effect function, whereas pretreatment with the nonselective 5-HT2A/2C antagonist 3-{2-[4-(4-fluorobenzoyl)piperidin-1-yl]ethyl}quinazoline-2,4(1H,3H)-dione (ketanserin) produced a parallel shift to the right in the DOI dose-response curve. Administration of the 5-HT2C agonist S-2-(chloro-5-fluoro-in-dol-L-yl)-1-methylethylamine (Ro 60-0175) noncompetitively inhibited DOI-elicited head-twitch behavior across the entire dose-effect function. Finally, pretreatment with the selective 5-HT2C antagonists 6-chloro-5-methyl-1-[(2-[2-methylpyrid-3-yloxy]pyrid-5yl)carbamoyl]indoline (SB242084) or 8-[5-(2,4-dimethoxy-5-(4-trifluoromethylphenylsulfonamido)phenyl-5-oxopentyl]-1,3,8-triazaspiro[4,5]decane-2,4-dione hydrochloride (RS 102221) did not alter DOI-elicited head-twitch behavior on the ascending limb of the dose-response curve but shifted the descending limb of the DOI dose-response function to the right. The results of these experiments provide strong evidence that DOI-elicited head-twitch behavior is a 5-HT2A agonist-mediated effect, with subsequent inhibition of head-twitch behavior being driven by competing 5-HT2C agonist activity.
C1 [Fantegrossi, W. E.; Zimmerman, S. M.; Henson, C. M.] Univ Arkansas Med Sci, Dept Pharmacol & Toxicol, Coll Med, Little Rock, AR 72205 USA.
   [Fantegrossi, W. E.; Simoneau, J.; Cohen, M. S.] Yerkes Natl Primate Res Ctr, Div Neurosci, Atlanta, GA USA.
   [Rice, K. C.] NIDA, Chem Biol Res Branch, NIH, Bethesda, MD 20892 USA.
   [Rice, K. C.] NIAAA, NIH, Bethesda, MD USA.
   [Woods, J. H.] Univ Michigan, Sch Med, Dept Pharmacol, Ann Arbor, MI 48109 USA.
RP Fantegrossi, WE (reprint author), Univ Arkansas Med Sci, Dept Pharmacol & Toxicol, Coll Med, 4301 W Markham St Mail Slot 638, Little Rock, AR 72205 USA.
EM wefantegrossi@uams.edu
FU National Institutes of Health National Institute on Drug Abuse and
   National Institute on Alcohol Abuse and Alcoholism; National Institutes
   of Health National Institute on Drug Abuse [DA020645]; National
   Institutes of Health National Center for Research Resources [RR020146,
   RR00165]; College on Problems of Drug Dependence; American Society for
   Pharmacology and Experimental Therapeutics
FX This work was supported in part by the Intramural Research program of
   the National Institutes of Health National Institute on Drug Abuse and
   National Institute on Alcohol Abuse and Alcoholism; the National
   Institutes of Health National Institute on Drug Abuse [Grant DA020645];
   the National Institutes of Health National Center for Research Resources
   [Grants RR020146, RR00165]; the College on Problems of Drug Dependence;
   and the American Society for Pharmacology and Experimental Therapeutics
   [Summer Undergraduate Research Fellowship (to C.M.H.)].
NR 35
TC 36
Z9 37
U1 1
U2 2
PU AMER SOC PHARMACOLOGY EXPERIMENTAL THERAPEUTICS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3995 USA
SN 0022-3565
J9 J PHARMACOL EXP THER
JI J. Pharmacol. Exp. Ther.
PD DEC
PY 2010
VL 335
IS 3
BP 728
EP 734
DI 10.1124/jpet.110.172247
PG 7
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA 681JS
UT WOS:000284308800023
PM 20858706
ER

PT J
AU Dahan, E
   Soukhoroukova, A
   Spann, M
AF Dahan, Ely
   Soukhoroukova, Arina
   Spann, Martin
TI New Product Development 2.0: Preference Markets - How Scalable
   Securities Markets Identify Winning Product Concepts and Attributes
SO JOURNAL OF PRODUCT INNOVATION MANAGEMENT
LA English
DT Article
ID EFFICIENT CAPITAL-MARKETS; VIRTUAL STOCK MARKETS; RATIONAL-EXPECTATIONS;
   PREDICTION MARKETS; CHOICE; INFORMATION; CUSTOMER; ACCURACY; CONSUMER;
   OPINIONS
AB Preference markets address the need for scalable, fast, and engaging market research in new product development. The Web 2.0 paradigm, in which users contribute numerous ideas that may lead to new products, requires new methods of screening those ideas for their marketability, and preference markets offer just such a mechanism. For faster new product development decisions, a flexible prioritization methodology is implemented for product features and concepts, one that scales up in the number of testable alternatives, limited only by the number of participants. New product preferences for concepts, attributes, and attribute levels are measured by trading stocks whose prices are based upon share of choice of new products and features. A conceptual model of scalable preference markets is developed and tested experimentally. Benefits of the methodology are found to include speed (less than one hour per trading experiment), scalability (question capacity grows linearly in the number of traders), flexibility (features and concepts can be tested simultaneously), and respondent enthusiasm for the method.
C1 [Dahan, Ely] Univ Calif Los Angeles, Sch Med, NIH, Los Angeles, CA 90077 USA.
   [Spann, Martin] Univ Munich, Munich Sch Management, D-80539 Munich, Germany.
RP Dahan, E (reprint author), Univ Calif Los Angeles, Sch Med, NIH, 2542 Cardigan Court, Los Angeles, CA 90077 USA.
EM elydahan@gmail.com
RI Spann, Martin/F-9636-2011
NR 55
TC 13
Z9 13
U1 3
U2 20
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0737-6782
J9 J PROD INNOVAT MANAG
JI J. Prod. Innov. Manage.
PD DEC
PY 2010
VL 27
IS 7
BP 937
EP 954
DI 10.1111/j.1540-5885.2010.00763.x
PG 18
WC Business; Engineering, Industrial; Management
SC Business & Economics; Engineering
GA 665XZ
UT WOS:000283072500002
ER

PT J
AU Das, S
   Bosley, AD
   Ye, XY
   Chan, KC
   Chu, I
   Green, JE
   Issaq, HJ
   Veenstra, TD
   Andresson, T
AF Das, Sudipto
   Bosley, Allen D.
   Ye, Xiaoying
   Chan, King C.
   Chu, Isabel
   Green, Jeffery E.
   Issaq, Haleem J.
   Veenstra, Timothy D.
   Andresson, Thorkell
TI Comparison of Strong Cation Exchange and SDS-PAGE Fractionation for
   Analysis of Multiprotein Complexes
SO JOURNAL OF PROTEOME RESEARCH
LA English
DT Article
DE Strong cation exchange; immunoprecipitation; protein complex isolation;
   mass spectrometry; FLAG
ID MASS-SPECTROMETRY; INTERACTION NETWORKS; QUANTITATIVE PROTEOMICS;
   PROTEIN COMPLEXES
AB Affinity purification of protein complexes followed by identification using liquid chromatography/mass spectrometry (LC-MS/MS) is a robust method to study the fundamental process of protein interaction Although affinity isolation reduces the complexity of the sample, fractionation prior to LC-MS/MS analysis is still necessary to maximize protein coverage In this study, we compared the protein coverage obtained via LC-MS/MS analysis of protein complexes prefractionated using two commonly employed methods, SDS-PAGE and strong cation exchange chromatography (SCX) The two complexes analyzed focused on the nuclear proteins Bmi 1 and GATA3 that were expressed within the cells at low and high levels respectively Prefractionation of the complexes at the peptide level using SCX consistently resulted in the identification of approximately 3 fold more proteins compared to separation at the protein level using SDS-PAGE The increase in the number of identified proteins was especially pronounced for the Bmi-1 complex, where the target protein was expressed at a low level The data show that prefractionation of affinity isolated protein complexes using SCX prior to LC-MS/MS analysis significantly increases the number of identified proteins and individual protein coverage particularly for target proteins expressed at low levels
C1 [Das, Sudipto; Bosley, Allen D.; Ye, Xiaoying; Chan, King C.; Issaq, Haleem J.; Veenstra, Timothy D.; Andresson, Thorkell] SAIC Frederick Inc, Adv Technol Program, Lab Prote & Analyt Technol, NCI Frederick, Frederick, MD 21702 USA.
   [Chu, Isabel; Green, Jeffery E.] NCI, Lab Canc Biol & Genet, NIH, Bethesda, MD 20892 USA.
RP Andresson, T (reprint author), SAIC Frederick Inc, Adv Technol Program, Lab Prote & Analyt Technol, NCI Frederick, Frederick, MD 21702 USA.
FU National Cancer Institute, National Institutes of Health
   [HHSN261200800001E]
FX This project has been funded in whole or in part with federal funds from
   the National Cancer Institute, National Institutes of Health under
   Contract HHSN261200800001E The content of this publication does not
   necessarily reflect the views or policies of the Department of Health
   and Human Services nor does mention of trade names commercial products
   or organizations Imply endorsement by the United States Government
NR 19
TC 12
Z9 12
U1 1
U2 5
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 DEC
PY 2010
VL 9
IS 12
BP 6696
EP 6704
DI 10.1021/pr100843x
PG 9
WC Biochemical Research Methods
SC Biochemistry & Molecular Biology
GA 688NI
UT WOS:000284856200052
PM 20968308
ER

PT J
AU Pagura, J
   Stein, MB
   Bolton, JM
   Cox, BJ
   Grant, B
   Sareen, J
AF Pagura, Jina
   Stein, Murray B.
   Bolton, James M.
   Cox, Brian J.
   Grant, Bridget
   Sareen, Jitender
TI Comorbidity of borderline personality disorder and posttraumatic stress
   disorder in the U.S. population
SO JOURNAL OF PSYCHIATRIC RESEARCH
LA English
DT Article
DE Posttraumatic stress disorder; Borderline personality disorder;
   Comorbidity; Epidemiology; Suicide attempt
ID DEXAMETHASONE-SUPPRESSION TEST; PSYCHIATRIC DIAGNOSTIC MODULES;
   DIALECTICAL BEHAVIOR-THERAPY; CHILDHOOD SEXUAL-ABUSE;
   ALCOHOL-USE-DISORDER; AXIS-I COMORBIDITY; SUICIDAL-BEHAVIOR; FOLLOW-UP;
   RISK-FACTORS; MAJOR DEPRESSION
AB While placed on different axes of the DSM classification system, borderline personality disorder (BPD) and posttraumatic stress disorder (PTSD) have important relationships with trauma, and overlap between these disorders has long been recognized. The current study is the first to examine comorbidity of PTSD and BPD in a large nationally representative sample using a reliable and valid method of assessing Axis I and II mental disorders. Data came from the National Epidemiologic Survey on Alcohol and Related Conditions (NESARC) Wave II (N = 34,653; response rate 70.2%). Multiple regression models were used to examine differences in psychopathology, traumatic events and health-related quality of life across individuals with PTSD alone (n = 1820), BPD alone (n = 1290) and those with comorbid PTSD-BPD (n = 643). The lifetime prevalence of PTSD and BPD were 6.6% and 5.9%, respectively. Of individuals with BPD, 30.2% were also diagnosed with PTSD, whereas 24.2% of individuals with PTSD were also diagnosed with BPD. Individuals with comorbid PTSD-BPD had a poorer quality of life, more comorbidity with other Axis I conditions, increased odds of a lifetime suicide attempt, and a higher prevalence of repeated childhood traumatic events than individuals with either condition alone. These results show that PTSD and BPD have a high degree of lifetime co-occurrence but are not entirely overlapping. Their concurrence is associated with poorer functioning compared to either diagnosis alone, emphasizing the clinical utility of diagnosing both conditions. Future research should explore the determinants of having either or both diagnoses with an aim toward improved identification, prevention, and intervention. (C) 2010 Elsevier Ltd. All rights reserved.
C1 [Pagura, Jina; Bolton, James M.; Cox, Brian J.; Sareen, Jitender] Univ Manitoba, Dept Psychiat, Winnipeg, MB R3E 3N4, Canada.
   [Pagura, Jina; Bolton, James M.; Cox, Brian J.; Sareen, Jitender] Univ Manitoba, Dept Psychol, Winnipeg, MB R3E 3N4, Canada.
   [Cox, Brian J.; Sareen, Jitender] Univ Manitoba, Dept Community Hlth Sci, Winnipeg, MB R3E 3N4, Canada.
   [Stein, Murray B.] Univ Calif San Diego, Dept Psychiat, La Jolla, CA 92093 USA.
   [Stein, Murray B.] Univ Calif San Diego, Dept Family & Prevent Med, La Jolla, CA 92093 USA.
   [Grant, Bridget] NIAAA, Lab Epidemiol & Biometry, Div Intramural Clin & Biol Res, NIH, Bethesda, MD USA.
RP Sareen, J (reprint author), Univ Manitoba, Dept Psychiat, PZ 430 771 Bannatyne Ave, Winnipeg, MB R3E 3N4, Canada.
EM sareen@cc.umanitoba.ca
FU National Institute on Alcohol and Related Conditions (NIAAA); National
   Institute on Drug Abuse; Social Sciences and Humanities Research Council
   (SSHRC) Canada; Manitoba Health Research Council (MHRC); Canada Research
   Chairs program; Canadian Institutes of Health Research (CIHR); Swampy
   Cree Suicide Prevention Team CIHR [82894]; US National Institute of
   Mental Health [MH64122]
FX The NESARC was supported by the National Institute on Alcohol and
   Related Conditions (NIAAA) and the National Institute on Drug Abuse. The
   research was supported by a Social Sciences and Humanities Research
   Council (SSHRC) Canada Graduate Scholarship (Pagura), a Manitoba Health
   Research Council (MHRC) operating grant (Bolton), the Canada Research
   Chairs program (Cox), a Canadian Institutes of Health Research (CIHR)
   New Investigator Award (Sareen), the Swampy Cree Suicide Prevention Team
   CIHR Operating Grant #82894, and MH64122 from the US National Institute
   of Mental Health (Stein). These funding sources had no role in study
   design, analysis or interpretation of data, writing of the manuscript or
   the decision to submit the paper for publication.
NR 58
TC 65
Z9 66
U1 1
U2 17
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0022-3956
J9 J PSYCHIATR RES
JI J. Psychiatr. Res.
PD DEC
PY 2010
VL 44
IS 16
BP 1190
EP 1198
DI 10.1016/j.jpsychires.2010.04.016
PG 9
WC Psychiatry
SC Psychiatry
GA 703CP
UT WOS:000285952000010
PM 20537660
ER

PT J
AU Schaefer, KL
   Baumann, J
   Rich, BA
   Luckenbaugh, DA
   Zarate, CA
AF Schaefer, Kathryn L.
   Baumann, Jacqueline
   Rich, Brendan A.
   Luckenbaugh, David A.
   Zarate, Carlos A., Jr.
TI Perception of facial emotion in adults with bipolar or unipolar
   depression and controls
SO JOURNAL OF PSYCHIATRIC RESEARCH
LA English
DT Article
DE Bipolar disorder (BPD); Cognition; Facial expression; Emotion
   perception; Unipolar depression
ID SUSTAINED ATTENTION-DEFICIT; MAJOR DEPRESSION; PSYCHOSOCIAL DISABILITY;
   AFFECT RECOGNITION; LABELING DEFICITS; REMITTED PATIENTS; II DISORDER;
   EXPRESSIONS; CHILDREN; IMPAIRMENT
AB Previous research indicates that patients with depression display deficits in their ability to perceive emotions. However, few studies have used animated facial stimuli or explored sensitivity to facial expressions in depressed individuals. Moreover, limited research is available on facial processing in unipolar versus bipolar depression. In this study, 34 patients with DSM-IV major depressive disorder (MDD), 21 patients with DSM-IV bipolar disorder (BPD) in the depressed phase, and 24 never-depressed controls completed the Emotional Expression Multimorph Task, which presents facial emotions in gradations from neutral to 100% emotional expression (happy, sad, surprised, fearful, angry, and disgusted). Groups were compared in terms of sensitivity and accuracy in identifying emotions. Our preliminary findings suggest that subjects with bipolar depression may have emotional processing abnormalities relative to controls. Published by Elsevier Ltd.
C1 [Baumann, Jacqueline; Luckenbaugh, David A.; Zarate, Carlos A., Jr.] NIMH, Expt Therapeut Mood & Anxiety Disorders Program, NIH, US Dept HHS, Bethesda, MD 20892 USA.
   [Rich, Brendan A.] Catholic Univ Amer, Dept Psychol, Washington, DC 20064 USA.
   [Schaefer, Kathryn L.] Univ Maryland, Dept Counseling & Personnel Serv, College Pk, MD 20742 USA.
RP Zarate, CA (reprint author), CRC, 10 Ctr Dr,Unit 7 SE,Room 7-3445, Bethesda, MD 20892 USA.
EM zaratec@mail.nih.gov
FU National Institute of Mental Health, National Institutes of Health,
   Department of Health and Human Services (IRP-NIMH-NIH-DHHS); NARSAD
FX Funding for this work was supported by the Intramural Research Program
   of the National Institute of Mental Health, National Institutes of
   Health, Department of Health and Human Services (IRP-NIMH-NIH-DHHS) and
   by a NARSAD Award (CAZ). The NIMH had no further role in study design;
   in the collection, analysis and interpretation of data; in the writing
   of the manuscript; or in the decision to submit the paper for
   publication.
NR 46
TC 30
Z9 33
U1 4
U2 12
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0022-3956
J9 J PSYCHIATR RES
JI J. Psychiatr. Res.
PD DEC
PY 2010
VL 44
IS 16
BP 1229
EP 1235
DI 10.1016/j.jpsychires.2010.04.024
PG 7
WC Psychiatry
SC Psychiatry
GA 703CP
UT WOS:000285952000015
PM 20510425
ER

PT J
AU Mueller, SC
   Ng, P
   Temple, V
   Hardin, MG
   Pine, DS
   Leibenluft, E
   Ernst, M
AF Mueller, Sven C.
   Ng, Pamela
   Temple, Veronica
   Hardin, Michael G.
   Pine, Daniel S.
   Leibenluft, Ellen
   Ernst, Monique
TI Perturbed reward processing in pediatric bipolar disorder: an
   antisaccade study
SO JOURNAL OF PSYCHOPHARMACOLOGY
LA English
DT Article
DE bipolar disorder; reward; antisaccade; cognitive control; emotion; ADHD
ID SACCADIC EYE-MOVEMENTS; DEFICIT HYPERACTIVITY DISORDER; SEVERE MOOD
   DYSREGULATION; COGNITIVE CONTROL; DEPRESSED ADOLESCENTS; VOLUNTARY
   CONTROL; SCHIZOPHRENIA; TASK; PSYCHOPATHOLOGY; CONTINGENCIES
AB Pediatric bipolar disorder is a severe and impairing illness. Characterizing the impact of pediatric bipolar disorder on cognitive function might aid in understanding the phenomenology of the disorder. While previous studies of pediatric bipolar disorder have reported deficits in cognitive control and reward behavior, little is understood about how affective processes influence behavioral control. Relative to prior studies using manual-response paradigms, eye movement tasks provide a more precise assessment of reward sensitivity and cognitive and motor control. The current study compares 20 youths with bipolar disorder (mean age = 13.9 years +/- 2.22) and 23 healthy subjects (mean age = 13.8 years +/- 2.49) on a mixed pro-antisaccade task with monetary incentives. On both types of saccades, participants were presented with three types of incentives: those where subjects can win money, lose money, or neither win nor lose money. Impaired reward processing was found in youths with bipolar disorder relative to controls, particularly on antisaccades. This difference was reflected in lower error rates during incentive trials in the control but not in the bipolar disorder group. By comparison, no group differences were found on prosaccade trials. The results provide further evidence for deficits in cognitive and reward processing in bipolar disorder.
C1 [Mueller, Sven C.; Ng, Pamela; Temple, Veronica; Hardin, Michael G.; Pine, Daniel S.; Ernst, Monique] NIMH, Sect Dev & Affect Neurosci, NIH, Bethesda, MD 20814 USA.
   [Leibenluft, Ellen] NIMH, Sect Bipolar Spectrum Disorders, NIH, Bethesda, MD 20814 USA.
RP Mueller, SC (reprint author), NIMH, Sect Dev & Affect Neurosci, NIH, 15K N Dr, Bethesda, MD 20814 USA.
EM msven@mail.nih.gov
FU NIMH, NIH
FX This work was supported by the intramural program of the NIMH, NIH.
NR 31
TC 22
Z9 22
U1 3
U2 14
PU SAGE PUBLICATIONS LTD
PI LONDON
PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND
SN 0269-8811
J9 J PSYCHOPHARMACOL
JI J. Psychopharmacol.
PD DEC
PY 2010
VL 24
IS 12
BP 1779
EP 1784
DI 10.1177/0269881109353462
PG 6
WC Clinical Neurology; Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA 690XX
UT WOS:000285044500007
PM 20080923
ER

PT J
AU Arevalo, O
   Chattopadhyay, A
   Lester, H
   Skelton, J
AF Arevalo, Oscar
   Chattopadhyay, Amit
   Lester, Harold
   Skelton, Judy
TI Mobile dental operations: capital budgeting and long-term viability
SO JOURNAL OF PUBLIC HEALTH DENTISTRY
LA English
DT Article
DE oral health; financial management; access; mobile units; Medicaid
AB Objective:
   The University of Kentucky College of Dentistry (UKCD) runs a large mobile dental operation. Economic conditions dictate that as the mobile units age it will be harder to find donors willing or able to provide the financial resources for asset replacement. In order to maintain current levels of access for the underserved, consideration of replacement is paramount. A financial analysis for a new mobile unit was conducted to determine self-sustainability, return on investment (ROI), and feasibility of generating a cash reserve for its replacement in 12 years.
   Methods:
   Information on clinical income, operational and replacement costs, and capital costs was collected. A capital budgeting analysis (CBA) was conducted using the Net Present Value (NPV) methodology in four different scenarios. Depreciation funding was calculated by transferring funds from cash inflows and reinvested to offset depreciation at fixed compound interest.
   Results:
   A positive ROI was obtained for two scenarios. He depreciation fund did not generate a cash reserve sufficient to replace the mobile unit.
   Conclusions:
   Mobile dental programs can play a vital role in providing access to care to underserved populations and ensuring their mission requires long-term planning. Careful financial viability and CBA based on sound assumptions are excellent decision-making tools.
C1 [Arevalo, Oscar] Univ Puerto Rico, Sch Dent Med, San Juan, PR 00936 USA.
   [Chattopadhyay, Amit] NIDCR, Off Sci Policy & Anal, NIH, Bethesda, MD USA.
   [Lester, Harold; Skelton, Judy] Univ Kentucky, Coll Dent, Lexington, KY 40506 USA.
RP Arevalo, O (reprint author), Univ Puerto Rico, Sch Dent Med, San Juan, PR 00936 USA.
EM oscar.arevalo@upr.edu
RI Chattopadhyay, Amit/L-1919-2013
OI Chattopadhyay, Amit/0000-0003-3278-7525
FU Kentucky Department for Public Health; Steele Reese Foundation; Kentucky
   Colonels; Chatios Foundation; Appalachian Regional Commission; Christian
   Appalachian project; Special Olympics/Special Smiles; Ronald McDonald's
   Charities of the Blue Grass; Ronald McDonald Care Mobile Program; Fifth
   Third Bank; Johnson and Johnson Corporation
FX On behalf of the University of Kentucky College of Dentistry, the
   authors would like to acknowledge the following agencies and foundations
   that have supported our mobile dental operation throughout its
   existence: Kentucky Department for Public Health, Steele Reese
   Foundation, Kentucky Colonels, Chatios Foundation, Appalachian Regional
   Commission, Christian Appalachian project, Special Olympics/Special
   Smiles, Ronald McDonald's Charities of the Blue Grass, Ronald McDonald
   Care Mobile Program, Fifth Third Bank, and the Johnson and Johnson
   Corporation. In addition, the authors want to express their gratitude to
   Dr. Paul Childs from the Gatton School of Business and Economics at the
   University of Kentucky for his helpful comments and guidance in the
   development of the analysis.
NR 19
TC 2
Z9 2
U1 0
U2 4
PU AAPHD NATIONAL OFFICE
PI PORTLAND
PA 3760 SW LYLE COURT, PORTLAND, OR 97221 USA
SN 0022-4006
J9 J PUBLIC HEALTH DENT
JI J. Public Health Dent.
PD WIN
PY 2010
VL 70
IS 1
BP 28
EP 34
DI 10.1111/j.1752-7325.2009.00140.x
PG 7
WC Dentistry, Oral Surgery & Medicine; Public, Environmental & Occupational
   Health
SC Dentistry, Oral Surgery & Medicine; Public, Environmental & Occupational
   Health
GA 563PR
UT WOS:000275145700004
PM 19694936
ER

PT J
AU Birnbaumer, L
   Zurita, AR
AF Birnbaumer, Lutz
   Zurita, Adolfo R.
TI On the roles of Mg in the activation of G proteins
SO JOURNAL OF RECEPTORS AND SIGNAL TRANSDUCTION
LA English
DT Review
DE Octahedral coordination shell; regulatory GTPase; GTPase fold;
   transition state
ID SIGNAL-TRANSDUCTION; CYCLASE
AB In this review, we highlight the evolution of our knowledge about the way Mg(2+) participates in the activation of heterotrimeric G proteins, beginning with its requirement in hormonal stimulation of fat cell adenylyl cyclase (1969) and ending with knowledge that incorporates information obtained from site directed mutagenesis and examination of the crystal structures of G proteins (2010). Our current view is that, as it seeks to fill its octahedral coordination shell, Mg acts as a keystone locking the G protein-alpha subunits into a conformation in which G alpha dissociates from the G beta gamma dimer, is competent in regulating effectors, and acquires GTPase activity. The latter is the result of moving the backbone carbonyl group of the Mg-coordinating threonine into a location in space that positions the hydrolytic water so as to facilitate the water's nucleophilic attack that leads to hydrolysis of the link between the beta and gamma phosphates of guanosine triphosphate (GTP). The role of the backbone carbonyl group of the Mg-coordinating threonine is equi-hierarchical with a similar and long-recognized role of the Switch II glutamine delta amide carbonyl group. Disruption of either leads to loss of GTPase activity.
C1 [Birnbaumer, Lutz; Zurita, Adolfo R.] NIEHS, Neurobiol Lab, NIH, DHHS, Res Triangle Pk, NC 27709 USA.
RP Birnbaumer, L (reprint author), NIEHS, Neurobiol Lab, NIH, DHHS, 111 TW Aexander Dr, Res Triangle Pk, NC 27709 USA.
EM birnbau1@niehs.nih.gov
FU NIH [Z01-ES-101643]
FX Supported by the Intramural Research Program of the NIH (Z01-ES-101643).
NR 7
TC 5
Z9 5
U1 0
U2 7
PU INFORMA HEALTHCARE
PI LONDON
PA TELEPHONE HOUSE, 69-77 PAUL STREET, LONDON EC2A 4LQ, ENGLAND
SN 1079-9893
J9 J RECEPT SIG TRANSD
JI J. Recept. Signal Transduct.
PD DEC
PY 2010
VL 30
IS 6
SI SI
BP 372
EP 375
DI 10.3109/10799893.2010.508165
PG 4
WC Biochemistry & Molecular Biology; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA 685DX
UT WOS:000284609700002
PM 20731539
ER

PT J
AU Weisman, M
   Learch, TJ
   Baraliakos, X
   Chandran, V
   Gladman, DD
   Raychaudhuri, SP
   Xu, HJ
   Collantes-Estevez, E
   Vazquez-Mellado, J
   Mease, PJ
   Sieper, J
   Deodhar, AA
   Colbert, RA
   Clegg, DO
AF Weisman, Michael
   Learch, Thomas J.
   Baraliakos, Xenofon
   Chandran, Vinod
   Gladman, Dafna D.
   Raychaudhuri, Siba P.
   Xu, Huji
   Collantes-Estevez, Eduardo
   Vazquez-Mellado, Jantzia
   Mease, Philip J.
   Sieper, Joachim
   Deodhar, Atul A.
   Colbert, Robert A.
   Clegg, Daniel O.
CA SPARTAN Grp
TI Current Controversies in Spondyloarthritis: SPARTAN
SO JOURNAL OF RHEUMATOLOGY
LA English
DT Editorial Material
DE ANKYLOSING SPONDYLITIS; EPIDEMIOLOGY; SPONDYLOARTHRITIS;
   SPONDYLOARTHROPATHIES
ID RESONANCE-IMAGING EXAMINATIONS; PLACEBO-CONTROLLED TRIAL;
   ANKYLOSING-SPONDYLITIS; SPINAL MOBILITY; RADIOGRAPHIC PROGRESSION;
   CLASSIFICATION CRITERIA; RHEUMATOID-ARTHRITIS; METROLOGY INDEX; OMERACT
   FILTER; DOUBLE-BLIND
AB The Spondyloarthritis Research and Therapy Network (SPARTAN), founded in 2003 to promote research, education, and treatment of ankylosing spondylitis (AS) and related forms of spondyloarthritis (SpA), held its 7th Annual Research and Education Meeting in July 2009 in Houston, Texas. Current controversies in SpA discussed during the meeting included an update on the epidemiology of AS, axial SpA, and inflammatory back pain; the adequacy of the mSASS to assess radiographic involvement; the helpfulness of magnetic resonance imaging in assessing disease progression; the reliability of metrology in assessing damage; and whether biologic agents alter the course of AS. Presentations also were made on psoriasis in the SCID mouse model; the challenges and opportunities of SpA in China; a discussion of the special needs in managing SpA in Ibero-America, and the SPARK Survey in Europe and North America. (J Rheumatol 2010; 37:2617-23; doi:3899/jrheum.100890)
C1 [Clegg, Daniel O.] Univ Utah, Sch Med, Salt Lake City, UT 84132 USA.
   Cedars Sinai Med Ctr, Los Angeles, CA 90048 USA.
   [Baraliakos, Xenofon] Ruhr Univ Bochum, Rheumazentrum Ruhrgebiet Herne, Bochum, Germany.
   [Chandran, Vinod; Gladman, Dafna D.] Univ Toronto, Toronto, ON, Canada.
   [Raychaudhuri, Siba P.] Univ Calif Davis, Davis, CA 95616 USA.
   [Xu, Huji] Second Mil Med Univ, Shanghai Changzheng Hosp, Shanghai, Peoples R China.
   [Collantes-Estevez, Eduardo] Univ Hosp Cordoba, Cordoba, Spain.
   [Vazquez-Mellado, Jantzia] Hosp Gen Mexico City, Mexico City, DF, Mexico.
   [Mease, Philip J.] Univ Washington, Seattle, WA 98195 USA.
   [Mease, Philip J.] Swedish Med Ctr, Seattle, WA USA.
   [Sieper, Joachim] Charite Campus Benjamin Franklin, Berlin, Germany.
   [Deodhar, Atul A.] Oregon Hlth & Sci Univ, Portland, OR 97201 USA.
   [Colbert, Robert A.] NIH, Bethesda, MD 20892 USA.
RP Clegg, DO (reprint author), Univ Utah, Sch Med, 50 N Med Dr, Salt Lake City, UT 84132 USA.
EM Daniel.Clegg@hsc.utah.edu
OI Collantes Estevez, Eduardo/0000-0002-7647-6289
NR 58
TC 6
Z9 6
U1 1
U2 3
PU J RHEUMATOL PUBL CO
PI TORONTO
PA 365 BLOOR ST E, STE 901, TORONTO, ONTARIO M4W 3L4, CANADA
SN 0315-162X
EI 1499-2752
J9 J RHEUMATOL
JI J. Rheumatol.
PD DEC
PY 2010
VL 37
IS 12
BP 2617
EP 2623
DI 10.3899/jrheum.100890
PG 7
WC Rheumatology
SC Rheumatology
GA 694CM
UT WOS:000285272600025
PM 21123334
ER

PT J
AU Baldwin, LM
   Chan, L
   Andrilla, CHA
   Huff, ED
   Hart, LG
AF Baldwin, Laura-Mae
   Chan, Leighton
   Andrilla, C. Holly A.
   Huff, Edwin D.
   Hart, L. Gary
TI Quality of Care for Myocardial Infarction in Rural and Urban Hospitals
SO JOURNAL OF RURAL HEALTH
LA English
DT Article
DE Medicare; myocardial infarction; quality of care; rural hospitals
ID COOPERATIVE CARDIOVASCULAR PROJECT; MEDICARE PATIENTS; UNITED-STATES;
   GUIDELINES; BENEFICIARIES; ASSOCIATION; PROGRAM; HEALTH; VOLUME
AB Background: In the mid-1990s, significant gaps existed in the quality of acute myocardial infarction (AMI) care between rural and urban hospitals. Since then, overall AMI care quality has improved. This study uses more recent data to determine whether rural-urban AMI quality gaps have persisted.
   Methods: Using inpatient records data for 34,776 Medicare beneficiaries with AMI from 2000-2001, unadjusted and logistic regression analysis compared receipt of 5 recommended treatments between admissions to urban, large rural, small rural, and isolated small rural hospitals as defined by Rural Urban Commuting Area codes.
   Results: Substantial proportions of hospital admissions in all areas did not receive guideline-recommended treatments (eg, 17.0% to 23.6% without aspirin within 24 hours of admission, 30.8% to 46.6% without beta-blockers at arrival/discharge). Admissions to small rural and isolated small rural hospitals were least likely to receive most treatments (eg, 69.2% urban, 68.3% large rural, 59.9% small rural, 53.4% isolated small rural received discharge beta-blocker prescriptions). Adjusted analyses found no treatment differences between admissions to large rural and urban area hospitals, but admissions to small rural and isolated small rural hospitals had lower rates of discharge prescriptions such as aspirin and beta-blockers than urban hospital admissions.
   Conclusions: Many simple guidelines that improve AMI outcomes are inadequately implemented, regardless of geographic location. In small rural and isolated small rural hospitals, addressing barriers to prescription of beneficial discharge medications is particularly important. The best quality improvement practices should be identified and translated to the broadest range of institutions and providers.
C1 [Baldwin, Laura-Mae; Andrilla, C. Holly A.] Univ Washington, Sch Med, Dept Family Med, WWAMI Rural Hlth Res Ctr, Seattle, WA 98195 USA.
   [Chan, Leighton] NIH, Dept Rehabil Med, Bethesda, MD 20892 USA.
   [Huff, Edwin D.] Ctr Medicare & Medicaid Serv, Boston Reg Off, Div Qual Improvement, Boston, MA USA.
   [Hart, L. Gary] Univ Arizona Mel & Enid Zuckerman, Coll Publ Hlth, Rural Hlth Off, Tucson, AZ USA.
RP Baldwin, LM (reprint author), Univ Washington, Sch Med, Dept Family Med, WWAMI Rural Hlth Res Ctr, Box 354982, Seattle, WA 98195 USA.
EM lmb@u.washington.edu
FU Office of Rural Health Policy; Health Resources and Services
   Administration; Department of Health and Human Services; National
   Institutes of Health
FX This study was funded by the federal Office of Rural Health Policy,
   Health Resources and Services Administration, Department of Health and
   Human Services, and by the Intramural Research Program of the National
   Institutes of Health. The Centers for Medicare & Medicaid Services
   provided the de-identified study database linked to Rural Urban
   Commuting Area Codes. The authors thank Shelli Beaver, MS, from the
   Centers for Medicare & Medicaid Services and Richard F. Maclehose, PhD,
   from the National Institute of Environmental Health Sciences for serving
   as resources in the use of the Medicare Quality Improvement Organization
   data, and Beth Jackson, PhD, for her help in developing the database
   used in this study.
NR 23
TC 11
Z9 11
U1 2
U2 4
PU WILEY-BLACKWELL PUBLISHING, INC
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0890-765X
J9 J RURAL HEALTH
JI J. Rural Health
PD WIN
PY 2010
VL 26
IS 1
BP 51
EP 57
DI 10.1111/j.1748-0361.2009.00265.x
PG 7
WC Health Care Sciences & Services; Health Policy & Services; Public,
   Environmental & Occupational Health
SC Health Care Sciences & Services; Public, Environmental & Occupational
   Health
GA 540EJ
UT WOS:000273313500008
PM 20105268
ER

PT J
AU Krishna, SS
   Aravind, L
AF Krishna, S. Sri
   Aravind, L.
TI The bridge-region of the Ku superfamily is an atypical zinc ribbon
   domain
SO JOURNAL OF STRUCTURAL BIOLOGY
LA English
DT Article
DE NHEJ; Zinc finger; Zinc ribbon; Protein flexibility; Segment-swapping
ID DOUBLE-STRAND BREAKS; NONHOMOLOGOUS END; DNA-END; STRUCTURAL
   CLASSIFICATION; BINDING DOMAIN; PSI-BLAST; PROTEIN; DATABASE; REPAIR;
   MOTIF
AB Members of the Ku superfamily are DNA-end-binding proteins involved in non-homologous end-joining (NHEJ) DNA repair. The published crystal structure of human Ku-DNA complex reveals a heterodimer that forms a ring around dsDNA by means of the Ku core modules. These modules contain a highly conserved seven-stranded beta-barrel, which in turn contains an insertion, termed the bridge-region, between its second and third beta-strands. The bridge-region adopts an unusual beta-strand-rich structure critical for dsDNA-binding and Ku function, but its provenance remains unclear. Here, we demonstrate that the bridge-region of Ku is a novel member of the diverse Zn-ribbon fold group. Sequence analysis reveals that Ku from several Gram-positive bacteria and bacteriophages retain metal-chelating motifs, whereas they have been lost in the versions from most other organisms. Structural comparisons suggest that the Zn-ribbon from Ku-bridge-region is the first example of a circularly permuted, segment-swapped Zn-ribbon. This finding helps explain how Ku is likely to bind DNA as an obligate dimer. Further, we hypothesize that retention of the unusual conformation of the turns of the Zn-ribbons, despite loss of the Zn-binding sites, provides clues regarding the mechanism by which the Ku-bridge-regions sense the DNA state. (C) 2010 Elsevier Inc. All rights reserved.
C1 [Krishna, S. Sri] CSIR, Inst Microbial Technol, Chandigarh 160036, India.
   [Krishna, S. Sri] Univ Calif San Diego, Ctr Res Biol Syst, La Jolla, CA 92093 USA.
   [Aravind, L.] NIH, Natl Ctr Biotechnol Informat, Natl Lib Med, Bethesda, MD 20894 USA.
RP Krishna, SS (reprint author), CSIR, Inst Microbial Technol, Chandigarh 160036, India.
EM krishna@sdsc.edu; aravind@ncbi.nlm.nih.gov
OI Krishna, Sanjeev/0000-0003-0066-0634
FU National Library of Medicine, NIH; Council of Scientific and Industrial
   Research (CSIR), India
FX LA is supported by the intramural funds of the National Library of
   Medicine, NIH. SSK is supported by the Council of Scientific and
   Industrial Research (CSIR), India. The content is solely the
   responsibility of the authors and does not necessarily represent the
   official views of the National Institutes of Health or the Council of
   Scientific and Industrial Research.
NR 47
TC 7
Z9 7
U1 1
U2 2
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 1047-8477
J9 J STRUCT BIOL
JI J. Struct. Biol.
PD DEC
PY 2010
VL 172
IS 3
BP 294
EP 299
DI 10.1016/j.jsb.2010.05.011
PG 6
WC Biochemistry & Molecular Biology; Biophysics; Cell Biology
SC Biochemistry & Molecular Biology; Biophysics; Cell Biology
GA 677BL
UT WOS:000283964000011
PM 20580930
ER

PT J
AU Rauch, SL
   Britton, JC
AF Rauch, Scott L.
   Britton, Jennifer C.
TI Developmental Neuroimaging Studies of OCD: The Maturation of a Field
SO JOURNAL OF THE AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY
LA English
DT Editorial Material
ID OBSESSIVE-COMPULSIVE DISORDER; ADOLESCENTS; CHILDREN
C1 [Rauch, Scott L.] McLean Hosp, Belmont, MA 02478 USA.
   [Britton, Jennifer C.] NIMH, Bethesda, MD 20892 USA.
RP Rauch, SL (reprint author), McLean Hosp, 115 Mill St, Belmont, MA 02478 USA.
EM srauch@partners.org
RI Britton, Jennifer/J-4501-2013
NR 9
TC 0
Z9 0
U1 0
U2 7
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0890-8567
J9 J AM ACAD CHILD PSY
JI J. Am. Acad. Child Adolesc. Psychiatr.
PD DEC
PY 2010
VL 49
IS 12
BP 1186
EP 1188
DI 10.1016/j.jaac.2010.08.016
PG 3
WC Psychology, Developmental; Pediatrics; Psychiatry
SC Psychology; Pediatrics; Psychiatry
GA 689HH
UT WOS:000284918200003
PM 21093768
ER

PT J
AU Wu, PA
   Turner, ML
   Cowen, EW
   Wilson, E
   Shea, YR
   Jancel, T
   Freeman, AF
AF Wu, Peggy A.
   Turner, Maria L.
   Cowen, Edward W.
   Wilson, Eleanor
   Shea, Yvonne R.
   Jancel, Timothy
   Freeman, Alexandra F.
TI Sixty-year-old man with slowly expanding nodular plaque on the thigh
SO JOURNAL OF THE AMERICAN ACADEMY OF DERMATOLOGY
LA English
DT Article
DE chromoblastomycosis; Fonsecaea pedisoi; fungal infection; Medlar bodies;
   posaconazole
ID TOPICAL HEAT THERAPY; FONSECAEA-PEDROSOI; LIQUID-NITROGEN;
   CHROMOBLASTOMYCOSIS; CHROMOMYCOSIS; ITRACONAZOLE; POSACONAZOLE;
   PHEOHYPHOMYCOSIS; TERBINAFINE; CRYOSURGERY
C1 [Turner, Maria L.; Cowen, Edward W.] NCI, Dermatol Branch, Ctr Canc Res, Bethesda, MD 20892 USA.
   [Wu, Peggy A.] Washington Univ, Div Dermatol, St Louis, MO USA.
   [Wilson, Eleanor; Jancel, Timothy] NIAID, NIH, Bethesda, MD 20892 USA.
   [Shea, Yvonne R.] NIH, Microbiol Serv, Dept Lab Med, Ctr Clin, Bethesda, MD 20892 USA.
   [Jancel, Timothy] NIH, Dept Pharm, Ctr Clin, Bethesda, MD 20892 USA.
   [Freeman, Alexandra F.] NIAID, Lab Clin Infect Dis, NIH, Bethesda, MD 20892 USA.
RP Cowen, EW (reprint author), NCI, Dermatol Branch, Ctr Canc Res, Bldg 10,Room 12N238,10 Ctr Dr,MSC 1908, Bethesda, MD 20892 USA.
OI Wilson, Eleanor/0000-0002-4855-514X
FU National Institutes of Health; Center for Cancer Research National
   Cancer Institute; National Institute of Allergy and Infectious Diseases
FX Supported by the Intramural Program of National Institutes of Health
   Center for Cancer Research National Cancer Institute and the National
   Institute of Allergy and Infectious Diseases Conflicts of interest None
   declared
NR 37
TC 2
Z9 2
U1 0
U2 0
PU MOSBY-ELSEVIER
PI NEW YORK
PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0190-9622
J9 J AM ACAD DERMATOL
JI J. Am. Acad. Dermatol.
PD DEC
PY 2010
VL 63
IS 6
BP 1083
EP 1087
DI 10.1016/j.jaad.2010.06.029
PG 5
WC Dermatology
SC Dermatology
GA 689YX
UT WOS:000284968100018
PM 21093663
ER

PT J
AU Gary Rozier, R
   Adair, S
   Graham, F
   Iafolla, T
   Kingman, A
   Kohn, W
   Krol, D
   Levy, S
   Pollick, H
   Whitford, G
   Strock, S
   Hawley, JF
   Aravamudhan, K
   Meyer, DM
AF Gary Rozier, R.
   Adair, Steven
   Graham, Frank
   Iafolla, Timothy
   Kingman, Albert
   Kohn, William
   Krol, David
   Levy, Steven
   Pollick, Howard
   Whitford, Gary
   Strock, Sheila
   Hawley, Julie Frantsve
   Aravamudhan, Krishna
   Meyer, Daniel M.
TI Evidence-based clinical recommendations on the prescription of dietary
   fluoride supplements for caries prevention A report of the American
   Dental Association Council on Scientific Affairs
SO JOURNAL OF THE AMERICAN DENTAL ASSOCIATION
LA English
DT Article
DE Fluoride supplements caries prevention fluorosis; evidence based
   dentistry clinical recommendations
ID PERMANENT 1ST MOLARS; MAXILLARY CENTRAL INCISORS; POSTERUPTION WATER
   FLUORIDE; SOUTH AUSTRALIAN CHILDREN; ENAMEL FLUOROSIS; CHEWABLE TABLETS;
   PRESCHOOL-CHILDREN; SCHOOL-CHILDREN; CRITICAL PERIOD; DRINKING-WATER
AB Background This article presents evidence based clinical recommendations for the prescription of dietary fluoride supplements The recommendations were developed by an expert panel convened by the American Dental Association (ADA) Council on Scientific Affairs (CSA) The panel addressed the following questions when and for whom should fluoride supplements be prescribed and what should be the recommended dosage schedule for dietary fluoride supplements?
   Types of Studies Reviewed A panel of experts convened by the ADA CSA m collaboration with staff of the ADA Center for Evidence based Dentistry conducted a MEDLINE search to identify publications that addressed the research questions systematic reviews as well as clinical studies published since the systematic reviews were conducted (June 1 2006)
   Results The panel concluded that dietary fluoride supplements should be prescribed only for children who are at high risk of developing canes and whose primary source of drinking water is deficient m fluoride
   Clinical Implications These recommendations are a resource for practitioners to consider in the clinical decision making process As part of the evidence based approach to care these clinical recommendations should be integrated with the practitioners professional judgment and the patients needs and preferences Providers should carefully monitor the patient s adherence to the fluoride dosing schedule to maximize the potential therapeutic benefit
C1 [Hawley, Julie Frantsve; Aravamudhan, Krishna] Amer Dent Assoc, Div Sci, Ctr Evidence Based Dent, Chicago, IL 60611 USA.
   [Hawley, Julie Frantsve] Amer Dent Assoc, Div Sci, Res Inst, Chicago, IL 60611 USA.
   [Gary Rozier, R.] Univ N Carolina, Gillings Sch Global Publ Hlth, Chapel Hill, NC USA.
   [Adair, Steven] FORBA Dent Management, Nashville, TN USA.
   [Adair, Steven] Med Coll Georgia, Sch Dent, Dept Pediat Dent, Augusta, GA 30912 USA.
   [Graham, Frank] Montefiore Med Ctr, Dept Dent, Bronx, NY 10467 USA.
   [Graham, Frank] Amer Dent Assoc, Council Dent Practice, Chicago, IL 60611 USA.
   [Iafolla, Timothy] Natl Inst Dent & Craniofacial Res, Off Sci Policy & Anal, NIH, Bethesda, MD USA.
   [Kohn, William] Ctr Dis Control & Prevent, Div Oral Hlth, Atlanta, GA USA.
   [Krol, David] Robert Wood Johnson Fdn, Princeton, NJ 08540 USA.
   [Levy, Steven] Univ Iowa, Coll Dent, Dept Prevent & Community Dent, Iowa City, IA 52242 USA.
   [Levy, Steven] Univ Iowa, Coll Publ Hlth, Dept Epidemiol, Iowa City, IA 52242 USA.
   [Pollick, Howard] Univ Calif San Francisco, Sch Dent, Dept Prevent & Restorat Dent Sci, San Francisco, CA 94143 USA.
   [Whitford, Gary] Med Coll Georgia, Sch Dent, Dept Oral Biol, Augusta, GA 30912 USA.
   [Strock, Sheila] Amer Dent Assoc, Council Access Prevent & Interprofess Relat, Chicago, IL 60611 USA.
RP Hawley, JF (reprint author), Amer Dent Assoc, Div Sci, Ctr Evidence Based Dent, 211 E Chicago Ave, Chicago, IL 60611 USA.
NR 74
TC 0
Z9 1
U1 2
U2 7
PU AMER DENTAL ASSOC
PI CHICAGO
PA 211 E CHICAGO AVE, CHICAGO, IL 60611 USA
SN 0002-8177
EI 1943-4723
J9 J AM DENT ASSOC
JI J. Am. Dent. Assoc.
PD DEC
PY 2010
VL 141
IS 12
BP 1480
EP 1489
PG 10
WC Dentistry, Oral Surgery & Medicine
SC Dentistry, Oral Surgery & Medicine
GA 695LR
UT WOS:000285372100022
ER

PT J
AU Kitahara, CM
AF Kitahara, Cari M.
TI Low-Glycemic Load Diets: How Does the Evidence for Prevention of Disease
   Measure Up?
SO JOURNAL OF THE AMERICAN DIETETIC ASSOCIATION
LA English
DT Editorial Material
ID DENSITY-LIPOPROTEIN CHOLESTEROL; C-REACTIVE PROTEIN; METABOLIC SYNDROME;
   US ADULTS; INDEX; RISK; CARBOHYDRATE; METAANALYSIS; MANAGEMENT; CANCER
C1 [Kitahara, Cari M.] NCI, Div Canc Epidemiol & Genet, NIH, Rockville, MD USA.
RP Kitahara, CM (reprint author), 6120 Execut Blvd,EPS 7051, Rockville, MD 20852 USA.
EM meinholdc@mail.nih.gov
RI Kitahara, Cari/R-8267-2016
FU Intramural NIH HHS [Z99 CA999999]
NR 21
TC 1
Z9 2
U1 0
U2 2
PU AMER DIETETIC ASSOC
PI CHICAGO
PA 120 S RIVERSIDE PLZ, STE 2000, CHICAGO, IL 60606-6995 USA
SN 0002-8223
J9 J AM DIET ASSOC
JI J. Am. Diet. Assoc.
PD DEC
PY 2010
VL 110
IS 12
BP 1818
EP 1819
DI 10.1016/j.jada.2010.09.018
PG 2
WC Nutrition & Dietetics
SC Nutrition & Dietetics
GA 689HI
UT WOS:000284918300010
PM 21111091
ER

PT J
AU Liggins, C
   Pryor, L
   Bernard, MA
AF Liggins, Charlene
   Pryor, Lisa
   Bernard, Marie A.
TI Challenges and Opportunities in Advancing Models of Care for Older
   Adults: An Assessment of the National Institute on Aging Research
   Portfolio
SO JOURNAL OF THE AMERICAN GERIATRICS SOCIETY
LA English
DT Article
DE models of care; elderly; organization and delivery of care; chronic
   care; and outcomes of care
ID OUTPATIENT GERIATRIC EVALUATION; MANAGEMENT; TRIAL; FRAIL; INTERVENTION;
   OUTCOMES; WALKING; DISEASE; COST
AB OBJECTIVES
   To identify existing projects supported by the National Institute on Aging (NIA) that may relate to the recommendations for models of care (MOCs) presented in the 2008 Institute of Medicine Report, Retooling for an Aging America: Building the Healthcare Workforce.
   DESIGN
   Cross-sectional analysis of NIA's grant portfolio.
   SETTING
   NIA.
   PARTICIPANTS
   NIA grantees.
   MEASUREMENTS
   NIA's grant portfolio was queried for the period 1999 to 2008 using a variety of search terms related to MOCs. Inclusion criteria were adherence to guiding principles for MOCs (comprehensive care, efficient care, older person as an active partner) or focus on innovative feature(s) of MOCs (interdisciplinary care, care management, chronic disease self-management, pharmaceutical management, preventive home visits, proactive rehabilitation, transitional care). Exclusion criteria were lack of focus on an intervention and focus on informal caregivers. Expert NIA staff reviewed and validated projects.
   RESULTS
   One hundred thirty-five grants were identified. These grants represent fewer than 1% of the approximate number of grants NIA has funded over this same period of time (similar to 24,000 grants). Forty-four percent focused on components of comprehensive care and 34% on active involvement of older adults. Approximately half specifically focused on innovative features of MOCs, ranging from chronic disease self-management (32%) and proactive rehabilitation (26%) to preventive home visits (1%) and transitional care (1%). The majority of projects were investigator-initiated grants (46%).
   CONCLUSION
   NIA has supported the development of many interventions that include components of MOCs related to recommendations from the IOM report. The challenge for the future will be determining which of the many components of comprehensive care systems are most effective for which subsets of the elderly population and assessing opportunities for enhanced collaboration between public and private aging research stakeholders.
C1 [Liggins, Charlene] NIA, Dept Hlth & Human Serv, NIH, Bethesda, MD 20892 USA.
RP Liggins, C (reprint author), NIA, Dept Hlth & Human Serv, NIH, Bldg 31,5C-05,31 Ctr Dr,MSC 2292, Bethesda, MD 20892 USA.
EM ligginsc@mail.nih.gov
FU National Institute on Aging
FX The National Institute on Aging, through salary support of the authors,
   supported the design, collection of data, and analysis and preparation
   of the manuscript. This manuscript was developed as a part of the
   official duties of these employees.
NR 23
TC 4
Z9 4
U1 1
U2 9
PU WILEY-BLACKWELL PUBLISHING, INC
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0002-8614
J9 J AM GERIATR SOC
JI J. Am. Geriatr. Soc.
PD DEC
PY 2010
VL 58
IS 12
BP 2345
EP 2349
DI 10.1111/j.1532-5415.2010.03157.x
PG 5
WC Geriatrics & Gerontology; Gerontology
SC Geriatrics & Gerontology
GA 692MI
UT WOS:000285156500011
PM 21070194
ER

PT J
AU Lloyd, JR
   Hess, S
AF Lloyd, John R.
   Hess, Sonja
TI Peptide Fragmentation by Corona Discharge Induced Electrochemical
   Ionization
SO JOURNAL OF THE AMERICAN SOCIETY FOR MASS SPECTROMETRY
LA English
DT Article
ID ELECTRON-CAPTURE DISSOCIATION; MOLECULAR RADICAL CATIONS;
   ATMOSPHERIC-PRESSURE PHOTOIONIZATION; MOBILE PROTON MODEL;
   MASS-SPECTROMETRY; GAS-PHASE; AUXILIARY LIGAND; STAINLESS-STEEL;
   ION-SOURCE; B-IONS
AB Fundamental studies have greatly improved our understanding of electrospray, including the underlying electrochemical reactions Generally regarded as disadvantageous, we have recently shown that corona discharge (CD) can be used as an effective method to create a radical cation species [M], thus optimizing the electrochemical reactions that occur on the surface of the stainless steel (SS) electrospray capillary tip This technique is known as CD initiated electrochemical ionization (CD-ECI) Here, we report on the fundamental studies using CD-ECI to induce analytically useful in-source fragmentation of a range of molecules that complex transition metals Compounds that have been selectively fragmented using CD-ECI include enolate forming phenylglycine containing peptides, glycopeptides, nucleosides, and phosphopeptides Collision induced dissociation (CID) or other activation techniques were not necessary for CD-ECI fragmentation A four step mechanism was proposed (1) complexation using either Fe in the SS capillary tip material or Cu(II) as an offline complexation reagent, (2) electrochemical oxidation of the complexed metal and thus formation of a radical cation (e g, Fe - e(-) -> Fe(+)), (3) radical fragmentation of the complexed compound, (4) electrospray ionization of the fragmented neutrals Fragmentation patterns resembling b- and y-type ions were observed and allowed the localization of the phosphorylation sites (J Am Soc Mass Spectrom 2010, 21, 2051-2061) (C) 2010 American Society for Mass Spectrometry
C1 [Hess, Sonja] CALTECH, Proteome Explorat Lab, Pasadena, CA 91125 USA.
   [Lloyd, John R.] NIDDK, Prote & Mass Spectrometry Facil, NIH, Bethesda, MD USA.
RP Hess, S (reprint author), CALTECH, Proteome Explorat Lab, Bl 211,MC139 74, Pasadena, CA 91125 USA.
RI Hess, Sonja/K-4842-2013
OI Hess, Sonja/0000-0002-5904-9816
FU National Institute of Diabetes and Digestive and Kidney Diseases [Z01
   DK070004-04]; Beckman Institute; Gordon and Betty Moore Foundation
FX This article is dedicated to Dr Henry M Fales, National Heart, Lung, and
   Blood Institute, National Institutes of Health The authors acknowledge
   research support from the National Institute of Diabetes and Digestive
   and Kidney Diseases (Z01 DK070004-04), the Beckman Institute, and the
   Gordon and Betty Moore Foundation is gratefully acknowledged The authors
   thank War-Ming Yau for synthesizing peptide UP14R They thank Anastasia
   Kalli and Robert Graham for critical review of the manuscript
NR 57
TC 4
Z9 4
U1 0
U2 12
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1044-0305
J9 J AM SOC MASS SPECTR
JI J. Am. Soc. Mass Spectrom.
PD DEC
PY 2010
VL 21
IS 12
BP 2051
EP 2061
DI 10.1016/j.jasms.2010.08.018
PG 11
WC Biochemical Research Methods; Chemistry, Analytical; Chemistry,
   Physical; Spectroscopy
SC Biochemistry & Molecular Biology; Chemistry; Spectroscopy
GA 690EL
UT WOS:000284985200012
PM 20869880
ER

PT J
AU Contreras, G
   Hu, B
   Astor, BC
   Greene, T
   Erlinger, T
   Kusek, JW
   Lipkowitz, M
   Lewis, JA
   Randall, OS
   Hebert, L
   Wright, JT
   Kendrick, CA
   Gassman, J
   Bakris, G
   Kopple, JD
   Appel, LJ
AF Contreras, Gabriel
   Hu, Bo
   Astor, Brad C.
   Greene, Tom
   Erlinger, Thomas
   Kusek, John W.
   Lipkowitz, Michael
   Lewis, Julia A.
   Randall, Otelio S.
   Hebert, Lee
   Wright, Jackson T., Jr.
   Kendrick, Cynthia A.
   Gassman, Jennifer
   Bakris, George
   Kopple, Joel D.
   Appel, Lawrence J.
CA African Amer Study Kidney Dis Hype
TI Malnutrition-Inflammation Modifies the Relationship of Cholesterol with
   Cardiovascular Disease
SO JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY
LA English
DT Article
ID CHRONIC KIDNEY-DISEASE; C-REACTIVE PROTEIN; TYPE-2 DIABETES-MELLITUS;
   CHRONIC-RENAL-FAILURE; HEMODIALYSIS-PATIENTS; BLOOD-PRESSURE;
   HYPERTENSION AASK; AFRICAN-AMERICAN; IN-VIVO; MORTALITY
AB In moderate and severe CKD, the association of cholesterol with subsequent cardiovascular disease (CVD) is weak. We examined whether malnutrition or inflammation (M-I) modifies the risk relationship between cholesterol levels and CVD events in African Americans with hypertensive CKD and a GFR between 20 and 65 ml/min per 1.73 m(2). We stratified 990 participants by the presence or absence of M-I, defined as body mass index <23 kg/m(2) or C-reactive protein >10 mg/L at baseline. The primary composite outcome included cardiovascular death or first hospitalization for coronary artery disease, stroke, or congestive heart failure occurring during a median follow-up of 77 months. Baseline total cholesterol (212 +/- 48 versus 212 +/- 44 mg/dl) and overall incidence of the primary CVD outcome (19 versus 21%) were similar in participants with (n = 304) and without (n = 686) M-I. In adjusted analyses, the CVD composite outcome exhibited a significantly stronger relationship with total cholesterol for participants without M-I than for participants with M-I at baseline (P < 0.02). In the non M-I group, the cholesterol-adjusted hazard ratio (HR) for CVD increased progressively across cholesterol levels: HR = 1.19 [95% CI; 0.77, 1.84] and 2.18 [1.43, 3.33] in participants with cholesterol 200 to 239 and >= 240 mg/dl, respectively (reference: cholesterol <200). In the M-I group, the corresponding HRs did not vary significantly by cholesterol level. In conclusion, the presence of M-I modifies the risk relationship between cholesterol level and CVD in African Americans with hypertensive CKD.
C1 [Contreras, Gabriel] Univ Miami, Miller Sch Med, Div Nephrol & Hypertens, Dept Med, Miami, FL 33136 USA.
   [Hu, Bo; Kendrick, Cynthia A.; Gassman, Jennifer] Cleveland Clin Fdn, Dept Quantitat Hlth Sci, Cleveland, OH 44195 USA.
   [Astor, Brad C.; Appel, Lawrence J.] Johns Hopkins Univ, Sch Med, Welch Ctr Prevent Epidemiol & Clin Res, Baltimore, MD USA.
   [Astor, Brad C.; Appel, Lawrence J.] Bloomberg Sch Publ Hlth, Baltimore, MD USA.
   [Greene, Tom] Univ Utah, Dept Internal Med, Div Epidemiol, Salt Lake City, UT 84112 USA.
   [Erlinger, Thomas] Seton Hosp, Dept Med, Austin, TX USA.
   [Kusek, John W.] Natl Inst Diabet & Kidney Dis, Bethesda, MD USA.
   [Lipkowitz, Michael] Mt Sinai Sch Med, Dept Med, New York, NY USA.
   [Lewis, Julia A.] Vanderbilt Univ, Dept Med, Nashville, TN USA.
   [Randall, Otelio S.] Howard Univ, Dept Med, Washington, DC 20059 USA.
   [Hebert, Lee] Ohio State Univ, Dept Med, Columbus, OH 43210 USA.
   [Wright, Jackson T., Jr.] Case Western Reserve Univ, Dept Med, Cleveland, OH 44106 USA.
   [Bakris, George] Univ Chicago, Pritzker Sch Med, Dept Prevent Med, Chicago, IL 60637 USA.
   [Kopple, Joel D.] Univ Calif Los Angeles, Dept Med, David Geffen Sch Med, Harbor Univ Calif Los Angeles Med Ctr, Torrance, CA USA.
   [Kopple, Joel D.] Univ Calif Los Angeles, David Geffen Sch Med, Dept Med, Harbor Univ Calif Los Angeles Med Ctr, Los Angeles, CA 90095 USA.
   [Kopple, Joel D.] Univ Calif Los Angeles, Sch Publ Hlth, Torrance, CA USA.
   [Kopple, Joel D.] Univ Calif Los Angeles, Sch Publ Hlth, Los Angeles, CA 90024 USA.
RP Contreras, G (reprint author), Univ Miami, Miller Sch Med, Div Nephrol & Hypertens, Dept Med, 1120 NW 14th St,Suite 360E, Miami, FL 33136 USA.
EM gcontrer@med.miami.edu; hub@ccf.org
FU National Institute of Health [U01 DK048652, UL1 RR024989, M01 RR-00080,
   5M01 RR-00071, M0100032, P20-RR11145, M01 RR00827, M01 RR00052, 2P20
   RR11104, DK 2818-02]; National Institute of Diabetes and Digestive and
   Kidney Diseases (NIDDK); General Clinical Research Center; Office of
   Research in Minority Health; King Pharmaceuticals; Pfizer; AstraZeneca
   Pharmaceuticals
FX Drs. Contreras, Hu, Astor, Greene, Wang, Gassman, and Appel have full
   access to all of the data and take responsibility for the integrity of
   the data and the accuracy of the data analysis. This study was supported
   by National Institute of Health Grants U01 DK048652 and UL1 RR024989. In
   addition to funding under a cooperative agreement from the National
   Institute of Diabetes and Digestive and Kidney Diseases (NIDDK), this
   work was supported in part by the following institutional General
   Clinical Research Center and other National Institutes of Health grants:
   M01 RR-00080, 5M01 RR-00071, M0100032, P20-RR11145, M01 RR00827, M01
   RR00052, 2P20 RR11104, and DK 2818-02. We also gratefully acknowledge
   support from the Office of Research in Minority Health (now the National
   Center on Minority Health and Health Disparities [NCMHD]) and the
   donation of drugs and some financial support to NIDDK by King
   Pharmaceuticals, Pfizer, and AstraZeneca Pharmaceuticals. A special
   acknowledgment is extended to the AASK participants for their time and
   commitment to the trial and cohort.
NR 47
TC 18
Z9 20
U1 0
U2 4
PU AMER SOC NEPHROLOGY
PI WASHINGTON
PA 1725 I ST, NW STE 510, WASHINGTON, DC 20006 USA
SN 1046-6673
J9 J AM SOC NEPHROL
JI J. Am. Soc. Nephrol.
PD DEC
PY 2010
VL 21
IS 12
BP 2131
EP 2142
DI 10.1681/ASN.2009121285
PG 12
WC Urology & Nephrology
SC Urology & Nephrology
GA 697RJ
UT WOS:000285533300019
PM 20864686
ER

PT J
AU Fox, CS
   Gona, P
   Larson, MG
   Selhub, J
   Tofler, G
   Hwang, SJ
   Meigs, JB
   Levy, D
   Wang, TJ
   Jacques, PF
   Benjamin, EJ
   Vasan, RS
AF Fox, Caroline S.
   Gona, Philimon
   Larson, Martin G.
   Selhub, Jacob
   Tofler, Geoffrey
   Hwang, Shih-Jen
   Meigs, James B.
   Levy, Daniel
   Wang, Thomas J.
   Jacques, Paul F.
   Benjamin, Emelia J.
   Vasan, Ramachandran S.
TI A Multi-Marker Approach to Predict Incident CKD and Microalbuminuria
SO JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY
LA English
DT Article
ID CHRONIC KIDNEY-DISEASE; GLOMERULAR-FILTRATION-RATE; RISK-ASSESSMENT
   STRATEGIES; BRAIN NATRIURETIC PEPTIDE; CORONARY-HEART-DISEASE; SERUM
   CYSTATIN-C; CARDIOVASCULAR OUTCOMES; RENAL-INSUFFICIENCY; VULNERABLE
   PATIENT; HYPERTENSIVE-RATS
AB Traditional risk factors do not adequately identify individuals at risk for CKD. We related a multi-marker panel consisting of the following seven circulating biomarkers to the incidence of CKD and microalbuminuria (MA) in 2345 participants who attended the sixth Framingham Offspring Study examination (1995 to 1998): C-reactive protein, aldosterone, renin, B-type natriuretic peptide (BNP), plasminogen-activator inhibitor type 1, fibrinogen, and homocysteine. We defined CKD at follow-up (2005 to 2008) as estimated GFR (eGFR) <60 ml/min per 1.73 m(2); we defined MA as urine albumin-to-creatinine ratio >= 25 (women) or 17 (men) mg/g on spot urine samples. We identified a parsimonious set of markers related to outcomes adjusting for standard risk factors and baseline renal function, and we assessed their incremental predictive utility. During a mean 9.5-year follow-up, 213 participants developed CKD and 186 developed MA. In multivariable logistic regression models, the multi-marker panel was associated with incident CKD (P < 0.001) and MA (P = 0.003). Serum homocysteine and aldosterone both were significantly associated with CKD incidence, and log-transformed aldosterone, BNP, and homocysteine were significantly associated with incident MA. Biomarkers improved risk prediction as measured by improvements in the c-statistics for both CKD and MA and by a 7% increase in net risk reclassification. In conclusion, circulating homocysteine, aldosterone, and BNP provide incremental information regarding risk for incident CKD and MA beyond traditional risk factors.
C1 [Fox, Caroline S.; Gona, Philimon; Larson, Martin G.; Hwang, Shih-Jen; Levy, Daniel; Benjamin, Emelia J.; Vasan, Ramachandran S.] NHLBI, Framingham Heart Study, Framingham, MA 01702 USA.
   [Fox, Caroline S.; Hwang, Shih-Jen; Levy, Daniel] NHLBI, Ctr Populat Studies, Bethesda, MD 20892 USA.
   [Fox, Caroline S.] Brigham & Womens Hosp, Dept Med, Div Endocrinol Metab & Diabet, Boston, MA 02115 USA.
   [Selhub, Jacob; Jacques, Paul F.] Tufts Univ, USDA, Human Nutr Res Ctr, Boston, MA 02111 USA.
   [Tofler, Geoffrey] Univ Sydney, Royal N Shore Hosp, Sydney, NSW 2006, Australia.
   [Meigs, James B.] Massachusetts Gen Hosp, Div Gen Internal Med, Boston, MA 02114 USA.
   [Wang, Thomas J.] Massachusetts Gen Hosp, Div Cardiol, Boston, MA 02114 USA.
   [Benjamin, Emelia J.; Vasan, Ramachandran S.] Boston Univ, Sch Med, Div Cardiol & Prevent Med, Boston, MA 02118 USA.
RP Fox, CS (reprint author), NHLBI, Framingham Heart Study, 73 Mt Wayte Ave,Suite 2, Framingham, MA 01702 USA.
EM foxca@nhlbi.nih.gov
OI Larson, Martin/0000-0002-9631-1254; Ramachandran,
   Vasan/0000-0001-7357-5970; Benjamin, Emelia/0000-0003-4076-2336
FU National Heart, Lung and Blood Institute's Framingham Heart Study
   [N01-HC-25195, 2-K24-HL04334, R01-HL-077477, R01-DK-080739, 1R01
   AG028321]
FX This study was supported by National Heart, Lung and Blood Institute's
   Framingham Heart Study (N01-HC-25195) Grants 2-K24-HL04334,
   R01-HL-077477, R01-DK-080739, and 1R01 AG028321.
NR 44
TC 43
Z9 44
U1 0
U2 5
PU AMER SOC NEPHROLOGY
PI WASHINGTON
PA 1725 I ST, NW STE 510, WASHINGTON, DC 20006 USA
SN 1046-6673
J9 J AM SOC NEPHROL
JI J. Am. Soc. Nephrol.
PD DEC
PY 2010
VL 21
IS 12
BP 2143
EP 2149
DI 10.1681/ASN.2010010085
PG 7
WC Urology & Nephrology
SC Urology & Nephrology
GA 697RJ
UT WOS:000285533300020
PM 20966127
ER

PT J
AU Baker, SG
   Sargent, DJ
AF Baker, Stuart G.
   Sargent, Daniel J.
TI Designing a Randomized Clinical Trial to Evaluate Personalized Medicine:
   A New Approach Based on Risk Prediction
SO JOURNAL OF THE NATIONAL CANCER INSTITUTE
LA English
DT Editorial Material
ID ADAPTIVE SIGNATURE DESIGN; CANCER
AB We define personalized medicine as the administration of treatment to only persons thought most likely to benefit, typically those at high risk for mortality or another detrimental outcome. To evaluate personalized medicine, we propose a new design for a randomized trial that makes efficient use of high-throughput data (such as gene expression microarrays) and clinical data (such as tumor stage) collected at baseline from all participants. Under this design for a randomized trial involving experimental and control arms with a survival outcome, investigators first estimate the risk of mortality in the control arm based on the high-throughput and clinical data. Then investigators use data from both randomization arms to estimate both the effect of treatment among all participants and among participants in the highest prespecified category of risk. This design requires only an 18.1% increase in sample size compared with a standard randomized trial. A trial based on this design that has a 90% power to detect a realistic increase in survival from 70% to 80% among all participants, would also have a 90% power to detect an increase in survival from 50% to 73% in the highest quintile of risk.
C1 [Baker, Stuart G.] NCI, Biometry Res Grp, Canc Prevent Div, Bethesda, MD 20892 USA.
   [Sargent, Daniel J.] Mayo Clin, Div Biomed Stat & Informat, Rochester, MN USA.
RP Baker, SG (reprint author), NCI, Biometry Res Grp, Canc Prevent Div, EPN 3131,6130 Execut Blvd,MSC 7354, Bethesda, MD 20892 USA.
EM sb16i@nih.gov
OI Sargent, Daniel/0000-0002-2684-4741
FU NCI NIH HHS [CA15083]
NR 16
TC 9
Z9 9
U1 0
U2 1
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0027-8874
J9 J NATL CANCER I
JI J. Natl. Cancer Inst.
PD DEC
PY 2010
VL 102
IS 23
BP 1756
EP 1759
DI 10.1093/jnci/djq427
PG 4
WC Oncology
SC Oncology
GA 689SU
UT WOS:000284950200006
PM 21044964
ER

PT J
AU Hadley, J
   Yabroff, KR
   Barrett, MJ
   Penson, DF
   Saigal, CS
   Potosky, AL
AF Hadley, Jack
   Yabroff, K. Robin
   Barrett, Michael J.
   Penson, David F.
   Saigal, Christopher S.
   Potosky, Arnold L.
TI Comparative Effectiveness of Prostate Cancer Treatments: Evaluating
   Statistical Adjustments for Confounding in Observational Data
SO JOURNAL OF THE NATIONAL CANCER INSTITUTE
LA English
DT Article
ID ANDROGEN DEPRIVATION THERAPY; INSTRUMENTAL VARIABLE METHODS; HEALTH
   INTERVIEW SURVEY; PROPENSITY SCORE; RADICAL PROSTATECTOMY;
   BREAST-CANCER; MEDICARE CLAIMS; SELF-SELECTION; LUNG-CANCER; MEN
AB Background Using observational data to assess the relative effectiveness of alternative cancer treatments is limited by patient selection into treatment, which often biases interpretation of outcomes. We evaluated methods for addressing confounding in treatment and survival of patients with early-stage prostate cancer in observational data and compared findings with those from a benchmark randomized clinical trial. Methods We selected 14 302 early-stage prostate cancer patients who were aged 66-74 years and had been treated with radical prostatectomy or conservative management from linked Surveillance, Epidemiology, and End Results-Medicare data from January 1, 1995, through December 31, 2003. Eligibility criteria were similar to those from a clinical trial used to benchmark our analyses. Survival was measured through December 31, 2007, by use of Cox proportional hazards models. We compared results from the benchmark trial with results from models with observational data by use of traditional multivariable survival analysis, propensity score adjustment, and instrumental variable analysis.
   Results Prostate cancer patients receiving conservative management were more likely to be older, nonwhite, and single and to have more advanced disease than patients receiving radical prostatectomy. In a multivariable survival analysis, conservative management was associated with greater risk of prostate cancer-specific mortality ( hazard ratio [HR] = 1.59, 95% confidence interval [CI] = 1.27 to 2.00) and all-cause mortality ( HR = 1.47, 95% CI = 1.35 to 1.59) than radical prostatectomy. Propensity score adjustments resulted in similar patient characteristics across treatment groups, although survival results were similar to traditional multivariable survival analyses. Results for the same comparison from the instrumental variable approach, which theoretically equalizes both observed and unobserved patient characteristics across treatment groups, differed from the traditional multivariable and propensity score results but were consistent with findings from the subset of elderly patient with early-stage disease in the trial (ie, conservative management vs radical prostatectomy: for prostate cancer-specific mortality, HR = 0.73, 95% CI = 0.08 to 6.73; for all-cause mortality, HR = 1.09, 95% CI = 0.46 to 2.59).
   Conclusion Instrumental variable analysis may be a useful technique in comparative effectiveness studies of cancer treatments if an acceptable instrument can be identified.
C1 [Hadley, Jack] George Mason Univ, Coll Hlth & Human Serv, Off Dean, Fairfax, VA 22030 USA.
   [Hadley, Jack] George Mason Univ, Coll Hlth & Human Serv, Dept Hlth Adm & Policy, Fairfax, VA 22030 USA.
   [Yabroff, K. Robin] NCI, Div Canc Control & Populat Sci, Bethesda, MD 20892 USA.
   [Barrett, Michael J.] Informat Management Serv Inc, Rockville, MD USA.
   [Penson, David F.] Vanderbilt Univ, Dept Urol Surg, Ctr Surg Qual & Outcomes Res, Nashville, TN USA.
   [Saigal, Christopher S.] Univ Calif Los Angeles, David Geffen Sch Med, Dept Urol, Los Angeles, CA 90095 USA.
   [Potosky, Arnold L.] Georgetown Univ, Dept Oncol, Lombardi Canc Ctr, Washington, DC USA.
RP Hadley, J (reprint author), George Mason Univ, Coll Hlth & Human Serv, Off Dean, 4400 Univ Dr,MS 2G7, Fairfax, VA 22030 USA.
EM jhadley1@gmu.edu
OI Yabroff, K. Robin/0000-0003-0644-5572
FU National Cancer Institute [HHSN2612007003 39P]
FX National Cancer Institute (HHSN2612007003 39P).
NR 55
TC 65
Z9 66
U1 0
U2 6
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0027-8874
J9 J NATL CANCER I
JI J. Natl. Cancer Inst.
PD DEC
PY 2010
VL 102
IS 23
BP 1780
EP 1793
DI 10.1093/jnci/djq393
PG 14
WC Oncology
SC Oncology
GA 689SU
UT WOS:000284950200009
PM 20944078
ER

PT J
AU Safaeian, M
   Quint, K
   Schiffman, M
   Rodriguez, AC
   Wacholder, S
   Herrero, R
   Hildesheim, A
   Viscidi, RP
   Quint, W
   Burk, RD
AF Safaeian, Mahboobeh
   Quint, Koen
   Schiffman, Mark
   Cecilia Rodriguez, Ana
   Wacholder, Sholom
   Herrero, Rolando
   Hildesheim, Allan
   Viscidi, Raphael P.
   Quint, Wim
   Burk, Robert D.
TI Chlamydia trachomatis and Risk of Prevalent and Incident Cervical
   Premalignancy in a Population-Based Cohort
SO JOURNAL OF THE NATIONAL CANCER INSTITUTE
LA English
DT Article
ID HUMAN-PAPILLOMAVIRUS INFECTION; SQUAMOUS-CELL CARCINOMA; NESTED
   CASE-CONTROL; COSTA-RICA; INTRAEPITHELIAL NEOPLASIA; HPV INFECTION;
   10000 WOMEN; CANCER; DNA; SEROPREVALENCE
AB Background Cofactors might affect the risk of the rare progression from infection with carcinogenic human papillomavirus (HPV) to cervical premalignancy to invasive cancer. Some studies have observed that Chlamydia trachomatis infection is associated with increased risk for cervical cancer. In a large prospective cohort, we assessed the role of C trachomatis in cervical premalignancy and addressed confounding by HPV.
   Methods We identified 182 women with prevalent and 132 women with incident histological cervical intraepithelial neoplasia grade 2 (CIN2), grade 3 (CIN3), or cervical cancer (CIN2+) in the Costa Rica HPV Natural History Study. Control subjects were 995 (approximately 10% of the 10 049) subjects who were randomly selected from the same study. Cervical HPV status at enrollment was determined by MY09/MY11 polymerase chain reaction amplification and dot-blot hybridization. The presence of C trachomatis DNA in cervical exfoliated cells at enrollment was determined by a novel serovar-specific polymerase chain reaction-based C trachomatis detection and genotyping assay. Plasma drawn at enrollment from each subject was used to determine C trachomatis immunoglobulin G (IgG) status. Logistic regression was used to examine the association between C trachomatis and CIN2+, taking into account possible confounding by HPV.
   Results C trachomatis positivity at enrollment was associated with CIN2+ and concurrent and subsequent carcinogenic HPV infection. To account for confounding by HPV status, we restricted the analysis to women positive for carcinogenic HPV DNA at enrollment and found no association between C trachomatis status (as assessed by DNA or IgG) at enrollment and combined prevalent and/or incident CIN2+ (for C trachomatis DNA positivity, odds ratio = 0.77, 95% confidence interval = 0.42 to 1.41; for C trachomatis seropositivity, odds ratio = 1.09, 95% confidence interval = 0.85 to 1.41).
   Conclusions We found no association between C trachomatis status, as assessed by DNA or IgG, and risk of cervical premalignancy, after controlling for carcinogenic HPV-positive status. Previous positive associations between C trachomatis and cervical premalignancy could have been caused, in part, by an increased susceptibility to HPV infection.
C1 [Safaeian, Mahboobeh] NCI, Div Canc Epidemiol & Genet, Infect & Immunoepidemiol Branch, Rockville, MD 20852 USA.
   [Quint, Koen; Quint, Wim] DDL Diagnost Labs, Voorburg, Netherlands.
   [Cecilia Rodriguez, Ana; Herrero, Rolando] Fdn INCIENSA, Proyecto Epidemiol Guanacaste, San Jose, Costa Rica.
   [Viscidi, Raphael P.] Johns Hopkins Univ, Sch Med, Dept Pediat, Baltimore, MD 21205 USA.
   [Burk, Robert D.] Albert Einstein Coll Med, Dept Pediat, Dept Microbiol & Immunol, Dept Epidemiol & Populat Hlth, Bronx, NY 10467 USA.
   [Burk, Robert D.] Albert Einstein Coll Med, Dept Obstet & Gynecol & Womens Hlth, Bronx, NY 10467 USA.
RP Safaeian, M (reprint author), NCI, Div Canc Epidemiol & Genet, Infect & Immunoepidemiol Branch, 6120 Execut Blvd,Ste 550, Rockville, MD 20852 USA.
EM safaeianm@mail.nih.gov
RI Hildesheim, Allan/B-9760-2015
OI Hildesheim, Allan/0000-0003-0257-2363
FU National Institutes of Health [N01-CP-21081, N01-CP-33061, N01-CP-40542,
   N01-CP-50535, N01-CP-81023, CA78527]; National Cancer Institute,
   National Institutes of Health, Department of Health and Human Services
FX National Institutes of Health (N01-CP-21081, N01-CP-33061, N01-CP-40542,
   N01-CP-50535, N01-CP-81023, and CA78527 to R.D.B.). The Guanacaste
   cohort (design and conduct of the study, sample collection, management,
   analysis, and interpretation of the data) for the enrollment and
   follow-up phases were supported by the National Cancer Institute,
   National Institutes of Health, Department of Health and Human Services.
NR 32
TC 34
Z9 36
U1 0
U2 7
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0027-8874
J9 J NATL CANCER I
JI J. Natl. Cancer Inst.
PD DEC
PY 2010
VL 102
IS 23
BP 1794
EP 1804
DI 10.1093/jnci/djq436
PG 11
WC Oncology
SC Oncology
GA 689SU
UT WOS:000284950200010
PM 21098758
ER

PT J
AU Elmets, CA
   Viner, JL
   Pentland, AP
   Cantrell, W
   Lin, HY
   Bailey, H
   Kang, S
   Linden, KG
   Heffernan, M
   Duvic, M
   Richmond, E
   Elewski, BE
   Umar, A
   Bell, W
   Gordon, GB
AF Elmets, Craig A.
   Viner, Jaye L.
   Pentland, Alice P.
   Cantrell, Wendy
   Lin, Hui-Yi
   Bailey, Howard
   Kang, Sewon
   Linden, Kenneth G.
   Heffernan, Michael
   Duvic, Madeleine
   Richmond, Ellen
   Elewski, Boni E.
   Umar, Asad
   Bell, Walter
   Gordon, Gary B.
TI Chemoprevention of Nonmelanoma Skin Cancer With Celecoxib: A Randomized,
   Double-Blind, Placebo-Controlled Trial
SO JOURNAL OF THE NATIONAL CANCER INSTITUTE
LA English
DT Article
ID SQUAMOUS-CELL CARCINOMA; NONSTEROIDAL ANTIINFLAMMATORY DRUGS; FAMILIAL
   ADENOMATOUS POLYPOSIS; REGULAR SUNSCREEN USE; LOW-FAT DIET; BASAL-CELL;
   SOLAR KERATOSES; CYCLOOXYGENASE-2 INHIBITOR; XERODERMA-PIGMENTOSUM;
   COLORECTAL ADENOMAS
AB Background Preclinical studies indicate that the enzyme cyclooxygenase 2 plays an important role in ultraviolet-induced skin cancers. We evaluated the efficacy and safety of celecoxib, a cyclooxygenase 2 inhibitor, as a chemopreventive agent for actinic keratoses, the premalignant precursor of nonmelanoma skin cancers, and for nonmelanoma skin cancers, including cutaneous squamous cell carcinomas (SCCs) and basal cell carcinomas (BCCs).
   Methods A double-blind placebo-controlled randomized trial involving 240 subjects aged 37-87 years with 10-40 actinic keratoses was conducted at eight US academic medical centers. Patients were randomly assigned to receive 200 mg of celecoxib or placebo administered orally twice daily for 9 months. Subjects were evaluated at 3, 6, 9 (ie, completion of treatment), and 11 months after randomization. The primary endpoint was the number of new actinic keratoses at the 9-month visit as a percentage of the number at the time of randomization. In an intent-to-treat analysis, the incidence of actinic keratoses was compared between the two groups using t tests. In exploratory analyses, we evaluated the number of nonmelanoma skin cancers combined and SCCs and BCCs separately per patient at 11 months after randomization using Poisson regression, after adjustment for patient characteristics and time on study. The numbers of adverse events in the two treatment arms were compared using chi(2) or Fisher exact tests. All statistical tests were two-sided.
   Results There was no difference in the incidence of actinic keratoses between the two groups at 9 months after randomization. However, at 11 months after randomization, there were fewer nonmelanoma skin cancers in the celecoxib arm than in the placebo arm (mean cumulative tumor number per patient 0.14 vs 0.35; rate ratio [RR] = .43, 95% confidence interval [CI] = 0.24 to 0.75; P = .003). After adjusting for age, sex, Fitzpatrick skin type, history of actinic keratosis at randomization, nonmelanoma skin cancer history, and patient time on study, the number of nonmelanoma skin cancers was lower in the celecoxib arm than in the placebo arm (RR = 0.41, 95% CI = 0.23 to 0.72, P = .002) as were the numbers of BCCs (RR = 0.40, 95% CI = 0.18 to 0.93, P = .032) and SCCs (RR = 0.42, 95% CI = 0.19 to 0.93, P = .032). Serious and cardiovascular adverse events were similar in the two groups.
   Conclusions Celecoxib may be effective for prevention of SCCs and BCCs in individuals who have extensive actinic damage and are at high risk for development of nonmelanoma skin cancers.
C1 [Elmets, Craig A.; Cantrell, Wendy; Lin, Hui-Yi; Elewski, Boni E.] Univ Alabama, Dept Dermatol, Skin Dis Res Ctr, Birmingham, AL 35294 USA.
   [Elmets, Craig A.; Cantrell, Wendy; Lin, Hui-Yi; Elewski, Boni E.; Bell, Walter] Univ Alabama, Ctr Comprehens Canc, Birmingham, AL 35294 USA.
   [Lin, Hui-Yi] Univ S Florida, H Lee Moffitt Canc Ctr, Tampa, FL 33682 USA.
   [Lin, Hui-Yi] Res Inst, Tampa, FL USA.
   [Elmets, Craig A.] Vet Affairs Med Ctr, Birmingham, AL USA.
   [Bell, Walter] Univ Alabama, Dept Pathol, Skin Dis Res Ctr, Birmingham, AL 35294 USA.
   [Viner, Jaye L.] MedImmune Inc, Gaithersburg, MD USA.
   [Viner, Jaye L.; Richmond, Ellen; Umar, Asad] NCI, Div Canc Canc Prevent, Bethesda, MD 20892 USA.
   [Pentland, Alice P.] Univ Rochester, Sch Med & Dent, Dept Dermatol, Rochester, NY 14642 USA.
   [Bailey, Howard] Univ Wisconsin, Dept Med, Madison, WI USA.
   [Kang, Sewon] Johns Hopkins Univ, Baltimore, MD USA.
   [Kang, Sewon] Univ Michigan, Dept Dermatol, Ann Arbor, MI 48109 USA.
   [Linden, Kenneth G.] Univ Calif Irvine, Dept Dermatol, Irvine, CA 92717 USA.
   [Heffernan, Michael] Wright State Univ, Dayton, OH 45435 USA.
   [Heffernan, Michael] Washington Univ, Sch Med, Dept Med, St Louis, MO 63110 USA.
   [Duvic, Madeleine] Univ Texas MD Anderson Canc Ctr, Dept Dermatol, Houston, TX 77030 USA.
   [Gordon, Gary B.] Abbott Labs, Abbott Pk, IL 60064 USA.
   [Gordon, Gary B.] GD Searle & Co, Oncol Immunodeficiency Res & Dev, Skokie, IL 60077 USA.
RP Elmets, CA (reprint author), Univ Alabama, Dept Dermatol, Skin Dis Res Ctr, 1530 3rd Ave S,EFH 414, Birmingham, AL 35294 USA.
EM celmets@uab.edu
FU National Cancer Institute (NCI) [N01-CN-85183, P30 CA013148]; Pfizer,
   Inc; Division of Cancer Prevention of the National Cancer Institute;
   National Institute of Arthritis and Musculoskeletal and Skin Diseases
   [P30 AR050948]; Veterans Administration; National Institutes of Health;
   corporations marketing Celebrex (celecoxib)
FX The study was funded by National Cancer Institute (NCI) (N01-CN-85183 to
   C. A. E.); Pfizer, Inc, also partially funded this study through a
   clinical trials agreement with the Division of Cancer Prevention of the
   National Cancer Institute; the National Institute of Arthritis and
   Musculoskeletal and Skin Diseases (P30 AR050948 to C. A. E.); NCI (P30
   CA013148) (Edward Partridge, UAB Comprehensive Cancer Center Director);
   and by the Veterans Administration (C.A.E.).; J. L. Viner is now
   employed by MedImmune, Inc. A. P. Pentland receives research grant
   support jointly from National Institutes of Health and corporations
   marketing Celebrex (celecoxib). G. B. Gordon owns stock in Pfizer, the
   manufacturer of Celebrex. Pfizer, Inc, had no role in the collection,
   analysis, or interpretation of the data, nor did Pfizer have any
   participation in the preparation, review, or approval of the manuscript.
   The National Cancer Institute contributed to the development of the
   protocol (Drs Viner and Hawk) and to the review of the manuscript (Drs
   Viner, Umar, and Ms. Richmond).
NR 59
TC 97
Z9 99
U1 0
U2 11
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0027-8874
J9 J NATL CANCER I
JI J. Natl. Cancer Inst.
PD DEC
PY 2010
VL 102
IS 24
BP 1835
EP 1844
DI 10.1093/jnci/djq442
PG 10
WC Oncology
SC Oncology
GA 696CP
UT WOS:000285419800009
PM 21115882
ER

PT J
AU Atz, AM
   Travison, TG
   Williams, IA
   Pearson, GD
   Laussen, PC
   Mahle, WT
   Cook, AL
   Kirsh, JA
   Sklansky, M
   Khaikin, S
   Goldberg, C
   Frommelt, M
   Krawczeski, C
   Puchalski, MD
   Jacobs, JP
   Baffa, JM
   Rychik, J
   Ohye, RG
AF Atz, Andrew M.
   Travison, Thomas G.
   Williams, Ismee A.
   Pearson, Gail D.
   Laussen, Peter C.
   Mahle, William T.
   Cook, Amanda L.
   Kirsh, Joel A.
   Sklansky, Mark
   Khaikin, Svetlana
   Goldberg, Caren
   Frommelt, Michele
   Krawczeski, Catherine
   Puchalski, Michael D.
   Jacobs, Jeffrey P.
   Baffa, Jeanne M.
   Rychik, Jack
   Ohye, Richard G.
CA Pediat Heart Network Investigators
TI Prenatal diagnosis and risk factors for preoperative death in neonates
   with single right ventricle and systemic outflow obstruction: Screening
   data from the Pediatric Heart Network Single Ventricle Reconstruction
   Trial
SO JOURNAL OF THORACIC AND CARDIOVASCULAR SURGERY
LA English
DT Article
ID NORWOOD PROCEDURE; DISEASE; INFANTS; OUTCOMES; EXPERIENCE; MANAGEMENT;
   MORTALITY; IMPACT
AB Objectives: The purpose of this analysis was to assess preoperative risk factors before the first-stage Norwood procedure in infants with hypoplastic left heart syndrome and related single-ventricle lesions and to evaluate practice patterns in prenatal diagnosis, as well as the role of prenatal diagnosis in outcome.
   Methods: Data from all live births with morphologic single right ventricle and systemic outflow obstruction screened for the Pediatric Heart Network's Single Ventricle Reconstruction Trial were used to investigate prenatal diagnosis and preoperative risk factors. Demographics, gestational age, prenatal diagnosis status, presence of major extracardiac congenital abnormalities, and preoperative mortality rates were recorded.
   Results: Of 906 infants, 677 (75%) had prenatal diagnosis, 15% were preterm (<37 weeks' gestation), and 16% were low birth weight (<2500 g). Rates of prenatal diagnosis varied by study site (59% to 85%, P < .0001). Major extracardiac congenital abnormalities were less prevalent in those born after prenatal diagnosis (6% vs 10%, P = .03). There were 26 (3%) deaths before Norwood palliation; preoperative mortality did not differ by prenatal diagnosis status (P = .49). In multiple logistic regression models, preterm birth (P = .02), major extracardiac congenital abnormalities (P < .0001), and obstructed pulmonary venous return (P = .02) were independently associated with preoperative mortality.
   Conclusions: Prenatal diagnosis occurred in 75%. Preoperative death was independently associated with preterm birth, obstructed pulmonary venous return, and major extracardiac congenital abnormalities. Adjusted for gestational age and the presence of obstructed pulmonary venous return, the estimated odds of preoperative mortality were 10 times greater for subjects with a major extracardiac congenital abnormality. (J Thorac Cardiovasc Surg 2010;140:1245-50)
C1 [Atz, Andrew M.] Med Univ S Carolina, Dept Pediat Cardiol, Charleston, SC 29425 USA.
   [Travison, Thomas G.] New England Res Inst, Watertown, MA 02172 USA.
   [Williams, Ismee A.] Columbia Univ, Div Pediat Cardiol, Med Ctr, New York, NY USA.
   [Pearson, Gail D.] NHLBI, Div Cardiovasc Dis, Bethesda, MD 20892 USA.
   [Laussen, Peter C.] Childrens Hosp, Dept Cardiol, Boston, MA 02115 USA.
   [Mahle, William T.] Emory Univ, Div Pediat Cardiol, Atlanta, GA 30322 USA.
   [Cook, Amanda L.] Wake Forest Univ, Div Pediat Cardiol, Winston Salem, NC 27109 USA.
   [Kirsh, Joel A.; Khaikin, Svetlana] Hosp Sick Children, Div Cardiol, Toronto, ON M5G 1X8, Canada.
   [Sklansky, Mark] Childrens Hosp Los Angeles, Div Cardiol, Los Angeles, CA 90027 USA.
   [Goldberg, Caren] Univ Michigan, Dept Pediat & Communicable Dis, Ann Arbor, MI 48109 USA.
   [Ohye, Richard G.] Univ Michigan, Dept Surg, Ann Arbor, MI 48109 USA.
   [Frommelt, Michele] Childrens Hosp Wisconsin, Div Cardiol, Milwaukee, WI 53201 USA.
   [Krawczeski, Catherine] Cincinnati Childrens Hosp, Med Ctr, Div Cardiol, Cincinnati, OH USA.
   Univ Utah, Salt Lake City, UT USA.
   [Puchalski, Michael D.] Primary Childrens Med Ctr, Div Pediat Cardiol, Salt Lake City, UT 84103 USA.
   [Jacobs, Jeffrey P.] Congenital Heart Inst Florida, Div Pediat Heart Surg, St Petersburg, FL USA.
   [Baffa, Jeanne M.] Alfred I Dupont Inst, Div Pediat Cardiol, Nemours Cardiac Ctr, Wilmington, DE 19899 USA.
   [Rychik, Jack] Childrens Hosp Philadelphia, Div Cardiol, Philadelphia, PA 19104 USA.
RP Atz, AM (reprint author), Med Univ S Carolina, Dept Pediat Cardiol, 171 Ashley Ave, Charleston, SC 29425 USA.
EM atzam@musc.edu
FU National Heart, Lung, and Blood Institute [HL068269, HL068270, HL068279,
   HL068281, HL068285, HL068292, HL068290, HL068288, HL085057]
FX Supported by U01 grants from the National Heart, Lung, and Blood
   Institute (HL068269, HL068270, HL068279, HL068281, HL068285, HL068292,
   HL068290, HL068288, and HL085057).
NR 22
TC 40
Z9 40
U1 2
U2 5
PU MOSBY-ELSEVIER
PI NEW YORK
PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0022-5223
J9 J THORAC CARDIOV SUR
JI J. Thorac. Cardiovasc. Surg.
PD DEC
PY 2010
VL 140
IS 6
BP 1245
EP 1250
DI 10.1016/j.jtcvs.2010.05.022
PG 6
WC Cardiac & Cardiovascular Systems; Respiratory System; Surgery
SC Cardiovascular System & Cardiology; Respiratory System; Surgery
GA 679GG
UT WOS:000284149200007
PM 20561642
ER

PT J
AU Klapper, JA
   Davis, JL
   Ripley, RT
   Smith, FO
   Nguyen, DM
   Kwong, KF
   Mercedes, L
   Kemp, CD
   Mathur, A
   White, DE
   Dudley, ME
   Wunderlich, JR
   Rosenberg, SA
   Schrump, DS
AF Klapper, Jacob A.
   Davis, Jeremy L.
   Ripley, R. Taylor
   Smith, Franz O.
   Nguyen, Dao M.
   Kwong, King F.
   Mercedes, Leandro
   Kemp, Clinton D.
   Mathur, Aarti
   White, Donald E.
   Dudley, Mark E.
   Wunderlich, John R.
   Rosenberg, Steven A.
   Schrump, David S.
TI Thoracic metastasectomy for adoptive immunotherapy of melanoma: A
   single-institution experience
SO JOURNAL OF THORACIC AND CARDIOVASCULAR SURGERY
LA English
DT Article
ID PULMONARY METASTATIC MELANOMA; PROGNOSTIC FACTORS; IMPROVED SURVIVAL;
   CELL THERAPY; LUNG-CANCER; RESECTION; INTERLEUKIN-2; CHEMOTHERAPY;
   REGRESSION; ANTIGEN-4
AB Objectives: Although refractory to chemotherapy, metastatic melanoma may respond to adoptive immunotherapy. As novel treatments evolve, surgeons may be asked to perform metastasectomy not only for palliation or potential cure but also for isolation of tumor-infiltrating lymphocytes. This study was undertaken to examine outcomes of patients with melanoma undergoing thoracic metastasectomy in preparation for investigational immunotherapy.
   Methods: A retrospective review identified 107 consecutive patients who underwent 116 thoracic metastasectomy procedures from April 1998 to July 2009. Indications for surgical intervention included procurement of tumor-infiltrating lymphocytes, rendering of patients to no evaluable disease status, palliation, and diagnosis. Response Evaluation Criteria in Solid Tumors criteria were used to assess tumor response.
   Results: Thoracotomy, lobectomy, and video-assisted thoracoscopic surgery with nonanatomic resection were the most common procedures. Major complications included 1 death and 1 coagulopathy-induced hemothorax. Seventeen patients were rendered to no evaluable disease status. Virtually all patients with residual disease had tumor specimens cultured for tumor-infiltrating lymphocytes; approximately 70% of tumor-infiltrating lymphocyte cultures exhibited antitumor reactivity. Of the 91 patients with residual or recurrent disease, 24 (26%) underwent adoptive cell transfer of tumor-infiltrating lymphocytes, of whom 7 exhibited objective responses (29% response rate and 8% based on intent to treat). Rapid disease progression precluded tumor-infiltrating lymphocyte therapy in most cases. Actuarial 1- and 5-year survival rates for patients rendered to no evaluable disease status or receiving or not receiving tumor-infiltrating lymphocytes were 93% and 76%, 64% and 33%, and 43% and 0%, respectively.
   Conclusions: Relatively few patients currently having thoracic metastasectomy undergo adoptive cell transfer. Continued refinement of tumor-infiltrating lymphocyte expansion protocols and improved patient selection might increase the number of patients with melanoma benefiting from these interventions. (J Thorac Cardiovasc Surg 2010;140:1276-82)
C1 [Ripley, R. Taylor; Nguyen, Dao M.; Kwong, King F.; Mercedes, Leandro; Kemp, Clinton D.; Mathur, Aarti; Schrump, David S.] NCI, Thorac Oncol Sect, Surg Branch, Ctr Canc Res,NIH, Bethesda, MD 20892 USA.
   [Klapper, Jacob A.; Davis, Jeremy L.; Smith, Franz O.; White, Donald E.; Dudley, Mark E.; Wunderlich, John R.; Rosenberg, Steven A.] NCI, Tumor Immunol Sect, Surg Branch, Ctr Canc Res,NIH, Bethesda, MD 20892 USA.
RP Schrump, DS (reprint author), NCI, Thorac Oncol Sect, Surg Branch, Ctr Canc Res,NIH, Bldg 10,Rm 4-3942,10 Ctr Dr, Bethesda, MD 20892 USA.
EM David_Schrump@nih.gov
NR 25
TC 5
Z9 5
U1 0
U2 0
PU MOSBY-ELSEVIER
PI NEW YORK
PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0022-5223
J9 J THORAC CARDIOV SUR
JI J. Thorac. Cardiovasc. Surg.
PD DEC
PY 2010
VL 140
IS 6
BP 1276
EP 1282
DI 10.1016/j.jtcvs.2010.05.020
PG 7
WC Cardiac & Cardiovascular Systems; Respiratory System; Surgery
SC Cardiovascular System & Cardiology; Respiratory System; Surgery
GA 679GG
UT WOS:000284149200012
PM 20584535
ER

PT J
AU Shimizu, Y
   Kinoshita, I
   Kikuchi, J
   Nishimura, M
   Birrer, MJ
   Dosaka-Akita, H
AF Shimizu, Yasushi
   Kinoshita, Ichiro
   Kikuchi, Junko
   Nishimura, Masaharu
   Birrer, Michael J.
   Dosaka-Akita, Hirotoshi
TI Growth Inhibition of Non-Small Cell Lung Cancer Cells by Blockade of
   AP-1 and Phosphatidylinositol 3-Kinase Pathway
SO JOURNAL OF THORACIC ONCOLOGY
LA English
DT Meeting Abstract
C1 [Shimizu, Yasushi; Kinoshita, Ichiro; Dosaka-Akita, Hirotoshi] Hokkaido Univ, Grad Sch Med, Dept Med Oncol, Sapporo, Hokkaido 060, Japan.
   [Kikuchi, Junko; Nishimura, Masaharu] Hokkaido Univ, Grad Sch Med, Dept Internal Med, Sapporo, Hokkaido 060, Japan.
   [Birrer, Michael J.] NCI, Dept Cell & Canc Biol, Bethesda, MD 20892 USA.
RI Akita, Hirotoshi/E-1356-2012
NR 0
TC 0
Z9 0
U1 0
U2 2
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1556-0864
J9 J THORAC ONCOL
JI J. Thorac. Oncol.
PD DEC
PY 2010
VL 5
IS 12
SU 5
BP S420
EP S421
PG 2
WC Oncology; Respiratory System
SC Oncology; Respiratory System
GA 690HO
UT WOS:000284993900173
ER

PT J
AU Ujhazy, P
   Garon, EB
AF Ujhazy, Peter
   Garon, Edward B.
TI Proapoptotic Agents in Lung Cancer
SO JOURNAL OF THORACIC ONCOLOGY
LA English
DT Article
C1 [Ujhazy, Peter] NCI, Div Canc Treatment & Diagnosis, Translat Res Program, Bethesda, MD 20892 USA.
   [Garon, Edward B.] Univ Calif Los Angeles, Los Angeles, CA USA.
RP Ujhazy, P (reprint author), NCI, Div Canc Treatment & Diagnosis, Translat Res Program, Bethesda, MD 20892 USA.
NR 2
TC 0
Z9 1
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1556-0864
J9 J THORAC ONCOL
JI J. Thorac. Oncol.
PD DEC
PY 2010
VL 5
IS 12
SU 6
BP S480
EP S481
DI 10.1097/01.JTO.0000391375.79129.e3
PG 2
WC Oncology; Respiratory System
SC Oncology; Respiratory System
GA 690HP
UT WOS:000284994000015
PM 21102248
ER

PT J
AU Ullmann, CD
AF Ullmann, Claudio Dansky
TI Cancer Stem Cells and Targeting Embryonic Signaling Pathways
SO JOURNAL OF THORACIC ONCOLOGY
LA English
DT Article
ID LUNG-CANCER; IDENTIFICATION
C1 NCI, Canc Therapy Evaluat Program, Bethesda, MD 20892 USA.
RP Ullmann, CD (reprint author), NCI, Canc Therapy Evaluat Program, Bethesda, MD 20892 USA.
NR 9
TC 1
Z9 1
U1 0
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1556-0864
J9 J THORAC ONCOL
JI J. Thorac. Oncol.
PD DEC
PY 2010
VL 5
IS 12
SU 6
BP S492
EP S494
DI 10.1097/01.JTO.0000391380.01932.50
PG 3
WC Oncology; Respiratory System
SC Oncology; Respiratory System
GA 690HP
UT WOS:000284994000020
PM 21102253
ER

PT J
AU Xiang, X
   Feng, M
   Ho, M
AF Xiang, X.
   Feng, M.
   Ho, M.
TI HN125: A Novel High Affinity Human Immunoadhesin to CA125/MUC16
SO JOURNAL OF THORACIC ONCOLOGY
LA English
DT Meeting Abstract
C1 [Xiang, X.; Feng, M.; Ho, M.] Natl Canc Inst, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1556-0864
J9 J THORAC ONCOL
JI J. Thorac. Oncol.
PD DEC
PY 2010
VL 5
IS 12
SU 7
BP S543
EP S543
PG 1
WC Oncology; Respiratory System
SC Oncology; Respiratory System
GA 690HQ
UT WOS:000284994100111
ER

PT J
AU Romero, R
AF Romero, Roberto
TI A Tribute to Beryl Benacerraf, Editor-in-Chief of the Journal of
   Ultrasound in Medicine, 2001-2010
SO JOURNAL OF ULTRASOUND IN MEDICINE
LA English
DT Biographical-Item
C1 [Romero, Roberto] NICHD, Perinatol Res Branch, NIH, Bethesda, MD 20892 USA.
   [Romero, Roberto] Wayne State Univ, Detroit, MI 48202 USA.
   [Romero, Roberto] Michigan State Univ, Bethesda, MD USA.
   [Romero, Roberto] Michigan State Univ, Detroit, MI USA.
RP Romero, R (reprint author), NICHD, Perinatol Res Branch, NIH, Bethesda, MD 20892 USA.
NR 1
TC 0
Z9 0
U1 0
U2 0
PU AMER INST ULTRASOUND MEDICINE
PI LAUREL
PA SUBSCRIPTION DEPT, 14750 SWEITZER LANE, STE 100, LAUREL, MD 20707-5906
   USA
SN 0278-4297
J9 J ULTRAS MED
JI J. Ultrasound Med.
PD DEC
PY 2010
VL 29
IS 12
BP 1684
EP 1686
PG 3
WC Acoustics; Radiology, Nuclear Medicine & Medical Imaging
SC Acoustics; Radiology, Nuclear Medicine & Medical Imaging
GA 699ZU
UT WOS:000285702700002
PM 21098838
ER

PT J
AU Miller, DC
   Ruterbusch, J
   Colt, JS
   Davis, FG
   Linehan, WM
   Chow, WH
   Schwartz, K
AF Miller, David C.
   Ruterbusch, Julie
   Colt, Joanne S.
   Davis, Faith G.
   Linehan, W. Marston
   Chow, Wong-Ho
   Schwartz, Kendra
TI Contemporary Clinical Epidemiology of Renal Cell Carcinoma: Insight From
   a Population Based Case-Control Study
SO JOURNAL OF UROLOGY
LA English
DT Article
DE kidney; carcinoma; renal cell; epidemiology; African Americans; European
   continental ancestry group
ID KIDNEY CANCER; SURVIVAL; TUMORS; SURVEILLANCE; VALIDATION; MASSES; RATES
AB Purpose: To clarify the contemporary clinical epidemiology of renal cell carcinoma we present trends in clinical presentation and treatment in patients enrolled in a population based case-control study.
   Materials and Methods: The National Cancer Institute performed a population based case-control study in metropolitan Detroit and Chicago from 2002 through 2007. In 1,136 patients with renal cell carcinoma who consented to an epidemiological interview and medical record review we ascertained detailed information on social and medical history, methods of renal cell carcinoma detection and diagnosis, cancer severity and treatment(s) received. From these data we assessed the demographic and cancer specific characteristics of study cases, and trends in clinical presentation, diagnosis and treatment.
   Results: Most patients with renal cell carcinoma had localized or regional tumors, including 52% with tumors 4 cm or less. The proportion of asymptomatic cases increased from 35% in 2002 to 50% in 2007 (p < 0.001). Hypertension and diabetes were common in patients (58% and 17%, respectively) and 24% had at least 2 significant comorbid conditions at cancer diagnosis. While the use of laparoscopic surgery increased with time (p < 0.001), fewer than 1/5 patients underwent nephron sparing surgery.
   Conclusions: The proportion of patients presenting with small, asymptomatic renal cell carcinoma continues to increase. Most of these cases are still treated with radical nephrectomy, although increasingly via a laparoscopic approach. Since most patients with small renal cell carcinomas have 1 or more renal function relevant comorbidities, there is an imperative to increase the use of nephron sparing surgery.
C1 [Miller, David C.] Univ Michigan, Dept Urol, Ann Arbor, MI 48109 USA.
   [Miller, David C.] Vet Affairs Ctr Clin Management Res, Ann Arbor, MI USA.
   [Ruterbusch, Julie] Wayne State Univ, Sch Med, Karmanos Canc Inst, Detroit, MI USA.
   [Schwartz, Kendra] Wayne State Univ, Sch Med, Dept Family Med & Publ Hlth Sci, Detroit, MI USA.
   [Colt, Joanne S.; Chow, Wong-Ho] Natl Canc Inst, Div Canc Epidemiol & Genet, Bethesda, MD USA.
   [Linehan, W. Marston] Natl Canc Inst, Urol Oncol Branch, Bethesda, MD USA.
   [Davis, Faith G.] Univ Illinois, Chicago Sch Publ Hlth, Dept Epidemiol, Chicago, IL USA.
RP Miller, DC (reprint author), Univ Michigan, Dept Urol, 3875 Taubman Ctr,1500 E Med Ctr, Ann Arbor, MI 48109 USA.
EM dcmiller@umich.edu
FU National Institutes of Health [NIH-N02-CP-11004]; New York Academy of
   Medicine
FX Supported by National Institutes of Health NIH-N02-CP-11004, and the
   Edwin Beer Research Fellowship in Urology and Urology-Related Fields
   from the New York Academy of Medicine (DCM).
NR 24
TC 36
Z9 38
U1 0
U2 1
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0022-5347
J9 J UROLOGY
JI J. Urol.
PD DEC
PY 2010
VL 184
IS 6
BP 2254
EP 2258
DI 10.1016/j.juro.2010.08.018
PG 5
WC Urology & Nephrology
SC Urology & Nephrology
GA 677ZY
UT WOS:000284037900009
PM 20952033
ER

PT J
AU Price, DK
   Chau, CH
   Till, C
   Goodman, PJ
   Baum, CE
   Ockers, SB
   English, BC
   Minasian, L
   Parnes, HL
   Hsing, AW
   Reichardt, JKV
   Hoque, A
   Tangen, CM
   Kristal, AR
   Thompson, IM
   Figg, WD
AF Price, Douglas K.
   Chau, Cindy H.
   Till, Cathee
   Goodman, Phyllis J.
   Baum, Caitlin E.
   Ockers, Sandy B.
   English, Bevin C.
   Minasian, Lori
   Parnes, Howard L.
   Hsing, Ann W.
   Reichardt, Juergen K. V.
   Hoque, Ashraful
   Tangen, Catherine M.
   Kristal, Alan R.
   Thompson, Ian M.
   Figg, William D.
TI Androgen Receptor CAG Repeat Length and Association With Prostate Cancer
   Risk: Results From the Prostate Cancer Prevention Trial
SO JOURNAL OF UROLOGY
LA English
DT Article
DE prostate; receptors; androgen; prostatic neoplasms; African continental
   ancestry group; European continental ancestry group
ID VITAMIN-D-RECEPTOR; GENETIC-VARIATION; INDIAN POPULATION; POLYMORPHIC
   CAG; SUSCEPTIBILITY; ONSET; MEN; AGE
AB Purpose: We investigated the association between the length of the polymorphic trinucleotide CAG microsatellite repeats in exon 1 of the AR gene and the risk of prostate cancer.
   Materials and Methods: This is a nested case-control study of 1,159 cases and 1,353 controls from the Prostate Cancer Prevention Trial, a randomized, placebo controlled trial testing whether the 5 alpha-reductase inhibitor finasteride could decrease the 7-year prevalence of prostate cancer. During the course of the trial men underwent annual digital rectal examination and prostate specific antigen measurement. Prostate biopsy was recommended in all men with abnormal digital rectal examination or finasteride adjusted prostate specific antigen greater than 4.0 ng/ml. Cases were drawn from men with biopsy determined prostate cancer identified by for cause or end of study biopsy. Controls were selected from men who completed the end of study biopsy.
   Results: Mean CAG repeat length did not differ between cases and controls. The frequency distribution of cases and controls for the AR CAG repeat length was similar. There were no significant associations of CAG repeat length with prostate cancer risk when stratified by treatment arm (finasteride or placebo), or when combined. There was also no significant association between CAG repeat length and the risk of low or high grade prostate cancer.
   Conclusions: There is no association of AR CAG repeat length with prostate cancer risk. Knowledge of AR CAG repeat length provides no clinically useful information to predict prostate cancer risk.
C1 [Figg, William D.] NCI, Ctr Canc Res, Med Oncol Branch, Bethesda, MD 20892 USA.
   [Minasian, Lori; Parnes, Howard L.] NCI, Canc Prevent Div, Bethesda, MD 20892 USA.
   [Hsing, Ann W.] NCI, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA.
   [Till, Cathee; Goodman, Phyllis J.] Fred Hutchinson Canc Res Ctr, Canc Prevent Program, Seattle, WA 98104 USA.
   [Kristal, Alan R.] Univ Washington, Dept Epidemiol, Seattle, WA 98195 USA.
   [Reichardt, Juergen K. V.] Univ Sydney, Plunkett Chair Mol Biol Med, Sydney, NSW 2006, Australia.
   [Hoque, Ashraful] Univ Texas MD Anderson Canc Ctr, Dept Clin Canc Prevent, Houston, TX 77030 USA.
   [Thompson, Ian M.] Univ Texas Hlth Sci Ctr San Antonio, Dept Urol, San Antonio, TX 78229 USA.
RP Figg, WD (reprint author), NCI, Ctr Canc Res, Med Oncol Branch, Bldg 10,Room 5A01,9000 Rockville Pike, Bethesda, MD 20892 USA.
EM wdfigg@helix.nih.gov
RI Figg Sr, William/M-2411-2016; 
OI Kristal, Alan/0000-0002-7329-1617; Reichardt,
   Juergen/0000-0001-6458-2773
FU National Cancer Institute [CA108964]; National Institutes of Health;
   American College of Clinical Pharmacy/Research Institute; National
   Institutes of Health National Center for Minority Health and Health
   Disparity; American Association for Cancer Research; Mission Pharmacal
FX Supported by the National Cancer Institute, National Institutes of
   Health Intramural Research Program, American College of Clinical
   Pharmacy/Research Institute, National Institutes of Health National
   Center for Minority Health and Health Disparity, and National Cancer
   Institute Prostate Cancer Prevention Trial PO1 Grant CA108964.;
   Financial interest and/or other relationship with American Association
   for Cancer Research.; Financial interest and/or other relationship with
   Mission Pharmacal.
NR 30
TC 22
Z9 23
U1 0
U2 1
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0022-5347
EI 1527-3792
J9 J UROLOGY
JI J. Urol.
PD DEC
PY 2010
VL 184
IS 6
BP 2297
EP 2302
DI 10.1016/j.juro.2010.08.005
PG 6
WC Urology & Nephrology
SC Urology & Nephrology
GA 677ZY
UT WOS:000284037900027
PM 20952028
ER

PT J
AU Olin, JW
   Allie, DE
   Belkin, M
   Bonow, RO
   Casey, DE
   Creager, MA
   Gerber, TC
   Hirsch, AT
   Jaff, MR
   Kaufman, JA
   Lewis, CA
   Martin, ET
   Martin, LG
   Sheehan, P
   Stewart, KJ
   Treat-Jacobson, D
   White, CJ
   Zheng, ZJ
AF Olin, Jeffrey W.
   Allie, David E.
   Belkin, Michael
   Bonow, Robert O.
   Casey, Donald E., Jr.
   Creager, Mark A.
   Gerber, Thomas C.
   Hirsch, Alan T.
   Jaff, Michael R.
   Kaufman, John A.
   Lewis, Curtis A.
   Martin, Edward T.
   Martin, Louis G.
   Sheehan, Peter
   Stewart, Kerry J.
   Treat-Jacobson, Diane
   White, Christopher J.
   Zheng, Zhi-Jie
TI ACCF/AHA/ACR/SCAI/SIR/SVM/SVN/SVS 2010 performance measures for adults
   with peripheral artery disease
SO JOURNAL OF VASCULAR SURGERY
LA English
DT Article
ID ABDOMINAL AORTIC-ANEURYSM; ANKLE-BRACHIAL INDEX; QUALITY-OF-LIFE;
   REHABILITATION/SECONDARY PREVENTION SERVICES; ELEVATION
   MYOCARDIAL-INFARCTION; MEASURES WRITING COMMITTEE; ASSOCIATION
   TASK-FORCE; CARDIOVASCULAR-DISEASE; INTERMITTENT CLAUDICATION;
   AMERICAN-COLLEGE
C1 [Lewis, Curtis A.] Amer Coll Radiol, Reston, VA USA.
   [Zheng, Zhi-Jie] NHLBI, Bethesda, MD 20892 USA.
RI White, Christopher/J-6686-2012
OI White, Christopher/0000-0001-8618-7539
NR 73
TC 8
Z9 8
U1 1
U2 2
PU MOSBY-ELSEVIER
PI NEW YORK
PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0741-5214
J9 J VASC SURG
JI J. Vasc. Surg.
PD DEC
PY 2010
VL 52
IS 6
BP 1616
EP 1652
DI 10.1016/j.jvs.2010.10.065
PG 37
WC Surgery; Peripheral Vascular Disease
SC Surgery; Cardiovascular System & Cardiology
GA 696GS
UT WOS:000285430500028
ER

PT J
AU Abend, JR
   Uldrick, T
   Ziegelbauer, JM
AF Abend, Johanna R.
   Uldrick, Thomas
   Ziegelbauer, Joseph M.
TI Regulation of Tumor Necrosis Factor-Like Weak Inducer of Apoptosis
   Receptor Protein (TWEAKR) Expression by Kaposi's Sarcoma-Associated
   Herpesvirus MicroRNA Prevents TWEAK-Induced Apoptosis and Inflammatory
   Cytokine Expression
SO JOURNAL OF VIROLOGY
LA English
DT Article
ID NF-KAPPA-B; HUMAN-IMMUNODEFICIENCY-VIRUS; ENDOTHELIAL-CELLS;
   GENE-EXPRESSION; HUMAN-HERPESVIRUS-8 INFECTION; MULTIFUNCTIONAL
   CYTOKINE; FUNCTIONAL EXPRESSION; CHEMOKINE PRODUCTION; ENCODED
   MICRORNAS; FN14
AB Kaposi's sarcoma (KS)-associated herpesvirus (KSHV) is the causative agent of KS, the second most common AIDS-associated malignancy. KSHV expresses at least 18 different mature microRNAs (miRNAs) during latency. To identify cellular targets of KSHV miRNAs, we have analyzed a previously reported series of microarrays examining changes in cellular gene expression in the presence of KSHV miRNAs. Tumor necrosis factor (TNF)-like weak inducer of apoptosis (TWEAK) receptor (TWEAKR) was among the most consistently and robustly downregulated genes in the presence of KSHV miR-K12-10a (miR-K10a). Results from luciferase assays with reporter plasmids containing the 3' untranslated region (UTR) of TWEAKR suggest a targeting of TWEAKR by miR-K10a. The mutation of two predicted miR-K10a recognition sites within the 3' UTR of TWEAKR completely disrupts inhibition by miR-K10a. The expression of TWEAKR was downregulated in cells transfected with miR-K10a as well as during de novo KSHV infection. In a KS tumor-derived endothelial cell line, the downregulation of TWEAKR by miR-K10a resulted in reduced levels of TWEAK-induced caspase activation. In addition, cells transfected with miR-K10a showed less induction of apoptosis by annexin V staining and terminal deoxynucleotidyltransferase-mediated dUTP-biotin nick end labeling (TUNEL) assays. Finally, the downregulation of TWEAKR by miR-K10a in primary human endothelial cells resulted in a decrease in levels of expression of the proinflammatory cytokines interleukin-8 (IL-8) and monocyte chemoattractant protein 1 (MCP-1) in response to TWEAK. These results identify and validate an important cellular target of KSHV miRNAs. Furthermore, we demonstrate that a viral miRNA protects cells from apoptosis and suppresses a proinflammatory response, which may have significant implications in the complex context of KS lesions.
C1 [Abend, Johanna R.; Uldrick, Thomas; Ziegelbauer, Joseph M.] NCI, HIV & AIDS Malignancy Branch, NIH, Bethesda, MD 20892 USA.
RP Ziegelbauer, JM (reprint author), Bldg 10,Room 6N106 MSC 1868,10 Ctr Dr, Bethesda, MD 20892 USA.
EM ziegelbauerjm@mail.nih.gov
OI Ziegelbauer, Joseph/0000-0001-6464-6941
FU Ziegelbauer laboratory; Center for Cancer Research, National Cancer
   Institute, National Institutes of Health
FX We thank Patricia Valdez for assistance with the Bio-Plex assays and
   Barbara Taylor and the NCI FACS core for assistance with annexin V and
   TUNEL assays. We thank Don Ganem for sharing unpublished microarray
   data. We thank members of the Ziegelbauer laboratory for help and
   support and Bob Yarchoan and Thomas Zheng for critical reviews of the
   manuscript.; This work was supported by the Intramural Research Program
   of the Center for Cancer Research, National Cancer Institute, National
   Institutes of Health.
NR 54
TC 73
Z9 76
U1 2
U2 5
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 0022-538X
J9 J VIROL
JI J. Virol.
PD DEC
PY 2010
VL 84
IS 23
BP 12139
EP 12151
DI 10.1128/JVI.00884-10
PG 13
WC Virology
SC Virology
GA 675BT
UT WOS:000283799500004
PM 20844036
ER

PT J
AU McLellan, JS
   Chen, M
   Chang, JS
   Yang, YP
   Kim, A
   Graham, BS
   Kwong, PD
AF McLellan, Jason S.
   Chen, Man
   Chang, Jung-San
   Yang, Yongping
   Kim, Albert
   Graham, Barney S.
   Kwong, Peter D.
TI Structure of a Major Antigenic Site on the Respiratory Syncytial Virus
   Fusion Glycoprotein in Complex with Neutralizing Antibody 101F
SO JOURNAL OF VIROLOGY
LA English
DT Article
ID MONOCLONAL-ANTIBODIES; F-PROTEIN; CRYSTAL-STRUCTURE; YOUNG-CHILDREN;
   INFECTION; DISEASE; MOTAVIZUMAB; INFANTS; EPITOPE; IDENTIFICATION
AB Respiratory syncytial virus (RSV) is a major cause of pneumonia and bronchiolitis in infants and elderly people. Currently there is no effective vaccine against RSV, but passive prophylaxis with neutralizing antibodies reduces hospitalizations. To investigate the mechanism of antibody-mediated RSV neutralization, we undertook structure-function studies of monoclonal antibody 101F, which binds a linear epitope in the RSV fusion glycoprotein. Crystal structures of the 101F antigen-binding fragment in complex with peptides from the fusion glycoprotein defined both the extent of the linear epitope and the interactions of residues that are mutated in antibody escape variants. The structure allowed for modeling of 101F in complex with trimers of the fusion glycoprotein, and the resulting models suggested that 101F may contact additional surfaces located outside the linear epitope. This hypothesis was supported by surface plasmon resonance experiments that demonstrated 101F bound the peptide epitope similar to 16,000-fold more weakly than the fusion glycoprotein. The modeling also showed no substantial clashes between 101F and the fusion glycoprotein in either the pre- or postfusion state, and cell-based assays indicated that 101F neutralization was not associated with blocking virus attachment. Collectively, these results provide a structural basis for RSV neutralization by antibodies that target a major antigenic site on the fusion glycoprotein.
C1 [McLellan, Jason S.; Chen, Man; Chang, Jung-San; Yang, Yongping; Kim, Albert; Graham, Barney S.; Kwong, Peter D.] NIAID, Vaccine Res Ctr, NIH, Bethesda, MD 20892 USA.
RP McLellan, JS (reprint author), NIAID, Vaccine Res Ctr, NIH, 40 Convent Dr,Bldg 40,Rm 2613B, Bethesda, MD 20892 USA.
EM mclellanja@mail.nih.gov
RI McLellan, Jason/A-6874-2010
FU National Institute of Allergy and Infectious Diseases; U.S. Department
   of Energy, Basic Energy Sciences, Office of Science [W-31-109-Eng-38]
FX Support for this work was provided by the Intramural Research Program
   (National Institute of Allergy and Infectious Diseases). Use of sector
   22 (SER-CAT) at the Advanced Photon Source was supported by the U.S.
   Department of Energy, Basic Energy Sciences, Office of Science, under
   contract W-31-109-Eng-38.
NR 46
TC 39
Z9 40
U1 14
U2 18
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 0022-538X
J9 J VIROL
JI J. Virol.
PD DEC
PY 2010
VL 84
IS 23
BP 12236
EP 12244
DI 10.1128/JVI.01579-10
PG 9
WC Virology
SC Virology
GA 675BT
UT WOS:000283799500012
PM 20881049
ER

PT J
AU Xiang, Y
   Baxa, U
   Zhang, Y
   Steven, AC
   Lewis, GL
   Van Etten, JL
   Rossmann, MG
AF Xiang, Ye
   Baxa, Ulrich
   Zhang, Ying
   Steven, Alasdair C.
   Lewis, Gentry L.
   Van Etten, James L.
   Rossmann, Michael G.
TI Crystal Structure of a Virus-Encoded Putative Glycosyltransferase
SO JOURNAL OF VIROLOGY
LA English
DT Article
ID PROTEIN GLYCOSYLATION; CHLORELLA; TRANSFERASE; ANNOTATION; CATALYSIS;
   SEQUENCE; ENZYME; PBCV-1
AB The chloroviruses (family Phycodnaviridae), unlike most viruses, encode some, if not most, of the enzymes involved in the glycosylation of their structural proteins. Annotation of the gene product B736L from chlorovirus NY-2A suggests that it is a glycosyltransferase. The structure of the recombinantly expressed B736L protein was determined by X-ray crystallography to 2.3-angstrom resolution, and the protein was shown to have two nucleotide-binding folds like other glycosyltransferase type B enzymes. This is the second structure of a chlorovirus-encoded glycosyltransferase and the first structure of a chlorovirus type B enzyme to be determined. B736L is a retaining enzyme and belongs to glycosyltransferase family 4. The donor substrate was identified as GDP-mannose by isothermal titration calorimetry and was shown to bind into the cleft between the two domains in the protein. The active form of the enzyme is probably a dimer in which the active centers are separated by about 40 angstrom.
C1 [Xiang, Ye; Zhang, Ying; Rossmann, Michael G.] Purdue Univ, Dept Biol Sci, W Lafayette, IN 47907 USA.
   [Baxa, Ulrich; Steven, Alasdair C.] NIAMSD, Struct Biol Lab, NIH, Bethesda, MD 20892 USA.
   [Lewis, Gentry L.; Van Etten, James L.] Univ Nebraska, Dept Plant Pathol, Lincoln, NE 68583 USA.
   [Lewis, Gentry L.; Van Etten, James L.] Univ Nebraska, Nebraska Ctr Virol, Lincoln, NE 68583 USA.
RP Rossmann, MG (reprint author), Purdue Univ, Dept Biol Sci, 915 W State St, W Lafayette, IN 47907 USA.
EM mr@purdue.edu
FU NIH [AI11219]; Public Health Service [GM32441]; NIH, National Center for
   Research Resources [P20RR15635]; NIAMS
FX The work was supported by NIH grant AI11219 to M. G. R., in part by
   Public Health Service grant GM32441 (to J.L.V.E.) and NIH grant
   P20RR15635 from the COBRE program of the National Center for Research
   Resources (to J.L.V.E.), and in part by the NIAMS Intramural Research
   Program.
NR 41
TC 7
Z9 7
U1 1
U2 5
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 0022-538X
J9 J VIROL
JI J. Virol.
PD DEC
PY 2010
VL 84
IS 23
BP 12265
EP 12273
DI 10.1128/JVI.01303-10
PG 9
WC Virology
SC Virology
GA 675BT
UT WOS:000283799500015
PM 20861263
ER

PT J
AU Jahnke, M
   Holmes, EC
   Kerr, PJ
   Wright, JD
   Strive, T
AF Jahnke, Marlene
   Holmes, Edward C.
   Kerr, Peter J.
   Wright, John D.
   Strive, Tanja
TI Evolution and Phylogeography of the Nonpathogenic Calicivirus RCV-A1 in
   Wild Rabbits in Australia
SO JOURNAL OF VIROLOGY
LA English
DT Article
ID HEMORRHAGIC-DISEASE VIRUS; GENETIC DIVERSITY; POPULATION; HOST;
   RECOMBINATION; EPIDEMIOLOGY; LAGOVIRUS; SEQUENCES; INFERENCE
AB Despite its potential importance for the biological control of European rabbits, relatively little is known about the evolution and molecular epidemiology of rabbit calicivirus Australia 1 (RCV-A1). To address this issue we undertook an extensive evolutionary analysis of 36 RCV-A1 samples collected from wild rabbit populations in southeast Australia between 2007 and 2009. Based on phylogenetic analysis of the entire capsid sequence, six clades of RCV-A1 were defined, each exhibiting strong population subdivision. Strikingly, our estimates of the time to the most recent common ancestor of RCV-A1 coincide with the introduction of rabbits to Australia in the mid-19th century. Subsequent divergence events visible in the RCV-A1 phylogenies likely reflect key moments in the history of the European rabbit in Australia, most notably the bottlenecks in rabbit populations induced by the two viral biocontrol agents used on the Australian continent, myxoma virus and rabbit hemorrhagic disease virus (RHDV). RCV-A1 strains therefore exhibit strong phylogeographic separation and may constitute a useful tool to study recent host population dynamics and migration patterns, which in turn could be used to monitor rabbit control in Australia.
C1 [Jahnke, Marlene; Kerr, Peter J.; Wright, John D.; Strive, Tanja] Commonwealth Sci & Ind Res Org, Canberra, ACT 2600, Australia.
   [Jahnke, Marlene; Wright, John D.; Strive, Tanja] 3D1 Univ Canberra, Invas Anim Cooperat Res Ctr, Canberra, ACT 2601, Australia.
   [Holmes, Edward C.] Penn State Univ, Dept Biol, Ctr Infect Dis Dynam, University Pk, PA 16802 USA.
   [Holmes, Edward C.] NIH, Fogarty Int Ctr, Bethesda, MD 20892 USA.
RP Strive, T (reprint author), CSIRO, Ecosyst Sci, GPO Box 1700, Canberra, ACT 2601, Australia.
EM Tanja.Strive@csiro.au
RI Strive, Tanja/C-1486-2008; Kerr, Peter/C-2463-2009; 
OI Holmes, Edward/0000-0001-9596-3552
FU Australian Department of Agriculture, Fisheries and Forestry; National
   Institutes of Health [R01 GM080533]
FX This work was supported by a Wildlife Exotic Disease Preparedness
   Program grant from the Australian Department of Agriculture, Fisheries
   and Forestry. E.C.H. is supported in part by grant R01 GM080533 from the
   National Institutes of Health.
NR 43
TC 23
Z9 23
U1 0
U2 9
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 0022-538X
J9 J VIROL
JI J. Virol.
PD DEC
PY 2010
VL 84
IS 23
BP 12397
EP 12404
DI 10.1128/JVI.00777-10
PG 8
WC Virology
SC Virology
GA 675BT
UT WOS:000283799500028
PM 20861266
ER

PT J
AU Smith, JL
   Pathak, VK
AF Smith, Jessica L.
   Pathak, Vinay K.
TI Identification of Specific Determinants of Human APOBEC3F, APOBEC3C, and
   APOBEC3DE and African Green Monkey APOBEC3F That Interact with HIV-1 Vif
SO JOURNAL OF VIROLOGY
LA English
DT Article
ID HUMAN-IMMUNODEFICIENCY-VIRUS; VIRION INFECTIVITY FACTOR; AMINO-ACID
   DIFFERENCE; FUSION INHIBITOR T-20; E3 UBIQUITIN LIGASE; TYPE-1 VIF;
   REVERSE TRANSCRIPTION; CYTIDINE DEAMINASE; ANTIVIRAL ACTIVITY;
   ANTIRETROVIRAL ACTIVITY
AB Human APOBEC3F (hA3F) and human APOBEC3G (hA3G) are potent anti-human immunodeficiency virus (anti-HIV) host factors that suppress viral replication by hypermutating the viral genome, inhibiting reverse transcription, and hindering integration. To overcome hA3F and hA3G, HIV-1 encodes Vif, which binds and targets these host proteins for proteasomal degradation. Previously, we reported that the hA3F-Vif interactions that lead to hA3F degradation are located in the region comprising amino acids 283 to 300. We have now performed mutational analysis of this region and found that the (289)EFLARH(294) amino acids contribute to hA3F-Vif binding and are critical for A3F's sensitivity to Vif. Mutants in which E289 is mutated significantly increase hA3F's ability to inhibit viral infectivity in the presence of Vif, and coimmunoprecipitation assays show that binding of Vif to the E289K mutant is decreased. We examined the role of the EFLARH sequence in other A3 proteins, including human A3C (hA3C), human A3DE (hA3DE), African green monkey A3F (agmA3F), and rhesus macaque A3F (rhA3F). hA3C, hA3DE, and agmA3F were all susceptible to degradation induced by HIV-1 Vif, while rhA3F was not. Mutagenesis of the glutamate in the EFLARH sites of hA3C, hA3DE, and agmA3F decreases the susceptibilities of these proteins to Vif-induced degradation. Together, these results indicate that the EFLARH region in hA3F, hA3C, hA3DE, and agmA3F interacts with HIV-1 Vif and that this interaction plays a role in the Vif-mediated proteasomal degradation of these A3 proteins. These studies identify a conserved region in 3 of 7 human A3 proteins that is critical for degradation mediated by HIV-1 Vif and provide structural insights into the hA3F-Vif interactions that could facilitate the development of a novel class of anti-HIV agents.
C1 [Smith, Jessica L.; Pathak, Vinay K.] NCI, Viral Mutat Sect, HIV Drug Resistance Program, Ctr Canc Res, Frederick, MD 21702 USA.
RP Pathak, VK (reprint author), NCI, Viral Mutat Sect, HIV Drug Resistance Program, Ctr Canc Res, POB B,Bldg 535,Rm 334, Frederick, MD 21702 USA.
EM vinay.pathak@nih.gov
FU NIH, National Cancer Institute, Center for Cancer Research
FX This research was supported in part by the Intramural Research Program
   of the NIH, National Cancer Institute, Center for Cancer Research.
NR 70
TC 36
Z9 38
U1 0
U2 3
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 0022-538X
J9 J VIROL
JI J. Virol.
PD DEC
PY 2010
VL 84
IS 24
BP 12599
EP 12608
DI 10.1128/JVI.01437-10
PG 10
WC Virology
SC Virology
GA 683IN
UT WOS:000284469600013
PM 20943965
ER

PT J
AU Hayward, JJ
   Dubovi, EJ
   Scarlett, JM
   Janeczko, S
   Holmes, EC
   Parrish, CR
AF Hayward, Jessica J.
   Dubovi, Edward J.
   Scarlett, Janet M.
   Janeczko, Stephanie
   Holmes, Edward C.
   Parrish, Colin R.
TI Microevolution of Canine Influenza Virus in Shelters and Its Molecular
   Epidemiology in the United States
SO JOURNAL OF VIROLOGY
LA English
DT Article
ID EQUINE INFLUENZA; A VIRUSES; SIALIC-ACID; HOST-RANGE; PHYLOGENETIC
   ANALYSIS; RESPIRATORY-DISEASE; SEROLOGICAL SURVEY; CELL GLYCOLIPIDS;
   RECEPTOR-BINDING; DOGS
AB Canine influenza virus (CIV) emerged around 2000 when an equine influenza virus (EIV) was transmitted to dogs in Florida. After 2003, the canine virus was carried by infected greyhounds to various parts of the United States and then became established in several large animal shelters, where it has continued to circulate. To better understand the evolution of CIV since its emergence, and particularly its microevolution in spatially restricted populations, we examined multiple gene segments of CIV from dogs resident in two large animal shelters in New York City during the period 2006 to 2009. In particular, we focused on viruses circulating in the two shelters in 2008 and 2009, which we found shared a common ancestor. While viruses in each shelter were generally monophyletic, we observed some gene flow between them. These shelter sequences were compared to earlier CIV isolates. The shelter viruses differed in 1 to 6 amino acids in each gene segment compared to viruses isolated in Florida between 2003 and 2005 and in Colorado in 2006 and 2008. A comparison of the sequences of equine and canine viruses revealed amino acid replacements that distinguished the viruses from the two hosts, but no clear evidence of positive selection indicative of host adaptation was detected, suggesting that any host range adaptation in CIV occurred early in the emergence of this virus or even before it transferred to dogs.
C1 [Hayward, Jessica J.; Parrish, Colin R.] Cornell Univ, Baker Inst Anim Hlth, Coll Vet Med, Ithaca, NY 14853 USA.
   [Dubovi, Edward J.; Scarlett, Janet M.; Janeczko, Stephanie] Cornell Univ, Dept Populat Med, Coll Vet Med, Ithaca, NY 14853 USA.
   [Holmes, Edward C.] Penn State Univ, Ctr Infect Dis Dynam, Dept Biol, University Pk, PA 16802 USA.
   [Holmes, Edward C.] NIH, Fogarty Int Ctr, Bethesda, MD 20892 USA.
RP Parrish, CR (reprint author), Cornell Univ, Baker Inst Anim Hlth, Coll Vet Med, Ithaca, NY 14853 USA.
EM crp3@cornell.edu
OI Holmes, Edward/0000-0001-9596-3552
FU NIH [GM080533-03]
FX This work was supported by NIH grant GM080533-03 to E.C.H. and C.R.P.
NR 55
TC 26
Z9 27
U1 1
U2 5
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 0022-538X
J9 J VIROL
JI J. Virol.
PD DEC
PY 2010
VL 84
IS 24
BP 12636
EP 12645
DI 10.1128/JVI.01350-10
PG 10
WC Virology
SC Virology
GA 683IN
UT WOS:000284469600017
PM 20943966
ER

PT J
AU Cho, WK
   Jang, MK
   Huang, K
   Pise-Masison, CA
   Brady, JN
AF Cho, Won-Kyung
   Jang, Moon Kyoo
   Huang, Keven
   Pise-Masison, Cynthia A.
   Brady, John N.
TI Human T-Lymphotropic Virus Type 1 Tax Protein Complexes with P-TEFb and
   Competes for Brd4 and 7SK snRNP/HEXIM1 Binding
SO JOURNAL OF VIROLOGY
LA English
DT Article
ID RNA-POLYMERASE-II; CARBOXY-TERMINAL DOMAIN; HTLV-I; TRANSCRIPTIONAL
   ELONGATION; CREB BINDING; DEPENDENT TRANSCRIPTION; REGULATORY ELEMENTS;
   MYELOPATHY HAM/TSP; COACTIVATOR CBP; GENE-EXPRESSION
AB Positive transcription elongation factor b (P-TEFb) plays an important role in stimulating RNA polymerase II elongation for viral and cellular gene expression. P-TEFb is found in cells in either an active, low-molecular-weight (LMW) form or an inactive, high-molecular-weight (HMW) form. We report here that human T-lymphotropic virus type 1 (HTLV-1) Tax interacts with the cyclin T1 subunit of P-TEFb, forming a distinct Tax/P-TEFb LMW complex. We demonstrate that Tax can play a role in regulating the amount of HMW complex present in the cell by decreasing the binding of 7SK snRNP/HEXIM1 to P-TEFb. This is seen both in vitro using purified Tax protein and in vivo in cells transduced with Tax expression constructs. Further, we find that a peptide of cyclin T1 spanning the Tax binding domain inhibits the ability of Tax to disrupt HMW P-TEFb complexes. These results suggest that the direct interaction of Tax with cyclin T1 can dissociate P-TEFb from the P-TEFb/7SK snRNP/HEXIM1 complex for activation of the viral long terminal repeat (LTR). We also show that Tax competes with Brd4 for P-TEFb binding. Chromatin immunoprecipitation (ChIP) assays demonstrated that Brd4 and P-TEFb are associated with the basal HTLV-1 LTR, while Tax and P-TEFb are associated with the activated template. Furthermore, the knockdown of Brd4 by small interfering RNA (siRNA) activates the HTLV-1 LTR promoter, which results in an increase in viral expression and production. Our studies have identified Tax as a regulator of P-TEFb that is capable of affecting the balance between its association with the large inactive complex and the small active complex.
C1 [Cho, Won-Kyung; Huang, Keven; Pise-Masison, Cynthia A.; Brady, John N.] NCI, Virus Tumor Biol Sect, Cellular Oncol Lab, Ctr Canc Res, Bethesda, MD 20892 USA.
   [Jang, Moon Kyoo] NIAID, Viral Dis Lab, NIH, Bethesda, MD 20892 USA.
RP Cho, WK (reprint author), NCI, Virus Tumor Biol Sect, Cellular Oncol Lab, Ctr Canc Res, 41 Medlars Dr,Bldg 41,Room B303, Bethesda, MD 20892 USA.
EM wonkyungc@gmail.com; masisonc@mail.nih.gov
FU National Institutes of Health, National Cancer Institute, Center for
   Cancer Research
FX This research was supported by the Intramural Research Program of the
   National Institutes of Health, National Cancer Institute, Center for
   Cancer Research.
NR 61
TC 10
Z9 10
U1 0
U2 1
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 0022-538X
J9 J VIROL
JI J. Virol.
PD DEC
PY 2010
VL 84
IS 24
BP 12801
EP 12809
DI 10.1128/JVI.00943-10
PG 9
WC Virology
SC Virology
GA 683IN
UT WOS:000284469600033
PM 20926576
ER

PT J
AU Baliji, S
   Liu, QP
   Kozak, CA
AF Baliji, Surendranath
   Liu, Qingping
   Kozak, Christine A.
TI Common Inbred Strains of the Laboratory Mouse That Are Susceptible to
   Infection by Mouse Xenotropic Gammaretroviruses and the Human-Derived
   Retrovirus XMRV
SO JOURNAL OF VIROLOGY
LA English
DT Article
ID MURINE LEUKEMIA VIRUSES; CELL-SURFACE RECEPTOR; MAJOR GLYCOPROTEINS
   GP70; MUS-MUSCULUS-MOLOSSINUS; HOST-RANGE; C VIRUSES; IN-VITRO; MICE;
   ORIGIN; LOCI
AB Laboratory mouse strains carry endogenous copies of the xenotropic mouse leukemia viruses (X-MLVs), named for their inability to infect cells of the laboratory mouse. This resistance to exogenous infection is due to a nonpermissive variant of the XPR1 gammaretrovirus receptor, a resistance that also limits in vivo expression of germ line X-MLV proviruses capable of producing infectious virus. Because laboratory mice vary widely in their proviral contents and in their virus expression patterns, we screened inbred strains for sequence and functional variants of the XPR1 receptor. We also typed inbred strains and wild mouse species for an endogenous provirus, Bxv1, that is capable of producing infectious X-MLV and that also contributes to the generation of pathogenic recombinant MLVs. We identified the active Bxv1 provirus in many common inbred strains and in some Japanese Mus molossinus mice but in none of the other wild mouse species that carry X-MLVs. Our screening for Xpr1 variants identified the permissive Xpr1(sxv) allele in 7 strains of laboratory mice, including a Bxv1-positive strain, F/St, which is characterized by lifelong X-MLV viremia. Cells from three strains carrying Xpr1(sxv), namely, SWR, SJL, and SIM.R, were shown to be infectable by X-MLV and XMRV; these strains carry different alleles at Fv1 and vary in their sensitivities to specific X/P-MLV isolates and XMRV. Several strains with Xpr1(sxv) lack the active Bxv1 provirus or other endogenous X-MLVs and may provide a useful model system to evaluate the in vivo spread of these gammaretroviruses and their disease potential in their natural host.
C1 [Kozak, Christine A.] NIAID, NIH, LMM, Bethesda, MD 20892 USA.
RP Kozak, CA (reprint author), NIAID, NIH, LMM, Bldg 4,Room 329,4 Ctr Dr,MSC 0460, Bethesda, MD 20892 USA.
EM ckozak@niaid.nih.gov
FU NIAID, NIH
FX This research was supported by the Intramural Research Program of the
   NIAID, NIH.
NR 52
TC 20
Z9 20
U1 0
U2 6
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 0022-538X
J9 J VIROL
JI J. Virol.
PD DEC
PY 2010
VL 84
IS 24
BP 12841
EP 12849
DI 10.1128/JVI.01863-10
PG 9
WC Virology
SC Virology
GA 683IN
UT WOS:000284469600037
PM 20943975
ER

PT J
AU Mens, H
   Kearney, M
   Wiegand, A
   Shao, W
   Schonning, K
   Gerstoft, J
   Obel, N
   Maldarelli, F
   Mellors, JW
   Benfield, T
   Coffin, JM
AF Mens, Helene
   Kearney, Mary
   Wiegand, Ann
   Shao, Wei
   Schonning, Kristian
   Gerstoft, Jan
   Obel, Niels
   Maldarelli, Frank
   Mellors, John W.
   Benfield, Thomas
   Coffin, John M.
TI HIV-1 Continues To Replicate and Evolve in Patients with Natural Control
   of HIV Infection
SO JOURNAL OF VIROLOGY
LA English
DT Article
ID HUMAN-IMMUNODEFICIENCY-VIRUS; ACTIVE ANTIRETROVIRAL THERAPY; LOW-LEVEL
   VIREMIA; CD4(+) T-CELLS; ELITE SUPPRESSORS; REVERSE-TRANSCRIPTASE;
   RALTEGRAVIR INTENSIFICATION; NEUTRALIZING ANTIBODY; PLASMA VIRUS; TYPE-1
AB Elucidating mechanisms leading to the natural control of HIV-1 infection is of great importance for vaccine design and for understanding viral pathogenesis. Rare HIV-1-infected individuals, termed HIV-1 controllers, have plasma HIV-1 RNA levels below the limit of detection by standard clinical assays (<50 to 75 copies/ml) without antiretroviral therapy. Although several recent studies have documented persistent low-grade viremia in HIV-1 controllers at a level not significantly different from that in HIV-1-infected individuals undergoing treatment with combination antiretroviral therapy (cART), it is unclear if plasma viruses are undergoing full cycles of replication in vivo or if the infection of new cells is completely blocked by host immune mechanisms. We studied a cohort of 21 HIV-1 controllers with a median level of viremia below 1 copy/ml, followed for a median of 11 years. Less than half of the cohort carried known protective HLA types (B*57/27). By isolating HIV-1 RNA from large volumes of plasma, we amplified single genome sequences of both pro-rt and env longitudinally. This study is the first to document that HIV-1 pro-rt and env evolve in this patient group, albeit at rates somewhat lower than in HIV-1 noncontrollers, in HLA B*57/27-positive, as well as HLA B*57/27-negative, individuals. Viral diversity and adaptive events associated with immune escape were found to be restricted in HIV-1 controllers, suggesting that replication occurs in the face of less overall immune selection.
C1 [Mens, Helene; Kearney, Mary; Wiegand, Ann; Maldarelli, Frank; Coffin, John M.] NCI, HIV Drug Resistance Program, NIH, Frederick, MD 21702 USA.
   [Mens, Helene; Benfield, Thomas] Copenhagen Univ Hosp, Dept Infect Dis, Hvidovre, Denmark.
   [Mens, Helene; Benfield, Thomas] Copenhagen Univ Hosp, Clin Res Ctr, Hvidovre, Denmark.
   [Shao, Wei] NCI, ISP Adv Biomed Comp Ctr, SAIC Frederick Inc, Frederick, MD 21702 USA.
   [Schonning, Kristian] Copenhagen Univ Hosp, Dept Clin Microbiol, Hvidovre, Denmark.
   [Gerstoft, Jan; Obel, Niels] Rigshosp, Dept Infect Dis, Copenhagen, Denmark.
   [Mellors, John W.] Univ Pittsburgh, Div Infect Dis, Pittsburgh, PA USA.
   [Coffin, John M.] Tufts Univ, Boston, MA 02111 USA.
RP Mens, H (reprint author), NCI, HIV Drug Resistance Program, NIH, Bldg 535, Frederick, MD 21702 USA.
EM helene.mens@gmail.com
FU Danish Medical Research Council [271-07-0371]; F.M. Kirby Foundation
FX The study was partly funded by The Danish Medical Research Council
   (271-07-0371). J.M.C. was a Research Professor of the American Cancer
   Society with support from the F.M. Kirby Foundation.
NR 67
TC 51
Z9 51
U1 0
U2 2
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 0022-538X
J9 J VIROL
JI J. Virol.
PD DEC
PY 2010
VL 84
IS 24
BP 12971
EP 12981
DI 10.1128/JVI.00387-10
PG 11
WC Virology
SC Virology
GA 683IN
UT WOS:000284469600049
PM 20926564
ER

PT J
AU Zhi, N
   Wan, ZH
   Liu, XH
   Wong, S
   Kim, DJ
   Young, NS
   Kajigaya, S
AF Zhi, Ning
   Wan, Zhihong
   Liu, Xiaohong
   Wong, Susan
   Kim, Dong Joo
   Young, Neal S.
   Kajigaya, Sachiko
TI Codon Optimization of Human Parvovirus B19 Capsid Genes Greatly
   Increases Their Expression in Nonpermissive Cells
SO JOURNAL OF VIROLOGY
LA English
DT Article
ID PROTEIN; IMMUNOGENICITY; REPLICATION; INFECTIVITY
AB Parvovirus B19 (B19V) is pathogenic for humans and has an extreme tropism for human erythroid progenitors. We report cell type-specific expression of the B19V capsid genes (VP1 and VP2) and greatly increased B19V capsid protein production in nonpermissive cells by codon optimization. Codon usage limitation, rather than promoter type and the 3' untranslated region of the capsid genes, appears to be a key factor in capsid protein production in nonpermissive cells. Moreover, B19 virus-like particles were successfully generated in nonpermissive cells by transient transfection of a plasmid carrying both codon-optimized VP1 and VP2 genes.
C1 [Zhi, Ning; Wan, Zhihong; Liu, Xiaohong; Wong, Susan; Kim, Dong Joo; Young, Neal S.; Kajigaya, Sachiko] NHLBI, Hematol Branch, NIH, Bethesda, MD 20892 USA.
RP Zhi, N (reprint author), NHLBI, Hematol Branch, NIH, Bldg 10CRC Rm 3E-5272,900 Rockville Pike, Bethesda, MD 20892 USA.
EM zhin@nhlbi.nih.gov
FU NIH, NHLBI
FX This study was supported by the Intramural Research Program of the NIH,
   NHLBI.
NR 11
TC 17
Z9 21
U1 0
U2 0
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 0022-538X
J9 J VIROL
JI J. Virol.
PD DEC
PY 2010
VL 84
IS 24
BP 13059
EP 13062
DI 10.1128/JVI.00912-10
PG 4
WC Virology
SC Virology
GA 683IN
UT WOS:000284469600059
PM 20943969
ER

PT J
AU Kumar, S
   Collins, PL
   Samal, SK
AF Kumar, Sachin
   Collins, Peter L.
   Samal, Siba K.
TI Identification of Simian Agent 10 as Human Parainfluenza Virus Type 3
   Suggests Transmission of a Human Virus to an African Monkey
SO JOURNAL OF VIROLOGY
LA English
DT Letter
C1 [Kumar, Sachin; Samal, Siba K.] Univ Maryland, Virginia Maryland Reg Coll Vet Med, College Pk, MD 20742 USA.
   [Collins, Peter L.] NIAID, Infect Dis Lab, Bethesda, MD 20892 USA.
RP Samal, SK (reprint author), Univ Maryland, Virginia Maryland Reg Coll Vet Med, College Pk, MD 20742 USA.
EM ssamal@umd.edu
FU Intramural NIH HHS; PHS HHS [N01A060009]
NR 12
TC 3
Z9 3
U1 1
U2 2
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 0022-538X
J9 J VIROL
JI J. Virol.
PD DEC
PY 2010
VL 84
IS 24
BP 13068
EP 13070
DI 10.1128/JVI.01928-10
PG 3
WC Virology
SC Virology
GA 683IN
UT WOS:000284469600061
PM 20881043
ER

PT J
AU Beydoun, HA
   Dail, J
   Tamim, H
   Ugwu, B
   Beydoun, MA
AF Beydoun, Hind A.
   Dail, Jessica
   Tamim, Hala
   Ugwu, Bethrand
   Beydoun, May A.
TI Gender and Age Disparities in the Prevalence of Chlamydia Infection
   Among Sexually Active Adults in the United States
SO JOURNAL OF WOMENS HEALTH
LA English
DT Article
ID SIMPLEX-VIRUS TYPE-2; TRANSMITTED INFECTIONS; DRUG-USE;
   NEISSERIA-GONORRHOEAE; BACTERIAL VAGINOSIS; YOUNG-ADULTS; RISK-FACTORS;
   SEX WORK; TRACHOMATIS; WOMEN
AB Background: Chlamydia trachomatis (CT) causes a costly and potentially recurrent bacterial infection that accounts for a considerable proportion of sexually transmitted infections (STIs) in the United States. Disparities by gender and age group in CT prevalence have been reported previously. The current study evaluates demographic, socioeconomic, and behavioral risk and protective factors that may account for gender/age disparities in CT infections among sexually active young adults in the United States.
   Methods: Secondary analyses were performing using the 1999-2006 National Health and Nutrition Examination Survey (NHANES) data.
   Results: A total sample of 5611 adults, 20-39 years of age, who participated in the 1999-2006 NHANES, reported lifetime sexual experience, and had valid laboratory-based CT status, was analyzed. CT prevalence did not differ significantly by gender and was estimated to be 1.6%. It was slightly higher for people <25 years vs. those >= 25 years of age; age disparities were reduced after controlling for demographic, socioeconomic, and behavioral characteristics. Among those <25 years, non-Hispanic blacks had a higher odds of CT infection compared with other groups. Among those >= 25 years of age, not having had unprotected sex in the past month reduced the odds for CT infection, whereas non-Hispanic black race and never married status increased the odds for CT infection.
   Conclusions: Among sexually active adults, no gender disparities were observed in CT prevalence. Age group disparities were partly explained by personal characteristics associated with risk of STIs.
C1 [Beydoun, Hind A.; Dail, Jessica; Ugwu, Bethrand] Eastern Virginia Med Sch, Grad Program Publ Hlth, Norfolk, VA 23501 USA.
   [Tamim, Hala] York Univ, Sch Kinesiol & Hlth Sci, Toronto, ON M3J 2R7, Canada.
   [Beydoun, May A.] NIA, Baltimore, MD 21224 USA.
RP Beydoun, HA (reprint author), Eastern Virginia Med Sch, Grad Program Publ Hlth, 700 Olney Rd,POB 1980, Norfolk, VA 23501 USA.
EM baydouha@evms.edu
FU National Institutes of Health, National Institute on Aging
FX This research was supported in part by the intramural research program
   of the National Institutes of Health, National Institute on Aging.
NR 31
TC 5
Z9 5
U1 0
U2 4
PU MARY ANN LIEBERT INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 1540-9996
J9 J WOMENS HEALTH
JI J. Womens Health
PD DEC
PY 2010
VL 19
IS 12
BP 2183
EP 2190
DI 10.1089/jwh.2010.1975
PG 8
WC Public, Environmental & Occupational Health; Medicine, General &
   Internal; Obstetrics & Gynecology; Women's Studies
SC Public, Environmental & Occupational Health; General & Internal
   Medicine; Obstetrics & Gynecology; Women's Studies
GA 685KF
UT WOS:000284626900007
PM 20950136
ER

PT J
AU Croteau, DL
   de Souza-Pinto, NC
   Harboe, C
   Keijzers, G
   Zhang, YQ
   Becker, K
   Sheng, S
   Bohr, VA
AF Croteau, Deborah L.
   de Souza-Pinto, Nadja C.
   Harboe, Charlotte
   Keijzers, Guido
   Zhang, Yongqing
   Becker, Kevin
   Sheng, Shan
   Bohr, Vilhelm A.
TI DNA Repair and the Accumulation of Oxidatively Damaged DNA Are Affected
   by Fruit Intake in Mice
SO JOURNALS OF GERONTOLOGY SERIES A-BIOLOGICAL SCIENCES AND MEDICAL
   SCIENCES
LA English
DT Article
DE Aging; Oxidative stress; DNA repair; DNA damage; Dietary intervention
ID BASE EXCISION-REPAIR; MITOCHONDRIA; GLYCOSYLASES; VEGETABLES; RADIATION;
   PATHWAY; PLUMS
AB AGING is associated with elevated oxidative stress and DNA damage. To achieve healthy aging, we must begin to understand how diet affects cellular processes. We postulated that fruit-enriched diets might initiate a program of enhanced DNA repair and thereby improve genome integrity. C57Bl/6 J mice were fed for 14 weeks a control diet or a diet with 8% peach or nectarine extract. The activities of DNA repair enzymes, the level of DNA damage, and gene expression changes were measured. Our study showed that repair of various oxidative DNA lesions was more efficient in liver extracts derived from mice fed fruit-enriched diets. In support of these findings, gas chromatography-mass spectrometry analysis revealed that there was a decrease in the levels of formamidopyrimidines in peach-fed mice compared with the controls. Additionally, microarray analysis revealed that NTH1 was upregulated in peach-fed mice. Taken together, these results suggest that an increased intake of fruits might modulate the efficiency of DNA repair, resulting in altered levels of DNA damage.
C1 [Croteau, Deborah L.; de Souza-Pinto, Nadja C.; Harboe, Charlotte; Keijzers, Guido; Bohr, Vilhelm A.] NIA, Lab Mol Gerontol, NIH, Baltimore, MD 21224 USA.
   [Zhang, Yongqing; Becker, Kevin; Sheng, Shan] NIA, Res Resources Branch, NIH, Baltimore, MD 21224 USA.
RP Bohr, VA (reprint author), NIA, Lab Mol Gerontol, NIH, 251 Bayview Blvd,Suite 100,Rm 06B133, Baltimore, MD 21224 USA.
EM vbohr@nih.gov
RI Souza-Pinto, Nadja/C-3462-2013; 3, INCT/H-4497-2013; Redoxoma,
   Inct/H-9962-2013; 
OI Souza-Pinto, Nadja/0000-0003-4206-964X; Becker,
   Kevin/0000-0002-6794-6656
FU National Institute on Aging; National Fruit Tree Association; National
   Institutes of Health, USA
FX This work was funded in part by the Intramural Research Program of the
   National Institute on Aging, National Institutes of Health, USA, and a
   grant from the National Fruit Tree Association from the California Tree
   Fruit Agreement to V.A.B., which also provided the fruit samples used in
   this study.
NR 34
TC 5
Z9 5
U1 0
U2 1
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 1079-5006
J9 J GERONTOL A-BIOL
JI J. Gerontol. Ser. A-Biol. Sci. Med. Sci.
PD DEC
PY 2010
VL 65
IS 12
BP 1300
EP 1311
DI 10.1093/gerona/glq157
PG 12
WC Geriatrics & Gerontology; Gerontology
SC Geriatrics & Gerontology
GA 685PD
UT WOS:000284639700004
PM 20847039
ER

PT J
AU Chang, ML
   Jonsson, PV
   Snaedal, J
   Bjornsson, S
   Saczynski, JS
   Aspelund, T
   Eiriksdottir, G
   Jonsdottir, MK
   Lopez, OL
   Harris, TB
   Gudnason, V
   Launer, LJ
AF Chang, Milan
   Jonsson, Palmi V.
   Snaedal, Jon
   Bjornsson, Sigurbjorn
   Saczynski, Jane S.
   Aspelund, Thor
   Eiriksdottir, Gudny
   Jonsdottir, Maria K.
   Lopez, Oscar L.
   Harris, Tamara B.
   Gudnason, Vilmundur
   Launer, Lenore J.
TI The Effect of Midlife Physical Activity on Cognitive Function Among
   Older Adults: AGES-Reykjavik Study
SO JOURNALS OF GERONTOLOGY SERIES A-BIOLOGICAL SCIENCES AND MEDICAL
   SCIENCES
LA English
DT Article
DE Physical activity; Cognitive function; Longitudinal study
ID INTERNATIONAL NEUROPSYCHIATRIC INTERVIEW; APOLIPOPROTEIN-E;
   RISK-FACTORS; ALZHEIMERS-DISEASE; DSM-IV; DEMENTIA; EXERCISE; HEALTH;
   BRAIN; MINI
AB There are few studies on the long-term associations of physical activity (PA) to cognition. Here, we examine the association of midlife PA to late-life cognitive function and dementia.
   The sample consisted of a population-based cohort of men and women (born in 1907-1935) participating in the Age Gene/Environment Susceptibility-Reykjavik Study. The interval between the midlife ascertainment of PA and late-life cognitive function was 26 years. Composite scores of speed of processing, memory, and executive function were assessed with a battery of neuropsychological tests, and dementia was diagnosed according to international guidelines. There were 4,761 nondemented participants and 184 (3.7%) with a diagnosis of dementia, with complete data for the analysis.
   Among the participants, no midlife PA was reported by 68.8%, < 5 hours PA by 26.5%, and > 5 hours PA by 4.5%. Excluding participants with dementia compared with the no PA group, both PA groups had significantly faster speed of processing (< 5 hours, beta = .22; > 5 hours, beta = .32, p trend < .0001), better memory (< 5 hours, beta = .15; > 5 hours, beta = .18, p trend < .0001), and executive function (< 5 hours, beta = .09; > 5 hours, beta = .18, p trend < .0001), after controlling for demographic and cardiovascular factors. The < 5 hours PA group was significantly less likely to have dementia in late life (odds ratio: 0.6, 95% confidence interval: 0.40-0.88) after adjusting for confounders.
   Midlife PA may contribute to maintenance of cognitive function and may reduce or delay the risk of late-life dementia.
C1 [Harris, Tamara B.; Launer, Lenore J.] NIA, Lab Epidemiol Demog & Biometry, NIH, Bethesda, MD 20892 USA.
   [Chang, Milan; Jonsson, Palmi V.; Snaedal, Jon; Bjornsson, Sigurbjorn; Jonsdottir, Maria K.] Landspitali Univ Hosp, Geriatr Res Ctr, Reykjavik, Iceland.
   [Jonsson, Palmi V.; Snaedal, Jon; Gudnason, Vilmundur] Univ Iceland, Fac Med, Reykjavik, Iceland.
   [Saczynski, Jane S.] Univ Massachusetts, Sch Med, Div Geriatr Med, Worcester, MA USA.
   [Saczynski, Jane S.] Univ Massachusetts, Sch Med, Meyers Primary Care Inst, Worcester, MA USA.
   [Aspelund, Thor; Eiriksdottir, Gudny; Gudnason, Vilmundur] Iceland Heart Assoc, Kopavogur, Iceland.
   [Aspelund, Thor] Univ Iceland, Fac Sci, Reykjavik, Iceland.
   [Jonsdottir, Maria K.] Univ Iceland, Fac Psychol, Reykjavik, Iceland.
   [Lopez, Oscar L.] Univ Pittsburgh, Dept Psychiat & Neurol, Pittsburgh, PA 15260 USA.
RP Launer, LJ (reprint author), NIA, Lab Epidemiol Demog & Biometry, NIH, Gateway Bldg,3C309,7201 Wisconsin Ave, Bethesda, MD 20892 USA.
EM launerl@nia.nih.gov
RI Aspelund, Thor/F-4826-2011; Aspelund, Thor/C-5983-2008; Gudnason,
   Vilmundur/K-6885-2015
OI Aspelund, Thor/0000-0002-7998-5433; Gudnason,
   Vilmundur/0000-0001-5696-0084
FU National Institutes of Health [N01-AG-12100]; National Institute on
   Aging; Icelandic Heart Association; Icelandic Parliament; Icelandic
   Center for Research
FX This study was funded by National Institutes of Health contract
   N01-AG-12100, the National Institute on Aging Intramural Research
   Program, the Icelandic Heart Association, the Icelandic Parliament, and
   the Icelandic Center for Research.
NR 43
TC 46
Z9 51
U1 2
U2 23
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 1079-5006
J9 J GERONTOL A-BIOL
JI J. Gerontol. Ser. A-Biol. Sci. Med. Sci.
PD DEC
PY 2010
VL 65
IS 12
BP 1369
EP 1374
DI 10.1093/gerona/glq152
PG 6
WC Geriatrics & Gerontology; Gerontology
SC Geriatrics & Gerontology
GA 685PD
UT WOS:000284639700012
PM 20805238
ER

PT J
AU Schaefer, GO
   Wertheimer, A
AF Schaefer, G. Owen
   Wertheimer, Alan
TI The Right to Withdraw from Research
SO KENNEDY INSTITUTE OF ETHICS JOURNAL
LA English
DT Article
AB The right to withdraw from participation in research is recognized in virtually all national and international guidelines for research on human subjects. It is therefore surprising that there has been little justification for that right in the literature. We argue that the right to withdraw should protect research participants from information imbalance, inability to hedge, inherent uncertainty, and untoward bodily invasion, and it serves to bolster public trust in the research enterprise. Although this argument is not radical, it provides a useful way to determine how the right should be applied in various cases.
C1 [Schaefer, G. Owen] Univ Oxford St Cross Coll, Fac Philosophy, Oxford OX1 3LZ, England.
   [Schaefer, G. Owen; Wertheimer, Alan] NIH, Dept Bioeth, Ctr Clin, NIH, Bethesda, MD 20892 USA.
RP Schaefer, GO (reprint author), Univ Oxford St Cross Coll, Fac Philosophy, Oxford OX1 3LZ, England.
NR 25
TC 8
Z9 8
U1 0
U2 1
PU JOHNS HOPKINS UNIV PRESS
PI BALTIMORE
PA JOURNALS PUBLISHING DIVISION, 2715 NORTH CHARLES ST, BALTIMORE, MD
   21218-4363 USA
SN 1054-6863
J9 KENNEDY INST ETHIC J
JI Kennedy Inst. Ethics J.
PD DEC
PY 2010
VL 20
IS 4
BP 329
EP 352
PG 24
WC Ethics; Philosophy; Social Issues
SC Social Sciences - Other Topics; Philosophy; Social Issues
GA 712QU
UT WOS:000286682100002
PM 21338028
ER

PT J
AU Wendler, D
   Abdoler, E
AF Wendler, David
   Abdoler, Emily
TI Does it Matter Whether Investigators Intend to Benefit Research
   Subjects?
SO KENNEDY INSTITUTE OF ETHICS JOURNAL
LA English
DT Article
ID I CANCER TRIALS; INFORMED-CONSENT; CLINICAL-TRIALS; ONCOLOGY
AB There has been long-standing, albeit largely implicit, debate over whether investigator intentions are relevant to the ethical appropriateness of clinical research. Some commentators argue that whether investigators intend to collect generalizable knowledge or to benefit subjects is central to the ethics of clinical research. Others do not even mention investigator intentions when evaluating what makes clinical research ethical. To shed light on this debate, the present paper considers the reasons why investigator intentions might be ethically relevant. This analysis reveals that investigator intentions are related to, but distinct from three ethical requirements: whether subjects understand that they are contributing to a project to help others, whether the included interventions have an appropriate risk/benefit ratio, and whether subjects' interests are adequately protected. Provided these three requirements are satisfied, the ethical appropriateness of clinical research does not depend on what intentions investigators have in conducting it.
C1 [Wendler, David] NIH, Unit Vulnerable Populat, Dept Bioeth, Ctr Clin, Bethesda, MD 20892 USA.
   [Abdoler, Emily] Univ Michigan, Sch Med, Ann Arbor, MI 48109 USA.
RP Wendler, D (reprint author), NIH, Unit Vulnerable Populat, Dept Bioeth, Ctr Clin, Bldg 10, Bethesda, MD 20892 USA.
NR 23
TC 3
Z9 3
U1 0
U2 1
PU JOHNS HOPKINS UNIV PRESS
PI BALTIMORE
PA JOURNALS PUBLISHING DIVISION, 2715 NORTH CHARLES ST, BALTIMORE, MD
   21218-4363 USA
SN 1054-6863
J9 KENNEDY INST ETHIC J
JI Kennedy Inst. Ethics J.
PD DEC
PY 2010
VL 20
IS 4
BP 353
EP 370
PG 18
WC Ethics; Philosophy; Social Issues
SC Social Sciences - Other Topics; Philosophy; Social Issues
GA 712QU
UT WOS:000286682100003
PM 21338029
ER

PT J
AU Leelahavanichkul, A
   Yan, Q
   Hu, XZ
   Eisner, C
   Huang, YN
   Chen, R
   Mizel, D
   Zhou, H
   Wright, EC
   Kopp, JB
   Schnermann, J
   Yuen, PST
   Star, RA
AF Leelahavanichkul, Asada
   Yan, Qin
   Hu, Xuzhen
   Eisner, Christoph
   Huang, Yuning
   Chen, Richard
   Mizel, Diane
   Zhou, Hua
   Wright, Elizabeth C.
   Kopp, Jeffrey B.
   Schnermann, Juergen
   Yuen, Peter S. T.
   Star, Robert A.
TI Angiotensin II overcomes strain-dependent resistance of rapid CKD
   progression in a new remnant kidney mouse model
SO KIDNEY INTERNATIONAL
LA English
DT Article
DE angiotensin II; blood pressure; glomerulosclerosis; interstitial
   fibrosis; telemetry
ID CHRONIC-RENAL-FAILURE; FOCAL SEGMENTAL GLOMERULOSCLEROSIS;
   ARTERIAL-BLOOD-PRESSURE; LOW-BIRTH-WEIGHT; 9 GENE MYH9;
   CARDIAC-HYPERTROPHY; AFRICAN-AMERICANS; GROWTH-FACTOR;
   MOLECULAR-MECHANISMS; INDUCED HYPERTENSION
AB The remnant kidney model in C57BL/6 mice does not develop progressive chronic kidney disease (CKD). In this study we modified the model to mimic features of human CKD and to define accelerants of disease progression using three strains of mice. Following the procedure, there was a progressive increase in albuminuria, progressive loss in renal function, severe glomerulosclerosis and interstitial fibrosis, hypertension, cardiac fibrosis, and anemia by 4 weeks in CD-1 mice and by 12 weeks in 129S3 mice. In contrast, even after 16 weeks, the C57BL/6 mice with a remnant kidney had modestly increased albuminuria without increased blood pressure and without developing CKD or cardiac fibrosis. The baseline blood pressure, determined by radiotelemetry in conscious animals, correlated with CKD progression rates in each strain. Administering angiotensin II overcame the resistance of C57BL/6 mice to CKD following renal mass reduction, displaying high blood pressure and albuminuria, severe glomerulosclerosis, and loss of renal function by 4 weeks. Decreasing blood pressure with olmesartan, but not hydralazine, in CD-1 mice with a remnant kidney reduced CKD progression and cardiac fibrosis. C57BL/6 mice with a remnant kidney and DOCA-salt hypertension developed modest CKD. Each strain had similar degrees of interstitial fibrosis in three different normotensive models of renal fibrosis. Thus, reducing renal mass in CD-1 or 129S3 mice mimics many features of human CKD. Angiotensin II can convert the C57BL/6 strain from CKD resistant to susceptible in this disease model. Kidney International (2010) 78, 1136-1153; doi: 10.1038/ki.2010.287; published online 25 August 2010
C1 [Leelahavanichkul, Asada; Hu, Xuzhen; Zhou, Hua; Yuen, Peter S. T.; Star, Robert A.] NIDDKD, Renal Diagnost & Therapeut Unit, NIH, Bethesda, MD 20892 USA.
   [Leelahavanichkul, Asada; Yan, Qin; Hu, Xuzhen; Eisner, Christoph; Huang, Yuning; Mizel, Diane; Zhou, Hua; Kopp, Jeffrey B.; Schnermann, Juergen; Yuen, Peter S. T.; Star, Robert A.] NIDDKD, Kidney Dis Branch, NIH, Bethesda, MD 20892 USA.
   [Leelahavanichkul, Asada] Chulalongkorn Univ, Fac Grad Sch, Interdept Program BioMed Sci, Bangkok, Thailand.
RP Yuen, PST (reprint author), NIDDKD, Renal Diagnost & Therapeut Unit, NIH, Bldg 10,Room 3N108,10 Ctr Dr,MSC 1268, Bethesda, MD 20892 USA.
EM py@nih.gov
RI Yuen, Peter/B-1954-2008; 
OI Yuen, Peter/0000-0001-9557-3909; Kopp, Jeffrey/0000-0001-9052-186X
FU NIH, NIDDK
FX This research was supported by the Intramural Research Program of the
   NIH, NIDDK. We thank Kantima Leelahavanichkul for suggesting the cut
   kidney remnant ratio, Kent Doi for suggesting the chronic post-I/R
   model, Constance Noguchi for EPO advice, Talearnsak Kanjanabuch for
   technical advice on pathology scoring, Hiroshi Kajiyama for technical
   advice on NIH Image J, and Xiongce Zhao for advice on statistics.
NR 80
TC 36
Z9 36
U1 2
U2 4
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 0085-2538
J9 KIDNEY INT
JI Kidney Int.
PD DEC
PY 2010
VL 78
IS 11
BP 1136
EP 1153
DI 10.1038/ki.2010.287
PG 18
WC Urology & Nephrology
SC Urology & Nephrology
GA 679PM
UT WOS:000284173300013
PM 20736988
ER

PT J
AU Ren, RQ
   Willis, MS
   Fedoriw, Y
AF Ren, Rongqin
   Willis, Monte S.
   Fedoriw, Yuri
TI Episodic Fever and Neutropenia in a 22-Year-Old Male
SO LABMEDICINE
LA English
DT Editorial Material
DE Genetics; Hematology; Hematopathology; Clinical Pathology; Chemistry
ID SEVERE CONGENITAL NEUTROPENIA; UNFOLDED PROTEIN RESPONSE; ONSET CYCLIC
   NEUTROPENIA; BREAST-CANCER PATIENTS; X-LINKED NEUTROPENIA; INDUCED
   AGRANULOCYTOSIS; FOLLOW-UP; LEVAMISOLE; MUTATIONS; ELASTASE
C1 [Willis, Monte S.; Fedoriw, Yuri] Univ N Carolina, Dept Pathol & Lab Med, Chapel Hill, NC 27515 USA.
   [Ren, Rongqin] Natl Inst Environm Hlth Sci, Res Triangle Pk, NC USA.
RP Fedoriw, Y (reprint author), Univ N Carolina, Dept Pathol & Lab Med, Chapel Hill, NC 27515 USA.
NR 42
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC CLINICAL PATHOLOGY
PI CHICAGO
PA 2100 W HARRISON ST, CHICAGO, IL 60612 USA
SN 0007-5027
J9 LABMEDICINE
JI Labmedicine
PD DEC
PY 2010
VL 41
IS 12
BP 708
EP 712
DI 10.1309/LM6BB0G1VYT0SFNF
PG 5
WC Medical Laboratory Technology
SC Medical Laboratory Technology
GA 686FH
UT WOS:000284681700001
ER

PT J
AU Browne, SK
   Holland, SM
AF Browne, Sarah K.
   Holland, Steven M.
TI Anticytokine autoantibodies in infectious diseases: pathogenesis and
   mechanisms
SO LANCET INFECTIOUS DISEASES
LA English
DT Review
ID PULMONARY ALVEOLAR PROTEINOSIS; COLONY-STIMULATING FACTOR;
   MYASTHENIA-GRAVIS PATIENTS; CHRONIC MUCOCUTANEOUS CANDIDIASIS;
   ANTI-CYTOKINE AUTOANTIBODIES; SYSTEMIC-LUPUS-ERYTHEMATOSUS; HYPER-IGE
   SYNDROME; RED-CELL APLASIA; INTERFERON-GAMMA AUTOANTIBODY;
   RESPIRATORY-DISTRESS-SYNDROME
AB Autoantibodies to cytokines occur in many different conditions and situations and can cause a wide range of disease, including pulmonary alveolar proteinosis, disseminated non-tuberculous mycobacterial disease, pure red-cell aplasia, and chronic mucocutaneous candidiasis. Anticytokine autoantibodies may also develop against exogenously administered cytokines, sometimes diminishing their effects or inhibiting the activity of the endogenous cytokine. Unlike primary congenital immunodeficiencies, autoantibodies may develop over time, wax and wane, and may change in titre or avidity. Naturally occurring autoantibodies to interferons alpha, beta, and gamma, interleukins 1 alpha, 2, 6, and 10, tumour necrosis factor, and granulocyte-macrophage colony-stimulating factor have been reported in healthy individuals and have been identified in rheumatological diseases, graft-versus-host disease, and cancer. Therapeutic antibodies, growth factors, other biological agents, and cytokines used to treat acute, chronic, malignant, and immune diseases may elicit or overcome autoantibodies, hence influencing the primary intended therapy. The increasing number of biologically active anticytokine autoantibodies being reported suggests that currently "idiopathic" diseases may someday be explained by neutralising or agonising autoantibodies. Their protean roles in causing, treating, preventing, and responding to disease, as well as simply maintaining normal homoeostasis, offer fascinating insights into the biology of immunity, inflammation, and infection.
C1 [Browne, Sarah K.; Holland, Steven M.] NIAID, Lab Clin Infect Dis, NIH, Bethesda, MD 20892 USA.
RP Holland, SM (reprint author), B3-4141,MSC 1684, Bethesda, MD 20892 USA.
EM smh@nih.gov
FU Division of Intramural Research, National Institute of Allergy and
   Infectious Diseases, US National Institutes of Health
FX We would like to thank Thomas Fleisher for the thoughtful review and
   commentary he provided in creation of this Review. This work was
   supported by the Division of Intramural Research, National Institute of
   Allergy and Infectious Diseases, US National Institutes of Health.
NR 144
TC 39
Z9 42
U1 0
U2 4
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1473-3099
J9 LANCET INFECT DIS
JI Lancet Infect. Dis.
PD DEC
PY 2010
VL 10
IS 12
BP 875
EP 885
DI 10.1016/S1473-3099(10)70196-1
PG 11
WC Infectious Diseases
SC Infectious Diseases
GA 697QP
UT WOS:000285530600022
PM 21109174
ER

PT J
AU Fojo, T
   Wilkerson, J
AF Fojo, Tito
   Wilkerson, Julia
TI Bevacizumab and breast cancer the E2100 outlier
SO LANCET ONCOLOGY
LA English
DT Editorial Material
ID PROGRESSION-FREE-SURVIVAL; PACLITAXEL PLUS BEVACIZUMAB;
   DRUG-DEVELOPMENT; GOLD-STANDARD; GROWTH-FACTOR; SURROGATE
C1 [Fojo, Tito; Wilkerson, Julia] NCI, Med Oncol Branch, NIH, Bethesda, MD 20892 USA.
RP Fojo, T (reprint author), NCI, Med Oncol Branch, NIH, Bethesda, MD 20892 USA.
OI Wilkerson, Julia/0000-0002-6965-0867
NR 10
TC 12
Z9 12
U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1470-2045
J9 LANCET ONCOL
JI Lancet Oncol.
PD DEC
PY 2010
VL 11
IS 12
BP 1117
EP 1119
DI 10.1016/S1470-2045(10)70259-X
PG 3
WC Oncology
SC Oncology
GA 694TJ
UT WOS:000285321600008
PM 21126685
ER

PT J
AU Wilson, WH
   Connor, OAO
   Czuczman, MS
   LaCasce, AS
   Gerecitano, JF
   Leonard, JP
   Tulpule, A
   Dunleavy, K
   Xiong, H
   Chiu, YL
   Cui, Y
   Busman, T
   Elmore, SW
   Rosenberg, SH
   Krivoshik, AP
   Enschede, SH
   Humerickhouse, RA
AF Wilson, Wyndham H.
   Connor, Owen A. O.
   Czuczman, Myron S.
   LaCasce, Ann S.
   Gerecitano, John F.
   Leonard, John P.
   Tulpule, Anil
   Dunleavy, Kieron
   Xiong, Hao
   Chiu, Yi Lin
   Cui, Yue
   Busman, Todd
   Elmore, Steven W.
   Rosenberg, Saul H.
   Krivoshik, Andrew P.
   Enschede, Sari H.
   Humerickhouse, Rod A.
TI Navitoclax, a targeted high-affinity inhibitor of BCL-2, in lymphoid
   malignancies: a phase 1 dose-escalation study of safety,
   pharmacokinetics, pharmacodynamics, and antitumour activity
SO LANCET ONCOLOGY
LA English
DT Article
ID CHRONIC LYMPHOCYTIC-LEUKEMIA; NON-HODGKINS-LYMPHOMA; PAN-BCL-2 FAMILY
   ANTAGONIST; B-CELL LYMPHOMA; INTERNATIONAL WORKSHOP; OBATOCLAX GX15-070;
   SOLID TUMORS; PROTEIN; APOPTOSIS; DEATH
AB Background Proteins of the BCL 2 family regulate clonal selection and survival of lymphocytes, and are frequently overexpressed in lymphomas Navitoclax is a targeted high affinity small molecule that inhibits the anti apoptotic activity of BCL 2 and BCL XL We aimed to assess the safety and antitumour activity of navitoclax in patients with lymphoid tumours and establish the drug's pharmacokinetic and pharmacodynamic profiles
   Methods In this phase 1 dose escalation study patients (aged >= 18 years) with relapsed or refractory lymphoid malignancies were enrolled and treated at seven sites in the USA between November 2006 and November 2009 A modified Fibonacci 3+3 design was used to assign patients to receive oral navitoclax once daily by one of two dosing schedules intermittently for the first 14 days of a 21 day cycle (14/21) at doses of 10 20 40 80 110, 160, 225, 315 or 440 mg/day or continuously for 21 days of a 21 day cycle (21/21) at doses of 200, 275, 325 or 425 mg/day Study endpoints were safety, maximum tolerated dose, pharmacokinetic profile pharmacodynamic effects on platelets and T cells and antitumour activity This trial is registered with ClinicalTrials gov number NCT00406809
   Findings 55 patients were enrolled (median age 59 years IQR 51-67), 38 to receive the 14/21 dosing schedule and 17 to receive the 21/21 dosing schedule Common toxic effects included grade 1 or 2 anaemia (41 patients) infection (39) diarrhoea (31) nausea (29) and fatigue (21) and grade 3 or 4 thrombocytopenia (29) lymphocytopenia (18) and neutropenia (18) On the Intermittent 14/21 schedule, dose limiting toxic effects were hospital admissions for bronchitis (one) and pleural effusion (one) grade 3 increase in aminotransferases (one) grade 4 thrombocytopenia (one), and grade 3 cardiac arrhythmia (one) To reduce platelet nadir associated with intermittent 14/21 dosing we assessed a 150 mg/day lead in dose followed by a continuous 21/21 dosing schedule On the 21/21 dosing schedule two patients did not complete the first cycle and were excluded from assessment of dose-limiting toxic effects dose-limiting toxic effects were grade 4 thrombocytopenia (one), grade 3 increase m aminotransferases (one) and grade 3 gastrointestinal bleeding (one) Navitoclax showed a pharmacodynamic effect on circulating platelets and T cells Clinical responses occurred across the range of doses and in several tumour types Ten of 46 patients with assessable disease had a partial response and these responders had median progression free survival of 455 days (IQR 40-218)
   Interpretation Navitoclax has a novel mechanism of peripheral thrombocytopenia and T cell lymphopenia attributable to high affinity inhibition of BCL XL and BCL 2 respectively On the basis of these findings a 150 mg 7 day lead in dose followed by a 325 mg dose administered on a continuous 21/21 dosing schedule was selected for phase 2 study
C1 [Wilson, Wyndham H.] NCI, Lymphoma Therapeut Sect, Metab Branch, Ctr Canc Res,NIH, Bethesda, MD 20892 USA.
   [Connor, Owen A. O.] NYU Langone Med Ctr, NYU Canc Inst, New York, NY USA.
   [Czuczman, Myron S.] Roswell Pk Canc Inst, Buffalo, NY 14263 USA.
   [LaCasce, Ann S.] Dana Farber Canc Inst, Boston, MA 02115 USA.
   [Gerecitano, John F.] Mem Sloan Kettering Canc Ctr, New York, NY 10021 USA.
   [Leonard, John P.] Cornell Univ, New York, NY 10021 USA.
   [Tulpule, Anil] Univ So Calif, Los Angeles, CA USA.
   [Xiong, Hao; Chiu, Yi Lin; Cui, Yue; Busman, Todd; Elmore, Steven W.; Rosenberg, Saul H.; Krivoshik, Andrew P.; Enschede, Sari H.; Humerickhouse, Rod A.] Abbott Labs, Abbott Pk, IL 60064 USA.
RP Wilson, WH (reprint author), NCI, Lymphoma Therapeut Sect, Metab Branch, Ctr Canc Res,NIH, Bethesda, MD 20892 USA.
RI Jones, Jeffrey/E-9827-2013
FU Abbott Laboratories; Genentech; National Cancer Institute National
   Institutes of Health
FX Abbott Laboratories Genentech and National Cancer Institute National
   Institutes of Health
NR 38
TC 272
Z9 275
U1 4
U2 19
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1470-2045
J9 LANCET ONCOL
JI Lancet Oncol.
PD DEC
PY 2010
VL 11
IS 12
BP 1149
EP 1159
DI 10.1016/S1470.2045(10)70261.8
PG 11
WC Oncology
SC Oncology
GA 694TJ
UT WOS:000285321600018
PM 21094089
ER

PT J
AU Zhao, FH
   Lin, MJ
   Chen, F
   Hu, SY
   Zhang, R
   Belinson, JL
   Sellors, JW
   Franceschi, S
   Qiao, YL
   Castle, PE
AF Zhao, Fang Hui
   Lin, Margaret Jane
   Chen, Feng
   Hu, Shang Ying
   Zhang, Rong
   Belinson, Jerome L.
   Sellors, John W.
   Franceschi, Silvia
   Qiao, You Lin
   Castle, Philip E.
CA Cervical Canc Screening Grp China
TI Performance of high-risk human papillomavirus DNA testing as a primary
   screen for cervical cancer: a pooled analysis of individual patient data
   from 17 population-based studies from China
SO LANCET ONCOLOGY
LA English
DT Article
ID REPUBLIC-OF-CHINA; SHANXI PROVINCE; RURAL CHINA; CONVENTIONAL CYTOLOGY;
   VISUAL INSPECTION; ACETIC-ACID; ACCURACY; TRIAL; SPECIFICITY;
   SENSITIVITY
AB Background Controversy remains over whether high risk human papillomavirus (HPV) DNA testing should be used as a primary screen for cervical cancer The aims of our study were to assess whether HPV DNA testing could be applied to cervical cancer screening programmes in China as well as other similar developing countries
   Methods We did a pooled analysis of population based cervical cancer screening studies done in mainland China from 1999 to 2008 with concurrent HPV DNA testing (Hybrid Capture 2 assay Qiagen, Gaithersburg MD USA) liquid based cytology (LBC), and visual inspection with acetic acid (VIA) Eligible women were sexually active not pregnant had an Intact uterus and had no history of cervical intraepithelial neoplasia (CIN) cervical cancer or pelvic irradiation All women positive for any test were referred for colposcopy and biopsy Cervical lesions were diagnosed by directed or random biopsy We assessed the diagnostic accuracy of HPV DNA testing for the detection of CIN grade 3 or greater
   Findings 30371 women from 17 cross sectional population based studies m various parts of China were screened 1523 women were subsequently excluded because of inadequate HPV DNA specimens or they did not have a biopsy taken which included women with atypical squamous cells of undetermined significance, low grade squamous intraepithelial lesion or worse positive HPV negative cytology and missing or positive colposcopy results and unsatisfactory cytology results HPV DNA testing had a higher sensitivity of 97 5% (95% CI 95 7-98 7) for detection of CIN grade 3 or worse and a lower specificity of 85 1% (82 3-87 9) compared with cytology (sensitivity 87 9% [95% CI 84 7-90 7], specificity 94 7% [93 5-96 0]) and VIA (54 6% [48 0-61 2] 89 9% [86 8-93 0]) Sensitivity did not vary by study or age (<35 years 35-49 years >= 50 years) however specificity did vary with age (p<0 0001) and was highest in women younger than 35 years (89 4% 95% CI 86 1-91 5) An increase in the positive cutoff point from the manufacturer recommended 1 pg/mL to 2 pg/mL led to a decrease m the overall HPV DNA positivity from 16 3% to 13 9% (p<0 0001) which could result m a decrease in referral rates although sensitivity was slightly lower (97 5% to 95 2%) An increase in the cutoff point to 10 pg/mL m women younger than 35 years maintained a high sensitivity 97 7% (95% CI 87 7-99 9) and increased specificity to 93 5% (95% CI 91 9-94 6)
   Interpretation HPV DNA testing is highly sensitive and moderately specific for CIN grade 3 or worse with consistent results across study sites and age groups-including women younger than 35 years A rise in the cutoff point might be beneficial for future screening programmes in China especially when screening women younger than 35 years
C1 [Zhao, Fang Hui; Chen, Feng; Hu, Shang Ying; Zhang, Rong; Qiao, You Lin] Chinese Acad Med Sci, Peking Union Med Coll, Canc Inst & Hosp, Beijing 100037, Peoples R China.
   [Lin, Margaret Jane] Washington Univ, Sch Med, St Louis, MO USA.
   [Belinson, Jerome L.] Prevent Oncol Int Inc, Cleveland, OH USA.
   [Belinson, Jerome L.] Cleveland Clin, Cleveland, OH 44106 USA.
   [Sellors, John W.] McMaster Univ, Hamilton, ON, Canada.
   [Franceschi, Silvia] Int Agcy Res Canc, F-69372 Lyon, France.
   [Castle, Philip E.] NCI, NIH, Bethesda, MD 20892 USA.
RP Qiao, YL (reprint author), 17 S Panjiayuan Lane,POB 2258, Beijing 100021, Peoples R China.
RI Qiao, You-Lin/B-4139-2012
OI Qiao, You-Lin/0000-0001-6380-0871
FU Fogarty International Center, US National Institutes of Health; Beijing
   Municipal Commission of Education [XK100230447]; Cancer Institute and
   Hospital of the Chinese Academy of Medical Sciences; CICAMS [JK2007]
FX Fogarty International Clinical Research Scholars Program (Fogarty
   International Center, US National Institutes of Health through the
   International Clinical Research Fellows Program at Vanderbilt
   University) Academic Capacity Development Program of the Beijing
   Municipal Commission of Education and Cancer Institute and Hospital of
   the Chinese Academy of Medical Sciences; This study was funded the
   Fogarty International Clinical Research Scholars Program (Fogarty
   International Center US National Institutes of Health through the
   International Clinical Research Fellows Program at Vanderbilt
   University) the Academic Capacity Development Program of the Beijing
   Municipal Commission of Education grant (No XK100230447) and CICAMS
   research grant (No JK2007) We thank the local doctors and the women who
   participated m our study from Beijing Gansu Guangdong Jiangsu Jiangxi
   Henan Shanghai Shanxi and Xinjiang as well as the Bill & Melinda Gates
   Foundation the International Agency for Research on Cancer and the
   Cleveland Clinic for their generous support
NR 41
TC 66
Z9 88
U1 0
U2 16
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1470-2045
J9 LANCET ONCOL
JI Lancet Oncol.
PD DEC
PY 2010
VL 11
IS 12
BP 1160
EP 1171
DI 10.1016/S1470.2045(10)70256.4
PG 12
WC Oncology
SC Oncology
GA 694TJ
UT WOS:000285321600019
PM 21075054
ER

PT J
AU Estvold, SK
   Mordini, F
   Zhou, YF
   Yu, ZX
   Sachdev, V
   Arai, A
   Horvath, KA
AF Estvold, Soren K.
   Mordini, Frederico
   Zhou, Yifu
   Yu, Zu X.
   Sachdev, Vandana
   Arai, Andrew
   Horvath, Keith A.
TI Does Laser Type Impact Myocardial Function Following Transmyocardial
   Laser Revascularization?
SO LASERS IN SURGERY AND MEDICINE
LA English
DT Article
DE CO(2) laser; Ho:YAG laser; myocardial function; laser-tissue interaction
ID REFRACTORY ANGINA-PECTORIS; RANDOMIZED-TRIAL; MEDICAL THERAPY; HOLMIUM;
   CO2; CO2-LASER; HEART
AB Background: Transmyocardial laser revascularization (TMR) is currently clinically performed with either a CO(2) or Ho:YAG laser for the treatment of severe angina. While both lasers provide symptomatic relief, there are significant differences in the laser-tissue interactions specific to each device that may impact their ability to enhance the perfusion of myocardium and thereby improve contractile function of the ischemic heart.
   Methods: A porcine model of chronic myocardial ischemia was employed. After collecting baseline functional data with cine magnetic resonance imaging (MRI) and dobutamine stress echo (DSE), 14 animals underwent TMR with either a CO(2) or Ho: YAG laser. Transmural channels were created with each laser in a distribution of 1/cm(2) in the ischemic zone. Six weeks post-treatment repeat MRI as well as DSE were obtained after which the animals were sacrificed. Histology was preformed to characterize the laser-tissue interaction.
   Results: CO(2) TMRled to improvement in wall thickening in the ischemic area as seen with cine MRI(40.3% vs. baseline, P < 0.05) and DSE (20.2% increase vs. baseline, P < 0.05). Ho: YAG treated animals had no improvement in wall thickening by MRI (-11.6% vs. baseline, P = .67) and DSE ( 16.7% vs. baseline, P = 0.08). Correlative semi-quantitative histology revealed a significantly higher fibrosis index in Ho: YAG treated myocardium versus CO(2) (1.81 vs. 0.083, P < 0.05).
   Conclusions: In a side-by-side comparison CO(2) TMR resulted in improved function of ischemic myocardium as assessed by MRI and echocardiography. Ho:YAG TMRled to no improvement in regional function likely due to concomitant increase in fibrosis in the lasered area. Lasers Surg. Med. 42:746-751, 2010. (C) 2010 Wiley-Liss, Inc.
C1 [Horvath, Keith A.] NHLBI, Cardiothorac Surg Res Program, NIH, Magnuson Clin Ctr, Bethesda, MD 20892 USA.
RP Horvath, KA (reprint author), NHLBI, Cardiothorac Surg Res Program, NIH, Magnuson Clin Ctr, Bldg 10,B1D47,10 Ctr Dr,MSC 1550, Bethesda, MD 20892 USA.
EM horvathka@mail.nih.gov
FU Division of Intramural Research; National Heart, Lung and Blood
   Institute, NIH, Bethesda, MD
FX Contract grant sponsor: Division of Intramural Research; Contract grant
   sponsor: National Heart, Lung and Blood Institute, NIH, Bethesda, MD.
NR 24
TC 4
Z9 5
U1 0
U2 1
PU WILEY-BLACKWELL PUBLISHING, INC
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0196-8092
J9 LASER SURG MED
JI Lasers Surg. Med.
PD DEC
PY 2010
VL 42
IS 10
BP 746
EP 751
DI 10.1002/lsm..21012
PG 6
WC Dermatology; Surgery
SC Dermatology; Surgery
GA 709LS
UT WOS:000286440100007
PM 21246579
ER

PT J
AU Zuurbier, L
   Homminga, I
   Calvert, V
   Winkel, MLT
   Buijs-Gladdines, JGCAM
   Kooi, C
   Smits, WK
   Sonneveld, E
   Veerman, AJP
   Kamps, WA
   Horstmann, M
   Petricoin, EF
   Pieters, R
   Meijerink, JPP
AF Zuurbier, L.
   Homminga, I.
   Calvert, V.
   Winkel, M. L. Te
   Buijs-Gladdines, J. G. C. A. M.
   Kooi, C.
   Smits, W. K.
   Sonneveld, E.
   Veerman, A. J. P.
   Kamps, W. A.
   Horstmann, M.
   Petricoin, E. F., III
   Pieters, R.
   Meijerink, J. P. P.
TI NOTCH1 and/or FBXW7 mutations predict for initial good prednisone
   response but not for improved outcome in pediatric T-cell acute
   lymphoblastic leukemia patients treated on DCOG or COALL protocols
SO LEUKEMIA
LA English
DT Article
DE pediatric T-ALL; NOTCH1; FBXW7; TLX3; prednisone response; outcome
AB Aberrant activation of the NOTCH1 pathway by inactivating and activating mutations in NOTCH1 or FBXW7 is a frequent phenomenon in T-cell acute lymphoblastic leukemia (T-ALL). We retrospectively investigated the relevance of NOTCH1/FBXW7 mutations for pediatric T-ALL patients enrolled on Dutch Childhood Oncology Group (DCOG) ALL7/8 or ALL9 or the German Co-Operative Study Group for Childhood Acute Lymphoblastic Leukemia study (COALL-97) protocols. NOTCH1-activating mutations were identified in 63% of patients. NOTCH1 mutations affected the heterodimerization, the juxtamembrane and/or the PEST domains, but not the RBP-J-kappa-associated module, the ankyrin repeats or the transactivation domain. Reverse-phase protein microarray data confirmed that NOTCH1 and FBXW7 mutations resulted in increased intracellular NOTCH1 levels in primary T-ALL biopsies. Based on microarray expression analysis, NOTCH1/FBXW7 mutations were associated with activation of NOTCH1 direct target genes including HES1, DTX1, NOTCH3, PTCRA but not cMYC. NOTCH1/FBXW7 mutations were associated with TLX3 rearrangements, but were less frequently identified in TAL1- or LMO2-rearranged cases. NOTCH1-activating mutations were less frequently associated with mature T-cell developmental stage. Mutations were associated with a good initial in vivo prednisone response, but were not associated with a superior outcome in the DCOG and COALL cohorts. Comparing our data with other studies, we conclude that the prognostic significance for NOTCH1/FBXW7 mutations is not consistent and may depend on the treatment protocol given. Leukemia (2010) 24, 2014-2022; doi:10.1038/leu.2010.204; published online 23 September 2010
C1 [Meijerink, J. P. P.] Erasmus Univ, Sophia Childrens Hosp, Dept Pediat Oncol Hematol, Med Ctr,ZH, NL-3015 GJ Rotterdam, Netherlands.
   [Calvert, V.; Petricoin, E. F., III] George Mason Univ, Ctr Appl Prote & Mol Med, Manassas, VA USA.
   [Sonneveld, E.; Veerman, A. J. P.; Kamps, W. A.] Dutch Childhood Oncol Grp, The Hague, Netherlands.
   [Kamps, W. A.] Univ Groningen, Univ Med Ctr Groningen, Beatrix Childrens Hosp, Dept Pediat Oncol, Groningen, Netherlands.
   [Horstmann, M.] German Cooperat Study Grp Childhood Acute Lymphob, Hamburg, Germany.
   [Horstmann, M.] Univ Med Ctr Hamburg Eppendorf, Res Inst Childrens Canc Ctr Hamburg, Clin Pediat Hematol & Oncol, Hamburg, Germany.
   [Petricoin, E. F., III] NCI, FDA Clin Prote Program, US FDA, Bethesda, MD USA.
RP Meijerink, JPP (reprint author), Erasmus Univ, Sophia Childrens Hosp, Dept Pediat Oncol Hematol, Med Ctr,ZH, Room Sp2456,Dr Molewaterpl 60, NL-3015 GJ Rotterdam, Netherlands.
EM j.meijerink@erasmusmc.nl
RI Meijerink, Jules/D-4393-2017
OI Meijerink, Jules/0000-0002-6860-798X
FU Stichting Kinderen Kankervrij (KiKa) [KiKa 2007-012, KiKa 2008-029];
   Dutch Cancer Society Dutch Cancer Society (KWF-EMCR) [2006-3500]; German
   Jose Carreras Leukemia Foundation [SP 04/03]
FX LZ and WKS were financed by the Stichting Kinderen Kankervrij (KiKa;
   Grant no. KiKa 2007-012). IH was financed by the Dutch Cancer Society
   Dutch Cancer Society (KWF-EMCR 2006-3500) CK was financed by KiKa (Grant
   no. KiKa 2008-029). We thank the German Jose Carreras Leukemia
   Foundation (Grant no. SP 04/03 to MH).
NR 44
TC 64
Z9 66
U1 0
U2 6
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0887-6924
EI 1476-5551
J9 LEUKEMIA
JI Leukemia
PD DEC
PY 2010
VL 24
IS 12
BP 2014
EP 2022
DI 10.1038/leu.2010.204
PG 9
WC Oncology; Hematology
SC Oncology; Hematology
GA 695OF
UT WOS:000285380900005
PM 20861909
ER

PT J
AU Parks, CG
   Biagini, RE
   Cooper, GS
   Gilkeson, GS
   Dooley, MA
AF Parks, C. G.
   Biagini, R. E.
   Cooper, G. S.
   Gilkeson, G. S.
   Dooley, M. A.
TI Total serum IgE levels in systemic lupus erythematosus and associations
   with childhood onset allergies
SO LUPUS
LA English
DT Article
DE allergy; atopy; autoantibodies; autoimmunity; hygiene hypothesis;
   immunoglobulins; nephritis; population-based; systemic lupus
   erythematosus
ID IMMUNOGLOBULIN-E LEVELS; C-REACTIVE PROTEIN; VITAMIN-D;
   AUTOIMMUNE-DISEASES; HYGIENE HYPOTHESIS; ATOPIC DISORDERS; RISK-FACTORS;
   EARLY-LIFE; POPULATION; ASTHMA
AB Elevated serum IgE has been described in systemic lupus erythematosus (SLE), but associations with disease risk and characteristics remain unresolved. We assessed total serum IgE levels and atopy (IgE > 100 IU/ml) in recently diagnosed SLE patients (n = 228) compared with population controls (n = 293) and in relation to disease activity, autoantibodies, clinical features, total immunoglobulins, C-reactive protein, and allergy history. Multivariate models estimated determinants of IgE and atopy in patients and controls, and associations of SLE with allergy and atopy. Total IgE levels were higher in patients than controls (median = 42 vs. 29 IU/ml); 32% of patients and 25% of controls were atopic (p = 0.06). IgE levels were significantly higher in non-Whites and patients reporting childhood onset (< 18 years) asthma and hives, and in controls reporting childhood asthma, hay fever, eczema, and adult onset hives. After accounting for racial differences, atopy was not associated with SLE, nephritis, or other clinical and laboratory parameters. In sum, our findings provide limited evidence of a direct association between total serum IgE and SLE overall or with other disease characteristics after adjusting for demographic characteristics and allergy history. Future studies may want to explore potentially shared risk factors for development of allergy, atopy, and SLE. Lupus (2010) 19, 1614-1622.
C1 [Parks, C. G.] NIEHS, Epidemiol Branch, NIH, Dept Hlth & Human Serv, Durham, NC USA.
   [Biagini, R. E.] NIOSH, Ctr Dis Control & Prevent, Dept Hlth & Human Serv, Cincinnati, OH 45226 USA.
   [Cooper, G. S.] US EPA, Washington, DC 20460 USA.
   [Gilkeson, G. S.] Med Univ S Carolina, Charleston, SC 29425 USA.
   [Dooley, M. A.] Univ N Carolina, Div Rheumatol, Chapel Hill, NC USA.
RP Parks, CG (reprint author), NIEHS, Epidemiol Branch, A3-05,POB 12233, Res Triangle Pk, NC 27599 USA.
EM Parks1@mail.nih.gov
OI Parks, Christine/0000-0002-5734-3456
FU NIH; National Institute of Environmental Health Sciences; National
   Institute for Occupational Safety and Health; NIOSH [Y1-ES-0001-Clinical
   Immunotoxicity]; National Institute of Environmental Health Sciences
   (NIEHS) [Y1-ES-0001-Clinical Immunotoxicity]
FX This work was supported in part by the intramural research program of
   the NIH, National Institute of Environmental Health Sciences, by the
   National Institute for Occupational Safety and Health, and by an
   interagency agreement between NIOSH and National Institute of
   Environmental Health Sciences (NIEHS) (grant number Y1-ES-0001-Clinical
   Immunotoxicity).
NR 48
TC 12
Z9 12
U1 0
U2 0
PU SAGE PUBLICATIONS LTD
PI LONDON
PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND
SN 0961-2033
J9 LUPUS
JI Lupus
PD DEC
PY 2010
VL 19
IS 14
BP 1614
EP 1622
DI 10.1177/0961203310379870
PG 9
WC Rheumatology
SC Rheumatology
GA 685IA
UT WOS:000284621200005
PM 20937624
ER

PT J
AU Lu, HB
   Leoni, R
   Silva, AC
   Stein, EA
   Yang, YH
AF Lu, Hanbing
   Leoni, Renata
   Silva, Afonso C.
   Stein, Elliot A.
   Yang, Yihong
TI High-Field Continuous Arterial Spin Labeling with Long Labeling
   Duration: Reduced Confounds from Blood Transit Time and Postlabeling
   Delay
SO MAGNETIC RESONANCE IN MEDICINE
LA English
DT Article
DE perfusion; blood transit time; brain; cerebral blood flow
ID RAT-BRAIN PERFUSION; FAIR TECHNIQUE; QUIPSS II; FLOW; WATER; MRI;
   STIMULATION; INVERSION; QUANTIFICATION; SATURATION
AB In quantitative perfusion imaging using arterial spin labeling, variable blood transit times and postlabeling delays are two confounding factors that may compromise the accuracy of perfusion quantifications. In this study, theoretical analyses and experimental data at 9.4 T demonstrate that increasing labeling duration not only enhances the contrast of the arterial spin labeling signal but also minimizes the effect of variable postlabeling delays in multislice arterial spin labeling acquisitions. With a labeling duration of 6.4 sec, arterial spin labeling signal acquired in multislice mode (11 slices) is very similar to that acquired in single-slice mode. Previous studies have shown that inserting a delay between the spin labeling pulse and the image acquisition pulse could reduce confounds resulting from variable blood transit times at the expense of arterial spin labeling sensitivity. Our simulations suggest that enhancing the contrast of arterial spin labeling signal offers the opportunity for extending the postlabeling delay to a longer duration, minimizing systematic errors associated with a wide range of blood transit times, which could have significant implications for applying arterial spin labeling techniques to perfusion imaging of pathological conditions in animal models. Magn Reson Med 64:1557-1566, 2010. (C) 2010 Wiley-Liss, Inc.
C1 [Lu, Hanbing; Stein, Elliot A.; Yang, Yihong] Natl Inst Drug Abuse, Neuroimaging Res Branch, Intramural Res Programs, NIH, Baltimore, MD 21224 USA.
   [Leoni, Renata; Silva, Afonso C.] Natl Inst Neurol Disorders & Stroke, Cerebral Microcirculat Unit, Intramural Res Programs, NIH, Baltimore, MD USA.
RP Lu, HB (reprint author), Natl Inst Drug Abuse, Neuroimaging Res Branch, Intramural Res Programs, NIH, 251 Bayview Blvd,Suite 200, Baltimore, MD 21224 USA.
EM luha@intra.nida.nih.gov
RI Leoni, Renata/J-3182-2012
OI Leoni, Renata/0000-0002-4568-0746
FU National Institute on Drug Abuse; National Institute of Neurological
   Disorders and Stroke; National Institutes of Health
FX Grant sponsors: Intramural Research Programs of the National Institute
   on Drug Abuse, The National Institute of Neurological Disorders and
   Stroke, National Institutes of Health.
NR 41
TC 7
Z9 7
U1 1
U2 6
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0740-3194
J9 MAGN RESON MED
JI Magn. Reson. Med.
PD DEC
PY 2010
VL 64
IS 6
BP 1557
EP 1566
DI 10.1002/mrm.22576
PG 10
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA 685WR
UT WOS:000284659300003
PM 20715292
ER

PT J
AU Derbyshire, JA
   Herzka, DA
   McVeigh, ER
   Lederman, RJ
AF Derbyshire, J. Andrew
   Herzka, Daniel A.
   McVeigh, Elliot R.
   Lederman, Robert J.
TI Efficient Implementation of Hardware-Optimized Gradient Sequences for
   Real-Time Imaging
SO MAGNETIC RESONANCE IN MEDICINE
LA English
DT Article
DE MRI; hardware-optimized; gradient; waveform; realtime; imaging; FISP;
   bSSFP
ID PULSE SEQUENCES; OBLIQUE PLANES; DEAD-PERIODS; MRI
AB This work improves the performance of interactive real-time imaging with balanced steady-state free precession. The method employs hardware-optimized gradient pulses, together with a novel phase-encoding strategy that simplifies the design and implementation of the optimized gradient waveforms. In particular, the waveforms for intermediate phase-encode steps are obtained by simple linear combination, rather than separate optimized waveform calculations. Gradient waveforms are redesigned in real time as the scan plane is manipulated, and the resulting sequence operates at the specified limits of the MRI gradient subsystem for each new scan-plane orientation. The implementation provides 14-25% improvement in the sequence pulse repetition time over the vendor-supplied interactive real-time imaging sequence for similar scan parameters on our MRI scanner. Magn Reson Med 64:1814-1820, 2010. (C) 2010 Wiley-Liss, Inc.
C1 [Derbyshire, J. Andrew; Herzka, Daniel A.; McVeigh, Elliot R.; Lederman, Robert J.] NHLBI, Translat Med Branch, Div Intramural Res, NIH,DHHS, Bethesda, MD 20892 USA.
   [Herzka, Daniel A.; McVeigh, Elliot R.] Johns Hopkins Univ, Sch Med, Dept Biomed Engn, Baltimore, MD 21205 USA.
RP Derbyshire, JA (reprint author), NHLBI, Translat Med Branch, Div Intramural Res, NIH,DHHS, Bldg 10,Room B1D416, Bethesda, MD 20892 USA.
EM jad11@nih.gov
OI lederman, robert/0000-0003-1202-6673; Herzka, Daniel/0000-0002-9400-7814
FU Intramural NIH HHS [ZIA HL006039-01, ZIA HL005062-08]
NR 10
TC 2
Z9 2
U1 0
U2 0
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0740-3194
J9 MAGN RESON MED
JI Magn. Reson. Med.
PD DEC
PY 2010
VL 64
IS 6
BP 1814
EP 1820
DI 10.1002/mrm.22211
PG 7
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA 685WR
UT WOS:000284659300031
PM 20878764
ER

PT J
AU Owen, N
   Sparling, PB
   Healy, GN
   Dunstan, DW
   Matthews, CE
AF Owen, Neville
   Sparling, Phillip B.
   Healy, Genevieve N.
   Dunstan, David W.
   Matthews, Charles E.
TI Sedentary Behavior: Emerging Evidence for a New Health Risk
SO MAYO CLINIC PROCEEDINGS
LA English
DT Editorial Material
ID AMERICAN-HEART-ASSOCIATION; TELEVISION VIEWING TIME; PHYSICAL-ACTIVITY;
   LIFE-STYLE; CARDIOVASCULAR-DISEASE; PLASMA-GLUCOSE; METABOLIC RISK;
   SITTING TIME; OBESITY; ADULTS
C1 [Sparling, Phillip B.] Georgia Inst Technol, Sch Appl Physiol, Atlanta, GA 30332 USA.
   [Owen, Neville; Healy, Genevieve N.] Univ Queensland, Sch Populat Hlth, Canc Prevent Res Ctr, Herston, Qld, Australia.
   [Matthews, Charles E.] NCI, Div Canc Epidemiol & Genet, Nutr Epidemiol Branch, Rockville, MD USA.
RP Sparling, PB (reprint author), Georgia Inst Technol, Sch Appl Physiol, Atlanta, GA 30332 USA.
EM phil.sparling@gatech.edu
RI Healy, Genevieve/A-7408-2008; Owen, Neville/K-5986-2012; matthews,
   Charles/E-8073-2015; Dunstan, David/E-8473-2010; 
OI Healy, Genevieve/0000-0001-7093-7892; matthews,
   Charles/0000-0001-8037-3103; Dunstan, David/0000-0003-2629-9568; Owen,
   Neville/0000-0003-2784-4820
NR 27
TC 140
Z9 141
U1 1
U2 34
PU MAYO CLINIC PROCEEDINGS
PI ROCHESTER
PA 660 SIEBENS BLDG MAYO CLINIC, ROCHESTER, MN 55905 USA
SN 0025-6196
J9 MAYO CLIN PROC
JI Mayo Clin. Proc.
PD DEC
PY 2010
VL 85
IS 12
BP 1138
EP 1141
DI 10.4065/mcp.2010.0444
PG 4
WC Medicine, General & Internal
SC General & Internal Medicine
GA 694HA
UT WOS:000285284400010
PM 21123641
ER

PT J
AU Chien, AT
   Kirchhoff, AC
   Schaefer, CT
   Huang, ES
   Brown, SES
   Heuer, L
   Graber, J
   Tang, H
   Casalino, LP
   Chin, MH
AF Chien, Alyna T.
   Kirchhoff, Anne C.
   Schaefer, Cynthia T.
   Huang, Elbert S.
   Brown, Sydney E. S.
   Heuer, Loretta
   Graber, Jessica
   Tang, Hui
   Casalino, Lawrence P.
   Chin, Marshall H.
TI Positive and Negative Spillovers of the Health Disparities
   Collaboratives in Federally Qualified Health Centers Staff Perceptions
SO MEDICAL CARE
LA English
DT Article
DE quality; quality improvement; federally qualified health centers; cost
ID UNINTENDED CONSEQUENCES; DIABETES CARE; QUALITY
AB Introduction: Quality improvement (QI) interventions are usually evaluated for their intended effect; little is known about whether they generate significant positive or negative spillovers.
   Methods: We mailed a 39-item self-administered survey to the 1256 staff at 135 federally qualified health centers (FQHC) implementing the Health Disparities Collaboratives (HDC), a large-scale QI collaborative intervention. We asked about the extent to which the HDC yielded improvements or detriments beyond its condition(s) of focus, particularly for non-HDC aspects of patient care and FQHC function.
   Results: Response rate was 68.7%. The HDC was perceived to improve non-HDC patient care and general FQHC functioning more often than it was regarded as diminishing them. In all, 45% of respondents indicated that the HDC improved the quality of care for chronic conditions not being emphasized by the HDC; 5% responded that the HDC diminished that quality. Seventy-five percent stated that the HDC improved care provided to patients with multiple chronic conditions; 4% signified that the HDC diminished it. Fifty-five percent of respondents indicated that the HDC improved their FQHC's ability to move patients through their center, and 80% indicated that the HDC improved their FQHC's QI plan as a whole; 8% and 2% indicated that the HDC diminished these, respectively.
   Discussion: On balance, the HDC was perceived to yield more positive spillovers than negative ones. This QI intervention appears to have generated effects beyond its condition of focus; QI's unintended effects should be included in evaluations to develop a better understanding of QI's net impact.
C1 [Chien, Alyna T.] Harvard Univ, Div Gen Pediat, Childrens Hosp Boston, Dept Pediat,Sch Med, Boston, MA 02115 USA.
   [Kirchhoff, Anne C.] Univ Washington, Sch Publ Hlth, Dept Hlth Serv, Seattle, WA 98195 USA.
   [Kirchhoff, Anne C.] Fred Hutchinson Canc Res Ctr, Div Clin Res, Seattle, WA 98104 USA.
   [Schaefer, Cynthia T.; Heuer, Loretta] MidWest Clinicians Network Inc, Lansing, MI USA.
   [Schaefer, Cynthia T.; Huang, Elbert S.; Heuer, Loretta; Tang, Hui; Chin, Marshall H.] Univ Chicago, Ctr Diabet Res & Training, Chicago, IL 60637 USA.
   [Schaefer, Cynthia T.] Univ Evansville, Dunigan Family Dept Nursing & Hlth Sci, Evansville, IN USA.
   [Huang, Elbert S.; Tang, Hui; Chin, Marshall H.] Univ Chicago, Dept Med, Gen Internal Med Sect, Chicago, IL 60637 USA.
   [Huang, Elbert S.; Chin, Marshall H.] Univ Chicago, Ctr Hlth & Social Sci, Chicago, IL 60637 USA.
   [Brown, Sydney E. S.] Univ Penn, Ctr Biostat & Epidemiol, Philadelphia, PA 19104 USA.
   [Heuer, Loretta] N Dakota State Univ, Coll Pharm Nursing & Allied Sci, Fargo, ND 58105 USA.
   [Graber, Jessica] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Natl Childrens Study, Bethesda, MD USA.
   [Casalino, Lawrence P.] Weill Cornell Med Coll, Dept Publ Hlth, Div Outcomes & Effectiveness Res, New York, NY USA.
RP Chien, AT (reprint author), Harvard Univ, Div Gen Pediat, Childrens Hosp Boston, Dept Pediat,Sch Med, 21 Autumn St,Room 223, Boston, MA 02115 USA.
EM alyna.chien@childrens.harvard.edu
FU Agency for Healthcare Research and Quality [1 U01 HS13635, R01 HS10479,
   K08 HS017146]; Health Resources and Services Administration [1 U01
   HS13635]; National Institute of Diabetes and Digestive and Kidney
   Diseases Diabetes Research and Training Center [P60 DK20595]; Robert
   Wood Johnson Clinical Scholars Program; National Institute of Diabetes
   and Digestive and Kidney Diseases [K24 DK071933]
FX Supported by the Agency for Healthcare Research and Quality, with
   support from the Health Resources and Services Administration (grant 1
   U01 HS13635). Additional support came from the Agency for Healthcare
   Research and Quality (R01 HS10479), and the National Institute of
   Diabetes and Digestive and Kidney Diseases Diabetes Research and
   Training Center (P60 DK20595). Also supported by the Robert Wood Johnson
   Clinical Scholars Program and the Agency for Healthcare Research and
   Quality (K08 HS017146) (to A.T.C.), and by a Midcareer Investigator
   Award in Patient-Oriented Research from the National Institute of
   Diabetes and Digestive and Kidney Diseases (K24 DK071933) (to M.H.C.).
NR 18
TC 6
Z9 6
U1 2
U2 10
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0025-7079
J9 MED CARE
JI Med. Care
PD DEC
PY 2010
VL 48
IS 12
BP 1050
EP 1056
DI 10.1097/MLR.0b013e3181f37d46
PG 7
WC Health Care Sciences & Services; Health Policy & Services; Public,
   Environmental & Occupational Health
SC Health Care Sciences & Services; Public, Environmental & Occupational
   Health
GA 682DN
UT WOS:000284380200002
PM 20966782
ER

PT J
AU Pourat, N
   Kagawa-Singer, M
   Breen, N
   Sripipatana, A
AF Pourat, Nadereh
   Kagawa-Singer, Marjorie
   Breen, Nancy
   Sripipatana, Alek
TI Access Versus Acculturation Identifying Modifiable Factors to Promote
   Cancer Screening Among Asian American Women
SO MEDICAL CARE
LA English
DT Article
DE cancer screening; Asian American; acculturation; access; navigation
ID BREAST-CANCER; PATIENT NAVIGATION; UNITED-STATES; WOMEN; HEALTH; CARE;
   MAMMOGRAPHY; CALIFORNIA; MORTALITY; US
AB Background: Asian Americans (AA) have the lowest rates of cancer screening of all ethnic groups. Reasons for these low rates of screening frequently include low acculturation levels. However, screening rates remain low for most AA populations despite differences in acculturation levels, suggesting presence of other important modifiers such as access barriers.
   Objectives: To compare the relative impact of access versus acculturation on breast and cervical cancer screening for AA subgroups.
   Research Design: Multiple regressions models, controlling for sociodemographics, were developed for each AA subgroup.
   Subjects: Women ages 18 and older from the 2003 California Health Interview Survey were included in this study. We included women with Chinese, Filipino, Japanese, Korean, South Asian, and Vietnamese origins.
   Measures: The dependent variables included clinical breast examination in the past year, mammogram in the past 2 years, and Pap test in the past 3 years. Independent variables included AA subgroup, access indicators, acculturation indicators, and other sociodemographics.
   Results: Access explained more variation that acculturation alone in cancer screening for most AA women. The exceptions were in mammograms for Japanese, Koreans and South Asians and Pap test among Japanese. No insurance reduced the likelihood of clinical breast examination for immigrant Chinese and Filipinos, and no usual source of care reduced likelihood of Pap test for Japanese and South Asians compared with US born.
   Conclusions: Access indicators represent the ability to navigate the US health care system but have a differential impact on AA groups. These differences should be integrated into interventions designed to improve cancer screening rates.
C1 [Pourat, Nadereh; Kagawa-Singer, Marjorie; Sripipatana, Alek] Univ Calif Los Angeles, Sch Publ Hlth, Dept Hlth Serv, Los Angeles, CA 90024 USA.
   [Pourat, Nadereh] Univ Calif Los Angeles, Ctr Hlth Policy Res, Dept Community Hlth Sci, Los Angeles, CA 90024 USA.
   [Kagawa-Singer, Marjorie] Univ Calif Los Angeles, Dept Asian Amer Studies, Los Angeles, CA 90024 USA.
   [Breen, Nancy] NCI, Div Canc Control & Populat Sci, Rockville, MD USA.
RP Pourat, N (reprint author), Univ Calif Los Angeles, Sch Publ Hlth, Dept Hlth Serv, 10960 Wilshire Blvd,Suite 1550, Los Angeles, CA 90024 USA.
EM Pourat@ucla.edu
FU Susan G. Komen Foundation [POP0402910]
FX Supported by Susan G. Komen Foundation (POP0402910).
NR 43
TC 36
Z9 36
U1 1
U2 9
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0025-7079
J9 MED CARE
JI Med. Care
PD DEC
PY 2010
VL 48
IS 12
BP 1088
EP 1096
PG 9
WC Health Care Sciences & Services; Health Policy & Services; Public,
   Environmental & Occupational Health
SC Health Care Sciences & Services; Public, Environmental & Occupational
   Health
GA 682DN
UT WOS:000284380200007
PM 20966779
ER

PT J
AU Chen, XJ
   Udupa, JK
   Alavi, A
   Torigian, DA
AF Chen, Xinjian
   Udupa, Jayaram K.
   Alavi, Abass
   Torigian, Drew A.
TI Automatic anatomy recognition via multiobject oriented active shape
   models
SO MEDICAL PHYSICS
LA English
DT Article
DE object recognition; image segmentation; active shape models; live wire
ID IMAGE SEGMENTATION; LEVEL SET; CT IMAGES; KNOWLEDGE; ATLAS;
   CONSTRUCTION; FRAMEWORK; PRIORS
AB Purpose: This paper studies the feasibility of developing an automatic anatomy recognition (AAR) system in clinical radiology and demonstrates its operation on clinical 2D images.
   Methods: The anatomy recognition method described here consists of two main components: (a) multiobject generalization of OASM and (b) object recognition strategies. The OASM algorithm is generalized to multiple objects by including a model for each object and assigning a cost structure specific to each object in the spirit of live wire. The delineation of multiobject boundaries is done in MOASM via a three level dynamic programming algorithm, wherein the first level is at pixel level which aims to find optimal oriented boundary segments between successive landmarks, the second level is at landmark level which aims to find optimal location for the landmarks, and the third level is at the object level which aims to find optimal arrangement of object boundaries over all objects. The object recognition strategy attempts to find that pose vector (consisting of translation, rotation, and scale component) for the multiobject model that yields the smallest total boundary cost for all objects. The delineation and recognition accuracies were evaluated separately utilizing routine clinical chest CT, abdominal CT, and foot MRI data sets. The delineation accuracy was evaluated in terms of true and false positive volume fractions (TPVF and FPVF). The recognition accuracy was assessed (1) in terms of the size of the space of the pose vectors for the model assembly that yielded high delineation accuracy, (2) as a function of the number of objects and objects' distribution and size in the model, (3) in terms of the interdependence between delineation and recognition, and (4) in terms of the closeness of the optimum recognition result to the global optimum.
   Results: When multiple objects are included in the model, the delineation accuracy in terms of TPVF can be improved to 97%-98% with a low FPVF of 0.1%-0.2%. Typically, a recognition accuracy of >= 90% yielded a TPVF >= 95% and FPVF <= 0.5%. Over the three data sets and over all tested objects, in 97% of the cases, the optimal solutions found by the proposed method constituted the true global optimum.
   Conclusions: The experimental results showed the feasibility and efficacy of the proposed automatic anatomy recognition system. Increasing the number of objects in the model can significantly improve both recognition and delineation accuracy. More spread out arrangement of objects in the model can lead to improved recognition and delineation accuracy. Including larger objects in the model also improved recognition and delineation. The proposed method almost always finds globally optimum solutions. c 2010 American Association of Physicists in Medicine. [DOI: 10.1118/1.3515751]
C1 [Udupa, Jayaram K.] UPENN, Dept Radiol, Med Imaging Proc Grp, Philadelphia, PA 19104 USA.
   [Chen, Xinjian] NIH, Ctr Clin, Bethesda, MD 20892 USA.
   [Alavi, Abass; Torigian, Drew A.] UPENN, Dept Radiol, Hosp UPENN, Philadelphia, PA 19104 USA.
RP Udupa, JK (reprint author), UPENN, Dept Radiol, Med Imaging Proc Grp, Philadelphia, PA 19104 USA.
EM jay@mail.med.upenn.edu
RI Chen, Xinjian/E-8592-2016; 
OI Chen, Xinjian/0000-0001-9627-6009
FU NIH [EB004395]
FX The authors' work is supported by NIH Grant No. EB004395.
NR 31
TC 8
Z9 8
U1 0
U2 2
PU AMER ASSOC PHYSICISTS MEDICINE AMER INST PHYSICS
PI MELVILLE
PA STE 1 NO 1, 2 HUNTINGTON QUADRANGLE, MELVILLE, NY 11747-4502 USA
SN 0094-2405
J9 MED PHYS
JI Med. Phys.
PD DEC
PY 2010
VL 37
IS 12
BP 6390
EP 6401
DI 10.1118/1.3515751
PG 12
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA 701UR
UT WOS:000285849400030
PM 21302796
ER

PT J
AU Mastro, MA
   Hardy, AW
   Boasso, A
   Shearer, GM
   Eddy, CR
   Kub, FJ
AF Mastro, Michael A.
   Hardy, Andrew W.
   Boasso, Adriano
   Shearer, Gene M.
   Eddy, Charles R., Jr.
   Kub, Francis J.
TI Non-toxic inhibition of HIV-1 replication with silver-copper
   nanoparticles
SO MEDICINAL CHEMISTRY RESEARCH
LA English
DT Article
DE HIV; Nanoparticles; Silver; Copper
ID GP120; CELLS; SULFADIAZINE; APOPTOSIS; SIZE
AB Cu and Ag-Cu mixed alloy nanoparticles displayed significant inhibition to HIV-1 replication with limited toxicity to human cells at relatively low concentrations of metal. A previous study (Elechiguerra et al. in J Nanobiotechnol 3:6-16, 2005) suggested a size-specific Ag nanoparticle can be tailored to block or damage the glycoprotein (gp) 120/gp41 spike or, more specifically, the invariant epitope at the gp120 binding site. Two different protocols were employed to test whether nanoparticles block entry of HIV-1, and in both instances the nanoparticles acted at some point other than initial binding. This work shows that Ag, Cu, and Ag-Cu mixed alloy metals display a chemically dependent inactivation of the target virus.
C1 [Mastro, Michael A.; Eddy, Charles R., Jr.; Kub, Francis J.] USN, Res Lab, Div Elect Sci & Technol, Washington, DC 20375 USA.
   [Hardy, Andrew W.] Vitae Pharmaceut, Ft Washington, PA USA.
   [Boasso, Adriano; Shearer, Gene M.] NCI, Expt Immunol Branch, NIH, Bethesda, MD 20910 USA.
RP Mastro, MA (reprint author), USN, Res Lab, Div Elect Sci & Technol, Code 6882,4555 Overlook Ave SW, Washington, DC 20375 USA.
EM michael.mastro@nrl.navy.mil
OI Boasso, Adriano/0000-0001-9673-6319
FU Office of Naval Research
FX This research was supported by the Office of Naval Research.
NR 24
TC 5
Z9 5
U1 2
U2 6
PU BIRKHAUSER BOSTON INC
PI CAMBRIDGE
PA 675 MASSACHUSETTS AVE, CAMBRIDGE, MA 02139 USA
SN 1054-2523
J9 MED CHEM RES
JI Med. Chem. Res.
PD DEC
PY 2010
VL 19
IS 9
BP 1074
EP 1081
DI 10.1007/s00044-009-9253-1
PG 8
WC Chemistry, Medicinal
SC Pharmacology & Pharmacy
GA 682VV
UT WOS:000284432000006
ER

PT J
AU Belcher, BR
   Berrigan, D
   Dodd, KW
   Emken, BA
   Chou, CP
   Spruijt-Metz, D
AF Belcher, Britni R.
   Berrigan, David
   Dodd, Kevin W.
   Emken, B. Adar
   Chou, Chih-Ping
   Spruijt-Metz, Donna
TI Physical Activity in US Youth: Effect of Race/Ethnicity, Age, Gender,
   and Weight Status
SO MEDICINE AND SCIENCE IN SPORTS AND EXERCISE
LA English
DT Article
DE NHANES; MODERATE TO VIGOROUS; ACCELEROMETER; BMI; ADOLESCENT
ID BODY-MASS INDEX; UNITED-STATES; SEDENTARY BEHAVIORS; ADOLESCENTS;
   CHILDREN; OBESITY; OVERWEIGHT; GIRLS; BMI; ACCELEROMETER
AB BELCHER, B. R., D. BERRIGAN, K. W. DODD, B. A EMKEN, C.-P. CHOU, and D. SPRUIJT-METZ. Physical Activity in US Youth: Effect of Race/Ethnicity, Age, Gender, and Weight Status. Med. Sci. Sports Exerc., Vol. 42, No. 12, pp. 2211-2221, 2010. Purpose: To describe physical activity (PA) levels by race/ethnicity, age, gender, and weight status in a representative sample of US youth. Methods: Cross-sectional data from the 2003-2004 and 2005-2006 National Health and Nutrition Examination Survey were combined and analyzed. Youth aged 6-19 yr with at least four 10-h days of PA measured by accelerometry were included (n = 3106). Outcomes included mean counts per minute and minutes spent in moderate-to-vigorous PA (MVPA). Results: Among the groups, the 6- to 11-yr-olds spent more time (88 min.d(-1)) in MVPA than the 12- to 15-yr-olds (33 min.d(-1)) and 16- to 19-yr-olds (26 min.d(-1); P < 0.001 for both). Females spent fewer minutes per day in MVPA than males (P < 0.001). Overall, obese youth spent 16 fewer minutes per day in MVPA than normal-weight youth. However, non-Hispanic white males spent three to four fewer minutes per day in vigorous PA than Mexican American (MA; P = 0.004) and non-Hispanic black (P < 0.001) males but had lower obesity rates and obese 12- to 15-yr-old MA recorded similar minutes in MVPA per day as normal-weight MA (P > 0.050). There was a significant three-way age-body mass index-race/ethnicity interaction for mean minutes per day in MVPA (P < 0.001). Adjustment for total energy intake did not qualitatively alter these results. Conclusions: Females and older youth were the least active groups. Obese youth were generally less active, but this did not hold uniformly across race/ethnic groups. Cultural or biological factors could moderate the association between PA and obesity in youth.
C1 [Belcher, Britni R.; Emken, B. Adar; Chou, Chih-Ping; Spruijt-Metz, Donna] Univ So Calif, Keck Sch Med, Dept Prevent Med, Los Angeles, CA 90033 USA.
   [Berrigan, David; Dodd, Kevin W.] NCI, NIH, Bethesda, MD 20892 USA.
RP Spruijt-Metz, D (reprint author), Univ So Calif, Inst Hlth Promot & Dis Prevent, 1000 S Fremont,Unit 8,Room 4101, Alhambra, CA 91803 USA.
EM dmetz@usc.edu
FU University of Southern California Center for Transdisciplinary Research
   on Energetics and Cancer [NCI U54 CA 116848]
FX This work was supported by the University of Southern California Center
   for Transdisciplinary Research on Energetics and Cancer (NCI U54 CA
   116848). The National Cancer Institute reviewed and approved this
   article before submission.
NR 47
TC 90
Z9 92
U1 3
U2 34
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0195-9131
J9 MED SCI SPORT EXER
JI Med. Sci. Sports Exerc.
PD DEC
PY 2010
VL 42
IS 12
BP 2211
EP 2221
DI 10.1249/MSS.0b013e3181e1fba9
PG 11
WC Sport Sciences
SC Sport Sciences
GA 681WG
UT WOS:000284353500009
PM 21084930
ER

PT J
AU Peters, TM
   Shu, XO
   Moore, SC
   Xiang, YB
   Yang, G
   Ekelund, U
   Liu, DK
   Tan, YT
   Ji, BT
   Schatzkin, AS
   Zheng, W
   Chow, WH
   Matthews, CE
   Leitzmann, MF
AF Peters, Tricia M.
   Shu, Xiao-Ou
   Moore, Steven C.
   Xiang, Yong Bing
   Yang, Gong
   Ekelund, Ulf
   Liu, Da-Ke
   Tan, Yu-Ting
   Ji, Bu-Tian
   Schatzkin, Arthur S.
   Zheng, Wei
   Chow, Wong Ho
   Matthews, Charles E.
   Leitzmann, Michael F.
TI Validity of a Physical Activity Questionnaire in Shanghai
SO MEDICINE AND SCIENCE IN SPORTS AND EXERCISE
LA English
DT Article
DE CHINA; MOTOR ACTIVITY; SELF-REPORT METHODS; REPRODUCIBILITY OF RESULTS
ID RETEST RELIABILITY; ACTIVITY PATTERNS; WOMENS HEALTH; UNITED-STATES;
   MENS HEALTH; TIME SPENT; CHINA; REPRODUCIBILITY; RECALL; ACCELEROMETER
AB PETERS, T. M., X.-O. SHU, S. C. MOORE, Y.B. XIANG, G. YANG, U. EKELUND, D.-K. LIU, Y.-T. TAN, B.-T. JI, A. S. SCHATZKIN, W. ZHENG, W. H. CHOW, C. E. MATTHEWS, and M. F. LEITZMANN. Validity of a Physical Activity Questionnaire in Shanghai. Med. Sci. Sports Exerc., Vol. 42, No. 12, pp. 2222-2230, 2010. Purpose: In large epidemiologic studies, physical activity (PA) is often assessed using PA questionnaires (PAQ). Because available PAQ may not capture the full range of PA in which urban Chinese adults engage, a PAQ was developed for this purpose. We examined the validity of this PAQ and the 1-yr stability of PA in 545 urban Shanghai adults. Methods: The PAQ was interview-administered twice, approximately 1 yr apart, and participants also wore an accelerometer and completed a PA-log for seven consecutive days every 3 months during the same year. The intraclass correlation coefficient (ICC) was used to evaluate the stability of PA across questionnaire administrations, and Spearman correlation coefficients (rho) and mean differences and 95% limits of agreement were used to examine the validity of the questionnaire compared against accelerometry and the PA-log. Results: When measured by accelerometry, estimates of time spent in moderate-to-vigorous PA were lower and estimates of time spent sedentary were higher than when self-reported on the PAQ (P < 0.001). Total PA (ICC = 0.65) and PA domains (ICC = 0.45-0.85) showed moderate to high stability across PAQ administrations. Total PA (rho = 0.30), moderate-to-vigorous activity (rho = 0.17), light activity (rho = 0.36), and sedentary behavior (rho = 0.16) assessed by PAQ and by accelerometry were significantly and positively correlated, and correlations of the PAQ with the PA-log (rho = 0.36-0.85) were stronger than those observed with accelerometry. Conclusions: The PAQ significantly overestimated time spent in moderate-to-vigorous activity and underestimated time spent in light activity and sedentary behavior compared with accelerometry, but it performed well at ranking participants according to PA level.
C1 [Peters, Tricia M.; Ekelund, Ulf] Addenbrookes Hosp, Inst Metab Sci, MRC Epidemiol Unit, Cambridge CB2 0QQ, England.
   [Peters, Tricia M.; Moore, Steven C.; Ji, Bu-Tian; Schatzkin, Arthur S.; Chow, Wong Ho; Matthews, Charles E.] NCI, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA.
   [Shu, Xiao-Ou; Yang, Gong; Zheng, Wei] Vanderbilt Univ, Sch Med, Vanderbilt Ingram Canc Ctr,Div Epidemiol, Inst Med & Publ Hlth,Vanderbilt Epidemiol Ctr,Dep, Nashville, TN 37212 USA.
   [Xiang, Yong Bing; Liu, Da-Ke; Tan, Yu-Ting] Shanghai Canc Inst, Shanghai, Peoples R China.
   [Leitzmann, Michael F.] Univ Med Ctr Regensburg, Dept Epidemiol & Prevent Med, Regensburg, Germany.
RP Ekelund, U (reprint author), Addenbrookes Hosp, Inst Metab Sci, MRC Epidemiol Unit, Box 285,Hills Rd, Cambridge CB2 0QQ, England.
EM ulf.ekelund@mrc-epid.cam.ac.uk
RI matthews, Charles/E-8073-2015; Moore, Steven/D-8760-2016
OI matthews, Charles/0000-0001-8037-3103; Moore, Steven/0000-0002-8169-1661
FU National Institutes of Health (NIH) (Shanghai Women's Health Study) [R01
   CA70867]; National Institutes of Health (NIH) (Shanghai Men's Health
   Study) [RO1 CA82729]
FX The study was supported in part by the Intramural Research Program of
   the National Institutes of Health (NIH) and by NIH grants R01 CA70867
   (Shanghai Women's Health Study) and RO1 CA82729 (Shanghai Men's Health
   Study), which supported the parent cohort studies. The ActiGraph
   accelerometer is a product of MTI ActiGraph, Fort Walton, FL.
NR 41
TC 10
Z9 12
U1 0
U2 4
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0195-9131
J9 MED SCI SPORT EXER
JI Med. Sci. Sports Exerc.
PD DEC
PY 2010
VL 42
IS 12
BP 2222
EP 2230
DI 10.1249/MSS.0b013e3181e1fcd5
PG 9
WC Sport Sciences
SC Sport Sciences
GA 681WG
UT WOS:000284353500010
PM 20404770
ER

PT J
AU Sumner, AE
   Harman, JL
   Buxbaum, SG
   Miller, BV
   Tambay, AV
   Wyatt, SB
   Taylor, HA
   Rotimi, CN
   Sarpong, DF
AF Sumner, Anne E.
   Harman, Jane L.
   Buxbaum, Sarah G.
   Miller, Bernard V., III
   Tambay, Anita V.
   Wyatt, Sharon B.
   Taylor, Herman A.
   Rotimi, Charles N.
   Sarpong, Daniel F.
TI The Triglyceride/High-Density Lipoprotein Cholesterol Ratio Fails to
   Predict Insulin Resistance in African-American Women: An Analysis of
   Jackson Heart Study
SO METABOLIC SYNDROME AND RELATED DISORDERS
LA English
DT Article
ID DIABETES-MELLITUS; GLUCOSE; MARKERS; ADULTS
AB Background: Compared to whites, insulin-resistant African Americans have worse outcomes. Screening programs that could identify insulin resistance early enough for intervention to affect outcome often rely on triglyceride (TG) and high-density lipoprotein cholesterol (HDL-C) levels. Racial differences in TG and HDL-C may compromise the efficacy of these programs in African Americans. A recommendation currently exists to use the TG/HDL-C ratio >= 2.0 to predict insulin resistance in African Americans. The validity of this recommendation needs examination. Therefore, our aim was to determine the ability of TG/HDL-C ratio to predict insulin resistance in African Americans.
   Methods: In 1,903 African Americans [895 men, 1,008 women, age 55 +/- 12 years, mean +/- standard deviation (SD), range 35-80 years, body mass index (BMI) 31.0 +/- 6.4 kg/m(2), range 18.5-55 kg/m2] participating in the Jackson Heart Study, a population-based study of African Americans, Jackson, Mississippi tricounty region, insulin resistance was defined by the upper quartile (>= 4.43) of homeostasis model assessment of insulin resistance (HOMA-IR). An area under the receiver operating characteristic curve (AUC-ROC) of >0.70 was required for prediction of insulin resistance by TG/HDL-C. The optimal test cutoff was determined by the Youden index.
   Results: HOMA-IR was similar in men and women (3.40 +/- 2.03 vs. 3.80 +/- 2.46, P = 0.60). Women had lower TG (94 +/- 49 vs. 109 +/- 65 mg/dL P < 0.001) and TG/HDL-C (1.9 +/- 1.4 vs. 2.7 +/- 2.1, P < 0.001). For men, AUC-ROC for prediction of insulin resistance by TG/HDL-C was: 0.77 +/- 0.01, mean +/- standard error (SE), with an optimal cutoff of >= 2.5. For women, the AUC-ROC was 0.66 +/- 0.01, rendering an optimal cutoff indefinable. When women were divided in two groups according to age, 35-50 years and 51-80 years, the results did not change.
   Conclusions: In African-American men, the recommended TG/HDL-C threshold of 2.0 should be adjusted upward to 2.5. In African-American women, TG/HDL-C cannot identify insulin resistance. The Jackson Heart Study can help determine the efficacy of screening programs in African Americans.
C1 [Sumner, Anne E.; Miller, Bernard V., III; Tambay, Anita V.] NIDDKD, Clin Endocrinol Branch, NIH, Bethesda, MD 20892 USA.
   [Harman, Jane L.] NHLBI, Div Cardiovasc Sci, Bethesda, MD 20892 USA.
   [Buxbaum, Sarah G.; Sarpong, Daniel F.] Jackson State Univ, Jackson, MS USA.
   [Wyatt, Sharon B.] Univ Mississippi, Med Ctr, Sch Nursing, Jackson, MS 39216 USA.
   [Taylor, Herman A.] Univ Mississippi, Med Ctr, Dept Med, Jackson, MS 39216 USA.
   [Rotimi, Charles N.] NHGRI, Ctr Res Genom & Global Hlth, Bethesda, MD 20892 USA.
RP Sumner, AE (reprint author), NIDDKD, Clin Endocrinol Branch, NIH, 9000 Rockville Pike, Bethesda, MD 20892 USA.
EM annes@intra.niddk.nih.gov
RI Buxbaum, Sarah/E-1970-2013
OI Buxbaum, Sarah/0000-0002-4886-3564
FU National Heart, Lung, and Blood Institute (NHLBI), National Institutes
   of Health [N01-HC-95170, N01-HC-95171, N01-HC-95172]; National Center on
   Minority Health and Health Disparities (NCMHD), , National Institutes of
   Health [N01-HC-95170, N01-HC-95171, N01-HC-95172]; National Institute of
   Biomedical Imaging and Bioengineering (NIBIB), , National Institutes of
   Health [N01-HC-95170, N01-HC-95171, N01-HC-95172]; Naitonal Institute of
   Diabetes and Digestive and Kidney Diseases (NIDDK)
FX The Jackson Heart Study is conducted by the Jackson State University,
   the University of Mississippi Medical Center, and Tougaloo College, and
   is supported by National Institutes of Health contracts N01-HC-95170,
   N01-HC-95171, and N01-HC-95172 from the National Heart, Lung, and Blood
   Institute (NHLBI), National Center on Minority Health and Health
   Disparities (NCMHD), and National Institute of Biomedical Imaging and
   Bioengineering (NIBIB). Anne E. Sumner, Anita V. Tambay, and Bernard V.
   Miller are supported by the Intramural Program of Naitonal Institute of
   Diabetes and Digestive and Kidney Diseases (NIDDK).
NR 16
TC 30
Z9 30
U1 0
U2 0
PU MARY ANN LIEBERT INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 1540-4196
J9 METAB SYNDR RELAT D
JI Metab. Syndr. Relat. Disord.
PD DEC
PY 2010
VL 8
IS 6
BP 511
EP 514
DI 10.1089/met.2010.0028
PG 4
WC Medicine, Research & Experimental
SC Research & Experimental Medicine
GA 688GN
UT WOS:000284837900008
PM 20715971
ER

PT J
AU King, NB
   Harper, S
   Meersman, SC
   Reichman, ME
   Breen, N
   Lynch, J
AF King, Nicholas B.
   Harper, Sam
   Meersman, Stephen C.
   Reichman, Marsha E.
   Breen, Nancy
   Lynch, John
TI We'll Take the Red Pill: A Reply to Asada
SO MILBANK QUARTERLY
LA English
DT Editorial Material
ID PERCEPTIONS; INEQUALITY; JUDGMENTS
C1 [King, Nicholas B.; Harper, Sam] McGill Univ, Dept Epidemiol Biostat & Occupat Hlth, Montreal, PQ H3A 1A2, Canada.
   [King, Nicholas B.] McGill Univ, Biomed Eth Unit, Montreal, PQ H3A 1A2, Canada.
   [King, Nicholas B.] Case Western Reserve Univ, Dept Bioeth, Cleveland, OH 44106 USA.
   [Meersman, Stephen C.] NCI, Surveillance Res Program, Bethesda, MD 20892 USA.
   [Reichman, Marsha E.] NCI, Div Canc Control & Populat Sci, Bethesda, MD 20892 USA.
   [Breen, Nancy] NCI, Appl Res Program, Bethesda, MD 20892 USA.
   [Lynch, John] Univ S Australia, Sansom Inst Hlth Res, Adelaide, SA 5001, Australia.
   [Lynch, John] Univ Bristol, Bristol BS8 1TH, Avon, England.
RP Harper, S (reprint author), McGill Univ, Dept Epidemiol Biostat & Occupat Hlth, 1020 Pine Ave W,Room 34, Montreal, PQ H3A 1A2, Canada.
EM sam.harper@mcgill.ca
RI Harper, Sam/A-3406-2008; 
OI Harper, Sam/0000-0002-2767-1053; King, Nicholas/0000-0002-2093-3380
NR 8
TC 3
Z9 3
U1 1
U2 2
PU WILEY-BLACKWELL PUBLISHING, INC
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0887-378X
J9 MILBANK Q
JI Milbank Q.
PD DEC
PY 2010
VL 88
IS 4
BP 623
EP 627
DI 10.1111/j.1468-0009.2010.00617.x
PG 5
WC Health Care Sciences & Services; Health Policy & Services
SC Health Care Sciences & Services
GA 696MV
UT WOS:000285446400009
ER

PT J
AU Changolkar, LN
   Singh, G
   Cui, KR
   Berletch, JB
   Zhao, KJ
   Disteche, CM
   Pehrson, JR
AF Changolkar, Lakshmi N.
   Singh, Geetika
   Cui, Kairong
   Berletch, Joel B.
   Zhao, Keji
   Disteche, Christine M.
   Pehrson, John R.
TI Genome-Wide Distribution of MacroH2A1 Histone Variants in Mouse Liver
   Chromatin
SO MOLECULAR AND CELLULAR BIOLOGY
LA English
DT Article
ID INACTIVE X-CHROMOSOME; GENE-EXPRESSION; CORE HISTONE; HETEROCHROMATIN;
   TRANSCRIPTION; LOCALIZATION; ISOFORMS; SUBTYPES; REVEALS; DOMAINS
AB Studies of macroH2A histone variants indicate that they have a role in regulating gene expression. To identify direct targets of the macroH2A1 variants, we produced a genome-wide map of the distribution of macroH2A1 nucleosomes in mouse liver chromatin using high-throughput DNA sequencing. Although macroH2A1 nucleosomes are widely distributed across the genome, their local concentration varies over a range of 100-fold or more. The transcribed regions of most active genes are depleted of macroH2A1, often in sharply localized domains that show depletion of 4-fold or more relative to bulk mouse liver chromatin. We used macroH2A1 enrichment to help identify genes that appear to be directly regulated by macroH2A1 in mouse liver. These genes functionally cluster in the area of lipid metabolism. All but one of these genes has increased expression in macroH2A1 knockout mice, indicating that macroH2A1 functions primarily as a repressor in adult liver. This repressor activity is further supported by the substantial and relatively uniform macroH2A1 enrichment along the inactive X chromosome, which averages 4-fold. Genes that escape X inactivation stand out as domains of macroH2A1 depletion. The rarity of such genes indicates that few genes escape X inactivation in mouse liver, in contrast to what has been observed in human cells.
C1 [Changolkar, Lakshmi N.; Singh, Geetika; Pehrson, John R.] Univ Penn, Sch Vet Med, Dept Anim Biol, Philadelphia, PA 19104 USA.
   [Cui, Kairong; Zhao, Keji] NHLBI, Lab Mol Immunol, NIH, Bethesda, MD 20892 USA.
   [Berletch, Joel B.; Disteche, Christine M.] Univ Washington, Dept Pathol, Seattle, WA 98195 USA.
   [Berletch, Joel B.; Disteche, Christine M.] Univ Washington, Dept Med, Seattle, WA 98195 USA.
RP Pehrson, JR (reprint author), Univ Penn, Sch Vet Med, Dept Anim Biol, Philadelphia, PA 19104 USA.
EM pehrson@vet.upenn.edu
FU National Institute of General Medical Sciences [GM49351, GM046883];
   Division of Intramural Research Program of the National Heart, Lung and
   Blood Institute, NIH; NRSA [1F32HD060402-01A1]
FX This work was supported by Public Health Service grants GM49351 (J.R.P.)
   and GM046883 (C. M. D.) from the National Institute of General Medical
   Sciences, by the Division of Intramural Research Program of the National
   Heart, Lung and Blood Institute, NIH (K.Z.), and by NRSA
   1F32HD060402-01A1 (J.B.B.).
NR 39
TC 32
Z9 32
U1 0
U2 1
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 0270-7306
J9 MOL CELL BIOL
JI Mol. Cell. Biol.
PD DEC
PY 2010
VL 30
IS 23
BP 5473
EP 5483
DI 10.1128/MCB.00518-10
PG 11
WC Biochemistry & Molecular Biology; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA 675QG
UT WOS:000283844900002
PM 20937776
ER

PT J
AU Gmeiner, WH
   Reinhold, WC
   Pommier, Y
AF Gmeiner, William H.
   Reinhold, William C.
   Pommier, Yves
TI Genome-Wide mRNA and microRNA Profiling of the NCI 60 Cell-Line Screen
   and Comparison of FdUMP[10] with Fluorouracil, Floxuridine, and
   Topoisomerase 1 Poisons
SO MOLECULAR CANCER THERAPEUTICS
LA English
DT Article
ID THYMIDYLATE SYNTHASE INHIBITION; ANTICANCER DRUG SCREEN; EXPRESSION
   PROFILES; BREAST-CANCER; PANEL; SENSITIVITY; GENES; 5-FLUOROURACIL;
   BIOSYNTHESIS; DETERMINANTS
AB A profile of microRNA (miRNA) and mRNA expression patterns across the NCI-60 cell-line screen was analyzed to identify expression signatures that correlate with sensitivity to FdUMP[10], fluorouracil (5FU), floxuridine (FdU), topotecan, and irinotecan. Genome-wide profile analyses revealed FdUMP[10] resembles FdU most closely and shows dissimilarities with 5FU. FdUMP[10] had the largest dynamic range of any of these drugs across the NCI-60 indicative of cancer cell-specific activity. Genes involved in endocytosis, such as clathrin (CLTC), SNF8, annexin A6 (ANXA6), and amyloid protein-binding 2 (APPBP2) uniquely correlated with sensitivity to FdUMP[10], consistent with a protein-mediated cellular uptake of FdUMP[10]. Genes involved in nucleotide metabolism were enriched for the three fluoropyrimidine drugs, with the expression profile for 5FU correlated to an RNA-mediated cytotoxic mechanism, whereas expression of glycosyltransferases (XYLT2) that use UDP sugars as substrates and the nucleoside diphosphatase and metastasis suppressor NM23 (NME1) were associated with FdUMP[10] sensitivity. Topotecan and irinotecan had significant negative correlations with miR-24, a miRNA with a high aggregate P(CT) score for topoisomerase 1 (Top1). Our results reveal significant new correlations between FdUMP[10] and Top1 poisons, as well as new information on the unique cytotoxic mechanism and genomic signature of FdUMP[10]. Mol Cancer Ther; 9(12); 3105-14. (C) 2010 AACR.
C1 [Gmeiner, William H.] Wake Forest Univ, Sch Med, Dept Canc Biol, Winston Salem, NC 27157 USA.
   [Reinhold, William C.; Pommier, Yves] NCI, Mol Pharmacol Lab, Ctr Canc Res, Bethesda, MD 20892 USA.
RP Gmeiner, WH (reprint author), Wake Forest Univ, Sch Med, Dept Canc Biol, Winston Salem, NC 27157 USA.
EM bgmeiner@wfubmc.edu
FU NIH-NCI [CA102532]; NIH, National Cancer Institute, Center for Cancer
   Research [Z01 BC 006161-17LMP]
FX This work was supported by NIH-NCI CA102532 (W.H. Gmeiner) and by the
   NIH Intramural Program, National Cancer Institute, Center for Cancer
   Research (Z01 BC 006161-17LMP).
NR 38
TC 44
Z9 44
U1 0
U2 4
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1535-7163
J9 MOL CANCER THER
JI Mol. Cancer Ther.
PD DEC
PY 2010
VL 9
IS 12
BP 3105
EP 3114
DI 10.1158/1535-7163.MCT-10-0674
PG 10
WC Oncology
SC Oncology
GA 694KL
UT WOS:000285296300001
PM 21159603
ER

PT J
AU Zhu, BK
   Bai, R
   Kennett, MJ
   Kang, BH
   Gonzalez, FJ
   Peters, JM
AF Zhu, Bokai
   Bai, Robert
   Kennett, Mary J.
   Kang, Boo-Hyon
   Gonzalez, Frank J.
   Peters, Jeffrey M.
TI Chemoprevention of Chemically Induced Skin Tumorigenesis by Ligand
   Activation of Peroxisome Proliferator-Activated Receptor-beta/delta and
   Inhibition of Cyclooxygenase 2
SO MOLECULAR CANCER THERAPEUTICS
LA English
DT Article
ID PPAR-BETA/DELTA; GENE-EXPRESSION; CELL-PROLIFERATION; DIFFERENTIATION;
   INFLAMMATION; MICE; CARCINOGENESIS; KERATINOCYTES; MODULATION; GROWTH
AB Ligand activation of peroxisome proliferator-activated receptor-beta/delta (PPAR beta/delta) and inhibition of cyclooxygenase-2 (COX2) activity by nonsteroidal anti-inflammatory drugs (NSAID) can both attenuate skin tumorigenesis. The present study examined the hypothesis that combining ligand activation of PPAR beta/delta with inhibition of COX2 activity will increase the efficacy of chemoprevention of chemically induced skin tumorigenesis over that observed with either approach alone. To test this hypothesis, wildtype and Ppar beta/delta-null mice were initiated with 7,12-dimethylbenz[a] anthracene (DMBA), topically treated with 12-O-tetradecanoylphorbol-13-acetate to promote tumorigenesis, and then immediately treated with topical application of the PPAR beta/delta ligand GW0742, dietary administration of the COX2 inhibitor nimesulide, or both GW0742 and nimesulide. Ligand activation of PPAR beta/delta with GW0742 caused a PPAR beta/delta-dependent delay in the onset of tumor formation. Nimesulide also delayed the onset of tumor formation and caused inhibition of tumor multiplicity (46%) in wild-type mice but not in Ppar beta/delta-null mice. Combining ligand activation of PPAR beta/delta with dietary nimesulide resulted in a further decrease of tumor multiplicity (58%) in wild-type mice but not in Ppar beta/delta-null mice. Biochemical and molecular analysis of skin and tumor samples show that these effects were due to the modulation of terminal differentiation, attenuation of inflammatory signaling, and induction of apoptosis through both PPAR beta/delta-dependent and PPAR beta/delta-independent mechanisms. Increased levels and activity of PPAR beta/delta by nimesulide were also observed. These studies support the hypothesis that combining ligand activation of PPAR beta/delta with inhibition of COX2 activity increases the efficacy of preventing chemically induced skin tumorigenesis as compared with either approach alone. Mol Cancer Ther; 9(12); 3267-77. (C) 2010 AACR.
C1 [Zhu, Bokai; Bai, Robert; Kennett, Mary J.; Peters, Jeffrey M.] Penn State Univ, Dept Vet & Biomed Sci, University Pk, PA 16802 USA.
   [Zhu, Bokai; Bai, Robert; Kennett, Mary J.; Peters, Jeffrey M.] Penn State Univ, Ctr Mol Toxicol & Carcinogenesis, University Pk, PA 16802 USA.
   [Zhu, Bokai; Peters, Jeffrey M.] Penn State Univ, Integrat Biosci Grad Program, Huck Inst Life Sci, University Pk, PA 16802 USA.
   [Kang, Boo-Hyon] Preclin Res Ctr, Yongin, Gyeonggi Do, South Korea.
   [Gonzalez, Frank J.] NCI, Lab Metab, Bethesda, MD 20892 USA.
RP Peters, JM (reprint author), Penn State Univ, Dept Vet Sci, University Pk, PA 16802 USA.
EM jmp21@psu.edu
RI Peters, Jeffrey/D-8847-2011; 
OI Zhu, Bokai/0000-0003-0827-5757
FU National Institutes of Health [CA124533, CA126826, CA141029, CA140369]
FX This work supported in part by National Institutes of Health (CA124533,
   CA126826, CA141029, and CA140369 to J.M. Peters)
NR 35
TC 7
Z9 7
U1 0
U2 1
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1535-7163
J9 MOL CANCER THER
JI Mol. Cancer Ther.
PD DEC
PY 2010
VL 9
IS 12
BP 3267
EP 3277
DI 10.1158/1535-7163.MCT-10-0820
PG 11
WC Oncology
SC Oncology
GA 694KL
UT WOS:000285296300016
PM 21159610
ER

PT J
AU Bonzo, JA
   Patterson, AD
   Krausz, KW
   Gonzalez, FJ
AF Bonzo, Jessica A.
   Patterson, Andrew D.
   Krausz, Kristopher W.
   Gonzalez, Frank J.
TI Metabolomics Identifies Novel Hnf1 alpha-Dependent Physiological
   Pathways in Vivo
SO MOLECULAR ENDOCRINOLOGY
LA English
DT Article
ID HEPATOCYTE NUCLEAR FACTOR-1-ALPHA; PHENYLALANINE-HYDROXYLASE GENE;
   FUNCTIONAL-CHARACTERIZATION; TARGETED DISRUPTION; ALPHA-GENE;
   EXPRESSION; MICE; MOUSE; METABOLISM; MUTATIONS
AB Mutations in the HNF1A gene cause maturity-onset diabetes of the young type 3, one of the most common genetic causes of non-insulin-dependent (type 2) diabetes mellitus. Although the whole-body Hnf1a-null mouse recapitulates the low insulin levels and high blood glucose observed in human maturity-onset diabetes of the young type 3 patients, these mice also suffer from Laron dwarfism and aminoaciduria, suggesting a role for hepatocyte nuclear factor 1 alpha (Hnf1 alpha) in pathophysiologies distinct from non-insulin-dependent (type 2) diabetes mellitus. In an effort to identify pathways associated with inactivation of Hnf1 alpha, an ultraperformance liquid chromatography coupled to mass spectrometry-based metabolomics study was conducted on urine samples from wild-type and Hnf1a-null mice. An increase in phenylalanine metabolites is in agreement with the known regulation of the phenylalanine hydroxylase gene by Hnf1 alpha. This metabolomic approach also identified urinary biomarkers for three tissue-specific dysfunctions previously unassociated with Hnf1 alpha function. 1) Elevated indole-lactate coupled to decreased xanthurenic acid also indicated defects in the indole and kynurenine pathways of tryptophan metabolism, respectively. 2) An increase in the neutral amino acid proline in the urine of Hnf1a-null mice correlated with loss of renal apical membrane transporters of the Slc6a family. 3) Further investigation into the mechanism of aldosterone increase revealed an overactive adrenal gland in Hnf1a-null mice possibly due to inhibition of negative feedback regulation. Although the phenotype of the Hnf1a-null mouse is complex, metabolomics has opened the door to investigation of several physiological systems in which Hnf1 alpha may be a critical regulatory component. (Molecular Endocrinology 24: 2343-2355, 2010)
C1 [Gonzalez, Frank J.] Natl Canc Inst, Natl Inst Hlth, Ctr Canc Res, Lab Metab, Bethesda, MD 20892 USA.
RP Gonzalez, FJ (reprint author), Natl Canc Inst, Natl Inst Hlth, Ctr Canc Res, Lab Metab, Bldg 37,Room 3E24, Bethesda, MD 20892 USA.
EM gonzalef@mail.nih.gov
RI Patterson, Andrew/G-3852-2012
OI Patterson, Andrew/0000-0003-2073-0070
FU National Cancer Institute; Pharmacology Research Associate Program
FX This work was supported by the National Cancer Institute Intramural
   Research Program. J.A.B. was supported by the Pharmacology Research
   Associate Program administered through the National Institute of General
   Medical Sciences.
NR 43
TC 12
Z9 12
U1 0
U2 7
PU ENDOCRINE SOC
PI CHEVY CHASE
PA 8401 CONNECTICUT AVE, SUITE 900, CHEVY CHASE, MD 20815-5817 USA
SN 0888-8809
J9 MOL ENDOCRINOL
JI Mol. Endocrinol.
PD DEC
PY 2010
VL 24
IS 12
BP 2343
EP 2355
DI 10.1210/me.2010-0130
PG 13
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 684WF
UT WOS:000284585200009
PM 20943816
ER

PT J
AU Goldin, E
AF Goldin, Ehud
TI Gaucher disease and parkinsonism, a molecular link theory
SO MOLECULAR GENETICS AND METABOLISM
LA English
DT Editorial Material
DE Gaucher disease; Parkinson disease; Prion; Macrophage; Alpha-synuclein
ID MUTANT ALPHA-SYNUCLEIN; GLUCOCEREBROSIDASE; ACCUMULATION; AGGREGATION;
   DISORDERS; MUTATIONS; SPECTRUM; STORAGE; SYSTEM; MODEL
AB Mutant GBA was found recently to be the most prevalent risk factor for familial parkinsonism. The two diseases do not share common symptoms and there is no direct pathway to explain the mechanism by which GBA mutations can confer the risk. Increased burden on the degradative pathway caused by defective glucocerebrosidase, or toxic side effects of glycosylated lipids accumulation were proposed to explain brain damage. Both hypotheses are not sufficient to explain the linkage. In order to develop a more inclusive theory we introduced into the model the prion theory and the second hit. Other possibilities are also brought into consideration. Published by Elsevier Inc.
C1 NHGRI, Med Genet Branch, NIH, Bethesda, MD 20892 USA.
RP Goldin, E (reprint author), NHGRI, Med Genet Branch, NIH, 35 Convent Dr,Room 1A213, Bethesda, MD 20892 USA.
EM goldine@mail.nih.gov
FU Intramural NIH HHS [Z99 HG999999]
NR 34
TC 9
Z9 9
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 1096-7192
J9 MOL GENET METAB
JI Mol. Genet. Metab.
PD DEC
PY 2010
VL 101
IS 4
BP 307
EP 310
DI 10.1016/j.ymgme.2010.08.004
PG 4
WC Endocrinology & Metabolism; Genetics & Heredity; Medicine, Research &
   Experimental
SC Endocrinology & Metabolism; Genetics & Heredity; Research & Experimental
   Medicine
GA 690VU
UT WOS:000285037500002
PM 20801700
ER

PT J
AU Raben, N
   Ralston, E
   Chien, YH
   Baum, R
   Schreiner, C
   Hwu, WL
   Zaal, KJM
   Plotz, PH
AF Raben, Nina
   Ralston, Evelyn
   Chien, Yin-Hsiu
   Baum, Rebecca
   Schreiner, Cynthia
   Hwu, Wuh-Liang
   Zaal, Kristien J. M.
   Plotz, Paul H.
TI Differences in the predominance of lysosomal and autophagic pathologies
   between infants and adults with Pompe disease: implications for therapy
SO MOLECULAR GENETICS AND METABOLISM
LA English
DT Article
DE Myopathy; Glycogen storage disease; Autophagy; Lysosomal storage
ID ACID ALPHA-GLUCOSIDASE; ENZYME REPLACEMENT THERAPY; STORAGE-DISEASE;
   ALGLUCOSIDASE ALPHA; SKELETAL-MUSCLE; NATURAL COURSE; RECOMBINANT;
   GLYCOGEN; PATHWAYS; FIBERS
AB Pompe disease is a lysosomal storage disorder caused by the deficiency of acid alpha-glucosidase, the enzyme that degrades glycogen in the lysosomes. The disease manifests as a fatal cardiomyopathy and skeletal muscle myopathy in infants; in milder late-onset forms skeletal muscle is the major tissue affected. We have previously demonstrated that autophagic inclusions in muscle are prominent in adult patients and the mouse model. In this study we have evaluated the contribution of the autophagic pathology in infants before and 6 months after enzyme replacement therapy. Single muscle fibers, isolated from muscle biopsies, were stained for autophagosomal and lysosomal markers and analyzed by confocal microscopy. In addition, unstained bundles of fixed muscles were analyzed by second harmonic imaging. Unexpectedly, the autophagic component which is so prominent in juvenile and adult patients was negligible in infants; instead, the overwhelming characteristic was the presence of hugely expanded lysosomes. After 6 months on therapy, however, the autophagic buildup becomes visible as if unmasked by the clearance of glycogen. In most fibers, the two pathologies did not seem to coexist. These data point to the possibility of differences in the pathogenesis of Pompe disease in infants and adults. Published by Elsevier Inc.
C1 [Raben, Nina; Baum, Rebecca; Schreiner, Cynthia; Plotz, Paul H.] NIAMSD, Arthrit & Rheumatism Branch, NIH, Bethesda, MD 20892 USA.
   [Ralston, Evelyn; Zaal, Kristien J. M.] NIAMSD, Light Imaging Sect, Off Sci & Technol, NIH, Bethesda, MD 20892 USA.
   [Chien, Yin-Hsiu; Hwu, Wuh-Liang] Natl Taiwan Univ Hosp, Dept Pediat, Taipei 10016, Taiwan.
   [Chien, Yin-Hsiu; Hwu, Wuh-Liang] Natl Taiwan Univ Hosp, Dept Med Genet, Taipei 10016, Taiwan.
   [Chien, Yin-Hsiu; Hwu, Wuh-Liang] Natl Taiwan Univ, Sch Med, Taipei 10764, Taiwan.
RP Raben, N (reprint author), NIAMS, NIH, 50 South Dr,Bld 50-1345, Bethesda, MD 20892 USA.
EM rabenn@mail.nih.gov
OI HWU, WUH-LIANG/0000-0001-6690-4879; CHIEN, YIN-HSIU/0000-0001-8802-5728
FU Genzyme; NIH; NIAMS; Genzyme Corporation
FX Drs. Chien and Hwu received honoraria and research grant funding from
   Genzyme. Dr. Hwu is a member of the Pompe disease advisory board for
   Genzyme. Rebecca Baum's fellowship is supported by a Cooperative
   Research and Development Agreement (CRADA) between NIAMS and the Genzyme
   Corporation for studies related to Pompe disease. The other authors have
   no financial interests to disclose.; This research was supported by the
   Intramural Research Program of the NIAMS of the NIH.
NR 37
TC 27
Z9 29
U1 0
U2 1
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 1096-7192
J9 MOL GENET METAB
JI Mol. Genet. Metab.
PD DEC
PY 2010
VL 101
IS 4
BP 324
EP 331
DI 10.1016/j.ymgme.2010.08.001
PG 8
WC Endocrinology & Metabolism; Genetics & Heredity; Medicine, Research &
   Experimental
SC Endocrinology & Metabolism; Genetics & Heredity; Research & Experimental
   Medicine
GA 690VU
UT WOS:000285037500004
PM 20801068
ER

PT J
AU Hanson, RL
   Millis, MP
   Young, NJ
   Kobes, S
   Nelson, RG
   Knowler, WC
   DiStefano, JK
AF Hanson, Robert L.
   Millis, Meredith P.
   Young, Naomi J.
   Kobes, Sayuko
   Nelson, Robert G.
   Knowler, William C.
   DiStefano, Johanna K.
TI ELMO1 variants and susceptibility to diabetic nephropathy in American
   Indians
SO MOLECULAR GENETICS AND METABOLISM
LA English
DT Article
DE Association analysis; Candidate gene study; End stage renal disease;
   Genetic susceptibility; Pima Indians
ID STAGE RENAL-DISEASE; URINARY ALBUMIN EXCRETION; PIMA-INDIANS; GENE;
   MELLITUS; ASSOCIATION; PREVALENCE; IMPACT; ESRD
AB Variants in the engulfment and cell motility 1 gene, ELMO1, have previously been associated with kidney disease attributed to type 2 diabetes. The Pima Indians of Arizona have high rates of diabetic nephropathy, which is strongly dependent on genetic determinants; thus, we sought to investigate the role of ELMO1 polymorphisms in mediating susceptibility to this disease in this population. Genotype distributions were compared among 141 individuals with nephropathy and 416 individuals without heavy proteinuria in a family study of 257 sibships, and 107 cases with diabetic ESRD and 108 controls with long duration diabetes and no nephropathy. We sequenced 17.4 kb of ELMO1 and identified 19 variants. We genotyped 12 markers, excluding those in 100% genotypic concordance with other variants or with a minor allele frequency <0.05, plus 21 additional markers showing association with ESRD in earlier studies. In the family study, the strongest evidence for association was with rs1345365 (odds ratio [OR] = 2.42 per copy of A allele [1.35-4.32]; P=0.001) and rs10951509 (OR = 2.42 per copy of A allele [1.31-4.48]; P=0.002), both of which are located in intron 13 and are in strong pairwise linkage disequilibrium (r(2) = 0.97). These associations were in the opposite direction from those observed in African Americans, which suggests that the relationship between diabetic kidney disease and ELMO1 variation may involve as yet undiscovered functional variants or complex interactions with other biological variables. (C) 2010 Elsevier Inc. All rights reserved.
C1 [Millis, Meredith P.; Young, Naomi J.; DiStefano, Johanna K.] Translat Genom Res Inst, Diabet Cardiovasc & Metab Dis Div, Phoenix, AZ 85004 USA.
   [Hanson, Robert L.; Kobes, Sayuko; Nelson, Robert G.; Knowler, William C.] NIDDKD, Diabet Epidemiol & Clin Res Sect, NIH, Phoenix, AZ 85014 USA.
RP DiStefano, JK (reprint author), Translat Genom Res Inst, Diabet Cardiovasc & Metab Dis Div, 445 N 5th St, Phoenix, AZ 85004 USA.
EM jdistefano@tgen.org
RI Nelson, Robert/B-1470-2012; Hanson, Robert/O-3238-2015
OI Hanson, Robert/0000-0002-4252-7068
FU American Diabetes Association; National Institute of Diabetes and
   Digestive and Kidney Diseases
FX We thank the study members for their participation and Kimberly A.
   Yeatts for her technical contribution. We also thank Kim et al [21] for
   providing their data for the meta-analysis. This work is supported by
   the American Diabetes Association and by the Intramural Research Program
   of the National Institute of Diabetes and Digestive and Kidney Diseases.
NR 27
TC 19
Z9 19
U1 1
U2 3
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 1096-7192
J9 MOL GENET METAB
JI Mol. Genet. Metab.
PD DEC
PY 2010
VL 101
IS 4
BP 383
EP 390
DI 10.1016/j.ymgme.2010.08.014
PG 8
WC Endocrinology & Metabolism; Genetics & Heredity; Medicine, Research &
   Experimental
SC Endocrinology & Metabolism; Genetics & Heredity; Research & Experimental
   Medicine
GA 690VU
UT WOS:000285037500012
PM 20826100
ER

PT J
AU Lee, CR
   Cho, SH
   Kim, HJ
   Kim, M
   Peterkofsky, A
   Seok, YJ
AF Lee, Chang-Ro
   Cho, Seung-Hyon
   Kim, Hyun-Jin
   Kim, Miri
   Peterkofsky, Alan
   Seok, Yeong-Jae
TI Potassium mediates Escherichia coli enzyme IIANtr-dependent regulation
   of sigma factor selectivity
SO MOLECULAR MICROBIOLOGY
LA English
DT Article
ID GLOBAL REPRESSOR MLC; CORE RNA-POLYMERASE; PROTEIN H-NS;
   PHOSPHOTRANSFERASE SYSTEM; GENE-EXPRESSION; GLUCOSE-TRANSPORTER; FACTOR
   COMPETITION; OSMOTIC CONTROL; IN-VIVO; TRANSCRIPTION
AB P>An Escherichia coli mutant devoid of enzyme IIANtr (EIIANtr) of the nitrogen PTS is extremely sensitive to leucine-containing peptides due to decreased expression of acetohydroxy acid synthase. This decreased expression is due to defective potassium homeostasis. We further elucidate here the mechanism for regulation of gene expression by the intracellular level of K+. The leucine hypersensitivity of a ptsN (encoding EIIANtr) mutant was suppressed by deleting rpoS, encoding the stationary phase sigma factor. Despite intracellular levels of sigma factors comparable to the wild-type strain, most of the genes downregulated in a ptsN mutant are controlled by sigma 70, while all the upregulated genes are controlled by sigma S, implying that the balance of sigma activities is modified by ptsN deletion. This change of sigma factor activities in the deletion mutant was found to be due to increased levels of K+. In vitro transcription assays demonstrated that a sigma 70 controlled gene and a sigma S controlled gene were differentially affected by potassium concentration. Biochemical studies revealed that K+ is responsible for sigma factor competition by differentially influencing the binding of sigma 70 and sigma S to core RNA polymerase. Taken together, the data suggest that EIIANtr controls sigma factor selectivity by regulating the intracellular K+ level.
C1 [Lee, Chang-Ro; Cho, Seung-Hyon; Kim, Hyun-Jin; Kim, Miri; Seok, Yeong-Jae] Seoul Natl Univ, Lab Macromol Interact, Dept Biophys & Chem Biol, Seoul 151742, South Korea.
   [Lee, Chang-Ro; Cho, Seung-Hyon; Kim, Hyun-Jin; Kim, Miri; Seok, Yeong-Jae] Seoul Natl Univ, Inst Microbiol, Seoul 151742, South Korea.
   [Peterkofsky, Alan] NHLBI, Cell Biol Lab, NIH, Bethesda, MD 20892 USA.
RP Seok, YJ (reprint author), Seoul Natl Univ, Lab Macromol Interact, Dept Biophys & Chem Biol, Seoul 151742, South Korea.
EM yjseok@snu.ac.kr
FU WCU [R31-2009-000-10032-0]; National Research Foundation
   [KRF-2007-313-C00644, NRF 2010-0017384]; Ministry of Education, Science,
   and Technology, Republic of Korea [MG08-0201-1-0]; NHLBI
FX We thank M. Cashel for his assistance with the measurement of (p) ppGpp
   and H.-E. Choy for sharing strains. This work was supported by the WCU
   program (R31-2009-000-10032-0), National Research Foundation Grant
   (KRF-2007-313-C00644 and NRF 2010-0017384) and the 21C Frontier
   Microbial Genomics and Applications Center Program (MG08-0201-1-0)
   funded by Ministry of Education, Science, and Technology, Republic of
   Korea and, in part, by intramural funds from the NHLBI (to A.P.).
NR 64
TC 25
Z9 25
U1 0
U2 5
PU WILEY-BLACKWELL PUBLISHING, INC
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0950-382X
J9 MOL MICROBIOL
JI Mol. Microbiol.
PD DEC
PY 2010
VL 78
IS 6
BP 1468
EP 1483
DI 10.1111/j.1365-2958.2010.07419.x
PG 16
WC Biochemistry & Molecular Biology; Microbiology
SC Biochemistry & Molecular Biology; Microbiology
GA 692MJ
UT WOS:000285156600012
PM 21143318
ER

PT J
AU Kong, HS
   Lee, S
   Beebe, K
   Scroggins, B
   Gupta, G
   Lee, MJ
   Jung, YJ
   Trepel, J
   Neckers, L
AF Kong, Hye-Sik
   Lee, Sunmin
   Beebe, Kristin
   Scroggins, Bradley
   Gupta, Gopal
   Lee, Min-Jung
   Jung, Yun-Jin
   Trepel, Jane
   Neckers, Leonard
TI Emetine Promotes von Hippel-Lindau-Independent Degradation of
   Hypoxia-Inducible Factor-2 alpha in Clear Cell Renal Carcinoma
SO MOLECULAR PHARMACOLOGY
LA English
DT Article
ID TUMOR-SUPPRESSOR PROTEIN; RECEPTOR NUCLEAR TRANSLOCATOR; FACTOR-I;
   FUMARATE HYDRATASE; KIDNEY CANCER; UP-REGULATION; FACTOR-1-ALPHA;
   HIF-1-ALPHA; HIF-2-ALPHA; INHIBITORS
AB Inactivating mutations of the von Hippel-Lindau (VHL) tumor suppressor gene are associated with inherited VHL syndrome, which is characterized by susceptibility to a variety of neoplasms, including central nervous system hemangioblastoma and clear cell renal cell carcinoma (CCRCC). Mutations in the VHL gene are also found in the majority of sporadic clear cell renal carcinoma, the most common malignant neoplasm of the human kidney. Inactivation of VHL ubiquitin ligase is associated with normoxic stabilization of hypoxia-inducible factor-1 alpha and 2-alpha (HIF-1 alpha and HIF-2 alpha), transcriptional regulators of tumor angiogenesis, invasion, survival, and glucose utilization. HIF-2 alpha has been particularly implicated in the development of CCRCC. Although several inhibitors of HIF-1 alpha have been described, these drugs typically have a minimal affect on HIF-2 alpha. 786-O is a VHL-deficient CCRCC cell line that constitutively expresses only HIF-2 alpha and is therefore suitable for the screening of novel HIF-2 alpha inhibitors. Using this cell line, we have identified emetine as a specific inhibitor of HIF-2 alpha protein stability and transcriptional activity. Without altering HIF-2 alpha mRNA level, emetine rapidly and dramatically down-regulated HIF-2 alpha protein expression in 786-O cells. HIF-2 alpha down-regulation was accompanied by HIF-2 alpha ubiquitination and was reversed by proteasome inhibition. Emetine-induced HIF-2 alpha down-regulation was confirmed in three additional VHL-renal cancer cell lines, was insensitive to the prolyl hydroxylase inhibitor dimethyloxaloyl glycine, and did not require neural precursor cell expressed developmentally down-regulated-8, suggesting that emetine accesses a previously undescribed cullin-independent proteasome degradation pathway for HIF-2 alpha. These data support the use of emetine or structurally related compounds as useful leads for the identification of novel HIF-2 alpha inhibitors.
C1 [Kong, Hye-Sik; Beebe, Kristin; Scroggins, Bradley; Gupta, Gopal; Neckers, Leonard] NCI, Urol Oncol Branch, Ctr Canc Res, Bethesda, MD 20892 USA.
   [Lee, Sunmin; Lee, Min-Jung; Trepel, Jane] NCI, Med Oncol Branch, Ctr Canc Res, Bethesda, MD 20892 USA.
   [Kong, Hye-Sik] Georgetown Univ, Lombardi Comprehens Canc Ctr, Dept Oncol, Washington, DC USA.
   [Jung, Yun-Jin] Pusan Natl Univ, Coll Pharm, Lab Biomed Chem, Pusan, South Korea.
RP Neckers, L (reprint author), NCI, Urol Oncol Branch, Ctr Canc Res, Bethesda, MD 20892 USA.
EM neckersl@mail.nih.gov
NR 38
TC 9
Z9 10
U1 0
U2 0
PU AMER SOC PHARMACOLOGY EXPERIMENTAL THERAPEUTICS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3995 USA
SN 0026-895X
J9 MOL PHARMACOL
JI Mol. Pharmacol.
PD DEC
PY 2010
VL 78
IS 6
BP 1072
EP 1078
DI 10.1124/mol.110.066514
PG 7
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA 680WC
UT WOS:000284267200010
PM 20813864
ER

PT J
AU Schloesser, RJ
   Lehmann, M
   Martinowich, K
   Manji, HK
   Herkenham, M
AF Schloesser, R. J.
   Lehmann, M.
   Martinowich, K.
   Manji, H. K.
   Herkenham, M.
TI Environmental enrichment requires adult neurogenesis to facilitate the
   recovery from psychosocial stress
SO MOLECULAR PSYCHIATRY
LA English
DT Article
DE hippocampal neurogenesis; social stress; environmental enrichment;
   dentate gyrus; anxiety; depression
ID DENTATE GYRUS; HIPPOCAMPAL NEUROGENESIS; ANTIDEPRESSANT TREATMENT;
   LEARNED HELPLESSNESS; CELL-PROLIFERATION; PATTERN SEPARATION;
   DEPRESSIVE-ILLNESS; ANIMAL-MODELS; RAT; BRAIN
AB The subgranular zone of the adult hippocampal dentate gyrus contains a pool of neural stem cells that continuously divide and differentiate into functional granule cells. It has been shown that production of new hippocampal neurons is necessary for amelioration of stress-induced behavioral changes by antidepressants in animal models of depression. The survival of newly born hippocampal neurons is decreased by chronic psychosocial stress and increased by exposure to enriched environments. These observations suggest the existence of a link between hippocampal neurogenesis, stress-induced behavioral changes, and the beneficial effects of enriched environment. To show causality, we subjected transgenic mice with conditionally suppressed neurogenesis to psychosocial stress followed by environmental enrichment. First, we showed that repeated social defeat coupled with chronic exposure to an aggressor produces robust and quantifiable indices of submissive and depressive-like behaviors; second, subsequent exposure to an enriched environment led to extinction of the submissive phenotype, while animals exposed to an impoverished environment retained the submissive phenotype; and third, enrichment was not effective in reversing the submissive and depressive-like behaviors in transgenic mice lacking neurogenesis. Our data show two main findings. First, living in an enriched environment is highly effective in extinguishing submissive behavioral traits developed during chronic social stress, and second, these effects are critically dependent on adult neurogenesis, indicating that beneficial behavioral adaptations are dependent on intact adult neurogenesis. Molecular Psychiatry (2010) 15, 1152-1163; doi:10.1038/mp.2010.34; published online 23 March 2010
C1 [Lehmann, M.; Herkenham, M.] NIMH, Funct Neuroanat Sect, NIH, Bethesda, MD 20892 USA.
   [Schloesser, R. J.; Martinowich, K.; Manji, H. K.] NIMH, Mol Pathophysiol Lab, NIH, Bethesda, MD 20892 USA.
RP Lehmann, M (reprint author), NIMH, Funct Neuroanat Sect, NIH, Bldg 35,Room 1C911,35 Convent Dr, Bethesda, MD 20892 USA.
EM michael.lehmann@nih.gov
RI Martinowich, Keri/F-9841-2012; 
OI Martinowich, Keri/0000-0002-5237-0789; Herkenham,
   Miles/0000-0003-2228-4238; Lehmann, Michael/0000-0003-4476-8268
FU National Institute of Mental Health, NIH
FX The work was supported by the Intramural Research Program of the
   National Institute of Mental Health, NIH. We thank JB Lednak, DV Jimenez
   and KM Cardinale for technical assistance and animal maintenance.
NR 55
TC 104
Z9 108
U1 1
U2 12
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1359-4184
J9 MOL PSYCHIATR
JI Mol. Psychiatr.
PD DEC
PY 2010
VL 15
IS 12
BP 1152
EP 1163
DI 10.1038/mp.2010.34
PG 12
WC Biochemistry & Molecular Biology; Neurosciences; Psychiatry
SC Biochemistry & Molecular Biology; Neurosciences & Neurology; Psychiatry
GA 684CJ
UT WOS:000284524300004
PM 20308988
ER

PT J
AU Olive, M
   Goldfarb, LG
   Lee, HS
   Odgerel, Z
   Blokhin, A
   Gonzalez-Mera, L
   Moreno, D
   Laing, NG
   Sambuughin, N
AF Olive, Montse
   Goldfarb, Lev G.
   Lee, Hee-Suk
   Odgerel, Zagaa
   Blokhin, Andre
   Gonzalez-Mera, Laura
   Moreno, Dolores
   Laing, Nigel G.
   Sambuughin, Nyamkhishig
TI NEMALINE MYOPATHY TYPE 6: CLINICAL AND MYOPATHOLOGICAL FEATURES
SO MUSCLE & NERVE
LA English
DT Article
DE chromosome 15q; core-rod myopathy; nemaline myopathy; NEM6; Spanish
   family
ID CONGENITAL MYOPATHY; ALPHA-TROPOMYOSIN; RYANODINE RECEPTOR; NEBULIN
   GENE; MUSCLE; MUTATIONS; RODS; CARDIOMYOPATHY; PATHOLOGY; PHENOTYPE
AB Nemaline myopathy (NEM) is one of the most common congenital myopathies. A unique subtype, NEM6, maps to chromosome 15q21-q23 in two pedigrees, but the causative gene has not been determined. We conducted clinical examination and myopathological studies in a new NEM family. Genotyping and gene screening were accomplished by searching known and 18 new candidate genes. The disease started in childhood by affecting proximal and distal muscles and causing slowness of movements. Muscle biopsies showed numerous nemaline rods and core-like formations. Suggestive linkage to chromosome 15q22-q23 was established. Genes known to be mutated in NEM or core-rod myopathy were screened and excluded. No pathogenic mutations were identified in other candidate genes. The disease in this Spanish family was classified as NEM6. It is phenotypically similar and probably allelic to the two previously reported NEM6 pedigrees. Further studies of these families will lead to the identification of the NEM6 gene. Muscle Nerve 42: 901-907, 2010
C1 [Olive, Montse; Gonzalez-Mera, Laura; Moreno, Dolores] IDIBELL Hosp Bellvitge, Dept Pathol, Inst Neuropathol, Barcelona 08907, Spain.
   [Olive, Montse; Gonzalez-Mera, Laura; Moreno, Dolores] Hosp Llobregat, CIBERNED, Barcelona 08907, Spain.
   [Goldfarb, Lev G.; Lee, Hee-Suk; Odgerel, Zagaa] NINDS, NIH, Bethesda, MD 20892 USA.
   [Blokhin, Andre; Sambuughin, Nyamkhishig] Uniformed Serv Univ Hlth Sci, Bethesda, MD 20814 USA.
   [Laing, Nigel G.] Univ Western Australia, QEII Med Ctr, Western Australian Inst Med Res, Med Res Ctr, Perth, WA 6009, Australia.
RP Olive, M (reprint author), IDIBELL Hosp Bellvitge, Dept Pathol, Inst Neuropathol, Feixa Llarga S-N, Barcelona 08907, Spain.
EM 25169mop@comb.cat
OI Olive, Montse/0000-0001-5727-0165; Gonzalez-Mera,
   Laura/0000-0001-5691-0343
FU FIS [PI08-574]; USUHS [R080CD]; National Institute of Neurological
   Disorders and Stroke, National Institutes of Health; Australian National
   Health and Medical Research Council; Biomedical Instrumentation Center
   of the Uniformed Services University of the Health Sciences, Bethesda,
   Maryland
FX This work was supported in part by the FIS (Grant PI08-574 to M.O.); the
   USUHS (Grant R080CD to N.S.); the Intramural Research Program of the
   National Institute of Neurological Disorders and Stroke, National
   Institutes of Health (to L.G.G., H.S.L., and Z.O.); and the Australian
   National Health and Medical Research Council (Principal Research
   Fellowship 403904 to N.G.L.). The authors acknowledge the support of Dr.
   S. Muldoon and the Biomedical Instrumentation Center of the Uniformed
   Services University of the Health Sciences, Bethesda, Maryland. We are
   grateful to the patients and the members of the affected families for
   their enthusiastic participation in the study.
NR 30
TC 6
Z9 6
U1 2
U2 4
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0148-639X
J9 MUSCLE NERVE
JI Muscle Nerve
PD DEC
PY 2010
VL 42
IS 6
BP 901
EP 907
DI 10.1002/mus.21788
PG 7
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA 692RI
UT WOS:000285172400009
PM 21104864
ER

PT J
AU Valentine, CR
   Delongchamp, RR
   Pearce, MG
   Rainey, HF
   Dobrovolsky, VN
   Malling, HV
   Heflich, RH
AF Valentine, Carrie R.
   Delongchamp, Robert R.
   Pearce, Mason G.
   Rainey, Heather F.
   Dobrovolsky, Vasily N.
   Malling, Heinrich V.
   Heflich, Robert H.
TI In vivo mutation analysis using the Phi X174 transgenic mouse and
   comparisons with other transgenes and endogenous genes
SO MUTATION RESEARCH-REVIEWS IN MUTATION RESEARCH
LA English
DT Review
DE Transgenic mice; Somatic cell mutation; Germ cell mutation; Mutation
   frequency; Single-burst analysis
ID PAROXYSMAL-NOCTURNAL HEMOGLOBINURIA; MISMATCH REPAIR DEFICIENCY;
   ENU-INDUCED MUTATION; BIG BLUE(R) MICE; ESCHERICHIA-COLI; SPLENIC
   LYMPHOCYTES; MUTANT FREQUENCIES; MAMMALIAN-CELLS; NUCLEOTIDE-SEQUENCE;
   INDUCED MUTAGENESIS
AB The Phi X174 transgenic mouse was first developed as an in vivo Ames test, detecting base pair substitution (bps) at a single bp in a reversion assay. A forward mutational assay was also developed, which is a gain of function assay that also detects bps exclusively. Later work with both assays focused on establishing that a mutation was fixed in vivo using single-burst analysis: determining the number of mutant progeny virus from an electroporated cell by dividing the culture into aliquots before scoring mutants. We review results obtained from single-burst analysis, including testing the hypothesis that high mutant frequencies (MFs) of G:C to A:T mutation recovered by transgenic targets include significant numbers of unrepaired G:T mismatches. Comparison between the Phi X174 and lad transgenes in mouse spleen indicates that the spontaneous bps mutation frequency per nucleotide (mf(n)) is not significantly lower for Phi X174 than for lacl; the response to ENU is also comparable. For the lad transgene, the spontaneous bps mf(n) is highly age-dependent up to 12 weeks of age and the linear trend extrapolates at conception to a frequency close to the human bps mf(n) per generation of 1.7 x 10(-8). Unexpectedly, we found that the lad somatic (spleen) bps mf(n) per cell division at early ages was estimated to be the same as for the human germ-line. The bps mf(n) in bone marrow for the gpt transgene is comparable to spleen for the lad and Phi X174 transgenes. We conclude that the G:C to A:T transition is characteristic of spontaneous in vivo mutation and that the MFs measured in these transgenes at early ages reflect the expected accumulation of in vivo mutation typical of endogenous mammalian mutation rates. However, spontaneous and induced mf(n)s per nucleotide for the cif gene in spleen are 5-10 times higher than for these other transgenes. Published by Elsevier B.V.
C1 [Valentine, Carrie R.; Pearce, Mason G.; Rainey, Heather F.; Dobrovolsky, Vasily N.; Heflich, Robert H.] Natl Ctr Toxicol Res, Div Genet & Reprod Toxicol, Jefferson, AR 72079 USA.
   [Delongchamp, Robert R.] Univ Arkansas Med Sci, Dept Epidemiol, Coll Publ Hlth, Little Rock, AR 72205 USA.
   [Malling, Heinrich V.] NIEHS, Mammalian Mutagenesis Grp, Toxicol Lab, Environm Toxicol Program, Res Triangle Pk, NC 27709 USA.
RP Heflich, RH (reprint author), Natl Ctr Toxicol Res, Div Genet & Reprod Toxicol, 3900 NCTR Rd,HFT-120, Jefferson, AR 72079 USA.
EM robert.heflich@fda.hhs.gov
NR 87
TC 3
Z9 3
U1 0
U2 3
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 1383-5742
J9 MUTAT RES-REV MUTAT
JI Mutat. Res.-Rev. Mutat. Res.
PD DEC
PY 2010
VL 705
IS 3
BP 205
EP 216
DI 10.1016/j.mrrev.2010.07.001
PG 12
WC Biotechnology & Applied Microbiology; Genetics & Heredity; Toxicology
SC Biotechnology & Applied Microbiology; Genetics & Heredity; Toxicology
GA 701HF
UT WOS:000285808300006
PM 20637298
ER

PT J
AU Bhirde, AA
   Patel, S
   Sousa, AA
   Patel, V
   Molinolo, AA
   Ji, YM
   Leapman, RD
   Gutkind, JS
   Rusling, JF
AF Bhirde, Ashwin A.
   Patel, Sachin
   Sousa, Alioscka A.
   Patel, Vyomesh
   Molinolo, Alfredo A.
   Ji, Youngmi
   Leapman, Richard D.
   Gutkind, J. Silvio
   Rusling, James F.
TI Distribution and clearance of PEG-single-walled carbon nanotube cancer
   drug delivery vehicles in mice
SO NANOMEDICINE
LA English
DT Article
DE biodistribution; cancer; carbon nanotube; cisplatin; clearance; drug
   delivery; dynamic light scattering; growth factor; H & E staining;
   polyethylene glycol; Raman spectroscopy; STEM
ID IN-VIVO; RAMAN-SPECTROSCOPY; QUANTUM DOTS; CELLS; DISPERSION;
   NANOPARTICLES; NANOMATERIALS; CIRCULATION; MOLECULES; TOXICITY
AB Aims: To study the distribution and clearance of polyethylene glycol (PEG)-ylated single-walled carbon nanotube (SWCNTs) as drug delivery vehicles for the anticancer drug cisplatin in mice. Materials & methods: PEG layers were attached to SWCNTs and dispersed in aqueous media and characterized using dynamic light scattering, scanning transmission electron microscopy and Raman spectroscopy. Cytotoxicity was assessed in vitro using Annexin-V assay, and the distribution and clearance pathways in mice were studied by histological staining and Raman spectroscopy. Efficacy of PEG-SWCNT-cisplatin for tumor growth inhibition was studied in mice. Results & discussion: PEG-SWCNTs were efficiently dispersed in aqueous media compared with controls, and did not induce apoptosis in vitro. Hematoxylin and eosin staining, and Raman bands for SWCNTs in tissues from several vital organs from mice injected intravenously with nanotube bioconjugates revealed that control SWCNTs were lodged in lung tissue as large aggregates compared with the PEG-SWCNTs, which showed little or no accumulation. Characteristic SWCNT Raman bands in feces revealed the presence of bilary or renal excretion routes. Attachment of cisplatin on bioconjugates was visualized with Z-contrast scanning transmission electron microscopy. PEG-SWCNT-cisplatin with the attached targeting ligand EGF successfully inhibited growth of head and neck tumor xenografts in mice. Conclusions: PEG-SWCNTs, as opposed to control SWCNTs, form more highly dispersed delivery vehicles that, when loaded with both cisplatin and EGF, inhibit growth of squamous cell tumors.
C1 [Patel, Sachin; Patel, Vyomesh; Molinolo, Alfredo A.; Gutkind, J. Silvio] Natl Inst Dent & Craniofacial Res, Oral & Pharyngeal Canc Branch, NIH, Bethesda, MD 20892 USA.
   [Bhirde, Ashwin A.; Rusling, James F.] Univ Connecticut, Dept Chem, Storrs, CT USA.
   [Sousa, Alioscka A.; Leapman, Richard D.] Natl Inst Biomed Imaging & Bioengn, Lab Cellular Imaging & Macromol Biophys, NIH, Bethesda, MD 20892 USA.
   [Ji, Youngmi] NIAMSD, NIH, Bethesda, MD 20892 USA.
   [Rusling, James F.] Univ Connecticut, Ctr Hlth, Dept Cell Biol, Farmington, CT USA.
   [Rusling, James F.] Univ Connecticut, Inst Mat Sci, Storrs, CT USA.
RP Patel, V (reprint author), Natl Inst Dent & Craniofacial Res, Oral & Pharyngeal Canc Branch, NIH, Bethesda, MD 20892 USA.
RI Gutkind, J. Silvio/A-1053-2009
FU National Institute of Dental and Craniofacial Research; National
   Institute of Biomedical Imaging and Bioengineering, NIH; NIEHS/NIH
   [ES013557]; University of Connecticut
FX This research was supported by the Intramural Programs of the National
   Institute of Dental and Craniofacial Research and the National Institute
   of Biomedical Imaging and Bioengineering, NIH, and in part by PHS grant
   ES013557 from NIEHS/NIH to JFR, University of Connecticut. The authors
   have no other relevant affiliations or financial involvement with any
   organization or entity with a financial interest in or financial
   conflict with the subject matter or materials discussed in the
   manuscript apart from those disclosed.
NR 61
TC 65
Z9 67
U1 3
U2 43
PU FUTURE MEDICINE LTD
PI LONDON
PA UNITEC HOUSE, 3RD FLOOR, 2 ALBERT PLACE, FINCHLEY CENTRAL, LONDON, N3
   1QB, ENGLAND
SN 1743-5889
J9 NANOMEDICINE-UK
JI Nanomedicine
PD DEC
PY 2010
VL 5
IS 10
BP 1535
EP 1546
DI 10.2217/NNM.10.90
PG 12
WC Biotechnology & Applied Microbiology; Nanoscience & Nanotechnology
SC Biotechnology & Applied Microbiology; Science & Technology - Other
   Topics
GA 710UE
UT WOS:000286541700009
PM 21143032
ER

PT J
AU Metzger, MB
   Weissman, AM
AF Metzger, Meredith B.
   Weissman, Allan M.
TI Working on a chain: E3s ganging up for ubiquitylation
SO NATURE CELL BIOLOGY
LA English
DT Editorial Material
ID POLYUBIQUITINATION; UBIQUITINATION; DEGRADATION; PROTEASOME; INSIGHTS;
   LIGASES
AB Substrate specificity in ubiquitylation is conferred by ubiquitin ligases (E3s). Now, several ways that E3s can interact to mediate ubiquitylation are illustrated for Ubr1 (a RING finger E3) and Ufd4 (a HECT domain E3), in Saccharomyces cerevisiae. These interactions and the related concept of E4 activity are discussed.
C1 [Metzger, Meredith B.; Weissman, Allan M.] NCI, Lab Prot Dynam & Signaling, Ctr Canc Res, NIH, Frederick, MD 21702 USA.
RP Metzger, MB (reprint author), NCI, Lab Prot Dynam & Signaling, Ctr Canc Res, NIH, Frederick, MD 21702 USA.
EM amw@nih.gov
NR 17
TC 10
Z9 10
U1 0
U2 7
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1465-7392
J9 NAT CELL BIOL
JI Nat. Cell Biol.
PD DEC
PY 2010
VL 12
IS 12
BP 1124
EP 1126
DI 10.1038/ncb1210-1124
PG 3
WC Cell Biology
SC Cell Biology
GA 688DY
UT WOS:000284831200002
PM 21124306
ER

PT J
AU Fujita, K
   Horikawa, I
   Mondal, AM
   Jenkins, LMM
   Appella, E
   Vojtesek, B
   Bourdon, JC
   Lane, DP
   Harris, CC
AF Fujita, Kaori
   Horikawa, Izumi
   Mondal, Abdul M.
   Jenkins, Lisa M. Miller
   Appella, Ettore
   Vojtesek, Borivoj
   Bourdon, Jean-Christophe
   Lane, David P.
   Harris, Curtis C.
TI Positive feedback between p53 and TRF2 during telomere-damage signalling
   and cellular senescence
SO NATURE CELL BIOLOGY
LA English
DT Article
ID DNA-DAMAGE; BETA-CATENIN; STEM-CELLS; IN-VIVO; TUMOR SUPPRESSION;
   PROTEIN; UBIQUITIN; CANCER; DYSFUNCTION; SIAH-1
AB The telomere-capping complex shelterin protects functional telomeres and prevents the initiation of unwanted DNA-damage-response pathways. At the end of cellular replicative lifespan, uncapped telomeres lose this protective mechanism and DNA-damage signalling pathways are triggered that activate p53 and thereby induce replicative senescence. Here, we identify a signalling pathway involving p53, Siah1 (a p53-inducible E3 ubiquitin ligase) and TRF2 (telomere repeat binding factor 2; a component of the shelterin complex). Endogenous Siah1 and TRF2 were upregulated and downregulated, respectively, during replicative senescence with activated p53. Experimental manipulation of p53 expression demonstrated that p53 induces Siah1 and represses TRF2 protein levels. The p53-dependent ubiquitylation and proteasomal degradation of TRF2 are attributed to the E3 ligase activity of Siah1. Knockdown of Siah1 stabilized TRF2 and delayed the onset of cellular replicative senescence, suggesting a role for Siah1 and TRF2 in p53-regulated senescence. This study reveals that p53, a downstream effector of telomere-initiated damage signalling, also functions upstream of the shelterin complex.
C1 [Fujita, Kaori; Horikawa, Izumi; Mondal, Abdul M.; Harris, Curtis C.] NCI, Human Carcinogenesis Lab, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
   [Jenkins, Lisa M. Miller; Appella, Ettore] NCI, Cell Biol Lab, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
   [Vojtesek, Borivoj] Masaryk Mem Canc Inst, Brno 65653, Czech Republic.
   [Bourdon, Jean-Christophe; Lane, David P.] Univ Dundee, Ninewells Hosp, Dept Surg & Mol Oncol, Inserm European Associated Lab, Dundee DD1 9SY, Scotland.
   [Lane, David P.] Inst Mol & Cell Biol, Singapore 138673, Singapore.
RP Harris, CC (reprint author), NCI, Human Carcinogenesis Lab, Ctr Canc Res, NIH, 37 Convent Dr, Bethesda, MD 20892 USA.
EM curtis_harris@nih.gov
RI ASTAR, IMCB/E-2320-2012; bourdon, jean-christophe/A-4439-2008; 
OI Bourdon, jean-christophe/0000-0003-4623-9386
FU NIH, NCI; Grant Agency of the Czech Republic [301/08/1468]; Internal
   Grant Agency of Health of Czech Republic [NS/9812-4]; Breast Cancer
   Campaign; Cancer-Research UK; Institut National de la Sante et de la
   Recherche Medicale
FX We thank M. Tainsky, B. Vogelstein and T. de Lange for cells and
   reagents. We also thank K. Kumamoto for carrying out Nutlin-3a
   treatment, A. Robles for carrying out doxorubicin treatment of
   lymphoblast cells, M. Yoneda for technical assistance and E. Spillare
   for continuous support. This research was supported in part by the
   Intramural Research Program of the NIH, NCI. B.V. was supported by the
   grants from the Grant Agency of the Czech Republic (number 301/08/1468)
   and the Internal Grant Agency of Health of Czech Republic (number
   NS/9812-4). J.C.B. was supported by Breast Cancer Campaign,
   Cancer-Research UK and the Institut National de la Sante et de la
   Recherche Medicale. D.L. is a Gibb fellow of Cancer-Research UK.
NR 59
TC 44
Z9 45
U1 0
U2 11
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1465-7392
J9 NAT CELL BIOL
JI Nat. Cell Biol.
PD DEC
PY 2010
VL 12
IS 12
BP 1205
EP U196
DI 10.1038/ncb2123
PG 21
WC Cell Biology
SC Cell Biology
GA 688DY
UT WOS:000284831200012
PM 21057505
ER

PT J
AU Smith, FD
   Langeberg, LK
   Cellurale, C
   Pawson, T
   Morrison, DK
   Davis, RJ
   Scott, JD
AF Smith, F. Donelson
   Langeberg, Lorene K.
   Cellurale, Cristina
   Pawson, Tony
   Morrison, Deborah K.
   Davis, Roger J.
   Scott, John D.
TI AKAP-Lbc enhances cyclic AMP control of the ERK1/2 cascade
SO NATURE CELL BIOLOGY
LA English
DT Article
ID PROTEIN-KINASE-A; SIGNALING PATHWAYS; IN-VIVO; B-RAF; ACTIVATION; CAMP;
   SCAFFOLD; INHIBITION; KSR
AB Mitogen-activated protein kinase (MAPK) cascades propagate a variety of cellular activities(1). Processive relay of signals through RAF-MEK-ERK modulates cell growth and proliferation(2,3). Signalling through this ERK cascade is frequently amplified in cancers, and drugs such as sorafenib (which is prescribed to treat renal and hepatic carcinomas) and PLX4720 (which targets melanomas) inhibit RAF kinases(4,5). Natural factors that influence ERK1/2 signalling include the second messenger cyclic AMP(6,7). However, the mechanisms underlying this cascade have been difficult to elucidate. We demonstrate that the A-kinase-anchoring protein AKAP-Lbc and the scaffolding protein kinase suppressor of Ras (KSR-1) form the core of a signalling network that efficiently relay signals from RAF, through MEK, and on to ERK1/2. AKAP-Lbc functions as an enhancer of ERK signalling by securing RAF in the vicinity of MEK1 and synchronizing protein kinase A (PKA)-mediated phosphorylation of Ser 838 on KSR-1. This offers mechanistic insight into cAMP-responsive control of ERK signalling events.
C1 [Smith, F. Donelson; Langeberg, Lorene K.; Scott, John D.] Univ Washington, Sch Med, Dept Pharmacol, Howard Hughes Med Inst, Seattle, WA 98195 USA.
   [Cellurale, Cristina; Davis, Roger J.] Univ Massachusetts, Howard Hughes Med Inst, Program Mol Med, Worcester, MA 01605 USA.
   [Pawson, Tony] Mt Sinai Hosp, Samuel Lunenfeld Res Inst, Toronto, ON M5G 1X5, Canada.
   [Morrison, Deborah K.] NCI, Lab Cell & Dev Signalling, Frederick, MD 21702 USA.
RP Scott, JD (reprint author), Univ Washington, Sch Med, Dept Pharmacol, Howard Hughes Med Inst, 1959 Pacific Ave NE, Seattle, WA 98195 USA.
EM scottjdw@u.washington.edu
RI Pawson, Tony/E-4578-2013
FU  [HL088366]
FX The authors wish to thank members of the Scott lab for critical
   evaluation of this work, M. Milnes for assistance in preparation of the
   manuscript, and K.L. Guan (UCSD) and R. Marais (ICR, London) for
   plasmids encoding KSR-1 and Flag-B-Raf. J.D.S. was supported in part by
   HL088366.
NR 27
TC 70
Z9 75
U1 0
U2 5
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1465-7392
J9 NAT CELL BIOL
JI Nat. Cell Biol.
PD DEC
PY 2010
VL 12
IS 12
BP 1242
EP U287
DI 10.1038/ncb2130
PG 16
WC Cell Biology
SC Cell Biology
GA 688DY
UT WOS:000284831200017
PM 21102438
ER

PT J
AU Jenkins, LMM
   Ott, DE
   Hayashi, R
   Coren, LV
   Wang, DY
   Xu, Q
   Schito, ML
   Inman, JK
   Appella, DH
   Appella, E
AF Jenkins, Lisa M. Miller
   Ott, David E.
   Hayashi, Ryo
   Coren, Lori V.
   Wang, Deyun
   Xu, Qun
   Schito, Marco L.
   Inman, John K.
   Appella, Daniel H.
   Appella, Ettore
TI Small-molecule inactivation of HIV-1 NCp7 by repetitive intracellular
   acyl transfer
SO NATURE CHEMICAL BIOLOGY
LA English
DT Article
ID VIRAL NUCLEOCAPSID PROTEIN; 2-MERCAPTOBENZAMIDE THIOESTERS;
   DRUG-RESISTANCE; ZINC FINGERS; INHIBITORS; SPECIFICITY; PARTICLES;
   INFECTION; TARGET
AB The zinc fingers of the HIV-1 nucleocapsid protein, NCp7, are prime targets for antiretroviral therapeutics. Here we show that S-acyl-2-mercaptobenzamide thioester (SAMT) chemotypes inhibit HIV by modifying the NCp7 region of Gag in infected cells, thereby blocking Gag processing and reducing infectivity. The thiol produced by SAMT reaction with NCp7 is acetylated by cellular enzymes to regenerate active SAMTs via a recycling mechanism unique among small-molecule inhibitors of HIV.
C1 [Jenkins, Lisa M. Miller; Hayashi, Ryo; Schito, Marco L.; Appella, Ettore] NCI, Cell Biol Lab, NIH, Bethesda, MD 20892 USA.
   [Ott, David E.; Coren, Lori V.] NCI, AIDS & Canc Virus Program, SAIC Frederick Inc, Frederick, MD 21701 USA.
   [Wang, Deyun; Xu, Qun; Appella, Daniel H.] NIDDKD, Bioorgan Chem Lab, Bethesda, MD 20892 USA.
   [Inman, John K.] NIAID, Bethesda, MD 20892 USA.
RP Jenkins, LMM (reprint author), NCI, Cell Biol Lab, NIH, Bldg 37, Bethesda, MD 20892 USA.
EM appellae@mail.nih.gov
RI Xu, Qun /C-6996-2011
FU US National Institutes of Health; National Institute of Diabetes and
   Digestive and Kidney Diseases; US National Cancer Institute
   [HHSN261200800001E, N01-CO-12400]
FX The authors thank T. Hartman (ImQuest Biosciences) for antiviral assays,
   E. Chertova (US National Cancer Institute at Frederick) for HPLC
   separation of Gag and P. Srivastava (US National Cancer Institute) for
   synthesis of <SUP>14</SUP>C-SAMT-247. The authors thank J.A. Turpin and
   P.F. Kiser for helpful discussion. This research was supported by the US
   National Institutes of Health Intramural AIDS Targeted Antiretroviral
   Program (L.M.M.J., R.H., M.L.S., E.A.), the Intramural Research Program
   of the National Institute of Diabetes and Digestive and Kidney Diseases
   (D.W., Q.X., D.H.A.) and with federal funds from the US National Cancer
   Institute under Contracts No. HHSN261200800001E and No. N01-CO-12400
   (D.E.O., L.V.C.).
NR 24
TC 15
Z9 15
U1 0
U2 14
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1552-4450
J9 NAT CHEM BIOL
JI Nat. Chem. Biol.
PD DEC
PY 2010
VL 6
IS 12
BP 887
EP 889
DI 10.1038/NCHEMBIO.456
PG 3
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 680EH
UT WOS:000284214700017
ER

PT J
AU Sotoodehnia, N
   Isaacs, A
   de Bakker, PIW
   Dorr, M
   Newton-Cheh, C
   Nolte, IM
   van der Harst, P
   Muller, M
   Eijgelsheim, M
   Alonso, A
   Hicks, AA
   Padmanabhan, S
   Hayward, C
   Smith, AV
   Polasek, O
   Giovannone, S
   Fu, JY
   Magnani, JW
   Marciante, KD
   Pfeufer, A
   Gharib, SA
   Teumer, A
   Li, M
   Bis, JC
   Rivadeneira, F
   Aspelund, T
   Kottgen, A
   Johnson, T
   Rice, K
   Sie, MPS
   Wang, YA
   Klopp, N
   Fuchsberger, C
   Wild, SH
   Leach, IM
   Estrada, K
   Volker, U
   Wright, AF
   Asselbergs, FW
   Qu, JX
   Chakravarti, A
   Sinner, MF
   Kors, JA
   Petersmann, A
   Harris, TB
   Soliman, EZ
   Munroe, PB
   Psaty, BM
   Oostra, BA
   Cupples, LA
   Perz, S
   de Boer, RA
   Uitterlinden, AG
   Volzke, H
   Spector, TD
   Liu, FY
   Boerwinkle, E
   Dominiczak, AF
   Rotter, JI
   van Herpen, G
   Levy, D
   Wichmann, HE
   van Gilst, WH
   Witteman, JCM
   Kroemer, HK
   Kao, WHL
   Heckbert, SR
   Meitinger, T
   Hofman, A
   Campbell, H
   Folsom, AR
   van Veldhuisen, DJ
   Schwienbacher, C
   O'Donnell, CJ
   Volpato, CB
   Caulfield, MJ
   Connell, JM
   Launer, L
   Lu, XW
   Franke, L
   Fehrmann, RSN
   Meerman, GT
   Groen, HJM
   Weersma, RK
   van den Berg, LH
   Wijmenga, C
   Ophoff, RA
   Navis, G
   Rudan, I
   Snieder, H
   Wilson, JF
   Pramstaller, PP
   Siscovick, DS
   Wang, TJ
   Gudnason, V
   van Duijn, CM
   Felix, SB
   Fishman, GI
   Jamshidi, Y
   Stricker, BHC
   Samani, NJ
   Kaab, S
   Arking, DE
AF Sotoodehnia, Nona
   Isaacs, Aaron
   de Bakker, Paul I. W.
   Doerr, Marcus
   Newton-Cheh, Christopher
   Nolte, Ilja M.
   van der Harst, Pim
   Mueller, Martina
   Eijgelsheim, Mark
   Alonso, Alvaro
   Hicks, Andrew A.
   Padmanabhan, Sandosh
   Hayward, Caroline
   Smith, Albert Vernon
   Polasek, Ozren
   Giovannone, Steven
   Fu, Jingyuan
   Magnani, Jared W.
   Marciante, Kristin D.
   Pfeufer, Arne
   Gharib, Sina A.
   Teumer, Alexander
   Li, Man
   Bis, Joshua C.
   Rivadeneira, Fernando
   Aspelund, Thor
   Koettgen, Anna
   Johnson, Toby
   Rice, Kenneth
   Sie, Mark P. S.
   Wang, Ying A.
   Klopp, Norman
   Fuchsberger, Christian
   Wild, Sarah H.
   Leach, Irene Mateo
   Estrada, Karol
   Voelker, Uwe
   Wright, Alan F.
   Asselbergs, Folkert W.
   Qu, Jiaxiang
   Chakravarti, Aravinda
   Sinner, Moritz F.
   Kors, Jan A.
   Petersmann, Astrid
   Harris, Tamara B.
   Soliman, Elsayed Z.
   Munroe, Patricia B.
   Psaty, Bruce M.
   Oostra, Ben A.
   Cupples, L. Adrienne
   Perz, Siegfried
   de Boer, Rudolf A.
   Uitterlinden, Andre G.
   Voelzke, Henry
   Spector, Timothy D.
   Liu, Fang-Yu
   Boerwinkle, Eric
   Dominiczak, Anna F.
   Rotter, Jerome I.
   van Herpen, Ge
   Levy, Daniel
   Wichmann, H-Erich
   van Gilst, Wiek H.
   Witteman, Jacqueline C. M.
   Kroemer, Heyo K.
   Kao, W. H. Linda
   Heckbert, Susan R.
   Meitinger, Thomas
   Hofman, Albert
   Campbell, Harry
   Folsom, Aaron R.
   van Veldhuisen, Dirk J.
   Schwienbacher, Christine
   O'Donnell, Christopher J.
   Volpato, Claudia Beu
   Caulfield, Mark J.
   Connell, John M.
   Launer, Lenore
   Lu, Xiaowen
   Franke, Lude
   Fehrmann, Rudolf S. N.
   Meerman, Gerard te
   Groen, Harry J. M.
   Weersma, Rinse K.
   van den Berg, Leonard H.
   Wijmenga, Cisca
   Ophoff, Roel A.
   Navis, Gerjan
   Rudan, Igor
   Snieder, Harold
   Wilson, James F.
   Pramstaller, Peter P.
   Siscovick, David S.
   Wang, Thomas J.
   Gudnason, Vilmundur
   van Duijn, Cornelia M.
   Felix, Stephan B.
   Fishman, Glenn I.
   Jamshidi, Yalda
   Stricker, Bruno H. Ch
   Samani, Nilesh J.
   Kaeaeb, Stefan
   Arking, Dan E.
TI Common variants in 22 loci are associated with QRS duration and cardiac
   ventricular conduction
SO NATURE GENETICS
LA English
DT Article
ID GENOME-WIDE ASSOCIATION; QT INTERVAL DURATION; RICH REPEAT PROTEIN;
   HEART-RATE; TRANSCRIPTION FACTOR; GENE-EXPRESSION; PR INTERVAL; SYSTEM;
   DISEASE; ELECTROCARDIOGRAM
AB The QRS interval, from the beginning of the Q wave to the end of the S wave on an electrocardiogram, reflects ventricular depolarization and conduction time and is a risk factor for mortality, sudden death and heart failure. We performed a genomewide association meta-analysis in 40,407 individuals of European descent from 14 studies, with further genotyping in 7,170 additional Europeans, and we identified 22 loci associated with QRS duration ( P < 5 x 10(-8)). These loci map in or near genes in pathways with established roles in ventricular conduction such as sodium channels, transcription factors and calcium-handling proteins, but also point to previously unidentified biologic processes, such as kinase inhibitors and genes related to tumorigenesis. We demonstrate that SCN10A, a candidate gene at the most significantly associated locus in this study, is expressed in the mouse ventricular conduction system, and treatment with a selective SCN10A blocker prolongs QRS duration. These findings extend our current knowledge of ventricular depolarization and conduction.
C1 [Sotoodehnia, Nona] Univ Washington, Dept Med, Div Cardiol, Seattle, WA 98195 USA.
   [Sotoodehnia, Nona; Marciante, Kristin D.; Bis, Joshua C.; Psaty, Bruce M.; Siscovick, David S.] Univ Washington, Dept Med, Cardiovasc Hlth Res Unit, Seattle, WA USA.
   [Isaacs, Aaron; Sie, Mark P. S.; van Duijn, Cornelia M.] Erasmus Med Ctr MC, Genet Epidemiol Unit, Dept Epidemiol, Rotterdam, Netherlands.
   [Isaacs, Aaron; Oostra, Ben A.; van Duijn, Cornelia M.] Ctr Med Syst Biol, Leiden, Netherlands.
   [de Bakker, Paul I. W.] Harvard Univ, Brigham & Womens Hosp, Sch Med, Div Genet,Dept Med, Boston, MA 02115 USA.
   [de Bakker, Paul I. W.] Broad Inst, Program Med & Populat Genet, Cambridge, MA USA.
   [de Bakker, Paul I. W.] Univ Med Ctr, Dept Med Genet, Utrecht, Netherlands.
   [de Bakker, Paul I. W.] Univ Med Ctr, Julius Ctr Hlth Sci & Primary Care, Utrecht, Netherlands.
   [Doerr, Marcus; Felix, Stephan B.] Ernst Moritz Arndt Univ Greifswald, Dept Internal Med B, Greifswald, Germany.
   [Newton-Cheh, Christopher] Massachusetts Gen Hosp, Ctr Human Genet Res, Boston, MA 02114 USA.
   [Newton-Cheh, Christopher; Wang, Thomas J.] Massachusetts Gen Hosp, Div Cardiol, Boston, MA 02114 USA.
   [Newton-Cheh, Christopher; Magnani, Jared W.; Wang, Ying A.; Cupples, L. Adrienne; Levy, Daniel; O'Donnell, Christopher J.; Wang, Thomas J.] NHLBI, Framingham Heart Study, Framingham, MA USA.
   [Nolte, Ilja M.; Fu, Jingyuan; Asselbergs, Folkert W.; Lu, Xiaowen; Snieder, Harold] Univ Groningen, Univ Med Ctr Groningen, Dept Epidemiol, Unit Genet Epidemiol & Bioinformat, Groningen, Netherlands.
   [van der Harst, Pim; Leach, Irene Mateo; Asselbergs, Folkert W.; de Boer, Rudolf A.; van Gilst, Wiek H.; van Veldhuisen, Dirk J.] Univ Groningen, Univ Med Ctr Groningen, Dept Cardiol, Groningen, Netherlands.
   [Mueller, Martina] Univ Munich, Chair Epidemiol, Inst Med Informat Biometry & Epidemiol, Munich, Germany.
   [Mueller, Martina; Sinner, Moritz F.] Univ Munich, Dept Med 1, Univ Hosp Grosshadern, Munich, Germany.
   [Mueller, Martina; Klopp, Norman; Wichmann, H-Erich] German Res Ctr Environm Hlth, Helmholtz Zentrum Munchen, Inst Epidemiol, Neuherberg, Germany.
   [Eijgelsheim, Mark; Rivadeneira, Fernando; Uitterlinden, Andre G.; Witteman, Jacqueline C. M.; Hofman, Albert; Stricker, Bruno H. Ch] Erasmus MC, Dept Epidemiol, Rotterdam, Netherlands.
   [Alonso, Alvaro; Folsom, Aaron R.] Univ Minnesota, Sch Publ Hlth, Div Epidemiol & Community Hlth, Minneapolis, MN USA.
   [Hicks, Andrew A.; Fuchsberger, Christian; Schwienbacher, Christine; Volpato, Claudia Beu; Pramstaller, Peter P.] European Acad Bozen Bolzano EURAC, Inst Med Genet, Bolzano, Italy.
   [Hicks, Andrew A.; Pfeufer, Arne; Fuchsberger, Christian; Schwienbacher, Christine; Volpato, Claudia Beu; Pramstaller, Peter P.] Univ Lubeck, Affiliated Inst, Lubeck, Germany.
   [Padmanabhan, Sandosh; Dominiczak, Anna F.] Univ Glasgow, Inst Cardiovasc & Med Sci, Coll Med Vet & Life Sci, Glasgow, Lanark, Scotland.
   [Hayward, Caroline; Wright, Alan F.] MRC, Human Genet Unit, Inst Genet & Mol Med, Edinburgh, Midlothian, Scotland.
   [Smith, Albert Vernon; Aspelund, Thor; Gudnason, Vilmundur] Iceland Heart Assoc, Kopavogur, Iceland.
   [Smith, Albert Vernon; Aspelund, Thor; Gudnason, Vilmundur] Univ Iceland, Reykjavik, Iceland.
   [Polasek, Ozren] Univ Zagreb, Sch Med, Andrija Stampar Sch Publ Hlth, Zagreb 41001, Croatia.
   [Giovannone, Steven; Qu, Jiaxiang; Liu, Fang-Yu; Fishman, Glenn I.] NYU, Sch Med, Leon H Charney Div Cardiol, New York, NY USA.
   [Fu, Jingyuan; Fehrmann, Rudolf S. N.; Meerman, Gerard te; Wijmenga, Cisca] Univ Groningen, Univ Med Ctr Groningen, Dept Genet, NL-9700 AB Groningen, Netherlands.
   [Magnani, Jared W.] Boston Univ, Sch Med, Sect Cardiovasc Med, Boston, MA 02118 USA.
   [Pfeufer, Arne; Meitinger, Thomas] German Res Ctr Environm Hlth, Helmholtz Zentrum Munchen, Inst Human Genet, Neuherberg, Germany.
   [Pfeufer, Arne; Meitinger, Thomas] Tech Univ Munich, Klinikum Rechts Isar, Inst Human Genet, D-8000 Munich, Germany.
   [Gharib, Sina A.] Univ Washington, Dept Med, Ctr Lung Biol, Seattle, WA USA.
   [Teumer, Alexander; Voelker, Uwe] Ernst Moritz Arndt Univ Greifswald, Interfac Inst Genet & Funct Gen, Greifswald, Germany.
   [Li, Man; Koettgen, Anna; Kao, W. H. Linda] Johns Hopkins Univ, Dept Epidemiol, Baltimore, MD USA.
   [Li, Man; Kao, W. H. Linda] Johns Hopkins Univ, Welch Ctr Prevent Epidemiol & Clin Res, Baltimore, MD USA.
   [Rivadeneira, Fernando; Estrada, Karol] Erasmus MC, Dept Internal Med, Rotterdam, Netherlands.
   [Johnson, Toby; Munroe, Patricia B.; Caulfield, Mark J.] Queen Mary Univ London, Barts & London Sch Med, William Harvey Res Inst, Clin Pharmacol & Barts & London Genome Ctr, London, England.
   [Johnson, Toby; Munroe, Patricia B.; Caulfield, Mark J.] Barts & London Natl Inst Hlth Res, Cardiovasc Biomed Res Unit, London, England.
   [Rice, Kenneth] Univ Washington, Dept Biostat, Seattle, WA 98195 USA.
   [Wang, Ying A.; Cupples, L. Adrienne] Boston Univ, Sch Publ Hlth, Dept Biostat, Boston, MA 02118 USA.
   [Wild, Sarah H.; Rudan, Igor; Wilson, James F.] Univ Edinburgh, Ctr Populat Hlth Sci, Edinburgh, Midlothian, Scotland.
   [Asselbergs, Folkert W.] Univ Med Ctr Utrecht, Div Heart & Lungs, Dept Cardiol, Utrecht, Netherlands.
   [Chakravarti, Aravinda; Arking, Dan E.] Johns Hopkins Univ, Sch Med, McKusick Nathans Inst Genet Med, Baltimore, MD USA.
   [Kors, Jan A.; van Herpen, Ge; Stricker, Bruno H. Ch] Erasmus MC, Dept Med Informat, Rotterdam, Netherlands.
   [Petersmann, Astrid] Ernst Moritz Arndt Univ Greifswald, Inst Clin Chem & Lab Med, Greifswald, Germany.
   [Harris, Tamara B.; Launer, Lenore] NIA, Lab Epidemiol Demog & Biometry, NIH, Bethesda, MD 20892 USA.
   [Soliman, Elsayed Z.] Wake Forest Univ, Sch Med, Epidemiol Cardiol Res Ctr EPICARE, Winston Salem, NC 27109 USA.
   [Psaty, Bruce M.] Univ Washington, Dept Epidemiol, Seattle, WA 98195 USA.
   [Psaty, Bruce M.] Univ Washington, Dept Hlth Serv, Seattle, WA 98195 USA.
   [Psaty, Bruce M.; Heckbert, Susan R.] Grp Hlth Cooperat Puget Sound, Gup Hlth Res Inst, Seattle, WA 98121 USA.
   [Oostra, Ben A.] Erasmus MC, Dept Clin Genet, Rotterdam, Netherlands.
   [Perz, Siegfried] German Res Ctr Environm Hlth, Helmholtz Zentrum Munchen, Inst Biol & Med Imaging, Neuherberg, Germany.
   [Uitterlinden, Andre G.; Witteman, Jacqueline C. M.; Hofman, Albert; van Duijn, Cornelia M.; Stricker, Bruno H. Ch] NCHA, NGI, Rotterdam, Netherlands.
   [Voelzke, Henry] Ernst Moritz Arndt Univ Greifswald, Inst Community Med, Greifswald, Germany.
   [Spector, Timothy D.; Snieder, Harold; Jamshidi, Yalda] St Thomas Hosp, Kings Coll London, Dept Twin Res, London, England.
   [Spector, Timothy D.; Snieder, Harold; Jamshidi, Yalda] St Thomas Hosp, Kings Coll London, Genet Epidemiol Unit, London, England.
   [Boerwinkle, Eric] Univ Texas Houston, Hlth Sci Ctr, Ctr Human Genet, Houston, TX USA.
   [Boerwinkle, Eric] Univ Texas Houston, Hlth Sci Ctr, Inst Mol Med, Houston, TX USA.
   [Rotter, Jerome I.] Cedars Sinai Med Ctr, Inst Med Genet, Los Angeles, CA 90048 USA.
   [Levy, Daniel; O'Donnell, Christopher J.] NHLBI, Bethesda, MD 20892 USA.
   [Wichmann, H-Erich] Univ Munich, Klinikum Grosshadern, D-8000 Munich, Germany.
   [Kroemer, Heyo K.] Ernst Moritz Arndt Univ Greifswald, Dept Pharmacol, Ctr Pharmacol & Expt Therapeut, Greifswald, Germany.
   [Schwienbacher, Christine] Univ Ferrara, Dept Expt & Diagnost Med, I-44100 Ferrara, Italy.
   [Connell, John M.] Univ Dundee, Ninewells Hosp & Med Sch, Dundee DD1 9SY, Scotland.
   [Franke, Lude] Queen Mary Univ London, Barts & London Sch Med & Dent, Blizard Inst Cell & Mol Sci, London, England.
   [Groen, Harry J. M.] Univ Groningen, Univ Med Ctr Groningen, Dept Pulmonol, NL-9700 AB Groningen, Netherlands.
   [Weersma, Rinse K.] Univ Groningen, Univ Med Ctr Groningen, Dept Gastroenterol & Hepatol, NL-9700 AB Groningen, Netherlands.
   [van den Berg, Leonard H.] Univ Utrecht, Dept Neurol, Rudolf Magnus Inst, Univ Med Ctr Utrecht, NL-3584 CX Utrecht, Netherlands.
   [Ophoff, Roel A.] Univ Med Ctr Utrecht, Dept Med Genet, Utrecht, Netherlands.
   [Ophoff, Roel A.] Univ Calif Los Angeles, Ctr Neurobehav Genet, Los Angeles, CA USA.
   [Navis, Gerjan] Univ Groningen, Univ Med Ctr Groningen, Dept Internal Med, NL-9700 AB Groningen, Netherlands.
   [Rudan, Igor] Univ Split, Ctr Global Hlth, Sch Med, Split, Croatia.
   [Rudan, Igor] Gen Info Ltd, Zagreb, Croatia.
   [Pramstaller, Peter P.] Gen Cent Hosp, Dept Neurol, Bolzano, Italy.
   [Pramstaller, Peter P.] Med Univ Lubeck, Dept Neurol, D-23538 Lubeck, Germany.
   [Jamshidi, Yalda] St Georges Univ London, Div Clin Dev Sci, London, England.
   [Stricker, Bruno H. Ch] Inspectorate Hlth Care, The Hague, Netherlands.
   [Samani, Nilesh J.] Univ Leicester, Dept Cardiovasc Sci, Leicester, Leics, England.
   [Samani, Nilesh J.] Glenfield Gen Hosp, Leicester NIHR Biomed Res Unit Cardiovasc Dis, Leicester LE3 9QP, Leics, England.
RP Sotoodehnia, N (reprint author), Univ Washington, Dept Med, Div Cardiol, Seattle, WA 98195 USA.
EM nsotoo@u.washington.edu; skaab@med.lmu.de; arking@jhmi.edu
RI Pfeufer, Arne/B-6634-2013; van Veldhuisen, Dirk Jan/E-8967-2014;
   Wijmenga, Cisca/D-2173-2009; Pramstaller, Peter/C-2357-2008; Gudnason,
   Vilmundur/K-6885-2015; Wilson, James F/A-5704-2009; Meitinger,
   Thomas/O-1318-2015; Rivadeneira, Fernando/O-5385-2015; Smith,
   Albert/K-5150-2015; Hayward, Caroline/M-8818-2016; Franke,
   Lude/P-7036-2016; Padmanabhan, Sandosh/S-3963-2016; Hicks,
   Andrew/E-9518-2017; Rudan, Igor/I-1467-2012; Rice, Kenneth/A-4150-2013;
   de Bakker, Paul/B-8730-2009; van Gilst, Wiek/C-3828-2008; Polasek,
   Ozren/B-6002-2011; Alonso, Alvaro/A-4917-2010; Soliman,
   Elsayed/D-8124-2011; Fehrmann, Rudolf/E-2551-2011; Fuchsberger,
   Christian/C-9646-2010; Aspelund, Thor/F-4826-2011; Aspelund,
   Thor/C-5983-2008; Kottgen, Anna/D-2920-2012; Kaab, Stefan/H-3915-2012
OI Cupples, L. Adrienne/0000-0003-0273-7965; Fuchsberger,
   Christian/0000-0002-5918-8947; Johnson, Toby/0000-0002-5998-3270;
   Padmanabhan, Sandosh/0000-0003-3869-5808; Jamshidi,
   Yalda/0000-0003-0151-6482; Wijmenga, Cisca/0000-0002-5635-1614;
   Gudnason, Vilmundur/0000-0001-5696-0084; Wilson, James
   F/0000-0001-5751-9178; Rivadeneira, Fernando/0000-0001-9435-9441; Smith,
   Albert/0000-0003-1942-5845; Hayward, Caroline/0000-0002-9405-9550;
   Franke, Lude/0000-0002-5159-8802; Hicks, Andrew/0000-0001-6320-0411;
   Rudan, Igor/0000-0001-6993-6884; Rice, Kenneth/0000-0001-5779-4495; de
   Bakker, Paul/0000-0001-7735-7858; Polasek, Ozren/0000-0002-5765-1862;
   Alonso, Alvaro/0000-0002-2225-8323; Soliman,
   Elsayed/0000-0001-5632-8150; Fehrmann, Rudolf/0000-0002-7516-315X;
   Aspelund, Thor/0000-0002-7998-5433; 
FU Biotechnology and Biological Sciences Research Council [G20234]; British
   Heart Foundation [06/094, PG/02/128, RG/07/005/23633, SP/08/005/25115];
   Chief Scientist Office [, CZB/4/710]; Department of Health; Intramural
   NIH HHS; Medical Research Council [G0400874, G9521010, G9521010D,
   MC_U127561128]; NCRR NIH HHS [M01-RR00425, UL1RR025005]; NHGRI NIH HHS
   [U01HG004402]; NHLBI NIH HHS [N01-HC-55020, HL80025, K23HL80025, L30
   HL097675, N01 HC-15103, N01 HC-55222, N01-HC-25195, N01-HC-35129,
   N01-HC-45133, N01-HC-55015, N01-HC-55016, N01-HC-55018, N01-HC-55019,
   N01-HC-55021, N01-HC-55022, N01-HC-75150, N01-HC-85079, N01-HC-85080,
   N01-HC-85081, N01-HC-85082, N01-HC-85083, N01-HC-85084, N01-HC-85085,
   N01-HC-85086, N02-HL-6-4278, R01 HL082727, R01 HL087652, R01 HL088456,
   R01 HL088456-04, R01HL086694, R01HL087641, R01HL59367, R01HL64757, U01
   HL080295]; NIA NIH HHS [N01-AG-12100]; NIDDK NIH HHS [DK063491]; NINDS
   NIH HHS [NS058980]; PHS HHS [HHSN268200625226C]; Wellcome Trust
   [076113/B/04/Z]
NR 66
TC 141
Z9 142
U1 1
U2 18
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1061-4036
J9 NAT GENET
JI Nature Genet.
PD DEC
PY 2010
VL 42
IS 12
BP 1068
EP U62
DI 10.1038/ng.716
PG 11
WC Genetics & Heredity
SC Genetics & Heredity
GA 684UZ
UT WOS:000284578800009
PM 21076409
ER

PT J
AU Elks, CE
   Perry, JRB
   Sulem, P
   Chasman, DI
   Franceschini, N
   He, CY
   Lunetta, KL
   Visser, JA
   Byrne, EM
   Cousminer, DL
   Gudbjartsson, DF
   Esko, T
   Feenstra, B
   Hottenga, JJ
   Koller, DL
   Kutalik, Z
   Lin, P
   Mangino, M
   Marongiu, M
   McArdle, PF
   Smith, AV
   Stolk, L
   Van Wingerden, SH
   Zhao, JH
   Albrecht, E
   Corre, T
   Ingelsson, E
   Hayward, C
   Magnusson, PKE
   Smith, EN
   Ulivi, S
   Warrington, NM
   Zgaga, L
   Alavere, H
   Amin, N
   Aspelund, T
   Bandinelli, S
   Barroso, I
   Berenson, GS
   Bergmann, S
   Blackburn, H
   Boerwinkle, E
   Buring, JE
   Busonero, F
   Campbell, H
   Chanock, SJ
   Chen, W
   Cornelis, MC
   Couper, D
   Coviello, AD
   d'Adamo, P
   de Faire, U
   de Geus, EJC
   Deloukas, P
   Doring, A
   Smith, GD
   Easton, DF
   Eiriksdottir, G
   Emilsson, V
   Eriksson, J
   Ferrucci, L
   Folsom, AR
   Foroud, T
   Garcia, M
   Gasparini, P
   Geller, F
   Gieger, C
   Gudnason, V
   Hall, P
   Hankinson, SE
   Ferreli, L
   Heath, AC
   Hernandez, DG
   Hofman, A
   Hu, FB
   Illig, T
   Jarvelin, MR
   Johnson, AD
   Karasik, D
   Khaw, KT
   Kiel, DP
   Kilpelainen, TO
   Kolcic, I
   Kraft, P
   Launer, LJ
   Laven, JSE
   Li, SX
   Liu, JJ
   Levy, D
   Martin, NG
   McArdle, WL
   Melbye, M
   Mooser, V
   Murray, JC
   Murray, SS
   Nalls, MA
   Navarro, P
   Nelis, M
   Ness, AR
   Northstone, K
   Oostra, BA
   Peacock, M
   Palmer, LJ
   Palotie, A
   Pare, G
   Parker, AN
   Pedersen, NL
   Peltonen, L
   Pennell, CE
   Pharoah, P
   Polasek, O
   Plump, AS
   Pouta, A
   Porcu, E
   Rafnar, T
   Rice, JP
   Ring, SM
   Rivadeneira, F
   Rudan, I
   Sala, C
   Salomaa, V
   Sanna, S
   Schlessinger, D
   Schork, NJ
   Scuteri, A
   Segre, AV
   Shuldiner, AR
   Soranzo, N
   Sovio, U
   Srinivasan, SR
   Strachan, DP
   Tammesoo, ML
   Tikkanen, E
   Toniolo, D
   Tsui, K
   Tryggvadottir, L
   Tyrer, J
   Uda, M
   van Dam, RM
   van Meurs, JBJ
   Vollenweider, P
   Waeber, G
   Wareham, NJ
   Waterworth, DM
   Weedon, MN
   Wichmann, HE
   Willemsen, G
   Wilson, JF
   Wright, AF
   Young, L
   Zhai, GJ
   Zhuang, WV
   Bierut, LJ
   Boomsma, DI
   Boyd, HA
   Crisponi, L
   Demerath, EW
   van Duijn, CM
   Econs, MJ
   Harris, TB
   Hunter, DJ
   Loos, RJF
   Metspalu, A
   Montgomery, GW
   Ridker, PM
   Spector, TD
   Streeten, EA
   Stefansson, K
   Thorsteinsdottir, U
   Uitterlinden, AG
   Widen, E
   Murabito, JM
   Ong, KK
   Murray, A
AF Elks, Cathy E.
   Perry, John R. B.
   Sulem, Patrick
   Chasman, Daniel I.
   Franceschini, Nora
   He, Chunyan
   Lunetta, Kathryn L.
   Visser, Jenny A.
   Byrne, Enda M.
   Cousminer, Diana L.
   Gudbjartsson, Daniel F.
   Esko, Tonu
   Feenstra, Bjarke
   Hottenga, Jouke-Jan
   Koller, Daniel L.
   Kutalik, Zoltan
   Lin, Peng
   Mangino, Massimo
   Marongiu, Mara
   McArdle, Patrick F.
   Smith, Albert V.
   Stolk, Lisette
   Van Wingerden, Sophie H.
   Zhao, Jing Hua
   Albrecht, Eva
   Corre, Tanguy
   Ingelsson, Erik
   Hayward, Caroline
   Magnusson, Patrik K. E.
   Smith, Erin N.
   Ulivi, Shelia
   Warrington, Nicole M.
   Zgaga, Lina
   Alavere, Helen
   Amin, Najaf
   Aspelund, Thor
   Bandinelli, Stefania
   Barroso, Ines
   Berenson, Gerald S.
   Bergmann, Sven
   Blackburn, Hannah
   Boerwinkle, Eric
   Buring, Julie E.
   Busonero, Fabio
   Campbell, Harry
   Chanock, Stephen J.
   Chen, Wei
   Cornelis, Marilyn C.
   Couper, David
   Coviello, Andrea D.
   d'Adamo, Pio
   de Faire, Ulf
   de Geus, Eco J. C.
   Deloukas, Panos
   Doering, Angela
   Smith, George Davey
   Easton, Douglas F.
   Eiriksdottir, Gudny
   Emilsson, Valur
   Eriksson, Johan
   Ferrucci, Luigi
   Folsom, Aaron R.
   Foroud, Tatiana
   Garcia, Melissa
   Gasparini, Paolo
   Geller, Frank
   Gieger, Christian
   Gudnason, Vilmundur
   Hall, Per
   Hankinson, Susan E.
   Ferreli, Liana
   Heath, Andrew C.
   Hernandez, Dena G.
   Hofman, Albert
   Hu, Frank B.
   Illig, Thomas
   Jaervelin, Marjo-Riitta
   Johnson, Andrew D.
   Karasik, David
   Khaw, Kay-Tee
   Kiel, Douglas P.
   Kilpelaeinen, Tuomas O.
   Kolcic, Ivana
   Kraft, Peter
   Launer, Lenore J.
   Laven, Joop S. E.
   Li, Shengxu
   Liu, Jianjun
   Levy, Daniel
   Martin, Nicholas G.
   McArdle, Wendy L.
   Melbye, Mads
   Mooser, Vincent
   Murray, Jeffrey C.
   Murray, Sarah S.
   Nalls, Michael A.
   Navarro, Pau
   Nelis, Mari
   Ness, Andrew R.
   Northstone, Kate
   Oostra, Ben A.
   Peacock, Munro
   Palmer, Lyle J.
   Palotie, Aarno
   Pare, Guillaume
   Parker, Alex N.
   Pedersen, Nancy L.
   Peltonen, Leena
   Pennell, Craig E.
   Pharoah, Paul
   Polasek, Ozren
   Plump, Andrew S.
   Pouta, Anneli
   Porcu, Eleonora
   Rafnar, Thorunn
   Rice, John P.
   Ring, Susan M.
   Rivadeneira, Fernando
   Rudan, Igor
   Sala, Cinzia
   Salomaa, Veikko
   Sanna, Serena
   Schlessinger, David
   Schork, Nicholas J.
   Scuteri, Angelo
   Segre, Ayellet V.
   Shuldiner, Alan R.
   Soranzo, Nicole
   Sovio, Ulla
   Srinivasan, Sathanur R.
   Strachan, David P.
   Tammesoo, Mar-Liis
   Tikkanen, Emmi
   Toniolo, Daniela
   Tsui, Kim
   Tryggvadottir, Laufey
   Tyrer, Jonathon
   Uda, Manuela
   van Dam, Rob M.
   van Meurs, Joyce B. J.
   Vollenweider, Peter
   Waeber, Gerard
   Wareham, Nicholas J.
   Waterworth, Dawn M.
   Weedon, Michael N.
   Wichmann, H. Erich
   Willemsen, Gonneke
   Wilson, James F.
   Wright, Alan F.
   Young, Lauren
   Zhai, Guangju
   Zhuang, Wei Vivian
   Bierut, Laura J.
   Boomsma, Dorret I.
   Boyd, Heather A.
   Crisponi, Laura
   Demerath, Ellen W.
   van Duijn, Cornelia M.
   Econs, Michael J.
   Harris, Tamara B.
   Hunter, David J.
   Loos, Ruth J. F.
   Metspalu, Andres
   Montgomery, Grant W.
   Ridker, Paul M.
   Spector, Tim D.
   Streeten, Elizabeth A.
   Stefansson, Kari
   Thorsteinsdottir, Unnur
   Uitterlinden, Andre G.
   Widen, Elisabeth
   Murabito, Joanne M.
   Ong, Ken K.
   Murray, Anna
CA GIANT Consortium
TI Thirty new loci for age at menarche identified by a meta-analysis of
   genome-wide association studies
SO NATURE GENETICS
LA English
DT Article
ID FOLLICLE-STIMULATING-HORMONE; ENERGY-BALANCE; SEQUENCE VARIANTS;
   INHIBIN-B; PUBERTY; WOMEN; GIRLS; GENE; EPIDEMIOLOGY; HERITABILITY
AB To identify loci for age at menarche, we performed a meta-analysis of 32 genome-wide association studies in 87,802 women of European descent, with replication in up to 14,731 women. In addition to the known loci at LIN28B (P = 5.4 x 10(-60)) and 9q31.2 (P = 2.2 x 10(-33)), we identified 30 new menarche loci (all P < 5 x 10(-8)) and found suggestive evidence for a further 10 loci (P < 1.9 x 10(-6)). The new loci included four previously associated with body mass index (in or near FTO, SEC16B, TRA2B and TMEM18), three in or near other genes implicated in energy homeostasis (BSX, CRTC1 and MCHR2) and three in or near genes implicated in hormonal regulation (INHBA, PCSK2 and RXRG). Ingenuity and gene-set enrichment pathway analyses identified coenzyme A and fatty acid biosynthesis as biological processes related to menarche timing.
C1 [Lunetta, Kathryn L.; Johnson, Andrew D.; Levy, Daniel; Murabito, Joanne M.] NHLBI, Framingham Heart Study, Framingham, MA USA.
   [Elks, Cathy E.; Zhao, Jing Hua; Kilpelaeinen, Tuomas O.; Li, Shengxu; Wareham, Nicholas J.; Loos, Ruth J. F.; Montgomery, Grant W.; Ong, Ken K.] Addenbrookes Hosp, Epidemiol Unit, MRC, Inst Metab Sci, Cambridge, England.
   [Perry, John R. B.; Weedon, Michael N.; Ridker, Paul M.; Murray, Anna] Univ Exeter, Peninsula Med Sch, Exeter EX4 4QJ, Devon, England.
   [Sulem, Patrick; Gudbjartsson, Daniel F.; Rafnar, Thorunn; Stefansson, Kari; Thorsteinsdottir, Unnur] deCODE Genet, Reykjavik, Iceland.
   [Chasman, Daniel I.; Buring, Julie E.; Pare, Guillaume; Ridker, Paul M.; Ong, Ken K.] Brigham & Womens Hosp, Div Prevent Med, Boston, MA 02115 USA.
   [Chasman, Daniel I.; Buring, Julie E.; Pare, Guillaume; Peltonen, Leena; Ridker, Paul M.] Harvard Univ, Sch Med, Boston, MA USA.
   [Elks, Cathy E.; Perry, John R. B.; Sulem, Patrick; Franceschini, Nora] Univ N Carolina, Dept Epidemiol, Gillings Sch Global Publ Hlth, Chapel Hill, NC USA.
   [He, Chunyan] Indiana Univ, Sch Med, Dept Publ Hlth, Indiana, PA USA.
   [He, Chunyan] Indiana Univ, Melvin & Bren Simon Canc Ctr, Indiana, PA USA.
   [Lunetta, Kathryn L.; Zhuang, Wei Vivian] Boston Univ, Sch Publ Hlth, Dept Biostat, Boston, MA USA.
   [Visser, Jenny A.; Stolk, Lisette; Rivadeneira, Fernando; van Meurs, Joyce B. J.; Uitterlinden, Andre G.] Erasmus Med Ctr MC, Dept Internal Med, Rotterdam, Netherlands.
   [Byrne, Enda M.] Queensland Inst Med Res, Brisbane, Qld 4006, Australia.
   [Byrne, Enda M.] Univ Queensland, Brisbane, Qld, Australia.
   [Cousminer, Diana L.; Palotie, Aarno; Peltonen, Leena; Tikkanen, Emmi; Widen, Elisabeth] Univ Helsinki, Inst Mol Med Finland FIMM, FIN-00014 Helsinki, Finland.
   [Esko, Tonu; Alavere, Helen; Nelis, Mari; Tammesoo, Mar-Liis; Metspalu, Andres] Univ Tartu, Estonian Genome Ctr, EE-50090 Tartu, Estonia.
   [Esko, Tonu; Nelis, Mari; Metspalu, Andres] Univ Tartu, Inst Mol & Cell Biol, Dept Biotechnol, EE-50090 Tartu, Estonia.
   [Esko, Tonu; Nelis, Mari; Metspalu, Andres] Estonian Bioctr, Genotyping Core Facil, Tartu, Estonia.
   [Feenstra, Bjarke; Geller, Frank; Melbye, Mads; Boyd, Heather A.] Statens Serum Inst, Dept Epidemiol Res, DK-2300 Copenhagen, Denmark.
   [Hottenga, Jouke-Jan; de Geus, Eco J. C.; Willemsen, Gonneke; Boomsma, Dorret I.] Vrije Univ Amsterdam, Dept Biol Psychol, Amsterdam, Netherlands.
   [Koller, Daniel L.; Foroud, Tatiana] Indiana Univ, Sch Med, Dept Med & Mol Genet, Indianapolis, IN 46202 USA.
   [Kutalik, Zoltan; Bergmann, Sven] Univ Lausanne, Dept Med Genet, Lausanne, Switzerland.
   [Kutalik, Zoltan; Bergmann, Sven] Swiss Inst Bioinformat, Lausanne, Switzerland.
   [Lin, Peng; Rice, John P.; Bierut, Laura J.] Washington Univ, Sch Med, Dept Psychiat, St Louis, MO 63110 USA.
   [Mangino, Massimo; Soranzo, Nicole; Zhai, Guangju; Spector, Tim D.] Kings Coll London, Dept Twin Res & Genet Epidemiol, London WC2R 2LS, England.
   [Marongiu, Mara; Busonero, Fabio; Ferreli, Liana; Porcu, Eleonora; Sanna, Serena; Scuteri, Angelo; Uda, Manuela; Crisponi, Laura] CNR, Ist Neurogenet & Neurofarmacol, Cagliari, Italy.
   [McArdle, Patrick F.; Shuldiner, Alan R.; Streeten, Elizabeth A.] Univ Maryland, Sch Med, Div Endocrinol Diabet & Nutr, Baltimore, MD 21201 USA.
   [Smith, Albert V.; Aspelund, Thor; Eiriksdottir, Gudny; Gudnason, Vilmundur] Iceland Heart Assoc, Kopavogur, Iceland.
   [Smith, Albert V.; Aspelund, Thor; Gudnason, Vilmundur; Econs, Michael J.] Univ Iceland, Reykjavik, Iceland.
   [Stolk, Lisette; Hofman, Albert; Rivadeneira, Fernando; van Meurs, Joyce B. J.; van Duijn, Cornelia M.; Uitterlinden, Andre G.] Netherlands Consortium Healthy Aging, Rotterdam, Netherlands.
   [Van Wingerden, Sophie H.; Amin, Najaf; Oostra, Ben A.; van Duijn, Cornelia M.] Erasmus Univ, Dept Epidemiol, Med Ctr, Genet Epidemiol Unit, Rotterdam, Netherlands.
   [Albrecht, Eva; Doering, Angela; Gieger, Christian; Illig, Thomas; Wichmann, H. Erich] German Res Ctr Environm Hlth, Helmholtz Zentrum Munchen, Inst Epidemiol, Neuherberg, Germany.
   [Corre, Tanguy; Sala, Cinzia; Toniolo, Daniela] Ist Sci San Raffaele, Div Genet & Cell Biol, I-20132 Milan, Italy.
   [Ingelsson, Erik; Magnusson, Patrik K. E.; Hall, Per; Pedersen, Nancy L.] Karolinska Inst, Dept Med Epidemiol & Biostat, Stockholm, Sweden.
   [Hayward, Caroline; Navarro, Pau; Wright, Alan F.] Western Gen Hosp, Inst Genet & Mol Med, MRC Human Genet Unit, Edinburgh EH4 2XU, Midlothian, Scotland.
   [Smith, Erin N.; Murray, Sarah S.; Schork, Nicholas J.] Scripps Genom Med, La Jolla, CA USA.
   [Smith, Erin N.; Murray, Sarah S.; Schork, Nicholas J.] Scripps Translat Sci Inst, La Jolla, CA USA.
   [Smith, Erin N.; Murray, Sarah S.; Schork, Nicholas J.] Scripps Res Inst, La Jolla, CA 92037 USA.
   [Ulivi, Shelia; d'Adamo, Pio; Gasparini, Paolo] Univ Trieste, Dept Reprod Sci & Dev, Trieste, Italy.
   [Warrington, Nicole M.; Palmer, Lyle J.] Univ Western Australia, Ctr Genet Epidemiol & Biostat, Crawley, WA, Australia.
   [Zgaga, Lina; Campbell, Harry; Rudan, Igor; Wilson, James F.] Univ Edinburgh, Ctr Populat Hlth Sci, Edinburgh, Midlothian, Scotland.
   [Bandinelli, Stefania] Azienda Sanit Firenze, Geriatr Unit, Florence, Italy.
   [Barroso, Ines; Blackburn, Hannah; Deloukas, Panos; Palotie, Aarno; Peltonen, Leena; Soranzo, Nicole] Wellcome Trust Sanger Inst, Cambridge, England.
   [Berenson, Gerald S.; Chen, Wei; Srinivasan, Sathanur R.] Tulane Univ, New Orleans, LA 70118 USA.
   [Boerwinkle, Eric] Univ Texas Houston, Hlth Sci Ctr, Ctr Human Genet, Houston, TX USA.
   [Buring, Julie E.; Hankinson, Susan E.; Hu, Frank B.; Kraft, Peter; Hunter, David J.; Ridker, Paul M.] Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA.
   [Chanock, Stephen J.; Hunter, David J.] NCI, Div Canc Epidemiol & Genet, NIH, Dept Hlth & Human Serv, Bethesda, MD 20892 USA.
   [Cornelis, Marilyn C.; Hu, Frank B.; Kraft, Peter; van Dam, Rob M.; Hunter, David J.] Harvard Univ, Sch Publ Hlth, Dept Nutr, Boston, MA 02115 USA.
   [Couper, David] Univ N Carolina, Dept Biostat, Gillings Sch Global Publ Hlth, Collaborat Studies Coordinating Ctr, Chapel Hill, NC USA.
   [Coviello, Andrea D.; Murabito, Joanne M.] Boston Univ, Sch Med, Dept Med, Sect Gen Internal Med Prevent Med & Endocrinol, Boston, MA 02118 USA.
   [de Faire, Ulf] Karolinska Inst, Inst Environm Med, S-10401 Stockholm, Sweden.
   [Smith, George Davey] Univ Bristol, Dept Social Med, MRC Ctr Causal Anal Translat Epidemiol, Bristol, Avon, England.
   [Easton, Douglas F.; Pharoah, Paul; Tyrer, Jonathon] Univ Cambridge, Dept Publ Hlth & Primary Care, Ctr Canc Genet Epidemiol, Cambridge, England.
   [Easton, Douglas F.; Pharoah, Paul; Tyrer, Jonathon] Univ Cambridge, Dept Oncol, Strangeways Res Labs, Cambridge, England.
   [Emilsson, Valur] Merck & Co Inc, MPRI, Rahway, NJ 07065 USA.
   [Eriksson, Johan; Peltonen, Leena; Pouta, Anneli; Salomaa, Veikko; Tikkanen, Emmi] Natl Inst Hlth & Welf, Helsinki, Finland.
   [Eriksson, Johan] Univ Helsinki, Dept Gen Practice & Primary Hlth Care, Helsinki, Finland.
   [Eriksson, Johan] Univ Helsinki, Cent Hosp, Unit Gen Practice, Helsinki, Finland.
   [Eriksson, Johan] Folkhalsan Res Ctr, Helsinki, Finland.
   [Ferrucci, Luigi] NIA, Longitudinal Studies Sect, Clin Res Branch, Baltimore, MD 21224 USA.
   [Folsom, Aaron R.; Demerath, Ellen W.] Univ Minnesota, Sch Publ Hlth, Div Epidemiol & Community Hlth, Minneapolis, MN USA.
   [Garcia, Melissa; Launer, Lenore J.; Harris, Tamara B.] NIA, Lab Epidemiol Demog & Biometry, Intramural Res Program, Bethesda, MD 20892 USA.
   [Hankinson, Susan E.; Hu, Frank B.; Kraft, Peter; Hunter, David J.] Brigham & Womens Hosp, Dept Med, Channing Lab, Boston, MA 02115 USA.
   [Hankinson, Susan E.; Hu, Frank B.; Karasik, David; Kiel, Douglas P.; Kraft, Peter; Hunter, David J.] Harvard Univ, Sch Med, Boston, MA USA.
   [Heath, Andrew C.] Washington Univ, Sch Med, Dept Psychiat, St Louis, MO 63110 USA.
   [Hernandez, Dena G.] NIA, Neurogenet Lab, Bethesda, MD 20892 USA.
   [Hofman, Albert; Rivadeneira, Fernando; Uitterlinden, Andre G.] Erasmus MC, Dept Epidemiol, Rotterdam, Netherlands.
   [Jaervelin, Marjo-Riitta; Sovio, Ulla] Univ London Imperial Coll Sci Technol & Med, Dept Epidemiol & Biostat, Sch Publ Hlth, London, England.
   [Johnson, Andrew D.; Levy, Daniel] NHLBI, Ctr Populat Studies, Bethesda, MD 20892 USA.
   [Karasik, David; Kiel, Douglas P.] Harvard Univ, Hebrew Senior Life Inst Aging Res, Boston, MA 02115 USA.
   [Khaw, Kay-Tee] Univ Cambridge, Inst Publ Hlth, Dept Publ Hlth & Primary Care, Cambridge, England.
   [Kolcic, Ivana; Polasek, Ozren] Univ Zagreb, Sch Med, Zagreb 41001, Croatia.
   [Laven, Joop S. E.] Erasmus, MC, Dept Obstet & Gynaecol, Rotterdam, Netherlands.
   [Liu, Jianjun] Genome Inst Singapore, Singapore, Singapore.
   [Levy, Daniel] Boston Univ, Sch Med, Div Cardiol, Boston, MA 02118 USA.
   [Martin, Nicholas G.; Montgomery, Grant W.] Queensland Inst Med Res, Brisbane, Qld 4006, Australia.
   [McArdle, Wendy L.; Northstone, Kate; Ring, Susan M.] Univ Bristol, Dept Social Med, ALSPAC, Bristol, Avon, England.
   [Mooser, Vincent; Waterworth, Dawn M.] GlaxoSmithKline, Div Genet, King Of Prussia, PA USA.
   [Murray, Jeffrey C.] Univ Iowa, Dept Pediat, Iowa City, IA 52242 USA.
   [Nalls, Michael A.] NIA, Neurogenet Lab, Intramural Res Program, Bethesda, MD 20892 USA.
   [Ness, Andrew R.] Univ Bristol, Dept Oral & Dent Sci, Bristol, Avon, England.
   [Oostra, Ben A.] Erasmus Univ, Dept Clin Genet, Med Ctr, NL-3000 DR Rotterdam, Netherlands.
   [Peacock, Munro; Econs, Michael J.] Indiana Univ, Sch Med, Dept Med, Indianapolis, IN USA.
   [Palotie, Aarno; Peltonen, Leena; Segre, Ayellet V.] Broad Inst Harvard & MIT, Cambridge, MA USA.
   [Pare, Guillaume] McMaster Univ, Genet & Mol Epidemiol Lab, Hamilton, ON, Canada.
   [Parker, Alex N.; Tsui, Kim; Young, Lauren] Amgen Inc, Cambridge, MA USA.
   [Pennell, Craig E.] Univ Western Australia, Sch Womens & Infants Hlth, Crawley, WA, Australia.
   [Polasek, Ozren] Gen Info Ltd, Zagreb, Croatia.
   [Plump, Andrew S.] Merck Res Lab, Rahway, NJ USA.
   [Rudan, Igor] Univ Split, Croatian Ctr Global Hlth, Sch Med, Split, Croatia.
   [Schlessinger, David] NIA, Gerontol Res Ctr, Bethesda, MD 20892 USA.
   [Scuteri, Angelo] IRCCS, INRCA, Unita Operativa Geriatr, Rome, Italy.
   [Segre, Ayellet V.] Massachusetts Gen Hosp, Dept Mol Biol, Boston, MA 02114 USA.
   [Shuldiner, Alan R.] Vet Adm Med Ctr, Geriatr Res & Educ Clin Ctr, Baltimore, MD 21218 USA.
   [Strachan, David P.] Univ London, Div Community Hlth Sci, London, England.
   [Tryggvadottir, Laufey] Iceland Canc Registry, Reykjavik, Iceland.
   [van Dam, Rob M.] Natl Univ Singapore, Yong Loo Lin Sch Med, Dept Epidemiol & Publ Hlth, Singapore 117595, Singapore.
   [van Dam, Rob M.] Natl Univ Singapore, Dept Med, Singapore 117595, Singapore.
   [Vollenweider, Peter; Waeber, Gerard] BH 10 Ctr Hosp Univ Vaudois CHUV, Dept Internal Med, Lausanne, Switzerland.
   [Wichmann, H. Erich] Univ Munich, Chair Epidemiol, Inst Med Informat Biometry & Epidemiol, Munich, Germany.
   [Wichmann, H. Erich] Univ Munich, Klinikum Grosshadern, D-8000 Munich, Germany.
   Brigham & Womens Hosp, Div Cardiol, Boston, MA 02115 USA.
   [Stefansson, Kari; Thorsteinsdottir, Unnur] Univ Iceland, Fac Med, Reykjavik, Iceland.
   [Ong, Ken K.] Univ Cambridge, Dept Paediat, Cambridge, England.
RP Murabito, JM (reprint author), NHLBI, Framingham Heart Study, Framingham, MA USA.
EM murabito@bu.edu; ken.ong@mrc-epid.cam.ac.uk; anna.murray@pms.ac.uk
RI Hayward, Caroline/M-8818-2016; Davey Smith, George/A-7407-2013;
   Magnusson, Patrik/C-4458-2017; Kolcic, Ivana/E-2713-2017; Byrne,
   Enda/J-6068-2014; Ness, Andy/M-7612-2013; d'Adamo, Adamo
   Pio/G-4064-2011; Lin, P/G-7702-2014; Palmer, Lyle/K-3196-2014;
   Warrington, Nicole/P-4868-2014; Gudnason, Vilmundur/K-6885-2015; Wilson,
   James F/A-5704-2009; de Geus, Eco/M-9318-2015; Montgomery,
   Grant/B-7148-2008; Rivadeneira, Fernando/O-5385-2015; Smith,
   Albert/K-5150-2015; mangino, massimo/F-5134-2011; Johnson,
   Andrew/G-6520-2013; Ulivi, Sheila/H-3700-2013; Colaus,
   PsyColaus/K-6607-2013; van Dam, Rob/F-9674-2010; Northstone,
   Kate/A-8165-2011; Polasek, Ozren/B-6002-2011; Smith, Erin/E-5933-2011;
   Aspelund, Thor/F-4826-2011; Aspelund, Thor/C-5983-2008; Visser, Jenny
   /F-8156-2011; Kilpelainen, Tuomas/F-8569-2012; Rudan, Igor/I-1467-2012;
   Deloukas, Panos/B-2922-2013; 
OI Martin, Nicholas/0000-0003-4069-8020; Gieger,
   Christian/0000-0001-6986-9554; Kiel, Douglas/0000-0001-8474-0310;
   Karasik, David/0000-0002-8826-0530; Jarvelin,
   Marjo-Riitta/0000-0002-2149-0630; Eriksson, Johan/0000-0002-2516-2060;
   Bergmann, Sven/0000-0002-6785-9034; Hayward,
   Caroline/0000-0002-9405-9550; Davey Smith, George/0000-0002-1407-8314;
   Kolcic, Ivana/0000-0001-7918-6052; Byrne, Enda/0000-0002-9491-7797;
   Murabito, Joanne/0000-0002-0192-7516; Lunetta,
   Kathryn/0000-0002-9268-810X; Soranzo, Nicole/0000-0003-1095-3852; Zgaga,
   Lina/0000-0003-4089-9703; Murray, Anna/0000-0002-2351-2522; Esko,
   Tonu/0000-0003-1982-6569; Ness, Andy/0000-0003-3548-9523; d'Adamo, Adamo
   Pio/0000-0001-9367-4909; Palmer, Lyle/0000-0002-1628-3055; Warrington,
   Nicole/0000-0003-4195-775X; Gudnason, Vilmundur/0000-0001-5696-0084;
   Wilson, James F/0000-0001-5751-9178; de Geus, Eco/0000-0001-6022-2666;
   Montgomery, Grant/0000-0002-4140-8139; Rivadeneira,
   Fernando/0000-0001-9435-9441; Smith, Albert/0000-0003-1942-5845;
   mangino, massimo/0000-0002-2167-7470; Ulivi, Sheila/0000-0003-3606-835X;
   van Dam, Rob/0000-0002-7354-8734; Northstone, Kate/0000-0002-0602-1983;
   Polasek, Ozren/0000-0002-5765-1862; Aspelund, Thor/0000-0002-7998-5433;
   Rudan, Igor/0000-0001-6993-6884; Deloukas, Panos/0000-0001-9251-070X;
   sanna, serena/0000-0002-3768-1749; Gudbjartsson,
   Daniel/0000-0002-5222-9857; Monsalve, Beatriz Elena/0000-0002-5994-866X;
   MARONGIU, MARA/0000-0002-7321-2384; Tryggvadottir,
   Laufey/0000-0001-8067-9030
FU Academy of Finland (Finnish Centre of Excellence in Complex Disease
   Genetics) [129680, 120315, 129287, 129494]; Affymetrix [N02-HL-6-4278];
   Agency of Science, Technology and Research of Singapore (A*STAR);
   Althingi (the Icelandic Parliament); American Heart Association
   [0855082E]; Amgen; Augustinus Foundation; Australian National Health and
   Medical Research Council [241944, 339462, 389927, 389875, 389891,
   389892, 389938, 442915, 442981, 496739, 552485, 552498, 619667];
   Australian Research Council [A7960034, A79801419, A79906588, DP0212016,
   DP0343921, DP0770096]; Baltimore Veterans Administration Medical Center
   Geriatrics Research; Canadian Institutes of Health Research [166067];
   Cancer Research United Kingdom; Cariplo Foundation; Center for Disease
   Control and Prevention (USA), Centre for Medical Systems Biology (CMSB);
   Chief Scientist Office of the Scottish Government; Clinical Nutrition
   Research Unit of Maryland [P30 DK072488]; Danish National Research
   Foundation; Danish Pharmacists' Fund; Egmont Foundation; Erasmus Medical
   Center; Erasmus University; Estonian Government [SF0180142s08]; European
   Commision [212111 BBMRI, 205419 ECOGENE, 201413 ENGAGE,
   HEALTH-F2-2008-201865-GEFOS, HEALTH-F2-2008-35627,
   HEALTH-F4-2007-201413, HEALTH-F4-2007-201550 HYPERGENES, 245536
   OPENGENE, TREAT-OA, QLG2-CT-2002-01254, EU/QLRT-2001-01254, ERC-230374];
   European Union [LSHG-CT-2006-018947, LSHM-CT-2003-503041]; European
   Regional Development Fund; Faculty of Biology and Medicine of Lausanne,
   Switzerland; Fondazione Compagnia di San Paolo Health Ministry,
   Framingham Heart Study [N01-HC-25195]; GENEVA Coordinating Center
   [U01HG004446]; German Federal Ministry of Education and Research; German
   National Genome Research Network [NGFN-2, 01GS0823]; Giorgi-Cavaglieri
   Foundation; GlaxoSmithKline; Health Fund of the Danish Health Insurance
   Societies; Helmholtz Zentrum Munchen-German Research Center for
   Environmental Health; Hjartavernd (the Icelandic Heart Association);
   Italian Ministry of Health [ICS110.1/RF97.71, RF-FSR-2007-647201];
   Juvenile Diabetes Research Foundation International (JDRF); Leenaards
   Foundation; March of Dimes Birth Defects Foundation; Medical Research
   Council [G0000934, G0500539, G0701863]; National Cancer Institute
   [CA40356, CA98233, P01CA087969, P01CA055075, CA047988, CA63464, CA54281,
   CA136792, CA089392, CA104021]; Munich Center of Health Sciences (MC
   Health, LMUinnovativ); National Health and Medical Research Council of
   Australia [572613, 003209]; National Heart, Lung, and Blood Institute
   [HL043851, HL087679, HL69757, N01-HC-55015, N01-HC-55016, N01-HC-55018,
   N01-HC-55019, N01-HC-55020, N01-HC-55021, N01-HC-55022, R01HL087641,
   R01HL59367, R01HL086694, RC2 HL102419]; National Human Genome Research
   Institute (NHGRI); National Institute of Aging [263 MD 9164, 263 MD
   821336, N.1-AG-1-1, N.1-AG-1-2111, N01-AG-5-0002, AG-16592,
   R21AG032598]; National Institute of Arthritis and Musculoskeletal and
   Skin Diseases and National Institute on Aging ((NIAMS/NIA) [R01 AR/AG
   41398)]; National Institute of Child Health and Human Development
   [HD-061437]; National Institute of Diabetes and Digestive and Kidney
   Diseases (NIDDK) [R01DK058845, U01 DK062418]; National Institute on
   Alcohol Abuse and Alcoholism (NIAAA); National Institute of Allergy and
   Infectious Diseases (NIAID); National Institute on Drug Abuse (NIDA);
   National Institutes of Health [U01HG004446, AA07535, AA10248, AA13320,
   AA13321, AA13326, AA14041, HHSN268200782096C, M01 RR-00750, MH66206,
   N01-AG-12100, N01-AG-1-2109, P01-AG-18397, R01-088119, R01-DA013423,
   RFAHG006033, U01DE018993, U01DE018903, U01HG004422, U01HL72515, U01
   HL84756, U01HG004399, U01HG004402, U01HG004415, U01HG004423,
   U01HG004436, U01HG004438, U01HG004726, U01HG004728, U01HG004729,
   U01HG004735, U01HG004738, U01HG04424, U10AA008401, U54RR025204-01,
   UL1RR025005, UL1 RR025774, Z01CP010200, HHSN268200625226C]; National
   Institute for Health Research Cambridge Biomedical Research Centre;
   Netherlands Organization for Scientific Research [904-61-193,
   575-25-006, 480-04-004, 56-464-14192, NWO 480-05-003, 175.010.2005.011,
   911-03-012, 014-93-015]; Netherlands Genomic Initiative (NGI)
   [050-060-810]; National Institute on Aging (NIA); Laboratory of
   Neurogenetics; US National Institutes of Health Genes, Environment and
   Health Initiative; Republic of Croatia Ministry of Science, Education
   and Sports [108-1080315-0302]; Robert Dawson Evans Endowment; Royal
   Society, Royal Swedish Academy of Science; State of Bavaria, Germany;
   Susan G. Komen Breast Cancer Foundation; Swedish Foundation for
   Strategic Research (SSF); Swedish Heart-Lung Foundation; Swedish
   Ministry of Higher Education and Research; Swedish Research Council;
   Swedish Society of Medicine; Swiss National Science Foundation
   [33CSCO-122661, 3100AO-116323/1]; University of Bristol, University of
   Maryland General Clinical Research Center [M01 RR 16500]; Wellcome Trust
   [068545/Z/02, 076467/Z/05/Z, 077016/Z/05/Z, 89061/Z/09/Z, 079895];
   Western Australian DNA Bank; Western Australian Genetic Epidemiology
   Resource
FX Academy of Finland (Finnish Centre of Excellence in Complex Disease
   Genetics 129680, 120315, 129287, 129494); Affymetrix (N02-HL-6-4278);
   Agency of Science, Technology and Research of Singapore (A*STAR);
   Althingi (the Icelandic Parliament); American Heart Association
   (0855082E); Amgen; Augustinus Foundation; Australian National Health and
   Medical Research Council (241944, 339462, 389927, 389875, 389891,
   389892, 389938, 442915, 442981, 496739, 552485, 552498, 619667);
   Australian Research Council (A7960034, A79801419, A79906588, DP0212016,
   DP0343921, DP0770096); Baltimore Veterans Administration Medical Center
   Geriatrics Research; Canadian Institutes of Health Research (grant ID
   166067); Cancer Research United Kingdom; the Cariplo Foundation; Center
   for Disease Control and Prevention (USA), Centre for Medical Systems
   Biology (CMSB); the Chief Scientist Office of the Scottish Government;
   Clinical Nutrition Research Unit of Maryland (P30 DK072488); Danish
   National Research Foundation; Danish Pharmacists' Fund; the Egmont
   Foundation; Erasmus Medical Center; Erasmus University; Estonian
   Government (SF0180142s08); the European Commision (212111 BBMRI, 205419
   ECOGENE, 201413 ENGAGE, HEALTH-F2-2008-201865-GEFOS,
   HEALTH-F2-2008-35627, HEALTH-F4-2007-201413, HEALTH-F4-2007-201550
   HYPERGENES, 245536 OPENGENE, TREAT-OA, GenomEUtwin Project
   QLG2-CT-2002-01254, EU/QLRT-2001-01254; ERC-230374); European Union
   framework program 6 EUROSPAN project (LSHG-CT-2006-018947,
   LSHM-CT-2003-503041); European Regional Development Fund; Faculty of
   Biology and Medicine of Lausanne, Switzerland; Fondazione Compagnia di
   San Paolo Health Ministry, Framingham Heart Study (N01-HC-25195); GENEVA
   Coordinating Center (U01HG004446); German Federal Ministry of Education
   and Research; German National Genome Research Network (NGFN-2 and
   NGFNPlus: 01GS0823); Giorgi-Cavaglieri Foundation; GlaxoSmithKline;
   Health Fund of the Danish Health Insurance Societies; Helmholtz Zentrum
   Munchen-German Research Center for Environmental Health; Hjartavernd
   (the Icelandic Heart Association); Italian Ministry of Health
   (ICS110.1/RF97.71, RF-FSR-2007-647201); Juvenile Diabetes Research
   Foundation International (JDRF); Leenaards Foundation; March of Dimes
   Birth Defects Foundation; the Medical Research Council (G0000934,
   G0500539, G0701863); National Cancer Institute (CA40356, CA98233,
   P01CA087969, P01CA055075, CA047988, CA63464, CA54281, CA136792,
   CA089392, CA104021); Munich Center of Health Sciences (MC Health,
   LMUinnovativ); National Health and Medical Research Council of Australia
   (572613 and 003209); National Heart, Lung, and Blood Institute
   (HL043851, HL087679, HL69757, N01-HC-55015, N01-HC-55016, N01-HC-55018,
   N01-HC-55019, N01-HC-55020, N01-HC-55021, N01-HC-55022, R01HL087641,
   R01HL59367, R01HL086694, RC2 HL102419); National Human Genome Research
   Institute (NHGRI); National Institute of Aging (263 MD 9164, 263 MD
   821336, N.1-AG-1-1, N.; 1-AG-1-2111, N01-AG-5-0002, AG-16592, Genetics
   of Reproductive Life Period and Health Outcomes R21AG032598); National
   Institute of Arthritis and Musculoskeletal and Skin Diseases and
   National Institute on Aging ((NIAMS/NIA) R01 AR/AG 41398); National
   Institute of Child Health and Human Development (HD-061437); National
   Institute of Diabetes and Digestive and Kidney Diseases (NIDDK,
   R01DK058845, U01 DK062418); National Institute on Alcohol Abuse and
   Alcoholism (NIAAA); National Institute of Allergy and Infectious
   Diseases (NIAID); National Institute on Drug Abuse (NIDA); National
   Institutes of Health (AA07535, AA10248, AA13320, AA13321, AA13326,
   AA14041, HHS268200782096C, M01 RR-00750, MH66206, N01-AG-12100,
   N01-AG-1-2109, P01-AG-18397, R01-088119, R01-DA013423, RFAHG006033,
   U01DE018993, U01DE018903, U01HG004422, U01HG004446, U01HL72515, U01
   HL84756, U01HG004399, U01HG004402, U01HG004415, U01HG004423,
   U01HG004436, U01HG004438, U01HG004402, U01HG004446, U01HG004726,
   U01HG004728, U01HG004729, U01HG004735, U01HG004738, U01HG04424,
   U10AA008401, U54RR025204-01, UL1RR025005, UL1 RR025774, Z01CP010200,
   HHSN268200625226C); the National Institute for Health Research Cambridge
   Biomedical Research Centre; Netherlands Organization for Scientific
   Research (904-61-193, 575-25-006, 480-04-004, 56-464-14192, NWO
   480-05-003, 175.010.2005.011, 911-03-012, 014-93-015); Netherlands
   Genomic Initiative (NGI, 050-060-810), National Institute on Aging (NIA)
   Intramural Research Program; and Laboratory of Neurogenetics; US
   National Institutes of Health Genes, Environment and Health Initiative;
   Republic of Croatia Ministry of Science, Education and Sports
   (108-1080315-0302); Robert Dawson Evans Endowment; the Royal Society,
   Royal Swedish Academy of Science; State of Bavaria, Germany; Susan G.
   Komen Breast Cancer Foundation; Swedish Foundation for Strategic
   Research (SSF); Swedish Heart-Lung Foundation; Swedish Ministry of
   Higher Education and Research; Swedish Research Council; Swedish Society
   of Medicine; Swiss National Science Foundation (Ref: 33CSCO-122661,
   3100AO-116323/1); the University of Bristol, University of Maryland
   General Clinical Research Center (M01 RR 16500); the Wellcome Trust
   (068545/Z/02, 076467/Z/05/Z, 077016/Z/05/Z, 89061/Z/09/Z, strategic
   award 079895); Western Australian DNA Bank; Western Australian Genetic
   Epidemiology Resource (see Supplementary Note for extended
   acknowledgments).
NR 44
TC 218
Z9 222
U1 1
U2 39
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1061-4036
J9 NAT GENET
JI Nature Genet.
PD DEC
PY 2010
VL 42
IS 12
BP 1077
EP U73
DI 10.1038/ng.714
PG 11
WC Genetics & Heredity
SC Genetics & Heredity
GA 684UZ
UT WOS:000284578800010
PM 21102462
ER

PT J
AU Belkaid, Y
   Chen, WJ
AF Belkaid, Yasmine
   Chen, WanJun
TI Regulatory ripples
SO NATURE IMMUNOLOGY
LA English
DT Editorial Material
ID T-CELLS; INFECTIOUS TOLERANCE; IL-35; INDUCTION; CYTOKINE; FOXP3
AB Regulatory T cells come in many different forms depending on their mode of action or developmental origin. Data now show that interleukin 35, an immunomodulatory cytokine secreted by regulatory T cells, and interleukin 10 induce so-called 'iT(R)35 cells', which may have an important role in the phenomenon of infectious tolerance.
C1 [Belkaid, Yasmine] NIAID, Mucosal Immunol Unit, Parasit Dis Lab, NIH, Bethesda, MD 20892 USA.
   [Chen, WanJun] Natl Inst Dent & Craniofacial Res, Mucosal Immunol Unit, NIH, Bethesda, MD USA.
RP Belkaid, Y (reprint author), NIAID, Mucosal Immunol Unit, Parasit Dis Lab, NIH, 9000 Rockville Pike, Bethesda, MD 20892 USA.
EM ybelkaid@niaid.nih.gov
FU Intramural NIH HHS [Z99 DE999999, ZIA DE000101-07]
NR 14
TC 17
Z9 19
U1 0
U2 1
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1529-2908
J9 NAT IMMUNOL
JI Nat. Immunol.
PD DEC
PY 2010
VL 11
IS 12
BP 1077
EP 1078
DI 10.1038/ni1210-1077
PG 2
WC Immunology
SC Immunology
GA 680UX
UT WOS:000284262200004
PM 21079629
ER

PT J
AU Zink, CF
   Weinberger, DR
AF Zink, Caroline F.
   Weinberger, Daniel R.
TI Cracking the moody brain The rewards of self starvation
SO NATURE MEDICINE
LA English
DT Editorial Material
ID ANOREXIA-NERVOSA; DOPAMINE
C1 [Zink, Caroline F.; Weinberger, Daniel R.] NIMH, Clin Brain Disorders Branch, Genes Cognit & Psychosis Program, US Natl Inst Hlth, Bethesda, MD 20892 USA.
RP Zink, CF (reprint author), NIMH, Clin Brain Disorders Branch, Genes Cognit & Psychosis Program, US Natl Inst Hlth, Bethesda, MD 20892 USA.
EM weinberd@mail.nih.gov
NR 12
TC 29
Z9 29
U1 0
U2 6
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1078-8956
J9 NAT MED
JI Nat. Med.
PD DEC
PY 2010
VL 16
IS 12
BP 1382
EP 1383
DI 10.1038/nm1210-1382
PG 2
WC Biochemistry & Molecular Biology; Cell Biology; Medicine, Research &
   Experimental
SC Biochemistry & Molecular Biology; Cell Biology; Research & Experimental
   Medicine
GA 690ZH
UT WOS:000285048900028
PM 21135849
ER

PT J
AU Nabel, GJ
   Fauci, AS
AF Nabel, Gary J.
   Fauci, Anthony S.
TI Induction of unnatural immunity: prospects for a broadly protective
   universal influenza vaccine
SO NATURE MEDICINE
LA English
DT Article
ID A VIRUS; MICE; NEUTRALIZATION; HEMAGGLUTININ; ANTIBODIES; CHALLENGE;
   INFECTION; EPITOPE
AB The immune system normally responds to influenza virus by making neutralizing antibodies to regions of the viral spike, the hemagglutinin, that vary year to year. This natural response protects against circulating subtypes but necessitates production of new vaccines annually. Newer vaccine approaches have succeeded in eliciting broadly neutralizing antibodies to highly conserved yet vulnerable regions of the hemagglutinin and suggest potential pathways for the development of universal influenza vaccines. (C) 2010 Nature America, Inc. All rights reserved.
C1 [Nabel, Gary J.; Fauci, Anthony S.] NIAID, US Natl Inst Hlth, Bethesda, MD 20892 USA.
   [Nabel, Gary J.] US Natl Inst Hlth, Vaccine Res Ctr, Inst Allergy & Infect Dis, Bethesda, MD USA.
RP Nabel, GJ (reprint author), NIAID, US Natl Inst Hlth, 9000 Rockville Pike, Bethesda, MD 20892 USA.
EM gnabel@nih.gov
NR 19
TC 78
Z9 84
U1 2
U2 17
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1078-8956
J9 NAT MED
JI Nat. Med.
PD DEC
PY 2010
VL 16
IS 12
BP 1389
EP 1391
DI 10.1038/nm1210-1389
PG 3
WC Biochemistry & Molecular Biology; Cell Biology; Medicine, Research &
   Experimental
SC Biochemistry & Molecular Biology; Cell Biology; Research & Experimental
   Medicine
GA 690ZH
UT WOS:000285048900030
PM 21135852
ER

PT J
AU Schneider, G
   Guttmann, P
   Heim, S
   Rehbein, S
   Mueller, F
   Nagashima, K
   Heymann, JB
   Muller, WG
   McNally, JG
AF Schneider, Gerd
   Guttmann, Peter
   Heim, Stefan
   Rehbein, Stefan
   Mueller, Florian
   Nagashima, Kunio
   Heymann, J. Bernard
   Mueller, Waltraud G.
   McNally, James G.
TI Three-dimensional cellular ultrastructure resolved by X-ray microscopy
SO NATURE METHODS
LA English
DT Article
ID COMPUTED-TOMOGRAPHY; RESOLUTION; CELLS; BSOFT
AB We developed an X-ray microscope using partially coherent object illumination instead of previously used quasi-incoherent illumination. The design permitted the incorporation of a cryogenic tilt stage, enabling tomography of frozen-hydrated, intact adherent cells. We obtained three-dimensional reconstructions of mouse adenocarcinoma cells at similar to 36-nm (Rayleigh) and similar to 70-nm (Fourier ring correlation) resolution, which allowed us to visualize the double nuclear membrane, nuclear pores, nuclear membrane channels, mitochondrial cristae and lysosomal inclusions.
C1 [Schneider, Gerd; Guttmann, Peter; Heim, Stefan; Rehbein, Stefan] Helmholtz Zentrum Berlin Mat & Energie GmbH, Berlin, Germany.
   [Mueller, Florian; Mueller, Waltraud G.; McNally, James G.] NCI, Lab Receptor Biol & Gene Express, NIH, Bethesda, MD 20892 USA.
   [Nagashima, Kunio] NCI, Electron Microscopy Lab, SAIC Frederick Inc, NIH, Frederick, MD 21701 USA.
   [Heymann, J. Bernard] NIAMSD, Struct Biol Lab, NIH, Bethesda, MD 20892 USA.
RP Schneider, G (reprint author), Helmholtz Zentrum Berlin Mat & Energie GmbH, Wilhelm Conrad Rontgen Campus, Berlin, Germany.
EM gerd.schneider@helmholtz-berlin.de; mcnallyj@exchange.nih.gov
RI Heymann, Bernard/F-6825-2011; Mueller, Florian/C-9075-2012; Guttmann,
   Peter/H-9869-2015; 
OI Mueller, Florian/0000-0002-9622-4396; Guttmann,
   Peter/0000-0002-0534-238X; Heymann, Bernard/0000-0002-8872-5326
FU Human Frontier Science Program [RGP0053/2005-C]; German Federal Ministry
   of Education and Research [05KS4BY1/7]; US National Institutes of
   Health; National Institute of Arthritis and Musculoskeletal and Skin
   Diseases, and the National Cancer Institute, Center for Cancer Research
   [HHSN26120080001E]
FX We thank B. Niemann for support and A. Leis for help with learning
   cryopreservation. This work was funded in part by the Human Frontier
   Science Program Research grant RGP0053/2005-C, the German Federal
   Ministry of Education and Research under contract 05KS4BY1/7, the
   intramural program of the US National Institutes of Health, including
   the National Institute of Arthritis and Musculoskeletal and Skin
   Diseases, and the National Cancer Institute, Center for Cancer Research,
   including Science Applications International Corporations Frederick
   contract HHSN26120080001E.
NR 15
TC 133
Z9 134
U1 8
U2 63
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1548-7091
J9 NAT METHODS
JI Nat. Methods
PD DEC
PY 2010
VL 7
IS 12
BP 985
EP U116
DI 10.1038/NMETH.1533
PG 4
WC Biochemical Research Methods
SC Biochemistry & Molecular Biology
GA 686HB
UT WOS:000284686300013
PM 21076419
ER

PT J
AU Li, SL
   Overman, JJ
   Katsman, D
   Kozlov, SV
   Donnelly, CJ
   Twiss, JL
   Giger, RJ
   Coppola, G
   Geschwind, DH
   Carmichael, ST
AF Li, Songlin
   Overman, Justine J.
   Katsman, Diana
   Kozlov, Serguei V.
   Donnelly, Christopher J.
   Twiss, Jeffery L.
   Giger, Roman J.
   Coppola, Giovanni
   Geschwind, Daniel H.
   Carmichael, S. Thomas
TI An age-related sprouting transcriptome provides molecular control of
   axonal sprouting after stroke
SO NATURE NEUROSCIENCE
LA English
DT Article
ID CENTRAL-NERVOUS-SYSTEM; MYELIN-ASSOCIATED GLYCOPROTEIN;
   GROWTH-ASSOCIATED GENE; CAT STRIATE CORTEX; NEURITE OUTGROWTH; IN-VIVO;
   CORTICAL INFARCT; DNA METHYLATION; NOGO RECEPTOR; NEURONS
AB Stroke is an age-related disease. Recovery after stroke is associated with axonal sprouting in cortex adjacent to the infarct. The molecular program that induces a mature cortical neuron to sprout a new connection after stroke is not known. We selectively isolated neurons that sprout a new connection in cortex after stroke and compared their whole-genome expression profile to that of adjacent, non-sprouting neurons. This 'sprouting transcriptome' identified a neuronal growth program that consists of growth factor, cell adhesion, axonal guidance and cytoskeletal modifying molecules that differed by age and time point. Gain and loss of function in three distinct functional classes showed new roles for these proteins in epigenetic regulation of axonal sprouting, growth factor-dependent survival of neurons and, in the aged mouse, paradoxical upregulation of myelin and ephrin receptors in sprouting neurons. This neuronal growth program may provide new therapeutic targets and suggest mechanisms for age-related differences in functional recovery.
C1 [Li, Songlin; Overman, Justine J.; Katsman, Diana; Coppola, Giovanni; Geschwind, Daniel H.; Carmichael, S. Thomas] Univ Calif Los Angeles, David Geffen Sch Med, Dept Neurol, Los Angeles, CA 90095 USA.
   [Kozlov, Serguei V.] NCI, Canc & Dev Biol Lab, Frederick, MD 21701 USA.
   [Donnelly, Christopher J.; Twiss, Jeffery L.] Drexel Univ, Dept Biol, Philadelphia, PA 19104 USA.
   [Giger, Roman J.] Univ Michigan, Dept Cell & Dev Biol, Ann Arbor, MI 48109 USA.
   [Giger, Roman J.] Univ Michigan, Dept Neurol, Ann Arbor, MI 48109 USA.
RP Carmichael, ST (reprint author), Univ Calif Los Angeles, David Geffen Sch Med, Dept Neurol, Los Angeles, CA 90095 USA.
EM scarmichael@mednet.ucla.edu
RI Li, Songlin/D-7768-2011; LI, Songlin/O-8512-2016; 
OI Donnelly, Christopher/0000-0002-2383-9015; Carmichael, S
   Thomas/0000-0002-1169-9203
FU US National Institutes of Health [NS045729, NS04733, NS049041, AHA
   09SDG2310180, 0525144Y]; US Department of Veterans Affairs; Larry L
   Hillblom Foundation; Dr. Miriam and Sheldon G. Adelson Medical Research
   Foundation; American Federation of Aging Research
FX We thank S. Raike (University of Michigan) for help with obtaining NgR2
   mutant mice. This research was funded by US National Institutes of
   Health NS045729, NS04733, NS049041, AHA 09SDG2310180 and 0525144Y; the
   US Department of Veterans Affairs; the Larry L Hillblom Foundation; the
   Dr. Miriam and Sheldon G. Adelson Medical Research Foundation and the
   American Federation of Aging Research.
NR 50
TC 121
Z9 121
U1 2
U2 12
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1097-6256
J9 NAT NEUROSCI
JI Nat. Neurosci.
PD DEC
PY 2010
VL 13
IS 12
BP 1496
EP U82
DI 10.1038/nn.2674
PG 11
WC Neurosciences
SC Neurosciences & Neurology
GA 684CW
UT WOS:000284525800014
PM 21057507
ER

PT J
AU Chou, JY
   Jun, HS
   Mansfield, BC
AF Chou, Janice Y.
   Jun, Hyun Sik
   Mansfield, Brian C.
TI Glycogen storage disease type I and G6Pase-beta deficiency: etiology and
   therapy
SO NATURE REVIEWS ENDOCRINOLOGY
LA English
DT Review
ID PUTATIVE GLUCOSE-6-PHOSPHATE TRANSLOCASE; PHOSPHOHISTIDINE-ENZYME
   INTERMEDIATE; SEVERE CONGENITAL NEUTROPENIA; DONOR
   LIVER-TRANSPLANTATION; ACUTE MYELOGENOUS LEUKEMIA; COLONY-STIMULATING
   FACTOR; MEDIATED GENE-THERAPY; OF-THE-LITERATURE; HEPATOCELLULAR
   ADENOMA; RENAL-DISEASE
AB Glycogen storage disease type I (GSD-I) consists of two subtypes: GSD-Ia, a deficiency in glucose-6-phosphatase-alpha (G6Pase-alpha) and GSD-Ib, which is characterized by an absence of a glucose-6-phosphate (G6P) transporter (G6PT). A third disorder, G6Pase-beta deficiency, shares similarities with this group of diseases. G6Pase-alpha and G6Pase-beta are G6P hydrolases in the membrane of the endoplasmic reticulum, which depend on G6PT to transport G6P from the cytoplasm into the lumen. A functional complex of G6PT and G6Pase-alpha maintains interprandial glucose homeostasis, whereas G6PT and G6Pase-beta act in conjunction to maintain neutrophil function and homeostasis. Patients with GSD-Ia and those with GSD-Ib exhibit a common metabolic phenotype of disturbed glucose homeostasis that is not evident in patients with G6Pase-beta deficiency. Patients with a deficiency in G6PT and those lacking G6Pase-beta display a common myeloid phenotype that is not shared by patients with GSD-Ia. Previous studies have shown that neutrophils express the complex of G6PT and G6Pase-beta to produce endogenous glucose. Inactivation of either G6PT or G6Pase-beta increases neutrophil apoptosis, which underlies, at least in part, neutrophil loss (neutropenia) and dysfunction in GSD-Ib and G6Pase-beta deficiency. Dietary and/or granulocyte colony-stimulating factor therapies are available; however, many aspects of the diseases are still poorly understood. This Review will address the etiology of GSD-Ia, GSD-Ib and G6Pase-beta deficiency and highlight advances in diagnosis and new treatment approaches, including gene therapy.
C1 [Chou, Janice Y.; Jun, Hyun Sik; Mansfield, Brian C.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Sect Cellular Differentiat, Program Dev Endocrinol & Genet, NIH, Bethesda, MD 20892 USA.
RP Chou, JY (reprint author), Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Sect Cellular Differentiat, Program Dev Endocrinol & Genet, NIH, Bldg 10,Room 9D42,10 Ctr Dr, Bethesda, MD 20892 USA.
EM chouja@mail.nih.gov
RI Jun, Hyun Sik/C-6799-2013
FU National Institute of Child Health & Human Development (NICHD), NIH
FX The authors were supported by the Intramural Research Program of the
   National Institute of Child Health & Human Development (NICHD), NIH.
NR 121
TC 47
Z9 51
U1 3
U2 20
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1759-5029
J9 NAT REV ENDOCRINOL
JI Nat. Rev. Endocrinol.
PD DEC
PY 2010
VL 6
IS 12
BP 676
EP 688
DI 10.1038/nrendo.2010.189
PG 13
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 684UY
UT WOS:000284578700007
PM 20975743
ER

PT J
AU Cookson, MR
AF Cookson, Mark R.
TI The role of leucine-rich repeat kinase 2 (LRRK2) in Parkinson's disease
SO NATURE REVIEWS NEUROSCIENCE
LA English
DT Article
ID AUTOSOMAL-DOMINANT PARKINSONISM; ALPHA-SYNUCLEIN;
   LEUCINE-RICH-REPEAT-KINASE-2 LRRK2; CYTOPLASMIC LOCALIZATION; 14-3-3
   BINDING; ROC DOMAIN; MUTATIONS; PROTEIN; PHOSPHORYLATION; GENE
AB Parkinson's disease, like many common age-related conditions, is now recognized to have a substantial genetic component. Here, I discuss how mutations in a large complex gene-leucine-rich repeat kinase 2 (LRRK2) - affect protein function, and I review recent evidence that LRRK2 mutations affect pathways that involve other proteins that have been implicated in Parkinson's disease, specifically a-synuclein and tau. These concepts can be used to understand disease processes and to develop therapeutic opportunities for the treatment of Parkinson's disease.
C1 NIA, Neurogenet Lab, NIH, Bethesda, MD 20982 USA.
RP Cookson, MR (reprint author), NIA, Neurogenet Lab, NIH, Bldg 35,Room 1A116,MSC 3707,35 Convent Dr, Bethesda, MD 20982 USA.
EM Cookson@mail.nih.gov
RI Turton, Jessica/K-6879-2013
FU National Institutes of Health (NIH), National Institute on Aging
FX I would like to thank E. Greggio and J.-M. Taymans for critically
   reading the manuscript. This research was supported by the Intramural
   Research Program of the National Institutes of Health (NIH), National
   Institute on Aging.
NR 74
TC 218
Z9 220
U1 3
U2 44
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1471-003X
J9 NAT REV NEUROSCI
JI Nat. Rev. Neurosci.
PD DEC
PY 2010
VL 11
IS 12
BP 791
EP 797
DI 10.1038/nrn2935
PG 7
WC Neurosciences
SC Neurosciences & Neurology
GA 682KN
UT WOS:000284402500001
PM 21088684
ER

PT J
AU Vaughan, CK
   Neckers, L
   Piper, PW
AF Vaughan, Cara K.
   Neckers, Len
   Piper, Peter W.
TI Understanding of the Hsp90 molecular chaperone reaches new heights
SO NATURE STRUCTURAL & MOLECULAR BIOLOGY
LA English
DT Editorial Material
ID HEAT-SHOCK-PROTEIN; CAENORHABDITIS-ELEGANS; STRUCTURAL BASIS; ATP
   BINDING; RESISTANCE; COCHAPERONE; EXPRESSION; COMPLEXES; TARGETS; CANCER
C1 [Vaughan, Cara K.] Birkbeck Coll, Inst Struct Mol Biol, London, England.
   [Neckers, Len] NCI, Bethesda, MD 20892 USA.
   [Piper, Peter W.] Univ Sheffield, Sheffield, S Yorkshire, England.
RP Vaughan, CK (reprint author), Birkbeck Coll, Inst Struct Mol Biol, London, England.
EM peter.piper@sheffield.ac.uk
NR 35
TC 16
Z9 17
U1 1
U2 9
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1545-9993
J9 NAT STRUCT MOL BIOL
JI Nat. Struct. Mol. Biol.
PD DEC
PY 2010
VL 17
IS 12
BP 1400
EP 1404
DI 10.1038/nsmb1210-1400
PG 5
WC Biochemistry & Molecular Biology; Biophysics; Cell Biology
SC Biochemistry & Molecular Biology; Biophysics; Cell Biology
GA 689QB
UT WOS:000284942200002
PM 21127511
ER

PT J
AU Di, LJ
   Fernandez, AG
   De Siervi, A
   Longo, DL
   Gardner, K
AF Di, Li-Jun
   Fernandez, Alfonso G.
   De Siervi, Adriana
   Longo, Dan L.
   Gardner, Kevin
TI Transcriptional regulation of BRCA1 expression by a metabolic switch
SO NATURE STRUCTURAL & MOLECULAR BIOLOGY
LA English
DT Article
ID BREAST-CANCER CELLS; MESSENGER-RNA; HUMAN GENOME;
   OXIDATIVE-PHOSPHORYLATION; BIDIRECTIONAL PROMOTERS; COREPRESSOR CTBP;
   ESTROGEN; PROTEIN; BINDING; GENES
AB Though the linkages between germline mutations of BRCA1 and hereditary breast cancer are well known, recent evidence suggests that altered BRCA1 transcription may also contribute to sporadic forms of breast cancer. Here we show that BRCA1 expression is controlled by a dynamic equilibrium between transcriptional coactivators and co-repressors that govern histone acetylation and DNA accessibility at the BRCA1 promoter. Eviction of the transcriptional co-repressor and metabolic sensor, C terminal-binding protein (CtBP), has a central role in this regulation. Loss of CtBP from the BRCA1 promoter through estrogen induction, depletion by RNA interference or increased NAD(+)/NADH ratio leads to HDAC1 dismissal, elevated histone acetylation and increased BRCA1 transcription. The active control of chromatin marks, DNA accessibility and gene expression at the BRCA1 promoter by this 'metabolic switch' provides an important molecular link between caloric intake and tumor suppressor expression in mammary cells.
C1 [Di, Li-Jun; Fernandez, Alfonso G.; Gardner, Kevin] NCI, Lab Receptor Biol & Gene Express, Bethesda, MD 20892 USA.
   [De Siervi, Adriana] Univ Buenos Aires, Sch Sci, Dept Biol Chem, Buenos Aires, DF, Argentina.
   [Longo, Dan L.] NIA, Immunol Lab, Baltimore, MD 21224 USA.
RP Gardner, K (reprint author), NCI, Lab Receptor Biol & Gene Express, Bethesda, MD 20892 USA.
EM gardnerk@mail.nih.gov
RI Di, Li-jun/D-6160-2013; Di, Li-jun/B-3352-2011
FU US National Institutes of Health; US National Cancer Institute; US
   National Institute on Aging; Argentinean Agency of Science and
   Technology (ANPCyT) [PICT 2006-00228]
FX This research was supported by the Intramural Research Program of the US
   National Institutes of Health, the US National Cancer Institute, the US
   National Institute on Aging and the Argentinean Agency of Science and
   Technology (ANPCyT, PICT 2006-00228). We thank P. M. Glazer (Yale
   University) for the gift of the BRCA1 promoter dual reporter.
NR 58
TC 40
Z9 40
U1 1
U2 9
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1545-9985
J9 NAT STRUCT MOL BIOL
JI Nat. Struct. Mol. Biol.
PD DEC
PY 2010
VL 17
IS 12
BP 1406
EP U1500
DI 10.1038/nsmb.1941
PG 9
WC Biochemistry & Molecular Biology; Biophysics; Cell Biology
SC Biochemistry & Molecular Biology; Biophysics; Cell Biology
GA 689QB
UT WOS:000284942200003
PM 21102443
ER

PT J
AU Liu, SX
   Harada, BT
   Miller, JT
   Le Grice, SFJ
   Zhuang, XW
AF Liu, Shixin
   Harada, Bryan T.
   Miller, Jennifer T.
   Le Grice, Stuart F. J.
   Zhuang, Xiaowei
TI Initiation complex dynamics direct the transitions between distinct
   phases of early HIV reverse transcription
SO NATURE STRUCTURAL & MOLECULAR BIOLOGY
LA English
DT Article
ID RNA SECONDARY STRUCTURE; VIRUS TYPE-1 VIRIONS; HUMAN-IMMUNODEFICIENCY;
   NUCLEOCAPSID PROTEIN; NUCLEIC-ACID; IN-VITRO; DNA-SYNTHESIS; EFFICIENT
   INITIATION; PRIMER TRNA(3)(LYS); SINGLE MOLECULES
AB Human immunodeficiency virus (HIV) initiates reverse transcription of its viral RNA (vRNA) genome from a cellular tRNA(3)(Lys) primer. This process is characterized by a slow initiation phase with specific pauses, followed by a fast elongation phase. We report a single-molecule study that monitors the dynamics of individual initiation complexes, comprised of vRNA, tRNA and HIV reverse transcriptase (RT). RT transitions between two opposite binding orientations on tRNA-vRNA complexes, and the prominent pausing events are related to RT binding in a flipped orientation opposite to the polymerization-competent configuration. A stem-loop structure within the vRNA is responsible for maintaining the enzyme predominantly in this flipped orientation. Disruption of the stem-loop structure triggers the initiation-to-elongation transition. These results highlight the important role of the structural dynamics of the initiation complex in directing transitions between early reverse transcription phases. (C) 2010 Nature America, Inc. All rights reserved.
C1 [Liu, Shixin; Zhuang, Xiaowei] Harvard Univ, Dept Chem & Chem Biol, Cambridge, MA 02138 USA.
   [Harada, Bryan T.] Harvard Univ, Grad Program Biophys, Cambridge, MA 02138 USA.
   [Miller, Jennifer T.; Le Grice, Stuart F. J.] NCI, HIV Drug Resistance Program, Frederick, MD 21701 USA.
   [Zhuang, Xiaowei] Harvard Univ, Dept Phys, Cambridge, MA 02138 USA.
   [Zhuang, Xiaowei] Howard Hughes Med Inst, Cambridge, MA USA.
RP Zhuang, XW (reprint author), Harvard Univ, Dept Chem & Chem Biol, Cambridge, MA 02138 USA.
EM zhuang@chemistry.harvard.edu
RI Liu, Shixin/A-4560-2012; 
OI Harada, Bryan/0000-0002-9683-782X
FU US National Institutes of Health (NIH) [GM 068518]; Center for Cancer
   Research, NCI; NIH/National Institute of General Medical Sciences
   [GM008313]
FX We thank J. Wu and E. Abbondanzieri for helpful discussions and R.
   Gorelick (National Cancer Institute (NCI), Frederick, Maryland, USA) for
   providing NC proteins. This work is supported in part by the US National
   Institutes of Health (NIH; GM 068518 to X.Z.) and the Intramural
   Research Program of the Center for Cancer Research, NCI (to S. F. J. L.
   G.). B. T. H. was supported by a NIH/National Institute of General
   Medical Sciences Molecular Biophysics Training Grant (GM008313 to the
   Harvard Biophysics Program). X.Z. is a Howard Hughes Medical Institute
   investigator.
NR 55
TC 29
Z9 29
U1 0
U2 15
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1545-9985
J9 NAT STRUCT MOL BIOL
JI Nat. Struct. Mol. Biol.
PD DEC
PY 2010
VL 17
IS 12
BP 1453
EP U83
DI 10.1038/nsmb.1937
PG 9
WC Biochemistry & Molecular Biology; Biophysics; Cell Biology
SC Biochemistry & Molecular Biology; Biophysics; Cell Biology
GA 689QB
UT WOS:000284942200009
PM 21102446
ER

PT J
AU Cravedi, P
   Maggiore, U
   Mannon, RB
AF Cravedi, Paolo
   Maggiore, Umberto
   Mannon, Roslyn B.
TI Low-density array PCR analysis of reperfusion biopsies: an adjunct to
   histological analysis
SO NEPHROLOGY DIALYSIS TRANSPLANTATION
LA English
DT Article
DE gene expression; integrin beta 2; kidney transplant; predictor;
   reperfusion biopsy
ID RENAL-ALLOGRAFT REJECTION; DELAYED GRAFT FUNCTION; DONOR KIDNEYS;
   GENE-EXPRESSION; MULTICENTER TRIAL; TRANSPLANTATION; IMPLANTATION;
   COMPLEMENT; MICROARRAY; INTEGRINS
AB Background. Histologic evaluation of baseline kidney biopsies is an inconsistent tool to predict graft outcomes, which might be assisted by gene expression analysis.
   Methods. We evaluated 49 consecutive kidney graft biopsies obtained post-reperfusion in 18 deceased donors (DD) and 31 living donors (LD) at our center. Biopsies were evaluated and scored using Banff criteria. Low-density real-time polymerase chain reaction arrays were used to measure intragraft expression of 95 genes associated with programmed cell death, fibrosis, innate and adaptive immunity and oxidative stress signaling. A pool of 25 normal kidney biopsies was used as control. We applied a stepwise forward selection procedure to build a multiple regression model predicting estimated glomerular filtration rate (eGFR) at 1 year after transplant using baseline clinical characteristics and gene expression levels.
   Results. DD grafts displayed a pattern of gene expression remarkably different from LD, including an increased expression of complement protein C3, and chemokines, CXCL1 and CXCL2, consistent with the proinflammatory setting of ischaemia-reperfusion injury. There was no association between any of the reperfusion biopsy histological features and either renal function at 1 year post-transplant or risk of acute rejection. Conversely, older donor age (R(2) = 0.17, P < 0.001) and higher integrin beta 2 gene expression levels (incremental R(2) versus Donor Age-only model = 0.23, P < 0.001) jointly predicted lower eGFR at 1 year after transplant (multiple regression R(2) = 0.40). Patients with higher ITG beta 2 expression levels in baseline biopsies showed lower eGFR, higher levels of proteinuria and more transplant glomerulopathy on the 1-year per-protocol biopsies.
   Conclusion. ITG beta 2 gene expression in reperfusion biopsies may represent a prognostic marker for kidney transplant recipients, potentially helpful in shaping patients' treatment. Further studies are needed to confirm our findings.
C1 [Cravedi, Paolo] Mario Negri Inst Pharmacol Res, I-24100 Bergamo, Italy.
   [Cravedi, Paolo; Mannon, Roslyn B.] NIDDKD, Transplantat Branch, NIH, Bethesda, MD 20892 USA.
   [Maggiore, Umberto] Univ Parma, UO Nefrol, Azienda Osped, I-43100 Parma, Italy.
   [Mannon, Roslyn B.] Univ Alabama, Dept Med, Div Nephrol, Birmingham, AL 35294 USA.
RP Cravedi, P (reprint author), Mario Negri Inst Pharmacol Res, Via Gavazzeni 11, I-24100 Bergamo, Italy.
EM p.cravedi@gmail.com
FU National Institute of Diabetes, Digestive, and Kidney Diseases of the
   National Institutes of Health [1Z01DK062008-05 DIR];  [U01AI058013]; 
   [U01AI084150]
FX This work was supported by the Intramural Research Program of the
   National Institute of Diabetes, Digestive, and Kidney Diseases of the
   National Institutes of Health (1Z01DK062008-05 DIR). Dr. R.B.M. is
   further supported by U01AI058013 and U01AI084150. The authors wish to
   thank Drs. Allan Kirk and David Kleiner for their clinical participation
   and thoughtful discussions.
NR 30
TC 4
Z9 4
U1 0
U2 1
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0931-0509
J9 NEPHROL DIAL TRANSPL
JI Nephrol. Dial. Transplant.
PD DEC
PY 2010
VL 25
IS 12
BP 4077
EP 4086
DI 10.1093/ndt/gfq297
PG 11
WC Transplantation; Urology & Nephrology
SC Transplantation; Urology & Nephrology
GA 685PK
UT WOS:000284640400043
PM 20504838
ER

PT J
AU Teider, N
   Scott, DK
   Neiss, A
   Weeraratne, SD
   Amani, VM
   Wang, YF
   Marquez, VE
   Cho, YJ
   Pomeroy, SL
AF Teider, Natalia
   Scott, Deborah K.
   Neiss, Adrianne
   Weeraratne, S. Dilhan
   Amani, Vladimir M.
   Wang, Yifei
   Marquez, Victor E.
   Cho, Yoon-Jae
   Pomeroy, Scott L.
TI Neuralized1 causes apoptosis and downregulates Notch target genes in
   medulloblastoma
SO NEURO-ONCOLOGY
LA English
DT Article
DE deazaneplanocin; Jagged1; Neuralized1; Notch; tumor suppressor
ID EMBRYONIC STEM-CELLS; TUMOR-SUPPRESSOR; DEVELOPMENTAL REGULATORS;
   HISTONE MODIFICATIONS; COLORECTAL-CANCER; UBIQUITIN LIGASE; DNA
   METHYLATION; PLASMA-MEMBRANE; BRAIN-TUMORS; POLYCOMB
AB Neuralized (Neurl) is a highly conserved E3 ubiquitin ligase, which in Drosophila acts upon Notch ligands to regulate Notch pathway signaling. Human Neuralized1 (NEURL1) was investigated as a potential tumor suppressor in medulloblastoma (MB). The gene is located at 10q25.1, a region demonstrating frequent loss of heterozygosity in tumors. In addition, prior publications have shown that the Notch pathway is functional in a proportion of MB tumors and that Neurl1 is only expressed in differentiated cells in the developing cerebellum. In this study, NEURL1 expression was downregulated in MB compared with normal cerebellar tissue, with the lowest levels of expression in hedgehog-activated tumors. Control of gene expression by histone modification was implicated mechanistically; loss of 10q, sequence mutation, and promoter hypermethylation did not play major roles. NEURL1-transfected MB cell lines demonstrated decreased population growth, colony-forming ability, tumor sphere formation, and xenograft growth compared with controls, and a significant increase in apoptosis was seen on cell cycle and cell death analysis. Notch pathway inhibition occurred on the exogenous expression of NEURL1, as shown by decreased expression of the Notch ligand, Jagged1, and the target genes, HES1 and HEY1. From these studies, we conclude that NEURL1 is a candidate tumor suppressor in MB, at least in part through its effects on the Notch pathway.
C1 [Teider, Natalia; Scott, Deborah K.; Neiss, Adrianne; Weeraratne, S. Dilhan; Amani, Vladimir M.; Wang, Yifei; Cho, Yoon-Jae; Pomeroy, Scott L.] Childrens Hosp, Dept Neurol, Boston, MA 02115 USA.
   [Marquez, Victor E.] NCI, Med Chem Lab, Ctr Canc Res, Frederick, MD 21701 USA.
RP Pomeroy, SL (reprint author), Childrens Hosp, Dept Neurol, 3 Blackfan Circle,CLS 14060, Boston, MA 02115 USA.
EM scott.pomeroy@childrens.harvard.edu
OI Neiss, Adrianne/0000-0001-5329-782X
FU NIH [CA, R01CA109467, P30 HD018655]; NIH, Center for Cancer Research,
   NCI-Frederick; American Brain Tumor Association
FX This work was supported by NIH grant CA; the Intramural Research Program
   of the NIH, Center for Cancer Research, NCI-Frederick; and an American
   Brain Tumor Association Fellowship, in memory of Stephanie Lee Kramer.
   This work was also supported by NIH grants R01CA109467 and P30 HD018655.
NR 49
TC 11
Z9 12
U1 0
U2 7
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 1522-8517
J9 NEURO-ONCOLOGY
JI Neuro-Oncology
PD DEC
PY 2010
VL 12
IS 12
BP 1244
EP +
DI 10.1093/neuonc/noq091
PG 13
WC Oncology; Clinical Neurology
SC Oncology; Neurosciences & Neurology
GA 682UR
UT WOS:000284429000002
PM 20847082
ER

PT J
AU Hummel, FC
   Heise, K
   Celnik, P
   Floel, A
   Gerloff, C
   Cohen, LG
AF Hummel, Friedhelm C.
   Heise, Kirstin
   Celnik, Pablo
   Floel, Agnes
   Gerloff, Christian
   Cohen, Leonardo G.
TI Facilitating skilled right hand motor function in older subjects by
   anodal polarization over the left primary motor cortex
SO NEUROBIOLOGY OF AGING
LA English
DT Article
DE Healthy ageing; Sensorimotor; Complex movements; Brain stimulation;
   Transcranial direct current stimulation; tDCS; Activities of daily
   living
ID DIRECT-CURRENT STIMULATION; AGE-RELATED-CHANGES; NONINVASIVE CORTICAL
   STIMULATION; TRANSCRANIAL DC STIMULATION; DEPENDENT CHANGES; FINGERTIP
   FORCES; STROKE PATIENTS; LIMB MOVEMENTS; AGING BRAIN; EXCITABILITY
AB Healthy ageing is accompanied by limitations in performance of activities of daily living and personal independence. Recent reports demonstrated improvements in motor function induced by noninvasive anodal direct current stimulation (tDCS) of the primary motor cortex (M1) in young healthy adults. Here we tested the hypothesis that a single session of anodal tDCS over left M1 could facilitate performance of right upper extremity tasks required for activities of daily living (Jebsen-Taylor hand function test, JTT) in older subjects relative to Sham in a double-blind cross-over study design. We found (a) significant improvement in JTT function with tDCS relative to Sham that outlasted the stimulation period by at least 30 min, (b) that the older the subjects the more prominent this improvement appeared and (c) that consistent with previous results in younger subjects, these effects were not accompanied by any overt undesired side effect. We conclude that anodal tDCS applied over M1 can facilitate performance of skilled hand functions required for activities of daily living in older subjects. (C) 2008 Elsevier Inc. All rights reserved.
C1 [Hummel, Friedhelm C.; Heise, Kirstin; Gerloff, Christian] Univ Med Ctr Hamburg Eppendorf, Dept Neurol, Brain Imaging & Neurostimulat BINS Lab, D-20246 Hamburg, Germany.
   [Hummel, Friedhelm C.; Celnik, Pablo; Cohen, Leonardo G.] NINDS, Human Cort Physiol Sect, NIH, Bethesda, MD 20892 USA.
   [Floel, Agnes] Univ Hosp Munster, Dept Neurol, Munster, Germany.
RP Hummel, FC (reprint author), Univ Med Ctr Hamburg Eppendorf, Dept Neurol, Brain Imaging & Neurostimulat BINS Lab, Martinistr 52, D-20246 Hamburg, Germany.
EM f.hummel@uke.uni-hamburg.de; cohenl@ninds.nih.gov
RI Floel, Agnes/A-9426-2017; 
OI Heise, Kirstin-Friederike/0000-0003-3666-8531
FU NINDS; Alexander von Humboldt Foundation; FFM of the University of
   Hamburg [NWF04/07]
FX This research was supported by the intramural program of the NINDS and
   from a grant from the Alexander von Humboldt Foundation (Feodor-Lynen)
   to F.H and by the FFM of the University of Hamburg (NWF04/07 to F.H.
NR 75
TC 64
Z9 65
U1 3
U2 11
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0197-4580
J9 NEUROBIOL AGING
JI Neurobiol. Aging
PD DEC
PY 2010
VL 31
IS 12
BP 2160
EP 2168
DI 10.1016/j.neurobiolaging.2008.12.008
PG 9
WC Geriatrics & Gerontology; Neurosciences
SC Geriatrics & Gerontology; Neurosciences & Neurology
GA 677VE
UT WOS:000284019500013
PM 19201066
ER

PT J
AU Fitzgerald, PJ
   Barkus, C
   Feyder, M
   Wiedholz, LM
   Chen, YC
   Karlsson, RM
   Machado-Vieira, R
   Graybeal, C
   Sharp, T
   Zarate, C
   Harvey-White, J
   Du, J
   Sprengel, R
   Gass, P
   Bannerman, D
   Holmes, A
AF Fitzgerald, Paul J.
   Barkus, Chris
   Feyder, Michael
   Wiedholz, Lisa M.
   Chen, Yi-Chyan
   Karlsson, Rose-Marie
   Machado-Vieira, Rodrigo
   Graybeal, Carolyn
   Sharp, Trevor
   Zarate, Carlos
   Harvey-White, Judith
   Du, Jing
   Sprengel, Rolf
   Gass, Peter
   Bannerman, David
   Holmes, Andrew
TI Does gene deletion of AMPA GluA1 phenocopy features of schizoaffective
   disorder?
SO NEUROBIOLOGY OF DISEASE
LA English
DT Article
DE Glutamate; Mouse; Stress; Anxiety; Mania; Dopamine; Open field test;
   Elevated plus-maze
ID STRESS-INDUCED HYPERTHERMIA; ELEVATED PLUS-MAZE; BIPOLAR DISORDER; MOOD
   DISORDERS; SEROTONIN TRANSPORTER; RECEPTOR ANTAGONISTS;
   LOCOMOTOR-ACTIVITY; STRAIN DIFFERENCES; SIGNALING PATHWAY;
   SOCIAL-BEHAVIOR
AB Glutamatergic dysfunction is strongly implicated in schizophrenia and mood disorders. GluA1 knockout KO mice display schizophrenia- and depression-related abnormalities. Here, we asked whether GluA1 KO show mania-related abnormalities. KO were tested for behavior in approach/avoid conflict tests, responses to repeated forced swim exposure, and locomotor responses under stress and after psychostimulant treatment. The effects of rapid dopamine depletion and treatment with lithium or a GSK-3 beta inhibitor (SB216763) on KO locomotor hyperactivity were tested. Results showed that KO exhibited novelty- and stress-induced locomotor hyperactivity, reduced forced swim immobility and alterations in approach/avoid conflict tests. Psychostimulant treatment and dopamine depletion exacerbated KO locomotor hyperactivity. Lithium, but not SB216763, treatment normalized KO anxiety-related behavior and partially reversed hyperlocomotor behavior, and also reversed elevated prefrontal cortex levels of phospho-MARCKS and phospho-neuromodulin. Collectively, these findings demonstrate mania-related abnormalities in GluA1 KO and, combined with previous findings, suggest this mutant may provide a novel model of features of schizoaffective disorder. (C) 2010 Elsevier Inc. All rights reserved.
C1 [Fitzgerald, Paul J.; Feyder, Michael; Wiedholz, Lisa M.; Karlsson, Rose-Marie; Graybeal, Carolyn; Holmes, Andrew] NIAAA, Sect Behav Sci & Genet, Lab Integrat Neurosci, Bethesda, MD 20852 USA.
   [Barkus, Chris; Bannerman, David] Univ Oxford, Dept Expt Psychol, Oxford OX1 2JD, England.
   [Chen, Yi-Chyan] Buddhist Tzu Chi Gen Hosp, Taipei Branch, Dept Psychiat, Taipei, Taiwan.
   [Machado-Vieira, Rodrigo; Du, Jing] NIMH, Lab Mol Pathol, Bethesda, MD 20892 USA.
   [Sharp, Trevor] Univ Oxford, Dept Pharmacol, Oxford OX1 2JD, England.
   [Zarate, Carlos] NIMH, Mood & Anxiety Disorders Res Program, Bethesda, MD 20892 USA.
   [Harvey-White, Judith] NIAAA, Neuroendocrinol Sect, Lab Physiol Studies, Bethesda, MD 20852 USA.
   [Sprengel, Rolf] Max Planck Inst Med Res, Heidelberg, Germany.
   [Gass, Peter] Cent Inst Mental Hlth, Dept Psychiat & Psychotherapy, D-6800 Mannheim, Germany.
RP Fitzgerald, PJ (reprint author), NIAAA, Sect Behav Sci & Genet, Lab Integrat Neurosci, 5625 Fishers Lane Room 2N09, Bethesda, MD 20852 USA.
EM fitzpj@mail.nih.gov
RI MACHADO-VIEIRA, RODRIGO/D-8293-2012
OI MACHADO-VIEIRA, RODRIGO/0000-0002-4830-1190
FU NIH (National Institute on Alcohol Abuse and Alcoholism, NIAAA)
   [Z01-AA000411]; Deutsche Forschungsgemeinschaft [GA427/8-1, SP602/2-1];
   Wellcome Trust [074385, 087736]; BBSRC/GSK
FX We are very grateful to Guoxiang Luo for genotyping. This research was
   supported (in part) by the Intramural Research Program of the NIH
   (National Institute on Alcohol Abuse and Alcoholism, NIAAA,
   Z01-AA000411). P.G. and R.S. received grants from the Deutsche
   Forschungsgemeinschaft (GA427/8-1 to P.G. and SP602/2-1 to R.S.). D.B.
   holds a Wellcome Trust Senior Research Fellowship (074385 and 087736).
   C.B. is funded by a BBSRC/GSK CASE studentship.
NR 74
TC 37
Z9 37
U1 1
U2 7
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0969-9961
J9 NEUROBIOL DIS
JI Neurobiol. Dis.
PD DEC
PY 2010
VL 40
IS 3
BP 608
EP 621
DI 10.1016/j.nbd.2010.08.005
PG 14
WC Neurosciences
SC Neurosciences & Neurology
GA 675NH
UT WOS:000283836900011
PM 20699120
ER

PT J
AU Palkovits, M
   Usdin, TB
   Makara, GB
   Dobolyi, A
AF Palkovits, M.
   Usdin, T. B.
   Makara, G. B.
   Dobolyi, A.
TI Tuberoinfundibular Peptide of 39 Residues- Immunoreactive Fibers in the
   Zona Incerta and the Supraoptic Decussations Terminate in the
   Neuroendocrine Hypothalamus
SO NEUROCHEMICAL RESEARCH
LA English
DT Article
DE Paraventricular nucleus; Arcuate nucleus; Dorsomedial nucleus; Preoptic
   area; Supraoptic decussations; Hypothalamic deafferentation
ID AUDIOGENIC STRESS; EFFERENT PROJECTIONS; RAT; NEURONS; SYSTEM; BRAIN;
   CONNECTIONS; ANTEROGRADE; EXPRESSION; FOREBRAIN
AB Tuberoinfundibular peptide of 39 residues (TIP39) is expressed by neurons in the subparafascicular area, the posterior intralaminar complex of the thalamus and the pontine medial paralemniscal nucleus. TIP39-positive fibers from these areas do not form individual bundles or fascicles, they join other pathways to reach their innervated brain areas. Fibers arise from TIP39 perikarya located in the subparafascicular area and the posterior intralaminar complex of the thalamus could be followed to the hypothalamus. After uni- and bilateral posterolateral surgical deafferentations of the hypothalamus, accumulation of TIP39 immunoreactivity was observed in the fibers caudal to the knife cut, while it disappeared completely rostral to the transection. In serial sections of the forebrain, we could follow TIP39-ir fibers coursing within the zona incerta and the supraoptic decussations. TIP39-positive fibers that join the incerto-hypothalamic pathway reach the medio-dorsal part of the hypothalamus and form moderate to high density networks in the dorsomedial and paraventricular nuclei. The other set of TIP39-positive axons from the subthalamic area join the fibers of the supraoptic decussations and run in an antero-medial direction through the most ventral portion of the hypothalamus up to the retrochiasmatic area, where they crossover. A certain portion of these TIP39-positive fibers terminates in the territories of the arcuate and the medial preoptic nuclei, as well as in the retrochiasmatic area.
C1 [Palkovits, M.; Dobolyi, A.] Semmelweis Univ, Dept Anat Histol & Embryol, Neuromorphol & Neuroendocrine Res Lab, H-1094 Budapest, Hungary.
   [Usdin, T. B.] NIMH, Sect Fundamental Neurosci, NIH, Bethesda, MD 20892 USA.
   [Makara, G. B.] Hungarian Acad Sci, Inst Expt Med, H-1450 Budapest, Hungary.
   [Palkovits, M.; Dobolyi, A.] Hungarian Acad Sci, H-1094 Budapest, Hungary.
RP Palkovits, M (reprint author), Semmelweis Univ, Dept Anat Histol & Embryol, Neuromorphol & Neuroendocrine Res Lab, Tuzolto Utca 58, H-1094 Budapest, Hungary.
EM palkovits@ana.sote.hu
RI Palkovits, Miklos/F-2707-2013; Makara, Gabor/H-8397-2013; 
OI Makara, Gabor/0000-0001-9220-0373; Palkovits, Miklos/0000-0003-0578-0387
FU Hungarian Science Foundation (OTKA) [NK72929]; Hungarian Academy of
   Sciences; NIH, National Institute of Mental Health
FX This article is dedicated to Abel Lajtha. Abel and I met first in 1987
   at a meeting in the United States. There, I had the opportunity to
   introduce myself to him who was a world-famous person, one of the
   leaders in neurochemistry. Abel was, as usual, very kind. After a long
   and friendly conversation, we both agreed that there was a need for
   mapping amino acids and various enzymes in the human, as well as in rat
   brains. Thus, we decided to do a little work together. We therefore
   pooled our expertise and entered upon a several-year journey in
   neuroscience that was both fascinating and somewhat exhausting. We
   eventually succeeded in publishing 15 articles. The high number of
   citations of these publications is a clear indication that our
   expectations were fulfilled. We are still interacting in neuroscience,
   hopefully we will continue these studies in the future. Abel is a great
   friend, always kind and very helpful. It is always an intellectual
   experience for me to meet him either in New York, or Budapest, or
   somewhere in the globe. I enjoy his great sense of humor and his
   attitude towards life. He is always positive, optimistic, never
   complaining-not like me. I feel lucky and privileged to have him for a
   scientific partner and be a friend of him. With profound appreciation, I
   wish Abel good health and further creative activity in research. The
   work was supported by the Hungarian Science Foundation (OTKA): grant No.
   NK72929 for MP, the Bolyai Janos Fellowship Grant of the Hungarian
   Academy of Sciences for AD, and Intramural Research Program of the NIH,
   National Institute of Mental Health for TBU.
NR 29
TC 5
Z9 5
U1 0
U2 4
PU SPRINGER/PLENUM PUBLISHERS
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0364-3190
J9 NEUROCHEM RES
JI Neurochem. Res.
PD DEC
PY 2010
VL 35
IS 12
SI SI
BP 2078
EP 2085
DI 10.1007/s11064-010-0292-2
PG 8
WC Biochemistry & Molecular Biology; Neurosciences
SC Biochemistry & Molecular Biology; Neurosciences & Neurology
GA 695IX
UT WOS:000285364900024
PM 20972828
ER

PT J
AU Pick, CG
   Rachmany, L
   Rubovitch, V
   Tweedie, D
   Li, Y
   Greig, NH
AF Pick, C. G.
   Rachmany, L.
   Rubovitch, V.
   Tweedie, D.
   Li, Y.
   Greig, N. H.
TI THE THERAPEUTIC IMPACT OF EXENDIN-4 ON COGNITIVE IMPAIRMENTS IN MICE
   AFTER MTBI
SO NEUROPEPTIDES
LA English
DT Meeting Abstract
CT 7th Joint Meeting of the European Neuropeptide Club and the
   American-Summer-Neuropeptide Conference
CY JUN 21-24, 2010
CL Pecs, HUNGARY
SP European Neuropeptide Club, Amer Summer Neuropeptide
C1 [Pick, C. G.; Rachmany, L.; Rubovitch, V.] Tel Aviv Univ, Sackler Fac Med, Dept Anat & Anthropol, Tel Aviv, Israel.
   [Tweedie, D.; Li, Y.; Greig, N. H.] NIA, Drug Design & Dev Sect, Neurosci Lab, Intramural Res Program, Baltimore, MD 21224 USA.
RI Pick, Chaim/D-4789-2009
NR 0
TC 0
Z9 0
U1 0
U2 0
PU CHURCHILL LIVINGSTONE
PI EDINBURGH
PA JOURNAL PRODUCTION DEPT, ROBERT STEVENSON HOUSE, 1-3 BAXTERS PLACE,
   LEITH WALK, EDINBURGH EH1 3AF, MIDLOTHIAN, SCOTLAND
SN 0143-4179
J9 NEUROPEPTIDES
JI Neuropeptides
PD DEC
PY 2010
VL 44
IS 6
BP 535
EP 535
PG 1
WC Endocrinology & Metabolism; Neurosciences
SC Endocrinology & Metabolism; Neurosciences & Neurology
GA 692QK
UT WOS:000285170000065
ER

PT J
AU Lauro, LJR
   Reis, J
   Cohen, LG
   Cecchetto, C
   Papagno, C
AF Lauro, Leonor J. Romero
   Reis, Janine
   Cohen, Leonardo G.
   Cecchetto, Carlo
   Papagno, Costanza
TI A case for the involvement of phonological loop in sentence
   comprehension
SO NEUROPSYCHOLOGIA
LA English
DT Article
DE Phonological loop; Verbal short-term memory; Sentence comprehension; TMS
ID SHORT-TERM-MEMORY; TRANSCRANIAL MAGNETIC STIMULATION; WORKING-MEMORY;
   CONDUCTION APHASIA; PREMOTOR CORTEX; NEGATIVE AFFECT; BROCAS AREA;
   LANGUAGE; RTMS; TMS
AB The specific role of the phonological loop in sentence comprehension is still a matter of debate.
   We tested the behavioural consequences of activity disruption in left BA40 and BA44, key regions of the phonological loop, on language comprehension using 1 Hz rTMS. Comprehension was assessed by means of two tasks: a sentence-to-picture matching task, with sentences varying in length and syntactic complexity (Experiment 1), and a sentence verification task (Experiment 2). rTMS over left BA40 significantly reduced accuracy for syntactically complex sentences and long, but syntactically simpler sentences, while rTMS over left BA44 significantly reduced accuracy only for syntactically complex sentences. rTMS applied over left BA40 also impaired performance on sentences in which word order was crucial.
   We suggest that the neural correlates of the phonological loop, left BA40 and BA44, are both involved in the comprehension of syntactically complex sentences, while only left BA40, corresponding to the short-term store, is recruited for the comprehension of long but syntactically simple sentences. Therefore, in contrast with the dominant view, we showed that sentence comprehension is a function of the phonological loop. (C) 2010 Elsevier Ltd. All rights reserved.
C1 [Lauro, Leonor J. Romero; Cecchetto, Carlo; Papagno, Costanza] Univ Milano Bicocca, Dept Psychol, I-20126 Milan, Italy.
   [Lauro, Leonor J. Romero; Reis, Janine; Cohen, Leonardo G.] NINDS, Human Cort Physiol Sect, NIH, Bethesda, MD 20892 USA.
   [Lauro, Leonor J. Romero; Reis, Janine; Cohen, Leonardo G.] NINDS, Stroke Neurorehabil Sect, NIH, Bethesda, MD 20892 USA.
   [Reis, Janine] Univ Freiburg, Dept Neurol, D-7800 Freiburg, Germany.
RP Lauro, LJR (reprint author), Univ Milano Bicocca, Dept Psychol, Piazza Ateneo Nuovo 1,Edificio U6, I-20126 Milan, Italy.
EM l.romerolauro@gmail.com
RI papagno, costanza/K-8460-2012; 
OI papagno, costanza/0000-0002-3659-6294; Romero Lauro, Leonor
   Josefina/0000-0002-6478-2502
FU MUR; NINDS, NIH
FX This work was supported by a grant from the MUR to CP and by the
   Intramural Research Program of NINDS, NIH.
NR 43
TC 6
Z9 6
U1 2
U2 18
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0028-3932
J9 NEUROPSYCHOLOGIA
JI Neuropsychologia
PD DEC
PY 2010
VL 48
IS 14
BP 4003
EP 4011
DI 10.1016/j.neuropsychologia.2010.10.019
PG 9
WC Behavioral Sciences; Neurosciences; Psychology, Experimental
SC Behavioral Sciences; Neurosciences & Neurology; Psychology
GA 699MT
UT WOS:000285668200004
PM 20969883
ER

PT J
AU Giedd, JN
   Stockman, M
   Weddle, C
   Liverpool, M
   Alexander-Bloch, A
   Wallace, GL
   Lee, NR
   Lalonde, F
   Lenroot, RK
AF Giedd, Jay N.
   Stockman, Michael
   Weddle, Catherine
   Liverpool, Maria
   Alexander-Bloch, Aaron
   Wallace, Gregory L.
   Lee, Nancy R.
   Lalonde, Francois
   Lenroot, Rhoshel K.
TI Anatomic Magnetic Resonance Imaging of the Developing Child and
   Adolescent Brain and Effects of Genetic Variation
SO NEUROPSYCHOLOGY REVIEW
LA English
DT Review
DE Magnetic resonance imaging; Brain; Development; Genes; Twins
ID HUMAN PREFRONTAL CORTEX; CORPUS-CALLOSUM; CEREBRAL-CORTEX; ENVIRONMENT
   INTERACTIONS; CORTICAL DEVELOPMENT; MONOZYGOTIC TWINS; WHITE-MATTER;
   LIFE-SPAN; MORPHOLOGY; EXPRESSION
AB Magnetic resonance imaging studies have begun to map effects of genetic variation on trajectories of brain development. Longitudinal studies of children and adolescents demonstrate a general pattern of childhood peaks of gray matter followed by adolescent declines, functional and structural increases in connectivity and integrative processing, and a changing balance between limbic/subcortical and frontal lobe functions, which extends well into young adulthood. Twin studies have demonstrated that genetic factors are responsible for a significant amount of variation in pediatric brain morphometry. Longitudinal studies have shown specific genetic polymorphisms affect rates of cortical changes associated with maturation. Although over-interpretation and premature application of neuroimaging findings for diagnostic purposes remains a risk, converging data from multiple imaging modalities is beginning to elucidate the influences of genetic factors on brain development and implications of maturational changes for cognition, emotion, and behavior.
C1 [Giedd, Jay N.] NIMH, Brain Imaging Unit Child Psychiat Branch, Bethesda, MD 20892 USA.
   [Giedd, Jay N.; Stockman, Michael; Weddle, Catherine; Liverpool, Maria; Alexander-Bloch, Aaron; Wallace, Gregory L.; Lee, Nancy R.; Lalonde, Francois; Lenroot, Rhoshel K.] NIMH, Child Psychiat Branch, Bethesda, MD 20892 USA.
   [Lenroot, Rhoshel K.] Univ New S Wales & Neurosci Res Australia, Sydney, NSW, Australia.
RP Giedd, JN (reprint author), NIMH, Brain Imaging Unit Child Psychiat Branch, Bldg 10,Room 4C110,MSC 1367, Bethesda, MD 20892 USA.
EM jg@nih.gov
RI Lee, Nancy Raitano/F-2565-2011; Giedd, Jay/A-3080-2008; Giedd,
   Jay/B-7302-2012; Giedd, Jay/J-9644-2015; Lee, Nancy/M-7492-2016; 
OI Giedd, Jay/0000-0003-0827-3460; Giedd, Jay/0000-0003-2002-8978; Lee,
   Nancy/0000-0002-6663-0713; Alexander-Bloch, Aaron/0000-0001-6554-1893;
   Wallace, Gregory/0000-0003-0329-5054
FU National Institute of Mental Health, National Institutes of Health
FX This research was supported by the Intramural Program of the National
   Institute of Mental Health, National Institutes of Health.
NR 71
TC 53
Z9 54
U1 0
U2 11
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1040-7308
J9 NEUROPSYCHOL REV
JI Neuropsychol. Rev.
PD DEC
PY 2010
VL 20
IS 4
SI SI
BP 349
EP 361
DI 10.1007/s11065-010-9151-9
PG 13
WC Psychology, Clinical; Neurosciences
SC Psychology; Neurosciences & Neurology
GA 682TD
UT WOS:000284425000003
PM 21069466
ER

PT J
AU Wang, PS
   Insel, TR
AF Wang, Philip S.
   Insel, Thomas R.
TI NIMH-Funded Pragmatic Trials: Moving On
SO NEUROPSYCHOPHARMACOLOGY
LA English
DT Editorial Material
C1 [Wang, Philip S.; Insel, Thomas R.] NIMH, NIH, Bethesda, MD 20892 USA.
RP Insel, TR (reprint author), NIMH, NIH, 6001 Execut Blvd,Room 8235, Bethesda, MD 20892 USA.
EM tinsel@mail.nih.gov
NR 3
TC 7
Z9 7
U1 0
U2 2
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0893-133X
J9 NEUROPSYCHOPHARMACOL
JI Neuropsychopharmacology
PD DEC
PY 2010
VL 35
IS 13
BP 2489
EP 2490
DI 10.1038/npp.2010.161
PG 2
WC Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA 678TS
UT WOS:000284104400001
PM 21068745
ER

PT J
AU Evans, S
   Shergill, SS
   Averbeck, BB
AF Evans, Simon
   Shergill, Sukhwinder S.
   Averbeck, Bruno B.
TI Oxytocin Decreases Aversion to Angry Faces in an Associative Learning
   Task
SO NEUROPSYCHOPHARMACOLOGY
LA English
DT Article
DE decision making; behavior; computational neuroscience; oxytocin; emotion
ID NUCLEUS-ACCUMBENS DOPAMINE; MATERNAL-BEHAVIOR; MICROTUS-OCHROGASTER;
   PARTNER-PREFERENCE; NEURAL CIRCUITRY; SOCIAL-BEHAVIOR; PRAIRIE VOLES;
   HUMANS; AMYGDALA; REINFORCEMENT
AB Social and financial considerations are often integrated when real life decisions are made, and recent studies have provided evidence that similar brain networks are engaged when either social or financial information is integrated. Other studies, however, have suggested that the neuropeptide oxytocin can specifically affect social behaviors, which would suggest separable mechanisms at the pharmacological level. Thus, we examined the hypothesis that oxytocin would specifically affect social and not financial information in a decision making task, in which participants learned which of the two faces, one smiling and the other angry or sad, was most often being rewarded. We found that oxytocin specifically decreased aversion to angry faces, without affecting integration of positive or negative financial feedback or choices related to happy vs sad faces. Neuropsychopharmacology ( 2010) 35, 2502-2509; doi:10.1038/npp.2010.110; published online 15 September 2010
C1 [Averbeck, Bruno B.] NIMH, Neuropsychol Lab, NIH, Bethesda, MD 20892 USA.
   [Evans, Simon; Averbeck, Bruno B.] UCL, Sobell Dept Motor Neurosci & Movement Disorde, Inst Neurol, London, England.
   [Shergill, Sukhwinder S.] Inst Psychiat, Cognit Schizophrenia & Imaging Lab, London, England.
   [Shergill, Sukhwinder S.] Kings Coll London, Dept Psychiat, London WC2R 2LS, England.
RP Averbeck, BB (reprint author), NIMH, Neuropsychol Lab, NIH, Bldg 49,Room 1B-80, Bethesda, MD 20892 USA.
EM bruno.averbeck@nih.gov
RI Shergill, Sukhi/G-7725-2011
FU NIH; National Institute of Mental Health; Welcome Trust; MRC
FX This work was supported in part by the Intramural Program of the NIH,
   National Institute of Mental Health and a Welcome Trust Project Grant to
   BBA. SE was supported by an MRC 3 Year PhD fellowship in Neuroscience at
   UCL.
NR 51
TC 46
Z9 47
U1 2
U2 12
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0893-133X
J9 NEUROPSYCHOPHARMACOL
JI Neuropsychopharmacology
PD DEC
PY 2010
VL 35
IS 13
BP 2502
EP 2509
DI 10.1038/npp.2010.110
PG 8
WC Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA 678TS
UT WOS:000284104400003
PM 20844475
ER

PT J
AU Peng, XQ
   Xi, ZX
   Li, X
   Spiller, K
   Li, J
   Chun, L
   Wu, KM
   Froimowitz, M
   Gardner, EL
AF Peng, Xiao-Qing
   Xi, Zheng-Xiong
   Li, Xia
   Spiller, Krista
   Li, Jie
   Chun, Lauren
   Wu, Kuo-Ming
   Froimowitz, Mark
   Gardner, Eliot L.
TI Is Slow-Onset Long-Acting Monoamine Transport Blockade to Cocaine as
   Methadone is to Heroin? Implication for Anti-Addiction Medications
SO NEUROPSYCHOPHARMACOLOGY
LA English
DT Article
DE cocaine; addiction; heroin; methadone; 31,345; DA transporter
ID DRUG-SEEKING BEHAVIOR; HETEROLOGOUSLY EXPRESSING CELLS; HUMAN DOPAMINE
   TRANSPORTER; POTENTIAL MEDICATIONS; SURFACE EXPRESSION;
   BRAIN-STIMULATION; UPTAKE INHIBITORS; OPIOID AGONISTS; INDUCED RELAPSE;
   ABUSE
AB The success of methadone in treating opiate addiction has suggested that long-acting agonist therapies may be similarly useful for treating cocaine addiction. Here, we examined this hypothesis, using the slow-onset long-acting monoamine reuptake inhibitor 31,345, a trans-aminotetralin analog, in a variety of addiction-related animal models, and compared it with methadone's effects on heroin's actions in the same animal models. Systemic administration of 31,345 produced long-lasting enhancement of electrical brain-stimulation reward (BSR) and extracellular nucleus accumbens (NAc) dopamine (DA). Pretreatment with 31,345 augmented cocaine-enhanced BSR, prolonged cocaine-enhanced NAc DA, and produced a long-term (24-48 h) reduction in cocaine self-administration rate without obvious extinction pattern, suggesting an additive effect of 31,345 with cocaine. In contrast, methadone pretreatment not only dose-dependently inhibited heroin self-administration with an extinction pattern but also dose-dependently inhibited heroin-enhanced BSR and NAc DA, suggesting functional antagonism by methadone of heroin's actions. In addition, 31,345 appears to possess significant abuse liability, as it produces dose-dependent enhancement of BSR and NAc DA, maintains a low rate of self-administration behavior, and dose-dependently reinstates drug-seeking behavior. In contrast, methadone only partially maintains self-administration with an extinction pattern, and fails to induce reinstatement of drug-seeking behavior. These findings suggest that 31,345 is a cocaine-like slow-onset long-acting monoamine transporter inhibitor that may act as an agonist therapy for cocaine addiction. However, its pattern of action appears to be significantly different from that of methadone. Ideal agonist substitutes for cocaine should fully emulate methadone's actions, that is, functionally antagonizing cocaine's action while blocking monoamine transporters to augment synaptic DA. Neuropsychopharmacology (2010) 35, 2564-2578; doi:10.1038/npp.2010.133; published online 8 September 2010
C1 [Peng, Xiao-Qing; Xi, Zheng-Xiong; Li, Xia; Spiller, Krista; Li, Jie; Chun, Lauren; Gardner, Eliot L.] NIDA, Intramural Res Program, NIH, DHHS, Baltimore, MD 21224 USA.
   [Wu, Kuo-Ming; Froimowitz, Mark] Pharm Eco Labs, Devens, MA USA.
   [Froimowitz, Mark] DNAPrint Pharmaceut, Sarasota, FL USA.
RP Xi, ZX (reprint author), NIDA, Intramural Res Program, NIH, DHHS, Baltimore, MD 21224 USA.
EM zxi@intra.nida.nih.gov
OI PENG, XIAOQING/0000-0002-7272-5428
FU National Institute on Drug Abuse, National Institutes of Health
FX This research was supported by the Intramural Research Program of the
   National Institute on Drug Abuse, National Institutes of Health. We
   thank Drs Maarten EA Reith of New York University School of Medicine and
   Jonathan L Katz of the Intramural Research Program, National Institute
   on Drug Abuse for helpful discussions and suggestions.
NR 65
TC 9
Z9 9
U1 2
U2 5
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0893-133X
J9 NEUROPSYCHOPHARMACOL
JI Neuropsychopharmacology
PD DEC
PY 2010
VL 35
IS 13
BP 2564
EP 2578
DI 10.1038/npp.2010.133
PG 15
WC Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA 678TS
UT WOS:000284104400009
PM 20827272
ER

PT J
AU Missig, G
   Ayers, LW
   Schulkin, J
   Rosen, JB
AF Missig, Galen
   Ayers, Luke W.
   Schulkin, Jay
   Rosen, Jeffrey B.
TI Oxytocin Reduces Background Anxiety in a Fear-Potentiated Startle
   Paradigm
SO NEUROPSYCHOPHARMACOLOGY
LA English
DT Article
DE oxytocin; anxiety; fear; startle; PTSD
ID POSTTRAUMATIC-STRESS-DISORDER; AUTISM SPECTRUM DISORDERS; SPRAGUE-DAWLEY
   RATS; PREPULSE INHIBITION; VIETNAM VETERANS; BASE-LINE; INTRANASAL
   OXYTOCIN; ACOUSTIC STARTLE; CONTEXTUAL FEAR; CUED FEAR
AB Oxytocin reportedly decreases anxious feelings in humans and may therefore have therapeutic value for anxiety disorders, such as post-traumatic stress disorder (PTSD). As PTSD patients have exaggerated startle responses, a fear-potentiated startle paradigm in rats may have face validity as an animal model to examine the efficacy of oxytocin in treating these symptoms. Oxytocin (0, 0.01, 0.1, or 1.0 mu g, subcutaneously) was given either 30 min before fear conditioning, immediately after fear conditioning, or 30 min before fear-potentiated startle testing to assess its effects on acquisition, consolidation, and expression of conditioned fear, respectively. Startle both in the presence and absence of the fear-conditioned light was significantly diminished by oxytocin when administered at acquisition, consolidation, or expression. There was no specific effect of oxytocin on light fear-potentiated startle. In an additional experiment, oxytocin had no effects on acoustic startle without previous fear conditioning. Further, in a context-conditioned test, previous light-shock fear conditioning did not increase acoustic startle during testing when the fear-conditioned light was not presented. The data suggest that oxytocin did not diminish cue-specific conditioned nor contextually conditioned fear, but reduced background anxiety. This suggests that oxytocin has unique effects of decreasing background anxiety without affecting learning and memory of a specific traumatic event. Oxytocin may have antianxiety properties that are particularly germane to the hypervigilance and exaggerated startle typically seen in PTSD patients. Neuropsychopharmacology (2010) 35, 2607-2616; doi:10.1038/npp.2010.155; published online 15 September 2010
C1 [Missig, Galen; Ayers, Luke W.; Rosen, Jeffrey B.] Univ Delaware, Dept Psychol, Behav Neurosci Program, Newark, DE 19716 USA.
   [Schulkin, Jay] Georgetown Univ, Dept Neurosci, Washington, DC USA.
   [Schulkin, Jay] NIMH, Behav Endocrinol Sect, Bethesda, MD 20892 USA.
   [Schulkin, Jay] Amer Coll Obstetricians & Gynecologists, Res Dept, Washington, DC 20024 USA.
RP Rosen, JB (reprint author), Univ Delaware, Dept Psychol, Behav Neurosci Program, 108 Wolf Hall, Newark, DE 19716 USA.
EM jrosen@udel.edu
FU US Army Medical Research and Materiel Command [W81XWH-08-1-0182]
FX This work was supported by Grant W81XWH-08-1-0182 from the
   Congressionally Directed Medical Research Programs, US Army Medical
   Research and Materiel Command.
NR 75
TC 30
Z9 30
U1 5
U2 22
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0893-133X
J9 NEUROPSYCHOPHARMACOL
JI Neuropsychopharmacology
PD DEC
PY 2010
VL 35
IS 13
BP 2607
EP 2616
DI 10.1038/npp.2010.155
PG 10
WC Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA 678TS
UT WOS:000284104400013
PM 20844476
ER

PT J
AU Sokoloff, L
AF Sokoloff, Louis
TI Seymour Kaufman
SO NEUROPSYCHOPHARMACOLOGY
LA English
DT Biographical-Item
C1 NIH, Silver Spring, MD USA.
RP Sokoloff, L (reprint author), NIH, Silver Spring, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0893-133X
J9 NEUROPSYCHOPHARMACOL
JI Neuropsychopharmacology
PD DEC
PY 2010
VL 35
IS 13
BP 2651
EP 2651
DI 10.1038/npp.2010.162
PG 1
WC Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA 678TS
UT WOS:000284104400022
ER

PT J
AU Pages, N
   Maurois, P
   Delplanque, B
   Bac, P
   Stables, JP
   Tamariz, J
   Chamorro, G
   Vamecq, J
AF Pages, Nicole
   Maurois, Pierre
   Delplanque, Bernadette
   Bac, Pierre
   Stables, James P.
   Tamariz, Joaquin
   Chamorro, German
   Vamecq, Joseph
TI Activities of alpha-asarone in various animal seizure models and in
   biochemical assays might be essentially accounted for by antioxidant
   properties
SO NEUROSCIENCE RESEARCH
LA English
DT Article
DE alpha-Asarone; Seizure; Audiogenic test; Electroshock;
   Pentylenetetrazole; Picrotoxin; N-methyl-D-aspartate; Pilocarpine;
   Neuroprotection; Antioxidant; Magnesium deficiency; Epilepsy
ID ACORI GRAMINEI RHIZOMA; CENTRAL-NERVOUS-SYSTEM; REDOX MODULATORY SITE;
   RAT CORTICAL-NEURONS; SUPEROXIDE ANION; ESSENTIAL OIL; MICE; EPILEPSY;
   MAGNESIUM; EXTRACT
AB Anticonvulsant properties of alpha-asarone were studied in mice at three doses with different toxicity. The 100 mg/kg dose decreased both treadmill performance and locomotor activity, caused hypothermia, and potentiated pentobarbital-induced sleep. The last two effects and no toxicity were observed at 60 and 22 mg/kg, respectively. In chemical (pentylenetetrazole, picrotoxin, N-methyl-D-aspartate, pilocarpine) and electrical (maximal electroshock) seizure tests, neither seizures not death were prevented by 60 mg/kg alpha-asarone which, however, exhibited protective-like effects (delay in the onset of clonic and/or tonic seizures and/or in the death of mice). Magnesium deficiency-dependent audiogenic seizures responded to non-toxic doses of alpha-asarone (60 mg/kg and less): 22 mg/kg protecting 50% of tested animals. Because these seizures respond to both anti-seizure and antioxidant compounds, antioxidant properties of alpha-asarone were studied, indicating 5 Units of superoxide dismutase-like activity per mg alpha-asarone. Treatment of mice by alpha-asarone (daily dose of 100 mg/kg during 7 days) induced brain antioxidant enzymes (superoxide dismutase, glutathione peroxidase and reductase) in striatum and hippocampus and to a lesser extent in cortex. In view of recent findings about deleterious roles of chronic inflammatory/oxidant stresses in human epilepsy outcome, antioxidant and inductive properties of alpha-asarone are proposed to be coherent bases for traditional clinical efficacy. (C) 2010 Elsevier Ireland Ltd and the Japan Neuroscience Society. All rights reserved.
C1 [Pages, Nicole] Fac Pharm, Toxicol Lab, Illkirch Graffenstaden, France.
   [Pages, Nicole; Maurois, Pierre; Delplanque, Bernadette] Univ Paris 11, NMPA, Orsay, France.
   [Pages, Nicole; Maurois, Pierre; Delplanque, Bernadette] Univ Paris 11, INSERM, F-91405 Orsay, France.
   [Maurois, Pierre; Bac, Pierre] Univ Paris 11, Fac Pharm, Neuropharmacol Lab, F-92290 Chatenay Malabry, France.
   [Maurois, Pierre; Bac, Pierre] Ctr Chirurg Marie Lannelongue, CNRS, UMR 8162, IFR 13, F-92350 Le Plessis Robinson, France.
   [Stables, James P.] NINDS, Epilepsy Branch, NIH, Ctr Neurosci, Bethesda, MD 20892 USA.
   [Tamariz, Joaquin] IPN, Natl Sch Biol Sci, Dept Organ Chem, Mexico City 07738, DF, Mexico.
   [Chamorro, German] IPN, Natl Sch Biol Sci, Preclin Toxicol Lab, Mexico City 07738, DF, Mexico.
   [Vamecq, Joseph] CHRU Lille, Dept Biochem & Mol Biol, Lab Endocrinol, Oncol Biol Pathol Ctr, F-59037 Lille, France.
   [Vamecq, Joseph] INSERM, F-59037 Lille, France.
RP Vamecq, J (reprint author), Univ Lille 2, Fac Med, Res Branch, INSERM,EA 1046, 4th Floor,1 Pl Verdun, F-59045 Lille, France.
EM joseph.vamecq@inserm.fr
OI Chamorro Cevallos, German/0000-0002-8935-9831
FU French Inserm
FX This work was supported by the french Inserm (JV and BD).
NR 40
TC 19
Z9 19
U1 1
U2 13
PU ELSEVIER IRELAND LTD
PI CLARE
PA ELSEVIER HOUSE, BROOKVALE PLAZA, EAST PARK SHANNON, CO, CLARE, 00000,
   IRELAND
SN 0168-0102
EI 1872-8111
J9 NEUROSCI RES
JI Neurosci. Res.
PD DEC
PY 2010
VL 68
IS 4
BP 337
EP 344
DI 10.1016/j.neures.2010.08.011
PG 8
WC Neurosciences
SC Neurosciences & Neurology
GA 690VK
UT WOS:000285036500010
PM 20833211
ER

PT J
AU Zhang, ZL
   Hancock, B
   Leen, S
   Ramaswamy, S
   Sollott, SJ
   Boheler, KR
   Juhaszova, M
   Lakatta, EG
   Spencer, RG
   Fishbein, KW
AF Zhang, Zhuoli
   Hancock, Brynne
   Leen, Stephanie
   Ramaswamy, Sharan
   Sollott, Steven J.
   Boheler, Kenneth R.
   Juhaszova, Magdalena
   Lakatta, Edward G.
   Spencer, Richard G.
   Fishbein, Kenneth W.
TI Compatibility of Superparamagnetic Iron Oxide Nanoparticle Labeling for
   H-1 MRI Cell Tracking with P-31 MRS for Bioenergetic Measurements
SO NMR IN BIOMEDICINE
LA English
DT Article
DE stem cells; bioenergetics; phosphorus; P31 NMR; SPIO; MRI; cell
   labeling; viability
ID EMBRYONIC STEM-CELLS; MAGNETIC-RESONANCE; IN-VIVO; MUSCLE; MOUSE; HEART;
   MAGNETOPHORESIS; NMR; DIFFERENTIATION; CARDIOMYOCYTES
AB Labeling of cells with superparamagnetic iron oxide nanoparticles permits cell tracking by H-1 MRI while P-31 MRS allows non-invasive evaluation of cellular bioenergetics. We evaluated the compatibility of these two techniques by obtaining P-31 NMR spectra of iron-labeled and unlabeled immobilized C2C12 myoblast cells in vitro. Broadened but usable P-31 spectra were obtained and peak area ratios of resonances corresponding to intracellular metabolites showed no significant differences between labeled and unlabeled cell populations. We conclude that P-31 NMR spectra can be obtained from cells labeled with sufficient iron to permit visualization by H-1 imaging protocols and that these spectra have sufficient quality to be used to assess metabolic status. This result introduces the possibility of using localized P-31 MRS to evaluate the viability of iron-labeled therapeutic cells as well as surrounding host tissue in vivo. Published in 2010 by John Wiley & Sons, Ltd.
C1 [Zhang, Zhuoli; Hancock, Brynne; Leen, Stephanie; Ramaswamy, Sharan; Spencer, Richard G.; Fishbein, Kenneth W.] NIA, Clin Invest Lab, Intramural Res Program, NIH, Baltimore, MD 21224 USA.
   [Zhang, Zhuoli; Sollott, Steven J.; Boheler, Kenneth R.; Juhaszova, Magdalena; Lakatta, Edward G.] NIA, Cardiovasc Sci Lab, Intramural Res Program, NIH, Baltimore, MD 21224 USA.
RP Fishbein, KW (reprint author), NIA, Clin Invest Lab, Intramural Res Program, NIH, GRC 4D-08,5600 Nathan Shock Dr, Baltimore, MD 21224 USA.
EM kf31x@nih.gov
FU NIH National Institute on Aging
FX The authors thank Chiara Dell'Agnola for her assistance with the flow
   cytometry assays. This study was supported by the Intramural Research
   Program of the NIH National Institute on Aging.
NR 35
TC 3
Z9 4
U1 1
U2 10
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0952-3480
J9 NMR BIOMED
JI NMR Biomed.
PD DEC
PY 2010
VL 23
IS 10
BP 1166
EP 1172
DI 10.1002/nbm.1545
PG 7
WC Biophysics; Radiology, Nuclear Medicine & Medical Imaging; Spectroscopy
SC Biophysics; Radiology, Nuclear Medicine & Medical Imaging; Spectroscopy
GA 703BJ
UT WOS:000285948600006
PM 20853523
ER

PT J
AU Yadav, M
   Jain, S
   Tomar, R
   Prasad, GBKS
   Yadav, H
AF Yadav, Mukesh
   Jain, Shalini
   Tomar, Radha
   Prasad, G. B. K. S.
   Yadav, Hariom
TI Medicinal and biological potential of pumpkin: an updated review
SO NUTRITION RESEARCH REVIEWS
LA English
DT Review
DE Pumpkin; Herbal medicine; Anti-diabetic properties; Antioxidants;
   Anti-carcinogens; Phytochemicals
ID INDUCED DIABETIC-RATS; CUCURBITA-FICIFOLIA; SEEDS; MOSCHATA; PROTEIN;
   PURIFICATION; FRUIT; INHIBITOR; EXTRACTS; MELLITUS
AB The use of herbal remedies individually or in combination with standard medicines has been used in various medical treatises for the cure of different diseases. Pumpkin is one of the well-known edible plants and has substantial medicinal properties due to the presence of unique natural edible substances. It contains several phyto-constituents belonging to the categories of alkaloids, flavonoids, and palmitic, oleic and linoleic acids. Various important medicinal properties including anti-diabetic, antioxidant, anti-carcinogenic, anti-inflammatory and others have been well documented. The purpose of the present article is to discuss various medicinal and biological potentials of pumpkin that can impart further research developments with this plant for human health benefits.
C1 [Jain, Shalini; Yadav, Hariom] NIDDKD, NIH, Bethesda, MD 20892 USA.
   [Yadav, Mukesh; Tomar, Radha] Jiwaji Univ, Sch Studies Chem, Gwalior 474011, MP, India.
   [Yadav, Mukesh] Coll Adv Studies, Datia, Madhya Pradesh, India.
   [Prasad, G. B. K. S.] Jiwaji Univ, Sch Studies Biotechnol, Gwalior 474011, MP, India.
RP Yadav, H (reprint author), NIDDKD, NIH, Bethesda, MD 20892 USA.
EM yadavh@mail.nih.gov
OI Yadav, Hariom/0000-0003-4504-1597
NR 65
TC 17
Z9 18
U1 6
U2 34
PU CAMBRIDGE UNIV PRESS
PI CAMBRIDGE
PA EDINBURGH BLDG, SHAFTESBURY RD, CB2 8RU CAMBRIDGE, ENGLAND
SN 0954-4224
EI 1475-2700
J9 NUTR RES REV
JI Nutr. Res. Rev.
PD DEC
PY 2010
VL 23
IS 2
BP 184
EP 190
DI 10.1017/S0954422410000107
PG 7
WC Nutrition & Dietetics
SC Nutrition & Dietetics
GA 686ST
UT WOS:000284716700002
PM 21110905
ER

PT J
AU Koster, A
   Stenholm, S
   Alley, DE
   Kim, LJ
   Simonsick, EM
   Kanaya, AM
   Visser, M
   Houston, DK
   Nicklas, BJ
   Tylavsky, FA
   Satterfield, S
   Goodpaster, BH
   Ferrucci, L
   Harris, TB
AF Koster, Annemarie
   Stenholm, Sari
   Alley, Dawn E.
   Kim, Lauren J.
   Simonsick, Eleanor M.
   Kanaya, Alka M.
   Visser, Marjolein
   Houston, Denise K.
   Nicklas, Barbara J.
   Tylavsky, Frances A.
   Satterfield, Suzanne
   Goodpaster, Bret H.
   Ferrucci, Luigi
   Harris, Tamara B.
CA Hlth ABC Study
TI Body Fat Distribution and Inflammation Among Obese Older Adults With and
   Without Metabolic Syndrome
SO OBESITY
LA English
DT Article
ID AGE-RELATED-CHANGES; ADIPOSE-TISSUE; WAIST CIRCUMFERENCE; RISK-FACTOR;
   POSTMENOPAUSAL WOMEN; GLUCOSE-TOLERANCE; ABDOMINAL OBESITY; US
   POPULATION; VISCERAL FAT; LIPID-LEVELS
AB The protective mechanisms by which some obese individuals escape the detrimental metabolic consequences of obesity are not understood. This study examined differences in body fat distribution and adipocytokines in obese older persons with and without metabolic syndrome. Additionally, we examined whether adipocytokines mediate the association between body fat distribution and metabolic syndrome. Data were from 729 obese men and women (BMI >= 30 kg/m(2)), aged 70-79 participating in the Health, Aging and Body Composition (Health ABC) study. Thirty-one percent of these obese men and women did not have metabolic syndrome. Obese persons with metabolic syndrome had significantly more abdominal visceral fat (men: P = 0.04; women: P < 0.01) and less thigh subcutaneous fat (men: P = 0.09; women: P < 0.01) than those without metabolic syndrome. Additionally, those with metabolic syndrome had significantly higher levels of interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-alpha), and plasminogen activator inhibitor-1 (PAI-1) than individuals without metabolic syndrome. Per standard deviation higher in visceral fat, the likelihood of metabolic syndrome significantly increased in women (odds ratio (OR): 2.16, 95% confidence interval (CI): 1.59-2.94). In contrast, the likelihood of metabolic syndrome decreased in both men (OR: 0.56, 95% CI: 0.39-0.80) and women (OR: 0.49, 95% CI: 0.34-0.69) with each standard deviation higher in thigh subcutaneous fat. These associations were partly mediated by adipocytokines; the association between thigh subcutaneous fat and metabolic syndrome was no longer significant in men. In summary, metabolically healthy obese older persons had a more favorable fat distribution, characterized by lower visceral fat and greater thigh subcutaneous fat and a more favorable inflammatory profile compared to their metabolically unhealthy obese counterparts.
C1 [Koster, Annemarie; Kim, Lauren J.; Harris, Tamara B.] NIA, Lab Epidemiol Demog & Biometry, Bethesda, MD 20892 USA.
   [Koster, Annemarie] Maastricht Univ, Sch Publ Hlth & Primary Care CAPHRI, Maastricht, Netherlands.
   [Stenholm, Sari; Simonsick, Eleanor M.; Ferrucci, Luigi] NIA, Clin Res Branch, Baltimore, MD 21224 USA.
   [Stenholm, Sari] Natl Inst Hlth & Welf, Dept Hlth Funct Capac & Welf, Turku, Finland.
   [Alley, Dawn E.] Univ Maryland, Sch Med, Dept Epidemiol & Prevent Med, Baltimore, MD 21201 USA.
   [Kanaya, Alka M.] Univ Calif San Francisco, Div Gen Internal Med, San Francisco, CA 94143 USA.
   [Visser, Marjolein] Vrije Univ Amsterdam, Fac Earth & Life Sci, EMGO Inst Hlth & Care Res, Amsterdam, Netherlands.
   [Visser, Marjolein] Vrije Univ Amsterdam, Dept Hlth Sci, Amsterdam, Netherlands.
   [Visser, Marjolein] Vrije Univ Amsterdam Med Ctr, EMGO Inst Hlth & Care Res, Dept Epidemiol & Biostat, Amsterdam, Netherlands.
   [Houston, Denise K.; Nicklas, Barbara J.] Wake Forest Univ, Sch Med, Sticht Ctr Aging, Dept Internal Med,Sect Gerontol & Geriatr, Winston Salem, NC 27109 USA.
   [Tylavsky, Frances A.; Satterfield, Suzanne] Univ Tennessee, Coll Med, Dept Prevent Med, Memphis, TN USA.
   [Goodpaster, Bret H.] Univ Pittsburgh, Med Ctr, Dept Med, Pittsburgh, PA USA.
RP Koster, A (reprint author), NIA, Lab Epidemiol Demog & Biometry, Bethesda, MD 20892 USA.
EM kostera@mail.nih.gov
RI Koster, Annemarie/E-7438-2010; Stenholm, Sari/G-6940-2011
FU National Institute on Aging [N01-AG-6-2101, N01-AG-6-2103,
   N01-AG-6-2106]; NIH, National Institute on Aging; Finnish Academy
   [125494]
FX This study was supported by National Institute on Aging contracts
   N01-AG-6-2101, N01-AG-6-2103, and N01-AG-6-2106. This research was
   supported (in part) by the Intramural Research Program of the NIH,
   National Institute on Aging. S.S. was supported in part by a grant from
   the Finnish Academy (no. 125494).
NR 44
TC 74
Z9 78
U1 3
U2 9
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1930-7381
J9 OBESITY
JI Obesity
PD DEC
PY 2010
VL 18
IS 12
BP 2354
EP 2361
DI 10.1038/oby.2010.86
PG 8
WC Endocrinology & Metabolism; Nutrition & Dietetics
SC Endocrinology & Metabolism; Nutrition & Dietetics
GA 684CM
UT WOS:000284524700017
PM 20395951
ER

PT J
AU Rossi, A
   Zoico, E
   Goodpaster, BH
   Sepe, A
   Di Francesco, V
   Fantin, F
   Pizzini, F
   Corzato, F
   Vitali, A
   Micciolo, R
   Harris, TB
   Cinti, S
   Zamboni, M
AF Rossi, Andrea
   Zoico, Elena
   Goodpaster, Bret H.
   Sepe, Anna
   Di Francesco, Vincenzo
   Fantin, Francesco
   Pizzini, Francesca
   Corzato, Francesca
   Vitali, Alessandra
   Micciolo, Rocco
   Harris, Tamara B.
   Cinti, Saverio
   Zamboni, Mauro
TI Quantification of Intermuscular Adipose Tissue in the Erector Spinae
   Muscle by MRI: Agreement With Histological Evaluation
SO OBESITY
LA English
DT Article
ID SKELETAL-MUSCLE; INSULIN-RESISTANCE; METABOLIC SYNDROME;
   BODY-COMPOSITION; OBESE MICE; WOMEN; FAT; MEN; SIZE; INFILTRATION
AB Deposition of fat between skeletal muscle bundles and beneath the muscle fascia, recently called intermuscular adipose tissue (IMAT), is gaining attention as potential contributor to insulin resistance, metabolic syndrome, muscle function impairment, and disability. The aim of this study was to compare IMAT as measured at the erector spinae level by magnetic resonance imaging (MRI), a well-recognized gold standard method to evaluate fat content inside muscles, and histology estimates. In 18 healthy elderly men and women with a wide range of BMI (25.05-35.58 kg/m(2)), undergoing elective vertebral surgery, IMAT within the erector spinae muscle was evaluated by MRI, by body composition using dual-energy X-ray absorptiometry and histological evaluation of intraoperative biopsy sample. The concordance between IMAT/total area (TA) ratio evaluated by MRI and histological examination was analyzed employing Lin's concordance correlation coefficient and the procedure proposed by Bland and Altman. Two thresholds to distinguish between muscle and IMAT calculated, respectively, by 20 and 10% reduction of the gray-level intensity evaluated by MRI from surrounding subcutaneous adipose tissue (SAT) were used. With a 20% reduction, calculated IMAT/TA as evaluated by MRI on average exceeds histological evaluation by 21.79%, whereas by reducing the threshold by 10% agreement between MRI and histology improved with a 12.42% difference. Our data show a good degree of concordance between IMAT assessment by MRI and histology and seems to show that agreement between the two methods could be improved by using a more restrictive threshold between muscle and fat.
C1 [Rossi, Andrea; Zoico, Elena; Sepe, Anna; Di Francesco, Vincenzo; Fantin, Francesco; Corzato, Francesca; Zamboni, Mauro] Univ Verona, Div Geriatr Med, Dept Biomed & Surg Sci, I-37100 Verona, Italy.
   [Goodpaster, Bret H.] Univ Pittsburgh, Dept Med, Div Endocrinol & Metab, Pittsburgh, PA USA.
   [Pizzini, Francesca] Borgo Trento City Hosp, Serv Neuroradiol, Verona, Italy.
   [Vitali, Alessandra] Univ Ancona, Inst Normal Human Morphol & Anat, Ancona, Italy.
   [Micciolo, Rocco] Univ Trent, Dept Stat, Trento, Italy.
   [Harris, Tamara B.] NIA, Lab Epidemiol Demog & Biometry, Geriatr Epidemiol Sect, Bethesda, MD 20892 USA.
RP Zamboni, M (reprint author), Univ Verona, Div Geriatr Med, Dept Biomed & Surg Sci, I-37100 Verona, Italy.
EM mauro.zamboni@univr.it
RI Pizzini, Francesca Bendetta/O-5291-2016; 
OI Pizzini, Francesca Bendetta/0000-0002-6285-0989; ZAMBONI,
   Mauro/0000-0001-6961-9483; ZOICO, Elena/0000-0002-5235-1545
FU NIA NIH HHS [Z01 AG006000-01]
NR 26
TC 18
Z9 18
U1 0
U2 1
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1930-7381
J9 OBESITY
JI Obesity
PD DEC
PY 2010
VL 18
IS 12
BP 2379
EP 2384
DI 10.1038/oby.2010.48
PG 6
WC Endocrinology & Metabolism; Nutrition & Dietetics
SC Endocrinology & Metabolism; Nutrition & Dietetics
GA 684CM
UT WOS:000284524700021
PM 20300085
ER

PT J
AU Gawrieh, S
   Baye, TM
   Carless, M
   Wallace, J
   Komorowski, R
   Kleiner, DE
   Andris, D
   Makladi, B
   Cole, R
   Charlton, M
   Curran, J
   Dyer, TD
   Charlesworth, J
   Wilke, R
   Blangero, J
   Kissebah, AH
   Olivier, M
AF Gawrieh, Samer
   Baye, Tesfaye M.
   Carless, Melanie
   Wallace, James
   Komorowski, Richard
   Kleiner, David E.
   Andris, Deborah
   Makladi, Bassem
   Cole, Regina
   Charlton, Michael
   Curran, Joanne
   Dyer, Thomas D.
   Charlesworth, Jac
   Wilke, Russell
   Blangero, John
   Kissebah, Ahmed H.
   Olivier, Michael
TI Hepatic Gene Networks in Morbidly Obese Patients With Nonalcoholic Fatty
   Liver Disease
SO OBESITY SURGERY
LA English
DT Article
DE Fatty liver; NAFLD; Genes; Gene networks; Gene expression; Pathogenesis
ID ACID-BINDING PROTEINS; PHOSPHATASE-INTERACTING PROTEINS;
   ENDOPLASMIC-RETICULUM STRESS; SUPPRESSES CELL-DEATH; INNATE
   IMMUNE-SYSTEM; CRYPTOGENIC CIRRHOSIS; INSULIN-RESISTANCE; UNITED-STATES;
   EXPRESSION; STEATOHEPATITIS
AB Background Genetic factors alter the risk for nonalcoholic fatty liver disease (NAFLD). We sought to identify NAFLD-associated genes and elucidate gene networks and pathways involved in the pathogenesis of NAFLD.
   Methods Quantitative global hepatic gene expression analysis was performed on 53 morbidly obese Caucasian subjects undergoing bariatric surgery (27 with NAFLD and 26 controls). After standardization of data, gene expression profiles were compared between patients with NAFLD and controls. The set of genes that significantly correlated with NAFLD was further analyzed by hierarchical clustering and ingenuity pathways analyses.
   Results There were 25,643 quantitative transcripts, of which 108 were significantly associated with NAFLD (p < 0.001). Canonical pathway analysis in the NAFLD-associated gene clusters showed that the hepatic fibrosis signaling was the most significant pathway in the up-regulated NAFLD gene cluster containing three (COL1A1, IL10, IGFBP3) significantly altered genes, whereas the endoplasmic reticulum stress and protein ubiquitination pathways were the most significant pathways in the down-regulated NAFLD gene cluster, with the first pathway containing one (HSPA5) and the second containing two (HSPA5, USP25) significantly altered genes. The four primary gene networks associated with NAFLD were involved in cell death, immunological disease, cellular movement, and lipid metabolism with several significantly altered "hub" genes in these networks.
   Conclusions This study reveals the canonical pathways and gene networks associated with NAFLD in morbidly obese Caucasians. The application of gene network analysis highlights the transcriptional relationships among NAFLD-associated genes and allows identification of hub genes that may represent high-priority candidates for NAFLD.
C1 [Gawrieh, Samer] Med Coll Wisconsin, Dept Med, Div Gastroenterol & Hepatol, Milwaukee, WI 53212 USA.
   [Wilke, Russell] Med Coll Wisconsin, Div Gen Internal Med, Milwaukee, WI 53212 USA.
   [Makladi, Bassem; Kissebah, Ahmed H.] Med Coll Wisconsin, Div Endocrinol, Milwaukee, WI 53212 USA.
   [Gawrieh, Samer] Zablocki VA Med Ctr, Milwaukee, WI USA.
   [Baye, Tesfaye M.; Cole, Regina; Wilke, Russell; Kissebah, Ahmed H.; Olivier, Michael] Med Coll Wisconsin, Human & Mol Genet Ctr, Milwaukee, WI 53212 USA.
   [Baye, Tesfaye M.; Cole, Regina; Olivier, Michael] Med Coll Wisconsin, Biotechnol & Bioengn Ctr, Milwaukee, WI 53212 USA.
   [Carless, Melanie; Curran, Joanne; Dyer, Thomas D.; Charlesworth, Jac; Blangero, John] SW Fdn Biomed Res, Dept Genet, San Antonio, TX USA.
   [Wallace, James; Andris, Deborah] Med Coll Wisconsin, Dept Surg, Milwaukee, WI 53212 USA.
   [Komorowski, Richard] Med Coll Wisconsin, Dept Pathol, Milwaukee, WI 53212 USA.
   [Kleiner, David E.] NCI, Pathol Lab, Bethesda, MD 20892 USA.
   [Charlton, Michael] Mayo Clin, Dept Gastroenterol & Hepatol, Rochester, MN USA.
   [Olivier, Michael] Med Coll Wisconsin, Dept Physiol, Milwaukee, WI 53212 USA.
RP Gawrieh, S (reprint author), Med Coll Wisconsin, Dept Med, Div Gastroenterol & Hepatol, 9200 W Wisconsin Ave, Milwaukee, WI 53212 USA.
EM sgawrieh@mcw.edu
OI Kleiner, David/0000-0003-3442-4453; Charlesworth,
   Jac/0000-0001-6201-3518
FU Biotechnology and Bioengineering Center of the Medical College of
   Wisconsin; Heart, Lung, and Blood Institute of the National Institutes
   of Health [HL74168]
FX This work was funded by a grant from the Biotechnology and
   Bioengineering Center of the Medical College of Wisconsin (SG and MO)
   and grant HL74168 from the Heart, Lung, and Blood Institute of the
   National Institutes of Health (MO).
NR 79
TC 12
Z9 14
U1 1
U2 7
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0960-8923
J9 OBES SURG
JI Obes. Surg.
PD DEC
PY 2010
VL 20
IS 12
BP 1698
EP 1709
DI 10.1007/s11695-010-0171-6
PG 12
WC Surgery
SC Surgery
GA 689VG
UT WOS:000284957600013
PM 20473581
ER

PT J
AU Burke, AE
   Barnhart, K
   Jensen, JT
   Creinin, MD
   Walsh, TL
   Wan, LS
   Westhoff, C
   Thomas, M
   Archer, D
   Wu, HS
   Liu, J
   Schlaff, W
   Carr, BR
   Blithe, D
AF Burke, Anne E.
   Barnhart, Kurt
   Jensen, Jeffrey T.
   Creinin, Mitchell D.
   Walsh, Terri L.
   Wan, Livia S.
   Westhoff, Carolyn
   Thomas, Michael
   Archer, David
   Wu, Hongsheng
   Liu, James
   Schlaff, William
   Carr, Bruce R.
   Blithe, Diana
TI Contraceptive Efficacy, Acceptability, and Safety of C31G and
   Nonoxynol-9 Spermicidal Gels A Randomized Controlled Trial
SO OBSTETRICS AND GYNECOLOGY
LA English
DT Article
ID IMMUNODEFICIENCY-VIRUS TYPE-1; MALE TOLERANCE; AGENT C31G; MICROBICIDE;
   EXPOSURE; SULFATE
AB OBJECTIVE: To estimate whether a gel containing the spermicide C31G was noninferior to a commercially available product containing nonoxynol-9.
   METHODS: Participants were healthy, sexually active women aged 18-40 years. Measured outcomes included pregnancy rates, continuation rates, adverse events, and acceptability. The primary study outcome was contraceptive efficacy. Sample size was calculated at a 2.5% significance level using a one-sided test based on assumed 6-month pregnancy probability of 15% in the nonoxynol-9 group. Sample size was sufficient to reject, with 80% power, the null hypothesis that pregnancy probability in the C31G arm would be more than 5% higher.
   RESULTS: Nine hundred thirty-two women were randomized in the C31G group and 633 in the nonoxynol-9 group. For randomized patients with at least one episode of coitus (modified intent-to-treat group), 6-month pregnancy probabilities were 12.0% (95% confidence interval [CI] 9.3-14.7%) and 12.0% (95% CI 8.7-15.3%) for C31G and nonoxynol-9, respectively. Twelve-month pregnancy probabilities were 13.8% (95% CI 7.6-20%) for C31G and 19.8% (95% CI 10.9-28.7%) for nonoxynol-9. Two serious adverse events were deemed possibly related to study product and neither occurred in the C31G group. Three fourths of users in either group reported that they liked their assigned study product. Approximately 40% of patients discontinued prematurely for reasons other than pregnancy with 11% lost to follow-up.
   CONCLUSION: C31G demonstrated noninferior contraceptive efficacy compared with nonoxynol-9. C31G may provide another marketable option for women seeking spermicidal contraception.
C1 [Burke, Anne E.] Johns Hopkins Univ, Sch Med, Baltimore, MD 21218 USA.
   Univ Penn, Sch Med, Philadelphia, PA 19104 USA.
   Calif Family Hlth Council, Los Angeles, CA USA.
   Oregon Hlth & Sci Univ, Portland, OR 97201 USA.
   Univ Pittsburgh, Sch Med, Pittsburgh, PA USA.
   NYU, New York, NY USA.
   Columbia Univ, Coll Phys & Surg, New York, NY USA.
   Univ Cincinnati, Sch Med, Cincinnati, OH USA.
   Eastern Virginia Med Sch, Norfolk, VA 23501 USA.
   Hlth Decis Inc, Chapel Hill, NC USA.
   Univ Hosp Cleveland, MacDonald Womens Hosp, Cleveland, OH 44106 USA.
   Univ Colorado, Hlth Sci Ctr, Denver, CO USA.
   Univ Texas Southwestern Med Sch, Dallas, TX USA.
   Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Bethesda, MD USA.
RP Burke, AE (reprint author), Johns Hopkins Univ, Sch Med, Baltimore, MD 21218 USA.
OI Jensen, Jeffrey/0000-0002-4733-1224
FU Eunice Kennedy Shriver National Institute of Child Health and Human
   Development, Bethesda, Maryland; Biosyn; Inc, Huntingdon Valley,
   Pennsylvania
FX Sponsored by the Eunice Kennedy Shriver National Institute of Child
   Health and Human Development, Bethesda, Maryland, and Biosyn, Inc,
   Huntingdon Valley, Pennsylvania.
NR 30
TC 16
Z9 17
U1 1
U2 6
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 0029-7844
J9 OBSTET GYNECOL
JI Obstet. Gynecol.
PD DEC
PY 2010
VL 116
IS 6
BP 1265
EP 1273
DI 10.1097/AOG.0b013e3181fc3b1a
PG 9
WC Obstetrics & Gynecology
SC Obstetrics & Gynecology
GA 683QT
UT WOS:000284491000005
PM 21099590
ER

PT J
AU Zhang, J
   Landy, HJ
   Branch, DW
   Burkman, R
   Haberman, S
   Gregory, KD
   Hatjis, CG
   Ramirez, MM
   Bailit, JL
   Gonzalez-Quintero, VH
   Hibbard, JU
   Hoffman, MK
   Kominiarek, M
   Learman, LA
   Van Veldhuisen, P
   Troendle, J
   Reddy, UM
AF Zhang, Jun
   Landy, Helain J.
   Branch, D. Ware
   Burkman, Ronald
   Haberman, Shoshana
   Gregory, Kimberly D.
   Hatjis, Christos G.
   Ramirez, Mildred M.
   Bailit, Jennifer L.
   Gonzalez-Quintero, Victor H.
   Hibbard, Judith U.
   Hoffman, Matthew K.
   Kominiarek, Michelle
   Learman, Lee A.
   Van Veldhuisen, Paul
   Troendle, James
   Reddy, Uma M.
CA Consortium Safe Labor
TI Contemporary Patterns of Spontaneous Labor With Normal Neonatal Outcomes
SO OBSTETRICS AND GYNECOLOGY
LA English
DT Article
ID ABNORMAL LABOR; ACTIVE LABOR; MANAGEMENT; CERVICOGRAPHS; PRIMIGRAVIDAE;
   INDUCTION; ALERT; LINE
AB OBJECTIVE: To use contemporary labor data to examine the labor patterns in a large, modern obstetric population in the United States.
   METHODS: Data were from the Consortium on Safe Labor, a multicenter retrospective study that abstracted detailed labor and delivery information from electronic medical records in 19 hospitals across the United States. A total of 62,415 parturients were selected who had a singleton term gestation, spontaneous onset of labor, vertex presentation, vaginal delivery, and a normal perinatal outcome. A repeated-measures analysis was used to construct average labor curves by parity. An interval-censored regression was used to estimate duration of labor, stratified by cervical dilation at admission and centimeter by centimeter.
   RESULTS: Labor may take more than 6 hours to progress from 4 to 5 cm and more than 3 hours to progress from 5 to 6 cm of dilation. Nulliparous and multiparous women appeared to progress at a similar pace before 6 cm. However, after 6 cm, labor accelerated much faster in multiparous than in nulliparous women. The 95(th) percentiles of the second stage of labor in nulliparous women with and without epidural analgesia were 3.6 and 2.8 hours, respectively. A partogram for nulliparous women is proposed.
   CONCLUSION: In a large, contemporary population, the rate of cervical dilation accelerated after 6 cm, and progress from 4 cm to 6 cm was far slower than previously described. Allowing labor to continue for a longer period before 6 cm of cervical dilation may reduce the rate of intrapartum and subsequent repeat cesarean deliveries in the United States. (Obstet Gynecol 2010;116:1281-7)
C1 Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, NIH, Bethesda, MD USA.
   Georgetown Univ Hosp, MedStar Hlth, Washington, DC 20007 USA.
   Univ Utah, Salt Lake City, UT USA.
   Intermt HealthCare, Salt Lake City, UT USA.
   Baystate Med Ctr, Springfield, MA USA.
   Maimonides Hosp, Brooklyn, NY 11219 USA.
   Cedars Sinai Med Ctr, Los Angeles, CA 90048 USA.
   Akron City Hosp, Summa Hlth Syst, Akron, OH USA.
   Univ Texas Hlth Sci Ctr Houston, Houston, TX USA.
   Metrohlth Med Ctr, Cleveland, OH USA.
   Univ Miami, Miami, FL USA.
   Univ Illinois, Chicago, IL USA.
   Christiana Care Hlth Syst, Wilmington, DE USA.
   Indiana Univ Clarian Hlth, Indianapolis, IN USA.
   EMMES Corp, Rockville, MD USA.
RP Zhang, J (reprint author), NICHD, Epidemiol Branch, NIH, Bldg 6100,Room 7B03, Bethesda, MD 20892 USA.
EM zhangj@mail.nih.gov
FU Eunice Kennedy Shriver National Institute of Child Health and Human
   Development; National Institutes of Health [HHSN267200603425C]
FX The Consortium on Safe Labor was supported by the Intramural Research
   Program of the Eunice Kennedy Shriver National Institute of Child Health
   and Human Development, National Institutes of Health, through a contract
   (contract HHSN267200603425C).
NR 18
TC 140
Z9 174
U1 2
U2 22
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0029-7844
J9 OBSTET GYNECOL
JI Obstet. Gynecol.
PD DEC
PY 2010
VL 116
IS 6
BP 1281
EP 1287
DI 10.1097/AOG.0b013e3181fdef6e
PG 7
WC Obstetrics & Gynecology
SC Obstetrics & Gynecology
GA 683QT
UT WOS:000284491000007
PM 21099592
ER

PT J
AU Berkowitz, Z
   Saraiya, M
   Benard, V
   Yabroff, KR
AF Berkowitz, Zahava
   Saraiya, Mona
   Benard, Vicki
   Yabroff, K. Robin
TI Common Abnormal Results of Pap and Human Papillomavirus Cotesting What
   Physicians Are Recommending for Management
SO OBSTETRICS AND GYNECOLOGY
LA English
DT Article
ID CERVICAL-CANCER; UNITED-STATES; PRIMARY-CARE; CYTOLOGY; PREVENTION;
   GUIDELINES; WOMEN; DNA
AB OBJECTIVE: To evaluate the association between physician and practice characteristics and adherence to management guidelines to better understand the factors associated with different screening recommendations by primary care physicians.
   METHODS: We used a cross-sectional nationally representative survey of 950 primary care physicians familiar with human papillomavirus (HPV) testing to assess adherence to management guidelines by analyzing responses to two clinical vignettes of a 35-year-old woman who had Pap and HPV tests results: 1) discordant (normal Pap and positive HPV) or 2) mildly abnormal (atypical squamous cells of undetermined significance Pap and negative HPV). Analyses included multivariable logistic regression.
   RESULTS: For the discordant test results, 54.3% (95% confidence interval [CI] 51-57.6%) of physicians recommended both Pap and HPV testing in 6-12 months, adhering to management guidelines. For the mildly abnormal results, only 12.2% (95% CI 10-14.7%) had a guideline-adherent recommendation of Pap testing in 12 months with no HPV test. In multivariable analyses, no significant difference among physicians' specialties was observed for the discordant results. For the mildly abnormal results, physician specialty was associated with guideline adherence in which obstetrician-gynecologists had the highest percent of adherence (19.8%) compared with family and general practitioners (9.3%) and internists (11%) (P<.001).
   CONCLUSION: Even for the most common abnormal results, many physicians reported recommendations that did not adhere to current management guidelines. Evidence-based interventions are needed to improve adherence to management guidelines for the newer HPV DNA test. (Obstet Gynecol 2010;116:1332-40)
C1 [Berkowitz, Zahava] Ctr Dis Control & Prevent, Div Canc Prevent & Control, Epidemiol & Appl Res Branch, Atlanta, GA 30341 USA.
   NCI, Div Canc Control & Populat Sci, Bethesda, MD 20892 USA.
RP Berkowitz, Z (reprint author), Ctr Dis Control & Prevent, Div Canc Prevent & Control, Epidemiol & Appl Res Branch, 4770 Buford Highway,Mailstop K-55, Atlanta, GA 30341 USA.
EM zab3@cdc.gov
OI Yabroff, K. Robin/0000-0003-0644-5572
FU National Cancer Institute [N02-PC-51308]; Centers for Disease Control
   and Prevention [Y3-PC-6017-01]; Agency for Healthcare Research and
   Quality [Y3-PC-5019-01, Y3-PC-5019-02]
FX Funding for this study was provided by the National Cancer Institute
   (contract N02-PC-51308), Centers for Disease Control and Prevention
   (interagency agreement Y3-PC-6017-01), and the Agency for Healthcare
   Research and Quality (interagency agreement Y3-PC-5019-01 and
   Y3-PC-5019-02).
NR 21
TC 11
Z9 11
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0029-7844
J9 OBSTET GYNECOL
JI Obstet. Gynecol.
PD DEC
PY 2010
VL 116
IS 6
BP 1332
EP 1340
DI 10.1097/AOG.0b013e3181fae4ca
PG 9
WC Obstetrics & Gynecology
SC Obstetrics & Gynecology
GA 683QT
UT WOS:000284491000014
PM 21099599
ER

PT J
AU Forsha, SJ
   Panyutin, IV
   Neumann, RD
   Panyutin, IG
AF Forsha, Stephen J.
   Panyutin, Irina V.
   Neumann, Ronald D.
   Panyutin, Igor G.
TI Intracellular Traffic of Oligodeoxynucleotides In and Out of the
   Nucleus: Effect of Exportins and DNA Structure
SO OLIGONUCLEOTIDES
LA English
DT Article
ID ANTISENSE OLIGONUCLEOTIDES; GENE-EXPRESSION; LEPTOMYCIN B; CELLS;
   INFLAMMASOME
AB The delivery of oligodeoxynucleotides (ODNs) into cells is widely utilized for antisense, antigene, aptamer, and similar approaches to regulate gene and protein activities based upon the ODNs' sequence-specific recognition. Short pieces of DNA can also be generated in biological processes, for example, after degradation of viral or bacterial DNA. However, the mechanisms that regulate intracellular trafficking and localization of ODNs are not fully understood. Here we study the effects of major transporters of microRNA, exportin-1 (Exp1) and exportin-5 (Exp5), on the transport of single-stranded ODNs in and out of the nucleus. For this, we employed a fluorescent microscopy-based assay to quantitatively measure the redistribution of ODNs between the nucleus and cytoplasm of live cells. By measuring the fluorescent signal of the nuclei we observed that after delivery into cells via cationic liposomes ODNs rapidly accumulated inside nuclei. However, after removal of the ODN/liposome containing media, we found re-localization of ODNs from the nuclei to cytoplasm of the cells over the time course of several hours. Downregulation of the Exp5 gene by siRNA resulted in a slight increase of ODN uptake into the nucleus, but the kinetics of ODN efflux to the cytoplasm was not affected. Inhibition of Exp1 with leptomycin B somewhat slowed down the clearance of ODNs from the nucleus; however, within 6 hours most of the ODN were still being cleared form the nucleus. ODNs that could form intramolecular G-quadruplex structures behaved differently. They also accumulated in nuclei, although at a lesser extent than unstructured ODN, but they remained there for up to 20 hours after transfection, causing significant cell death. We conclude that Exp1 and Exp5 are not the major transporters of our ODNs out of the nucleus, and that the transport of ODNs is strongly affected by their secondary structure.
C1 [Forsha, Stephen J.; Panyutin, Irina V.; Neumann, Ronald D.; Panyutin, Igor G.] NIH, Radiol & Imaging Sci Dept, Ctr Clin, Bethesda, MD 20892 USA.
RP Panyutin, IG (reprint author), NIH, Radiol & Imaging Sci Dept, Ctr Clin, Bldg 10, Bethesda, MD 20892 USA.
EM igorp@helix.nih.gov
FU NIH, Clinical Center
FX This research was supported by the Intramural Research Program of the
   NIH, Clinical Center.
NR 26
TC 5
Z9 5
U1 2
U2 5
PU MARY ANN LIEBERT INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 1545-4576
J9 OLIGONUCLEOTIDES
JI Oligonucleotides
PD DEC
PY 2010
VL 20
IS 6
BP 277
EP 284
DI 10.1089/oli.2010.0255
PG 8
WC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology
SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology
GA 695ZP
UT WOS:000285412000002
PM 20946012
ER

PT J
AU Mayeenuddin, LH
   Yu, Y
   Kang, Z
   Helman, LJ
   Cao, L
AF Mayeenuddin, L. H.
   Yu, Y.
   Kang, Z.
   Helman, L. J.
   Cao, L.
TI Insulin-like growth factor 1 receptor antibody induces rhabdomyosarcoma
   cell death via a process involving AKT and Bcl-x(L)
SO ONCOGENE
LA English
DT Article
DE IGF1R therapeutic antibody; apoptosis; tumor regression; predictive
   biomarker; Bcl-x(L); Bcl-2
ID FACTOR-I RECEPTOR; MONOCLONAL-ANTIBODY; IGF-I; CYTOCHROME-C;
   TUMOR-GROWTH; APOPTOSIS; CANCER; SURVIVAL; THERAPY; BCL-2
AB Insulin-like growth factors (IGFs) and their receptor, IGF-1 receptor (IGF1R), have important roles in growth, development, stress response, aging and cancer. There are many agents that inhibit IGF1R in oncology clinical development, and in some cases, they have been associated with rapid tumor regression. However, it is not clear by which process these targeted agents induce cancer cell death and how to predict such tumor responses. Here, we showed that IGF1R antibody led to rapid cell death and tumor regression in some rhabdomyosarcoma (RMS) cells. Mechanistic analysis revealed a rapid onset of mitochondrial-dependent apoptosis, including mitochondrial depolarization, cytochrome C release and the activation of specific caspases. The antibody sensitive cells had greater dependence on AKT for maintaining downstream signaling and the expression of a constitutively active AKT, which restored AKT-signaling in these cells, inhibited anti-IGF1R induced cell death. Further analysis showed IGF1R antibody-induced hypophosphorylation of BAD and activation of downstream BAX. Interestingly, the examination of RMS cell lines and tumors revealed an inverse correlation between elevated IGF1R and Bcl-2 level (P = 0.033), with the sensitive cells lacking Bcl-2 expression. The overexpression of BAD specific target, Bcl-x(L), conferred resistance, whereas Bcl-x(L) knockdown sensitized cells lacking Bcl-2 to anti-IGF1R-induced cell death. We propose that RMS pathogenesis involves increased IGF1R expression that enhances AKT and Bcl-x(L)-mediated cell survival, and the blockage of IGF1R results in inhibition of survival signal from Bcl-x(L) and cell death in the sensitive Bcl-2 negative cells. Oncogene (2010) 29, 6367-6377; doi:10.1038/onc.2010.364; published online 6 September 2010
C1 [Mayeenuddin, L. H.; Yu, Y.; Kang, Z.; Cao, L.] NCI, Genet Branch, Ctr Canc Res, Bethesda, MD 20892 USA.
   [Mayeenuddin, L. H.; Yu, Y.; Kang, Z.] NCI Frederick, Lab Prote & Analyt Technol, SAIC Frederick Inc, Frederick, MD USA.
   [Helman, L. J.] NCI, Pediat Oncol Branch, Ctr Canc Res, Bethesda, MD 20892 USA.
RP Cao, L (reprint author), NCI, Genet Branch, Ctr Canc Res, 37 Convent Dr,MSC 4265,Bldg 37,Room 6134, Bethesda, MD 20892 USA.
EM caoli@mail.nih.gov
FU US National Cancer Institute (NCI); NCI, NIH [N01-CO-12400]
FX We thank Dr Andrius Kazlauskas for providing the lentivirus expressing
   Bcl-x<INF>L</INF>, and Arnulfo Mendoza, Vanessa Moore, Susan Garfield
   and Barbara Taylor for excellent technical assistance. This research was
   supported by the Intramural Research Program of the US National Cancer
   Institute (NCI). This project was also funded in part with federal funds
   from the NCI, NIH, under contract N01-CO-12400.
NR 33
TC 18
Z9 20
U1 0
U2 2
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0950-9232
J9 ONCOGENE
JI Oncogene
PD DEC
PY 2010
VL 29
IS 48
BP 6367
EP 6377
DI 10.1038/onc.2010.364
PG 11
WC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics &
   Heredity
SC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics &
   Heredity
GA 688SW
UT WOS:000284874700007
PM 20818434
ER

PT J
AU Balzer, EM
   Whipple, RA
   Thompson, K
   Boggs, AE
   Slovic, J
   Cho, EH
   Matrone, MA
   Yoneda, T
   Mueller, SC
   Martin, SS
AF Balzer, E. M.
   Whipple, R. A.
   Thompson, K.
   Boggs, A. E.
   Slovic, J.
   Cho, E. H.
   Matrone, M. A.
   Yoneda, T.
   Mueller, S. C.
   Martin, S. S.
TI c-Src differentially regulates the functions of microtentacles and
   invadopodia
SO ONCOGENE
LA English
DT Article
DE microtentacle; invadopodia; Src; breast cancer; microtubule; actin
ID CANCER-CELLS; EXTRACELLULAR-MATRIX; TUMOR-CELLS; METASTASIS; PODOSOMES;
   INVASION; DEGRADATION; ADHESION; GROWTH; ACTIN
AB During metastasis, invading cells produce various actin-based membrane protrusions that promote directional migration and proteolysis of extracellular matrix (ECM). Observations of actin staining within thin, tubulin-based microtentacle (McTN) protrusions in suspended MDA-MB-231 tumor cells, prompted an investigation of whether McTNs are structural or functional analogs of invadopodia. We show here that MDA-MB-231 cells are capable of producing invadopodia and McTNs, both of which contain F-actin. Invadopodium formation was enhanced by the expression of a constitutively active c-Src kinase, and repressed by the expression of dominant-negative, catalytically inactive form of c-Src. In contrast, expression of inactive c-Src significantly increased McTN formation. Direct inhibition of c-Src with the SU6656 inhibitor compound also significantly enhanced McTN formation, but suppressed invadopodia, including the appearance of F-actin cores and phospho-cortactin foci, as well as completely blocking focal degradation of ECM. In addition, silencing of Tks5 in Src-transformed fibroblasts blocked invadopodia without affecting McTNs. Genetic modification of c-Src activity that promoted McTN formation augmented capillary retention of circulating tumor cells in vivo and rapid re-attachment of suspended cells in vitro, even though invadopodia were strongly suppressed. These results indicate that McTNs are capable of enhancing tumor cell reattachment, even in the absence of Tks5 and active Src, and define separate cytoskeletal mechanisms and functions for McTNs and invadopodia. Oncogene (2010) 29, 6402-6408; doi:10.1038/onc.2010.360; published online 18 October 2010
C1 [Balzer, E. M.; Whipple, R. A.; Thompson, K.; Cho, E. H.; Matrone, M. A.; Martin, S. S.] Univ Maryland, Sch Med, Marlene & Stewart Greenebaum NCI Canc Ctr, Dept Physiol, Baltimore, MD 21201 USA.
   [Balzer, E. M.; Boggs, A. E.; Slovic, J.; Cho, E. H.; Matrone, M. A.; Martin, S. S.] Univ Maryland, Sch Med, Program Mol Med, Baltimore, MD 21201 USA.
   [Yoneda, T.] Osaka Univ, Grad Sch Dent, Dept Biochem, Osaka, Japan.
   [Mueller, S. C.] Georgetown Univ, Sch Med, Lombardi Comprehens Canc Ctr, Dept Oncol, Washington, DC USA.
RP Martin, SS (reprint author), Univ Maryland, Sch Med, Marlene & Stewart Greenebaum NCI Canc Ctr, Dept Physiol, 655 W Baltimore St,Room 10-029, Baltimore, MD 21201 USA.
EM ssmartin@som.umaryland.edu
FU National Cancer Institute [R01-CA124704]; USA Medical Research and
   Materiel Command [BC061047]; Susan G Komen investigator-initiated grant
   [KG100240]
FX This study was supported by R01-CA124704 grant from the National Cancer
   Institute, Breast Cancer Idea Award from USA Medical Research and
   Materiel Command (BC061047) and a Susan G Komen investigator-initiated
   grant (KG100240). We are very grateful to Darren Seals and Sara
   Courtneidge for generously providing cell lines and reagents to examine
   the role of Tks5.
NR 20
TC 34
Z9 34
U1 0
U2 3
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0950-9232
J9 ONCOGENE
JI Oncogene
PD DEC
PY 2010
VL 29
IS 48
BP 6402
EP 6408
DI 10.1038/onc.2010.360
PG 7
WC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics &
   Heredity
SC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics &
   Heredity
GA 688SW
UT WOS:000284874700010
PM 20956943
ER

PT J
AU Deng, Y
   Liu, J
   Han, G
   Lu, SL
   Wang, SY
   Malkoski, S
   Tan, AC
   Deng, C
   Wang, XJ
   Zhang, Q
AF Deng, Y.
   Liu, J.
   Han, G.
   Lu, S-L
   Wang, S-Y
   Malkoski, S.
   Tan, A. C.
   Deng, C.
   Wang, X-J
   Zhang, Q.
TI Redox-dependent Brca1 transcriptional regulation by an NADH-sensor CtBP1
SO ONCOGENE
LA English
DT Article
DE Brca1; CtBP1; NADH; transcription; tumor suppressor; HNSCC
ID SQUAMOUS-CELL CARCINOMA; TERMINAL BINDING-PROTEIN; FANCONI-ANEMIA;
   NECK-CANCER; NEGATIVE MODULATION; ANTIOXIDANT TEMPOL; DOWN-REGULATION;
   BREAST-CANCER; E1A PROTEIN; RAT-LIVER
AB C-terminal binding protein 1 (CtBP1) is a transcriptional co-repressor and metabolic sensory protein, which often represses tumor suppressor genes. Hence, we sought to determine if CtBP1 affects expression of the tumor suppressor Brca1 in head and neck tissue, as downregulation of Brca1 begins at the early stages of head and neck squamous cell carcinomas (HNSCCs). We found that CtBP1 represses Brca1 transcription by binding to the E2F4 site of the Brca1 promoter. Additionally, the recruitment of CtBP1 to the Brca1 promoter is redox-dependent, that is, increased at high NADH levels in hypoxic conditions. Further, immunostaining using a human HNSCC tissue array revealed that nuclear CtBP1 staining began to accumulate in hyperplasic lesions and HNSCCs, this staining correlated with Brca1 downregulation in these lesions. Pharmacological disruption of CtBP1 binding to Brca1 promoter by the antioxidant Tempol, which reduces NADH levels, relieved CtBP1-mediated repression of Brca1, leading to increased DNA repair in HNSCC cells. As tumor cells are generally hypoxic with increased NADH levels, the dynamic control of Brca1 by a 'metabolic switch' found in this study not only provides an important link between tumor metabolism and tumor suppressor expression but also suggests a potential chemo preventative or therapeutic strategy for HNSCC by blocking NADH-dependent CtBP1 activity at early stages of HNSCC carcinogenesis. Oncogene (2010) 29, 6603-6608; doi:10.1038/onc.2010.406; published online 6 September 2010
C1 [Han, G.; Wang, X-J] Univ Colorado, Dept Pathol, Aurora, CO 80045 USA.
   [Deng, Y.; Liu, J.; Zhang, Q.] Univ Colorado, Dept Dermatol, Aurora, CO 80045 USA.
   [Lu, S-L] Univ Colorado, Dept Otolaryngol, Aurora, CO 80045 USA.
   [Wang, S-Y] Oregon Hlth & Sci Univ, Vollum Inst, Portland, OR 97201 USA.
   [Malkoski, S.] Univ Colorado, Dept Med, Div Pulm, Aurora, CO 80045 USA.
   [Tan, A. C.] Univ Colorado, Dept Med, Div Med Oncol, Aurora, CO 80045 USA.
   [Deng, C.] NIDDK, NIH, Bethesda, MD USA.
RP Wang, XJ (reprint author), Univ Colorado, Dept Pathol, Aurora, CO 80045 USA.
EM xj.wang@UCDenver.edu; Qinghong.Zhang@UCDenver.edu
RI Tan, Aik Choon/A-3135-2011; deng, chuxia/N-6713-2016; 
OI Tan, Aik Choon/0000-0003-2955-8369
FU NIH [R01DE15953, R01CA115468]
FX This work was supported by Grants from the NIH, R01DE15953 (to X-JW) and
   R01CA115468 (to QZ). We thank Dr Petra Boukamp for providing the normal
   human keratinocytes HaCaT cells and Dr James Mitchell for helpful
   discussions.
NR 44
TC 15
Z9 16
U1 0
U2 5
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0950-9232
J9 ONCOGENE
JI Oncogene
PD DEC
PY 2010
VL 29
IS 50
BP 6603
EP 6608
DI 10.1038/onc.2010.406
PG 6
WC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics &
   Heredity
SC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics &
   Heredity
GA 695OA
UT WOS:000285380200009
PM 20818429
ER

PT J
AU Smits, M
   Nilsson, J
   Mir, SE
   van der Stoop, PM
   Hulleman, E
   Niers, JM
   Hamer, PCDW
   Marquez, VE
   Cloos, J
   Krichevsky, AM
   Noske, DP
   Tannous, BA
   Wurdinger, T
AF Smits, Michiel
   Nilsson, Jonas
   Mir, Shahryar E.
   van der Stoop, Petra M.
   Hulleman, Esther
   Niers, Johanna M.
   Hamer, Phillip C. de Witt
   Marquez, Victor E.
   Cloos, Jacqueline
   Krichevsky, Anna M.
   Noske, David P.
   Tannous, Bakhos A.
   Wurdinger, Thomas
TI miR-101 is down-regulated in glioblastoma resulting in EZH2-induced
   proliferation, migration, and angiogenesis
SO ONCOTARGET
LA English
DT Article
DE cancer; microRNA; Policomb group; glioblastoma; angiogenesis
ID HISTONE METHYLTRANSFERASE ACTIVITY; H3 LYSINE-27 METHYLATION; GROUP
   PROTEIN EZH2; MOUSE DEVELOPMENT; PROSTATE-CANCER; CELL FATE; IN-VIVO;
   POLYCOMB; EXPRESSION; GENE
AB Background: Glioblastoma (GBM) is a malignant brain tumor with dismal prognosis. GBM patients have a median survival of less than 2 years. GBM is characterized by fast cell proliferation, infiltrative migration, and by the induction of angiogenesis. MicroRNAs and polycomb group (PcG) proteins have emerged as important regulators of gene expression.
   Methods: Here we determined that miR-101 is down-regulated in GBM, resulting in overexpression of the miR-101 target PcG protein EZH2, a histone methyltransferase affecting gene expression profiles in an epigenetic manner.
   Results: Inhibition of EZH2 in vitro by pre-miR-101, EZH2 siRNA, or small molecule DZNep, attenuated GBM cell growth, migration/invasion, and GBM-induced endothelial tubule formation. In addition, for each biological process we identified ontology-associated transcripts that significantly correlate with EZH2 expression. Inhibition of EZH2 in vivo by systemic DZNep administration in a U87-Fluc-mCherry GBM xenograft mouse imaging model resulted in reduced tumor growth.
   Conclusion: Our results indicate that EZH2 has a versatile function in GBM progression and that its overexpression is at least partly due to decreased miR-101 expression. Inhibition of EZH2 may be a potential therapeutic strategy to target GBM proliferation, migration, and angiogenesis.cancer, microRNA, Policomb group, glioblastoma, angiogenesis
C1 [Smits, Michiel; Nilsson, Jonas; Mir, Shahryar E.; van der Stoop, Petra M.; Hulleman, Esther; Hamer, Phillip C. de Witt; Cloos, Jacqueline; Noske, David P.; Wurdinger, Thomas] Vrije Univ Amsterdam Med Ctr, Canc Ctr Amsterdam, Dept Neurosurg, Neurooncol Res Grp, Amsterdam, Netherlands.
   [Smits, Michiel; Nilsson, Jonas; Mir, Shahryar E.; van der Stoop, Petra M.; Hulleman, Esther; Hamer, Phillip C. de Witt; Cloos, Jacqueline; Noske, David P.; Wurdinger, Thomas] Vrije Univ Amsterdam Med Ctr, Canc Ctr Amsterdam, Dept Pediat Oncol Hematol, Neurooncol Res Grp, Amsterdam, Netherlands.
   [Niers, Johanna M.; Tannous, Bakhos A.; Wurdinger, Thomas] Massachusetts Gen Hosp, Dept Neurol, Mol Neurogenet Unit, Boston, MA 02114 USA.
   [Niers, Johanna M.; Tannous, Bakhos A.; Wurdinger, Thomas] Massachusetts Gen Hosp, Dept Radiol, Mol Neurogenet Unit, Boston, MA 02114 USA.
   [Niers, Johanna M.; Tannous, Bakhos A.; Wurdinger, Thomas] Harvard Univ, Sch Med, Neurosci Program, Boston, MA 02115 USA.
   [Marquez, Victor E.] NCI, Med Chem Lab, Ctr Canc Res, Frederick, MD 21701 USA.
   [Krichevsky, Anna M.] Harvard Univ, Brigham & Womens Hosp, Sch Med, Dept Neurol, Boston, MA 02115 USA.
RP Nilsson, J (reprint author), Vrije Univ Amsterdam Med Ctr, Canc Ctr Amsterdam, Dept Neurosurg, Neurooncol Res Grp, Amsterdam, Netherlands.
EM j.nilsson@vumc.nl; t.wurdinger@vumc.nl
RI De Witt Hamer, Philip/E-7630-2013
OI De Witt Hamer, Philip/0000-0003-2988-8544
FU Dutch Cancer Foundation; Lion's Cancer Research Foundation; Umea
   University, Sweden; Stichting Translational Research CCA/VU University
   medical center; Swedish Research Counsil; NIH, National Cancer
   Institute, Center for Cancer Research
FX We thank X. O. Breakefield for helpful discussions and P. Van der Valk
   and L. Wedekind for technical assistance. This work was supported by the
   Dutch Cancer Foundation (S. E. M.), Lion's Cancer Research Foundation,
   Umea University, Sweden; Stichting Translational Research CCA/VU
   University medical center; Swedish Research Counsil (R.J.A.N.). This
   research was supported in part by the Intramural Research Program of the
   NIH, National Cancer Institute, Center for Cancer Research.
NR 45
TC 117
Z9 122
U1 1
U2 11
PU IMPACT JOURNALS LLC
PI ALBANY
PA 6211 TIPTON HOUSE, STE 6, ALBANY, NY 12203 USA
SN 1949-2553
J9 ONCOTARGET
JI Oncotarget
PD DEC
PY 2010
VL 1
IS 8
BP 710
EP 720
PG 11
WC Oncology; Cell Biology
SC Oncology; Cell Biology
GA 802JQ
UT WOS:000293506500003
PM 21321380
ER

PT J
AU Chernomordik, V
   Gandjbakhche, AH
   Hassan, M
   Pajevic, S
   Weiss, GH
AF Chernomordik, Victor
   Gandjbakhche, Amir H.
   Hassan, Moinuddin
   Pajevic, Sinisa
   Weiss, George H.
TI A CTRW-based model of time-resolved fluorescence lifetime imaging in a
   turbid medium
SO OPTICS COMMUNICATIONS
LA English
DT Article
DE Photon migration; Time-resolved; Optical imaging; Fluorescence
ID ANISOTROPIC RANDOM-WALKS; SCALING RELATIONSHIPS; PHOTON MIGRATION;
   BIOLOGICAL MEDIA; IN-VIVO; TISSUE; DOMAIN; TOMOGRAPHY; SCATTERING;
   CONTRAST
AB We develop an analytic model of time-resolved fluorescent imaging of photons migrating through a semi-infinite turbid medium bounded by an infinite plane in the presence of a single stationary point fluorophore embedded in the medium. In contrast to earlier models of fluorescent imaging in which photon motion is assumed to be some form of continuous diffusion process, the present analysis is based on a continuous-time random walk (CTRW) on a simple cubic lattice, the objective being to estimate the position and lifetime of the fluorophore This can provide information related to local variations in pH and temperature with potential medical significance Aspects of the theory were tested using time-resolved measurements of the fluorescence from small inclusions inside tissue-like phantoms The experimental results were found to be in good agreement with theoretical predictions provided that the fluorophore was not located too close to the planar boundary, a common problem in many diffusive systems Published by Elsevier B V
C1 [Pajevic, Sinisa; Weiss, George H.] NIH, Math & Stat Comp Lab, Div Computat Biosci, Ctr Informat Technol, Bethesda, MD 20892 USA.
   [Chernomordik, Victor; Gandjbakhche, Amir H.; Hassan, Moinuddin] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Sect Analyt & Funct Biophoton, Program Pediat Imaging & Tissue Sci, NIH, Bethesda, MD 20892 USA.
RP Pajevic, S (reprint author), NIH, Math & Stat Comp Lab, Div Computat Biosci, Ctr Informat Technol, Bethesda, MD 20892 USA.
FU Division of Computational Biosciences of the Center for Informational
   Technology; National Institute of Child Health and Human Development,
   NIH
FX We are grateful to Professor Leonardo Dagdug from Universidad Autonoma
   Metropolitana (UAM) for many helpful comments. This research was
   supported by the Division of Computational Biosciences of the Center for
   Informational Technology and the National Institute of Child Health and
   Human Development, NIH.
NR 32
TC 3
Z9 3
U1 0
U2 0
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0030-4018
J9 OPT COMMUN
JI Opt. Commun.
PD DEC 1
PY 2010
VL 283
IS 23
BP 4832
EP 4839
DI 10.1016/j.optcom.2010.06.099
PG 8
WC Optics
SC Optics
GA 674AF
UT WOS:000283704800044
PM 21057657
ER

PT J
AU Abrahao, AC
   Castilho, RM
   Squarize, CH
   Molinolo, AA
   dos Santos-Pinto, D
   Gutkind, JS
AF Abrahao, Aline Correa
   Castilho, Rogerio M.
   Squarize, Cristiane H.
   Molinolo, Alfredo A.
   dos Santos-Pinto, Decio, Jr.
   Gutkind, J. Silvio
TI A role for COX2-derived PGE2 and PGE2-receptor subtypes in head and neck
   squamous carcinoma cell proliferation
SO ORAL ONCOLOGY
LA English
DT Article
DE Head and neck cancer; Cyclooxygenase; Prostaglandin E2; PGE2 receptors;
   EP1; EP2; EP3; EP4; G protein-coupled receptors; Oral cancer; Cell
   proliferation
ID CYCLOOXYGENASE-2 EXPRESSION; PROSTAGLANDIN E-2; PROGNOSTIC-SIGNIFICANCE;
   CANCER; GROWTH; RECEPTORS; PATHWAY; COX-2; ANGIOGENESIS; CELECOXIB
AB The overexpression of cyclooxygenase (COX)-2 is a frequent event in squamous cell carcinomas of the head and neck (HNSCC), and non-steroidal anti-inflammatory drugs, which are potent inhibitors of COX-1 and COX-2, exert chemopreventive effects on HNSCC cancer development. COX-2 promotes the release of the pro-inflammatory mediator prostaglandin E2 (PGE2), which acts on its cell surface G protein-coupled receptors EP1, EP2, EP3, and EP4. Here, we investigated the role of PGE2 and its receptors in cellular proliferation in HNSCC. The expression of COX-2 and EP1-4 was examined in immortalized oral epithelial cells and in a representative panel of HNSCC cell lines, and based on these data EP1-EP3 and COX-2 expression were evaluated by immunohistochemistry in a large clinical sample collection using HNSCC tissue microarrays. The ability of selective COX-2 inhibition to block PGE2 secretion was measured by ELISA specific assays. The effects of PGE2 on cell proliferation were evaluated using PGE2, its stable analog, and EP2 and EP3-specific synthetic agonists. The results presented here show that HNSCC tumoral lesions and their derived cell lines constitutively express COX-2 and the EP1, EP2 and EP3 receptors for PGE2. HNSCC cells secrete PGE2, which can be suppressed by low concentrations of COX-2 selective inhibitors, without inhibiting cell proliferation. Exogenously added stable PGE2 and EP3-specific agonists induce DNA synthesis in all HNSCC cell lines tested. Overall, our study supports the emerging notion that PGE2 produced in the tumor microenvironment by the overexpression of COX-2 in tumoral and inflammatory cells may promote the growth of HNSCC cells in an autocrine and paracrine fashion by acting on PGE2 receptors that are widely expressed in most HNSCC cancer cells. In particular, our findings suggest that EP3 receptor may play a more prominent role in HNSCC cell growth promotion, thus providing a rationale for the future evaluation of this PGE2 receptor as a target for HNSCC prevention strategies. Published by Elsevier Ltd.
C1 [Castilho, Rogerio M.; Squarize, Cristiane H.; Molinolo, Alfredo A.; Gutkind, J. Silvio] Natl Inst Dent & Craniofacial Res, Oral & Pharyngeal Canc Branch, NIH, Bethesda, MD 20892 USA.
   [Abrahao, Aline Correa; dos Santos-Pinto, Decio, Jr.] Univ Sao Paulo, Dept Oral Pathol, Sch Dent, BR-05509000 Sao Paulo, Brazil.
   [Castilho, Rogerio M.; Squarize, Cristiane H.] Univ Michigan, Sch Dent, Dept Periodont & Oral Med, Ann Arbor, MI 48109 USA.
RP Gutkind, JS (reprint author), Natl Inst Dent & Craniofacial Res, Oral & Pharyngeal Canc Branch, NIH, 30 Convent Dr,Rm 211, Bethesda, MD 20892 USA.
EM sg39v@nih.gov
RI Gutkind, J. Silvio/A-1053-2009; Abrahao, Aline/G-1863-2012; Pinto,
   Decio/B-6041-2011
OI Abrahao, Aline/0000-0002-3397-3234; Pinto, Decio/0000-0001-6198-5155
FU CAPES (Coordenacao de Aperfeicoamento de Pessoal de Nivel Superior,
   Brazil); National Institutes of Dental and Craniofacial Research
   (NIDCR), National Institute of Health (NIH)
FX ACA was supported by CAPES (Coordenacao de Aperfeicoamento de Pessoal de
   Nivel Superior, Brazil). This work was supported by the Intramural
   Research Program, National Institutes of Dental and Craniofacial
   Research (NIDCR), National Institute of Health (NIH).
NR 28
TC 34
Z9 36
U1 0
U2 15
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 1368-8375
J9 ORAL ONCOL
JI Oral Oncol.
PD DEC
PY 2010
VL 46
IS 12
BP 880
EP 887
DI 10.1016/j.oraloncology.2010.09.005
PG 8
WC Oncology; Dentistry, Oral Surgery & Medicine
SC Oncology; Dentistry, Oral Surgery & Medicine
GA 682KS
UT WOS:000284403000007
PM 20951077
ER

PT J
AU Hesse, BW
   Johnson, LE
   Davis, KL
AF Hesse, Bradford William
   Johnson, Lenora Eulene
   Davis, Kia LaTrece
TI Extending the reach, effectiveness, and efficiency of communication:
   Evidence from the centers of excellence in cancer communication research
SO PATIENT EDUCATION AND COUNSELING
LA English
DT Editorial Material
ID HEALTH INFORMATION; SCIENCE
C1 [Hesse, Bradford William; Johnson, Lenora Eulene] NCI, Bethesda, MD 20892 USA.
   [Davis, Kia LaTrece] Harvard Univ, Sch Publ Hlth, Cambridge, MA 02138 USA.
RP Hesse, BW (reprint author), 6130 Execut Blvd,MSC 7365,EPN 4068, Bethesda, MD 20892 USA.
EM hesseb@mail.nih.gov
OI Davis, Kia/0000-0002-1338-3018; Hesse, Bradford/0000-0003-1142-1161
FU Intramural NIH HHS [Z99 CA999999]; NCI NIH HHS [CA-P20-137219,
   CA-P50-95815]
NR 25
TC 4
Z9 4
U1 0
U2 1
PU ELSEVIER IRELAND LTD
PI CLARE
PA ELSEVIER HOUSE, BROOKVALE PLAZA, EAST PARK SHANNON, CO, CLARE, 00000,
   IRELAND
SN 0738-3991
J9 PATIENT EDUC COUNS
JI Patient Educ. Couns.
PD DEC
PY 2010
VL 81
SU 1
BP S1
EP S5
DI 10.1016/j.pec.2010.11.002
PG 5
WC Public, Environmental & Occupational Health; Social Sciences,
   Interdisciplinary
SC Public, Environmental & Occupational Health; Social Sciences - Other
   Topics
GA 707OK
UT WOS:000286295700001
PM 21094014
ER

PT J
AU Cai, L
   He, L
   Xu, YR
   Zhao, YM
   Yang, X
AF Cai, Ling
   He, Lei
   Xu, Yiren
   Zhao, Yuming
   Yang, Xin
TI Multi-object detection and tracking by stereo vision
SO PATTERN RECOGNITION
LA English
DT Article
DE Stereo vision; Kernel density estimation; Multi-object detection and
   tracking; Clustering
ID OBJECT DETECTION; MEAN SHIFT; VIDEO; SEGMENTATION; FEATURES; SHADOWS;
   COLOR
AB This paper presents a new stereo vision-based model for multi-object detection and tracking in surveillance systems. Unlike most existing monocular camera-based systems, a stereo vision system is constructed in our model to overcome the problems of illumination variation, shadow interference, and object occlusion. In each frame, a sparse set of feature points are identified in the camera coordinate system, and then projected to the 2D ground plane. A kernel-based clustering algorithm is proposed to group the projected points according to their height values and locations on the plane. By producing clusters, the number, position, and orientation of objects in the surveillance scene can be determined for online multi-object detection and tracking. Experiments on both indoor and outdoor applications with complex scenes show the advantages of the proposed system. (C) 2010 Elsevier Ltd. All rights reserved.
C1 [He, Lei] NIH, Natl Lib Med, Bethesda, MD 20894 USA.
   [Cai, Ling; Xu, Yiren; Zhao, Yuming; Yang, Xin] Shanghai Jiao Tong Univ, Dept Automat, Shanghai 200340, Peoples R China.
RP Cai, L (reprint author), NIH, Natl Lib Med, Bethesda, MD 20894 USA.
EM cailing.cs@gmail.com; lei.he@nih.gov; xuyiren@gmail.com;
   arola_zym@sjtu.edu.cn; yangxin@sjtu.edu.cn
NR 44
TC 16
Z9 18
U1 2
U2 11
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 0031-3203
J9 PATTERN RECOGN
JI Pattern Recognit.
PD DEC
PY 2010
VL 43
IS 12
BP 4028
EP 4041
DI 10.1016/j.patcog.2010.06.012
PG 14
WC Computer Science, Artificial Intelligence; Engineering, Electrical &
   Electronic
SC Computer Science; Engineering
GA 657BC
UT WOS:000282384900010
ER

PT J
AU Keir, ST
   Maris, JM
   Lock, R
   Kolb, EA
   Gorlick, R
   Carol, H
   Morton, CL
   Reynolds, CP
   Kang, MH
   Watkins, A
   Houghton, PJ
   Smith, MA
AF Keir, Stephen T.
   Maris, John M.
   Lock, Richard
   Kolb, E. Anders
   Gorlick, Richard
   Carol, Hernan
   Morton, Christopher L.
   Reynolds, C. Patrick
   Kang, Min H.
   Watkins, Amy
   Houghton, Peter J.
   Smith, Malcolm A.
TI Initial Testing (Stage 1) of the Multi-Targeted Kinase Inhibitor
   Sorafenib by the Pediatric Preclinical Testing Program
SO PEDIATRIC BLOOD & CANCER
LA English
DT Article
DE developmental therapeutics; preclinical testing; tyrosine kinases
ID ACUTE LYMPHOBLASTIC-LEUKEMIA; MYELOID CELL LEUKEMIA-1; MULTIKINASE
   INHIBITOR; DOWN-REGULATION; ANTITUMOR-ACTIVITY;
   HEPATOCELLULAR-CARCINOMA; RAF/MEK/ERK PATHWAY; XENOGRAFT MODELS;
   TUMOR-GROWTH; BRAF GENE
AB Background. Sorafenib is an inhibitor of multiple kinases (e.g., VEGF receptors, PDGFR, FLT3, RET, BRAF, KIT) and is approved by FDA for treatment of two adult cancers. The activity of sorafenib was evaluated against the PPTP's in vitro and in vivo panels. Procedures. Sorafenib was evaluated against the PPTP in vitro panel using 96-hr exposure at concentrations ranging from 1.0 nM to 10.0 mu M. It was tested against the PPTP in vivo panels at a dose of 60 mg/kg administered by oral gavage daily for 5 days per week, repeated for 6 weeks. Results. In vitro sorafenib demonstrated cytotoxic activity, with a median IC(50) value of 4.3 mu M. Twenty of 23 cell lines had IC(50) values between 1.0 and 10.0 mu M. A single cell line (Kasumi-1) with an activating KIT mutation had an IC(50) value <1.0 mu M (IC(50) = 0.02 mu M). In vivo sorafenib induced significant differences in event-free survival (EFS) distribution compared to control in 27 of 36 (75%) of the evaluable solid tumor xenografts and in 1 of 8 (12.5%) of the evaluable ALL xenografts. Sorafenib induced tumor growth inhibition meeting criteria for intermediate activity (EFS T/C) in 15 of 34 (44%) evaluable solid tumor xenografts. No xenografts achieved an objective response. Conclusions. The primary in vitro activity of sorafenib was noted at concentrations above 1 mu M, with the exception of a more sensitive cell line with an activating KIT mutation. The primary in vivo effect for sorafenib was tumor growth inhibition, which was observed across multiple histotypes. Pediatr Blood Cancer. 2010;55:1126-1133. (C) 2010 Wiley-Liss, Inc.
C1 [Keir, Stephen T.] Duke Univ, Med Ctr, Dept Surg, Preston Robert Tisch Brain Tumor Ctr, Durham, NC 27710 USA.
   [Maris, John M.] Univ Penn, Childrens Hosp Philadelphia, Sch Med, Abramson Family Canc Res Inst, Philadelphia, PA 19104 USA.
   [Lock, Richard; Carol, Hernan] Childrens Canc Inst Australia Med Res, Randwick, NSW, Australia.
   [Kolb, E. Anders] Alfred I DuPont Hosp Children, Wilmington, DE USA.
   [Gorlick, Richard] Childrens Hosp Montefiore, Bronx, NY USA.
   [Morton, Christopher L.; Watkins, Amy] St Jude Childrens Hosp, Memphis, TN 38105 USA.
   [Reynolds, C. Patrick; Kang, Min H.] Texas Tech Univ, Hlth Sci Ctr, Lubbock, TX 79430 USA.
   [Houghton, Peter J.] Nationwide Childrens Hosp, Columbus, OH USA.
   [Smith, Malcolm A.] NCI, Canc Therapy Evaluat Program, Bethesda, MD 20892 USA.
RP Keir, ST (reprint author), Duke Univ, Med Ctr, Dept Surg, Preston Robert Tisch Brain Tumor Ctr, Durham, NC 27710 USA.
EM keir0001@mc.duke.edu
RI Houghton, Peter/E-3265-2011; Carol, Hernan/F-5750-2013; Lock,
   Richard/G-4253-2013; 
OI Carol, Hernan/0000-0002-9443-8032; Reynolds, C.
   Patrick/0000-0002-2827-8536
FU National Cancer Institute [NO1-CM-42216, CA21765, CA108786]
FX Grant sponsor: National Cancer Institute; Grant numbers: NO1-CM-42216,
   CA21765, CA108786.
NR 47
TC 23
Z9 29
U1 0
U2 3
PU WILEY-LISS
PI HOBOKEN
PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 1545-5009
J9 PEDIATR BLOOD CANCER
JI Pediatr. Blood Cancer
PD DEC 1
PY 2010
VL 55
IS 6
BP 1126
EP 1133
DI 10.1002/pbc.22712
PG 8
WC Oncology; Hematology; Pediatrics
SC Oncology; Hematology; Pediatrics
GA 674OT
UT WOS:000283757600016
PM 20672370
ER

PT J
AU Houghton, PJ
   Morton, CL
   Kang, M
   Reynolds, CP
   Billups, CA
   Favours, E
   Payne-Turner, D
   Tucker, C
   Smith, MA
AF Houghton, Peter J.
   Morton, Christopher L.
   Kang, Min
   Reynolds, C. Patrick
   Billups, Catherine A.
   Favours, Edward
   Payne-Turner, Debbie
   Tucker, Chandra
   Smith, Malcolm A.
TI Evaluation of Cytarabine Against Ewing Sarcoma Xenografts by the
   Pediatric Preclinical Testing Program
SO PEDIATRIC BLOOD & CANCER
LA English
DT Article
DE Ewings/PNET; oncogenes; pediatric hematology/oncology
ID CHILDRENS ONCOLOGY GROUP; PHASE-I TRIAL; PROTRACTED IRINOTECAN; SOLID
   TUMORS; VINCRISTINE; COMBINATION; NUCLEOSIDE; BORTEZOMIB; TOPOTECAN;
   STAGE-1
AB Treatment with the nucleoside analog cytarabine has been shown to mimic changes in gene expression associated with down-regulation of the EWS-FLI1 oncogene in Ewing sarcoma cell lines, selectively inhibit their growth in vitro, and cause tumor regression in athymic nude mice. For this report cytarabine was studied in vitro against a panel of 23 pediatric cancer cell lines and in vivo against 6 Ewing sarcoma xenografts. Acute lymphoblastic leukemia cell lines were the most sensitive to cytarabine in vitro (median IC(50) 9 nM), while Ewing sarcoma cell lines showed intermediate sensitivity (median IC(50) 232 nM). Cytarabine at a dose of 150 mg/kg administered daily 5x failed to significantly inhibit growth of five xenograft models, but reduced growth rate of the A673 xenograft by 50%. Cytarabine shows no differential in vitro activity against Ewing sarcoma cell lines and is ineffective in vivo against Ewing sarcoma xenografts at the dose and schedule studied. Pediatr Blood Cancer 2010;55:1224-1226 (C) 2010 Wiley-Liss, Inc.
C1 [Houghton, Peter J.] St Jude Childrens Hosp, Dept Mol Pharmacol, Memphis, TN 38105 USA.
   [Kang, Min; Reynolds, C. Patrick] Texas Tech Univ, Hlth Sci Ctr, Lubbock, TX 79430 USA.
   [Smith, Malcolm A.] NCI, Canc Therapy Evaluat Program, Bethesda, MD 20892 USA.
RP Houghton, PJ (reprint author), St Jude Childrens Hosp, Dept Mol Pharmacol, 332 N Lauderdale St, Memphis, TN 38105 USA.
EM peter.houghton@stjude.org
RI Houghton, Peter/E-3265-2011
FU National Cancer Institute [NO1-CM-42216];  [CA21765]
FX This work was supported by NO1-CM-42216 from the National Cancer
   Institute, and CA21765.
NR 17
TC 5
Z9 5
U1 0
U2 1
PU WILEY-LISS
PI HOBOKEN
PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 1545-5009
J9 PEDIATR BLOOD CANCER
JI Pediatr. Blood Cancer
PD DEC 1
PY 2010
VL 55
IS 6
BP 1224
EP 1226
DI 10.1002/pbc.22355
PG 3
WC Oncology; Hematology; Pediatrics
SC Oncology; Hematology; Pediatrics
GA 674OT
UT WOS:000283757600037
PM 20979180
ER

PT J
AU Cervia, JS
   Chantry, CJ
   Hughes, MD
   Alvero, C
   Meyer, WA
   Hodge, J
   Borum, P
   Moye, J
   Spector, SA
AF Cervia, Joseph S.
   Chantry, Caroline J.
   Hughes, Michael D.
   Alvero, Carmelita
   Meyer, William A., III
   Hodge, Janice
   Borum, Peggy
   Moye, Jack, Jr.
   Spector, Stephen A.
CA PACTG 1010 Team
TI Associations of Proinflammatory Cytokine Levels With Lipid Profiles,
   Growth, and Body Composition in HIV-infected Children Initiating or
   Changing Antiretroviral Therapy
SO PEDIATRIC INFECTIOUS DISEASE JOURNAL
LA English
DT Article
DE HIV; proinflammatory cytokines; children; antiretroviral therapy; lipid
   profile
ID HUMAN-IMMUNODEFICIENCY-VIRUS; FACTOR-I; HEALTHY; WATER; BORN; MASS
AB Objectives: To measure proinflammatory cytokines (PIC) in HIV-infected children beginning or changing antiretroviral therapy (ART), evaluating associations with virologic, immunologic, serum lipid, growth, and body composition measures, markers of growth hormone action and glucose metabolism.
   Methods: Forty-nine prepubertal HIV-infected children had measurements of viral load (VL), CD4(+) lymphocyte count and percentage, serum lipids, apolipoprotein AI/B, IGF-1, IGFBP-1, and IGFBP-3, anthropometry, bioelectrical impedance analysis, TNF-alpha, IL-1 beta, and IL-6 at baseline and 48 weeks of ART.
   Results: Baseline levels were detectable (>0.1 pg/mL) for IL-1 beta in 28 of 48, and for TNF-alpha and Il-6 in all 49 children. TNF-alpha decreased with ART (P < 0.001) and IL-6 demonstrated a similar trend (P = 0.065). Children with 48-week VL <400 copies/mL had greater declines in TNF-alpha (mean 45%) than subjects with higher VL (5%; P = 0.009). Each 10% improvement in CD4% was associated with 26% lower TNF-alpha (P = 0.002) and 31% lower IL-6 (P = 0.016). Greater reductions in TNF-alpha were associated with lower total/HDL cholesterol ratio (P = 0.003) at week 48.
   Conclusions: In HIV-infected children initiating or changing ART, PIC were detectable at baseline and decreased over 48 weeks. Better immunologic responses were associated with greater reductions in TNF-alpha and IL-6. Reductions in TNF-alpha were associated with improved total/HDL cholesterol ratio.
C1 [Cervia, Joseph S.] Albert Einstein Coll Med, Bronx, NY 10467 USA.
   [Chantry, Caroline J.] Univ Calif, Davis Med Ctr, Sacramento, CA USA.
   [Hughes, Michael D.; Alvero, Carmelita] Harvard Univ, Sch Publ Hlth, Ctr Biostat AIDS Res, Boston, MA 02115 USA.
   [Meyer, William A., III] Quest Diagnost, Baltimore, MD USA.
   [Hodge, Janice] Frontier Sci & Technol Res Fdn Inc, Amherst, NY USA.
   [Borum, Peggy] Univ Florida, Gainesville, FL USA.
   [Moye, Jack, Jr.] NICHD, NIH, Bethesda, MD USA.
   [Spector, Stephen A.] Univ Calif San Diego, La Jolla, CA 92093 USA.
RP Cervia, JS (reprint author), N Shore Univ Hosp, Div Infect Dis, 300 Community Dr, Manhasset, NY 11030 USA.
EM cervia@lij.edu
OI moye, john/0000-0001-9976-8586
FU National Institute of Allergy and Infectious Diseases (NIAID) [U01
   AI068632]; Eunice Kennedy Shriver National Institute of Child Health and
   Human Development (NICHD); National Institute of Mental Health (NIMH)
   [AI068632]; Statistical and Data Analysis Center at Harvard School of
   Public Health, under the National Institute of Allergy and Infectious
   Diseases [5 U01 AI41110]; Pediatric AIDS Clinical Trials Group (PACTG);
   IMPAACT Group [1 U01 AI068616]; NICHD [N01-DK-9-001/HHSN267200800001C]
FX Supported by the National Institute of Allergy and Infectious Diseases
   (NIAID) grant U01 AI068632, the Eunice Kennedy Shriver National
   Institute of Child Health and Human Development (NICHD), and the
   National Institute of Mental Health (NIMH) grant AI068632 (to the
   International Maternal Pediatric Adolescent AIDS Clinical Trials Group
   [IMPAACT]). Also supported by the Statistical and Data Analysis Center
   at Harvard School of Public Health, under the National Institute of
   Allergy and Infectious Diseases cooperative agreement number 5 U01
   AI41110 with the Pediatric AIDS Clinical Trials Group (PACTG) and number
   1 U01 AI068616 with the IMPAACT Group. Support of the sites was provided
   by the National Institute of Allergy and Infectious Diseases (NIAID) the
   NICHD International and Domestic Pediatric and Maternal HIV Clinical
   Trials Network funded by NICHD (contract number
   N01-DK-9-001/HHSN267200800001C).
NR 19
TC 11
Z9 11
U1 0
U2 2
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 0891-3668
EI 1532-0987
J9 PEDIATR INFECT DIS J
JI Pediatr. Infect. Dis. J.
PD DEC
PY 2010
VL 29
IS 12
BP 1118
EP 1122
DI 10.1097/INF.0b013e3181ed9f4c
PG 5
WC Immunology; Infectious Diseases; Pediatrics
SC Immunology; Infectious Diseases; Pediatrics
GA 683RI
UT WOS:000284492500013
PM 20631646
ER

PT J
AU Boghossian, NS
   Hansen, NI
   Bell, EF
   Stoll, BJ
   Murray, JC
   Laptook, AR
   Shankaran, S
   Walsh, MC
   Das, A
   Higgins, RD
AF Boghossian, Nansi S.
   Hansen, Nellie I.
   Bell, Edward F.
   Stoll, Barbara J.
   Murray, Jeffrey C.
   Laptook, Abbot R.
   Shankaran, Seetha
   Walsh, Michele C.
   Das, Abhik
   Higgins, Rosemary D.
CA Eunice Kennedy Shriver Natl Inst C
TI Survival and Morbidity Outcomes for Very Low Birth Weight Infants With
   Down Syndrome
SO PEDIATRICS
LA English
DT Article
DE neonatal mortality; neonatal morbidity; preterm infants; Down syndrome;
   trisomy 21
ID OXYGEN-INDUCED RETINOPATHY; ATHEROMA-FREE MODEL; UNITED-STATES;
   SUPEROXIDE-DISMUTASE; PRETERM INFANTS; SOLID TUMORS; RISK-FACTOR;
   GROWTH; ENDOSTATIN; CHILDREN
AB OBJECTIVE: Our objective was to compare survival and neonatal morbidity rates between very low birth weight (VLBW) infants with Down syndrome (DS) and VLBW infants with non-DS chromosomal anomalies, nonchromosomal birth defects (BDs), and no chromosomal anomaly or major BD.
   METHODS: Data were collected prospectively for infants weighing 401 to 1500 g who were born and/or cared for at one of the study centers participating in the Eunice Kennedy Shriver National Institute of Child Health and Human Development Neonatal Research Network in 1994-2008. Risk of death and morbidities, including patent ductus arteriosus (PDA), necrotizing enterocolitis (NEC), late-onset sepsis (LOS), retinopathy of prematurity, and bronchopulmonary dysplasia (BPD), were compared between VLBW infants with DS and infants in the other groups.
   RESULTS: Infants with DS were at increased risk of death (adjusted relative risk: 2.47 [95% confidence interval: 2.00-3.07]), PDA, NEC, LOS, and BPD, relative to infants with no BDs. Decreased risk of death (relative risk: 0.40 [95% confidence interval: 0.31-0.52]) and increased risks of NEC and LOS were observed when infants with DS were compared with infants with other non-DS chromosomal anomalies. Relative to infants with nonchromosomal BDs, infants with DS were at increased risk of PDA and NEC.
   CONCLUSION: The increased risk of morbidities among VLBW infants with DS provides useful information for counseling parents and for anticipating the need for enhanced surveillance for prevention of these morbidities. Pediatrics 2010;126:1132-1140
C1 [Boghossian, Nansi S.; Bell, Edward F.; Murray, Jeffrey C.] Univ Iowa Hlth Care, Dept Pediat, Iowa City, IA USA.
   [Hansen, Nellie I.] RTI Int, Stat & Epidemiol Div, Res Triangle Pk, NC USA.
   [Stoll, Barbara J.] Emory Univ, Sch Med, Dept Pediat, Atlanta, GA USA.
   [Stoll, Barbara J.] Childrens Healthcare Atlanta, Atlanta, GA USA.
   [Laptook, Abbot R.] Brown Univ, Dept Pediat, Sch Med, Providence, RI 02912 USA.
   [Shankaran, Seetha] Wayne State Univ, Sch Med, Dept Pediat, Detroit, MI 48201 USA.
   [Walsh, Michele C.] Case Western Reserve Univ, Sch Med, Dept Pediat, Cleveland, OH 44106 USA.
   [Das, Abhik] RTI Int, Rockville, MD USA.
   [Higgins, Rosemary D.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Pregnancy & Perinatol Branch, Ctr Dev Biol & Perinatal Med, Bethesda, MD USA.
RP Bell, EF (reprint author), Univ Iowa, Dept Pediat, 200 Hawkins Dr, Iowa City, IA 52242 USA.
EM edward-bell@uiowa.edu
FU National Institutes of Health (NIH) [U10 HD27904, U10 HD34167, GCRC M01
   RR80, U10 HD21364, GCRC M01 RR8084, U10 HD27853, GCRC M01 RR30, U10
   HD40492, GCRC M01 RR39, U10 HD27851, GCRC M01 RR54, U10 HD53119, GCRC
   M01 RR750, U10 HD27856, U10 HD36790, GCRC M01 RR70, U10 HD27880]
FX Funded by the National Institutes of Health (NIH).; Data collected at
   participating sites of the Eunice Kennedy Shriver National Institute of
   Child Health and Human Development NRN were transmitted to RTI
   International, the data coordinating center for the network, which
   stored, managed, and analyzed the data for this study. On behalf of the
   NRN, Dr Abhik Das (data coordinating center principal investigator) and
   Nellie Hansen (data coordinating center statistician) had full access to
   all of the data in the study and take responsibility for the integrity
   of the data and accuracy of the data analysis. The following
   investigators, in addition to those listed as authors, participated in
   this study: NRN Steering Committee Chair: Alan H. Jobe, MD, PhD,
   University of Cincinnati; Michael S. Caplan, MD, University of Chicago,
   Pritzker School of Medicine; Alpert Medical School of Brown University
   and Women and Infants Hospital of Rhode Island (National Institutes of
   Health grant U10 HD27904): William Oh, MD; Angelita M. Hensman, RN, BSN;
   Brigham and Women's Hospital, Children's Hospital Boston, Beth Israel
   Deaconess Medical Center, and Harvard Medical School (National
   Institutes of Health grant U10 HD34167): Ann R. Stark, MD; Kerri
   Fournier, RN; Stacy Dow, RN; Case Western Reserve University, Rainbow
   Babies and Children's Hospital (National Institutes of Health grants
   GCRC M01 RR80 and U10 HD21364): Avroy A. Fanaroff, MD; Nancy S. Newman,
   BA, RN; Cincinnati Children's Hospital Medical Center, University
   Hospital, and Good Samaritan Hospital (National Institutes of Health
   grants GCRC M01 RR8084 and U10 HD27853): Kurt Schibler, MD; Edward F.
   Donovan, MD; Kate Bridges, MD; Barbara Alexander, RN; Cathy Grisby, BSN,
   CCRC; Holly L. Mincey, RN, BSN; Jody Hessling, RN; Marcia Worley
   Mersmann, RN, CCRC; Duke University School of Medicine, University
   Hospital, Alamance Regional Medical Center, and Durham Regional Hospital
   (National Institutes of Health grants GCRC M01 RR30 and U10 HD40492):
   Ronald N. Goldberg, MD; C. Michael Cotten, MD, MHS; Kathy J. Auten,
   MSHS; Kimberley A. Fisher, PhD, FNP-BC, IBCLC; Katherine A. Foy, RN;
   Emory University, Children's Healthcare of Atlanta, Grady Memorial
   Hospital, and Emory University Hospital Midtown (National Institutes of
   Health grants GCRC M01 RR39 and U10 HD27851): David P. Carlton, MD;
   Lucky Jain, MD; Ira Adams-Chapman, MD; Ellen C. Hale, RN, BS, CCRC;
   Eunice Kennedy Shriver National Institute of Child Health and Human
   Development: Linda L. Wright, MD; Stephanie Wilson Archer, MA; Elizabeth
   M. McClure, MEd; Floating Hospital for Children at Tufts Medical Center
   (National Institutes of Health grants GCRC M01 RR54 and U10 HD53119):
   Ivan D. Frantz III, MD; John M. Fiascone, MD; Brenda L. MacKinnon, RNC;
   Anne Furey, MPH; Ellen Nylen, RN, BSN; Indiana University, Indiana
   University Hospital, Methodist Hospital, Riley Hospital for Children,
   and Wishard Health Services (National Institutes of Health grants GCRC
   M01 RR750 and U10 HD27856): Brenda B. Poindexter, MD, MS; James A.
   Lemons, MD; Diana D. Appel, RN, BSN; Dianne E. Herron, RN; Lucy C.
   Miller, RN, BSN, CCRC; Leslie Dawn Wilson, BSN, CCRC; RTI International
   (National Institutes of Health grant U10 HD36790): W. Kenneth Poole,
   PhD; Dennis Wallace, PhD; Jeanette O'Donnell Auman, BS; Margaret
   Cunningham, BS; Amanda R. Irene, BS; Betty K. Hastings; Carolyn M.
   Petrie Huitema, MS; James W. Pickett II, BS; Scott E. Schaefer, MS;
   Kristin M.; Zaterka-Baxter, RN, BSN; Stanford University, California
   Pacific Medical Center, Dominican Hospital, El Camino Hospital, and
   Lucile Packard Children's Hospital (National Institutes of Halth grants
   GCRC M01 RR70 and U10 HD27880): Krisa P. Van Meurs, MD; David K.
   Stevenson, MD; Charles E. Ahlfors, MD; Marian M. Adams, MD; M. Bethany
   Ball, BS, CCRC; Robert D. Stebbins, MD; Melinda S. Proud, RCP;
   University of Alabama at Birmingham Health System and Children's
   Hospital of Alabama (National Institutes of Health grants GCRC M01 RR32
   and U10 HD34216): Waldemar A. Carlo, MD; Namasivayam Ambalavanan, MD;
   Monica V. Collins, RN, BSN, MaEd; Shirley S. Cosby, RN, BSN; University
   of California, San Diego, Medical Center and Sharp Mary Birch Hospital
   for Women and Newborns (National Institutes of Health grant U10
   HD40461): Neil N. Finer, MD; Maynard R. Rasmussen, MD; Paul R. Wozniak,
   MD; Kathy Arnell, RNC; Renee Bridge, RN; Clarence Demetrio, RN; Chris
   Henderson, RCP, CRTT; Wade Rich, BSHS, RRT; University of Iowa
   Children's Hospital (National Institutes of Health grants GCRC M01 RR59
   and U10 HD53109): John A. Widness, MD; Karen J. Johnson, RN, BSN;
   University of Miami, Holtz Children's Hospital (National Institutes of
   Health grant U10 HD21397): Shahnaz Duara, MD; Charles R. Bauer, MD; Ruth
   Everett-Thomas, RN, MSN; Amy Mur Worth, RN, MS; University of New Mexico
   Health Sciences Center (National Institutes of Health grants GCRC M01
   RR997 and U10 HD53089): Kristi L. Watterberg, MD; Lu-Ann Papile, MD;
   Robin K. Ohls, MD; Conra Backstrom Lacy, RN; Julie Rohr, MSN, RNC, CNS;
   University of Rochester Medical Center, Golisano Children's Hospital
   (National Institutes of Health grants U10 HD40521, GCRC M01 RR44, and
   UL1 RR024160): Dale L. Phelps, MD; Linda J. Reubens, RN, CCRC; Erica
   Burnell, RN; Rosemary L. Jensen; Mary Rowan, RN; University of Tennessee
   Health Science Center (National Institutes of Health grant U10 HD21415):
   Sheldon B. Korones, MD; Henrietta S. Bada, MD; Tina Hudson, RN BSN;
   University of Texas Southwestern Medical Center at Dallas, Parkland
   Health and Hospital System, and Children's Medical Center Dallas
   (National Institutes of Health grants GCRC M01 RR633 and U10 HD40689):
   Pablo J. Sanchez, MD; Charles R. Rosenfeld, MD; Walid A. Salhab, MD; Jon
   E. Tyson, MD, MPH; Alicia Guzman; Gaynelle Hensley, RN; Melissa H. Leps,
   RN; Susie Madison, RN; Nancy A. Miller, RN; University of Texas Health
   Science Center at Houston Medical School, Children's Memorial Hermann
   Hospital, and Lyndon Baines Johnson General Hospital/Harris County
   Hospital District (National Institutes of Health grant U10 HD21373):
   Kathleen A. Kennedy, MD, MPH; Jon E. Tyson, MD, MPH; Esther G. Akpa, RN,
   BSN; Patty A. Cluff, RN; Beverly Foley Harris, RN, BSN; Claudia I.
   Franco, RNC, MSN; Anna E. Lis, RN, BSN; Sarah Martin, RN, BSN; Georgia
   E. McDavid, RN; Patti L. Pierce Tate, RCP; Maegan C. Simmons, RN;
   University of Utah, University Hospital, LDS Hospital, and Primary
   Children's Medical Center (National Institutes of Health grants CTSA UL1
   RR25764, GCRC M01 RR64, and U10 HD53124): Roger G. Faix, MD; Bradley A.
   Yoder, MD; Karen A. Osborne, RN, BSN, CCRC; Jennifer J. Jensen, RN, BSN;
   Cynthia Spencer, RNC; Kimberlee Weaver-Lewis, RN, BSN; Wake Forest
   University, Baptist Medical Center, Brenner Children's Hospital, and
   Forsyth Medical Center (National Institutes of Health grants U10 HD40498
   and GCRC M01 RR7122): T. Michael O'Shea, MD, MPH; Nancy J.; Peters, RN,
   CCRP; Wayne State University, Hutzel Women's Hospital, and Children's
   Hospital of Michigan (National Institutes of Health grant 10 HD21385):
   Rebecca Bara, RN, BSN; Geraldine Muran, RN, BSN; Yale University,
   Yale-New Haven Children's Hospital, and Bridgeport Hospital (National
   Institutes of Health grants CTSA UL1 RR24139, GCRC M01 RR125, GCRC M01
   RR6022, and U10 HD27871): Richard A. Ehrenkranz, MD; Harris Jacobs, MD;
   Patricia Cervone, RN; Patricia Gettner, RN; Monica Konstantino, RN, BSN;
   JoAnn Poulsen, RN; Janet Taft, RN, BSN.
NR 29
TC 11
Z9 12
U1 2
U2 2
PU AMER ACAD PEDIATRICS
PI ELK GROVE VILLAGE
PA 141 NORTH-WEST POINT BLVD,, ELK GROVE VILLAGE, IL 60007-1098 USA
SN 0031-4005
J9 PEDIATRICS
JI Pediatrics
PD DEC
PY 2010
VL 126
IS 6
BP 1132
EP 1140
DI 10.1542/peds.2010-1824
PG 9
WC Pediatrics
SC Pediatrics
GA 688EF
UT WOS:000284831900039
PM 21098157
ER

PT J
AU Patrick, AR
   Miller, M
   Barber, CW
   Wang, PS
   Canning, CF
   Schneeweiss, S
AF Patrick, Amanda R.
   Miller, Matthew
   Barber, Catherine W.
   Wang, Philip S.
   Canning, Claire F.
   Schneeweiss, Sebastian
TI Identification of hospitalizations for intentional self-harm when
   E-codes are incompletely recorded
SO PHARMACOEPIDEMIOLOGY AND DRUG SAFETY
LA English
DT Article
DE intentional self-harm; suicide; depression
ID SUICIDE; ADULTS; SAFETY; RISK
AB Context Suicidal behavior has gained attention as an adverse outcome of prescription drug use. Hospitalizations for intentional self-harm, including suicide, can be identified in administrative claims databases using external cause of injury codes (E-codes). However, rates of E-code completeness in US government and commercial claims databases are low due to issues with hospital billing software.
   Objective To develop an algorithm to identify intentional self-harm hospitalizations using recorded injury and psychiatric diagnosis codes in the absence of E-code reporting.
   Methods We sampled hospitalizations with an injury diagnosis (ICD-9 800-995) from two databases with high rates of E-coding completeness: 1999-2001 British Columbia, Canada data and the 2004 US Nationwide Inpatient Sample. Our gold standard for intentional self-harm was a diagnosis of E950-E958. We constructed algorithms to identify these hospitalizations using information on type of injury and presence of specific psychiatric diagnoses.
   Results The algorithm that identified intentional self-harm hospitalizations with high sensitivity and specificity was a diagnosis of poisoning, toxic effects, open wound to elbow, wrist, or forearm, or asphyxiation; plus a diagnosis of depression, mania, personality disorder, psychotic disorder, or adjustment reaction. This had a sensitivity of 63%, specificity of 99% and positive predictive value (PPV) of 86% in the Canadian database. Values in the US data were 74, 98, and 73%. PPV was highest (80%) in patients under 25 and lowest those over 65 (44%).
   Conclusions The proposed algorithm may be useful for researchers attempting to study intentional self-harm in claims databases with incomplete E-code reporting, especially among younger populations. Copyright (C) 2010 John Wiley & Sons, Ltd.
C1 [Patrick, Amanda R.; Canning, Claire F.; Schneeweiss, Sebastian] Harvard Univ, Brigham & Womens Hosp, Sch Med, Div Pharmacoepidemiol & Pharmacoecon,Dept Med, Boston, MA 02115 USA.
   [Miller, Matthew; Barber, Catherine W.] Harvard Univ, Sch Publ Hlth, Harvard Injury Control Res Ctr, Boston, MA 02115 USA.
   [Wang, Philip S.] NIMH, Bethesda, MD 20892 USA.
RP Patrick, AR (reprint author), Brigham & Womens Hosp, Div Pharmacoepidemiol, 1620 Tremont St,Suite 3030, Boston, MA 02120 USA.
EM arpatrick@partners.org
RI Schneeweiss, Sebastian/C-2125-2013
FU National Institute of Mental Health [RO1-MH078708]
FX This project was funded by a grant from the National Institute of Mental
   Health (RO1-MH078708). Amanda Patrick had full access to all of the data
   in the study and takes responsibility for the integrity of the data and
   the accuracy of the data analysis.
NR 24
TC 24
Z9 24
U1 0
U2 4
PU JOHN WILEY & SONS LTD
PI CHICHESTER
PA THE ATRIUM, SOUTHERN GATE, CHICHESTER PO19 8SQ, W SUSSEX, ENGLAND
SN 1053-8569
J9 PHARMACOEPIDEM DR S
JI Pharmacoepidemiol. Drug Saf.
PD DEC
PY 2010
VL 19
IS 12
BP 1263
EP 1275
DI 10.1002/pds.2037
PG 13
WC Public, Environmental & Occupational Health; Pharmacology & Pharmacy
SC Public, Environmental & Occupational Health; Pharmacology & Pharmacy
GA 699JO
UT WOS:000285659900009
PM 20922709
ER

PT J
AU Freidlin, B
   Korn, EL
AF Freidlin, Boris
   Korn, Edward L.
TI Biomarker-adaptive clinical trial designs
SO PHARMACOGENOMICS
LA English
DT Editorial Material
DE enrichment; interim monitoring; multi-arm trials; randomized clinical
   trials; targeted therapy
C1 [Freidlin, Boris; Korn, Edward L.] NCI, Biometr Res Branch, Div Canc Treatment & Diag, Bethesda, MD 20892 USA.
RP Freidlin, B (reprint author), NCI, Biometr Res Branch, Div Canc Treatment & Diag, EPN-8122, Bethesda, MD 20892 USA.
EM freidlinb@ctep.nci.nih.gov
NR 15
TC 15
Z9 15
U1 0
U2 2
PU FUTURE MEDICINE LTD
PI LONDON
PA UNITEC HOUSE, 3RD FLOOR, 2 ALBERT PLACE, FINCHLEY CENTRAL, LONDON, N3
   1QB, ENGLAND
SN 1462-2416
J9 PHARMACOGENOMICS
JI Pharmacogenomics
PD DEC
PY 2010
VL 11
IS 12
SI SI
BP 1679
EP 1682
DI 10.2217/PGS.10.153
PG 4
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA 742VS
UT WOS:000288974000006
PM 21142910
ER

PT J
AU Gao, ZG
   Ding, Y
   Jacobson, KA
AF Gao, Zhan-Guo
   Ding, Yi
   Jacobson, Kenneth A.
TI P2Y(13) receptor is responsible for ADP-mediated degranulation in
   RBL-2H3 rat mast cells
SO PHARMACOLOGICAL RESEARCH
LA English
DT Article
DE P2Y13 receptor; Nucleotide; Mast cell; Degranulation; Allergy; G
   protein-coupled receptor
ID NUCLEOTIDE RECEPTORS; ACTIVATION; RELEASE; ANTAGONIST; EXPRESSION;
   HISTAMINE; PATHWAYS; AGONIST
AB Extracellular ADP is known to play many important physiological roles In this study we identified the P2Y(13) receptor in a rat mast cell line (RBL-2H3) and explored the functional role of ADP its endogenous agonist ADP induced both intracellular calcium mobilization and release of hexosaminidase (Hex) In an assay of intracellular calcium ADP was 100-fold less potent than and equally efficacious as the P2Y(1) receptor-selective agonist MRS2365 However ADP was more potent and efficacious than MRS2365 in inducing Hex release and in enhancing antigen-induced Hex release ADP-induced intracellular calcium mobilization was blocked by phospholipase C inhibitor U73122 and by P2Y(1) receptor-selective antagonist MRS2500 but not by pertussis toxin (PTX) suggesting a mechanism mediated by the G(q)-coupled P2Y(1) receptor but not P2Y(13) (G(1)-coupled) or P2X receptors ADP-induced Hex release was blocked by PTX and a selective P2Y(13) receptor antagonist MRS2211 but not by MRS2500 or P2Y(1) receptor-specific siRNA suggesting a G(1)-coupled P2Y(13) receptor-related mechanism Measurement of gene expression confirmed high expression of both P2Y(1) and P2Y(13) receptors (in comparison to a previously reported P2Y(14) receptor) in RBL-2H3 cells Thus we demonstrated that ADP-mediated intracellular calcium mobilization and Hex release in RBL-2H3 cells are via P2Y(1) and P2Y(13) receptors respectively Selective antagonists of the P2Y(13) receptor might be novel therapeutic agents for various allergic conditions Published by Elsevier Ltd
C1 [Gao, Zhan-Guo; Jacobson, Kenneth A.] NIDDKD, Mol Recognit Sect, Bioorgan Chem Lab, NIH, Bethesda, MD 20892 USA.
   [Ding, Yi] NIH, Ctr Clin, Bethesda, MD 20892 USA.
RP Gao, ZG (reprint author), NIDDKD, Mol Recognit Sect, Bioorgan Chem Lab, NIH, Bldg 8A,Rm B1A-19, Bethesda, MD 20892 USA.
RI Jacobson, Kenneth/A-1530-2009
OI Jacobson, Kenneth/0000-0001-8104-1493
FU NIDDK, National Institutes of Health
FX Supported by the NIDDK Intramural Research Program National Institutes
   of Health
NR 29
TC 13
Z9 13
U1 0
U2 7
PU ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
PI LONDON
PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
SN 1043-6618
J9 PHARMACOL RES
JI Pharmacol. Res.
PD DEC
PY 2010
VL 62
IS 6
BP 500
EP 505
DI 10.1016/j.phrs.2010.08.003
PG 6
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA 689XZ
UT WOS:000284965700005
PM 20813187
ER

PT J
AU Pertwee, RG
   Howlett, AC
   Abood, ME
   Alexander, SPH
   Di Marzo, V
   Elphick, MR
   Greasley, PJ
   Hansen, HS
   Kunos, G
   Mackie, K
   Mechoulam, R
   Ross, RA
AF Pertwee, R. G.
   Howlett, A. C.
   Abood, M. E.
   Alexander, S. P. H.
   Di Marzo, V.
   Elphick, M. R.
   Greasley, P. J.
   Hansen, H. S.
   Kunos, G.
   Mackie, K.
   Mechoulam, R.
   Ross, R. A.
TI International Union of Basic and Clinical Pharmacology. LXXIX.
   Cannabinoid Receptors and Their Ligands: Beyond CB1 and CB2
SO PHARMACOLOGICAL REVIEWS
LA English
DT Review
ID PROTEIN-COUPLED-RECEPTOR; FREE FATTY-ACIDS; ANANDAMIDE-INDUCED
   VASORELAXATION; PROLIFERATOR-ACTIVATED RECEPTORS; VANILLOID TYPE-1
   RECEPTORS; CA2+-ACTIVATED K+ CHANNELS; TRIGEMINAL SENSORY NEURONS;
   DEPENDENT VASCULAR ACTIONS; POTENTIAL CATION CHANNELS;
   N-ARACHIDONOYL-DOPAMINE
AB There are at least two types of cannabinoid receptors (CB1 and CB2). Ligands activating these G protein-coupled receptors (GPCRs) include the phytocannabinoid Delta(9)-tetrahydrocannabinol, numerous synthetic compounds, and endogenous compounds known as endo-cannabinoids. Cannabinoid receptor antagonists have also been developed. Some of these ligands activate or block one type of cannabinoid receptor more potently than the other type. This review summarizes current data indicating the extent to which cannabinoid receptor ligands undergo orthosteric or allosteric interactions with non-CB1, non-CB2 established GPCRs, deorphanized receptors such as GPR55, ligand-gated ion channels, transient receptor potential (TRP) channels, and other ion channels or peroxisome proliferator-activated nuclear receptors. From these data, it is clear that some ligands that interact similarly with CB1 and/or CB2 receptors are likely to display significantly different pharmacological profiles. The review also lists some criteria that any novel "CB3" cannabinoid receptor or channel should fulfil and concludes that these criteria are not currently met by any non-CB1, non-CB2 pharmacological receptor or channel. However, it does identify certain pharmacological targets that should be investigated further as potential CB3 receptors or channels. These include TRP vanilloid 1, which possibly functions as an ionotropic cannabinoid receptor under physiological and/or pathological conditions, and some deorphanized GPCRs. Also discussed are 1) the ability of CB1 receptors to form heteromeric complexes with certain other GPCRs, 2) phylogenetic relationships that exist between CB1/CB2 receptors and other GPCRs, 3) evidence for the existence of several as-yet-uncharacterized non-CB1, non-CB2 cannabinoid receptors; and 4) current cannabinoid receptor nomenclature.
C1 [Pertwee, R. G.; Ross, R. A.] Univ Aberdeen, Inst Med Sci, Sch Med Sci, Aberdeen AB25 2ZD, Scotland.
   [Howlett, A. C.] Wake Forest Univ Hlth Sci, Dept Physiol & Pharmacol, Winston Salem, NC USA.
   [Abood, M. E.] Temple Univ, Ctr Subst Abuse Res, Philadelphia, PA 19122 USA.
   [Alexander, S. P. H.] Univ Nottingham, Sch Med, Sch Biomed Sci, Nottingham, England.
   [Di Marzo, V.] Univ Naples 2, Endocannabinoid Res Grp, Div Pharmacol L Donatelli, Dept Expt Med, Naples, Italy.
   [Elphick, M. R.] Queen Mary Univ London, Sch Biol & Chem Sci, London, England.
   [Greasley, P. J.] AstraZeneca R&D, Lead Generat Dept, Molndal, Sweden.
   [Hansen, H. S.] Univ Copenhagen, Fac Pharmaceut Sci, Dept Pharmacol & Pharmacotherapy, Copenhagen, Denmark.
   [Kunos, G.] NIAAA, Lab Physiol Studies, Bethesda, MD USA.
   [Mackie, K.] Indiana Univ, Gill Ctr Biomol Sci, Dept Psychol & Brain Sci, Bloomington, IN USA.
   [Mechoulam, R.] Hebrew Univ Jerusalem, Fac Med, Jerusalem, Israel.
RP Pertwee, RG (reprint author), Univ Aberdeen, Inst Med Sci, Sch Med Sci, Foresterhill, Aberdeen AB25 2ZD, Scotland.
EM rgp@abdn.ac.uk
RI Mackie, Kenneth/B-7358-2011; Pertwee, Roger/E-1312-2011; Mackie,
   Ken/E-3715-2013; Alexander, Steve/B-8105-2009; 
OI Mackie, Ken/0000-0001-8501-6199; Alexander, Steve/0000-0003-4417-497X;
   Elphick, Maurice/0000-0002-9169-0048; Hansen, Harald
   S./0000-0001-7360-7418; Howlett, Allyn/0000-0002-2810-0164; Pertwee,
   Roger/0000-0003-3227-2783; Di Marzo, Vincenzo/0000-0002-1490-3070
FU National Institutes of Health National Institute on Alcohol Abuse and
   Alcoholism; National Institutes of Health National Institute on Drug
   Abuse [DA009789, DA021696, DA023204, DA03672, DA03690, DA03934,
   DA05274]; UNIK program
FX This work was supported in part by the Intramural Research Program of
   the National Institutes of Health National Institute on Alcohol Abuse
   and Alcoholism (to G. K.); by the National Institutes of Health National
   Institute on Drug Abuse [Grants DA009789 (to R.G.P., V.D., R.A.R.,
   R.M.), DA021696 (to K.M.), DA023204 (to M.E.A.), DA03672 (to R.G.P.,
   R.A.R.), DA03690 (to A.C.H.), DA03934 (to R.G.P., R.A.R.), DA05274 (to
   M.E.A.)]; and by funding from the UNIK program "Food, Fitness and
   Pharma" (to H.S.H.).
NR 368
TC 561
Z9 569
U1 11
U2 79
PU AMER SOC PHARMACOLOGY EXPERIMENTAL THERAPEUTICS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3995 USA
SN 0031-6997
J9 PHARMACOL REV
JI Pharmacol. Rev.
PD DEC
PY 2010
VL 62
IS 4
BP 588
EP 631
DI 10.1124/pr.110.003004
PG 44
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA 680EJ
UT WOS:000284214900003
PM 21079038
ER

PT J
AU Banks, ML
   Folk, JE
   Rice, KC
   Negus, SS
AF Banks, Matthew L.
   Folk, John E.
   Rice, Kenner C.
   Negus, S. Stevens
TI Selective enhancement of fentanyl-induced antinociception by the delta
   agonist SNC162 but not by ketamine in rhesus monkeys: Further evidence
   supportive of delta agonists as candidate adjuncts to mu opioid
   analgesics
SO PHARMACOLOGY BIOCHEMISTRY AND BEHAVIOR
LA English
DT Article
DE Delta opioid receptor; Mu opioid receptor; NMDA receptor; Interaction;
   Antinociception; Rhesus monkey
ID SPINAL-CORD; QUANTITATIVE AUTORADIOGRAPHY; PHARMACOLOGICAL MODULATION;
   BEHAVIORAL PHARMACOLOGY; THERMAL NOCICEPTION; RAT-BRAIN; PAIN; MORPHINE;
   RECEPTORS; SNC80
AB Mu-opioid receptor agonists such as fentanyl are effective analgesics, but their clinical use is limited by untoward effects. Adjunct medications may improve the effectiveness and/or safety of opioid analgesics. This study compared interactions between fentanyl and either the noncompetitive N-methyl-D-aspartate (NMDA) glutamate receptor antagonist ketamine or the delta-opioid receptor agonist SNC162 [(+)-4-[(alphaR)-alpha-[(2S,5R)-2,5-dimethyl-4-(2-propenyl)-1-piperazinyl]-(3-phenyl)methyl]-N,N-diethylbenzamide] in two behavioral assays in rhesus monkeys. An assay of thermal nociception evaluated tail-withdrawal latencies from water heated to 50 and 54 C. An assay of schedule-controlled responding evaluated response rates maintained under a fixed-ratio 30 schedule of food presentation. Effects of each drug alone and of three mixtures of ketamine + fentanyl (22:1, 65:1. 195:1 ketamine/fentanyl) or SNC162 + fentanyl (59:1, 176:1, 528:1 SNC162/fentanyl) were evaluated in each assay. All drugs and mixtures dose-dependently decreased rates of food-maintained responding, and drug proportions in the mixtures were based on relative potencies in this assay. Ketamine and SNC162 were inactive in the assay of thermal antinociception, but fentanyl and all mixtures produced dose-dependent antinociception. Drug interactions were evaluated using dose-addition and dose-ratio analysis. Dose-addition analysis revealed that interactions for all ketamine/fentanyl mixtures were additive in both assays. SNC162/fentanyl interactions were usually additive, but one mixture (176:1) produced synergistic antinociception at 50 C. Dose-ratio analysis indicated that ketamine failed to improve the relative potency of fentanyl to produce antinociception vs. rate suppression, whereas two SNC162/fentanyl mixtures (59:1 and 176:1) increased the relative potency of fentanyl to produce antinociception. These results suggest that delta agonists may produce more selective enhancement than ketamine of mu agonist-induced antinociception. (C) 2010 Elsevier Inc. All rights reserved.
C1 [Banks, Matthew L.; Negus, S. Stevens] Virginia Commonwealth Univ, Dept Pharmacol & Toxicol, Richmond, VA 23298 USA.
   [Folk, John E.; Rice, Kenner C.] NIDA, Chem Biol Res Branch, NIH, DHHS, Bethesda, MD 20892 USA.
   [Folk, John E.; Rice, Kenner C.] NIAAA, NIH, DHHS, Bethesda, MD USA.
RP Negus, SS (reprint author), Virginia Commonwealth Univ, Dept Pharmacol & Toxicol, 410 N 12th St,POB 980613, Richmond, VA 23298 USA.
EM ssnegus@vcu.edu
RI Banks, Matthew/K-4429-2014
OI Banks, Matthew/0000-0003-4949-5246
FU  [R01-DA011460];  [T32-DA007027]
FX We appreciate the technical assistance of Ember Morrissey and Crystal
   Reyns. This research was supported by grants R01-DA011460 and
   T32-DA007027.
NR 43
TC 8
Z9 8
U1 0
U2 1
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0091-3057
J9 PHARMACOL BIOCHEM BE
JI Pharmacol. Biochem. Behav.
PD DEC
PY 2010
VL 97
IS 2
BP 205
EP 212
DI 10.1016/j.pbb.2010.07.019
PG 8
WC Behavioral Sciences; Neurosciences; Pharmacology & Pharmacy
SC Behavioral Sciences; Neurosciences & Neurology; Pharmacology & Pharmacy
GA 680ON
UT WOS:000284244400004
PM 20678514
ER

PT J
AU Schneider, EH
   Seifert, R
AF Schneider, Erich H.
   Seifert, Roland
TI Sf9 cells: A versatile model system to investigate the pharmacological
   properties of G protein-coupled receptors
SO PHARMACOLOGY & THERAPEUTICS
LA English
DT Review
DE Sf9 insect cells; GPCR; G-protein; Functional reconstitution;
   Constitutive activity; Protein expression
ID INFECTED INSECT CELLS; FORMYL PEPTIDE RECEPTOR; SCINTILLATION PROXIMITY
   ASSAY; HISTAMINE H-4 RECEPTOR; DOPAMINE D-1 RECEPTOR; MU-OPIOID
   RECEPTOR; BETA(2)-ADRENOCEPTOR-G(S-ALPHA) FUSION PROTEIN; MUSCARINIC
   CHOLINERGIC-RECEPTOR; AGONIST-INDUCED DESENSITIZATION; RECOMBINANT
   EXPRESSION SYSTEMS
AB The Sf9 cell/baculovirus expression system is widely used for high-level protein expression, often with the purpose of purification. However, proteins may also be functionally expressed in the defined Sf9 cell environment. According to the literature, the pharmacology of G-protein-coupled receptors (GPCRs) functionally reconstituted in 519 cells is similar to the receptor properties in mammalian cells. Sf9 cells express both recombinant GPCRs and G-proteins at much higher levels than mammalian cells. Sf9 cells can be grown in suspension culture, providing an inexpensive way of obtaining large protein amounts. Co-infection with various baculoviruses allows free combination of GPCRs with different G-proteins. The absence of constitutively active receptors in Sf9 cells provides an excellent signal-to background ratio in functional assays, allowing the detection of agonist-independent receptor activity and of small ligand-induced signals including partial agonistic and inverse agonistic effects. Insect cell G alpha(i)-like proteins mostly do not couple productively to mammalian GPCRs. Thus, unlike in mammalian cells, Sf9 cells do not require pertussis toxin treatment to obtain a G alpha(i)-free environment. Co-expression of GPCRs with G alpha(i1), G alpha(i2), G alpha(i3) or G alpha(o) in Sf9 cells allows the generation of a selectivity profile for these G alpha(i/o)-isoforms. Additionally. GPCR-G-protein combinations can be compared with defined 1:1 stoichiometry by expressing GPCR-G alpha fusion proteins. Sf9 cells can also be employed for ligand screening in medicinal chemistry programs, using radioligand binding assays or functional assays, like the steady-state GTPase- or [(35)S]GTP gamma S binding assay. This review shows that Sf9 cells are a versatile model system to investigate the pharmacological properties of GPCRs. (C) 2010 Elsevier Inc. All rights reserved.
C1 [Schneider, Erich H.] NIAID, Lab Mol Immunol, NIH, Bethesda, MD 20892 USA.
   [Seifert, Roland] Hannover Med Sch, Inst Pharmacol, D-30625 Hannover, Germany.
RP Schneider, EH (reprint author), NIAID, Lab Mol Immunol, NIH, Bldg 10,Room 11N107,9000 Rockville Pike, Bethesda, MD 20892 USA.
EM schneidere@mail.nih.gov
RI Schneider, Erich/B-9051-2016
OI Schneider, Erich/0000-0002-7905-4276
FU DFG [GRK 760]; European Comission [BM0806]
FX This work was supported by DFG (GRK 760).; This work was supported by
   the European Cooperation in the Field of Scientific and Technical
   Research (COST) action #BM0806 ("Recent advances in histamine receptor
   H4R research"), funded by the European Comission (7th European Framework
   Program).
NR 235
TC 31
Z9 33
U1 2
U2 18
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0163-7258
J9 PHARMACOL THERAPEUT
JI Pharmacol. Ther.
PD DEC
PY 2010
VL 128
IS 3
BP 387
EP 418
DI 10.1016/j.pharmthera.2010.07.005
PG 32
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA 686UO
UT WOS:000284721900001
PM 20705094
ER

PT J
AU Arnheiter, H
AF Arnheiter, Heinz
TI The discovery of the microphthalmia locus and its gene, Mitf
SO PIGMENT CELL & MELANOMA RESEARCH
LA English
DT Review
DE Mice; Mitf alleles; Microphthalmia; Hearing deficiency; Paula Hertwig
ID WAARDENBURG-SYNDROME TYPE-2; TRANSCRIPTION FACTOR MITF; MELANOCYTE
   DEVELOPMENT; EYE DEVELOPMENT; ZIPPER TRANSCRIPTION; MAST-CELLS; MOUSE;
   MUTATIONS; PROTEIN; CLONING
AB P>The history of the discovery of the microphthalmia locus and its gene, now called Mitf, is a testament to the triumph of serendipity. Although the first microphthalmia mutation was discovered among the descendants of a mouse that was irradiated for the purpose of mutagenesis, the mutation most likely was not radiation induced but occurred spontaneously in one of the parents of a later breeding. Although Mitf might eventually have been identified by other molecular genetic techniques, it was first cloned from a chance transgene insertion at the microphthalmia locus. And although Mitf was found to encode a member of a well-known transcription factor family, its analysis might still be in its infancy had Mitf not turned out to be of crucial importance for the physiology and pathology of many distinct organs, including eye, ear, immune system, bone, and skin, and in particular for melanoma. In fact, near seven decades of Mitf research have led to many insights about development, function, degeneration, and malignancies of a number of specific cell types, and it is hoped that these insights will one day lead to therapies benefitting those afflicted with diseases originating in these cell types.
C1 NINDS, Mammalian Dev Sect, NIH, Bethesda, MD 20892 USA.
RP Arnheiter, H (reprint author), NINDS, Mammalian Dev Sect, NIH, Bldg 36,Rm 4D04, Bethesda, MD 20892 USA.
EM ha3p@nih.gov
FU NIH, NINDS
FX I thank the many collaborators who have made this work possible and my
   host institute, NINDS, for allowing us to pursue investigations on Mitf.
   I also extend my thanks to Nancy Jenkins and Neal Copeland, Karen Steel,
   Harold Gainer, James Battey, Eirikur Steingrimsson, and Monique
   Dubois-Dalcq for invaluable comments on the manuscript. This work was
   supported by the intramural program of the NIH, NINDS.
NR 44
TC 24
Z9 29
U1 0
U2 11
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1755-1471
J9 PIGM CELL MELANOMA R
JI Pigment Cell Melanoma Res.
PD DEC
PY 2010
VL 23
IS 6
BP 729
EP 735
DI 10.1111/j.1755-148X.2010.00759.x
PG 7
WC Oncology; Cell Biology; Dermatology
SC Oncology; Cell Biology; Dermatology
GA 664QQ
UT WOS:000282977800005
PM 20807369
ER

PT J
AU Klug, HLP
   Tooze, JA
   Graff-Cherry, C
   Anver, MR
   Noonan, FP
   Fears, TR
   Tucker, MA
   De Fabo, EC
   Merlino, G
AF Klug, Heather L. P.
   Tooze, Janet A.
   Graff-Cherry, Cari
   Anver, Miriam R.
   Noonan, Frances P.
   Fears, Thomas R.
   Tucker, Margaret A.
   De Fabo, Edward C.
   Merlino, Glenn
TI Sunscreen prevention of melanoma in man and mouse
SO PIGMENT CELL & MELANOMA RESEARCH
LA English
DT Letter
ID CUTANEOUS MELANOMA; UNITED-STATES; SUN EXPOSURE; RISK
C1 [Klug, Heather L. P.] Univ Texas Hlth Sci Ctr San Antonio, Reg Acad Hlth Ctr Edinburg, Edinburg, TX USA.
   [Tooze, Janet A.] Wake Forest Univ, Sch Hlth Sci, Dept Biostat Sci, Winston Salem, NC 27109 USA.
   [Graff-Cherry, Cari; Anver, Miriam R.] NCI Frederick, Lab Anim Sci Program, SAIC Frederick Inc, Frederick, MD USA.
   [Noonan, Frances P.; De Fabo, Edward C.] George Washington Univ, Med Ctr, Sch Med & Hlth Sci, Dept Microbiol Immunol & Trop Med, Washington, DC 20037 USA.
   [Fears, Thomas R.; Tucker, Margaret A.] NCI, Div Canc Epidemiol & Genet, NIH, Bethesda, MD 20892 USA.
   [Merlino, Glenn] NCI, Lab Canc Biol & Genet, NIH, Bethesda, MD 20892 USA.
RP Klug, HLP (reprint author), Univ Texas Hlth Sci Ctr San Antonio, Reg Acad Hlth Ctr Edinburg, Edinburg, TX USA.
EM klug@uthscsa.edu
RI Tucker, Margaret/B-4297-2015
FU CCR NIH HHS [HHSN261200800001C]; Intramural NIH HHS; NCI NIH HHS
   [HHSN261200800001E]
NR 13
TC 9
Z9 9
U1 0
U2 3
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1755-1471
J9 PIGM CELL MELANOMA R
JI Pigment Cell Melanoma Res.
PD DEC
PY 2010
VL 23
IS 6
BP 835
EP 837
DI 10.1111/j.1755-148X.2010.00756.x
PG 3
WC Oncology; Cell Biology; Dermatology
SC Oncology; Cell Biology; Dermatology
GA 664QQ
UT WOS:000282977800018
PM 20726949
ER

PT J
AU Danoy, P
   Pryce, K
   Hadler, J
   Bradbury, LA
   Farrar, C
   Pointon, J
   Ward, M
   Weisman, M
   Reveille, JD
   Wordsworth, BP
   Stone, MA
   Maksymowych, WP
   Rahman, P
   Gladman, D
   Inman, RD
   Brown, MA
AF Danoy, Patrick
   Pryce, Karena
   Hadler, Johanna
   Bradbury, Linda A.
   Farrar, Claire
   Pointon, Jennifer
   Ward, Michael
   Weisman, Michael
   Reveille, John D.
   Wordsworth, B. Paul
   Stone, Millicent A.
   Maksymowych, Walter P.
   Rahman, Proton
   Gladman, Dafna
   Inman, Robert D.
   Brown, Matthew A.
CA Australo-Anglo-Amer
   Spondyloarthrit Res Consortium
TI Association of Variants at 1q32 and STAT3 with Ankylosing Spondylitis
   Suggests Genetic Overlap with Crohn's Disease
SO PLOS GENETICS
LA English
DT Article
ID GENOME-WIDE ASSOCIATION; INFLAMMATORY-BOWEL-DISEASE; SUSCEPTIBILITY
   LOCI; PSORIASIS; SACROILIITIS; PREVALENCE; SCAN
AB Ankylosing spondylitis (AS) is a common inflammatory arthritic condition. Overt inflammatory bowel disease (IBD) occurs in about 10% of AS patients, and in addition 70% of AS cases may have subclinical terminal ileitis. Spondyloarthritis is also common in IBD patients. We therefore tested Crohn's disease susceptibility genes for association with AS, aiming to identify pleiotropic genetic associations with both diseases. Genotyping was carried out using Sequenom and Applied Biosystems TaqMan and OpenArray technologies on 53 markers selected from 30 Crohn's disease associated genomic regions. We tested genotypes in a population of unrelated individual cases (n = 2,773) and controls (n = 2,215) of white European ancestry for association with AS. Statistical analysis was carried out using a Cochran-Armitage test for trend in PLINK. Strong association was detected at chr1q32 near KIF21B (rs11584383, P = 1.66 x 10(-10), odds ratio (OR) = 0.74, 95% CI: 0.68-0.82). Association with disease was also detected for 2 variants within STAT3 (rs6503695, P = 4.6 x 10(-4). OR = 0.86 (95% CI: 0.79-0.93); rs744166, P = 2.6 x 10(-5), OR = 0.84 (95% CI: 0.77-0.91)). Association was confirmed for IL23R (rs11465804, P = 1.2 x 10(-5), OR = 0.65 (95% CI: 0.54-0.79)), and further associations were detected for IL12B (rs10045431, P = 5.2 x 10(-5), OR = 0.83 (95% CI: 0.76-0.91)), CDKAL1 (rs6908425, P = 1.1 x 10(-4), OR = 0.82 (95% CI: 0.74-0.91)), LRRK2/MUC19 (rs11175593, P = 9.9 x 10(-5), OR = 1.92 (95% CI: 1.38-2.67)), and chr13q14 (rs3764147, P = 5.9 x 10(-4), OR = 1.19 (95% CI: 1.08-1.31)). Excluding cases with clinical IBD did not significantly affect these findings. This study identifies chr1q32 and STAT3 as ankylosing spondylitis susceptibility loci. It also further confirms association for IL23R and detects suggestive association with another 4 loci. STAT3 is a key signaling molecule within the Th17 lymphocyte differentiation pathway and further enhances the case for a major role of this T-lymphocyte subset in ankylosing spondylitis. Finally these findings suggest common aetiopathogenic pathways for AS and Crohn's disease and further highlight the involvement of common risk variants across multiple diseases.
C1 [Danoy, Patrick; Pryce, Karena; Hadler, Johanna; Bradbury, Linda A.; Brown, Matthew A.] Univ Queensland, Diamantina Inst, Brisbane, Qld, Australia.
   [Farrar, Claire; Pointon, Jennifer; Wordsworth, B. Paul; Brown, Matthew A.] Univ Oxford, Inst Musculoskeletal Sci, Oxford, England.
   [Farrar, Claire; Pointon, Jennifer; Wordsworth, B. Paul; Brown, Matthew A.] Nuffield Orthopaed Ctr, NIHR Biomed Res Ctr, Oxford OX3 7LD, England.
   [Ward, Michael] NIAMSD, NIH, Bethesda, MD 20892 USA.
   [Weisman, Michael] Cedars Sinai Med Ctr, Dept Med Rheumatol, Los Angeles, CA 90048 USA.
   [Reveille, John D.] Univ Texas Hlth Sci Ctr Houston, Houston, TX USA.
   [Stone, Millicent A.] Univ Bath, Bath BA2 7AY, Avon, England.
   [Maksymowych, Walter P.] Univ Alberta, Edmonton, AB, Canada.
   [Rahman, Proton] Mem Univ Newfoundland, St John, NF, Canada.
   [Gladman, Dafna; Inman, Robert D.] Univ Toronto, Toronto, ON, Canada.
RP Danoy, P (reprint author), Univ Queensland, Diamantina Inst, Brisbane, Qld, Australia.
EM matt.brown@uq.edu.au
OI Brown, Matthew A/0000-0003-0538-8211
FU National Institute of Arthritis and Musculoskeletal and Skin Diseases
   (NIAMS) [P01-052915, R01-AR046208]; University of Texas at Houston CTSA
   [UL1RR024188]; Cedars-Sinai GCRC [MO1-RR00425]; NIAMS/NIH; Rebecca
   Cooper Foundation (Australia); National Health and Medical Research
   Council (Australia); National Institute for Health Research (UK) Oxford
   Biomedical Research Centre [A91202]; NIHR Oxford Musculoskeletal
   Biomedical Research Unit; NIHR Thames Valley Collaborative Local
   Research Network; Princess Alexandra Hospital Research Foundation;
   Arthritis Research Campaign (UK) [19356, 18797]; Arthritis Society of
   Canada; National Ankylosing Spondylitis Society (UK)
FX This study was funded by the National Institute of Arthritis and
   Musculoskeletal and Skin Diseases (NIAMS) grants P01-052915 and
   R01-AR046208. Funding was also received from the University of Texas at
   Houston CTSA grant UL1RR024188, Cedars-Sinai GCRC grant MO1-RR00425,
   Intramural Research Program, NIAMS/NIH, and Rebecca Cooper Foundation
   (Australia). MAB is funded by the National Health and Medical Research
   Council (Australia). Support was also received from the National
   Institute for Health Research (UK) Oxford Biomedical Research Centre
   ankylosing spondylitis chronic disease cohort (Theme Code A91202), NIHR
   Oxford Musculoskeletal Biomedical Research Unit and the NIHR Thames
   Valley Collaborative Local Research Network, and Princess Alexandra
   Hospital Research Foundation. We would like to thank the National
   Ankylosing Spondylitis Society (UK) for assistance in patient
   recruitment and the Arthritis Research Campaign (UK) for financial
   support under grants 19356 and 18797. The Spondyloarthritis Research
   Consortium of Canada (SPARCC) is supported by a National Research
   Initiative (NRI) award from the Arthritis Society of Canada. The funders
   had no role in study design, data collection and analysis, decision to
   publish, or preparation of the manuscript.
NR 23
TC 90
Z9 93
U1 0
U2 9
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 185 BERRY ST, STE 1300, SAN FRANCISCO, CA 94107 USA
SN 1553-7390
J9 PLOS GENET
JI PLoS Genet.
PD DEC
PY 2010
VL 6
IS 12
AR e1001195
DI 10.1371/journal.pgen.1001195
PG 5
WC Genetics & Heredity
SC Genetics & Heredity
GA 698FM
UT WOS:000285578900002
PM 21152001
ER

PT J
AU Todd, PK
   Oh, SY
   Krans, A
   Pandey, UB
   Di Prospero, NA
   Min, KT
   Taylor, JP
   Paulson, HL
AF Todd, Peter K.
   Oh, Seok Yoon
   Krans, Amy
   Pandey, Udai B.
   Di Prospero, Nicholas A.
   Min, Kyung-Tai
   Taylor, J. Paul
   Paulson, Henry L.
TI Histone Deacetylases Suppress CGG Repeat-Induced Neurodegeneration Via
   Transcriptional Silencing in Models of Fragile X Tremor Ataxia Syndrome
SO PLOS GENETICS
LA English
DT Article
ID FMR1 MESSENGER-RNA; CEREBELLAR-TREMOR/ATAXIA-SYNDROME; PREMUTATION
   CARRIERS; DROSOPHILA MODEL; FULL MUTATION; MOUSE MODEL; MEDIATED
   NEURODEGENERATION; INTRANUCLEAR INCLUSIONS; PROTEIN EXPRESSION;
   PERIPHERAL-BLOOD
AB Fragile X Tremor Ataxia Syndrome (FXTAS) is a common inherited neurodegenerative disorder caused by expansion of a CGG trinucleotide repeat in the 5'UTR of the fragile X syndrome (FXS) gene, FMR1. The expanded CGG repeat is thought to induce toxicity as RNA, and in FXTAS patients mRNA levels for FMR1 are markedly increased. Despite the critical role of FMR1 mRNA in disease pathogenesis, the basis for the increase in FMR1 mRNA expression is unknown. Here we show that overexpressing any of three histone deacetylases (HDACs 3, 6, or 11) suppresses CGG repeat-induced neurodegeneration in a Drosophila model of FXTAS. This suppression results from selective transcriptional repression of the CGG repeat-containing transgene. These findings led us to evaluate the acetylation state of histones at the human FMR1 locus. In patient-derived lymphoblasts and fibroblasts, we determined by chromatin immunoprecipitation that there is increased acetylation of histones at the FMR1 locus in pre-mutation carriers compared to control or FXS derived cell lines. These epigenetic changes correlate with elevated FMR1 mRNA expression in pre-mutation cell lines. Consistent with this finding, histone acetyltransferase (HAT) inhibitors repress FMR1 mRNA expression to control levels in pre-mutation carrier cell lines and extend lifespan in CGG repeat-expressing Drosophila. These findings support a disease model whereby the CGG repeat expansion in FXTAS promotes chromatin remodeling in cis, which in turn increases expression of the toxic FMR1 mRNA. Moreover, these results provide proof of principle that HAT inhibitors or HDAC activators might be used to selectively repress transcription at the FMR1 locus.
C1 [Todd, Peter K.; Oh, Seok Yoon; Krans, Amy; Paulson, Henry L.] Univ Michigan, Dept Neurol, Ann Arbor, MI 48109 USA.
   [Pandey, Udai B.] Louisiana State Univ, Dept Genet, Hlth Sci Ctr, New Orleans, LA USA.
   [Di Prospero, Nicholas A.] NINDS, Neurogenet Branch, Bethesda, MD 20892 USA.
   [Min, Kyung-Tai] Indiana Univ, Dept Biol, Bloomington, IN USA.
   [Taylor, J. Paul] St Jude Childrens Hosp, Dept Dev Neurobiol, Memphis, TN 38105 USA.
RP Todd, PK (reprint author), Univ Michigan, Dept Neurol, Ann Arbor, MI 48109 USA.
EM petertod@umich.edu
OI min, kyung-tai/0000-0003-0983-4258
FU American Academy of Neurology; NIH [NS069809, NS053825, NS038712]; Bucky
   and Kristin Harris endowed Research Professorship
FX Work was funded by a clinical research training fellowship from the
   American Academy of Neurology to PKT, the Bucky and Kristin Harris
   endowed Research Professorship to PKT, and NIH grants to PKT (NS069809),
   JPT (NS053825), and HLP (NS038712). The funders had no role in study
   design, data collection and analysis, decision to publish, or
   preparation of the manuscript.
NR 73
TC 40
Z9 41
U1 1
U2 3
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 185 BERRY ST, STE 1300, SAN FRANCISCO, CA 94107 USA
SN 1553-7390
J9 PLOS GENET
JI PLoS Genet.
PD DEC
PY 2010
VL 6
IS 12
AR e1001240
DI 10.1371/journal.pgen.1001240
PG 17
WC Genetics & Heredity
SC Genetics & Heredity
GA 698FM
UT WOS:000285578900018
PM 21170301
ER

PT J
AU Wendte, JM
   Miller, MA
   Lambourn, DM
   Magargal, SL
   Jessup, DA
   Grigg, ME
AF Wendte, Jered M.
   Miller, Melissa A.
   Lambourn, Dyanna M.
   Magargal, Spencer L.
   Jessup, David A.
   Grigg, Michael E.
TI Self-Mating in the Definitive Host Potentiates Clonal Outbreaks of the
   Apicomplexan Parasites Sarcocystis neurona and Toxoplasma gondii
SO PLOS GENETICS
LA English
DT Article
ID ENHYDRA-LUTRIS-NEREIS; FREE-RANGE CHICKENS; EQUINE PROTOZOAL
   MYELOENCEPHALITIS; GENETIC DIVERSITY; INTERMEDIATE HOSTS; SEA OTTERS;
   MOLECULAR CHARACTERIZATION; CONGENITAL TOXOPLASMOSIS; SEXUAL
   RECOMBINATION; BACTERIAL PATHOGENS
AB Tissue-encysting coccidia, including Toxoplasma gondii and Sarcocystis neurona, are heterogamous parasites with sexual and asexual life stages in definitive and intermediate hosts, respectively. During its sexual life stage, T. gondii reproduces either by genetic out-crossing or via clonal amplification of a single strain through self-mating. Out-crossing has been experimentally verified as a potent mechanism capable of producing offspring possessing a range of adaptive and virulence potentials. In contrast, selfing and other life history traits, such as asexual expansion of tissue-cysts by oral transmission among intermediate hosts, have been proposed to explain the genetic basis for the clonal population structure of T. gondii. In this study, we investigated the contributing roles self-mating and sexual recombination play in nature to maintain clonal population structures and produce or expand parasite clones capable of causing disease epidemics for two tissue encysting parasites. We applied high-resolution genotyping against strains isolated from a T. gondii waterborne outbreak that caused symptomatic disease in 155 immune-competent people in Brazil and a S. neurona outbreak that resulted in a mass mortality event in Southern sea otters. In both cases, a single, genetically distinct clone was found infecting outbreak-exposed individuals. Furthermore, the T. gondii outbreak clone was one of several apparently recombinant progeny recovered from the local environment. Since oocysts or sporocysts were the infectious form implicated in each outbreak, the expansion of the epidemic clone can be explained by self-mating. The results also show that out-crossing preceded selfing to produce the virulent T. gondii clone. For the tissue encysting coccidia, self-mating exists as a key adaptation potentiating the epidemic expansion and transmission of newly emerged parasite clones that can profoundly shape parasite population genetic structures or cause devastating disease outbreaks.
C1 [Wendte, Jered M.; Magargal, Spencer L.; Grigg, Michael E.] NIAID, Mol Parasitol Unit, Parasit Dis Lab, NIH, Bethesda, MD 20892 USA.
   [Wendte, Jered M.; Grigg, Michael E.] Oklahoma State Univ, Dept Vet Pathobiol, Ctr Vet Hlth Sci, Stillwater, OK 74078 USA.
   [Wendte, Jered M.] Howard Hughes Med Inst, Natl Inst Hlth Res Scholars Program, Bethesda, MD 20817 USA.
   [Miller, Melissa A.; Jessup, David A.] Marine Wildlife Vet Care & Res Ctr CDFG OSPR, Santa Cruz, CA USA.
   [Lambourn, Dyanna M.] Washington Dept Fish & Wildlife, Lakewood, WA USA.
RP Wendte, JM (reprint author), NIAID, Mol Parasitol Unit, Parasit Dis Lab, NIH, 9000 Rockville Pike, Bethesda, MD 20892 USA.
EM griggm@niaid.nih.gov
FU NIH; NIAID [AI001018]; National Science Foundation [0525750]; Howard
   Hughes Medical Institute; Morris Animal Foundation [D10ZO-416]; NOAA;
   WDFW
FX The work was supported by the Intramural Research Program of the NIH and
   NIAID AI001018 and the National Science Foundation 0525750 (MEG); by the
   Howard Hughes Medical Institute Research Scholars Program and Morris
   Animal Foundation Wildlife Training Fellowship D10ZO-416 (JMW); by NOAA
   Fisheries Prescott grant program and WDFW (DML). The funders had no role
   in study design, data collection and analysis, decision to publish, or
   preparation of the manuscript.
NR 85
TC 43
Z9 44
U1 1
U2 13
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1553-7404
J9 PLOS GENET
JI PLoS Genet.
PD DEC
PY 2010
VL 6
IS 12
AR e1001261
DI 10.1371/journal.pgen.1001261
PG 13
WC Genetics & Heredity
SC Genetics & Heredity
GA 698FM
UT WOS:000285578900039
PM 21203443
ER

PT J
AU Vazquez-Prokopec, GM
   Kitron, U
   Montgomery, B
   Horne, P
   Ritchie, SA
AF Vazquez-Prokopec, Gonzalo M.
   Kitron, Uriel
   Montgomery, Brian
   Horne, Peter
   Ritchie, Scott A.
TI Quantifying the Spatial Dimension of Dengue Virus Epidemic Spread within
   a Tropical Urban Environment
SO PLOS NEGLECTED TROPICAL DISEASES
LA English
DT Article
ID STRUCTURED ADDITIVE REGRESSION; MARK-RELEASE-RECAPTURE; AEDES-AEGYPTI
   DIPTERA; SPACE-TIME ANALYSIS; NORTH QUEENSLAND; PUERTO-RICO; POINT
   PATTERNS; AUSTRALIA; DISPERSAL; INFECTION
AB Background: Dengue infection spread in naive populations occurs in an explosive and widespread fashion primarily due to the absence of population herd immunity, the population dynamics and dispersal of Ae. aegypti, and the movement of individuals within the urban space. Knowledge on the relative contribution of such factors to the spatial dimension of dengue virus spread has been limited. In the present study we analyzed the spatio-temporal pattern of a large dengue virus-2 (DENV-2) outbreak that affected the Australian city of Cairns (north Queensland) in 2003, quantified the relationship between dengue transmission and distance to the epidemic's index case (IC), evaluated the effects of indoor residual spraying (IRS) on the odds of dengue infection, and generated recommendations for city-wide dengue surveillance and control.
   Methods and Findings: We retrospectively analyzed data from 383 DENV-2 confirmed cases and 1,163 IRS applications performed during the 25-week epidemic period. Spatial (local k-function, angular wavelets) and space-time (Knox test) analyses quantified the intensity and directionality of clustering of dengue cases, whereas a semi-parametric Bayesian space-time regression assessed the impact of IRS and spatial autocorrelation in the odds of weekly dengue infection. About 63% of the cases clustered up to 800 m around the IC's house. Most cases were distributed in the NW-SE axis as a consequence of the spatial arrangement of blocks within the city and, possibly, the prevailing winds. Space-time analysis showed that DENV-2 infection spread rapidly, generating 18 clusters (comprising 65% of all cases), and that these clusters varied in extent as a function of their distance to the IC's residence. IRS applications had a significant protective effect in the further occurrence of dengue cases, but only when they reached coverage of 60% or more of the neighboring premises of a house.
   Conclusion: By applying sound statistical analysis to a very detailed dataset from one of the largest outbreaks that affected the city of Cairns in recent times, we not only described the spread of dengue virus with high detail but also quantified the spatio-temporal dimension of dengue virus transmission within this complex urban environment. In areas susceptible to non-periodic dengue epidemics, effective disease prevention and control would depend on the prompt response to introduced cases. We foresee that some of the results and recommendations derived from our study may also be applicable to other areas currently affected or potentially subject to dengue epidemics.
C1 [Vazquez-Prokopec, Gonzalo M.; Kitron, Uriel] Emory Univ, Dept Environm Studies, Atlanta, GA 30322 USA.
   [Vazquez-Prokopec, Gonzalo M.; Kitron, Uriel] NIH, Fogarty Int Ctr, Bethesda, MD 20892 USA.
   [Montgomery, Brian; Horne, Peter; Ritchie, Scott A.] Trop Publ Hlth Unit Network, Cairns, Qld, Australia.
   [Ritchie, Scott A.] James Cook Univ, Sch Publ Hlth Trop Med & Rehabil Sci, Cairns, Qld, Australia.
RP Vazquez-Prokopec, GM (reprint author), Emory Univ, Dept Environm Studies, Atlanta, GA 30322 USA.
EM gmvazqu@emory.edu
FU Emory University (Department of Environmental Studies); Science and
   Technology Directorate, U.S. Department of Homeland Security; Fogarty
   International Center, National Institutes of Health; Dr. Edward Koch
   Foundation
FX This work was supported in part by Emory University (Department of
   Environmental Studies internal support), Research and Policy for
   Infectious Disease Dynamics (RAPIDD) program of the Science and
   Technology Directorate, U.S. Department of Homeland Security, and the
   Fogarty International Center, National Institutes of Health. The Dr.
   Edward Koch Foundation funded Dr. Vazquez-Prokopec's travel to Cairns.
   The funders had no role in study design, data collection and analysis,
   decision to publish, or preparation of the manuscript.
NR 48
TC 64
Z9 65
U1 3
U2 29
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 185 BERRY ST, STE 1300, SAN FRANCISCO, CA 94107 USA
SN 1935-2727
J9 PLOS NEGLECT TROP D
JI Plos Neglect. Trop. Dis.
PD DEC
PY 2010
VL 4
IS 12
AR e920
DI 10.1371/journal.pntd.0000920
PG 14
WC Infectious Diseases; Parasitology; Tropical Medicine
SC Infectious Diseases; Parasitology; Tropical Medicine
GA 697VI
UT WOS:000285547000019
PM 21200419
ER

PT J
AU Heimann, E
   Jones, HA
   Resjo, S
   Manganiello, VC
   Stenson, L
   Degerman, E
AF Heimann, Emilia
   Jones, Helena A.
   Resjo, Svante
   Manganiello, Vincent C.
   Stenson, Lena
   Degerman, Eva
TI Expression and Regulation of Cyclic Nucleotide Phosphodiesterases in
   Human and Rat Pancreatic Islets
SO PLOS ONE
LA English
DT Article
ID INHIBITED CAMP-PHOSPHODIESTERASE; INSULIN-INDUCED PHOSPHORYLATION;
   PROTEIN-KINASE B; BETA-CELLS; ANTILIPOLYTIC ACTION; GLUCOSE-INTOLERANCE;
   ENERGY HOMEOSTASIS; IN-VITRO; SECRETION; 3B
AB As shown by transgenic mouse models and by using phosphodiesterase 3 (PDE3) inhibitors, PDE3B has an important role in the regulation of insulin secretion in pancreatic beta-cells. However, very little is known about the regulation of the enzyme. Here, we show that PDE3B is activated in response to high glucose, insulin and cAMP elevation in rat pancreatic islets and INS-1 (832/13) cells. Activation by glucose was not affected by the presence of diazoxide. PDE3B activation was coupled to an increase as well as a decrease in total phosphorylation of the enzyme. In addition to PDE3B, several other PDEs were detected in human pancreatic islets: PDE1, PDE3, PDE4C, PDE7A, PDE8A and PDE10A. We conclude that PDE3B is activated in response to agents relevant for beta-cell function and that activation is linked to increased as well as decreased phosphorylation of the enzyme. Moreover, we conclude that several PDEs are present in human pancreatic islets.
C1 [Heimann, Emilia; Jones, Helena A.; Resjo, Svante; Stenson, Lena; Degerman, Eva] Lund Univ, Dept Expt Med Sci, Div Diabet Metab & Endocrinol, Lund, Sweden.
   [Manganiello, Vincent C.] NHLBI, Pulm Crit Care Med Branch, NIH, Bethesda, MD 20892 USA.
RP Heimann, E (reprint author), Lund Univ, Dept Expt Med Sci, Div Diabet Metab & Endocrinol, Lund, Sweden.
EM emilia.heimann@med.lu.se
RI Jones, Helena/C-8847-2013
OI Jones, Helena/0000-0002-3948-161X
FU Swedish Research Council [3362]; Swedish Diabetes Association; Swedish
   Society of Medicine; A. Pahlsson foundation; P. Hakansson foundation;
   Novo Nordisk Foundation, Denmark; Royal Physiographic Society in Lund;
   Lund University Diabetes Center
FX This work was supported by the Swedish Research Council Project 3362 (to
   ED); the Swedish Diabetes Association (http://www.diabetes.se/); the
   Swedish Society of Medicine; the A. Pahlsson and P. Hakansson
   foundations; Novo Nordisk Foundation, Denmark
   (http://www.novonordiskfonden.dk/en/index.asp); the Royal Physiographic
   Society in Lund (http://www.fysiografen.se/); and Lund University
   Diabetes Center (http://www.ludc.med.lu.se/). The funders had no role in
   study design, data collection and analysis, decision to publish, or
   preparation of the manuscript.
NR 48
TC 15
Z9 16
U1 0
U2 1
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 185 BERRY ST, STE 1300, SAN FRANCISCO, CA 94107 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD DEC 1
PY 2010
VL 5
IS 12
AR e14191
DI 10.1371/journal.pone.0014191
PG 8
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 688AU
UT WOS:000284821300008
PM 21152070
ER

PT J
AU Moayeri, M
   Crown, D
   Newman, ZL
   Okugawa, S
   Eckhaus, M
   Cataisson, C
   Liu, SH
   Sastalla, I
   Leppla, SH
AF Moayeri, Mahtab
   Crown, Devorah
   Newman, Zachary L.
   Okugawa, Shu
   Eckhaus, Michael
   Cataisson, Christophe
   Liu, Shihui
   Sastalla, Inka
   Leppla, Stephen H.
TI Inflammasome Sensor Nlrp1b-Dependent Resistance to Anthrax Is Mediated
   by Caspase-1, IL-1 Signaling and Neutrophil Recruitment
SO PLOS PATHOGENS
LA English
DT Article
ID BACILLUS-ANTHRACIS; LETHAL TOXIN; STERNE STRAIN; KINASE-KINASE; MOUSE
   MODEL; IN-VIVO; MICE; MACROPHAGES; SPORES; SUSCEPTIBILITY
AB Bacillus anthracis infects hosts as a spore, germinates, and disseminates in its vegetative form. Production of anthrax lethal and edema toxins following bacterial outgrowth results in host death. Macrophages of inbred mouse strains are either sensitive or resistant to lethal toxin depending on whether they express the lethal toxin responsive or non-responsive alleles of the inflammasome sensor Nlrp1b (Nlrp1b(S/S) or Nlrp1b(R/R), respectively). In this study, Nlrp1b was shown to affect mouse susceptibility to infection. Inbred and congenic mice harboring macrophage-sensitizing Nlrp1b(S/S) alleles (which allow activation of caspase-1 and IL-1 beta release in response to anthrax lethal toxin challenge) effectively controlled bacterial growth and dissemination when compared to mice having Nlrp1b(R/R) alleles (which cannot activate caspase-1 in response to toxin). Nlrp1b(S)-mediated resistance to infection was not dependent on the route of infection and was observed when bacteria were introduced by either subcutaneous or intravenous routes. Resistance did not occur through alterations in spore germination, as vegetative bacteria were also killed in Nlrp1b(S/S) mice. Resistance to infection required the actions of both caspase-1 and IL-1 beta as Nlrp1b(S/S) mice deleted of caspase-1 or the IL-1 receptor, or treated with the Il-1 receptor antagonist anakinra, were sensitized to infection. Comparison of circulating neutrophil levels and IL-1 beta responses in Nlrp1b(S/S), Nlrp1b(R/R) and IL-1 receptor knockout mice implicated Nlrp1b and IL-1 signaling in control of neutrophil responses to anthrax infection. Neutrophil depletion experiments verified the importance of this cell type in resistance to B. anthracis infection. These data confirm an inverse relationship between murine macrophage sensitivity to lethal toxin and mouse susceptibility to spore infection, and establish roles for Nlrp1b(S), caspase-1, and IL-1 beta in countering anthrax infection.
C1 [Moayeri, Mahtab; Crown, Devorah; Newman, Zachary L.; Okugawa, Shu; Liu, Shihui; Sastalla, Inka; Leppla, Stephen H.] NIAID, Lab Bacterial Dis, Bacterial Toxins & Therapeut Sect, NIH, Bethesda, MD 20892 USA.
   [Eckhaus, Michael] NIH, Diagnost & Res Serv Branch, Div Vet Resources, Off Res Serv, Bethesda, MD 20892 USA.
   [Cataisson, Christophe] NCI, Lab Canc Biol & Genet, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
RP Moayeri, M (reprint author), NIAID, Lab Bacterial Dis, Bacterial Toxins & Therapeut Sect, NIH, 9000 Rockville Pike, Bethesda, MD 20892 USA.
EM sleppla@niaid.nih.gov
FU NIH, National Institute of Allergy and Infectious Diseases
FX This research was supported by the Intramural Research Program of the
   NIH, National Institute of Allergy and Infectious Diseases. The funders
   had no role in study design, data collection and analysis, decision to
   publish, or preparation of the manuscript.
NR 40
TC 56
Z9 58
U1 0
U2 3
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1553-7366
EI 1553-7374
J9 PLOS PATHOG
JI PLoS Pathog.
PD DEC
PY 2010
VL 6
IS 12
AR e1001222
DI 10.1371/journal.ppat.1001222
PG 9
WC Microbiology; Parasitology; Virology
SC Microbiology; Parasitology; Virology
GA 698IM
UT WOS:000285587500010
PM 21170303
ER

PT J
AU White, TA
   Bartesaghi, A
   Borgnia, MJ
   Meyerson, JR
   de la Cruz, MJV
   Bess, JW
   Nandwani, R
   Hoxie, JA
   Lifson, JD
   Milne, JLS
   Subramaniam, S
AF White, Tommi A.
   Bartesaghi, Alberto
   Borgnia, Mario J.
   Meyerson, Joel R.
   de la Cruz, M. Jason V.
   Bess, Julian W.
   Nandwani, Rachna
   Hoxie, James A.
   Lifson, Jeffrey D.
   Milne, Jacqueline L. S.
   Subramaniam, Sriram
TI Molecular Architectures of Trimeric SIV and HIV-1 Envelope Glycoproteins
   on Intact Viruses: Strain-Dependent Variation in Quaternary Structure
SO PLOS PATHOGENS
LA English
DT Article
ID SIMIAN IMMUNODEFICIENCY VIRUS; ANTIBODY-MEDIATED NEUTRALIZATION; GP120
   CORE; CD4; RECEPTOR; BINDING; CLASSIFICATION; VISUALIZATION;
   SENSITIVITY; TOMOGRAPHY
AB The initial step in target cell infection by human, and the closely related simian immunodeficiency viruses (HIV and SIV, respectively) occurs with the binding of trimeric envelope glycoproteins (Env), composed of heterodimers of the viral transmembrane glycoprotein (gp41) and surface glycoprotein (gp120) to target T-cells. Knowledge of the molecular structure of trimeric Env on intact viruses is important both for understanding the molecular mechanisms underlying virus-cell interactions and for the design of effective immunogen-based vaccines to combat HIV/AIDS. Previous analyses of intact HIV-1 BaL virions have already resulted in structures of trimeric Env in unliganded and CD4-liganded states at similar to 20 angstrom resolution. Here, we show that the molecular architectures of trimeric Env from SIVmneE11S, SIVmac239 and HIV-1 R3A strains are closely comparable to that previously determined for HIV-1 BaL, with the V1 and V2 variable loops located at the apex of the spike, close to the contact zone between virus and cell. The location of the V1/V2 loops in trimeric Env was definitively confirmed by structural analysis of HIV-1 R3A virions engineered to express Env with deletion of these loops. Strikingly, in SIV CP-MAC, a CD4-independent strain, trimeric Env is in a constitutively "open" conformation with gp120 trimers splayed out in a conformation similar to that seen for HIV-1 BaL Env when it is complexed with sCD4 and the CD4i antibody 17b. Our findings suggest a structural explanation for the molecular mechanism of CD4-independent viral entry and further establish that cryo-electron tomography can be used to discover distinct, functionally relevant quaternary structures of Env displayed on intact viruses.
C1 [White, Tommi A.; Bartesaghi, Alberto; Borgnia, Mario J.; Meyerson, Joel R.; de la Cruz, M. Jason V.; Nandwani, Rachna; Milne, Jacqueline L. S.; Subramaniam, Sriram] NCI, Cell Biol Lab, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
   [Bess, Julian W.; Lifson, Jeffrey D.] Natl Canc Inst Frederick, AIDS & Canc Virus Program, SAIC Frederick Inc, Frederick, MD USA.
   [Hoxie, James A.] Univ Penn, Dept Med, Philadelphia, PA 19104 USA.
RP White, TA (reprint author), NCI, Cell Biol Lab, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
EM ss1@nih.gov
RI Bess, Jr., Julian/B-5343-2012
FU National Cancer Institute; National Cancer Institute, NIH
   [HHSN261200800001E]
FX This work was supported by funds from the intramural program of the
   National Cancer Institute and in part with Federal funds from the
   National Cancer Institute, NIH, under contract HHSN261200800001E. The
   funders had no role in study design, data collection and analysis,
   decision to publish, or preparation of the manuscript.
NR 34
TC 104
Z9 104
U1 2
U2 25
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 185 BERRY ST, STE 1300, SAN FRANCISCO, CA 94107 USA
SN 1553-7366
J9 PLOS PATHOG
JI PLoS Pathog.
PD DEC
PY 2010
VL 6
IS 12
AR e1001249
DI 10.1371/journal.ppat.1001249
PG 14
WC Microbiology; Parasitology; Virology
SC Microbiology; Parasitology; Virology
GA 698IM
UT WOS:000285587500031
PM 21203482
ER

PT J
AU Wilham, JM
   Orru, CD
   Bessen, RA
   Atarashi, R
   Sano, K
   Race, B
   Meade-White, KD
   Taubner, LM
   Timmes, A
   Caughey, B
AF Wilham, Jason M.
   Orru, Christina D.
   Bessen, Richard A.
   Atarashi, Ryuichiro
   Sano, Kazunori
   Race, Brent
   Meade-White, Kimberly D.
   Taubner, Lara M.
   Timmes, Andrew
   Caughey, Byron
TI Rapid End-Point Quantitation of Prion Seeding Activity with Sensitivity
   Comparable to Bioassays
SO PLOS PATHOGENS
LA English
DT Article
ID TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY; CREUTZFELDT-JAKOB-DISEASE;
   SCRAPIE PRIONS; IN-VITRO; CYCLIC AMPLIFICATION; SEEDED CONVERSION;
   INFECTIOUS PRIONS; PROTEIN; BLOOD; PRP
AB A major problem for the effective diagnosis and management of prion diseases is the lack of rapid high-throughput assays to measure low levels of prions. Such measurements have typically required prolonged bioassays in animals. Highly sensitive, but generally non-quantitative, prion detection methods have been developed based on prions' ability to seed the conversion of normally soluble protease-sensitive forms of prion protein to protease-resistant and/or amyloid fibrillar forms. Here we describe an approach for estimating the relative amount of prions using a new prion seeding assay called real-time quaking induced conversion assay (RT-QuIC). The underlying reaction blends aspects of the previously described quaking-induced conversion (QuIC) and amyloid seeding assay (ASA) methods and involves prion-seeded conversion of the alpha helix-rich form of bacterially expressed recombinant PrP(C) to a beta sheet-rich amyloid fibrillar form. The RT-QuIC is as sensitive as the animal bioassay, but can be accomplished in 2 days or less. Analogous to end-point dilution animal bioassays, this approach involves testing of serial dilutions of samples and statistically estimating the seeding dose (SD) giving positive responses in 50% of replicate reactions (SD(50)). Brain tissue from 263K scrapie-affected hamsters gave SD(50) values of 10(11)-10(12)/g, making the RT-QuIC similar in sensitivity to end-point dilution bioassays. Analysis of bioassay-positive nasal lavages from hamsters affected with transmissible mink encephalopathy gave SD(50) values of 10(3.5)-10(5.7)/ml, showing that nasal cavities release substantial prion infectivity that can be rapidly detected. Cerebral spinal fluid from 263K scrapie-affected hamsters contained prion SD(50) values of 10(2.0)-10(2.9)/ml. RT-QuIC assay also discriminated deer chronic wasting disease and sheep scrapie brain samples from normal control samples. In principle, end-point dilution quantitation can be applied to many types of prion and amyloid seeding assays. End point dilution RT-QuIC provides a sensitive, rapid, quantitative, and high throughput assay of prion seeding activity.
C1 [Wilham, Jason M.; Orru, Christina D.; Race, Brent; Meade-White, Kimberly D.; Taubner, Lara M.; Timmes, Andrew; Caughey, Byron] NIAID, Rocky Mt Labs, Persistent Viral Dis Lab, Hamilton, MT 59840 USA.
   [Orru, Christina D.] Univ Cagliari, Dept Biomed Sci & Technol, Monserrato, Italy.
   [Bessen, Richard A.] Montana State Univ, Bozeman, MT 59717 USA.
   [Atarashi, Ryuichiro; Sano, Kazunori] Nagasaki Univ, Grad Sch Biomed Sci, Dept Mol Microbiol & Immunol, Nagasaki, Kyushu 852, Japan.
RP Wilham, JM (reprint author), NIAID, Rocky Mt Labs, Persistent Viral Dis Lab, Hamilton, MT 59840 USA.
EM BCAUGHEY@niaid.nih.gov
FU NIAID, NIH; NIH; Regione Sardegna (Italy)
FX This research was funded by the Intramural Research Program of the
   NIAID, NIH. J.M.W. was supported in part by the Undergraduate
   Scholarship Program of the NIH and C.D.O. was partially supported by the
   Master and Back Program of the Regione Sardegna (Italy). The funders had
   no role in study design, data collection and analysis, decision to
   publish, or preparation of the manuscript.
NR 48
TC 104
Z9 106
U1 0
U2 17
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 185 BERRY ST, STE 1300, SAN FRANCISCO, CA 94107 USA
SN 1553-7366
J9 PLOS PATHOG
JI PLoS Pathog.
PD DEC
PY 2010
VL 6
IS 12
AR e1001217
DI 10.1371/journal.ppat.1001217
PG 15
WC Microbiology; Parasitology; Virology
SC Microbiology; Parasitology; Virology
GA 698IM
UT WOS:000285587500006
PM 21152012
ER

PT J
AU Haaga, JG
AF Haaga, John G.
TI Violence and Social Orders: A Conceptual Framework for Interpreting
   Recorded Human History
SO POPULATION AND DEVELOPMENT REVIEW
LA English
DT Book Review
C1 [Haaga, John G.] NIA, Bethesda, MD 20892 USA.
RP Haaga, JG (reprint author), NIA, Bethesda, MD 20892 USA.
NR 3
TC 0
Z9 0
U1 0
U2 3
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0098-7921
EI 1728-4457
J9 POPUL DEV REV
JI Popul. Dev. Rev.
PD DEC
PY 2010
VL 36
IS 4
BP 841
EP 843
DI 10.1111/j.1728-4457.2010.00360.x
PG 3
WC Demography; Sociology
SC Demography; Sociology
GA 695GW
UT WOS:000285359600008
ER

PT J
AU Luk, JW
   Wang, J
   Simons-Morton, BG
AF Luk, Jeremy W.
   Wang, Jing
   Simons-Morton, Bruce G.
TI Bullying Victimization and Substance Use Among US Adolescents: Mediation
   by Depression
SO PREVENTION SCIENCE
LA English
DT Article
DE Victimization; Depression; Substance use; Mediation; Sex difference
ID PEER VICTIMIZATION; GENDER-DIFFERENCES; RISK-FACTORS; ASSOCIATION;
   YOUTH; SYMPTOMATOLOGY; PREVALENCE; BEHAVIORS; SYMPTOMS
AB This study examined the link between bullying victimization and substance use and tested the mediating role of depression in male and female adolescents. Cross-sectional data were collected from a national sample of 1,495 tenth graders who participated in the 2005/06 Health Behaviors in School-aged Children U.S. Survey. Victimization, depression and substance use were all measured as latent variables. Substance use was measured by drinking alcohol, being drunk, smoking cigarettes and using marijuana in the past 30 days. Multiple-group structural equation modeling showed that victimization was linked to substance use in both males and females. Among females, depression was positively associated with both victimization and substance use and mediated the association between the two latter variables. Among males, depression was associated with victimization but not with substance use. Results highlight the elevated risk for victimization and substance use problems that depression poses among adolescent females.
C1 [Luk, Jeremy W.] Univ Washington, Dept Psychol, Seattle, WA 98195 USA.
   [Wang, Jing; Simons-Morton, Bruce G.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Prevent Res Branch, Div Epidemiol Stat & Prevent Res, Bethesda, MD USA.
RP Luk, JW (reprint author), Univ Washington, Dept Psychol, Box 351525, Seattle, WA 98195 USA.
EM jwluk@uw.edu
OI Simons-Morton, Bruce/0000-0003-1099-6617
FU Intramural NIH HHS [Z99 HD999999]; NICHD NIH HHS [N01-HD-5-3401]
NR 26
TC 50
Z9 52
U1 3
U2 15
PU SPRINGER/PLENUM PUBLISHERS
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1389-4986
J9 PREV SCI
JI Prev. Sci.
PD DEC
PY 2010
VL 11
IS 4
BP 355
EP 359
DI 10.1007/s11121-010-0179-0
PG 5
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA 686AI
UT WOS:000284668800002
PM 20422288
ER

PT J
AU DeRoo, LA
   Vlastos, AT
   Mock, P
   Vlastos, G
   Morabia, A
AF DeRoo, Lisa A.
   Vlastos, Anne Therese
   Mock, Pascal
   Vlastos, Georges
   Morabia, Alfredo
TI Comparison of women's breast cancer risk factors in Geneva, Switzerland
   and Shanghai, China
SO PREVENTIVE MEDICINE
LA English
DT Article
DE China; Switzerland; Breast Cancer; Risk Factors
ID HORMONE REPLACEMENT THERAPY; ASIAN-AMERICAN WOMEN; COLLABORATIVE
   REANALYSIS; REPRODUCTIVE FACTORS; INDIVIDUAL DATA; CIGARETTE-SMOKING;
   HONG-KONG; MORTALITY; COUNTRIES; DISEASE
AB Background We compared the prevalence of known and suspected breast cancer risk factors among women in Geneva Switzerland where the annual incidence of breast cancer is high to women in Shanghai China where incidence is lower
   Methods Different translations of the same woman s health questionnaire were administered to women aged 35 to 74 years in Shanghai (n=631) and Geneva (n=1 212) during 1996-1997 and reproductive and lifestyle factors compared
   Results Shanghai women reported older age at menarche (median 15 vs 13 years) fewer nulliparity (7 3 vs 21 6%) younger age at first live birth (median 25 7 vs 284 years) and shorter duration of reproductive life (median 357 vs 384 years) Geneva women had a greater prevalence of current cigarette smoking (22 4 vs 1 8%) oral contraceptive use (61 1 vs 100%) hormone replacement therapy use (23 4 vs (1 8%) and family history of breast cancer (8 6 vs 1 4%) Among women who breastfed Shanghai women had more than twice the duration of breastfeeding than Geneva women (median 48 vs 21 weeks)
   Conclusions Differences in the prevalence of breast cancer risk factors in particular reproductive characteristics may contribute to the large contrast in cumulative risk between women living in Geneva and Shanghai Published by Elsevier Inc
C1 [DeRoo, Lisa A.; Morabia, Alfredo] Univ Hosp Geneva, Div Clin Epidemiol, Dept Community Med, Geneva, Switzerland.
   [Vlastos, Anne Therese; Mock, Pascal; Vlastos, Georges] Univ Hosp Geneva, Div Gynecol & Reprod Med, Dept Gynecol & Obstet, Geneva, Switzerland.
RP DeRoo, LA (reprint author), NIEHS, Epidemiol Branch, POB 12233,Mail Drop A3 05, Res Triangle Pk, NC 27709 USA.
FU Geneva League Against Cancer; Swiss National Research Federation; Swiss
   National Fund for Scientific Research [32-46142 95, 32-47219 96,
   32-49847 96]
FX This study was supported by the Geneva League Against Cancer the Swiss
   National Research Federation and the Swiss National Fund for Scientific
   Research (grants 32-46142 95 32-47219 96 32-49847 96)
NR 35
TC 4
Z9 5
U1 1
U2 4
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0091-7435
J9 PREV MED
JI Prev. Med.
PD DEC
PY 2010
VL 51
IS 6
BP 497
EP 501
DI 10.1016/j.ypmed.2010.09.013
PG 5
WC Public, Environmental & Occupational Health; Medicine, General &
   Internal
SC Public, Environmental & Occupational Health; General & Internal Medicine
GA 696LI
UT WOS:000285442500011
PM 20920521
ER

PT J
AU Bivona, L
   Zou, ZC
   Stutzman, N
   Sun, PD
AF Bivona, Louis
   Zou, Zhongcheng
   Stutzman, Nicole
   Sun, Peter D.
TI Influence of the second amino acid on recombinant protein expression
SO PROTEIN EXPRESSION AND PURIFICATION
LA English
DT Article
DE Recombinant expression; Second codon position; Ig alpha; Recombinant
   protein production; Codon usage; mRNA structure; Mutational analysis;
   Escherichia coli expression system
ID RNA SECONDARY STRUCTURE; ESCHERICHIA-COLI; INITIATION CODON;
   MESSENGER-RNA; TRANSLATION INITIATION; EFFICIENCY; GENE; SEQUENCE;
   RIBOSOME
AB Factors affecting protein expression have been intensely studied to the benefit of recombinant protein production. Through mutational analysis at the +2 amino acid position of recombinant Ig alpha, we examined the effect of all 20 amino acids on protein expression. The results showed that amino acids at the +2 position affected 10-fold in the recombinant protein expression. Specifically, Ala, Cys, Pro, Ser, Thr, and Lys at the +2 position resulted in significantly higher expression of recombinant Ig alpha than other amino acids, while Met, His and Glu resulted in greatly reduced protein expression. This expression difference depended on the amino acid instead of their codon usage. Consistent with the mutational results, a statistically significant enrichment in Ala and Ser at the +2 position was observed among highly expressed Escherichia coli genes. This work suggests a general approach to enhance protein expression by incorporating an Ala or Ser after the initiation codon. Published by Elsevier Inc.
C1 [Bivona, Louis; Zou, Zhongcheng; Stutzman, Nicole; Sun, Peter D.] NIAID, Immunogenet Lab, NIH, Rockville, MD 20852 USA.
RP Sun, PD (reprint author), NIAID, Immunogenet Lab, NIH, 12441 Parklawn Dr, Rockville, MD 20852 USA.
EM psun@nih.gov
FU National Institute of Allergy and Infectious Diseases; National
   Institutes of Health
FX We thank Dr. M. Gordon Joyce for insightful discussions of the
   experimental results. The work is supported by the intramural research
   funding of National Institute of Allergy and Infectious Diseases,
   National Institutes of Health.
NR 20
TC 2
Z9 2
U1 0
U2 6
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 1046-5928
J9 PROTEIN EXPRES PURIF
JI Protein Expr. Purif.
PD DEC
PY 2010
VL 74
IS 2
BP 248
EP 256
DI 10.1016/j.pep.2010.06.005
PG 9
WC Biochemical Research Methods; Biochemistry & Molecular Biology;
   Biotechnology & Applied Microbiology
SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology
GA 667PS
UT WOS:000283206700017
PM 20600944
ER

PT J
AU Shafrir, Y
   Durell, SR
   Anishkin, A
   Guy, HR
AF Shafrir, Yinon
   Durell, Stewart R.
   Anishkin, Andriy
   Guy, H. Robert
TI Beta-barrel models of soluble amyloid beta oligomers and annular
   protofibrils
SO PROTEINS-STRUCTURE FUNCTION AND BIOINFORMATICS
LA English
DT Article
DE Abeta; molecular models; structure prediction; Alzheimer's disease;
   protein structure; molecular dynamics; molecular assemblies
ID ALZHEIMERS-DISEASE; PROTEIN FIBRILLOGENESIS; HYDROGEN/DEUTERIUM
   EXCHANGE; PROTEOLYTIC FRAGMENTATION; STRUCTURAL DIFFERENCES;
   MOLECULAR-DYNAMICS; HYDROGEN-EXCHANGE; ION CHANNELS; PEPTIDE;
   NEUROTOXICITY
AB Both soluble and membrane-bound prefibrillar assemblies of Abeta (A beta) peptides have been associated with Alzheimer's disease (AD). The size and nature of these assemblies vary greatly and are affected by many factors. Here, we present models of soluble hexameric assemblies of A beta 42 and suggest how they can lead to larger assemblies and eventually to fibrils. The common element in most of these assemblies is a six-stranded beta-barrel formed by the last third of A beta 42, which is composed of hydrophobic residues and glycines. The hydrophobic core beta-barrels of the hexameric models are shielded from water by the N-terminus and central segments. These more hydrophilic segments were modeled to have either predominantly beta or predominantly alpha secondary structure. Molecular dynamics simulations were performed to analyze stabilities of the models. The hexameric models were used as starting points from which larger soluble assemblies of 12 and 36 subunits were modeled. These models were developed to be consistent with numerous experimental results.
C1 [Shafrir, Yinon; Durell, Stewart R.; Guy, H. Robert] NCI, Cell Biol Lab, CCR, NIH, Bethesda, MD 20892 USA.
   [Anishkin, Andriy] Univ Maryland, Dept Biol, College Pk, MD 20742 USA.
RP Guy, HR (reprint author), 6510 Tahawash St, Cochiti Lake, NM 87083 USA.
EM bg4y@nih.gov
FU NIH, National Cancer Institute, Center for Cancer Research
FX Grant sponsor: Intramural Research Program of the NIH, National Cancer
   Institute, Center for Cancer Research.
NR 57
TC 13
Z9 14
U1 1
U2 8
PU WILEY-LISS
PI HOBOKEN
PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 0887-3585
J9 PROTEINS
JI Proteins
PD DEC
PY 2010
VL 78
IS 16
BP 3458
EP 3472
DI 10.1002/prot.22832
PG 15
WC Biochemistry & Molecular Biology; Biophysics
SC Biochemistry & Molecular Biology; Biophysics
GA 678CK
UT WOS:000284046400019
PM 20830782
ER

PT J
AU Shafrir, Y
   Durell, S
   Arispe, N
   Guy, HR
AF Shafrir, Yinon
   Durell, Stewart
   Arispe, Nelson
   Guy, H. Robert
TI Models of membrane-bound Alzheimer's Abeta peptide assemblies
SO PROTEINS-STRUCTURE FUNCTION AND BIOINFORMATICS
LA English
DT Article
DE amyloid beta; Alzheimer's disease; membrane; channels; molecular models;
   structure prediction; protein structure; molecular dynamics; molecular
   assemblies
ID AMYLOID-BETA-PROTEIN; ION-CHANNEL; LIPID-BILAYERS; CRYSTAL-STRUCTURE;
   DISEASE; A-BETA-42; DISRUPTION; FIBRILS; NEURONS; DOMAIN
AB Although it is clear that amyloid beta (A beta) peptides play a pivotal role in the development of Alzheimer's disease, the precise molecular model of action remains unclear. A beta peptide forms assemble both in aqueous solution and in lipid membranes. It has been proposed that deleterious effects occur when the peptides interact with membranes, possibly by forming Ca(2+) permeant ion channels. In the accompanying manuscript, we propose models in which the C-terminus third of six A beta 42 peptides forms a six-stranded beta-barrel in highly toxic soluble oligomers. Here we extend this hypothesis to membrane-bound assemblies. In these A beta models, the hydrophobic beta-barrel of a hexamer may either reside on the surface of the bilayer, or span the bilayer. Transmembrane pores are proposed to form between several hexamers. Once the beta-barrels of six hexamers have spanned the bilayer, they may merge to form a more stable 36-stranded beta-barrel. We favor models in which parallel beta-barrels formed by N-terminus segments comprise the lining of the pores. These types of models explain why the channels are selective for cations and how metal ions, such as Zn(2+), synthetic peptides that contain histidines, and some small organic cations may block channels or inhibit formation of channels. Our models were developed to be consistent with microscopy studies of A beta assemblies in membranes, one of which is presented here for the first time.
C1 [Shafrir, Yinon; Durell, Stewart; Guy, H. Robert] NCI, Cell Biol Lab, NIH, Bethesda, MD 20892 USA.
   [Arispe, Nelson] Uniformed Serv Univ Sch Med, Dept Anat Physiol & Genet, Bethesda, MD 20814 USA.
   [Arispe, Nelson] Uniformed Serv Univ Sch Med, Inst Mol Med, Bethesda, MD 20814 USA.
RP Guy, HR (reprint author), 6510 Tahawash St, Cochiti Lake, NM 87083 USA.
EM bg4y@nih.gov
FU Intramural NIH HHS [Z01 BC010722-02, ZIA BC010722-04]
NR 75
TC 27
Z9 28
U1 3
U2 22
PU WILEY-LISS
PI HOBOKEN
PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 0887-3585
J9 PROTEINS
JI Proteins
PD DEC
PY 2010
VL 78
IS 16
BP 3473
EP 3487
DI 10.1002/prot.22853
PG 15
WC Biochemistry & Molecular Biology; Biophysics
SC Biochemistry & Molecular Biology; Biophysics
GA 678CK
UT WOS:000284046400020
PM 20939098
ER

PT J
AU Gonzales, DA
   De Torre, C
   Wang, HH
   Devor, CB
   Munson, PJ
   Ying, SX
   Kern, SJ
   Petraitiene, R
   Levens, DL
   Walsh, TJ
   Suffredini, AF
AF Gonzales, Denise A.
   De Torre, Carlos
   Wang, Honghui
   Devor, Christopher B.
   Munson, Peter J.
   Ying, Sai-Xia
   Kern, Steven J.
   Petraitiene, Ruta
   Levens, David L.
   Walsh, Thomas J.
   Suffredini, Anthony F.
TI Protein expression profiles distinguish between experimental invasive
   pulmonary aspergillosis and Pseudomonas pneumonia
SO PROTEOMICS
LA English
DT Article
DE Animal proteomics; Aspergillus fumigatus; Neutropenia; Pneumonia;
   Pseudomonas aeruginosa
ID C-REACTIVE PROTEIN; SERUM PROTEOMIC PATTERN; GALACTOMANNAN ANTIGENEMIA;
   BRONCHOALVEOLAR LAVAGE; PROSTATE-CANCER; BREAST-CANCER; SELDI-TOF;
   DIAGNOSIS; BLOOD; HAPTOGLOBIN
AB We hypothesized that invasive pulmonary aspergillosis (IPA) may generate a distinctive proteomic signature in plasma and bronchoalveolar lavage (BAL) Proteins in plasma and BAL from two neutropenic rabbit models of IPA and Pseudomonas pneumonia were analyzed by SELDI TOF MS Hierarchical clustering analysis of plasma time course spectra demonstrated two dusters of peaks that were differentially regulated between IPA and Pseudomonas pneumonia (57 and 34 peaks respectively p<0 001) PCA of plasma proteins demonstrated a time-dependent separation of the two infections A random forest analysis that ranked the top 30 spectral points distinguished between late Aspergillus and Pseudomonas pneumonias with 100% sensitivity and specificity Based on spectral data analysis three proteins were identified using SDS PAGE and LC/MS and quantified using reverse phase arrays Differences in the temporal sequence of plasma haptoglobin (p<0 001) apohpoprotem A1 (p<0 001) and transthyretin (p<0 038) were observed between IPA and Pseudomonas pneumonia as was C reactive protein (p < 0 001) In summary proteomic analysis of plasma and BAL proteins of experimental Aspergillus and Pseudomonas pneumonias demonstrates unique protein profiles with principal components and spectral regions that are shared in early infection and diverge at later stages of infection Haptoglobin apohpoprotem A1 transthyretin and C reactive protein are differentially expressed m these infections suggesting important contributions to host defense against IPA
C1 [Gonzales, Denise A.; De Torre, Carlos; Wang, Honghui; Kern, Steven J.; Suffredini, Anthony F.] NIH, Dept Crit Care Med, Ctr Clin, Bethesda, MD 20892 USA.
   [Devor, Christopher B.; Levens, David L.] NCI, Pathol Lab, NIH, Bethesda, MD 20892 USA.
   [Munson, Peter J.; Ying, Sai-Xia] NIH, Math & Stat Comp Lab, Ctr Informat Technol, Bethesda, MD 20892 USA.
   [Petraitiene, Ruta; Walsh, Thomas J.] NCI, Pediat Oncol Branch, NIH, Bethesda, MD 20892 USA.
   [Petraitiene, Ruta] SAIC Frederick, Lab Anim Sci Program, Frederick, MD USA.
RP Suffredini, AF (reprint author), NIH, Dept Crit Care Med, Ctr Clin, Bldg 10,Room 2C145,9000 Rockville Pike, Bethesda, MD 20892 USA.
RI Levens, David/C-9216-2009
OI Levens, David/0000-0002-7616-922X
FU National Institutes of Health Critical Care Medicine Department Clinical
   Center Laboratory of Pathology; Pediatric Oncology Branch National
   Cancer Institute
FX This research was supported by the Intramural Research Program of the
   National Institutes of Health Critical Care Medicine Department Clinical
   Center Laboratory of Pathology and Pediatric Oncology Branch National
   Cancer Institute
NR 47
TC 13
Z9 13
U1 0
U2 3
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1615-9853
EI 1615-9861
J9 PROTEOMICS
JI Proteomics
PD DEC
PY 2010
VL 10
IS 23
BP 4270
EP 4280
DI 10.1002/pmic.200900768
PG 11
WC Biochemical Research Methods; Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 701VK
UT WOS:000285851900012
PM 21089047
ER

PT J
AU Rodriguez, H
   Rivers, R
   Kinsinger, C
   Mesri, M
   Hiltke, T
   Rahbar, A
   Boja, E
AF Rodriguez, Henry
   Rivers, Robert
   Kinsinger, Christopher
   Mesri, Mehdi
   Hiltke, Tara
   Rahbar, Amir
   Boja, Emily
TI Reconstructing the pipeline by introducing multiplexed multiple reaction
   monitoring mass spectrometry for cancer biomarker verification: An
   NCI-CPTC initiative perspective
SO PROTEOMICS CLINICAL APPLICATIONS
LA English
DT Review
DE Biomarkers; Biomarker qualification (clinical validation); Biomarker
   verification (analytical validation); MRM-MS; Quantification
ID STABLE-ISOTOPE DILUTION; ABUNDANCE PROTEINS; PROTEOMIC ANALYSIS;
   DISCOVERY; PLASMA; ASSAYS; SERUM; QUANTIFICATION; DIAGNOSTICS;
   VALIDATION
AB Proteomics holds great promise in personalized medicine for cancer in the post-genomic era. In the past decade, clinical proteomics has significantly evolved in terms of technology development, optimization and standardization, as well as in advanced bioinformatics data integration and analysis. Great strides have been made for characterizing a large number of proteins qualitatively and quantitatively in a proteome, including the use of sample fractionation, protein microarrays and MS. It is believed that differential proteomic analysis of high-quality clinical biospecimen (tissue and biofluids) can potentially reveal protein/peptide biomarkers responsible for cancer by means of their altered levels of expression and/or PTMs. Multiple reaction monitoring, a multiplexed platform using stable isotope dilution-MS with sensitivity and reproducibility approaching that of traditional ELISAs commonly used in the clinical setting, has emerged as a potentially promising technique for next-generation high-throughput protein biomarker measurements for diagnostics and therapeutics.
C1 [Rodriguez, Henry; Rivers, Robert; Kinsinger, Christopher; Mesri, Mehdi; Hiltke, Tara; Rahbar, Amir; Boja, Emily] NCI, Off Canc Clin Prote Res, Ctr Strateg Sci Initiat, NIH, Bethesda, MD 20892 USA.
RP Boja, E (reprint author), Room 10A52,31 Ctr Dr,MSC 2580, Bethesda, MD 20892 USA.
EM bojae@mail.nih.gov
FU Intramural NIH HHS [Z99 CA999999]
NR 55
TC 24
Z9 24
U1 1
U2 17
PU WILEY-V C H VERLAG GMBH
PI WEINHEIM
PA PO BOX 10 11 61, D-69451 WEINHEIM, GERMANY
SN 1862-8346
J9 PROTEOM CLIN APPL
JI Proteom. Clin. Appl.
PD DEC
PY 2010
VL 4
IS 12
SI SI
BP 904
EP 914
DI 10.1002/prca.201000057
PG 11
WC Biochemical Research Methods; Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 702HR
UT WOS:000285885700005
PM 21137031
ER

PT J
AU Cuthbert, B
   Insel, T
AF Cuthbert, Bruce
   Insel, Thomas
TI The Data of Diagnosis: New Approaches to Psychiatric Classification
SO PSYCHIATRY-INTERPERSONAL AND BIOLOGICAL PROCESSES
LA English
DT Editorial Material
C1 [Cuthbert, Bruce; Insel, Thomas] NIMH, Bethesda, MD 20892 USA.
RP Cuthbert, B (reprint author), NIMH, 6001 Execut Blvd,MSC 9625, Bethesda, MD 20892 USA.
EM bcuthber@mail.nih.gov
NR 6
TC 39
Z9 39
U1 0
U2 10
PU GUILFORD PUBLICATIONS INC
PI NEW YORK
PA 72 SPRING STREET, NEW YORK, NY 10012 USA
SN 0033-2747
J9 PSYCHIATRY
JI Psychiatry-Interpers. Biol. Process.
PD WIN
PY 2010
VL 73
IS 4
BP 311
EP 314
DI 10.1521/psyc.2010.73.4.311
PG 4
WC Psychiatry
SC Psychiatry
GA 696NS
UT WOS:000285448700003
PM 21198381
ER

PT J
AU Gamaldo, AA
   Allaire, JC
   Whitfield, KE
AF Gamaldo, Alyssa A.
   Allaire, Jason C.
   Whitfield, Keith E.
TI Exploring the Within-Person Coupling of Sleep and Cognition in Older
   African Americans
SO PSYCHOLOGY AND AGING
LA English
DT Article
DE cognition sleep; within person coupling; older adults; African Americans
ID INTRAINDIVIDUAL VARIABILITY; DAYTIME SLEEPINESS; MEMORY FAILURES;
   QUALITY INDEX; PERFORMANCE; DEPRIVATION; INSOMNIA; ADULTS; POPULATION;
   IMPAIRMENT
AB This study examined the within person relationship between sleep and cognitive functioning Fifty community dwelling African Americans (age range = 50-80 years) were asked to report their sleep duration and quality the previous evening and to complete cognitive measures over 8 occasions within a 2-3 week period A within person daily change in sleep duration was significantly associated with woise global cognitive performance The greater an individual deviated away from his or her average sleep duration on a particular day the more likely his or her performance would decline These results demonstrate that the sleep cognition relationship can be observed at a within person level of analysis
C1 [Gamaldo, Alyssa A.] NIA, BRC, NIH, Intramural Res Program, Baltimore, MD 21224 USA.
   [Allaire, Jason C.] N Carolina State Univ, Dept Psychol, Raleigh, NC 27695 USA.
   [Whitfield, Keith E.] Duke Univ, Dept Psychol & Neurosci, Durham, NC 27706 USA.
RP Gamaldo, AA (reprint author), NIA, BRC, NIH, Intramural Res Program, 04B325 251 Bayview Blvd, Baltimore, MD 21224 USA.
FU Intramural NIH HHS; NIA NIH HHS [R01 AG024108-02S1, R01 AG024108, R01
   AG024108-01A1, R01 AG024108-01]
NR 50
TC 13
Z9 13
U1 1
U2 1
PU AMER PSYCHOLOGICAL ASSOC
PI WASHINGTON
PA 750 FIRST ST NE, WASHINGTON, DC 20002-4242 USA
SN 0882-7974
J9 PSYCHOL AGING
JI Psychol. Aging
PD DEC
PY 2010
VL 25
IS 4
BP 851
EP 857
DI 10.1037/a0021378
PG 7
WC Gerontology; Psychology, Developmental
SC Geriatrics & Gerontology; Psychology
GA 701IM
UT WOS:000285811600011
PM 21058868
ER

PT J
AU Wagner, EH
   Bowles, EJA
   Greene, SM
   Tuzzio, L
   Wiese, CJ
   Kirlin, B
   Clauser, SB
AF Wagner, Edward H.
   Bowles, Erin J. Aiello
   Greene, Sarah M.
   Tuzzio, Leah
   Wiese, Cheryl J.
   Kirlin, Beth
   Clauser, Steven B.
TI The quality of cancer patient experience: perspectives of patients,
   family members, providers and experts
SO QUALITY & SAFETY IN HEALTH CARE
LA English
DT Article
ID BREAST-CANCER; UNITED-STATES; CARE; INTERVENTION; INFORMATION; INTERNET;
   IMPROVE; WOMEN; WEB
AB Background Anecdotes and limited evidence suggest that a significant percentage of cancer patients encounter troublesome problems in the course of their care.
   Methods The authors collected data about barriers to and facilitators of high-quality cancer care and innovative solutions to improve quality from three sources: focus groups with patients, family members of cancer patients and providers; site visits to cancer care providers and organisations in three American communities; and expert interviews.
   Results The authors' respondents consistently described a similar list of problems facing the individual with a suspicion or diagnosis of cancer and his/her family: delays in and lack of coordination of care, patient information gaps and passivity, inadequate attention to emotional and social problems, and difficulty accessing services because of inadequate insurance, limited financial resources or rural residence. The fragmentation and uncertain accountability of cancer care contribute to these issues. Respondents recommended linking patients with a care navigator or manager, using computer technology to better inform and support patients and connect providers, and reforming provider reimbursement to encourage more patient-centred care.
   Conclusions Cancer patients and their families have urgent needs for information and support especially early in their course. To meet these needs, early cancer care must be better organised, integrated, and patient centred. The Institute of Medicine's Model for the Delivery of Psychosocial Services appears to provide a relevant guide to delivering cancer care that better meets patient and family needs.
C1 [Wagner, Edward H.; Bowles, Erin J. Aiello; Greene, Sarah M.; Tuzzio, Leah; Wiese, Cheryl J.; Kirlin, Beth] Grp Hlth Res Inst, Seattle, WA 98101 USA.
   [Clauser, Steven B.] NCI, Appl Res Program, Div Canc Control & Populat Sci, Bethesda, MD 20892 USA.
RP Wagner, EH (reprint author), Grp Hlth Res Inst, 1730 Minor Ave,Suite 1600, Seattle, WA 98101 USA.
EM wagner.e@ghc.org
FU National Cancer Institute [PO-263-MQ-516309, U19 CA79689]
FX This work was supported by a contract (PO-263-MQ-516309) and grant (U19
   CA79689) from the National Cancer Institute. There are no financial
   disclosures.
NR 32
TC 34
Z9 34
U1 0
U2 9
PU B M J PUBLISHING GROUP
PI LONDON
PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND
SN 1475-3898
J9 QUAL SAF HEALTH CARE
JI Qual. Saf. Health Care
PD DEC
PY 2010
VL 19
IS 6
BP 484
EP 489
DI 10.1136/qshc.2010.042374
PG 6
WC Health Care Sciences & Services
SC Health Care Sciences & Services
GA 705BL
UT WOS:000286103300070
PM 21127109
ER

PT J
AU Skryabin, AM
   Drozdovitch, V
   Belsky, Y
   Leshcheva, SV
   Mirkhaidarov, AK
   Voilleque, P
   Luckyanov, N
   Bouville, A
AF Skryabin, A. M.
   Drozdovitch, V.
   Belsky, Y.
   Leshcheva, S. V.
   Mirkhaidarov, A. K.
   Voilleque, P.
   Luckyanov, N.
   Bouville, A.
TI THYROID MASS IN CHILDREN AND ADOLESCENTS LIVING IN THE MOST EXPOSED
   AREAS TO CHERNOBYL FALLOUT IN BELARUS
SO RADIATION PROTECTION DOSIMETRY
LA English
DT Article
ID RECONSTRUCTION; ACCIDENT
AB This paper aims to determine the thyroid volumes in children and teenagers living in Gomel and Mogilev Oblasts, which are the areas of Belarus that were most affected by the Chernobyl accident. Results of thyroid volume measurements performed in 1991-1996 by the Sasakawa Memorial Health Foundation were used to evaluate the variation by age of the thyroid volumes for girls and boys aged from 5 to 16 y. Thyroid volumes for age groups without measurements were also estimated. For a given age and gender, the differences between children from Gomel and Mogilev Oblasts do not exceed 12 %, which is relatively small when the variability of individual values is considered. For children of a given age, the individual values show a variability characterised by geometric standard deviation (GSD) of 1.25-1.4. Values of thyroid mass that were derived from the measured thyroid volumes are being used within the framework of the on-going Belarusian-American cohort study of thyroid cancer and other thyroid diseases after the Chernobyl accident to estimate with more accuracy the thyroid doses that were received by the cohort members.
C1 [Drozdovitch, V.; Luckyanov, N.; Bouville, A.] NCI, DHHS, NIH, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA.
   [Skryabin, A. M.; Belsky, Y.; Leshcheva, S. V.; Mirkhaidarov, A. K.] Republican Res Ctr Radiat Med & Human Ecol, Gomel 246040, Byelarus.
   [Voilleque, P.] MJP Risk Assessment Inc, Denver, CO 80220 USA.
RP Drozdovitch, V (reprint author), NCI, DHHS, NIH, Div Canc Epidemiol & Genet, 6120 Execut Blvd, Bethesda, MD 20892 USA.
EM drozdovv@mail.nih.gov
FU National Institutes of Health, National Cancer Institute (USA)
   [N02-CP-45506]
FX This work was supported by the National Institutes of Health, National
   Cancer Institute (USA) within the framework of Belarus-US study of
   thyroid cancer and other diseases following the Chernobyl accident
   [N02-CP-45506]
NR 10
TC 8
Z9 8
U1 0
U2 0
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 2010
VL 142
IS 2-4
BP 292
EP 299
DI 10.1093/rpd/ncq209
PG 8
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 693AK
UT WOS:000285196800027
PM 20823035
ER

PT J
AU Bhatti, P
   Veiga, LHS
   Ronckers, CM
   Sigurdson, AJ
   Stovall, M
   Smith, SA
   Weathers, R
   Leisenring, W
   Mertens, AC
   Hammond, S
   Friedman, DL
   Neglia, JP
   Meadows, AT
   Donaldson, SS
   Sklar, CA
   Robison, LL
   Inskip, PD
AF Bhatti, Parveen
   Veiga, Lene H. S.
   Ronckers, Cecile M.
   Sigurdson, Alice J.
   Stovall, Marilyn
   Smith, Susan A.
   Weathers, Rita
   Leisenring, Wendy
   Mertens, Ann C.
   Hammond, Sue
   Friedman, Debra L.
   Neglia, Joseph P.
   Meadows, Anna T.
   Donaldson, Sarah S.
   Sklar, Charles A.
   Robison, Leslie L.
   Inskip, Peter D.
TI Risk of Second Primary Thyroid Cancer after Radiotherapy for a Childhood
   Cancer in a Large Cohort Study: An Update from the Childhood Cancer
   Survivor Study
SO RADIATION RESEARCH
LA English
DT Article
ID IONIZING-RADIATION; CHEMOTHERAPY; EXPOSURE; DISEASE; ACCIDENT; UKRAINE;
   CERVIX
AB Previous studies have indicated that thyroid cancer risk after a first childhood malignancy is curvilinear with radiation dose, increasing at low to moderate doses and decreasing at high doses. Understanding factors that modify the radiation dose response over the entire therapeutic dose range is challenging and requires large numbers of subjects. We quantified the long-term risk of thyroid cancer associated with radiation treatment among 12,547 5-year survivors of a childhood cancer (leukemia, Hodgkin lymphoma and non-Hodgkin lymphoma, central nervous system cancer, soft tissue sarcoma, kidney cancer, bone cancer, neuroblastoma) diagnosed between 1970 and 1986 in the Childhood Cancer Survivor Study using the most current cohort follow-up to 2005. There were 119 subsequent pathologically confirmed thyroid cancer cases, and individual radiation doses to the thyroid gland were estimated for the entire cohort. This cohort study builds on the previous case-control study in this population (69 thyroid cancer cases with follow-up to 2000) by allowing the evaluation of both relative and absolute risks. Poisson regression analyses were used to calculate standardized incidence ratios (SIR), excess relative risks (ERR) and excess absolute risks (EAR) of thyroid cancer associated with radiation dose. Other factors such as sex, type of first cancer, attained age, age at exposure to radiation, time since exposure to radiation, and chemotherapy (yes/no) were assessed for their effect on the linear and exponential quadratic terms describing the dose response relationship. Similar to the previous analysis, thyroid cancer risk increased linearly with radiation dose up to approximately 20 Gy, where the relative risk peaked at 14.6-fold (95% CI, 6.8-31.5). At thyroid radiation doses >20 Gy, a downturn in the dose response relationship was observed. The ERR model that best fit the data was linear-exponential quadratic. We found that age at exposure modified the ERR linear dose term (higher radiation risk with younger age) (P < 0.001) and that sex (higher radiation risk among females) (P = 0.008) and time since exposure (higher radiation risk with longer time) (P < 0.001) modified the EAR linear dose term. None of these factors modified the exponential quadratic (high dose) term. Sex, age at exposure and time since exposure were found to be significant modifiers of the radiation-related risk of thyroid cancer and as such are important factors to account for in clinical follow-up and thyroid cancer risk estimation among childhood cancer survivors. (C) 2010 by Radiation Research Society
C1 [Bhatti, Parveen] Fred Hutchinson Canc Res Ctr, Div Publ Hlth Sci, Program Epidemiol, Seattle, WA 98109 USA.
   [Bhatti, Parveen; Veiga, Lene H. S.; Ronckers, Cecile M.; Sigurdson, Alice J.; Inskip, Peter D.] NCI, Radiat Epidemiol Branch, Div Canc Epidemiol & Genet, NIH,DHHS, Bethesda, MD 20892 USA.
   [Ronckers, Cecile M.] Dutch Childhood Oncol Grp, Late Effects Childhood Canc LATER Registry, The Hague, Netherlands.
   [Stovall, Marilyn; Smith, Susan A.; Weathers, Rita] Univ Texas MD Anderson Canc Ctr, Dept Radiat Phys, Houston, TX 77030 USA.
   [Leisenring, Wendy] Fred Hutchinson Canc Res Ctr, Canc Prevent Res Program, Seattle, WA 98109 USA.
   [Mertens, Ann C.] Emory Univ, Atlanta, GA 30322 USA.
   [Hammond, Sue] Childrens Hosp, Dept Lab Med & Pathol, Columbus, OH 43205 USA.
   [Hammond, Sue] Ohio State Univ, Coll Med, Columbus, OH 43210 USA.
   [Friedman, Debra L.] Vanderbilt Ingram Canc Ctr, Canc Control & Prevent Program, Nashville, TN USA.
   [Neglia, Joseph P.] Univ Minnesota, Sch Med, Dept Pediat, Minneapolis, MN 55455 USA.
   [Meadows, Anna T.] Childrens Hosp Philadelphia, Philadelphia, PA 19104 USA.
   [Donaldson, Sarah S.] Stanford Canc Ctr, Dept Radiat Oncol, Stanford, CA USA.
   [Sklar, Charles A.] Mem Sloan Kettering Canc Ctr, Dept Pediat, New York, NY 10021 USA.
   [Robison, Leslie L.] St Jude Childrens Res Hosp, Dept Epidemiol & Canc Control, Memphis, TN 38105 USA.
RP Bhatti, P (reprint author), Fred Hutchinson Canc Res Ctr, Div Publ Hlth Sci, Program Epidemiol, POB 19024,M4-B874, Seattle, WA 98109 USA.
EM pbhatti@fhcrc.org
FU National Cancer Institute [U24 CA55727]; Children's Cancer Research
   Fund; Lance Armstrong Foundation [147149]; NIH, National Cancer
   Institute, Division of Cancer Epidemiology and Genetics
FX This study was funded by National Cancer Institute grant U24 CA55727,
   the Children's Cancer Research Fund, the Lance Armstrong Foundation
   grant 147149 and the Intramural Research Program of the NIH, National
   Cancer Institute, Division of Cancer Epidemiology and Genetics. We thank
   Drs. Ethel Gilbert, Dale Preston and Jay Lubin for their assistance with
   the statistical analysis and for helpful comments on the manuscript.
NR 29
TC 104
Z9 110
U1 0
U2 5
PU RADIATION RESEARCH SOC
PI LAWRENCE
PA 810 E TENTH STREET, LAWRENCE, KS 66044 USA
SN 0033-7587
EI 1938-5404
J9 RADIAT RES
JI Radiat. Res.
PD DEC
PY 2010
VL 174
IS 6
BP 741
EP 752
DI 10.1667/RR2240.1
PN 1
PG 12
WC Biology; Biophysics; Radiology, Nuclear Medicine & Medical Imaging
SC Life Sciences & Biomedicine - Other Topics; Biophysics; Radiology,
   Nuclear Medicine & Medical Imaging
GA 690TQ
UT WOS:000285031500009
PM 21128798
ER

PT J
AU Hatch, M
   Furukawa, K
   Brenner, A
   Olinjyk, V
   Ron, E
   Zablotska, L
   Terekhova, G
   McConnell, R
   Markov, V
   Shpak, V
   Ostroumova, E
   Bouville, A
   Tronko, M
AF Hatch, M.
   Furukawa, K.
   Brenner, A.
   Olinjyk, V.
   Ron, E.
   Zablotska, L.
   Terekhova, G.
   McConnell, R.
   Markov, V.
   Shpak, V.
   Ostroumova, E.
   Bouville, A.
   Tronko, M.
TI Prevalence of Hyperthyroidism after Exposure during Childhood or
   Adolescence to Radioiodines from the Chornobyl Nuclear Accident:
   Dose-Response Results from the Ukrainian-American Cohort Study
SO RADIATION RESEARCH
LA English
DT Article
ID THYROID-DISEASES; SUBCLINICAL HYPERTHYROIDISM; AUTOIMMUNE-THYROIDITIS;
   RADIATION; CHILDREN; CANCER; HYPOTHYROIDISM; FALLOUT; AUTOANTIBODIES;
   POPULATION
AB Relatively few data are available on the prevalence of hyperthyroidism (TSH concentrations of <0.3 mIU/liter, with normal or elevated concentrations of free T4) in individuals exposed to radioiodines at low levels. The accident at the Chornobyl (Chernobyl) nuclear plant in Ukraine on April 26, 1986 exposed large numbers of residents to radioactive fallout, principally to iodine-131 (I-131) (mean and median doses = 0.6 Gy and 0.2 Gy). We investigated the relationship between I-131 and prevalent hyperthyroidism among 11,853 individuals exposed as children or adolescents in Ukraine who underwent an in-depth, standardized thyroid gland screening examination 12-14 years later. Radioactivity measurements taken shortly after the accident were available for all subjects and were used to estimate individual thyroid doses. We identified 76 cases of hyperthyroidism (11 overt, 65 subclinical). Using logistic regression, we tested a variety of continuous risk models and conducted categorical analyses for all subjects combined and for females (53 cases, n = 5,767) and males (23 cases, n = 6,086) separately but found no convincing evidence of a dose-response relationship between I-131 and hyperthyroidism. There was some suggestion of elevated risk among females in an analysis based on a dichotomous dose model with a threshold of 0.5 Gy chosen empirically (OR = 1.86, P = 0.06), but the statistical significance level was reduced (P = 0.13) in a formal analysis with an estimated threshold. In summary, after a thorough exploration of the data, we found no statistically significant dose-response relationship between individual I-131 thyroid doses and prevalent hyperthyroidism. (C) 2010 by Radiation Research Society
C1 [Hatch, M.; Furukawa, K.; Brenner, A.; Ron, E.; Ostroumova, E.; Bouville, A.] NCI, Div Canc Epidemiol & Genet, NIH, DHHS, Rockville, MD 20852 USA.
   [Olinjyk, V.] Inst Endocrinol & Metab, Kiev, Ukraine.
   [Zablotska, L.] Univ Calif San Francisco, Dept Epidemiol & Biostat, San Francisco, CA 94143 USA.
   [McConnell, R.; Markov, V.; Shpak, V.; Tronko, M.] Columbia Univ, Thyroid Ctr, New York, NY USA.
RP Hatch, M (reprint author), NCI, Div Canc Epidemiol & Genet, NIH, DHHS, 6120 Execut Blvd,Room 7098, Rockville, MD 20852 USA.
EM hatchm@mail.nih.gov
FU U.S. National Cancer Institute; NIH; DHHS; Department of Energy; U.S.
   Nuclear Regulatory Commission; French Institute of Radioprotection and
   Nuclear Safety
FX This research was supported by the Intramural Research Program of the
   U.S. National Cancer Institute, NIH, DHHS, and the Department of Energy.
   The U.S. Nuclear Regulatory Commission and the French Institute of
   Radioprotection and Nuclear Safety provided the initial funds for
   purchase of equipment. We thank the Louise Hamilton Kyiv Data Management
   Center and its head, Oleksander Zvinchuk, for their excellent help with
   database management. The authors are also grateful to the late Drs.
   Ovisy Epshtein and Daniel Fink for their laboratory skills, insights and
   support, as well as to the late Dr. Jacob Robbins, who always encouraged
   the Chornobyl team to investigate functional disorders of the thyroid.
   Finally, we would like to thank the Journal's Associate Editor and
   anonymous reviewers for their valuable comments.
NR 38
TC 4
Z9 6
U1 0
U2 2
PU RADIATION RESEARCH SOC
PI LAWRENCE
PA 810 E TENTH STREET, LAWRENCE, KS 66044 USA
SN 0033-7587
EI 1938-5404
J9 RADIAT RES
JI Radiat. Res.
PD DEC
PY 2010
VL 174
IS 6
BP 763
EP 772
DI 10.1667/RR2003.1
PN 1
PG 10
WC Biology; Biophysics; Radiology, Nuclear Medicine & Medical Imaging
SC Life Sciences & Biomedicine - Other Topics; Biophysics; Radiology,
   Nuclear Medicine & Medical Imaging
GA 690TQ
UT WOS:000285031500011
PM 21128800
ER

PT J
AU Ron, E
   Jacob, P
AF Ron, Elaine
   Jacob, Peter
TI Late Health Effects of Ionizing Radiation: Bridging the Experimental and
   Epidemiologic Divide INTRODUCTION
SO RADIATION RESEARCH
LA English
DT Editorial Material
ID ATOMIC-BOMB SURVIVORS; MORTALITY; EXPOSURE; DISEASES; WORKERS; RISKS;
   COHORT; SYSTEM; DAMAGE
C1 [Jacob, Peter] German Res Ctr Environm Hlth, Inst Radiat Protect, Helmholtz Zentrum Munchen, D-85764 Neuherberg, Bayern, Germany.
   [Ron, Elaine] NCI, Radiat Epidemiol Branch, Div Canc Epidemiol & Genet, NIH,DHHS, Bethesda, MD 20892 USA.
RP Jacob, P (reprint author), German Res Ctr Environm Hlth, Inst Radiat Protect, Helmholtz Zentrum Munchen, Ingolstadter Landstr 1, D-85764 Neuherberg, Bayern, Germany.
EM jacob@helmholtz-muenchen.de
NR 24
TC 4
Z9 5
U1 0
U2 0
PU RADIATION RESEARCH SOC
PI LAWRENCE
PA 810 E TENTH STREET, LAWRENCE, KS 66044 USA
SN 0033-7587
J9 RADIAT RES
JI Radiat. Res.
PD DEC
PY 2010
VL 174
IS 6
BP 789
EP 792
DI 10.1667/RRXX24.1
PN 2
PG 4
WC Biology; Biophysics; Radiology, Nuclear Medicine & Medical Imaging
SC Life Sciences & Biomedicine - Other Topics; Biophysics; Radiology,
   Nuclear Medicine & Medical Imaging
GA 690TR
UT WOS:000285031600001
PM 21128804
ER

PT J
AU Linet, MS
   Kim, KP
   Miller, DL
   Kleinerman, RA
   Simon, SL
   de Gonzalez, AB
AF Linet, Martha S.
   Kim, Kwang Pyo
   Miller, Donald L.
   Kleinerman, Ruth A.
   Simon, Steven L.
   de Gonzalez, Amy Berrington
TI Historical Review of Occupational Exposures and Cancer Risks in Medical
   Radiation Workers
SO RADIATION RESEARCH
LA English
DT Review
ID US RADIOLOGIC TECHNOLOGISTS; NATIONAL DOSE REGISTRY; IONIZING-RADIATION;
   INTERVENTIONAL RADIOLOGY; UNITED-STATES; AMERICAN RADIOLOGISTS; BRITISH
   RADIOLOGISTS; STONE EXTRACTION; APLASTIC-ANEMIA; BRAIN CANCER
AB Epidemiological studies of medical radiation workers have found excess risks of leukemia, skin and female breast cancer in those employed before 1950 but little consistent evidence of cancer risk increases subsequently. Occupational radiation-related dose-response data and recent and lifetime cancer risk data are limited for radiologists and radiologic technologists and lacking for physicians and technologists performing fluoroscopically guided procedures. Survey data demonstrate that occupational doses to radiologists and radiologic technologists have declined over time. Eighty mostly small studies of cardiologists and fewer studies of other physicians reveal that effective doses to physicians per interventional procedure vary by more than an order of magnitude. For medical radiation workers, there is an urgent need to expand the limited information on average annual, time-trend and organ doses from occupational radiation exposures and to assess lifetime cancer risks of these workers. For physicians and technologists performing interventional procedures, more information about occupational doses should be collected and long-term follow-up studies of cancer and other serious disease risks should be initiated. Such studies will help optimize standardized protocols for radiologic procedures, determine whether current radiation protection measures for medical radiation workers are adequate, provide guidance on cancer screening needs, and yield valuable insights on cancer risks associated with chronic radiation exposure. (C) 2010 by Radiation Research Society
C1 [Linet, Martha S.] NCI, Div Canc Epidemiol & Genet, REB, DCEG, Bethesda, MD 20892 USA.
   [Kim, Kwang Pyo] Kyung Hee Univ, Dept Nucl Engn, Gyeonggi Do, South Korea.
   [Miller, Donald L.] Natl Naval Med Ctr, Dept Radiol, Bethesda, MD USA.
RP Linet, MS (reprint author), NCI, Div Canc Epidemiol & Genet, REB, DCEG, 6120 Execut Blvd,EPS 7048, Bethesda, MD 20892 USA.
EM linetm@mail.nih.gov
OI Kleinerman, Ruth/0000-0001-7415-2478
FU Division of Cancer Epidemiology and Genetics, National Cancer Institute,
   National Institutes of Health
FX We are grateful to Dr. Alice Sigurdson and Michele Doody, M.S., for
   their helpful suggestions, and to Annelie Landgren, MPH, for technical
   support. This review was supported by the Intramural Research Program of
   the Division of Cancer Epidemiology and Genetics, National Cancer
   Institute, National Institutes of Health.
NR 126
TC 45
Z9 48
U1 2
U2 14
PU RADIATION RESEARCH SOC
PI LAWRENCE
PA 810 E TENTH STREET, LAWRENCE, KS 66044 USA
SN 0033-7587
J9 RADIAT RES
JI Radiat. Res.
PD DEC
PY 2010
VL 174
IS 6
BP 793
EP 808
DI 10.1667/RR2014.1
PN 2
PG 16
WC Biology; Biophysics; Radiology, Nuclear Medicine & Medical Imaging
SC Life Sciences & Biomedicine - Other Topics; Biophysics; Radiology,
   Nuclear Medicine & Medical Imaging
GA 690TR
UT WOS:000285031600002
PM 21128805
ER

PT J
AU Preston, DL
   Krestinina, LY
   Sokolnikov, ME
   Ron, E
   Davis, FG
   Ostroumova, EV
   Gilbert, ES
AF Preston, D. L.
   Krestinina, L. Yu
   Sokolnikov, M. E.
   Ron, E.
   Davis, F. G.
   Ostroumova, E. V.
   Gilbert, E. S.
TI How Much Can We Say about Site-Specific Cancer Radiation Risks?
SO RADIATION RESEARCH
LA English
DT Article
ID TECHA RIVER COHORT; ATOMIC-BOMB SURVIVORS; SOLID CANCER; MORTALITY RISK;
   DOSIMETRY
AB Studies of Mayak workers and people who lived along the Techa River have demonstrated significant associations between low-dose-rate radiation exposure and increased solid cancer risk. It is of interest to use the long-term follow-up data from these cohorts to describe radiation effects for specific types of cancer; however, statistical variability in the site-specific risk estimates is large. The goal of this work is to describe this variability and provide Bayesian adjusted risk estimates. We assume that the site-specific estimates can be viewed as a sample from some underlying distribution and use Bayesian methods to produce adjusted excess relative risk per gray estimates in the Mayak and Techa River cohorts. The impact of the adjustment is compared to that seen in similar analyses in the atomic bomb survivors. Site-specific risk estimates in the Mayak and Techa River cohorts have large uncertainties. Unadjusted estimates vary from implausibly large decreases to large increases, with a range that greatly exceeds that found in the A-bomb survivors. The Bayesian adjustment markedly reduced the range of the site-specific estimates for the Techa River and Mayak studies. The extreme variability in the site-specific risk estimates is largely a consequence of the small number of excess cases. The adjusted estimates provide a useful perspective on variation in the actual risks. However, additional work on interpretation of the adjusted estimates, extension of the methods used in describing effect modification, and making more use of prior knowledge is needed to make these methods useful. (C) 2010 by Radiation Research Society
C1 [Preston, D. L.] Hirosoft Int, Eureka, CA USA.
   [Krestinina, L. Yu; Ostroumova, E. V.] Urals Res Ctr Radiat Med, Chelyabinsk, Russia.
   [Sokolnikov, M. E.] So Urals Biophys Inst, Ozyorsk, Russia.
   [Ron, E.; Gilbert, E. S.] NCI, Radiat Epidemiol Branch, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA.
   [Davis, F. G.] Univ Illinois, Dept Epidemiol & Biostat, Chicago, IL USA.
RP Preston, DL (reprint author), Hirosoft Int, Eureka, CA USA.
EM preston@hirosoft.net
FU Japanese Ministry of Health, Labor, and Welfare; U.S. Department of
   Energy through the U.S. National Academy of Sciences; NCI [N01-CP-41003,
   N01-CP-45505]; DOE [DE-FC02-04EH04014]; NIH; U.S. National Cancer
   Institute, National Institutes of Health, Department of Health and Human
   Services
FX This report makes use of data obtained from the Radiation Effects
   Research Foundation (RERF) in Hiroshima, Japan. RERF is a private
   foundation funded equally by the Japanese Ministry of Health, Labor, and
   Welfare and the U.S. Department of Energy through the U.S. National
   Academy of Sciences. The data include information obtained from the
   Hiroshima City, Hiroshima Prefecture, Nagasaki City, and Nagasaki
   Prefecture Tumor Registries and the Hiroshima and Nagasaki Tissue
   Registries. The conclusions in this report are those of the authors and
   do not necessarily reflect the scientific judgment of RERF or its
   funding agencies. The work described in this paper was carried out with
   support from NCI contracts N01-CP-41003 (MWC) and N01-CP-45505 (TRC),
   DOE contract DE-FC02-04EH04014 (TRC), and NIH intramural research
   program, and the intramural research program of the U.S. National Cancer
   Institute, National Institutes of Health, Department of Health and Human
   Services.
NR 20
TC 12
Z9 12
U1 0
U2 3
PU RADIATION RESEARCH SOC
PI LAWRENCE
PA 810 E TENTH STREET, LAWRENCE, KS 66044 USA
SN 0033-7587
EI 1938-5404
J9 RADIAT RES
JI Radiat. Res.
PD DEC
PY 2010
VL 174
IS 6
BP 816
EP 824
DI 10.1667/RR2024.1
PN 2
PG 9
WC Biology; Biophysics; Radiology, Nuclear Medicine & Medical Imaging
SC Life Sciences & Biomedicine - Other Topics; Biophysics; Radiology,
   Nuclear Medicine & Medical Imaging
GA 690TR
UT WOS:000285031600004
PM 21128806
ER

PT J
AU Ron, E
   Brenner, A
AF Ron, Elaine
   Brenner, Alina
TI Non-malignant Thyroid Diseases after a Wide Range of Radiation Exposures
SO RADIATION RESEARCH
LA English
DT Article
ID ATOMIC-BOMB SURVIVORS; DOSE-RESPONSE RELATIONSHIPS; CHILDHOOD-CANCER
   SURVIVOR; HANFORD NUCLEAR SITE; CHERNOBYL ACCIDENT;
   AUTOIMMUNE-THYROIDITIS; RADIOACTIVE IODINE; IONIZING-RADIATION;
   HODGKINS-DISEASE; TINEA-CAPITIS
AB The thyroid gland is one of the most radiosensitive human organs. While it is well known that radiation exposure increases the risk of thyroid cancer, less is known about its effects in relation to non-malignant thyroid diseases. The aim of this review is to evaluate the effects of high- and low-dose radiation on benign structural and functional diseases of the thyroid. We examined the results of major studies from cancer patients treated with high-dose radiotherapy or thyrotoxicosis patients treated with high doses of iodine-131, patients treated with moderate- to high-dose radiotherapy for benign diseases, persons exposed to low doses from environmental radiation, and survivors of the atomic bombings who were exposed to a range of doses. We evaluated radiation effects on structural (tumors, nodules), functional (hyper- and hypothyroidism), and autoimmune thyroid diseases. After a wide range of doses of ionizing radiation, an increased risk of thyroid adenomas and nodules was observed in a variety of populations and settings. The dose response appeared to be linear at low to moderate doses, but in one study there was some suggestion of a reduction in risk above 5 Gy. The elevated risk for benign tumors continues for decades after exposure. Considerably less consistent findings are available regarding functional thyroid diseases including autoimmune diseases. In general, associations for these outcomes were fairly weak, and significant radiation effects were most often observed after high doses, particularly for hypothyroidism. A significant radiation dose response relationship was demonstrated for benign nodules and follicular adenomas. The effects of radiation on functional thyroid diseases are less clear, partly due to the greater difficulties encountered in studying these diseases. (C) 2010 by Radiation Research Society
C1 [Brenner, Alina] NCI, Radiat Epidemiol Branch, Div Canc Epidemiol & Genet, NIH, Bethesda, MD 20892 USA.
RP Brenner, A (reprint author), NCI, Radiat Epidemiol Branch, Div Canc Epidemiol & Genet, NIH, Bethesda, MD 20892 USA.
EM brennera@mail.nih.gov
FU United States National Cancer Institute, NIH, DHHS
FX This work was supported by the Intramural Research Program of the United
   States National Cancer Institute, NIH, DHHS.
NR 75
TC 16
Z9 16
U1 2
U2 3
PU RADIATION RESEARCH SOC
PI LAWRENCE
PA 810 E TENTH STREET, LAWRENCE, KS 66044 USA
SN 0033-7587
EI 1938-5404
J9 RADIAT RES
JI Radiat. Res.
PD DEC
PY 2010
VL 174
IS 6
BP 877
EP 888
DI 10.1667/RR1953.1
PN 2
PG 12
WC Biology; Biophysics; Radiology, Nuclear Medicine & Medical Imaging
SC Life Sciences & Biomedicine - Other Topics; Biophysics; Radiology,
   Nuclear Medicine & Medical Imaging
GA 690TR
UT WOS:000285031600011
PM 21128812
ER

PT J
AU Stanko, JP
   Enoch, RR
   Rayner, JL
   Davis, CC
   Wolf, DC
   Malarkey, DE
   Fenton, SE
AF Stanko, Jason P.
   Enoch, Rolondo R.
   Rayner, Jennifer L.
   Davis, Christine C.
   Wolf, Douglas C.
   Malarkey, David E.
   Fenton, Suzanne E.
TI Effects of prenatal exposure to a low dose atrazine metabolite mixture
   on pubertal timing and prostate development of male Long-Evans rats
SO REPRODUCTIVE TOXICOLOGY
LA English
DT Article
DE Atrazine; Puberty; Prostate; Inflammation; Development; Rat;
   Metabolites; Mixture
ID MAMMARY-GLAND DEVELOPMENT; FEMALE WISTAR RATS; THYROID-FUNCTION;
   GESTATIONAL EXPOSURE; OVARIAN-FUNCTION; SPRAGUE-DAWLEY; UNITED-STATES;
   IN-UTERO; PITUITARY; ANDROGEN
AB The present study examines the postnatal reproductive development of male rats following prenatal exposure to an atrazine metabolite mixture (AMM) consisting of the herbicide atrazine and its environmental metabolites diaminochlorotriazine hydroxyatrazine deethylatrazine and deisopropylatrazine Pregnant Long-Evans rats were treated by gavage with 0 09 0 87 or 8 73 mg AMM/kg body weight (BW) vehicle or 100 mg ATR/kg BW positive control on gestation days 15-19 Preputial separation was significantly delayed in 0 87 mg and 8 73 mg AMM-exposed males AMM-exposed males demonstrated a significant treatment-related increase in incidence and severity of inflammation in the prostate on postnatal day (PND) 120 A dose-dependent increase in epididymal fat masses and prostate foci were grossly visible in AMM-exposed offspring These results indicate that a short late prenatal exposure to mixture of chlorotriazine metabolites can cause chronic prostatitis in male LE rats The mode of action for these effects is presently unclear Published by Elsevier Inc
C1 [Stanko, Jason P.; Fenton, Suzanne E.] US EPA, Reprod Toxicol Div, ORD NHEERL, Res Triangle Pk, NC 27711 USA.
   [Davis, Christine C.] US EPA, Hlth & Environm Impacts Div, OAR OAQPS, Res Triangle Pk, NC 27711 USA.
   [Wolf, Douglas C.] US EPA, ORD, Res Triangle Pk, NC 27711 USA.
   [Enoch, Rolondo R.] N Carolina Cent Univ, Dept Biol, Durham, NC 27707 USA.
   [Rayner, Jennifer L.] Univ N Carolina, Dept Environm Sci & Engn, Chapel Hill, NC 27599 USA.
   [Fenton, Suzanne E.] NIEHS, NIH, NTP, CMPB, Res Triangle Pk, NC 27709 USA.
RP Fenton, SE (reprint author), NIEHS, NIH, NTP, CMPB, 111 TW Alexander Dr,MD E1 08, Res Triangle Pk, NC 27709 USA.
FU U S EPA/NCCU [CT829460]; North Carolina Central University Durham [NC
   27707]; U S EPA NHEERL-DESE [CT826513]; University of North Carolina
   Chapel Hill [NC 27599]; U S Environmental Protection Agency; Division of
   Intramural Research of the NIH National Institute of Environmental
   Health Sciences
FX Financial support for Rolondo Enoch by U S EPA/NCCU Cooperative Research
   Training Grant No CT829460 North Carolina Central University Durham NC
   27707 and for Jennifer Rayner by U S EPA NHEERL-DESE Cooperative
   Training Agreement No CT826513 University of North Carolina Chapel Hill
   NC 27599 The U S Environmental Protection Agency and the Division of
   Intramural Research of the NIH National Institute of Environmental
   Health Sciences have funded the studies in this document The contents do
   not necessarily reflect the views of the Agency or the Institute nor
   does mention of trade names or commercial products constitute
   endorsement or recommendation for use Portions of these data were
   presented at the Society for the Study of Reproduction meeting in San
   Antonio TX July 2007
NR 46
TC 19
Z9 22
U1 2
U2 12
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0890-6238
J9 REPROD TOXICOL
JI Reprod. Toxicol.
PD DEC
PY 2010
VL 30
IS 4
BP 540
EP 549
DI 10.1016/j.reprotox.2010.07.006
PG 10
WC Reproductive Biology; Toxicology
SC Reproductive Biology; Toxicology
GA 690VI
UT WOS:000285036300005
PM 20727709
ER

PT J
AU Rider, LG
   Wu, L
   Mamyrova, G
   Targoff, IN
   Miller, FW
AF Rider, Lisa G.
   Wu, Lan
   Mamyrova, Gulnara
   Targoff, Ira N.
   Miller, Frederick W.
CA Childhood Myositis Heterogeneity C
TI Environmental factors preceding illness onset differ in phenotypes of
   the juvenile idiopathic inflammatory myopathies
SO RHEUMATOLOGY
LA English
DT Article
DE Juvenile myositis; Environmental factor; Phenotype; Myositis
   autoantibody; Infection; Medication
ID TRANSFER RNA-SYNTHETASES; CUTANEOUS PHOTOSENSITIVITY;
   RHEUMATOID-ARTHRITIS; GENE POLYMORPHISMS; TOXIC MYOPATHIES;
   RISK-FACTORS; DERMATOMYOSITIS; AUTOANTIBODIES; DISEASE; CHILDREN
AB Methods. Physicians completed questionnaires regarding documented infections, medications, immunizations and an open-ended question about other noted exposures within 6 months before illness onset for 285 patients with probable or definite JIIM. Medical records were reviewed for 81% of the patients. Phenotypes were defined by standard clinical and laboratory measures.
   Results. Sixty per cent of JIIM patients had a reported exposure within 6 months before illness onset. Most patients (62%) had one recorded exposure, 26% had two and 12% had three to five exposures. Patients older than the median age at diagnosis, those with a longer delay to diagnosis and those with anti-signal recognition particle autoantibodies had a higher frequency of documented exposures [odds ratios (ORs) 95% CI 3.4, 31]. Infections were the most common exposure and represented 44% of the total number of reported exposures. Non-infectious exposures included medications (18%), immunizations (11%), stressful life events (11%) and unusual sun exposure (7%). Exposures varied by age at diagnosis, race, disease course and the presence of certain myositis autoantibodies.
   Conclusion. The JIIMs may be related to multiple exposures and these appear to vary among phenotypes.
C1 [Rider, Lisa G.; Wu, Lan; Mamyrova, Gulnara; Miller, Frederick W.] NIEHS, Environm Autoimmun Grp, NIH, DHHS, Bethesda, MD 20892 USA.
   [Targoff, Ira N.] Univ Oklahoma, Hlth Sci Ctr, Vet Affairs Med Ctr, Oklahoma City, OK USA.
   [Targoff, Ira N.] Univ Oklahoma, Hlth Sci Ctr, Oklahoma Med Res Fdn, Oklahoma City, OK USA.
RP Rider, LG (reprint author), Natl Inst Environm Sci, Environm Autoimmun Grp, NIH, DHHS,Clin Res Ctr, Room 4-2352,10 Ctr Dr,MSC 1301, Bethesda, MD 20892 USA.
EM riderl@mail.nih.gov
OI Rider, Lisa/0000-0002-6912-2458; Miller, Frederick/0000-0003-2831-9593
FU National Institute of Environmental Health Sciences, National Institutes
   of Health [ES101074-08]; Center for Biologics Evaluation and Research,
   Food and Drug Administration; Cure JM Foundation; Myositis Association
FX This work was supported in part by the Intramural Research Programs of
   National Institute of Environmental Health Sciences, National Institutes
   of Health (project number ES101074-08) and Center for Biologics
   Evaluation and Research, Food and Drug Administration. G. M. was
   supported by the Cure JM Foundation and The Myositis Association. I.N.T.
   is a consultant to the Oklahoma Medical Research Foundation Clinical
   Immunology Laboratory.
NR 45
TC 15
Z9 15
U1 0
U2 2
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 1462-0324
J9 RHEUMATOLOGY
JI RHEUMATOLOGY
PD DEC
PY 2010
VL 49
IS 12
BP 2381
EP 2390
DI 10.1093/rheumatology/keq277
PG 10
WC Rheumatology
SC Rheumatology
GA 682WD
UT WOS:000284432800022
PM 20802007
ER

PT J
AU Abdi, K
   Singh, NJ
AF Abdi, K.
   Singh, N. J.
TI Antigen-Activated T Cells Induce IL-12p75 Production from Dendritic
   Cells in an IFN-gamma-Independent Manner
SO SCANDINAVIAN JOURNAL OF IMMUNOLOGY
LA English
DT Article
ID INTERFERON-GAMMA; INNATE RESISTANCE; ADAPTIVE IMMUNITY; HUMAN MONOCYTES;
   HELPER-CELLS; INTERLEUKIN-12; P35; EXPRESSION; CYTOKINE; REQUIRES
AB The addition of IL-12p75 to naive CD4(+) T cells promotes their differentiation towards a T(H)1-type cytokine pattern. Dendritic cells stimulated by LPS generate IL-12p75, but only if the environment also contains IFN-gamma. Thus, it appears that IFN-gamma is needed to start the response that will result in further production of IFN-gamma. We previously reported that paradoxically DCs produce IL-12p75 only after engaging primed, but not naive T cells. This study examines the mechanism by which primed T cells trigger IL-12p75 secretion and asks whether this induction is also dependent on the presence of IFN-gamma. Here, we show that, in contrast to LPS, primed T cells induce IL-12p75 in an IFN-gamma-independent manner. Addition of rIFN-gamma to cocultures of naive T cells with DCs did not induce IL-12p75. Moreover, antigen-activated CD4(+) T cells from wild type or IFN-gamma-deficient mice both initiated IL-12p75 production from DCs. Surprisingly, we found that synergies between three T-cell-derived factors - CD40 Ligand, IL-4 and GM-CSF - were necessary and sufficient for IL-12p75 production. These results suggest that there are at least two distinct pathways for IL-12p75 production in vivo. Furthermore, the T-cell-dependent pathway of IL-12p75 production employs molecules that are not classically associated with a T(H)1-type response.
C1 [Abdi, K.; Singh, N. J.] NIAID, Lab Cellular & Mol Immunol, NIH, Bethesda, MD 20892 USA.
RP Abdi, K (reprint author), NIAID, Lab Cellular & Mol Immunol, NIH, 9000 Rockville Pike,Bldg 4,Room 111,Msc 0420, Bethesda, MD 20892 USA.
EM kabdi@niaid.nih.gov
FU NIAID, NIH
FX We thank Dr Ronald Schwartz for critical review of the manuscript. We
   would also like to thank Dr Polly Matzinger for discussion and also her
   support, which made this work possible. This work was entirely supported
   by the intramural program of the NIAID, NIH.
NR 31
TC 6
Z9 7
U1 0
U2 0
PU WILEY-BLACKWELL PUBLISHING, INC
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0300-9475
J9 SCAND J IMMUNOL
JI Scand. J. Immunol.
PD DEC
PY 2010
VL 72
IS 6
BP 511
EP 521
DI 10.1111/j.1365-3083.2010.02467.x
PG 11
WC Immunology
SC Immunology
GA 677LE
UT WOS:000283993100005
PM 21044125
ER

PT J
AU Subrahmanyam, R
   Sen, R
AF Subrahmanyam, Ramesh
   Sen, Ranjan
TI RAGs' eye view of the immunoglobulin heavy chain gene locus
SO SEMINARS IN IMMUNOLOGY
LA English
DT Review
DE Immunoglobulin; Enhancer; Accessibility; Epigenetics
ID B-CELL DIFFERENTIATION; V-H GENE; I HYPERSENSITIVE SITES; TCR-BETA
   LOCUS; V(D)J RECOMBINATION; ALLELIC EXCLUSION; INTRONIC ENHANCER; PRE-B;
   TARGETED DELETION; VARIABLE REGION
AB The immunoglobulin heavy chain (IgH) gene locus is activated at a precise stage of B lymphocyte development to undergo gene rearrangements that assemble the functional gene. In this review we summarize our current understanding of the chromatin state of the IgH as it appears just prior to the initiation of V(D)J recombination, and the implications of this structure for regulation of recombination. We also examine the role of the intron enhancer, E mu, in establishing the pre-rearrangement chromatin structure. The emerging picture shows that the IgH locus consists of independently regulated domains, each of which requires multiple levels of epigenetic changes to reach the fully activated state. (C) 2010 Published by Elsevier Ltd.
C1 [Subrahmanyam, Ramesh; Sen, Ranjan] NIA, Gene Regulat Sect, Lab Cellular & Mol Biol, NIH, Baltimore, MD 21224 USA.
RP Sen, R (reprint author), NIA, Gene Regulat Sect, Lab Cellular & Mol Biol, NIH, 251 Bayview Blvd,Room 06C214, Baltimore, MD 21224 USA.
EM ranjan.sen@nih.gov
RI Subrahmanyam, Ramesh/K-5503-2012
FU National Institute on Aging (Baltimore, MD)
FX We thank Valerie Martin for editorial assistance. The authors are
   supported by the Intramural Research Program of the National Institute
   on Aging (Baltimore, MD).
NR 110
TC 12
Z9 12
U1 0
U2 2
PU ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
PI LONDON
PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
SN 1044-5323
J9 SEMIN IMMUNOL
JI Semin. Immunol.
PD DEC
PY 2010
VL 22
IS 6
BP 337
EP 345
DI 10.1016/j.smim.2010.08.003
PG 9
WC Immunology
SC Immunology
GA 686UN
UT WOS:000284721800005
PM 20864355
ER

PT J
AU Alexander, HR
   Pacak, K
AF Alexander, H. Richard, Jr.
   Pacak, Karel
TI Introduction: Endocrine Cancers
SO SEMINARS IN ONCOLOGY
LA English
DT Editorial Material
C1 [Alexander, H. Richard, Jr.] Univ Maryland, Sch Med, Dept Surg, Baltimore, MD 21201 USA.
   [Pacak, Karel] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Sect Med Neuroendocrinol, NIH, Bethesda, MD USA.
RP Alexander, HR (reprint author), Univ Maryland, Sch Med, Dept Surg, Baltimore, MD 21201 USA.
FU Intramural NIH HHS [Z01 HD008735-08]
NR 0
TC 0
Z9 0
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 2010
VL 37
IS 6
BP 556
EP 556
DI 10.1053/j.seminoncol.2010.10.009
PG 1
WC Oncology
SC Oncology
GA 700WT
UT WOS:000285775700003
PM 21167374
ER

PT J
AU Sharretts, JM
   Kebebew, E
   Simonds, WF
AF Sharretts, John M.
   Kebebew, Electron
   Simonds, William F.
TI Parathyroid Cancer
SO SEMINARS IN ONCOLOGY
LA English
DT Review
ID JAW TUMOR SYNDROME; FAMILIAL ISOLATED HYPERPARATHYROIDISM; ENDOCRINE
   NEOPLASIA TYPE-1; HRPT2 GENE; DIFFERENTIAL EXPRESSION; GERMLINE
   MUTATION; HEREDITARY HYPERPARATHYROIDISM; PARAFIBROMIN IMMUNOREACTIVITY;
   ENCODING PARAFIBROMIN; PULMONARY METASTASIS
C1 [Sharretts, John M.; Simonds, William F.] NIDDKD, Metab Dis Branch, NIH, Bethesda, MD 20892 USA.
   [Kebebew, Electron] NCI, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
RP Simonds, WF (reprint author), NIDDKD, Metab Dis Branch, NIH, Bldg 10,Room 8C-101,10 Ctr Dr,MSC 1752, Bethesda, MD 20892 USA.
EM wfs@helix.nih.gov
FU National Institute of Diabetes and Digestive and Kidney Diseases;
   National Cancer Institute
FX The Intramural Research Programs of the National Institute of Diabetes
   and Digestive and Kidney Diseases and the National Cancer Institute
   supported this research.
NR 121
TC 29
Z9 31
U1 0
U2 1
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 2010
VL 37
IS 6
BP 580
EP 590
DI 10.1053/j.seminoncol.2010.10.013
PG 11
WC Oncology
SC Oncology
GA 700WT
UT WOS:000285775700006
PM 21167377
ER

PT J
AU Balasubramaniam, S
   Fojo, T
AF Balasubramaniam, Sanjeeve
   Fojo, Tito
TI Practical Considerations in the Evaluation and Management of
   Adrenocortical Cancer
SO SEMINARS IN ONCOLOGY
LA English
DT Review
ID ADRENAL-CORTICAL CARCINOMA; POSITRON-EMISSION-TOMOGRAPHY;
   SOUTHWEST-ONCOLOGY-GROUP; LONG-TERM SURVIVAL; PHASE-II TRIAL; ADJUNCTIVE
   TREATMENT; COMPUTED-TOMOGRAPHY; MOLECULAR MARKERS; ADJUVANT MITOTANE;
   PLUS MITOTANE
C1 [Balasubramaniam, Sanjeeve; Fojo, Tito] NCI, Med Oncol Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
RP Fojo, T (reprint author), NCI, Med Oncol Branch, Ctr Canc Res, NIH, Bldg 10,Room 12N226,9000 Rockville Pike, Bethesda, MD 20892 USA.
EM fojot@mail.nih.gov
OI Balasubramaniam, Sanjeeve/0000-0002-0643-2117
NR 53
TC 14
Z9 15
U1 0
U2 2
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 0093-7754
J9 SEMIN ONCOL
JI Semin. Oncol.
PD DEC
PY 2010
VL 37
IS 6
BP 619
EP 626
DI 10.1053/j.seminoncol.2010.10.011
PG 8
WC Oncology
SC Oncology
GA 700WT
UT WOS:000285775700009
PM 21167380
ER

PT J
AU Fliedner, SMJ
   Lehnert, H
   Pacak, K
AF Fliedner, Stephanie M. J.
   Lehnert, Hendrik
   Pacak, Karel
TI Metastatic Paraganglioma
SO SEMINARS IN ONCOLOGY
LA English
DT Review
ID POSITRON-EMISSION-TOMOGRAPHY; SOMATOSTATIN RECEPTOR SUBTYPES; GLAND
   SCALED SCORE; B GENE-MUTATIONS; MALIGNANT PHEOCHROMOCYTOMA;
   SUCCINATE-DEHYDROGENASE; NECK PARAGANGLIOMAS; SDH MUTATIONS;
   ADRENAL-GLAND; PHASE-II
C1 [Fliedner, Stephanie M. J.; Pacak, Karel] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Program Reprod & Adult Endocrinol, NIH, Bethesda, MD USA.
   [Lehnert, Hendrik] Univ Lubeck, Dept Med 1, Lubeck, Germany.
RP Pacak, K (reprint author), NICHD, Reprod & Adult Endocrinol Program, NIH, Bldg 10,CRC,1 East,Room 1-3140,10 Ctr Dr,MSC 1109, Bethesda, MD 20892 USA.
EM karel@mail.nih.gov
RI Fliedner, Stephanie/D-3406-2012
FU Eunice Kennedy Shriver National Institute of Child Health and Human
   Development, National Institutes of Health, Bethesda, MD
FX Funding was provided by the Eunice Kennedy Shriver National Institute of
   Child Health and Human Development, National Institutes of Health,
   Bethesda, MD.
NR 111
TC 26
Z9 27
U1 1
U2 4
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 0093-7754
EI 1532-8708
J9 SEMIN ONCOL
JI Semin. Oncol.
PD DEC
PY 2010
VL 37
IS 6
BP 627
EP 637
DI 10.1053/j.seminoncol.2010.10.017
PG 11
WC Oncology
SC Oncology
GA 700WT
UT WOS:000285775700010
PM 21167381
ER

PT J
AU Carrasquillo, JA
   Chen, CC
AF Carrasquillo, Jorge A.
   Chen, Clara C.
TI Molecular Imaging of Neuroendocrine Tumors
SO SEMINARS IN ONCOLOGY
LA English
DT Review
ID SOMATOSTATIN RECEPTOR SCINTIGRAPHY; POSITRON-EMISSION-TOMOGRAPHY;
   MEDULLARY-THYROID CARCINOMA; MERKEL CELL-CARCINOMA; DIGESTIVE ENDOCRINE
   TUMORS; ELEVATED CALCITONIN LEVELS; ZOLLINGER-ELLISON-SYNDROME;
   LYMPH-NODE METASTASES; F-18-FDG PET-CT; FDG-PET
C1 [Carrasquillo, Jorge A.] Radiol Dept Mem Sloan Kettering, Nucl Med Serv, New York, NY USA.
   [Carrasquillo, Jorge A.] Weill Cornell Med Cente, Dept Radiol, New York, NY USA.
   [Chen, Clara C.] NIH, Dept Radiol & Imaging Sci, Ctr Clin, Bethesda, MD 20892 USA.
RP Chen, CC (reprint author), 1275 York Ave, New York, NY 10065 USA.
EM carrasj1@mskcc.org
OI Carrasquillo, Jorge/0000-0002-8513-5734
FU Intramural NIH HHS [Z99 CL999999]
NR 179
TC 20
Z9 22
U1 2
U2 10
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
EI 1532-8708
J9 SEMIN ONCOL
JI Semin. Oncol.
PD DEC
PY 2010
VL 37
IS 6
BP 662
EP 679
DI 10.1053/j.seminoncol.2010.10.015
PG 18
WC Oncology
SC Oncology
GA 700WT
UT WOS:000285775700013
PM 21167384
ER

PT J
AU Lodish, MB
   Stratakis, CA
AF Lodish, Maya B.
   Stratakis, Constantine A.
TI Rare and Unusual Endocrine Cancer Syndromes With Mutated Genes
SO SEMINARS IN ONCOLOGY
LA English
DT Review
ID FAMILIAL ADENOMATOUS POLYPOSIS; MACRONODULAR ADRENOCORTICAL DISEASE;
   PANCREATIC NEUROENDOCRINE TUMORS; NEUROFIBROMATOSIS TYPE-1 GENE;
   BECKWITH-WIEDEMANN-SYNDROME; TUBEROUS SCLEROSIS COMPLEX;
   CARNEY-STRATAKIS-SYNDROME; GASTRIC STROMAL SARCOMA;
   PEUTZ-JEGHERS-SYNDROME; LI-FRAUMENI-SYNDROME
C1 [Lodish, Maya B.; Stratakis, Constantine A.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Sect Endocrinol Genet, Program Dev Endocrinol Genet SEGDEN, Pediat Endocrinol Interinst Training Program,NIH, Bethesda, MD USA.
RP Lodish, MB (reprint author), 10 Ctr Dr,CRC Room 1-3330, Bethesda, MD 20892 USA.
EM lodishma@mail.nih.go
FU Eunice Kennedy Shriver NICHD Intramural Research of the National
   Institutes of Health
FX This work was supported by the Eunice Kennedy Shriver NICHD Intramural
   Research of the National Institutes of Health.
NR 122
TC 3
Z9 3
U1 1
U2 2
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 0093-7754
EI 1532-8708
J9 SEMIN ONCOL
JI Semin. Oncol.
PD DEC
PY 2010
VL 37
IS 6
BP 680
EP 690
DI 10.1053/j.seminoncol.2010.10.019
PG 11
WC Oncology
SC Oncology
GA 700WT
UT WOS:000285775700014
PM 21167385
ER

PT J
AU Horn, ME
   Landesman, B
   McFadden, TG
   Prieto, AG
   Rosenblatt, S
   Malinowski, T
AF Horn, Marguerite E.
   Landesman, Betty
   McFadden, T. G.
   Prieto, Adolfo G.
   Rosenblatt, Stephanie
   Malinowski, Teresa
TI Metadata
SO SERIALS REVIEW
LA English
DT Review
AB Marguerite E Horn reviews Metadata Betty Landesman reviews Content Licensing T G McFadden reviews This Book Is Overdue(1) Adolfo G Prieto reviews The Back Page and Stephanie Rosenblatt reviews Teaching Generation M Serials Review 2010 36 271-277 (C) 2010 Elsevier Inc All rights reserved
C1 [Horn, Marguerite E.] SUNY Albany, Lib Data & Syst Analyst, Off Lib & Informat Serv Syst Adm, Albany, NY 12246 USA.
   [Landesman, Betty] NIH Lib, Bethesda, MD 20892 USA.
   [McFadden, T. G.] Union Coll, Schaffer Lib, Schenectady, NY 12308 USA.
   [Prieto, Adolfo G.; Rosenblatt, Stephanie; Malinowski, Teresa] Calif State Univ Fullerton, Pollak Lib, Fullerton, CA 92834 USA.
RP Horn, ME (reprint author), SUNY Albany, Lib Data & Syst Analyst, Off Lib & Informat Serv Syst Adm, Albany, NY 12246 USA.
NR 6
TC 0
Z9 0
U1 1
U2 4
PU ELSEVIER INC
PI SAN DIEGO
PA 525 B STREET, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0098-7913
J9 SERIALS REV
JI Ser. Rev.
PD DEC
PY 2010
VL 36
IS 4
BP 271
EP 277
DI 10.1016/j.serrev.2010.08.012
PG 7
WC Information Science & Library Science
SC Information Science & Library Science
GA 690FY
UT WOS:000284989100010
ER

PT J
AU Marrazzo, JM
   Martin, DH
   Watts, DH
   Schulte, J
   Sobel, JD
   Hillier, SL
   Deal, C
   Fredricks, DN
AF Marrazzo, Jeanne M.
   Martin, David H.
   Watts, D. Heather
   Schulte, Joann
   Sobel, Jack D.
   Hillier, Sharon L.
   Deal, Carolyn
   Fredricks, David N.
TI Bacterial Vaginosis: Identifying Research Gaps Proceedings of a Workshop
   Sponsored by DHHS/NIH/NIAID
SO SEXUALLY TRANSMITTED DISEASES
LA English
DT Article
ID PELVIC-INFLAMMATORY-DISEASE; SEXUALLY-TRANSMITTED-DISEASE;
   IMMUNODEFICIENCY-VIRUS TYPE-1; VAGINAL FLORA; RISK-FACTORS;
   GARDNERELLA-VAGINALIS; INFECTED WOMEN; METRONIDAZOLE THERAPY; PRETERM
   PREDICTION; QUANTITATIVE PCR
AB The microbiota of the human vagina can affect the health of women, their fetuses, and newborns. Bacterial vaginosis (BV) is the most prevalent form of vaginal infection in women of reproductive age, affecting 8% to 23%, and is the most common etiology of vaginal symptoms prompting women to seek medical care. While traditional cultivation has identified numerous BV-associated bacteria involved in these processes, recent advances in molecular biology have facilitated the detection and identification of bacteria without cultivation, some of which have not previously been described or well characterized. A more complete understanding of vaginal microbial populations resulting from the adoption of molecular tools may lead to better strategies to maintain healthy vaginal microbial communities-thus enhancing women's health-and will create opportunities to explore the role of novel bacteria in reproductive tract diseases. On November 19-20, 2008, the NIH convened a workshop of experts in the field of research and clinical practice related to BV in order to discuss how these new advances should be interpreted and applied to research in progress and collaborations between relevant disciplines. This paper summarizes the presentations of this workshop and outlines general recommendations arising from the related discussions. Future studies of BV and its associated adverse outcomes should determine if specific combinations of organisms are more pathogenic than others, and causally associated with different adverse events. Moreover, determination of causality will depend not only on more precise categorization of the vaginal microbiota, but also on variations in the host environment that may be associated with changes in bacterial communities over time. In this report, we offer suggestions and recommendations that we hope will facilitate conduct of consistent approaches to collaborative efforts towards advancing our understanding of the vaginal microbiota and its impact on human health.
C1 [Marrazzo, Jeanne M.] Univ Washington, Harborview Med Ctr, Div Infect Dis, Seattle, WA 98104 USA.
   [Martin, David H.] Louisiana State Univ, Div Infect Dis, New Orleans, LA USA.
   [Watts, D. Heather] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Bethesda, MD USA.
   [Schulte, Joann; Deal, Carolyn] NIAID, Bethesda, MD 20892 USA.
   [Hillier, Sharon L.] Magee Womens Res Inst, Pittsburgh, PA USA.
   [Sobel, Jack D.] Wayne State Univ, Detroit, MI USA.
   [Fredricks, David N.] Fred Hutchinson Canc Res Ctr, Seattle, WA 98104 USA.
RP Marrazzo, JM (reprint author), Univ Washington, Harborview Med Ctr, Div Infect Dis, 325 9th Ave,Mailbox 359932, Seattle, WA 98104 USA.
EM jmm2@uw.edu
OI Marrazzo, Jeanne/0000-0002-9277-7364
FU National Institute of Allergy and Infectious Diseases
FX Supported by National Institute of Allergy and Infectious Diseases.
NR 84
TC 43
Z9 45
U1 0
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0148-5717
J9 SEX TRANSM DIS
JI Sex. Transm. Dis.
PD DEC
PY 2010
VL 37
IS 12
BP 732
EP 744
DI 10.1097/OLQ.0b013e3181fbbc95
PG 13
WC Infectious Diseases
SC Infectious Diseases
GA 682DS
UT WOS:000284380700001
PM 21068695
ER

PT J
AU Bernard, HR
   Hallett, T
   Iovita, A
   Johnsen, EC
   Lyerla, R
   McCarty, C
   Mahy, M
   Salganik, MJ
   Saliuk, T
   Scutelniciuc, O
   Shelley, GA
   Sirinirund, P
   Weir, S
   Stroup, DF
AF Bernard, H. Russell
   Hallett, Tim
   Iovita, Alexandrina
   Johnsen, Eugene C.
   Lyerla, Rob
   McCarty, Christopher
   Mahy, Mary
   Salganik, Matthew J.
   Saliuk, Tetiana
   Scutelniciuc, Otilia
   Shelley, Gene A.
   Sirinirund, Petchsri
   Weir, Sharon
   Stroup, Donna F.
TI Counting hard-to-count populations: the network scale-up method for
   public health
SO SEXUALLY TRANSMITTED INFECTIONS
LA English
DT Article
ID PERSONAL NETWORK; UNITED-STATES; HIV STATUS; SIZE; PEOPLE;
   SEROPREVALENCE; BEHAVIOR; KNOWS
AB Estimating sizes of hidden or hard-to-reach populations is an important problem in public health. For example, estimates of the sizes of populations at highest risk for HIV and AIDS are needed for designing, evaluating and allocating funding for treatment and prevention programmes. A promising approach to size estimation, relatively new to public health, is the network scale-up method (NSUM), involving two steps: estimating the personal network size of the members of a random sample of a total population and, with this information, estimating the number of members of a hidden subpopulation of the total population. We describe the method, including two approaches to estimating personal network sizes (summation and known population). We discuss the strengths and weaknesses of each approach and provide examples of international applications of the NSUM in public health. We conclude with recommendations for future research and evaluation.
C1 [Stroup, Donna F.] Data Solut Inc, Decatur, GA 30031 USA.
   [Bernard, H. Russell] Univ Florida, Dept Anthropol, Gainesville, FL 32611 USA.
   [Hallett, Tim] Univ London Imperial Coll Sci Technol & Med, Sch Publ Hlth, Dept Infect Dis Epidemiol, London, England.
   [Iovita, Alexandrina] UNAIDS, Kishinev, Moldova.
   [Johnsen, Eugene C.] Univ Calif Santa Barbara, Dept Math, Santa Barbara, CA 93106 USA.
   [Lyerla, Rob] NIH, Fogarty Int Ctr, Bethesda, MD 20892 USA.
   [McCarty, Christopher] Univ Florida, Bur Econ & Business Res, Gainesville, FL USA.
   [Mahy, Mary] UNAIDS, Div Monitoring & Evaluat, Geneva, Switzerland.
   [Salganik, Matthew J.] Princeton Univ, Dept Sociol, Princeton, NJ 08544 USA.
   [Salganik, Matthew J.] Princeton Univ, Off Populat Res, Princeton, NJ 08544 USA.
   [Saliuk, Tetiana] Natl Univ Kiev Mohyla Acad, Sch Publ Hlth, Kiev, Ukraine.
   [Saliuk, Tetiana] Natl Univ Kiev Mohyla Acad, Int HIV AIDS Alliance, Kiev, Ukraine.
   [Scutelniciuc, Otilia] Natl Ctr Hlth Management, Kishinev, Moldova.
   [Shelley, Gene A.] Georgia State Univ, Sch Publ Hlth, Atlanta, GA 30303 USA.
   [Sirinirund, Petchsri] Minist Publ Hlth, Bangkok, Thailand.
   [Weir, Sharon] Univ N Carolina, Dept Epidemiol, Chapel Hill, NC USA.
   [Weir, Sharon] Univ N Carolina, Carolina Populat Ctr, Chapel Hill, NC USA.
RP Stroup, DF (reprint author), Data Solut Inc, POB 894, Decatur, GA 30031 USA.
EM donnafstroup@dataforsolutions.com
RI Hallett, Timothy/A-2390-2011
FU UNAIDS; National Science Foundation; National Institutes of Health
   (NICHD), USA
FX The preparation of this article was partially supported by UNAIDS. Work
   to develop the NSUM method was supported by the National Science
   Foundation. MJS acknowledges funding from the National Institutes of
   Health (NICHD), USA.
NR 33
TC 7
Z9 8
U1 1
U2 5
PU BMJ PUBLISHING GROUP
PI LONDON
PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND
SN 1368-4973
J9 SEX TRANSM INFECT
JI Sex. Transm. Infect.
PD DEC
PY 2010
VL 86
SU 2
BP I11
EP I15
DI 10.1136/sti.2010.044446
PG 5
WC Infectious Diseases
SC Infectious Diseases
GA 684TR
UT WOS:000284572700002
PM 21106509
ER

PT J
AU Peng, KW
AF Peng, Kuo-Wei
TI Having Peace and Making Peace when Peace Is Broken: "Peace" in the
   Gospels
SO SINO-CHRISTIAN STUDIES
LA Chinese
DT Article
DE peace as a state of well-being; peace as a state of concord; prince of
   peace; gospels
AB This article explores the different ways that the theme of "peace" is presented in the Gospels and their relevance to today's world. The discussion starts with the use of the concept of "Prince of Peace" in the Synoptic Gospels and it introduces four different facets of the theme of "peace" revealed in the Gospels: (1) peace as a state of well-being, (2) peace as a state of concord, (3) the breaking of peace caused by the Prince of Peace, and (4) peace as a different kind of state of well-being The article is concluded with the relevance of these four facets of "peace" in the Gospels to today's socio-religious situations, which is the concern of this article.
C1 Amer Bible Soc, Nida Inst Bibl Scholarship, New York, NY USA.
RP Peng, KW (reprint author), Amer Bible Soc, Nida Inst Bibl Scholarship, New York, NY USA.
EM kpeng@americanbible.org
NR 13
TC 0
Z9 0
U1 0
U2 0
PU CHUNG YUAN CHRISTIAN UNIV
PI CHUNG LI
PA 200 CHUNG PEI RD, CHUNG LI, 32023 ROC, TAIWAN
SN 1990-2670
J9 SINO-CHRIST STUD
JI Sino-Christ. Stud.
PD DEC
PY 2010
IS 10
BP 65
EP 80
PG 16
WC Religion
SC Religion
GA 700GR
UT WOS:000285726500003
ER

PT J
AU Knutson, KM
   Krueger, F
   Koenigs, M
   Hawley, A
   Escobedo, JR
   Vasudeva, V
   Adolphs, R
   Grafman, J
AF Knutson, Kristine M.
   Krueger, Frank
   Koenigs, Michael
   Hawley, Angelina
   Escobedo, Jessica R.
   Vasudeva, Viren
   Adolphs, Ralph
   Grafman, Jordan
TI Behavioral norms for condensed moral vignettes
SO SOCIAL COGNITIVE AND AFFECTIVE NEUROSCIENCE
LA English
DT Article
DE moral cognition; moral judgment; norms
ID NEURAL BASIS; DECISION-MAKING; JUDGMENT; MONKEYS; FMRI; COGNITION;
   EMOTIONS; AMYGDALA; LESIONS; MULATTA
AB Moral judgment is an evaluation of the actions and character of a person made with respect to societal norms. Although many types of vignettes have been used in previous studies on moral beliefs and judgment, what is missing is a set of standardized common vignettes based in real life. The goal of this study was to provide researchers with stimuli that have values on several dimensions pertaining to moral judgment and whose underlying components are known. These values will allow researchers to select stimuli based on standardized ratings rather than on the results of pilot studies, while avoiding the limitations of the classic, abstract moral scenarios. Our study was composed of three phases, (i) collecting and shortening the vignettes, (ii) obtaining ratings of the vignettes on several dimensions including emotional intensity, degree of social norm violation, and level of harm or benefit caused and (iii) determining the underlying components of the vignettes by performing a factor analysis. We found three components that accounted for most of the variance: norm violation, social affect and intention. The resulting vignettes can be used in future parametric studies on moral judgment in behavioral, neuropsychological and functional imaging experiments.
C1 [Knutson, Kristine M.; Krueger, Frank; Grafman, Jordan] Natl Inst Neurol Disorders & Stroke, Cognit Neurosci Sect, NIH, Bethesda, MD 20892 USA.
   [Krueger, Frank] George Mason Univ, Krasnow Inst Adv Study, Fairfax, VA 22030 USA.
   [Koenigs, Michael] Univ Wisconsin, Dept Psychiat, Madison, WI 53706 USA.
   [Hawley, Angelina] Boston Coll, Dept Psychol, Chestnut Hill, MA 02167 USA.
   [Escobedo, Jessica R.; Adolphs, Ralph] CALTECH, Emot & Social Cognit Lab, Pasadena, CA 91125 USA.
   [Vasudeva, Viren] Med Coll Georgia, Sch Med, Augusta, GA 30912 USA.
RP Grafman, J (reprint author), Natl Inst Neurol Disorders & Stroke, Cognit Neurosci Sect, NIH, Bldg 10,Room 7D43,MSC 1440,10 Ctr Dr, Bethesda, MD 20892 USA.
EM grafmanj@ninds.nih.gov
OI Grafman, Jordan H./0000-0001-8645-4457; Knutson,
   Kristine/0000-0003-4626-4514; Koenigs, Michael/0000-0002-5799-4881
FU National Institute of Neurological Disorders and Stroke, National
   Institutes of Health
FX This study was supported by the Intramural Research Program of the
   National Institute of Neurological Disorders and Stroke, National
   Institutes of Health.
NR 37
TC 14
Z9 14
U1 1
U2 26
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 1749-5016
J9 SOC COGN AFFECT NEUR
JI Soc. Cogn. Affect. Neurosci.
PD DEC
PY 2010
VL 5
IS 4
BP 378
EP 384
DI 10.1093/scan/nsq005
PG 7
WC Neurosciences; Psychology; Psychology, Experimental
SC Neurosciences & Neurology; Psychology
GA 703VJ
UT WOS:000286009100003
PM 20154053
ER

PT J
AU Marsh, AA
   Kozak, MN
   Wegner, DM
   Reid, ME
   Yu, HH
   Blair, RJR
AF Marsh, Abigail A.
   Kozak, Megan N.
   Wegner, Daniel M.
   Reid, Marguerite E.
   Yu, Henry H.
   Blair, R. J. R.
TI The neural substrates of action identification
SO SOCIAL COGNITIVE AND AFFECTIVE NEUROSCIENCE
LA English
DT Article
DE fMRI; action identification; mentalize; ventral premotor cortex;
   extrastriate body area; amygdale
ID EXTRASTRIATE BODY AREA; TEMPORO-PARIETAL JUNCTION; VENTRAL PREMOTOR
   CORTEX; SOCIAL COGNITION; FACIAL EXPRESSIONS; EMPATHY; MIND; AMYGDALA;
   SYSTEM; BRAIN
AB Mentalization is the process by which an observer views a target as possessing higher cognitive faculties such as goals, intentions and desires. Mentalization can be assessed using action identification paradigms, in which observers choose mentalistic (goals-focused) or mechanistic (action-focused) descriptions of targets' actions. Neural structures that play key roles in inferring goals and intentions from others' observed or imagined actions include temporo-parietal junction, ventral premotor cortex and extrastriate body area. We hypothesized that these regions play a role in action identification as well. Data collected using functional magnetic resonance imaging (fMRI) confirmed our predictions that activity in ventral premotor cortex and middle temporal gyrus near the extrastriate body area varies both as a function of the valence of the target and the extent to which actions are identified as goal-directed. In addition, the inferior parietal lobule is preferentially engaged when participants identify the actions of mentalized targets. Functional connectivity analyses suggest support from other regions, including the medial prefrontal cortex and amygdala, during mentalization. We found correlations between action identification and Autism Quotient scores, suggesting that understanding the neural correlates of action identification may enhance our understanding of the underpinnings of essential social cognitive processes.
C1 [Marsh, Abigail A.] Georgetown Univ, Dept Psychol, Washington, DC 20057 USA.
   [Kozak, Megan N.] Pace Univ, Dept Psychol, New York, NY 10038 USA.
   [Wegner, Daniel M.] Harvard Univ, Dept Psychol, Cambridge, MA 02138 USA.
   [Reid, Marguerite E.; Yu, Henry H.; Blair, R. J. R.] NIMH, Mood & Anxiety Program, Bethesda, MA USA.
RP Marsh, AA (reprint author), Georgetown Univ, Dept Psychol, 37th & O St NW, Washington, DC 20057 USA.
EM aam72@georgetown.edu
FU Intramural Research Program at the National Institute of Mental Health
FX This research was supported by Intramural Research Program at the
   National Institute of Mental Health.
NR 61
TC 17
Z9 17
U1 3
U2 12
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 1749-5016
J9 SOC COGN AFFECT NEUR
JI Soc. Cogn. Affect. Neurosci.
PD DEC
PY 2010
VL 5
IS 4
BP 392
EP 403
DI 10.1093/scan/nsq004
PG 12
WC Neurosciences; Psychology; Psychology, Experimental
SC Neurosciences & Neurology; Psychology
GA 703VJ
UT WOS:000286009100005
PM 20150343
ER

PT J
AU Stover, DG
   Freeman, AF
   Wright, PW
   Hummell, DS
   Ness, RM
AF Stover, Daniel G.
   Freeman, Alexandra F.
   Wright, Patty W.
   Hummell, Donna S.
   Ness, Reid M.
TI Diverticulitis in a Young Man with Hyper-IgE Syndrome
SO SOUTHERN MEDICAL JOURNAL
LA English
DT Article
DE diverticulitis; hyper IgE syndrome; STAT3
ID HYPERIMMUNOGLOBULIN-E SYNDROME; COLON PERFORATION; CROHNS-DISEASE; JOBS
   SYNDROME; PATIENT; MUTATIONS
AB Autosomal dominant hyperimmunoglobulin E syndrome (HIES, or Job syndrome) is a rare primary immunodeficiency characterized by elevated immunoglobulin E (IgE), eosinophilia, recurrent skin and pulmonary infections, dermatitis, and connective tissue and skeletal abnormalities. A 26-year-old male with known HIES presented with abdominal pain and diarrhea. Imaging showed sigmoid diverticulitis without abscess or perforation. Conservative management with antibiotics failed, and he developed a peridiverticular abscess, which was percutaneously drained with plans for elective resection. He returned four days later with progression of his diverticulitis, requiring partial colectomy with primary anastomosis. To our knowledge, this is the first case of diverticulitis in HIES. Diverticulitis is rare in younger individuals, raising the possibility that the connective tissue abnormalities of HIES patients may predispose them to colonic diverticula. Although the majority of complications are sinopulmonary and skin infections, diverticulitis should be considered in the differential of intra-abdominal processes in HIES.
C1 NIAID, Dept Med, Bethesda, MD 20892 USA.
   NIAID, Lab Clin Infect Dis, Bethesda, MD 20892 USA.
   Vanderbilt Univ, Med Ctr, Div Infect Dis, Div Pediat Allergy Immunol & Pulm Med, Nashville, TN USA.
   Vanderbilt Univ, Med Ctr, Div Gastroenterol, Nashville, TN USA.
RP Ness, RM (reprint author), 1660 Vanderbilt Clin, 1301 Med Ctr Dr, Nashville, TN 37232 USA.
EM reid.ness@vanderbilt.edu
OI Stover, Daniel/0000-0001-9003-8165
FU NCCIH NIH HHS [R01 AT004660, R01 AT004660-03]; NCI NIH HHS [P50
   CA095103, P50 CA095103-090004]
NR 13
TC 2
Z9 2
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0038-4348
J9 SOUTH MED J
JI South.Med.J.
PD DEC
PY 2010
VL 103
IS 12
BP 1261
EP 1263
DI 10.1097/SMJ.0b013e3181fa5f0e
PG 3
WC Medicine, General & Internal
SC General & Internal Medicine
GA 684DZ
UT WOS:000284529600020
PM 21037522
ER

PT J
AU Abou-Kheir, WG
   Hynes, PG
   Martin, PL
   Pierce, R
   Kelly, K
AF Abou-Kheir, Wassim G.
   Hynes, Paul G.
   Martin, Philip L.
   Pierce, Rachel
   Kelly, Kathleen
TI Characterizing the Contribution of Stem/Progenitor Cells to
   Tumorigenesis in the Pten(-/-) TP53(-/-) Prostate Cancer Model
SO STEM CELLS
LA English
DT Article
DE PTEN; TP53; Cancer stem cells; Self-renewal; Differentiation; Prostate
ID STEM-CELLS; CELLULAR SENESCENCE; PROXIMAL REGION; SELF-RENEWAL;
   IN-VITRO; P53; DIFFERENTIATION; HETEROGENEITY; EXPRESSION; SUPPRESSION
AB Loss of PTEN is one of the most common mutations in prostate cancer, and loss of wild-type TP53 is associated with prostate cancer progression and castrate resistance. Modeling prostate cancer in the mouse has shown that while Pten deletion in prostate epithelial cells leads to adenocarcinoma, combined loss of Pten and TP53 results in rapidly developing disease with greater tumor burden and early death. TP53 contributes significantly to the regulation of stem cell self-renewal, and we hypothesized that loss of Pten/TP53 would result in measurable changes in prostate cancer stem/progenitor cell properties. Clonogenic assays that isolate progenitor function in primary prostate epithelial cells were used to measure self-renewal, differentiation, and tumorigenic potential. Pten/TP53 null as compared with wild-type protospheres showed increased self-renewal activity and modified lineage commitment. Orthotopic transplantation of Pten/TP53 null cells derived from protospheres produced invasive Prostatic Intraepithelial Neoplasia (PIN)/adenocarcinoma, recapitulating the pathology seen in primary tumors. Pten/TP53 null progenitors relative to wild type also demonstrated increased dependence on the AKT/mammalian target of rapamycin complex 1 (mTORC1) and androgen receptor (AR) pathways for clonogenic and tumorigenic growth. These data demonstrate roles for Pten/TP53 in prostate epithelial stem/progenitor cell function, and moreover, as seen in patients with castrate-resistant prostate cancer, suggest for the involvement of an AR-dependent axis in the clonogenic expansion of prostate cancer stem cells. STEM CELLS 2010; 28: 2129-2140
C1 [Abou-Kheir, Wassim G.; Hynes, Paul G.; Martin, Philip L.; Pierce, Rachel; Kelly, Kathleen] NCI, Cell & Canc Biol Branch, NIH, Bethesda, MD 20892 USA.
RP Kelly, K (reprint author), NCI, Cell & Canc Biol Branch, NIH, 37 Convent Dr,Room 1068, Bethesda, MD 20892 USA.
EM kellyka@mail.nih.gov
FU NIH, National Cancer Institute, Center for Cancer Research, USA
FX We acknowledge the support of the Intramural Research Program of the
   NIH, National Cancer Institute, Center for Cancer Research, USA. P. L.
   M. is currently affiliated with the Center for Advanced Preclinical
   Research, SAIC-NCI, Frederick, Maryland, USA.
NR 31
TC 20
Z9 20
U1 0
U2 5
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1066-5099
J9 STEM CELLS
JI Stem Cells
PD DEC
PY 2010
VL 28
IS 12
BP 2129
EP 2140
DI 10.1002/stem.538
PG 12
WC Cell & Tissue Engineering; Biotechnology & Applied Microbiology;
   Oncology; Cell Biology; Hematology
SC Cell Biology; Biotechnology & Applied Microbiology; Oncology; Hematology
GA 700LK
UT WOS:000285742700003
PM 20936707
ER

PT J
AU Kim, DH
   Vanella, L
   Inoue, K
   Burgess, A
   Gotlinger, K
   Manthati, VL
   Koduru, SR
   Zeldin, DC
   Falck, JR
   Schwartzman, ML
   Abraham, NG
AF Kim, Dong Hyun
   Vanella, Luca
   Inoue, Kazuyoshi
   Burgess, Angela
   Gotlinger, Katherine
   Manthati, Vijaya Lingam
   Koduru, Sreenivasulu Reddy
   Zeldin, Darryl C.
   Falck, John R.
   Schwartzman, Michal L.
   Abraham, Nader G.
TI Epoxyeicosatrienoic Acid Agonist Regulates Human Mesenchymal Stem
   Cell-Derived Adipocytes Through Activation of HO-1-pAKT Signaling and a
   Decrease in PPAR gamma
SO STEM CELLS AND DEVELOPMENT
LA English
DT Article
ID IMPROVES INSULIN SENSITIVITY; INCREASES ADIPONECTIN LEVELS; NF-KAPPA-B;
   HEME OXYGENASE-1; EPOXIDE HYDROLASE; ENDOTHELIAL-CELLS;
   ARACHIDONIC-ACID; 11,12-EPOXYEICOSATRIENOIC ACID; EPOXYGENASE
   METABOLITES; HYPERPOLARIZING FACTORS
AB Human mesenchymal stem cells (MSCs) expressed substantial levels of CYP2J2, a major CYP450 involved in epoxyeicosatrienoic acid (EET) formation. MSCs synthesized significant levels of EETs (65.8 +/- 5.8 pg/mg protein) and dihydroxyeicosatrienoic acids (DHETs) (15.83 +/- 1.62 pg/mg protein), suggesting the presence of soluble epoxide hydrolase (sEH). The addition of an sEH inhibitor to MSC culture decreased adipogenesis. EETs decreased MSC-derived adipocytes in a concentration-dependent manner, 8,9- and 14,15-EET having the maximum reductive effect on adipogenesis. We examined the effect of 12-(3-hexylureido) dodec-8(Z)-enoic acid, an EET agonist, on MSC-derived adipocytes and demonstrated an increased number of healthy small adipocytes, attenuated fatty acid synthase (FAS) levels (P < 0.01), and reduced PPAR gamma, C/EBP alpha, FAS, and lipid accumulation (P < 0.05). These effects were accompanied by increased levels of heme oxygenase (HO)-1 and adiponectin (P < 0.05), and increased glucose uptake (P < 0.05). Inhibition of HO activity or AKT by tin mesoporphyrin (SnMP) and LY2940002, respectively, reversed EET-induced inhibition of adipogenesis, suggesting that activation of the HO-1-adiponectin axis underlies EET effect in MSCs. These findings indicate that EETs decrease MSC-derived adipocyte stem cell differentiation by upregulation of HO-1-adiponectin-AKT signaling and play essential roles in the regulation of adipocyte differentiation by inhibiting PPAR gamma, C/EBP alpha, and FAS and in stem cell development. These novel observations highlight the seminal role of arachidonic acid metabolism in MSCs and suggest that an EET agonist may have potential therapeutic use in the treatment of dyslipidemia, diabetes, and the metabolic syndrome.
C1 [Kim, Dong Hyun; Vanella, Luca; Burgess, Angela; Abraham, Nader G.] Univ Toledo, Coll Med, Dept Physiol & Pharmacol, Toledo, OH 43614 USA.
   [Inoue, Kazuyoshi; Gotlinger, Katherine; Schwartzman, Michal L.] New York Med Coll, Dept Pharmacol, Valhalla, NY 10595 USA.
   [Manthati, Vijaya Lingam; Koduru, Sreenivasulu Reddy; Falck, John R.] Univ Texas SW Med Ctr Dallas, Dept Biochem & Pharmacol, Dallas, TX 75390 USA.
   [Zeldin, Darryl C.] NIEHS, Div Intramural Res, NIH, Res Triangle Pk, NC 27709 USA.
RP Abraham, NG (reprint author), Univ Toledo, Coll Med, Dept Physiol & Pharmacol, Toledo, OH 43614 USA.
EM nader.abraham@utoledo.edu
RI Vanella, Luca/J-7354-2016
OI Vanella, Luca/0000-0002-6314-6029
FU NIH [DK068134, HL55601, HL34300]; Robert A. Welch Foundation; NIH,
   National Institute of Environmental Health Sciences [Z01 ES025034];
   Beatrice Renfield Foundation;  [GM31278]
FX This work was supported by NIH grants DK068134, HL55601 (N.G.A.), and
   HL34300 (M.L.S.), and The Robert A. Welch Foundation and GM31278
   (J.R.F.). This research was also supported, in part, by the Intramural
   Research Program of the NIH, National Institute of Environmental Health
   Sciences (Z01 ES025034)(DZ). The authors are indebted to Dr. Attallah
   Kappas and The Beatrice Renfield Foundation for their support.
NR 52
TC 36
Z9 38
U1 0
U2 2
PU MARY ANN LIEBERT INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 1547-3287
J9 STEM CELLS DEV
JI Stem Cells Dev.
PD DEC
PY 2010
VL 19
IS 12
BP 1863
EP 1873
DI 10.1089/scd.2010.0098
PG 11
WC Cell & Tissue Engineering; Hematology; Medicine, Research &
   Experimental; Transplantation
SC Cell Biology; Hematology; Research & Experimental Medicine;
   Transplantation
GA 685KA
UT WOS:000284626400005
PM 20412023
ER

PT J
AU Jones, MB
   Chu, CH
   Pendleton, JC
   Betenbaugh, MJ
   Shiloach, J
   Baljinnyam, B
   Rubin, JS
   Shamblott, MJ
AF Jones, Meredith B.
   Chu, Chia H.
   Pendleton, James C.
   Betenbaugh, Michael J.
   Shiloach, Joseph
   Baljinnyam, Bolormaa
   Rubin, Jeffrey S.
   Shamblott, Michael J.
TI Proliferation and Pluripotency of Human Embryonic Stem Cells Maintained
   on Type I Collagen
SO STEM CELLS AND DEVELOPMENT
LA English
DT Article
ID FRIZZLED-RELATED PROTEIN-1; WNT SIGNALING PATHWAY; SERUM-FREE CULTURE;
   SELF-RENEWAL; UNDIFFERENTIATED GROWTH; DEFINED CONDITIONS;
   GENE-EXPRESSION; MOUSE; PROSTACYCLIN; DIFFERENTIATION
AB Human embryonic stem cells (hESC) require a balance of growth factors and signaling molecules to proliferate and retain pluripotency. Conditioned medium (CM) from a human embryonic germ-cell-derived cell culture, SDEC, was observed to support the growth of hESC on type I collagen (COL I) and on Matrigel (MAT) biomatricies. After 1 month, the population doubling of hESC grown in SDEC CM on COL I was equivalent to that of hESC grown in mouse embryonic fibroblast (MEF) CM on MAT. hESC grown in SDEC CM on COL I expressed OCT4, NANOG, SSEA-4, alkaline phosphatase (AP), and TRA-1-60; retained a normal karyotype; and were capable of forming teratomas. DNA microarray analysis was used to compare the transcriptional profiles of SDEC and the less supportive WI38 and Detroit 551 human cell lines. The mRNA level of secreted frizzled-related protein (sFRP-1), a known antagonist of the WNT/beta-catenin signaling pathway, was significantly reduced in SDEC as compared with the other 2 cell lines, whereas the mRNA levels of prostaglandin-endoperoxide synthase 2 (PTGS2 or COX-2) and prostaglandin I(2) synthase (PGIS), two prostaglandin biosynthesis genes, were significantly increased in SDEC. The level of sFRP-1 protein was significantly reduced, and levels of 2 prostaglandins that are downstream products of PTGS2 and PGIS, prostaglandin E2 and 6-keto-prostaglandin F(1 alpha), were significantly elevated in SDEC CM compared with WI38, Detroit 551, and MEF CM. Further, addition of purified sFRP-1 to SDEC CM reduced the proliferation of hESC grown on COL I as well as MAT in a dose-dependent manner.
C1 [Jones, Meredith B.; Chu, Chia H.; Betenbaugh, Michael J.] Johns Hopkins Univ, Dept Chem & Biomol Engn, Baltimore, MD USA.
   [Chu, Chia H.; Shiloach, Joseph] NIDDK, Bethesda, MD USA.
   [Pendleton, James C.; Shamblott, Michael J.] Johns Hopkins Univ, Sch Med, Hugo W Moser Res Inst Kennedy Krieger, Baltimore, MD USA.
   [Pendleton, James C.; Shamblott, Michael J.] Johns Hopkins Univ, Sch Med, Dept Neurol, Baltimore, MD USA.
   [Baljinnyam, Bolormaa; Rubin, Jeffrey S.] NCI, Bethesda, MD 20892 USA.
RP Shamblott, MJ (reprint author), 707 N Broadway,Suite 520, Baltimore, MD 21205 USA.
EM shamblott@kennedykrieger.org
RI Betenbaugh, Michael J./A-3252-2010
OI Betenbaugh, Michael J./0000-0002-6336-4659
FU Maryland Stem Cell Research Fund [2009MSCRF-E-0081]
FX Funding for the study described in this article was provided by Maryland
   Stem Cell Research Fund Award 2009MSCRF-E-0081.
NR 91
TC 9
Z9 10
U1 0
U2 19
PU MARY ANN LIEBERT INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 1547-3287
J9 STEM CELLS DEV
JI Stem Cells Dev.
PD DEC
PY 2010
VL 19
IS 12
BP 1923
EP 1935
DI 10.1089/scd.2009.0326
PG 13
WC Cell & Tissue Engineering; Hematology; Medicine, Research &
   Experimental; Transplantation
SC Cell Biology; Hematology; Research & Experimental Medicine;
   Transplantation
GA 685KA
UT WOS:000284626400010
PM 20367282
ER

PT J
AU Wallace, AD
   Cao, Y
   Chandramouleeswaran, S
   Cidlowski, JA
AF Wallace, Andrew D.
   Cao, Yan
   Chandramouleeswaran, Sindhu
   Cidlowski, John A.
TI Lysine 419 targets human glucocorticoid receptor for proteasomal
   degradation
SO STEROIDS
LA English
DT Article
DE Glucocorticoid receptor; Proteasome inhibitor; Dexamethasone; PEST
ID DOWN-REGULATION; ESTROGEN-RECEPTOR; MULTIPLE-MYELOMA; GENE-EXPRESSION;
   MESSENGER-RNA; 26S PROTEASOME; LIVING CELLS; PROTEIN; PHOSPHORYLATION;
   TRANSACTIVATION
AB Glucocorticoid receptors (GRs) are members of a highly conserved family of ligand dependent transcription factors which following hormone binding undergo homologous down-regulation reducing the levels of receptor protein. This decline in human GR (hGR) is due in part to a decrease in protein receptor stability that may limit cellular responsiveness to ligand. To examine the role of the proteasome protein degradation pathway in steroid-dependent hGR responsiveness, we utilized the proteasomal inhibitors MG-132, p-lactone, and epoxomicin. HeLa cells and COS cells were treated with proteasome inhibitors in the presence of the GR agonist dexamethasone (Dex), or were pretreated with proteasomal inhibitor and then Dex. Dexamethasone induced glucocorticoid responsive reporter activity significantly over untreated controls, whereas cells treated with proteasomal inhibitors and Dex together showed 2-3-fold increase in activity. Protein sequence analysis of the hGR protein identified several candidate protein degradation motifs including a PEST element. Mutagenesis of this element at lysine 419 was done and mutant K419A hGR failed to undergo ligand dependent down-regulation. Mutant K419A hGR displayed 2-3-fold greater glucocorticoid responsive reporter activity in the presence of Dex than wild type hGR. These differences in transcriptional activity were not due to altered subcellular localization, since when the mutant K419A hGR was fused with the green fluorescent protein (GFP) it was found to move in and out of the nucleus similarly to wild type hGR. Together these results suggest that the proteasome and the identified PEST degradation motif limit steroid-dependent human glucocorticoid receptor signaling. (C) 2010 Elsevier Inc. All rights reserved.
C1 [Wallace, Andrew D.; Cao, Yan; Chandramouleeswaran, Sindhu] N Carolina State Univ, Dept Environm & Mol Toxicol, Raleigh, NC 27695 USA.
   [Cidlowski, John A.] NIEHS, Mol Endocrinol Grp, Lab Signal Transduct, NIH, Res Triangle Pk, NC 27709 USA.
RP Wallace, AD (reprint author), N Carolina State Univ, Dept Environm & Mol Toxicol, 850 Main Campus Dr,Suite 1104,Campus Box 7633, Raleigh, NC 27695 USA.
EM adwallac@unity.ncsu.edu
FU National Institute of Environmental Health Sciences; North Carolina
   State University
FX The authors would like to thank Dr. Brian Necela for his technical
   assistance with the fluorescence microscopy and Dr. Yoav Timsit for the
   critical reading of this manuscript. This work was supported by the
   Intramural Research Program of the National Institute of Environmental
   Health Sciences and North Carolina State University (A.D.W.).
NR 48
TC 13
Z9 14
U1 0
U2 1
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0039-128X
J9 STEROIDS
JI Steroids
PD DEC
PY 2010
VL 75
IS 12
BP 1016
EP 1023
DI 10.1016/j.steroids.2010.06.015
PG 8
WC Biochemistry & Molecular Biology; Endocrinology & Metabolism
SC Biochemistry & Molecular Biology; Endocrinology & Metabolism
GA 651MT
UT WOS:000281932500030
PM 20619282
ER

PT J
AU Mathur, A
   Weng, J
   Moses, W
   Steinberg, SM
   Rahabari, R
   Kitano, M
   Khanafshar, E
   Ljung, BM
   Duh, QY
   Clark, OH
   Kebebew, E
AF Mathur, Aarti
   Weng, Julie
   Moses, Willieford
   Steinberg, Seth M.
   Rahabari, Reza
   Kitano, Mio
   Khanafshar, Elham
   Ljung, Britt-Marie
   Duh, Quan-Yang
   Clark, Orlo H.
   Kebebew, Electron
TI A prospective study evaluating the accuracy of using combined clinical
   factors and candidate diagnostic markers to refine the accuracy of
   thyroid fine needle aspiration biopsy
SO SURGERY
LA English
DT Article
ID BRAF MUTATION; MOLECULAR MARKERS; CANCER; PAPILLARY; NODULES
AB Background. Approximately 30% of fine needle aspiration biopsies of the thyroid have inconclusive results. We conducted a prospective trial to determine whether clinical and molecular markers could be used in combination to improve the accuracy of thyroid fine needle aspiration biopsy.
   Methods. Clinical, tumor genotyping for common somatic mutations (BRAF V600E, NRAS, KRAS, RET/PTC1, RET/PTC3, and NTRK1), and the gene expression levels of 6 candidate diagnostic markers were analyzed by univariate and multivariate methods in 341 patients to determine whether they could distinguish reliably benign from malignant thyroid neoplasms, and a scoring model was derived.
   Results. By a multivariate analysis, fine needle aspiration biopsy cytology classification, the presence of a NRAS mutation, and the tissue inhibitor of metalloproteinase 1 expression level were associated jointly with malignancy. The overall accuracy of the scoring model, including these 3 variables, to distinguish benign from malignant thyroid tumors was 91%, including 67% for the indeterminate and 77% for the suspicious FNA subgroups.
   Conclusion. Fine needle aspiration biopsy cytology classification, the presence of NRAS mutation, and tissue inhibitor of metalloproteinase 1 messenger RNA expression levels in combination provide a greater diagnostic accuracy than fine needle aspiration biopsy cytology alone to allow selection of more definitive initial operative treatment. The sensitivity of the scoring model, however, was too low to avoid the need for diagnostic thyroidectomies for indeterminate fine needle aspiration biopsy findings. (Surgery 2010; 148:1170-7.)
C1 [Mathur, Aarti; Steinberg, Seth M.; Rahabari, Reza; Kitano, Mio; Kebebew, Electron] NCI, Endocrine Oncol Sect, Surg Branch, Bethesda, MD 20892 USA.
   [Duh, Quan-Yang; Clark, Orlo H.] Univ Calif San Francisco, Dept Surg, San Francisco, CA 94143 USA.
   [Weng, Julie; Moses, Willieford; Khanafshar, Elham; Ljung, Britt-Marie] Univ Calif San Francisco, Dept Pathol, San Francisco, CA 94143 USA.
RP Kebebew, E (reprint author), 10 Ctr Dr,MSC 1201,CRC Room 4-5952, Bethesda, MD 20892 USA.
EM kebebewe@mail.nih.gov
FU Intramural NIH HHS [Z99 CA999999]
NR 21
TC 21
Z9 22
U1 0
U2 7
PU MOSBY-ELSEVIER
PI NEW YORK
PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0039-6060
J9 SURGERY
JI Surgery
PD DEC
PY 2010
VL 148
IS 6
BP 1170
EP 1176
DI 10.1016/j.surg.2010.09.025
PG 7
WC Surgery
SC Surgery
GA 704XM
UT WOS:000286088900029
PM 21134548
ER

PT J
AU Panuncialman, J
   Falanga, V
AF Panuncialman, Jaymie
   Falanga, Vincent
TI Unusual Causes of Cutaneous Ulceration
SO SURGICAL CLINICS OF NORTH AMERICA
LA English
DT Article
DE Inflammatory ulcers; Pyoderma gangrenosum; Vasculitis; Calciphylaxis;
   Cryofibrinogenemia
ID CHOLESTEROL CRYSTAL EMBOLIZATION; INDUCED SKIN NECROSIS; PERISTOMAL
   PYODERMA-GANGRENOSUM; CHRONIC-RENAL-FAILURE; INTRAVENOUS-SODIUM
   THIOSULFATE; OF-THE-LITERATURE; NECROBIOSIS LIPOIDICA;
   MYCOPHENOLATE-MOFETIL; TOPICAL TACROLIMUS; VASCULITIS UPDATE
AB Skin ulceration is a major source of morbidity and is often difficult to manage Ulcers caused by an inflammatory cause or microvascular occlusion are particularly challenging in terms of diagnosis and treatment The management of such ulcers requires careful assessment of associated systemic conditions and a thorough analysis of the ulcer's clinical and histologic findings In this article, the authors discuss several examples of inflammatory ulcers and the approach to the diagnosis and treatment of these ulcers
C1 [Panuncialman, Jaymie; Falanga, Vincent] Roger Williams Med Ctr, Dept Dermatol, Providence, RI 02908 USA.
   [Panuncialman, Jaymie; Falanga, Vincent] NIH, Roger Williams Med Ctr, Ctr Biomed Res Excellence, Providence, RI 02908 USA.
   [Falanga, Vincent] Boston Univ, Sch Med, Dept Dermatol, Boston, MA 02118 USA.
   [Falanga, Vincent] Boston Univ, Sch Med, Dept Biochem, Boston, MA 02118 USA.
RP Falanga, V (reprint author), Roger Williams Med Ctr, Dept Dermatol, 50 Maude St, Providence, RI 02908 USA.
FU NIH Center of Biomedical Research Excellence at Roger Williams Medical
   Center [P20RR018757]; NIH [P20RR018757-07]; Imaging core and Regulatory;
   GMP core
FX This work was supported by the NIH Center of Biomedical Research
   Excellence (P20RR018757) at Roger Williams Medical Center (PI FV); This
   work was made possible by NIH Grant P20RR018757-07 (PI Vincent Falanga)
   and by the grant's Imaging core and Regulatory and GMP core
NR 122
TC 6
Z9 8
U1 0
U2 3
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 0039-6109
J9 SURG CLIN N AM
JI Surg. Clin.-North Am.
PD DEC
PY 2010
VL 90
IS 6
BP 1161
EP +
DI 10.1016/j.suc.2010.08.006
PG 21
WC Surgery
SC Surgery
GA 694AV
UT WOS:000285268200006
PM 21074034
ER

PT J
AU Lane, DA
   Chan, J
   Lupica, CR
   Pickel, VM
AF Lane, Diane A.
   Chan, June
   Lupica, Carl R.
   Pickel, Virginia M.
TI Cannabinoid-1 Receptor Gene Deletion Has a Compartment-Specific Affect
   on the Dendritic and Axonal Availability of mu-Opioid Receptors and on
   Dopamine Axons in the Mouse Nucleus Accumbens
SO SYNAPSE
LA English
DT Article
DE development; mouse; reward; drug addiction; immunolabeling
ID VENTRAL TEGMENTAL AREA; CAUDATE-PUTAMEN NUCLEUS; LONG-TERM POTENTIATION;
   KNOCKOUT MICE; ULTRASTRUCTURAL-LOCALIZATION; ENDOCANNABINOID SYSTEM;
   SYNAPTIC PLASTICITY; PERFORATED SYNAPSES; PROJECTION NEURONS;
   BRAIN-DEVELOPMENT
AB Cannabinoid-type 1 (CB1) receptors are implicated in mu-opioid receptor (mu-OR)-dependent reward ascribed partially to mesolimbic dopamine release in the nucleus accumbens (Acb) shell. Thus, CB1 receptor gene deletion may preferentially alter the availability of mu-ORs and/or dopamine innervation in this brain region, which is functionally distinct from the motor-associated Acb core. To test this hypothesis, we examined the electron microscopic immunolabeling of the mu-OR and the dopamine-synthesizing enzyme, tyrosine hydroxylase (TH) in Acb shell, and core of adult C57BL/6J wild-type (WT) and CB1-knock-out (KO) mice. The mu-OR-immunogold particles were observed in the cytoplasm and on the plasmalemma in dendrites, dendritic spines, and axon terminals throughout the Acb. Compared to WT, the Acb shell of CB1-KO mice showed a lower cytoplasmic density of mu-ORs in dendrites and fewer mu-OR labeled, but not unlabeled, dendritic spines. In this region, the CB1-KO's had a significantly enhanced plasmalemmal density of mu-OR-immunogold in axon terminals, 70% of which formed excitatory-type synapses. However, the number of both mu-OR-labeled terminals and TH-labeled small varicosities was significantly reduced in the Acb shell of CB1-KO's. These adaptations were not seen in the Acb core, where CB1-KO's had a preferentially lower dendritic plasmalemmal and total spine density of mu -OR immunogold. Our results indicate that constitutive deletion of the CBI receptor gene has a major impact on the pre and postsynaptic availability of mu-ORs at axospinous synapses and on the dopamine innervation of the Acb shell as well as the dendritic surface expression of mu-ORs in Acb core of mature rodents. Synapse 64:886-897, 2010. (C)2010 Wiley-Liss, Inc.
C1 [Lane, Diane A.; Chan, June; Pickel, Virginia M.] Cornell Univ, Weill Med Coll, Dept Neurol & Neurosci, New York, NY 10021 USA.
   [Lupica, Carl R.] Natl Inst Drug Abuse, Electrophysiol Res Sect, Cellular Neurobiol Branch, Intramural Res Program, Baltimore, MD 21224 USA.
RP Pickel, VM (reprint author), Cornell Univ, Dept Neurol & Neurosci, Coll Med, 407 E 61st St, New York, NY 10065 USA.
EM vpickel@med.cornell.edu
FU NIH [DA 04600]; NIDA Center for Addiction [DA005130]; Rockefeller
   University; NIDA intramural Research
FX Contract grant sponsor: NIH; Contract grant number: DA 04600; Contract
   grant sponsor: NIDA Center for Addiction; Contract grant number:
   DA005130; Contract grant sponsors: Rockefeller University, NIDA
   intramural Research
NR 57
TC 10
Z9 11
U1 0
U2 1
PU WILEY-LISS
PI HOBOKEN
PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 0887-4476
J9 SYNAPSE
JI Synapse
PD DEC
PY 2010
VL 64
IS 12
BP 886
EP 897
DI 10.1002/syn.20807
PG 12
WC Neurosciences
SC Neurosciences & Neurology
GA 672UE
UT WOS:000283611600002
PM 20939059
ER

PT J
AU Driscoll, JJ
   DeChowdhury, R
AF Driscoll, James J.
   DeChowdhury, Roopa
TI Therapeutically targeting the SUMOylation, Ubiquitination and Proteasome
   pathways as a novel anticancer strategy
SO TARGETED ONCOLOGY
LA English
DT Review
DE Ubiquitin; Proteasome; Bortezomib; SUMOylation; NEDDylation
ID MULTIPLE-MYELOMA CELLS; PROTEIN-DEGRADATION; CANCER-THERAPY; 26S
   PROTEASOME; FISSION YEAST; 20S PROTEASOME; T-CELLS; CLASS-I; BORTEZOMIB;
   SUMO
AB The ubiquitin (Ub)+proteasome proteolytic pathway is responsible for the selective degradation of the majority of nuclear and cytosolic proteins. The proteasome is a high molecular weight multicatalytic protease that serves as the catalytic core of the complex Ub-dependent protein degradation pathway and is an exciting new target for the development of novel anticancer therapies. Inhibition of the proteasome, and consequently Ub-dependent proteolysis, with the small molecule pharmacologic agent bortezomib led to approval by the US Food and Drug Administration (FDA) for the treatment of multiple myeloma (MM) that has subsequently been extended to other hematologic malignancies. Inhibition of the proteasome results in the intracellular accumulation of many ubiquitinated proteins that control essential cellular functions such as cellular growth and apoptosis. The accumulation of high molecular weight Ub similar to protein conjugates eventually triggers apoptosis, with tumor cells more susceptible to proteasome inhibition than non-malignant cells. The defined mechanism of action for proteasome inhibitors has not been completely characterized, not all patients respond to proteasome inhibitor-based therapy, and inevitably patients develop resistance to proteasome inhibitors. Further investigation of the Ub+proteasome system (UPS) is needed to develop more effective inhibitors, to develop agents that overcome bortezomib resistance and to avoid adverse effects such as neuropathy. Furthermore, there are newly uncovered pathways, e.g., the SUMOylation and NEDDylation pathways, which similarly attach Ub-like proteins (ULPs) to protein substrates. The functional consequence of these modifications is only beginning to emerge, but these pathways have been linked to tumorigenesis and may similarly provide therapeutic targets. The immunoproteasome is a specialized form of the proteasome that produces peptides that are presented at the cell surface as major histocompatibility complex (MHC) class I antigens. Proteasome inhibitors decrease the presentation of antigenic peptides to reduce tumor cell recognition by cytotoxic T cells (CTLs) but unexpectedly increase tumor cell recognition by natural killer (NK) cells. Inhibitors of the UPS are validated, cytotoxic agents that may be further exploited in immunotherapy since they modulate tumor cell recognition by effectors of the immune system. Targeting the UPS, SUMOylation and NEDDylation pathways offers great promise in the treatment of hematologic and solid malignancies.
C1 [Driscoll, James J.; DeChowdhury, Roopa] NCI, Med Oncol Branch, Magnuson Canc Ctr, NIH, Bethesda, MD 20892 USA.
RP Driscoll, JJ (reprint author), NCI, Med Oncol Branch, Magnuson Canc Ctr, NIH, 10 Ctr Dr,Bldg 10,Room 12N-226, Bethesda, MD 20892 USA.
EM driscollj@mail.nih.gov
NR 69
TC 25
Z9 26
U1 1
U2 7
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 1776-2596
J9 TARGET ONCOL
JI Target. Oncol.
PD DEC
PY 2010
VL 5
IS 4
BP 281
EP 289
DI 10.1007/s11523-010-0165-2
PG 9
WC Oncology
SC Oncology
GA 693FA
UT WOS:000285208800007
PM 21125340
ER

PT J
AU Butler, PW
   Smith, SM
   Linderman, JD
   Brychta, RJ
   Alberobello, AT
   Dubaz, OM
   Luzon, JA
   Skarulis, MC
   Cochran, CS
   Wesley, RA
   Pucino, F
   Celi, FS
AF Butler, Peter W.
   Smith, Sheila M.
   Linderman, Joyce D.
   Brychta, Robert J.
   Alberobello, Anna Teresa
   Dubaz, Ornella M.
   Luzon, Javier A.
   Skarulis, Monica C.
   Cochran, Craig S.
   Wesley, Robert A.
   Pucino, Frank
   Celi, Francesco Saverio
TI The Thr92Ala 5 ' Type 2 Deiodinase Gene Polymorphism Is Associated with
   a Delayed Triiodothyronine Secretion in Response to the
   Thyrotropin-Releasing Hormone-Stimulation Test: A Pharmacogenomic Study
SO THYROID
LA English
DT Article
ID IODOTHYRONINE DEIODINASE; INSULIN-RESISTANCE; THYROXINE; DIO2;
   3,5,3'-TRIIODOTHYRONINE; 5'-DEIODINASE; PARAMETERS; THERAPY; VARIANT
AB Background: The common Thr92Ala D2 polymorphism has been associated with changes in pituitary-thyroid axis homeostasis, but published results are conflicting. To investigate the effects of the Thr92Ala polymorphism on intrathyroidal thyroxine (T4) to triiodothyronine (T3) conversion, we designed prospective pharmacogenomic intervention aimed to detect differences in T3 levels after thyrotropin (TSH)-releasing hormone (TRH)-mediated TSH stimulation of the thyroid gland.
   Methods: Eighty-three healthy volunteers were screened and genotyped for the Thr92Ala polymorphism. Fifteen volunteers of each genotype (Thr/Thr, Thr/Ala, and Ala/Ala) underwent a 500 mcg intravenous TRH stimulation test with serial measurements of serum total T3 (TT3), free T4, and TSH over 180 minutes.
   Results: No differences in baseline thyroid hormone levels were seen among the study groups. Compared to the Thr/Thr group, the Ala/Ala group showed a significantly lower TRH-stimulated increase in serum TT3 at 60 minutes (12.07 +/- 2.67 vs. 21.07 +/- 2.86 ng/dL, p = 0.029). Thr/Ala subjects showed an intermediate response. Compared to Thr/Thr subjects, the Ala/Ala group showed a blunted rate of rise in serum TT3 as measured by mean time to 50% maximum delta serum TT3 (88.42 +/- 6.84 vs. 69.56 +/- 6.06 minutes, p = 0.028). Subjects attained similar maximal (180 minutes) TRH-stimulated TT3 levels. TRH-stimulated TSH and free T4 levels were not significantly different among the three genotype groups.
   Conclusions: The commonly occurring Thr92Ala D2 variant is associated with a decreased rate of acute TSH-stimulated T3 release from the thyroid consistent with a decrease in intrathyroidal deiodination. These data provide a proof of concept that the Thr92Ala polymorphism is associated with subtle changes in thyroid hormone homeostasis.
C1 [Butler, Peter W.; Smith, Sheila M.; Linderman, Joyce D.; Brychta, Robert J.; Alberobello, Anna Teresa; Dubaz, Ornella M.; Luzon, Javier A.; Skarulis, Monica C.; Cochran, Craig S.; Pucino, Frank; Celi, Francesco Saverio] NIDDK, Clin Endocrinol Branch, NIH, Bethesda, MD 20892 USA.
   [Butler, Peter W.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Reprod & Adult Endocrinol Branch, NIH, Bethesda, MD USA.
   [Wesley, Robert A.] NIH, Warren G Magnuson Clin Ctr, Bethesda, MD 20892 USA.
RP Celi, FS (reprint author), NIDDK, Clin Endocrinol Branch, NIH, Bldg 10,CRC,RM 6-3940,10 Ctr Dr,MSC 1613, Bethesda, MD 20892 USA.
EM fc93a@nih.gov
FU NIDDK [Z01-DK047057-02]
FX The authors gratefully acknowledge the help and professionalism of the
   nursing, laboratory, and ancillary personnel of the NIH Clinical Center.
   This research could have not been accomplished without the selfless
   participation of the study volunteers. The authors are grateful to Dr.
   Douglas Forrest (NIDDK) for his invaluable encouragement, comments, and
   suggestions. Grant support: The Intramural Research Program of the
   NIDDK, project number Z01-DK047057-02. Clinical Trial Registration
   Number: NCT00812149.
NR 22
TC 24
Z9 25
U1 0
U2 0
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 2010
VL 20
IS 12
BP 1407
EP 1412
DI 10.1089/thy.2010.0244
PG 6
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 687CJ
UT WOS:000284751500012
PM 21054208
ER

PT J
AU Jonklaas, J
   Cooper, DS
   Ain, KB
   Bigos, T
   Brierley, JD
   Haugen, BR
   Ladenson, PW
   Magner, J
   Ross, DS
   Skarulis, MC
   Steward, DL
   Maxon, HR
   Sherman, SI
AF Jonklaas, Jacqueline
   Cooper, David S.
   Ain, Kenneth B.
   Bigos, Thomas
   Brierley, James D.
   Haugen, Bryan R.
   Ladenson, Paul W.
   Magner, James
   Ross, Douglas S.
   Skarulis, Monica C.
   Steward, David L.
   Maxon, Harry R.
   Sherman, Steven I.
CA NTCTCSG
TI Radioiodine Therapy in Patients with Stage I Differentiated Thyroid
   Cancer
SO THYROID
LA English
DT Letter
ID CARCINOMA
C1 [Jonklaas, Jacqueline] Georgetown Univ, Med Ctr, Div Endocrinol & Metab, Washington, DC 20007 USA.
   [Cooper, David S.; Ladenson, Paul W.] Johns Hopkins Univ, Sch Med, Baltimore, MD USA.
   [Ain, Kenneth B.] Univ Kentucky, Med Ctr, Lexington, KY USA.
   [Bigos, Thomas] Maine Med Ctr, Portland, ME 04102 USA.
   [Brierley, James D.] Princess Margaret Hosp, Toronto, ON M4X 1K9, Canada.
   [Haugen, Bryan R.] Univ Colorado, Denver, CO 80202 USA.
   [Haugen, Bryan R.] Hlth Sci Ctr, Aurora, CO USA.
   [Magner, James] Genzyme Corp, Cambridge, MA USA.
   [Ross, Douglas S.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
   [Skarulis, Monica C.] NIH, Bethesda, MD 20892 USA.
   [Steward, David L.; Maxon, Harry R.] Univ Cincinnati, Med Ctr, Cincinnati, OH 45267 USA.
   [Sherman, Steven I.] Univ Texas MD Anderson Canc Ctr, Houston, TX 77030 USA.
RP Jonklaas, J (reprint author), Georgetown Univ, Med Ctr, Div Endocrinol & Metab, Suite 230,Bldg D,4000 Reservoir Rd NW, Washington, DC 20007 USA.
EM jj@bc.georgetown.edu
OI Ain, Kenneth/0000-0002-2668-934X; Sherman, Steven/0000-0002-3079-5153
NR 5
TC 27
Z9 27
U1 0
U2 1
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 2010
VL 20
IS 12
BP 1423
EP 1424
DI 10.1089/thy.2010.0308
PG 2
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 687CJ
UT WOS:000284751500015
PM 21054207
ER

PT J
AU Thoolen, B
   Maronpot, RR
   Harada, T
   Nyska, A
   Rousseaux, C
   Nolte, T
   Malarkey, DE
   Kaufmann, W
   Kuttler, K
   Deschl, U
   Nakae, D
   Gregson, R
   Vinlove, MP
   Brix, AE
   Singh, B
   Belpoggi, F
   Ward, JM
AF Thoolen, Bob
   Maronpot, Robert R.
   Harada, Takanori
   Nyska, Abraham
   Rousseaux, Colin
   Nolte, Thomas
   Malarkey, David E.
   Kaufmann, Wolfgang
   Kuettler, Karin
   Deschl, Ulrich
   Nakae, Dai
   Gregson, Richard
   Vinlove, Michael P.
   Brix, Amy E.
   Singh, Bhanu
   Belpoggi, Fiorella
   Ward, Jerrold M.
TI Proliferative and Nonproliferative Lesions of the Rat and Mouse
   Hepatobiliary System
SO TOXICOLOGIC PATHOLOGY
LA English
DT Article
DE diagnostic pathology; hepatobiliary system; histopathology; liver;
   nomenclature; rodent pathology
ID DRUG-INDUCED PHOSPHOLIPIDOSIS; SPRAGUE-DAWLEY RATS; CHRONIC ACTIVE
   HEPATITIS; HEREDITARY HEMORRHAGIC TELANGIECTASIA; POLYCYSTIC
   KIDNEY-DISEASE; INDUCED PELIOSIS HEPATIS; CHOLESTEROL-CHOLIC-ACID;
   INDUCED LIVER-TUMORS; B6C3F1 MICE; CELL-PROLIFERATION
AB The INHAND Project (International Harmonization of Nomenclature and Diagnostic Criteria for Lesions in Rats and Mice) is a joint initiative of the Societies of Toxicologic Pathology from Europe (ESTP); Great Britain (BSTP), Japan (JSTP) and North America (STP) to develop an internationally-accepted nomenclature for proliferative and non-proliferative lesions in laboratory animals. The purpose of this publication is to provide a standardized nomenclature and differential diagnosis for classifying microscopic lesions observed in the hepatobiliary system of laboratory rats and mice, with color microphotographs illustrating examples of some lesions. The standardized nomenclature presented in this document is also available for society members electronically on the internet (http://goreni.org). Sources of material included histopathology databases from government, academia, and industrial laboratories throughout the world. Content includes spontaneous and aging lesions as well as lesions induced by exposure to test materials. A widely accepted and utilized international harmonization of nomenclature for lesions of the hepatobiliary system in laboratory animals will decrease confusion among regulatory and scientific research organizations in different countries and provide a common language to increase and enrich international exchanges of information among toxicologists and pathologists.
C1 [Thoolen, Bob] Global Pathol Support, NL-2596 BA The Hague, Netherlands.
   [Maronpot, Robert R.] Maronpot Consulting LLC, Raleigh, NC USA.
   [Harada, Takanori] Inst Environm Toxicol, Joso, Ibaraki, Japan.
   [Nolte, Thomas] Boehringer Ingelheim Pharma GmbH & Co KG, Biberach, Germany.
   [Malarkey, David E.] NIEHS, Natl Toxicol Program, Cellular & Mol Pathol Branch, Res Triangle Pk, NC 27709 USA.
   [Kaufmann, Wolfgang] Merck KGaA, Darmstadt, Germany.
   [Kuettler, Karin] BASF AG, Ludwigshafen, Germany.
   [Deschl, Ulrich] Boehringer Ingelheim Pharma GmbH & Co KG, Biberach, Germany.
   [Nakae, Dai] Tokyo Metropolitan Inst Publ Hlth, Shinjuku Ku, Tokyo 1690073, Japan.
   [Gregson, Richard] Charles River Labs, Dept Pathol, Senneville, PQ, Canada.
   [Vinlove, Michael P.] Pathol Associates Inc, Frederick, MD USA.
   [Brix, Amy E.] Expt Pathol Labs Inc, Res Triangle Pk, NC USA.
   [Singh, Bhanu] DuPont Haskell Global Ctr Hlth & Environm Sci, Newark, DE USA.
   [Belpoggi, Fiorella] Ramazzini Inst, Bentivoglio, BO, Italy.
   [Ward, Jerrold M.] Global VetPathol, Montgomery Village, MD USA.
RP Thoolen, B (reprint author), Global Pathol Support, Benoordenhoutseweg 23, NL-2596 BA The Hague, Netherlands.
EM bob.thoolen@gpstoxpath.com
NR 313
TC 101
Z9 103
U1 2
U2 7
PU SAGE PUBLICATIONS INC
PI THOUSAND OAKS
PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA
SN 0192-6233
EI 1533-1601
J9 TOXICOL PATHOL
JI Toxicol. Pathol.
PD DEC
PY 2010
VL 38
IS 7
SU S
BP 5S
EP 81S
DI 10.1177/0192623310386499
PG 77
WC Pathology; Toxicology
SC Pathology; Toxicology
GA 705XW
UT WOS:000286175000001
PM 21191096
ER

PT J
AU Yoshizawa, K
   Walker, NJ
   Nyska, A
   Kissling, GE
   Jokinen, MP
   Brix, AE
   Sells, DM
   Wyde, ME
AF Yoshizawa, Katsuhiko
   Walker, Nigel J.
   Nyska, Abraham
   Kissling, Grace E.
   Jokinen, Micheal P.
   Brix, Amy E.
   Sells, Donald M.
   Wyde, Michael E.
TI Thyroid Follicular Lesions Induced by Oral Treatment for 2 Years with
   2,3,7,8-Tetrachlorodibenzo-p-dioxin and Dioxin-like Compounds in Female
   Harlan Sprague-Dawley Rats
SO TOXICOLOGIC PATHOLOGY
LA English
DT Article
DE carcinogenesis; dioxin; follicular cell hypertrophy; rat; thyroid
ID TOXIC EQUIVALENCY FACTORS; POLYCHLORINATED-BIPHENYLS; CHLORINATED
   DIOXINS; POSTNATAL EXPOSURE; RISK ASSESSMENT; HORMONE STATUS; DOSE
   LEVELS; FOLLOW-UP; TCDD; CARCINOGENICITY
AB 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) and structurally-similar dioxin-like compounds affect thyroid function and morphology and thyroid hormone metabolism in animals and humans. The National Toxicology Program conducted eight 2-year gavage studies in female Harlan Sprague-Dawley rats to determine the relative potency of chronic toxicity and carcinogenicity of TCDD, 3,3',4,4',5-pentachlorobiphenyl (PCB126), 2,3,4,7,8-pentachlorodibenzofuran (PeCDF), 2,3',4,4',5-pentachlorobiphenyl (PCB118), 2,2',4,4',5,5'-hexachloro-biphenyl (PCB153), a tertiary mixture of TCDD/PCB126/PeCDF, and two binary mixtures (PCB126/PCB153 and PCB126/PCB118). Administration of these compounds was associated with increased incidences of thyroid follicular cell hypertrophy, variably observed in the 14-, 31-, and 53-week interim and 2-year sacrifice groups. In all studies, the incidences of follicular cell adenoma and carcinoma were not increased. Decreased levels of serum thyroxine were primarily noted in the 14-or-later - week interim groups of all chemicals. Serum triiodothyronine (T3) levels were increased in the TCDD, PCB126, PeCDF, TCDD/PCB126/PeCDF, and PCB126/PCB153 studies, while decreased levels were noted in the PCB153 and PCB126/PCB118 studies. TCDD, PCB126, PCB126/PCB153, and PCB126/PCB118 increased levels of serum thyroid-stimulating hormone almost in a dose-dependent manner in the 14-week groups. These data suggest that although dioxin-like compounds alter thyroid hormones and increase follicular cell hyperplasia, there is not an increase in thyroid adenoma or carcinoma in female Sprague-Dawley rats.
C1 [Kissling, Grace E.] NIEHS, Biostat Branch, Res Triangle Pk, NC 27709 USA.
   [Yoshizawa, Katsuhiko] Kansai Med Univ, Osaka, Japan.
   [Jokinen, Micheal P.] Pathol Associates Charles River Co, Durham, NC USA.
   [Brix, Amy E.] Expt Pathol Labs, Res Triangle Pk, NC USA.
   [Sells, Donald M.] Battelle Columbus Labs, Columbus, OH USA.
   [Walker, Nigel J.; Nyska, Abraham; Wyde, Michael E.] NIEHS, Natl Toxicol Program, Res Triangle Pk, NC 27709 USA.
RP Wyde, ME (reprint author), NIEHS, Natl Toxicol Program, POB 12233,Mail Drop EC 35,111 TW Alexander Dr, Res Triangle Pk, NC 27709 USA.
EM wyde@niehs.nih.gov
RI Walker, Nigel/D-6583-2012
OI Walker, Nigel/0000-0002-9111-6855
NR 61
TC 5
Z9 5
U1 1
U2 8
PU SAGE PUBLICATIONS INC
PI THOUSAND OAKS
PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA
SN 0192-6233
J9 TOXICOL PATHOL
JI Toxicol. Pathol.
PD DEC
PY 2010
VL 38
IS 7
BP 1037
EP 1050
DI 10.1177/0192623310382560
PG 14
WC Pathology; Toxicology
SC Pathology; Toxicology
GA 800QM
UT WOS:000293378600004
PM 20924081
ER

PT J
AU Chan, PC
   Ramot, Y
   Malarkey, DE
   Blackshear, P
   Kissling, GE
   Travlos, G
   Nyska, A
AF Chan, Po C.
   Ramot, Yuval
   Malarkey, David E.
   Blackshear, Pamela
   Kissling, Grace E.
   Travlos, Greg
   Nyska, Abraham
TI Fourteen-Week Toxicity Study of Green Tea Extract in Rats and Mice
SO TOXICOLOGIC PATHOLOGY
LA English
DT Article
DE green tea; toxicity; liver; nasal cavity
ID EPIGALLOCATECHIN GALLATE EGCG; ZERO DOSE CONTROL; INDUCED ASTHMA; WISTAR
   RATS; METABOLIZING-ENZYMES; CAMELLIA-SINENSIS; GENE-EXPRESSION; NASAL
   CAVITY; POLYPHENON-E; IN-VIVO
AB The toxicity of green tea extract (GTE) was evaluated in 14-week gavage studies in male and female F344/NTac rats and B6C3F1 mice at doses up to 1,000 mg/kg. In the rats, no treatment-related mortality was noted. In the mice, treatment-related mortality occurred in male and female mice in the 1,000 mg/kg dose groups. The cause of early deaths was likely related to liver necrosis. Treatment-related histopathological changes were seen in both species in the liver, nose, mesenteric lymph nodes, and thymus. In addition, in mice, changes were seen in the Peyer's patches, spleen, and mandibular lymph nodes. The no adverse effect level (NOAEL) for the liver in both species was 500 mg/kg. In the nose of rats, the NOAEL in males was 62.5 mg/kg, and in females no NOAEL was found. No NOAEL was found in the nose of female or male mice. The changes in the liver and nose were considered primary toxic effects of GTE, while the changes in other organs were considered to be secondary effects. The nose and liver are organs with high metabolic enzyme activity. The increased susceptibility of the nose and liver suggests a role for GTE metabolites in toxicity induction.
C1 [Nyska, Abraham] Toxicol Pathol, Timrat, Israel.
   [Nyska, Abraham] Tel Aviv Univ, Sackler Sch Med, IL-36576 Tel Aviv, Israel.
   [Chan, Po C.; Malarkey, David E.; Kissling, Grace E.; Travlos, Greg] Natl Inst Environm Hlth Sci, Res Triangle Pk, NC USA.
   [Ramot, Yuval] Hadassah Hebrew Univ Med Ctr, IL-91200 Jerusalem, Israel.
   [Blackshear, Pamela] Integrated Lab Syst ILS Inc, Res Triangle Pk, NC USA.
RP Nyska, A (reprint author), DVM, Toxicol Pathologist, Haharuv 18,POB 184, IL-36576 Timrat, Israel.
EM anyska@bezeqint.net
FU NIH, National Institute of Environmental Health Sciences and Pathology
   [N01-ES-55548 (HHSN291200555548C)]
FX This research was supported in part by the Intramural Research Program
   of the NIH, National Institute of Environmental Health Sciences and
   Pathology Support for the NIEHS, Contract # N01-ES-55548
   (HHSN291200555548C).
NR 83
TC 19
Z9 21
U1 0
U2 1
PU SAGE PUBLICATIONS INC
PI THOUSAND OAKS
PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA
SN 0192-6233
EI 1533-1601
J9 TOXICOL PATHOL
JI Toxicol. Pathol.
PD DEC
PY 2010
VL 38
IS 7
BP 1070
EP 1084
DI 10.1177/0192623310382437
PG 15
WC Pathology; Toxicology
SC Pathology; Toxicology
GA 800QM
UT WOS:000293378600008
PM 20884815
ER

PT J
AU Collins, BJ
   Stout, MD
   Levine, KE
   Kissling, GE
   Melnick, RL
   Fennell, TR
   Walden, R
   Abdo, K
   Pritchard, JB
   Fernando, RA
   Burka, LT
   Hooth, MJ
AF Collins, Bradley J.
   Stout, Matthew D.
   Levine, Keith E.
   Kissling, Grace E.
   Melnick, Ronald L.
   Fennell, Timothy R.
   Walden, Ramsey
   Abdo, Kamal
   Pritchard, John B.
   Fernando, Reshan A.
   Burka, Leo T.
   Hooth, Michelle J.
TI Exposure to Hexavalent Chromium Resulted in Significantly Higher Tissue
   Chromium Burden Compared With Trivalent Chromium Following Similar Oral
   Doses to Male F344/N Rats and Female B6C3F1 Mice
SO TOXICOLOGICAL SCIENCES
LA English
DT Article
DE National Toxicology Program; cancer; hexavalent chromium; trivalent
   chromium; chromium picolinate monohydrate; sodium dichromate dihydrate;
   disposition; rodent; inductively coupled plasma-mass spectrometry
ID DRINKING-WATER; ABSORPTION; CARCINOGENICITY; INGESTION; TOXICITY;
   HUMANS; PICOLINATE; CHROMATE; MECHANISMS; TRANSPORT
AB In National Toxicology Program 2-year studies, hexavalent chromium [Cr(VI)] administered in drinking water was clearly carcinogenic in male and female rats and mice, resulting in small intestine epithelial neoplasms in mice at a dose equivalent to or within an order of magnitude of human doses that could result from consumption of chromium-contaminated drinking water, assuming that dose scales by body weight(3/4) (body weight raised to the 3/4 power). In contrast, exposure to trivalent chromium [Cr(III)] at much higher concentrations may have been carcinogenic in male rats but was not carcinogenic in mice or female rats. As part of these studies, total chromium was measured in tissues and excreta of additional groups of male rats and female mice. These data were used to infer the uptake and distribution of Cr(VI) because Cr(VI) is reduced to Cr(III) in vivo, and no methods are available to speciate tissue chromium. Comparable external doses resulted in much higher tissue chromium concentrations following exposure to Cr(VI) compared with Cr(III), indicating that a portion of the Cr(VI) escaped gastric reduction and was distributed systemically. Linear or supralinear dose responses of total chromium in tissues were observed following exposure to Cr(VI), indicating that these exposures did not saturate gastric reduction capacity. When Cr(VI) exposure was normalized to ingested dose, chromium concentrations in the liver and glandular stomach were higher in mice, whereas kidney concentrations were higher in rats. In vitro studies demonstrated that Cr(VI), but not Cr(III), is a substrate of the sodium/sulfate cotransporter, providing a partial explanation for the greater absorption of Cr(VI).
C1 [Collins, Bradley J.; Stout, Matthew D.; Kissling, Grace E.; Melnick, Ronald L.; Abdo, Kamal; Burka, Leo T.; Hooth, Michelle J.] NIEHS, Natl Toxicol Program, Res Triangle Pk, NC 27709 USA.
   [Levine, Keith E.; Fennell, Timothy R.; Fernando, Reshan A.] RTI Int, Discovery & Analyt Sci, Res Triangle Pk, NC 27709 USA.
   [Walden, Ramsey; Pritchard, John B.] NIEHS, Pharmacol Lab, Res Triangle Pk, NC 27709 USA.
RP Hooth, MJ (reprint author), NIEHS, Natl Toxicol Program, 111 Alexander Dr,MD K2-13, Res Triangle Pk, NC 27709 USA.
EM hooth@niehs.nih.gov
RI Fennell, Tim/D-9936-2013
FU National Institutes of Health, National Institute of Environmental
   Health Sciences [ZO1 ES045004-11 BB, Z01 ES65554]
FX This research was supported (in part) by the Intramural Research Program
   of the National Institutes of Health, National Institute of
   Environmental Health Sciences under Research Project Number ZO1
   ES045004-11 BB and Z01 ES65554.
NR 48
TC 25
Z9 27
U1 0
U2 11
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 1096-6080
J9 TOXICOL SCI
JI Toxicol. Sci.
PD DEC
PY 2010
VL 118
IS 2
BP 368
EP 379
DI 10.1093/toxsci/kfq263
PG 12
WC Toxicology
SC Toxicology
GA 682WB
UT WOS:000284432600005
PM 20843897
ER

PT J
AU Lu, H
   Gonzalez, FJ
   Klaassen, C
AF Lu, Hong
   Gonzalez, Frank J.
   Klaassen, Curtis
TI Alterations in Hepatic mRNA Expression of Phase II Enzymes and
   Xenobiotic Transporters after Targeted Disruption of Hepatocyte Nuclear
   Factor 4 Alpha
SO TOXICOLOGICAL SCIENCES
LA English
DT Article
DE HNF4a; knockout; Ugt; Gst; Sult; transporter
ID CONSTITUTIVE ANDROSTANE RECEPTOR; PREGNANE-X-RECEPTOR; ORGANIC CATION
   TRANSPORTERS; LIVER GENE-EXPRESSION; TISSUE DISTRIBUTION; FACTOR
   4-ALPHA; UDP-GLUCURONOSYLTRANSFERASES; TRANSCRIPTIONAL REGULATION;
   MOUSE-LIVER; INTERINDIVIDUAL VARIABILITY
AB Hepatocyte nuclear factor 4 alpha (HNF4a) is a liver-enriched master regulator of liver function. HNF4a is important in regulating hepatic expression of certain cytochrome P450s. The purpose of this study was to use mice lacking HNF4a expression in liver (HNF4a-HNull) to elucidate the role of HNF4a in regulating hepatic expression of phase II enzymes and transporters in mice. Compared with male wild-type mice, HNF4a-HNull male mouse livers had (1) markedly lower messenger RNAs (mRNAs) encoding the uptake transporters sodium taurocholate cotransporting polypeptide, organic anion transporting polypeptide (Oatp) 1a1, Oatp2b1, organic anion transporter 2, sodium phosphate cotransporter type 1, sulfate anion transporter 1, sodium-dependent vitamin C transporter 1, the phase II enzymes Uridine 5'-diphospho (UDP)-glucuronosyltransferase (Ugt) 2a3, Ugt2b1, Ugt3a1, Ugt3a2, sulfotransferase (Sult) 1a1, Sult1b1, Sult5a1, the efflux transporters multidrug resistance-associated protein (Mrp) 6, and multidrug and toxin extrusion 1; (2) moderately lower mRNAs encoding Oatp1b2, organic cation transporter (Oct) 1, Ugt1a5, Ugt1a9, glutathione S-transferase (Gst) m4, Gstm6, and breast cancer resistance protein; but (3) higher mRNAs encoding Oatp1a4, Octn2, Ugt1a1, Sult1e1, Sult2a2, Gsta4, Gstm1-m3, multidrug resistance protein (Mdr) 1a, Mrp3, and Mrp4. Hepatic signaling of nuclear factor E2-related factor 2 and pregnane X receptor appear to be activated in HNF4a-HNull mice. In conclusion, HNF4a deficiency markedly alters hepatic mRNA expression of a large number of phase II enzymes and transporters, probably because of the loss of HNF4a, which is a transactivator and a determinant of gender-specific expression and/or adaptive activation of signaling pathways important in hepatic regulation of these phase II enzymes and transporters.
C1 [Lu, Hong; Klaassen, Curtis] Univ Kansas, Med Ctr, Dept Pharmacol Toxicol & Therapeut, Kansas City, KS 66103 USA.
   [Gonzalez, Frank J.] NCI, Lab Metab, Bethesda, MD 20892 USA.
RP Lu, H (reprint author), 3901 Rainbow Blvd, Kansas City, KS 66160 USA.
EM hlu@kumc.edu
FU National Institutes of Health [ES-009649, ES-009716, ES-013714,
   ES-019487, DK081461, RR021940]
FX National Institutes of Health (grants ES-009649, ES-009716, ES-013714,
   ES-019487, DK081461, and RR021940).
NR 82
TC 21
Z9 22
U1 0
U2 4
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 1096-6080
J9 TOXICOL SCI
JI Toxicol. Sci.
PD DEC
PY 2010
VL 118
IS 2
BP 380
EP 390
DI 10.1093/toxsci/kfq280
PG 11
WC Toxicology
SC Toxicology
GA 682WB
UT WOS:000284432600006
PM 20935164
ER

PT J
AU Qu, AJ
   Shah, YM
   Matsubara, T
   Yang, QA
   Gonzalez, FJ
AF Qu, Aijuan
   Shah, Yatrik M.
   Matsubara, Tsutomu
   Yang, Qian
   Gonzalez, Frank J.
TI PPAR alpha-Dependent Activation of Cell Cycle Control and DNA Repair
   Genes in Hepatic Nonparenchymal Cells
SO TOXICOLOGICAL SCIENCES
LA English
DT Article
DE PPAR alpha; peroxisome proliferators; hepatomegaly; DNA damage repair;
   carcinogenesis
ID CHECKPOINT KINASE CHK1; PEROXISOME PROLIFERATORS; DAMAGE;
   HEPATOCARCINOGENESIS; CLOFIBRATE; EXPRESSION; MECHANISM; LIVER
AB Peroxisome proliferator-activated receptor-alpha (PPAR alpha) mediates the diverse biological effects of peroxisome proliferator (PP) chemicals, including fatty acid catabolism, hepatomegaly, hepatocyte proliferation, and hepatocarcinogenesis in rodents. However, transgenic mice expressing a constitutively active PPAR alpha in hepatocytes (VP16PPAR alpha) do not develop hepatocellular carcinomas in spite of hepatocyte proliferation and hepatomegaly; this suggests that activation of genes in nonparenchymal cells may have a critical role in PP-induced carcinogenesis. VP16PPAR alpha mice exhibited massive peroxisome proliferation and hepatomegaly as well as increased mortality upon Wy-14,643 treatment. Several genes involved in cell cycle or DNA damage repair, such as Chek1, Prkdc, Mcm, and Rad51, were significantly induced to a similar extent between wild-type and VP16PPAR alpha mice after Wy-14,643 administration. This induction was completely abolished in Ppar alpha-null mice, suggesting a PPAR alpha-dependent pathway. These data revealed a DNA damage response signaling network as an early event upon PP treatment and provide novel putative mechanisms for PP-induced hepatocellular carcinoma.
C1 [Qu, Aijuan; Shah, Yatrik M.; Matsubara, Tsutomu; Yang, Qian; Gonzalez, Frank J.] NCI, Lab Metab, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
   [Shah, Yatrik M.] Univ Michigan, Sch Med, Dept Mol & Integrat Physiol, Ann Arbor, MI 48109 USA.
   [Shah, Yatrik M.] Univ Michigan, Sch Med, Dept Internal Med, Div Gastroenterol, Ann Arbor, MI 48109 USA.
RP Gonzalez, FJ (reprint author), NCI, Lab Metab, Ctr Canc Res, NIH, Bldg 37,Room 3106, Bethesda, MD 20892 USA.
EM gonzalef@mail.nih.gov
FU National Cancer Institute; National Institute of Health [CA148828]
FX National Cancer Institute Intramural Research Program to F.J.G.;
   National Institute of Health Grant CA148828 to Y.M.S.
NR 24
TC 12
Z9 12
U1 0
U2 0
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 1096-6080
J9 TOXICOL SCI
JI Toxicol. Sci.
PD DEC
PY 2010
VL 118
IS 2
BP 404
EP 410
DI 10.1093/toxsci/kfq259
PG 7
WC Toxicology
SC Toxicology
GA 682WB
UT WOS:000284432600008
PM 20813756
ER

PT J
AU Leung, MCK
   Goldstone, JV
   Boyd, WA
   Freedman, JH
   Meyer, JN
AF Leung, Maxwell C. K.
   Goldstone, Jared V.
   Boyd, Windy A.
   Freedman, Jonathan H.
   Meyer, Joel N.
TI Caenorhabditis elegans Generates Biologically Relevant Levels of
   Genotoxic Metabolites from Aflatoxin B-1 but Not Benzo[a]pyrene In Vivo
SO TOXICOLOGICAL SCIENCES
LA English
DT Article
DE Caenorhabditis elegans; cytochrome P450; aflatoxin B-1; benzo[a]pyrene;
   genotoxicity; nucleotide excision repair
ID NUCLEOTIDE EXCISION-REPAIR; ARYL-HYDROCARBON RECEPTOR; CYTOCHROME
   P450-DEPENDENT METABOLISM; POLYCYCLIC AROMATIC-HYDROCARBONS; POLYCHAETE
   NEREIS-VIRENS; DNA-DAMAGE; C-ELEGANS; XERODERMA-PIGMENTOSUM; NUCLEAR
   TRANSLOCATOR; INDUCED MUTATIONS
AB There is relatively little information regarding the critical xenobiotic-metabolizing cytochrome P450 (CYP) enzymes in Caenorhabditis elegans, despite this organism's increasing use as a model in toxicology and pharmacology. We carried out experiments to elucidate the capacity of C. elegans to metabolically activate important promutagens via CYPs. Phylogenetic comparisons confirmed an earlier report indicating a lack of CYP1 family enzymes in C. elegans. Exposure to aflatoxin B-1 (AFB(1)), which is metabolized in mammals by CYP1, CYP2, and CYP3 family enzymes, resulted in significant DNA damage in C. elegans. However, exposure to benzo[a]pyrene (BaP), which is metabolized in mammals by CYP1 family enzymes only, produced no detectable damage. To further test whether BaP exposure caused DNA damage, the toxicities of AFB(1) and BaP were compared in nucleotide excision repair (NER)-deficient (xpa-1) and NER-proficient (N2) strains of C. elegans. Exposure to AFB(1) inhibited growth more in xpa-1 than N2 nematodes, but the growth-inhibitory effects of BaP were indistinguishable in the two strains. Finally, a CYP-nicotinamide adenine dinucleotide phosphate reductase-deficient strain (emb-8) of C. elegans was found to be more resistant to the growth-inhibitory effect of AFB(1) exposure than N2, confirming that the AFB(1)-mediated growth inhibition resulted from CYP-mediated metabolism. Together, these results indicate that C. elegans lacks biologically significant CYP1 family-mediated enzymatic metabolism of xenobiotics. Interestingly, we also found that xpa-1 nematodes were slightly more sensitive to chlorpyrifos than were wild type. Our results highlight the importance of considering differences between xenobiotic metabolism in C. elegans and mammals when using this alternative model in pharmaceutical and toxicological research.
C1 [Leung, Maxwell C. K.; Meyer, Joel N.] Duke Univ, Nicholas Sch Environm, Durham, NC 27708 USA.
   [Goldstone, Jared V.] Woods Hole Oceanog Inst, Dept Biol, Woods Hole, MA 02543 USA.
   [Boyd, Windy A.] NIEHS, Biomol Screening Branch, Natl Toxicol Program, NIH, Res Triangle Pk, NC 27709 USA.
   [Freedman, Jonathan H.] NIEHS, Mol Toxicol Lab, NIH, Res Triangle Pk, NC 27709 USA.
RP Meyer, JN (reprint author), Duke Univ, Nicholas Sch Environm, Durham, NC 27708 USA.
EM joel.meyer@duke.edu
OI Goldstone, Jared/0000-0002-9618-4961; Leung, Maxwell/0000-0003-1530-3306
FU National Institutes of Health [R21 NS065468, R01-ES015912,
   5-P42-ES007381]; National Toxicology Program [Z01ES102046]; National
   Institute of Environmental Health Sciences [Z01ES102045]; Caenorhabditis
   Genetics Center, National Center for Research Resources
FX National Institutes of Health (R21 NS065468 to J.N.M.); National
   Toxicology Program (Z01ES102046 to W. A. B.); Intramural Research
   Program of the National Institute of Environmental Health Sciences
   (Z01ES102045 to J.H.F.); National Institutes of Health Grants to John
   Stegeman (R01-ES015912, Superfund Basic Research Program at Boston
   University 5-P42-ES007381) to J.V.G.; Caenorhabditis Genetics Center,
   National Center for Research Resources.
NR 80
TC 23
Z9 25
U1 0
U2 4
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 1096-6080
J9 TOXICOL SCI
JI Toxicol. Sci.
PD DEC
PY 2010
VL 118
IS 2
BP 444
EP 453
DI 10.1093/toxsci/kfq295
PG 10
WC Toxicology
SC Toxicology
GA 682WB
UT WOS:000284432600012
PM 20864627
ER

PT J
AU Kozlov, MM
   McMahon, HT
   Chernomordik, LV
AF Kozlov, Michael M.
   McMahon, Harvey T.
   Chernomordik, Leonid V.
TI Protein-driven membrane stresses in fusion and fission
SO TRENDS IN BIOCHEMICAL SCIENCES
LA English
DT Review
ID TUBULAR ENDOPLASMIC-RETICULUM; SYNAPTIC VESICLE FUSION; VIRAL FUSION;
   CA2+-TRIGGERED EXOCYTOSIS; INFLUENZA HEMAGGLUTININ; JUXTAMEMBRANE
   REGION; BIOLOGICAL-MEMBRANES; C2 DOMAINS; CURVATURE; DYNAMIN
AB Cellular membranes undergo continuous remodeling. Exocytosis and endocytosis, mitochondrial fusion and fission, entry of enveloped viruses into host cells and release of the newly assembled virions, cell-to-cell fusion and cell division, and budding and fusion of transport carriers all proceed via topologically similar, but oppositely ordered, membrane rearrangements. The biophysical similarities and differences between membrane fusion and fission become more evident if we disregard the accompanying biological processes and consider only remodeling of the lipid bilayer. The forces that determine the bilayer propensity to undergo fusion or fission come from proteins and in most cases from membrane-bound proteins. In this review, we consider the mechanistic principles underlying the fusion and fission reactions and discuss the current hypotheses on how specific proteins act in the two types of membrane remodeling.
C1 [Kozlov, Michael M.] Tel Aviv Univ, Sackler Fac Med, Dept Physiol & Pharmacol, IL-69978 Tel Aviv, Israel.
   [McMahon, Harvey T.] MRC Lab Mol Biol, Cambridge CB2 0QH, England.
   [Chernomordik, Leonid V.] Eunice Kennedy Shriver NICHD, Sect Membrane Biol, Lab Cellular & Mol Biophys, NIH, Bethesda, MD 20892 USA.
RP Kozlov, MM (reprint author), Tel Aviv Univ, Sackler Fac Med, Dept Physiol & Pharmacol, IL-69978 Tel Aviv, Israel.
EM michk@post.tau.ac.il; hmm@mrc-lmb.cam.ac.uk; chernoml@mail.nih.gov
FU Israel Science Foundation (ISF); Medical Research Council, UK; National
   Institute of Child Health and Human Development, National Institutes of
   Health; NIAID; National Institutes of Health Intramural Biodefense
   Research
FX Financial support for MMK from the Israel Science Foundation (ISF) and
   Marie Curie Network "Virus Entry", for HMM from the Medical Research
   Council, UK, and for LVC from the Intramural Research Program of the
   National Institute of Child Health and Human Development, National
   Institutes of Health and NIAID, and a National Institutes of Health
   Intramural Biodefense Research grant is gratefully acknowledged.
NR 81
TC 101
Z9 102
U1 0
U2 38
PU ELSEVIER SCIENCE LONDON
PI LONDON
PA 84 THEOBALDS RD, LONDON WC1X 8RR, ENGLAND
SN 0968-0004
J9 TRENDS BIOCHEM SCI
JI Trends Biochem.Sci.
PD DEC
PY 2010
VL 35
IS 12
BP 699
EP 706
DI 10.1016/j.tibs.2010.06.003
PG 8
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 693PZ
UT WOS:000285237300007
PM 20638285
ER

PT J
AU Lazarov, O
   Mattson, MP
   Peterson, DA
   Pimplikar, SW
   van Praag, H
AF Lazarov, Orly
   Mattson, Mark P.
   Peterson, Daniel A.
   Pimplikar, Sanjay W.
   van Praag, Henriette
TI When neurogenesis encounters aging and disease
SO TRENDS IN NEUROSCIENCES
LA English
DT Review
ID NEURAL STEM-CELLS; ADULT HIPPOCAMPAL NEUROGENESIS; FAMILIAL
   ALZHEIMERS-DISEASE; MOUSE DENTATE GYRUS; SPATIAL-PATTERN SEPARATION;
   GENERATED GRANULE CELLS; TRANSGENIC MICE; OLFACTORY-BULB; SYNAPTIC
   PLASTICITY; SUBVENTRICULAR ZONE
AB In this review, we consider the evidence that a reduction in neurogenesis underlies aging-related cognitive deficits and impairments in disorders such as Alzheimer's disease (AD). The molecular and cellular alterations associated with impaired neurogenesis in the aging brain are discussed. Dysfunction of presenilin-1, misprocessing of amyloid precursor protein and toxic effects of hyperphosphorylated tau and beta-amyloid probably contribute to impaired neurogenesis in AD. Because factors such as exercise, environmental enrichment and dietary energy restriction enhance neurogenesis, and protect against age-related cognitive decline and AD, knowledge of the underlying neurogenic signaling pathways could lead to novel therapeutic strategies for preserving brain function. In addition, manipulation of endogenous neural stem cells and stem cell transplantation, as stand-alone or adjunct treatments, seems promising.
C1 [Lazarov, Orly] Univ Illinois, Dept Anat & Cell Biol, Chicago, IL 60607 USA.
   [Mattson, Mark P.; van Praag, Henriette] NIA, Neurosci Lab, Intramural Res Program, Baltimore, MD USA.
   [Peterson, Daniel A.] Rosalind Franklin Univ Med & Sci, Ctr Stem Cell & Regenerat Med, N Chicago, IL USA.
   [Peterson, Daniel A.] Rosalind Franklin Univ Med & Sci, Dept Neurosci, N Chicago, IL USA.
   [Pimplikar, Sanjay W.] Cleveland Clin, Lerner Res Inst, Dept Neurosci, Cleveland, OH 44106 USA.
RP Lazarov, O (reprint author), Univ Illinois, Dept Anat & Cell Biol, Chicago, IL 60607 USA.
EM olazarov@uic.edu
RI Mattson, Mark/F-6038-2012; van Praag, Henriette/F-3939-2015; Lazarov,
   Orly/F-9406-2015
OI van Praag, Henriette/0000-0002-5727-434X; 
FU National Institutes of Health [AG033570, AG036208Z, AG20047, AG22555,
   AG026146]; National Institute on Aging; Alzheimer's Association;
   Illinois Department of Public Health; Brain Research Foundation
FX The authors' work was supported by the National Institutes of Health
   grants AG033570, AG036208Z (O.L.), AG20047 and AG22555 (D.A.P.) and
   AG026146 (S.W.P.); the Intramural Research Program of the National
   Institute on Aging (M.M. and H.v.P.); Alzheimer's Association Young
   Investigator Award, Alzheimer's disease Research Fund, the Illinois
   Department of Public Health, and the Brain Research Foundation (O.L.).
   The authors thank Archana Gadadhar, Yuan-shih Hu and Michael Demars for
   producing images presented in this manuscript. The authors thank KC
   Alexander and David J. Creer for figure preparation.
NR 119
TC 154
Z9 161
U1 6
U2 45
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 2010
VL 33
IS 12
BP 569
EP 579
DI 10.1016/j.tins.2010.09.003
PG 11
WC Neurosciences
SC Neurosciences & Neurology
GA 692CF
UT WOS:000285128400005
PM 20961627
ER

PT J
AU Su, TP
   Hayashi, T
   Maurice, T
   Buch, S
   Ruoho, AE
AF Su, Tsung-Ping
   Hayashi, Teruo
   Maurice, Tangui
   Buch, Shilpa
   Ruoho, Arnold E.
TI The sigma-1 receptor chaperone as an inter-organelle signaling modulator
SO TRENDS IN PHARMACOLOGICAL SCIENCES
LA English
DT Review
ID STEROL C-8-C-7 ISOMERASE; AMINO-ACID-RESIDUES; PIG BRAIN MEMBRANES;
   METHYL-D-ASPARTATE; DOMAIN-LIKE-I; LIGAND-BINDING; RAT-BRAIN;
   HIGH-AFFINITY; ENDOPLASMIC-RETICULUM; H-3 (+)-PENTAZOCINE
AB Inter-organelle signaling plays important roles in many physiological functions. Endoplasmic reticulum (ER)-mitochondrion signaling affects intramitochondrial calcium (Ca2+) homeostasis and cellular bioenergetics. ER-nucleus signaling attenuates ER stress. ER-plasma membrane signaling regulates cytosolic Ca2+ homeostasis and ER-mitochondrion-plasma membrane signaling regulates hippocampal dendritic spine formation. Here, we propose that the sigma-1 receptor (Sig-1R), an ER chaperone protein, acts as an inter-organelle signaling modulator. Sig-1Rs normally reside at the ER-mitochondrion contact called the MAM (mitochondrion-associated ER membrane), where Sig-1Rs regulate ER-mitochondrion signaling and ER-nucleus crosstalk. When cells are stimulated by ligands or undergo prolonged stress, Sig-1Rs translocate from the MAM to the ER reticular network and plasmalemma/plasma membrane to regulate a variety of functional proteins, including ion channels, receptors and kinases. Thus, the Sig-1R serves as an inter-organelle signaling modulator locally at the MAM and remotely at the plasmalemma/plasma membrane. Many pharmacological/physiological effects of Sig-1Rs might relate to this unique action of Sig-1Rs.
C1 [Su, Tsung-Ping; Hayashi, Teruo] NIDA, Cellular Pathobiol Sect, Intramural Res Program, NIH,DHHS, Baltimore, MD 21224 USA.
   [Maurice, Tangui] INSERM, U710, F-34095 Montpellier 5, France.
   [Maurice, Tangui] Univ Montpellier 2, F-34095 Montpellier 5, France.
   [Maurice, Tangui] EPHE, F-75017 Paris, France.
   [Buch, Shilpa] Univ Nebraska Med Ctr, Dept Pharmacol & Expt Neurosci, Omaha, NE 68198 USA.
   [Ruoho, Arnold E.] Univ Wisconsin, Dept Pharmacol, Sch Med & Publ Hlth, Madison, WI 53706 USA.
RP Su, TP (reprint author), NIDA, Cellular Pathobiol Sect, Intramural Res Program, NIH,DHHS, Suite 3304,333 Cassell Dr, Baltimore, MD 21224 USA.
EM TSU@intra.nida.nih.gov
OI Buch, Shilpa/0000-0002-3103-6685
FU National Institute on Drug Abuse/NIH Intramural Research Program;
   INSERM; Gates Millennium Foundation;  [MH-068212];  [DA-020392]; 
   [DA-023397];  [DA-024442];  [MH-065503];  [T32 GM08688];  [F31DA-022932]
FX The authors would like to acknowledge financial support from the
   following sources: National Institute on Drug Abuse/NIH Intramural
   Research Program (T-P.S., T.H.); INSERM (T.M.); MH-068212, DA-020392,
   DA-023397, DA-024442 (S.B.); MH-065503, T32 GM08688, F31DA-022932, Gates
   Millennium Foundation Award (A.E.R.). We would also like to thank the
   following collaborators: S-Y. Tsai, M. Fujimoto, J. Meunier (T-P.S.,
   T.H.); J. Meunier, V. Villard (T.M.); H.H. Yao (S.B.); U. Chu, D.
   Fontanilla, L. Guo (A.E.R.).
NR 108
TC 168
Z9 175
U1 4
U2 25
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 2010
VL 31
IS 12
BP 557
EP 566
DI 10.1016/j.tips.2010.08.007
PG 10
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA 694VM
UT WOS:000285327100001
PM 20869780
ER

PT J
AU Jacobson, KA
AF Jacobson, Kenneth A.
TI GPCR ligand-dendrimer (GLiDe) conjugates: future smart drugs?
SO TRENDS IN PHARMACOLOGICAL SCIENCES
LA English
DT Review
ID PROTEIN-COUPLED RECEPTORS; ADENOSINE RECEPTORS; P2Y(14) RECEPTOR;
   NUCLEOTIDE; CANCER; ANTAGONISTS; DISCOVERY; DELIVERY; AGONISTS; THERAPY
AB Unlike nanocarriers that are intended to release their drug cargo at the site of action, biocompatibile polyamidoamine (PAMAM) conjugates are designed to act at cell surface G protein-coupled receptors (GPCRs) without drug release. These multivalent GPCR ligand-dendrimer (GLiDe) conjugates display qualitatively different pharmacological properties in comparison with monomeric drugs. They might be useful as novel tools to study GPCR homodimers and heterodimers as well as higher aggregates. The structure of the conjugate determines the profile of biological activity, receptor selectivity, and physical properties such as water solubility. Prosthetic groups for characterization and imaging of receptors can be introduced without loss of affinity. The feasibility of targeting multiple adenosine and P2Y receptors for synergistic effects has been shown. Testing in vivo will be needed to explore the effects on pharmacokinetics and tissue targeting.
C1 NIDDKD, Mol Recognit Sect, Bioorgan Chem Lab, NIH, Bethesda, MD 20892 USA.
RP Jacobson, KA (reprint author), NIDDKD, Mol Recognit Sect, Bioorgan Chem Lab, NIH, Bethesda, MD 20892 USA.
EM kajacobs@helix.nih.gov
RI Jacobson, Kenneth/A-1530-2009
OI Jacobson, Kenneth/0000-0001-8104-1493
FU NIDDK, National institutes of Health (Bethesda, MD, USA)
FX Support from the NIDDK Intramural Research Program, National institutes
   of Health (Bethesda, MD, USA) is acknowledged.
NR 33
TC 8
Z9 8
U1 0
U2 10
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 2010
VL 31
IS 12
BP 575
EP 579
DI 10.1016/j.tips.2010.09.002
PG 5
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA 694VM
UT WOS:000285327100003
PM 20961625
ER

PT J
AU Olin, JW
   Allie, DE
   Belkin, M
   Bonow, RO
   Casey, DE
   Creager, MA
   Gerber, TC
   Hirsch, AT
   Jaff, MR
   Kaufman, JA
   Lewis, CA
   Martin, ET
   Martin, LG
   Sheehan, P
   Stewart, KJ
   Treat-Jacobson, D
   White, CJ
   Zheng, ZJ
AF Olin, Jeffrey W.
   Allie, David E.
   Belkin, Michael
   Bonow, Robert O.
   Casey, Donald E.
   Creager, Mark A.
   Gerber, Thomas C.
   Hirsch, Alan T.
   Jaff, Michael R.
   Kaufman, John A.
   Lewis, Curtis A.
   Martin, Edward T.
   Martin, Louis G.
   Sheehan, Peter
   Stewart, Kerry J.
   Treat-Jacobson, Diane
   White, Christopher J.
   Zheng, Zhi-Jie
TI ACCF/AHA/ACR/SCAI/SIR/SVM/SVN/SVS 2010 performance measures for adults
   with peripheral artery disease
SO VASCULAR MEDICINE
LA English
DT Article
DE ACCF/AHA Performance Measures; abdominal aortic aneurysm; ankle brachial
   index; peripheral arterial disease; secondary prevention; supervised
   exercise
ID ABDOMINAL AORTIC-ANEURYSM; ANKLE-BRACHIAL INDEX; QUALITY-OF-LIFE;
   REHABILITATION/SECONDARY PREVENTION SERVICES; ELEVATION
   MYOCARDIAL-INFARCTION; MEASURES WRITING COMMITTEE; ASSOCIATION
   TASK-FORCE; CARDIOVASCULAR-DISEASE; INTERMITTENT CLAUDICATION;
   AMERICAN-COLLEGE
C1 [Zheng, Zhi-Jie] NHLBI, Bethesda, MD 20892 USA.
RI White, Christopher/J-6686-2012
OI White, Christopher/0000-0001-8618-7539
NR 73
TC 12
Z9 13
U1 1
U2 2
PU SAGE PUBLICATIONS LTD
PI LONDON
PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND
SN 1358-863X
J9 VASC MED
JI Vasc. Med.
PD DEC
PY 2010
VL 15
IS 6
BP 481
EP 512
DI 10.1177/1358863X10390838
PG 32
WC Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 698EF
UT WOS:000285574400006
PM 21183653
ER

PT J
AU Padhi, A
   Ross, H
   Terwee, J
   VandeWoude, S
   Poss, M
AF Padhi, Abinash
   Ross, Howard
   Terwee, Julie
   VandeWoude, Sue
   Poss, Mary
TI Profound Differences in Virus Population Genetics Correspond to
   Protection from CD4 Decline Resulting from Feline Lentivirus Coinfection
SO VIRUSES-BASEL
LA English
DT Article
DE Lentivirus; dual infection; population genetics; genetic bottleneck;
   viral temporal dynamics; mutation rate
ID HUMAN-IMMUNODEFICIENCY-VIRUS; CHRONIC INFECTION; DNA POLYMORPHISM;
   SOFTWARE PACKAGE; HIV-1 INFECTION; MULLER RATCHET; IN-VIVO; EVOLUTION;
   TYPE-1; FITNESS
AB CD4 decline is a hallmark of disease onset in individuals infected with Feline Immunodeficiency Virus (FIV) or Human Immunodeficiency Virus type 1 (HIV-1). Cats that are infected with a poorly replicating, apathogenic FIV (PLV) prior to exposure to a virulent FIV strain (FIVC) maintain CD4 numbers by mechanisms that are not correlated with a measurable adaptive immune response or reduction in circulating viral load. We employed population genetic approaches based on the 3' portion of the viral genome to estimate the population structure of FIVC from single and dual infected cats. In dual infected cats, FIVC effective population size was decreased during the initial viral expansion phase, and after three weeks of infection, the population declined sharply. The FIVC population recovered to pre-bottleneck levels approximately seven weeks post-FIVC infection. However, the population emerging from the bottleneck in dual infected cats was distinct based on estimates of temporal population structure and substitution profiles. The transition to transversion rate ratio (kappa) increased from early to late phases in dual infected cats due primarily to a decrease in transversions whereas in single infected cats,. declined over time. Although one clone with extensive G to A substitutions, indicative of host cytidine deaminase editing, was recovered from a dual infected cat during the bottleneck, the post bottleneck population had an overall reduction in G to A substitutions. These data are consistent with a model of PLV-induced host restriction, putatively involving host DNA editing, that alters the dynamics of FIVC throughout the course of infection leading to disease attenuation.
C1 [Padhi, Abinash; Poss, Mary] Penn State Univ, Dept Biol, University Pk, PA 16802 USA.
   [Ross, Howard] Univ Auckland, Sch Biol Sci, Auckland 1142, New Zealand.
   [Terwee, Julie; VandeWoude, Sue] Colorado State Univ, Dept Microbiol Immunol & Pathol, Ft Collins, CO 80523 USA.
   [Poss, Mary] NIH, Fogarty Int Ctr, Bethesda, MD 20892 USA.
   [Poss, Mary] Penn State Univ, Ctr Infect Dis Dynam, Mueller Lab 208, University Pk, PA 16802 USA.
RP Poss, M (reprint author), Penn State Univ, Dept Biol, University Pk, PA 16802 USA.
EM aup17@psu.edu; h.ross@auckland.ac.nz; jat@lamar.colostate.edu;
   Sue.Vandewoude@colostate.edu; mposs@bx.psu.edu
FU NIH [R01 HL092791]; Science & Technology Directorate, Department of
   Homeland Security; Fogarty International Center, National Institutes of
   Health
FX This work was supported NIH R01 HL092791. MP was supported in part by
   the RAPIDD program of the Science & Technology Directorate, Department
   of Homeland Security, and the Fogarty International Center, National
   Institutes of Health. The authors thank Dan Nicholls for excellent
   technical support.
NR 61
TC 3
Z9 3
U1 1
U2 3
PU MDPI AG
PI BASEL
PA POSTFACH, CH-4005 BASEL, SWITZERLAND
SN 1999-4915
J9 VIRUSES-BASEL
JI Viruses-Basel
PD DEC
PY 2010
VL 2
IS 12
BP 2663
EP 2680
DI 10.3390/v2122663
PG 18
WC Virology
SC Virology
GA 700GI
UT WOS:000285725600006
PM 21994636
ER

PT J
AU Yin, ZQ
   Craigie, R
AF Yin, Zhiqi
   Craigie, Robert
TI Modeling the HIV-1 Intasome: A Prototype View of the Target of Integrase
   Inhibitors
SO VIRUSES-BASEL
LA English
DT Article
DE HIV-1; integrase; intasome
ID DNA-BINDING DOMAIN; CATALYTIC DOMAIN; STRAND TRANSFER; TRANSPOSITION;
   COMPLEX; VIRUS
AB The HIV-1 integrase enzyme is essential for integrating the viral DNA into the host chromosome. Infection is aborted in the absence of integration, making integrase an attractive antiviral target. Recently approved inhibitors of integrase bind tightly to integrase assembled in a nucleoprotein complex with the viral DNA ends (intasome), but have only low affinity for free integrase. High-resolution structures of HIV-1 intasomes are therefore required to understand the detailed mechanisms of inhibition and resistance. Although the structure of the HIV-1 intasome has not yet been determined, the structure of the related prototype foamy virus (PFV) intasome was recently solved. A new study [1] exploits the PFV structure to model the HIV-1 intasome. The model provides the most reliable picture to date of the active site region of the HIV-1 intasome and is an important advance in studies of inhibition of this essential HIV-1 enzyme.
C1 [Yin, Zhiqi; Craigie, Robert] NIDDKD, Mol Biol Lab, NIH, Bethesda, MD 20892 USA.
RP Craigie, R (reprint author), NIDDKD, Mol Biol Lab, NIH, Bethesda, MD 20892 USA.
EM bobc@helix.nih.gov
FU National Institute of Diabetes and Digestive and Kidney Diseases; NIH
FX This work was supported by the Intramural Research Program of the
   National Institute of Diabetes and Digestive and Kidney Diseases and by
   the NIH AIDS Targeted Antiviral Program.
NR 15
TC 8
Z9 8
U1 0
U2 2
PU MDPI AG
PI BASEL
PA KANDERERSTRASSE 25, CH-4057 BASEL, SWITZERLAND
SN 1999-4915
J9 VIRUSES-BASEL
JI Viruses-Basel
PD DEC
PY 2010
VL 2
IS 12
BP 2777
EP 2781
DI 10.3390/v2122777
PG 5
WC Virology
SC Virology
GA 700GI
UT WOS:000285725600011
PM 21994639
ER

PT J
AU Simeonov, I
   Gong, XY
   Kim, O
   Poss, M
   Chiaromonte, F
   Fricks, J
AF Simeonov, Ivan
   Gong, Xiaoyan
   Kim, Oekyung
   Poss, Mary
   Chiaromonte, Francesca
   Fricks, John
TI Exploratory Spatial Analysis of in vitro Respiratory Syncytial Virus
   Co-infections
SO VIRUSES-BASEL
LA English
DT Article
DE human respiratory syncytial virus; co-infections; spatial statistics
ID POINT-PROCESSES; INFECTIONS; EPIDEMICS; PATTERNS; CHILDREN; RSV
AB The cell response to virus infection and virus perturbation of that response is dynamic and is reflected by changes in cell susceptibility to infection. In this study, we evaluated the response of human epithelial cells to sequential infections with human respiratory syncytial virus strains A2 and B to determine if a primary infection with one strain will impact the ability of cells to be infected with the second as a function of virus strain and time elapsed between the two exposures. Infected cells were visualized with fluorescent markers, and location of all cells in the tissue culture well were identified using imaging software. We employed tools from spatial statistics to investigate the likelihood of a cell being infected given its proximity to a cell infected with either the homologous or heterologous virus. We used point processes, K-functions, and simulation procedures designed to account for specific features of our data when assessing spatial associations. Our results suggest that intrinsic cell properties increase susceptibility of cells to infection, more so for RSV-B than for RSV-A. Further, we provide evidence that the primary infection can decrease susceptibility of cells to the heterologous challenge virus but only at the 16 h time point evaluated in this study. Our research effort highlights the merits of integrating empirical and statistical approaches to gain greater insight on in vitro dynamics of virus-host interactions.
C1 [Simeonov, Ivan; Chiaromonte, Francesca; Fricks, John] Penn State Univ, Dept Stat, University Pk, PA 16802 USA.
   [Gong, Xiaoyan; Kim, Oekyung; Poss, Mary] Penn State Univ, Dept Biol, University Pk, PA 16802 USA.
   [Poss, Mary] NIH, Fogarty Int Ctr, Bethesda, MD 20892 USA.
RP Fricks, J (reprint author), Penn State Univ, Dept Stat, University Pk, PA 16802 USA.
EM fricks@stat.psu.edu
FU Science and Technology Directorate, Department of Homeland Security;
   Fogarty International Center, National Institutes of Health; Huck
   Institutes for the Life Sciences of the Pennsylvania State University;
   Eberly College of Science of the Pennsylvania State University; National
   Science Foundation [OCI-0821527]
FX We thank all members of our research group, and in particular Timothy
   Reluga, for discussion, ideas and comments that were instrumental in
   shaping this study. Mary Poss was supported in part by the RAPIDD
   program of the Science and Technology Directorate, Department of
   Homeland Security, and the Fogarty International Center, National
   Institutes of Health. Ivan Simeonov and Francesca Chiaromonte were
   supported in part by funding from the Huck Institutes for the Life
   Sciences of the Pennsylvania State University. John Fricks was partially
   supported by funds from the Eberly College of Science of the
   Pennsylvania State University. This work was also supported in part
   through instrumentation funded by the National Science Foundation grant
   OCI-0821527.
NR 22
TC 2
Z9 2
U1 1
U2 4
PU MDPI AG
PI BASEL
PA POSTFACH, CH-4005 BASEL, SWITZERLAND
SN 1999-4915
J9 VIRUSES-BASEL
JI Viruses-Basel
PD DEC
PY 2010
VL 2
IS 12
BP 2782
EP 2802
DI 10.3390/v2122782
PG 21
WC Virology
SC Virology
GA 700GI
UT WOS:000285725600012
PM 21994640
ER

PT J
AU Gill, JA
   Lowe, L
   Nguyen, J
   Liu, PP
   Blake, T
   Venkatesh, B
   Aplan, PD
AF Gill, James A.
   Lowe, Linda
   Nguyen, Joan
   Liu, P. Paul
   Blake, Trevor
   Venkatesh, Byrappa
   Aplan, Peter D.
TI Enforced Expression of Simian Virus 40 Large T-Antigen Leads to
   Testicular Germ Cell Tumors in Zebrafish
SO ZEBRAFISH
LA English
DT Article
ID MYCOBACTERIUM SPP.; TRANSGENIC MICE; DANIO-RERIO; MALIGNANCIES;
   FACILITIES; MUTANTS; CANCER; GENES
AB Testicular germ cell tumors (TGCTs) are the most common malignancy in young men. However, there are few in vivo animal models that have been developed to study this disease. We have used the pufferfish (fugu) lymphocyte-specific protein tyrosine kinase (flck) promoter, which has been shown to enforce high-level expression in the testes of transgenic mice, to express Simian virus 40 large T-antigen in zebrafish testes. Zebrafish that express T-antigen develop TGCTs after a long latency of >1 year. Although overt TGCTs are only evident in 20% of the fish, occult TGCTs can be detected in 90% of the transgenic fish by 36 month of age. The TGCTs resemble the human disease in terms of morphology and gene expression pattern, and can be transplanted to healthy wild-type recipient fish. In addition, enforced expression of the zebrafish stem cell leukemia (scl) gene in the zebrafish testes also generated TGCTs in transgenic fish. These results demonstrate the feasibility of studying TGCTs in a model organism.
C1 [Aplan, Peter D.] NCI, Genet Branch, Ctr Canc Res, NIH, Bethesda, MD 20889 USA.
   [Liu, P. Paul; Blake, Trevor] NHGRI, Genet & Mol Biol Branch, NIH, Bethesda, MD USA.
   [Venkatesh, Byrappa] ASTAR, Inst Mol & Cell Biol, Biopolis, Singapore.
RP Aplan, PD (reprint author), NCI, Genet Branch, Ctr Canc Res, NIH, Navy 8,Room 5101, Bethesda, MD 20889 USA.
EM aplanp@mail.nih.gov
RI ASTAR, IMCB/E-2320-2012; Liu, Paul/A-7976-2012; Aplan,
   Peter/K-9064-2016; 
OI Liu, Paul/0000-0002-6779-025X; Venkatesh, Byrappa/0000-0003-3620-0277
FU NCI, NIH; NHGRI, NIH
FX The authors thank Dennis Hickstein, Dave Caudell, and members of the
   Aplan lab for helpful discussions. The authors thank the Charles River
   Aquatic staff for excellent animal care. This research was supported by
   the Intramural Research Programs of the NCI and NHGRI, NIH.
NR 31
TC 11
Z9 11
U1 0
U2 0
PU MARY ANN LIEBERT, INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 1545-8547
EI 1557-8542
J9 ZEBRAFISH
JI Zebrafish
PD DEC
PY 2010
VL 7
IS 4
BP 333
EP 341
DI 10.1089/zeb.2010.0663
PG 9
WC Developmental Biology; Zoology
SC Developmental Biology; Zoology
GA 695AN
UT WOS:000285343100002
PM 21158563
ER

PT J
AU Murphy, AJ
   Remaley, AT
   Sviridov, D
AF Murphy, A. J.
   Remaley, A. T.
   Sviridov, D.
TI HDL Therapy: Two Kinds of Right?
SO CURRENT PHARMACEUTICAL DESIGN
LA English
DT Review
DE Cardiovascular disease; high density lipoprotein; apolipoprotein A-I;
   low density lipoprotein; lipids
ID HIGH-DENSITY-LIPOPROTEIN; APOLIPOPROTEIN-A-I; CHOLESTERYL ESTER
   TRANSFER; LIVER-X-RECEPTOR; CORONARY-HEART-DISEASE; RANDOMIZED
   CONTROLLED-TRIAL; E-DEFICIENT MICE; TRANSFER PROTEIN-INHIBITION; TYPE-2
   DIABETES-MELLITUS; DRAMATICALLY REDUCES ATHEROSCLEROSIS
AB Cardiovascular disease remains the leading cause of morbidity and mortality globally. The disease is largely controlled with interventions managing atherogenic lipids including LDL and triglycerides. However a number of studies have shown that increasing HDL levels is likely to provide better outcomes for patients suffering from this disease. There has been an extensive research effort into understanding how HDL levels are regulated in the body and which pathways can be targeted therapeutically. The HDL metabolic pathway is however overwhelmingly complex. This has provided only limited success in trialing drugs designed to raise HDL. To add to the complexity HDL itself is a heterogeneous population of particles and there is controversy surrounding which HDL particle is the most cardio-protective. In addition there are varying opinions on which of the HDL cellular receptors are more important in humans (as opposed to what has been discovered in mice) in regulating these effects. In this article we explore the evidence for and against using the currently suggested methods of raising HDL and provide some evidence for how the adverse effects of these drugs could be corrected.
C1 [Murphy, A. J.] Columbia Univ, Dept Med, Div Mol Med, New York, NY 10032 USA.
   [Remaley, A. T.] NHLBI, NIH, Bethesda, MD 20892 USA.
   [Sviridov, D.] Baker IDI Heart & Diabet Inst, Melbourne, Vic, Australia.
   [Sviridov, D.] Univ Western Australia, Sch Med & Pharmacol, Perth, WA 6009, Australia.
RP Murphy, AJ (reprint author), Columbia Univ, Dept Med, Div Mol Med, 630 W 168th St, New York, NY 10032 USA.
EM am3440@columbia.edu
NR 185
TC 8
Z9 8
U1 0
U2 0
PU BENTHAM SCIENCE PUBL LTD
PI SHARJAH
PA EXECUTIVE STE Y-2, PO BOX 7917, SAIF ZONE, 1200 BR SHARJAH, U ARAB
   EMIRATES
SN 1381-6128
J9 CURR PHARM DESIGN
JI Curr. Pharm. Design
PD DEC
PY 2010
VL 16
IS 37
BP 4134
EP 4147
PG 14
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA 721LW
UT WOS:000287357200008
PM 21247394
ER

PT J
AU Wu, N
   Wu, XW
   Agama, K
   Pommier, Y
   Du, J
   Li, D
   Gu, LQ
   Huang, ZS
   An, LK
AF Wu, Ning
   Wu, Xi-Wei
   Agama, Keli
   Pommier, Yves
   Du, Jun
   Li, Ding
   Gu, Lian-Quan
   Huang, Zhi-Shu
   An, Lin-Kun
TI A Novel DNA Topoisomerase I Inhibitor with Different Mechanism from
   Camptothecin Induces G2/M Phase Cell Cycle Arrest to K562 Cells
SO BIOCHEMISTRY
LA English
DT Article
ID ANTITUMOR-ACTIVITY; CARCINOMA-CELLS; G(2) ARREST; CLEAVAGE;
   CYTOTOXICITY; ANTICANCER; DRUGS; INTERCALATORS; DERIVATIVES; INDUCTION
AB DNA topoisomerase I (Top 1) is an essential nuclear enzyme and a validated target for anticancer agent screening. In a previous study, we found that indolizinoquinoline-5,12-dione derivatives show significant biological activity against several human cancer cell lines. To understand their mechanism of inhibition of cancer cell growth, one indolizinoquinoline-5,12-dione derivative, CY13II, was further studied as lead. Our present results indicate that CY13II shows more potent antiproliferative activity against K562 cells than camptothecin. Additionally, K562 cells were arrested in G2/M, and their growth rate decreased after treatment with CY13II at micromolar concentration. Biochemical Top1 assays indicate that CY13II exhibits a different inhibitory mechanism from camptothecin. Unlike camptothecin, CY13II specifically inhibits the catalytic cleavage activity of Top 1 instead of forming the drug-enzyme-DNA covalent ternary complex.
C1 [Wu, Ning; Wu, Xi-Wei; Li, Ding; Gu, Lian-Quan; Huang, Zhi-Shu; An, Lin-Kun] Sun Yat Sen Univ, Inst Med Chem, Guangzhou 510006, Guangdong, Peoples R China.
   [Du, Jun] Sun Yat Sen Univ, Sch Pharmaceut Sci, Dept Microbial & Biochem Pharmac, Guangzhou 510006, Guangdong, Peoples R China.
   [Agama, Keli; Pommier, Yves] NCI, Mol Pharmacol Lab, Ctr Canc Res, Bethesda, MD 20892 USA.
RP Gu, LQ (reprint author), Sun Yat Sen Univ, Inst Med Chem, Guangzhou 510006, Guangdong, Peoples R China.
EM cesglq@mail.sysu.edu.cn; lssalk@mail.sysu.edu.cn
FU National Natural Science Foundation of China [30801425]; National S & T
   Major Project [2009ZX09103-042]; Guangdong Natural Science Fund
   [10151008901000022]; Center for Cancer Research; National Cancer
   Institute, National Institutes of Health
FX This work was supported by the National Natural Science Foundation of
   China (No. 30801425), National S & T Major Project (No.
   2009ZX09103-042), and Guangdong Natural Science Fund (No.
   10151008901000022). Y. Pommier and K. Agama are supported by the Center
   for Cancer Research, intramural Program of the National Cancer
   Institute, National Institutes of Health.
NR 40
TC 27
Z9 28
U1 2
U2 13
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 30
PY 2010
VL 49
IS 47
BP 10131
EP 10136
DI 10.1021/bi1009419
PG 6
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 682YL
UT WOS:000284438800011
PM 21033700
ER

PT J
AU Thanassoulis, G
   Vasan, RS
AF Thanassoulis, George
   Vasan, Ramachandran S.
TI Genetic Cardiovascular Risk Prediction Will We Get There?
SO CIRCULATION
LA English
DT Review
DE cardiovascular disease; epidemiology; genetics; risk prediction; risk
   stratification
ID CORONARY-HEART-DISEASE; GENOME-WIDE ASSOCIATION; MIDDLE-AGED ADULTS;
   MYOCARDIAL-INFARCTION; ARTERY-DISEASE; CHROMOSOME 9P21.3; COMPLEX
   DISEASES; ATHEROSCLEROSIS RISK; BLOOD-PRESSURE; POPULATION
C1 [Vasan, Ramachandran S.] NHLBI, NIH, Framingham Heart Study, Framingham, MA 01702 USA.
   Boston Univ, Fac Med, Boston, MA 02215 USA.
RP Vasan, RS (reprint author), NHLBI, NIH, Framingham Heart Study, 73 Mt Wayte,2, Framingham, MA 01702 USA.
EM vasan@bu.edu
OI Ramachandran, Vasan/0000-0001-7357-5970
FU Canadian Institute of Health Research; Fonds de Recherche en Sante du
   Quebec; National Institutes of Health [NO1-HC-25195, RO1-HL93328]
FX Dr Thanassoulis is supported by a Research Fellowship from the Canadian
   Institute of Health Research and the Fonds de Recherche en Sante du
   Quebec. Dr Vasan is supported in part by National Institutes of Health
   contract NO1-HC-25195 and RO1-HL93328.
NR 97
TC 47
Z9 47
U1 0
U2 2
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 30
PY 2010
VL 122
IS 22
BP 2323
EP 2334
DI 10.1161/CIRCULATIONAHA.109.909309
PG 12
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 686JD
UT WOS:000284691700020
PM 21147729
ER

PT J
AU Fishman, GI
   Chugh, SS
   DiMarco, JP
   Albert, CM
   Anderson, ME
   Bonow, RO
   Buxton, AE
   Chen, PS
   Estes, M
   Jouven, X
   Kwong, R
   Lathrop, DA
   Mascette, AM
   Nerbonne, JM
   O'Rourke, B
   Page, RL
   Roden, DM
   Rosenbaum, DS
   Sotoodehnia, N
   Trayanova, NA
   Zheng, ZJ
AF Fishman, Glenn I.
   Chugh, Sumeet S.
   DiMarco, John P.
   Albert, Christine M.
   Anderson, Mark E.
   Bonow, Robert O.
   Buxton, Alfred E.
   Chen, Peng-Sheng
   Estes, Mark
   Jouven, Xavier
   Kwong, Raymond
   Lathrop, David A.
   Mascette, Alice M.
   Nerbonne, Jeanne M.
   O'Rourke, Brian
   Page, Richard L.
   Roden, Dan M.
   Rosenbaum, David S.
   Sotoodehnia, Nona
   Trayanova, Natalia A.
   Zheng, Zhi-Jie
TI Sudden Cardiac Death Prediction and Prevention Report From a National
   Heart, Lung, and Blood Institute and Heart Rhythm Society Workshop
SO CIRCULATION
LA English
DT Article
DE sudden cardiac death; prevention; epidemiology; electrophysiology;
   National Heart, Lung, and Blood Institute
ID LONG-QT SYNDROME; T-WAVE ALTERNANS; IMPLANTABLE
   CARDIOVERTER-DEFIBRILLATOR; CORONARY-ARTERY-DISEASE; ACUTE
   MYOCARDIAL-INFARCTION; VENTRICULAR SYSTOLIC DYSFUNCTION; SIGNAL-AVERAGED
   ELECTROCARDIOGRAM; NONINVASIVE RISK STRATIFICATION; SPATIALLY DISCORDANT
   ALTERNANS; MULTIPLE SOURCE SURVEILLANCE
C1 [Fishman, Glenn I.] NYU, Sch Med, Div Cardiol, New York, NY 10016 USA.
   [Chugh, Sumeet S.] Cedars Sinai Med Ctr, Los Angeles, CA 90048 USA.
   [DiMarco, John P.] Univ Virginia Hlth Syst, Charlottesville, VA USA.
   [Albert, Christine M.; Kwong, Raymond] Brigham & Womens Hosp, Boston, MA 02115 USA.
   [Anderson, Mark E.] Univ Iowa, Iowa City, IA USA.
   [Bonow, Robert O.] Northwestern Univ, Chicago, IL 60611 USA.
   [Buxton, Alfred E.] Rhode Isl Hosp, Providence, RI USA.
   [Chen, Peng-Sheng] Indiana Univ, Krannert Inst Cardiol, Indianapolis, IN 46204 USA.
   [Estes, Mark] Tufts Univ, Sch Med, Boston, MA 02111 USA.
   [Jouven, Xavier] Univ Paris 05, INSERM, U970, Paris, France.
   [Lathrop, David A.; Mascette, Alice M.; Zheng, Zhi-Jie] NHLBI, Bethesda, MD 20892 USA.
   [Nerbonne, Jeanne M.] Washington Univ, St Louis, MO USA.
   [O'Rourke, Brian] Johns Hopkins Univ Hosp, Baltimore, MD 21287 USA.
   [Page, Richard L.] Univ Wisconsin, Sch Med & Publ Hlth, Madison, WI USA.
   [Roden, Dan M.] Vanderbilt Univ, Sch Med, Nashville, TN 37212 USA.
   [Rosenbaum, David S.] Case Western Reserve Univ, Cleveland, OH 44106 USA.
   [Sotoodehnia, Nona] Univ Washington, Seattle, WA 98101 USA.
   [Trayanova, Natalia A.] Johns Hopkins Univ, Baltimore, MD USA.
RP Fishman, GI (reprint author), NYU, Sch Med, Div Cardiol, 522 1st Ave,Smilow 801, New York, NY 10016 USA.
EM glenn.fishman@med.nyu.edu
RI Trayanova, Natalia/A-3386-2010; Page, Richard/L-5501-2014
OI Page, Richard/0000-0001-5603-1330
FU National Institutes of Health (NIH) [HL068070, HL091069, HL78931,
   HL78932, HL71140, HL105170, HL088416, HL64757, HL82727, HL081336,
   HL034161, HL066388, HL65962, HL49989, RO1-HL54807, R01HL088456,
   HL082729]; Fondation Leducq Alliance for CaMKII Signaling in Heart
   [HL70250, HL079031, HL096652]; Medtronic-Zipes Endowment; Fondation
   Leducq Preventing Sudden Death Trans-Atlantic Alliance; National Science
   Foundation [CBET-0601935]; St. Jude Medical; Novartis; Medtronic and St.
   Jude Medical; Medtronic; Boston Scientific; New York State NYSTEM
FX Dr Albert received National Institutes of Health (NIH) research grants
   HL068070 and HL091069 and is the recipient of the American Heart
   Association Established Investigator Award; Dr Anderson received NIH
   research grants HL70250, HL079031 and HL096652 and funding from
   Fondation Leducq Alliance for CaMKII Signaling in Heart; Dr Chen
   received NIH research grants HL78931, HL78932, and HL71140 and funding
   from the Medtronic-Zipes Endowment; Dr Chugh received NIH research
   grants HL105170, HL088416, and HL088416; Dr Fishman received NIH
   research grants HL64757, HL82727, and HL081336; Dr Nerbonne received NIH
   research grants HL034161 and HL066388; Dr Roden received NIH research
   grants HL65962 and HL49989 and funding from Fondation Leducq Preventing
   Sudden Death Trans-Atlantic Alliance; Dr Rosenbaum received NIH research
   grant RO1-HL54807;Dr Sotoodehnia received NIH research grant
   R01HL088456; Dr Trayanova received NIH research grant HL082729 and
   National Science Foundation grant CBET-0601935.; Dr Albert received
   research grants from St. Jude Medical, is a consultant to Novartis, and
   is on the clinical trial end point committee of GlaxoSmithKline; Dr
   Buxton received honoraria from GE Healthcare and Medtronic; Dr Chen
   received research support from Medtronic and St. Jude Medical; Dr
   DiMarco received a research grant from Medtronic, a training grant from
   Boston Scientific, and honoraria from St. Jude Medical and is a
   consultant to Medtronic; Dr Estes received a research grant and
   honoraria from and is a consultant and expert witness for Boston
   Scientific; Dr Fishman received a New York State NYSTEM grant; Dr
   Lathrop is an employee of NIH; Dr Mascette is an employee of NIH and a
   member of the PRECISION Trial Executive Committee; Dr Roden is a
   consultant to Merck, Sanofi, Daiichi, and Vitae Pharmaceutical; Dr
   Rosenbaum is on the Cambridge Heart Advisory Board; Dr Trayanova is the
   cofounder of Cardiosolv LLC; and Dr Zheng is an employee of NIH.
NR 194
TC 196
Z9 203
U1 2
U2 18
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 30
PY 2010
VL 122
IS 22
BP 2335
EP 2348
DI 10.1161/CIRCULATIONAHA.110.976092
PG 14
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 686JD
UT WOS:000284691700021
PM 21147730
ER

PT J
AU Navarathna, DHMLP
   Roberts, DD
AF Navarathna, Dhammika H. M. L. P.
   Roberts, David D.
TI Candida albicans heme oxygenase and its product CO contribute to
   pathogenesis of candidemia and alter systemic chemokine and cytokine
   expression
SO FREE RADICAL BIOLOGY AND MEDICINE
LA English
DT Article
DE Candid albicans; Heme oxygenase; Antifungal immunity; Kidney; Virulence;
   Mouse model; Carbon monoxide; Free radicals
ID TUMOR-NECROSIS-FACTOR; GRAM-NEGATIVE BACTERIA; HOST-DEFENSE;
   CARBON-MONOXIDE; MOUSE MODEL; EXERCISE PERFORMANCE; ESCHERICHIA-COLI;
   IMMUNE-RESPONSES; ORAL CANDIDIASIS; INTERFERON-GAMMA
AB Mammalian heme oxygenases play important roles in immune regulation by producing immunosuppressive CO. The pathogenic yeast Candida albicans encodes a heme oxygenase, Hmx1, that is specifically induced by the host protein hemoglobin, suggesting a role in the pathogenesis of disseminated bloodstream infections. We show that exposing mice to therapeutic levels of CO increases C. albicans virulence, whereas an HMX1 null strain has decreased virulence in murine disseminated candidiasis. Levels of several regulatory cytokines and chemokines are decreased in mice infected with the null strain, and initial lesions in the kidney are more rapidly cleared after polymorphonuclear leukocyte infiltration. Reconstitution of one or both alleles restores virulence to the level of wild type. Growth in vitro and initial organ burdens in infected mice are not decreased and host iron overload does not restore virulence for the null strain, suggesting that early growth in the host is not limited by Hmx1-mediated iron scavenging. In contrast, inhaled CO partially reverses the virulence defect of the null strain and restores several host cytokine responses to wild-type levels. Collectively, these results show that C. albicans Hmx1 expression and CO production limit the host immune response and contribute to the pathogenesis of candidemia. Published by Elsevier Inc.
C1 [Navarathna, Dhammika H. M. L. P.; Roberts, David D.] NCI, Pathol Lab, Ctr Canc Res, NIH, Bethesda, MD 20982 USA.
RP Roberts, DD (reprint author), NCI, Pathol Lab, Ctr Canc Res, NIH, Bethesda, MD 20982 USA.
EM droberts@helix.nih.gov
RI Roberts, David/A-9699-2008
OI Roberts, David/0000-0002-2481-2981
FU Center for Cancer Research, National Cancer Institute, NIH
FX We are grateful to Jason Foley (NCI, Bethesda, MD, USA) and Michael
   Sanford (NCI, Frederick, MD, USA) for help with the Luminex assays and
   Dr. Joachim Morschhauser (University of Wurzburg, Germany) for kindly
   providing pSFS2A. This work was supported by the Intramural Research
   Program of the Center for Cancer Research, National Cancer Institute,
   NIH.
NR 59
TC 14
Z9 15
U1 0
U2 1
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0891-5849
EI 1873-4596
J9 FREE RADICAL BIO MED
JI Free Radic. Biol. Med.
PD NOV 30
PY 2010
VL 49
IS 10
BP 1561
EP 1573
DI 10.1016/j.freeradbiomed.2010.08.020
PG 13
WC Biochemistry & Molecular Biology; Endocrinology & Metabolism
SC Biochemistry & Molecular Biology; Endocrinology & Metabolism
GA 681VC
UT WOS:000284347900011
PM 20800092
ER

PT J
AU Elking, DM
   Perera, L
   Duke, R
   Darden, T
   Pedersen, LG
AF Elking, Dennis M.
   Perera, Lalith
   Duke, Robert
   Darden, Thomas
   Pedersen, Lee G.
TI Atomic Forces for Geometry-Dependent Point Multipole and Gaussian
   Multipole Models
SO JOURNAL OF COMPUTATIONAL CHEMISTRY
LA English
DT Article
DE multipole; Gaussian multipole; force; torque; Wigner function
ID POLARIZABLE MOLECULAR-MECHANICS; INITIO QUANTUM-CHEMISTRY; DYNAMICS
   SIMULATIONS; FLUCTUATING CHARGE; INTERMOLECULAR POTENTIALS; BIOMOLECULAR
   SIMULATIONS; INTERACTION ENERGIES; WATER; FIELD; DIPOLE
AB In standard treatments of atomic multipole models, interaction energies, total molecular forces, and total molecular torques are given for multipolar interactions between rigid molecules. However, if the molecules are assumed to be flexible, two additional multipolar atomic forces arise because of (1) the transfer of torque between neighboring atoms and (2) the dependence of multipole moment on internal geometry (bond lengths, bond angles, etc.) for geometry-dependent multipole models. In this study, atomic force expressions for geometry-dependent multipoles are presented for use in simulations of flexible molecules. The atomic forces are derived by first proposing a new general expression for Wigner function derivatives partial derivative D(m'm)(l)/partial derivative Omega. The force equations can be applied to electrostatic models based on atomic point multipoles or Gaussian multipole charge density. Hydrogen-bonded dimers are used to test the intermolecular electrostatic energies and atomic forces calculated by geometry-dependent multipoles fit to the ab initio electrostatic potential. The electrostatic energies and forces are compared with their reference ab initio values. It is shown that both static and geometry-dependent multipole models are able to reproduce total molecular forces and torques with respect to ab initio, whereas geometry-dependent multipoles are needed to reproduce ab initio atomic forces. The expressions for atomic force can be used in simulations of flexible molecules with atomic multipoles. In addition, the results presented in this work should lead to further development of next generation force fields composed of geometry-dependent multipole models. (C) 2010 Wiley Periodicals, Inc. J Comput Chem 31: 2702-2713, 2010
C1 [Elking, Dennis M.; Perera, Lalith; Duke, Robert; Pedersen, Lee G.] Natl Inst Environm Hlth Sci, Struct Biol Lab, Res Triangle Pk, NC 27709 USA.
   [Darden, Thomas] OpenEye Sci Software, Santa Fe, NM 87508 USA.
   [Pedersen, Lee G.] Univ N Carolina, Dept Chem, Chapel Hill, NC 27599 USA.
RP Pedersen, LG (reprint author), Natl Inst Environm Hlth Sci, Struct Biol Lab, Res Triangle Pk, NC 27709 USA.
EM lee_pedersen@unc.edu
RI perera, Lalith/B-6879-2012; Pedersen, Lee/E-3405-2013
OI perera, Lalith/0000-0003-0823-1631; Pedersen, Lee/0000-0003-1262-9861
FU NIH [HL06350]; NIEHS [Z01 ESO943010-23]; NSF [FRG DMR 0804549]
FX Contract/grant sponsor: Intramural Research Program of the NIH and
   NIEHS; contract/grant number: Z01 ESO943010-23; Contract/grant sponsor:
   NIH; contract/grant number: HL06350; Contract/grant sponsor: NSF;
   contract/grant number: FRG DMR 0804549
NR 74
TC 10
Z9 10
U1 2
U2 20
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0192-8651
J9 J COMPUT CHEM
JI J. Comput. Chem.
PD NOV 30
PY 2010
VL 31
IS 15
BP 2702
EP 2713
DI 10.1002/jcc.21563
PG 12
WC Chemistry, Multidisciplinary
SC Chemistry
GA 656EV
UT WOS:000282309900003
PM 20839297
ER

PT J
AU Van Prooyen, N
   Gold, H
   Andresen, V
   Schwartz, O
   Jones, K
   Ruscetti, F
   Lockett, S
   Gudla, P
   Venzon, D
   Franchini, G
AF Van Prooyen, Nancy
   Gold, Heather
   Andresen, Vibeke
   Schwartz, Owen
   Jones, Kathryn
   Ruscetti, Frank
   Lockett, Stephen
   Gudla, Prabhakar
   Venzon, David
   Franchini, Genoveffa
TI Human T-cell leukemia virus type 1 p8 protein increases cellular
   conduits and virus transmission
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
   AMERICA
LA English
DT Article
DE human leukemia retrovirus; orf-I
ID RECEPTOR SIGNAL-TRANSDUCTION; TROPICAL SPASTIC PARAPARESIS;
   HUMAN-IMMUNODEFICIENCY-VIRUS; LYMPHOTROPIC-VIRUS; P12(I) PROTEIN;
   IMMUNOLOGICAL SYNAPSE; TUNNELING NANOTUBULES; VIROLOGICAL-SYNAPSE;
   MEMBRANE NANOTUBES; ANIMAL-CELLS
AB The human T-cell leukemia virus type 1 (HTLV-1) is the cause of adult T-cell leukemia/lymphoma as well as tropical spastic paraparesis/HTLV-1-associated myelopathy. HTLV-1 is transmitted to T cells through the virological synapse and by extracellular viral assemblies. Here, we uncovered an additional mechanism of virus transmission that is regulated by the HTLV-1-encoded p8 protein. We found that the p8 protein, known to anergize T cells, is also able to increase T-cell contact through lymphocyte function-associated antigen-1 clustering. In addition, p8 augments the number and length of cellular conduits among T cells and is transferred to neighboring T cells through these conduits. p8, by establishing a T-cell network, enhances the envelope-dependent transmission of HTLV-1. Thus, the ability of p8 to simultaneously anergize and cluster T cells, together with its induction of cellular conduits, secures virus propagation while avoiding the host's immune surveillance. This work identifies p8 as a viral target for the development of therapeutic strategies that may limit the expansion of infected cells in HTLV-1 carriers and decrease HTLV-1-associated morbidity.
C1 [Van Prooyen, Nancy; Gold, Heather; Andresen, Vibeke; Franchini, Genoveffa] NCI, Anim Models Retroviral Vaccine Sect, Vaccine Branch, NIH, Bethesda, MD 20892 USA.
   [Van Prooyen, Nancy] Johns Hopkins Univ, Dept Biol, Baltimore, MD 21218 USA.
   [Schwartz, Owen] NIAID, NIH, Bethesda, MD 20892 USA.
   [Jones, Kathryn] NCI, Basic Res Program, Sci Applicat Int Corp Frederick, Frederick, MD 21702 USA.
   [Ruscetti, Frank] NCI, Expt Immunol Lab, Frederick, MD 21702 USA.
   [Lockett, Stephen] NCI, Opt Microscopy & Anal Lab, Frederick, MD 21702 USA.
   [Gudla, Prabhakar] NCI, Image Anal Lab, Res Tech Program, Sci Applicat Int Corp Frederick, Frederick, MD 21702 USA.
   [Venzon, David] NCI, Biostat & Data Management Sect, NIH, Bethesda, MD 20892 USA.
RP Franchini, G (reprint author), NCI, Anim Models Retroviral Vaccine Sect, Vaccine Branch, NIH, Bethesda, MD 20892 USA.
EM franchig@mail.nih.gov
FU National Institutes of Health [HHSN261200800001E]; National Cancer
   Institute [HHSN261200800001E]; Center for Cancer Research; Howard Hughes
   Medical Institute
FX We are dedicating this work to the memory of the late Dr. David Derse,
   as his very generous contribution of reagents greatly helped. We thank
   Drs. T. Misteli and Dustin Edwards for critical reading of the
   manuscript, Teresa Habina for editorial assistance, and Graham Myers for
   assistance in some of the experiments. We are grateful to Dr. K.
   Nagashima for transmission electron microscopy and to T. Karpova and J.
   McNally for help with the confocal microscopy. This work was supported
   by the Intramural Research Program of the National Institutes of Health,
   National Cancer Institute, Center for Cancer Research, and federal funds
   from the National Cancer Institute, National Institutes of Health, under
   Contract HHSN261200800001E. N.V.P. is a Gilliam graduate fellow of the
   Howard Hughes Medical Institute.
NR 47
TC 45
Z9 45
U1 0
U2 1
PU NATL ACAD SCIENCES
PI WASHINGTON
PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA
SN 0027-8424
J9 P NATL ACAD SCI USA
JI Proc. Natl. Acad. Sci. U. S. A.
PD NOV 30
PY 2010
VL 107
IS 48
BP 20738
EP 20743
DI 10.1073/pnas.1009635107
PG 6
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 687ET
UT WOS:000284762400031
PM 21076035
ER

PT J
AU Zhang, R
   Zhong, NN
   Liu, MG
   Yan, H
   Qiu, CA
   Han, Y
   Wang, W
   Hou, WK
   Liu, Y
   Gao, CG
   Guo, TW
   Lu, SM
   Deng, HW
   Ma, J
AF Zhang, Rui
   Zhong, Nan-Nan
   Liu, Mao-Gang
   Yan, Han
   Qiu, Chuan
   Han, Yan
   Wang, Wei
   Hou, Wei-Kun
   Liu, Yue
   Gao, Cheng-Ge
   Guo, Ting-Wei
   Lu, She-Min
   Deng, Hong-Wen
   Ma, Jie
TI Is the EFNB2 locus associated with schizophrenia? Single nucleotide
   polymorphisms and haplotypes analysis
SO PSYCHIATRY RESEARCH
LA English
DT Article
DE Schizophrenia; EFNB2; SNP; Haplotype; Association; NMDA
ID AMINO-ACID OXIDASE; CHINESE POPULATION; TRANSMISSION DISEQUILIBRIUM;
   G72/G30 POLYMORPHISMS; GENE-EXPRESSION; CANDIDATE GENES; NO ASSOCIATION;
   DAOA; LINKAGE; G72
AB Recently evidence of linkage of schizophrenia to chromosome 13q22-q34 has been demonstrated in multiple studies Based on structure and function EFNB2 may be considered as a compelling candidate gene for schizophrenia on chromosome 13q33 We genotyped three single-nucleotide polymorphisms (SNPs rs9520087 rs11069646 and rs8000078) in this region in 846 Han Chinese subjects (477 cases and 369 controls) Significant association between an allele of marker rs9520087 and schizophrenia was found Furthermore since no ID was observed in the three SNPs linkage disequilibrium estimation all three SNPs were used in multiple SNPs haplotype analysis and a strongly significant difference was found for the common haplotype TTC Overall our findings indicate that EFNB2 gene may be a candidate susceptibility gene for schizophrenia in the Han Chinese population and also provide further support for the potential importance of the NMDA receptor pathway in the etiology of schizophrenia (C) 2010 Elsevier Ireland Ltd All rights reserved
C1 [Zhang, Rui; Zhong, Nan-Nan; Han, Yan; Wang, Wei; Hou, Wei-Kun; Liu, Yue; Guo, Ting-Wei; Lu, She-Min; Ma, Jie] Xi An Jiao Tong Univ, Dept Genet & Mol Biol, Sch Med, Xian 710061, Shaanxi, Peoples R China.
   [Liu, Mao-Gang; Yan, Han; Qiu, Chuan; Deng, Hong-Wen] Xi An Jiao Tong Univ, Sch Life Sci & Technol, Xian 710061, Shaanxi, Peoples R China.
   [Gao, Cheng-Ge] Xi An Jiao Tong Univ, Sch Med, Affiliated Hosp 1, Xian 710061, Shaanxi, Peoples R China.
   [Guo, Ting-Wei] NIDDK, NIH, Phoenix, AZ USA.
RP Guo, TW (reprint author), Xi An Jiao Tong Univ, Dept Genet & Mol Biol, Sch Med, 76 W Yan Ta Rd, Xian 710061, Shaanxi, Peoples R China.
OI Lu, Shemin/0000-0001-8250-850X; Deng, Hong-Wen/0000-0002-0387-8818
FU Ministry of Education PRC [20090201120062]; National Natural Science
   Foundation of China [30800618]; Headmaster Fundation of Xi an Jiaotong
   University
FX We are deeply grateful to all of the families who participated in this
   study as well as to the psychiatrists and mental health workers who
   helped us with the identification of the families This work was
   supported by grants from the Ministry of Education PRC (No
   20090201120062) the National Natural Science Foundation of China (No
   30800618) and the Headmaster Fundation of Xi an Jiaotong University
NR 38
TC 10
Z9 11
U1 0
U2 2
PU ELSEVIER IRELAND LTD
PI CLARE
PA ELSEVIER HOUSE, BROOKVALE PLAZA, EAST PARK SHANNON, CO, CLARE, 00000,
   IRELAND
SN 0165-1781
J9 PSYCHIAT RES
JI Psychiatry Res.
PD NOV 30
PY 2010
VL 180
IS 1
BP 5
EP 9
DI 10.1016/j.psychres.2010.04.037
PG 5
WC Psychiatry
SC Psychiatry
GA 687QO
UT WOS:000284793200002
PM 20483485
ER

PT J
AU Schafer, MKH
   Mahata, SK
   Stroth, N
   Eiden, LE
   Weihe, E
AF Schafer, M. K. -H.
   Mahata, S. K.
   Stroth, N.
   Eiden, L. E.
   Weihe, E.
TI Cellular distribution of chromogranin A in excitatory, inhibitory,
   aminergic and peptidergic neurons of the rodent central nervous system
SO REGULATORY PEPTIDES
LA English
DT Article
DE GABAergic; Glutamatergic; WE14; Neurosecretion, chemical coding;
   Neurotransmission
ID VESICULAR ACETYLCHOLINE TRANSPORTER; SECRETORY GRANULE BIOGENESIS;
   DENSE-CORED VESICLES; RAT-BRAIN; MONOAMINE TRANSPORTER-2; CATECHOLAMINE
   RELEASE; CHOLINERGIC NEURONS; TARGETED ABLATION; SECRETOGRANIN-II;
   ADRENAL-MEDULLA
AB Immunoreactivity for both processed and unprocessed forms of chromogranin A (CGA) was examined, using an antibody recognizing the WE14 epitope, among terminal fields and cell bodies of anatomically defined GABAergic, glutamatergic, cholinergic, catecholaminergic, and peptidergic cell groups in the rodent central nervous system. CGA is ubiquitous within neuronal cell bodies, with no obvious anatomical or chemically-coded subdivision of the nervous system in which CGA is not expressed in most neurons. CGA expression is essentially absent from catecholaminergic terminal fields in the CNS, suggesting a relative paucity of large dense-core vesicles in CNS compared to peripheral catecholaminergic neurons. Extensive synaptic co-localization with classical transmitter markers is not observed even in areas such as amygdala, where CGA fibers are numerous, suggesting preferential segregation of CGA to peptidergic terminals in CNS. Localization of CGA in dendrites in some areas of CNS may indicate its involvement in regulation of dendritic release mechanisms. Finally, the ubiquitous presence of CGA in neuronal cell somata, especially pronounced in GABAergic neurons, suggests a second non-secretory vesicle-associated function for CGA in CNS. We propose that CGA may function in the CNS as a prohormone and granulogenic factor in some terminal fields, but also possesses as-yet unknown unique cellular functions within neuronal somata and dendrites. (C) 2009 Published by Elsevier B.V.
C1 [Stroth, N.; Eiden, L. E.] NIMH IRP, Mol Neurosci Sect, Bethesda, MD 20892 USA.
   [Schafer, M. K. -H.; Weihe, E.] Univ Marburg, Inst Anat & Cell Biol, Marburg, Germany.
   [Mahata, S. K.] Univ Calif San Diego, Dept Med, La Jolla, CA 92093 USA.
RP Eiden, LE (reprint author), NIMH IRP, Mol Neurosci Sect, Bethesda, MD 20892 USA.
EM eidenl@mail.nih.gov
OI Eiden, Lee/0000-0001-7524-944X
FU NIMH-IRP [Z01-MH002386-23]; NIH [R01DA011311-10]; University Clinics
   Giessen Marburg (UKGM); Volkswagen-Stiftung (LEE, EW)
FX This work was supported by NIMH-IRP Project Z01-MH002386-23 (LEE), NIH
   grant R01DA011311-10 (SM), University Clinics Giessen Marburg (UKGM)
   grant (MKHS) and a grant from the Volkswagen-Stiftung (LEE, EW). The
   technical assistance of Heidemarie Schneider, Michael Schneider, Barbara
   Wiegand, Marion Zibuschka, and David Huddleston is gratefully
   acknowledged.
NR 52
TC 3
Z9 3
U1 1
U2 2
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 30
PY 2010
VL 165
IS 1
SI SI
BP 36
EP 44
DI 10.1016/j.regpep.2009.11.021
PG 9
WC Endocrinology & Metabolism; Physiology
SC Endocrinology & Metabolism; Physiology
GA 705RP
UT WOS:000286155900007
PM 20005907
ER

PT J
AU Koshimizu, H
   Kim, T
   Cawley, NX
   Loh, YP
AF Koshimizu, Hisatsugu
   Kim, Taeyoon
   Cawley, Niamh X.
   Loh, Y. Peng
TI Reprint of: Chromogranin A: A new proposal for trafficking, processing
   and induction of granule biogenesis
SO REGULATORY PEPTIDES
LA English
DT Article
DE Chromogranin A; Granule biogenesis; AtT-20 cells; Protease Nexin-1;
   Secretogranin III
ID REGULATED SECRETORY PATHWAY; TRANS-GOLGI NETWORK; CHROMAFFIN GRANULES;
   SECRETOGRANIN-III; TARGETED ABLATION; SORTING RECEPTOR; BREFELDIN-A;
   CATHEPSIN-L; CELLS; PROHORMONE
AB Chromogranin A (CgA), a member of the granin family serves several important cell biological roles in (neuro) endocrine cells which are summarized in this review. CgA is a "prohormone" that is synthesized at the rough endoplasmic reticulum and transported into the cisternae of this organelle via its signal peptide. It is then trafficked to the Golgi complex and then to the trans-Golgi network (TGN) where CgA aggregates at low pH in the presence of calcium. The CgA aggregates provide the physical driving force to induce budding of the TGN membrane resulting in dense core granule (DCG) formation. Within the granule, a small amount of the CgA is processed to bioactive peptides, including a predicted C-terminal peptide, serpinin. Upon stimulation, DCGs undergo exocytosis and CgA and its derived peptides are released. Serpinin, acting extracellularly is able to signal the increase in transcription of a serine protease inhibitor, protease nexin-1 (PN-1) that protects DCG proteins against degradation in the Golgi complex, which then enhances DCG biogenesis to replenish those that were released. Thus CgA and its derived peptide, serpinin, plays a significant role in granule formation and regulation of granule biogenesis, respectively, in (neuro) endocrine cells. (C) 2010 Published by Elsevier B.V.
C1 [Koshimizu, Hisatsugu; Kim, Taeyoon; Cawley, Niamh X.; Loh, Y. Peng] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Cellular Neurobiol Sect, Program Dev Neurosci, NIH, Bethesda, MD 20892 USA.
RP Loh, YP (reprint author), Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Cellular Neurobiol Sect, Program Dev Neurosci, NIH, Bldg 49,Rm 5A-22,49 Convent Dr, Bethesda, MD 20892 USA.
EM lohp@mail.nih.gov
FU Eunice Kennedy Shriver National Institute of Child Health and Human
   Development, National Institutes of Health
FX This work was supported by Eunice Kennedy Shriver National Institute of
   Child Health and Human Development, National Institutes of Health
   intramural research programs.
NR 42
TC 3
Z9 3
U1 0
U2 1
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 30
PY 2010
VL 165
IS 1
SI SI
BP 95
EP 101
DI 10.1016/j.regpep.2010.09.006
PG 7
WC Endocrinology & Metabolism; Physiology
SC Endocrinology & Metabolism; Physiology
GA 705RP
UT WOS:000286155900014
PM 20920534
ER

PT J
AU Kozak, CA
AF Kozak, Christine A.
TI The mouse "xenotropic" gammaretroviruses and their XPR1 receptor
SO RETROVIROLOGY
LA English
DT Review
ID MURINE LEUKEMIA-VIRUS; CHRONIC-FATIGUE-SYNDROME; FOCUS-FORMING VIRUS;
   CELL-SURFACE RECEPTOR; MAJOR GLYCOPROTEINS GP70; PROSTATE
   CARCINOMA-CELLS; HOST-RANGE RESTRICTIONS; MUS-MUSCULUS-MOLOSSINUS; LONG
   TERMINAL REPEATS; HUMAN RETROVIRUS XMRV
AB The xenotropic/polytropic subgroup of mouse leukemia viruses (MLVs) all rely on the XPR1 receptor for entry, but these viruses vary in tropism, distribution among wild and laboratory mice, pathogenicity, strategies used for transmission, and sensitivity to host restriction factors. Most, but not all, isolates have typical xenotropic or polytropic host range, and these two MLV tropism types have now been detected in humans as viral sequences or as infectious virus, termed XMRV, or xenotropic murine leukemia virus-related virus. The mouse xenotropic MLVs (X-MLVs) were originally defined by their inability to infect cells of their natural mouse hosts. It is now clear, however, that X-MLVs actually have the broadest host range of the MLVs. Nearly all nonrodent mammals are susceptible to X-MLVs, and all species of wild mice and several common strains of laboratory mice are X-MLV susceptible. The polytropic MLVs, named for their apparent broad host range, show a more limited host range than the X-MLVs in that they fail to infect cells of many mouse species as well as many nonrodent mammals. The co-evolution of these viruses with their receptor and other host factors that affect their replication has produced a heterogeneous group of viruses capable of inducing various diseases, as well as endogenized viral genomes, some of which have been domesticated by their hosts to serve in antiviral defense.
C1 NIAID, Mol Microbiol Lab, Bethesda, MD 20892 USA.
RP Kozak, CA (reprint author), NIAID, Mol Microbiol Lab, Bethesda, MD 20892 USA.
EM ckozak@niaid.nih.gov
FU NIH, NIAID
FX This work was supported by the Intramural Research Program of the NIH,
   NIAID.
NR 212
TC 41
Z9 42
U1 0
U2 8
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1742-4690
J9 RETROVIROLOGY
JI Retrovirology
PD NOV 30
PY 2010
VL 7
AR 101
DI 10.1186/1742-4690-7-101
PG 17
WC Virology
SC Virology
GA 700ZS
UT WOS:000285784700002
PM 21118532
ER

PT J
AU Tooze, JA
   Kipnis, V
   Buckman, DW
   Carroll, RJ
   Freedman, LS
   Guenther, PM
   Krebs-Smith, SM
   Subar, AF
   Dodd, KW
AF Tooze, Janet A.
   Kipnis, Victor
   Buckman, Dennis W.
   Carroll, Raymond J.
   Freedman, Laurence S.
   Guenther, Patricia M.
   Krebs-Smith, Susan M.
   Subar, Amy F.
   Dodd, Kevin W.
TI A mixed-effects model approach for estimating the distribution of usual
   intake of nutrients: The NCI method
SO STATISTICS IN MEDICINE
LA English
DT Article
DE statistical distributions; diet surveys; nutrition assessment;
   mixed-effects model; nutrients; percentiles
ID EPISODICALLY CONSUMED FOODS; MULTIPLE-PASS METHOD; MEASUREMENT ERROR;
   POPULATION; BIOMARKER; VARIANCE; DESIGN
AB It is of interest to estimate the distribution of usual nutrient intake for a population from repeat 24-h dietary recall assessments. A mixed effects model and quantile estimation procedure, developed at the National Cancer Institute (NCI), may be used for this purpose. The model incorporates a Box-Cox parameter and covariates to estimate usual daily intake of nutrients; model parameters are estimated via quasi-Newton optimization of a likelihood approximated by the adaptive Gaussian quadrature. The parameter estimates are used in a Monte Carlo approach to generate empirical quantiles; standard errors are estimated by bootstrap. The NCI method is illustrated and compared with current estimation methods, including the individual mean and the semi-parametric method developed at the Iowa State University (ISU), using data from a random sample and computer simulations. Both the NCI and ISU methods for nutrients are superior to the distribution of individual means. For simple (no covariate) models, quantile estimates are similar between the NCI and ISU methods. The bootstrap approach used by the NCI method to estimate standard errors of quantiles appears preferable to Taylor linearization. One major advantage of the NCI method is its ability to provide estimates for subpopulations through the incorporation of covariates into the model. The NCI method may be used for estimating the distribution of usual nutrient intake for populations and subpopulations as part of a unified framework of estimation of usual intake of dietary constituents. Copyright (C) 2010 John Wiley & Sons, Ltd.
C1 [Tooze, Janet A.] Wake Forest Univ, Dept Biostat Sci, Sch Med, Winston Salem, NC 27157 USA.
   [Kipnis, Victor; Dodd, Kevin W.] NCI, Canc Prevent Div, Bethesda, MD 20892 USA.
   [Buckman, Dennis W.] Informat Management Serv Inc, Silver Spring, MD 20904 USA.
   [Carroll, Raymond J.] Texas A&M Univ, Dept Stat, College Stn, TX 77843 USA.
   [Freedman, Laurence S.] Sheba Med Ctr, Gertner Inst Epidemiol & Hlth Policy Res, IL-52161 Tel Hashomer, Israel.
   [Guenther, Patricia M.] Ctr Nutr Policy & Promot, USDA, Alexandria, VA 22302 USA.
   [Krebs-Smith, Susan M.; Subar, Amy F.] NCI, Appl Res Program, Div Canc Control & Populat Sci, Bethesda, MD 20892 USA.
RP Tooze, JA (reprint author), Wake Forest Univ, Dept Biostat Sci, Sch Med, Med Ctr Blvd, Winston Salem, NC 27157 USA.
EM jtooze@wfubmc.edu
FU NCI NIH HHS [R37 CA057030, R37 CA057030-23, R01 CA057030]
NR 23
TC 113
Z9 116
U1 0
U2 25
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0277-6715
J9 STAT MED
JI Stat. Med.
PD NOV 30
PY 2010
VL 29
IS 27
BP 2857
EP 2868
DI 10.1002/sim.4063
PG 12
WC Mathematical & Computational Biology; Public, Environmental &
   Occupational Health; Medical Informatics; Medicine, Research &
   Experimental; Statistics & Probability
SC Mathematical & Computational Biology; Public, Environmental &
   Occupational Health; Medical Informatics; Research & Experimental
   Medicine; Mathematics
GA 680BL
UT WOS:000284206400008
PM 20862656
ER

PT J
AU Jin, SM
   Lazarou, M
   Wang, CX
   Kane, LA
   Narendra, DP
   Youle, RJ
AF Jin, Seok Min
   Lazarou, Michael
   Wang, Chunxin
   Kane, Lesley A.
   Narendra, Derek P.
   Youle, Richard J.
TI Mitochondrial membrane potential regulates PINK1 import and proteolytic
   destabilization by PARL
SO JOURNAL OF CELL BIOLOGY
LA English
DT Article
ID RECESSIVE JUVENILE PARKINSONISM; SUBCELLULAR-LOCALIZATION; OXIDATIVE
   STRESS; DISEASE; MUTATIONS; MITOPHAGY; PROTEASES; MUTANTS;
   DROSOPHILA-PINK1; INACTIVATION
AB PINK1 is a mitochondrial kinase mutated in some familial cases of Parkinson's disease. It has been found to work in the same pathway as the E3 ligase Parkin in the maintenance of flight muscles and dopaminergic neurons in Drosophila melanogaster and to recruit cytosolic Parkin to mitochondria to mediate mitophagy in mammalian cells. Although PINK1 has a predicted mitochondrial import sequence, its cellular and submitochondrial localization remains unclear in part because it is rapidly degraded. In this study, we report that the mitochondrial inner membrane rhomboid protease presenilin-associated rhomboid-like protein (PARL) mediates cleavage of PINK1 dependent on mitochondrial membrane potential. In the absence of PARL, the constitutive degradation of PINK1 is inhibited, stabilizing a 60-kD form inside mitochondria. When mitochondrial membrane potential is dissipated, PINK1 accumulates as a 63-kD full-length form on the outer mitochondrial membrane, where it can recruit Parkin to impaired mitochondria. Thus, differential localization to the inner and outer mitochondrial membranes appears to regulate PINK1 stability and function.
C1 [Jin, Seok Min; Lazarou, Michael; Wang, Chunxin; Kane, Lesley A.; Narendra, Derek P.; Youle, Richard J.] NINDS, Biochem Sect, Surg Neurol Branch, NIH, Bethesda, MD 20892 USA.
   [Narendra, Derek P.] Univ Cambridge, MRC, Mitochondrial Biol Unit, Welcome Trust Med Res Council, Cambridge CB2 0XY, England.
RP Youle, RJ (reprint author), NINDS, Biochem Sect, Surg Neurol Branch, NIH, Bethesda, MD 20892 USA.
EM youler@ninds.nih.gov
RI Lazarou, Michael/G-7143-2011; Wang, Chunxin/B-9312-2016; 
OI Wang, Chunxin/0000-0001-6015-6806; Lazarou, Michael/0000-0003-2150-5545
FU National Institutes of Health
FX This work was supported by the National Institutes of Health intramural
   program.
NR 34
TC 334
Z9 345
U1 1
U2 28
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 29
PY 2010
VL 191
IS 5
BP 933
EP 942
DI 10.1083/jcb.201008084
PG 10
WC Cell Biology
SC Cell Biology
GA 690EK
UT WOS:000284985100007
PM 21115803
ER

PT J
AU Sens, KL
   Zhang, SL
   Jin, P
   Duan, R
   Zhang, GF
   Luo, FB
   Parachini, L
   Chen, EH
AF Sens, Kristin L.
   Zhang, Shiliang
   Jin, Peng
   Duan, Rui
   Zhang, Guofeng
   Luo, Fengbao
   Parachini, Lauren
   Chen, Elizabeth H.
TI An invasive podosome-like structure promotes fusion pore formation
   during myoblast fusion
SO JOURNAL OF CELL BIOLOGY
LA English
DT Article
ID CELL-CELL FUSION; DROSOPHILA-MELANOGASTER; IMMUNOGLOBULIN SUPERFAMILY;
   CYTOSKELETAL ORGANIZATION; TRANSCELLULAR DIAPEDESIS; ACTIN CYTOSKELETON;
   ROLLING-PEBBLES; PROTEIN; WASP; INVADOPODIA
AB Recent studies in Drosophila have implicated actin cytoskeletal remodeling in myoblast fusion, but the cellular mechanisms underlying this process remain poorly understood. Here we show that actin polymerization occurs in an asymmetric and cell type specific manner between a muscle founder cell and a fusion-competent myoblast (FCM). In the FCM, a dense F-actin enriched focus forms at the site of fusion, whereas a thin sheath of F-actin is induced along the apposing founder cell membrane. The FCM-specific actin focus invades the apposing founder cell with multiple finger-like protrusions, leading to the formation of a single-channel macro fusion pore between the two muscle cells. Two actin nucleation promoting factors of the Arp2/3 complex, WASP and Scar, are required for the formation of the F-actin foci, whereas WASP but not Scar promotes efficient foci invasion. Our studies uncover a novel invasive podosome-like structure (PLS) in a developing tissue and reveal a previously unrecognized function of PLSs in facilitating cell membrane juxtaposition and fusion.
C1 [Sens, Kristin L.; Zhang, Shiliang; Jin, Peng; Duan, Rui; Luo, Fengbao; Parachini, Lauren; Chen, Elizabeth H.] Johns Hopkins Univ, Dept Mol Biol & Genet, Sch Med, Baltimore, MD 21205 USA.
   [Zhang, Guofeng] Natl Inst Biomed Imaging & Bioengn, Lab Bioengn & Phys Sci, Bethesda, MD 20892 USA.
RP Chen, EH (reprint author), Johns Hopkins Univ, Dept Mol Biol & Genet, Sch Med, Baltimore, MD 21205 USA.
EM echen@jhmi.edu
FU National Institutes of Health; American Heart Association
FX This work was supported by grants from the National Institutes of Health
   and the American Heart Association. P. Jin is a predoctoral fellow of
   the American Heart Association. E.H. Chen is a Searle Scholar and a
   Packard Fellow.
NR 67
TC 74
Z9 76
U1 0
U2 7
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 29
PY 2010
VL 191
IS 5
BP 1013
EP 1027
DI 10.1083/jcb.201006006
PG 15
WC Cell Biology
SC Cell Biology
GA 690EK
UT WOS:000284985100013
PM 21098115
ER

PT J
AU Le Nouen, C
   Hillyer, P
   Munir, S
   Winter, CC
   McCarty, T
   Bukreyev, A
   Collins, PL
   Rabin, RL
   Buchholz, UJ
AF Le Nouen, Cyril
   Hillyer, Philippa
   Munir, Shirin
   Winter, Christine C.
   McCarty, Thomas
   Bukreyev, Alexander
   Collins, Peter L.
   Rabin, Ronald L.
   Buchholz, Ursula J.
TI Effects of Human Respiratory Syncytial Virus, Metapneumovirus,
   Parainfluenza Virus 3 and Influenza Virus on CD4+T Cell Activation by
   Dendritic Cells
SO PLOS ONE
LA English
DT Article
ID T-HELPER TYPE-1; IN-VITRO; YOUNG-CHILDREN; DIFFERENTIAL RESPONSE;
   FLOW-CYTOMETRY; CILIATED CELLS; TRACT DISEASE; HUMAN NAIVE; INFECTION;
   LYMPHOCYTES
AB Background: Human respiratory syncytial virus (HRSV), and to a lesser extent human metapneumovirus (HMPV) and human parainfluenza virus type 3 (HPIV3), re-infect symptomatically throughout life without antigenic change, suggestive of incomplete immunity. One causative factor is thought to be viral interference with dendritic cell (DC)-mediated stimulation of CD4+ T cells.
   Methodology, Principal Findings: We infected human monocyte-derived DC with purified HRSV, HMPV, HPIV3, or influenza A virus (IAV) and compared their ability to induce activation and proliferation of autologous CD4+ T cells in vitro. IAV was included because symptomatic re-infection without antigenic change is less frequent, suggesting that immune protection is more complete and durable. We examined virus-specific memory responses and superantigen-induced responses by multiparameter flow cytometry. Live virus was more stimulatory than inactivated virus in inducing DC-mediated proliferation of virus-specific memory CD4+ T cells, suggesting a lack of strong suppression by live virus. There were trends of increasing proliferation in the order: HMPV, HRSV, HPIV3, IAV, and greater production of interferon-gamma c and tumor necrosis factor-alpha by proliferating cells in response to IAV, but differences were not significant. Exposure of DC to HRSV, HPIV3, or IAV reduced CD4+ T cell proliferation in response to secondary stimulus with superantigen, but the effect was transitory and greatest for IAV. T cell cytokine production was similar, with no evidence of Th2 or Th17 skewing.
   Conclusions, Significance: Understanding the basis for the ability of HRSV in particular to symptomatically re-infect without significant antigenic change is of considerable interest. The present results show that these common respiratory viruses are similar in their ability to induce DC to activate CD4+ T cells. Thus, the results do not support the common model in which viral suppression of CD4+ T cell activation and proliferation by HRSV, HMPV, and HPIV3 is a major factor in the difference in re-infectability compared to IAV.
C1 [Le Nouen, Cyril; Munir, Shirin; Winter, Christine C.; McCarty, Thomas; Bukreyev, Alexander; Collins, Peter L.; Buchholz, Ursula J.] NIAID, Infect Dis Lab, NIH, Bethesda, MD 20892 USA.
   [Hillyer, Philippa; Rabin, Ronald L.] US FDA, Ctr Biol Evaluat & Res, Bethesda, MD USA.
RP Le Nouen, C (reprint author), NIAID, Infect Dis Lab, NIH, Bethesda, MD 20892 USA.
EM ubuchholz@niaid.nih.gov
OI Tripp, Ralph/0000-0002-2924-9956
FU NIAID, NIH
FX This research was supported by the Intramural Research Program of the
   NIAID, NIH. Disclaimer: The views expressed in this report are the
   personal opinions of the authors and are not the official opinion of the
   U.S. Food and Drug Administration, the National Institutes of Health, or
   the Department of Health and Human Services. The funders had no role in
   study design, data collection and analysis, decision to publish, or
   preparation of the manuscript.
NR 60
TC 18
Z9 18
U1 1
U2 7
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 185 BERRY ST, STE 1300, SAN FRANCISCO, CA 94107 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD NOV 29
PY 2010
VL 5
IS 11
AR e15017
DI 10.1371/journal.pone.0015017
PG 14
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 686HD
UT WOS:000284686500016
PM 21124776
ER

PT J
AU Pinton, G
   Thomas, W
   Bellini, P
   Manente, AG
   Favoni, RE
   Harvey, BJ
   Mutti, L
   Moro, L
AF Pinton, Giulia
   Thomas, Warren
   Bellini, Paolo
   Manente, Arcangela Gabriella
   Favoni, Roberto E.
   Harvey, Brian J.
   Mutti, Luciano
   Moro, Laura
TI Estrogen Receptor beta Exerts Tumor Repressive Functions in Human
   Malignant Pleural Mesothelioma via EGFR Inactivation and Affects
   Response to Gefitinib
SO PLOS ONE
LA English
DT Article
ID GROWTH-FACTOR RECEPTOR; ENDOCRINE THERAPY RESISTANCE; FACTOR SIGNALING
   PATHWAYS; PROSTATE-CANCER CELLS; MOLECULAR-MECHANISM; LUNG-CANCER;
   PHASE-II; TYROSINE KINASE; BREAST-CANCER; CROSS-TALK
AB Background: The role of estrogen and estrogen receptors in oncogenesis has been investigated in various malignancies. Recently our group identified estrogen receptor beta (ER beta) expression as an independent prognostic factor in the progression of human Malignant Pleural Mesothelioma (MMe), but the underlying mechanism by which ER beta expression in tumors determines clinical outcome remains largely unknown. This study is aimed at investigating the molecular mechanisms of ER beta action in MMe cells and disclosing the potential translational implications of these results.
   Methods: We modulated ER beta expression in REN and MSTO-211H MMe cell lines and evaluated cell proliferation and EGF receptor (EGFR) activation.
   Results: Our data indicate that ER beta knockdown in ER positive cells confers a more invasive phenotype, increases anchorage independent proliferation and elevates the constitutive activation of EGFR-coupled signal transduction pathways. Conversely, re-expression of ER beta in ER negative cells confers a more epithelioid phenotype, decreases their capacity for anchorage independent growth and down-modulates proliferative signal transduction pathways. We identify a physical interaction between ER beta, EGFR and caveolin 1 that results in an altered internalization and in a selective reduced activation of EGFR-coupled signaling, when ER beta is over-expressed. We also demonstrate that differential expression of ER beta influences MMe tumor cell responsiveness to the therapeutic agent: Gefitinib.
   Conclusions: This study describes a role for ER beta in the modulation of cell proliferation and EGFR activation and provides a rationale to facilitate the targeting of a subgroup of MMe patients who would benefit most from therapy with Gefitinib alone or in combination with Akt inhibitors.
C1 [Pinton, Giulia; Bellini, Paolo; Manente, Arcangela Gabriella; Moro, Laura] Univ Piemonte Orientale, Drug & Food Biotechnol Ctr, Dept Chem Food Pharmaceut & Pharmacol Sci, Novara, Italy.
   [Thomas, Warren; Harvey, Brian J.] Royal Coll Surgeons Ireland, Dept Mol Med, Dublin 2, Ireland.
   [Thomas, Warren; Harvey, Brian J.] Beaumont Hosp, Educ & Res Ctr, Dublin 9, Ireland.
   [Favoni, Roberto E.] Natl Canc Inst, Lab Expt Pharmacol, Genoa, Italy.
   [Mutti, Luciano] Dept Med, Local Hlth Unit 11, Vercelli, Italy.
RP Pinton, G (reprint author), Univ Piemonte Orientale, Drug & Food Biotechnol Ctr, Dept Chem Food Pharmaceut & Pharmacol Sci, Novara, Italy.
EM moro@pharm.unipmn.it
RI Harvey, Brian/A-5120-2010; Thomas, Warren/A-5477-2010
OI Harvey, Brian/0000-0002-7388-8034; 
FU MARF (Mesothelioma Applied Research Foundation); Fondazione Buzzi
   Unicem; Higher Education Authority of Ireland [PRTLI4]; Progetto
   Lagrange (Cassa di Risparmio di Torino)
FX This work was supported by MARF (Mesothelioma Applied Research
   Foundation), Fondazione Buzzi Unicem and Higher Education Authority of
   Ireland (PRTLI4) through the National Biophotonics and Imaging Platform.
   G. Pinton was supported by a PhD fellowship from Progetto Lagrange
   (Cassa di Risparmio di Torino). The funders had no role in study design,
   data collection and analysis, decision to publish, or preparation of the
   manuscript.
NR 40
TC 24
Z9 24
U1 0
U2 1
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 185 BERRY ST, STE 1300, SAN FRANCISCO, CA 94107 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD NOV 29
PY 2010
VL 5
IS 11
AR e14110
DI 10.1371/journal.pone.0014110
PG 10
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 686HD
UT WOS:000284686500005
PM 21124760
ER

PT J
AU Ghez, D
   Lepelletier, Y
   Jones, KS
   Pique, C
   Hermine, O
AF Ghez, David
   Lepelletier, Yves
   Jones, Kathryn S.
   Pique, Claudine
   Hermine, Olivier
TI Current concepts regarding the HTLV-1 receptor complex
SO RETROVIROLOGY
LA English
DT Review
ID T-CELL LEUKEMIA; VIRUS TYPE-I; HEPARAN-SULFATE PROTEOGLYCANS;
   GLUCOSE-TRANSPORTER GLUT-1; ENDOTHELIAL GROWTH-FACTOR; ENVELOPE-MEDIATED
   FUSION; SYNCYTIUM FORMATION; IMMUNODEFICIENCY-VIRUS; BINDING-PROTEIN;
   DENDRITIC CELLS
AB The identity of the Human T lymphotropic Virus type 1 (HTLV-1) receptor remained an unsolved puzzle for two decades, until the recent demonstration that three molecules, Glucose Transporter 1, Neuropilin-1 and Heparan Sulfate Proteoglycans are involved in HTLV-1 binding and entry. Despite these advances, several questions remain unanswered, including the precise role of each of these molecules during virus entry. In light of the most recent data, we propose a model of the HTLV-1 receptor complex and discuss its potential impact on HTLV-1 infection.
C1 [Ghez, David; Lepelletier, Yves; Hermine, Olivier] Univ Paris 05, CNRS, UMR8147, F-75743 Paris 15, France.
   [Ghez, David] Inst Gustave Roussy, Serv Hematol, F-94805 Villejuif, France.
   [Jones, Kathryn S.] NCI, SAIC Frederick Inc, Frederick, MD 21701 USA.
   [Pique, Claudine] Univ Paris 05, CNRS, UMR 8104, Inst Cochin, Paris, France.
   [Pique, Claudine] INSERM, U1016, Paris, France.
   [Hermine, Olivier] Hop Necker Enfants Malad, Serv Hematol Adulte, F-75743 Paris 15, France.
RP Ghez, D (reprint author), Univ Paris 05, CNRS, UMR8147, 161 Rue Sevres, F-75743 Paris 15, France.
EM david.ghez@igr.fr; ohermine@gmail.com
OI lepelletier, yves/0000-0001-7746-5170
FU French Foundation "Cent pour sang la Vie"; Institut National du cancer
   (INCA); Association de lutte contre le cancer; ligue nationale contre le
   cancer; canceropole d'ile de France; foundation pour la recherche
   medicale; foundation de France
FX The authors would like to thank the French Foundation "Cent pour sang la
   Vie", Institut National du cancer (INCA), Association de lutte contre le
   cancer, ligue nationale contre le cancer, canceropole d'ile de France,
   foundation pour la recherche medicale, foundation de France for the
   financial support of this work.
NR 92
TC 30
Z9 31
U1 0
U2 5
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1742-4690
J9 RETROVIROLOGY
JI Retrovirology
PD NOV 29
PY 2010
VL 7
AR 99
DI 10.1186/1742-4690-7-99
PG 11
WC Virology
SC Virology
GA 694JK
UT WOS:000285292800001
PM 21114861
ER

PT J
AU Beard, WA
   Batra, VK
   Wilson, SH
AF Beard, William A.
   Batra, Vinod K.
   Wilson, Samuel H.
TI DNA polymerase structure-based insight on the mutagenic properties of
   8-oxoguanine
SO MUTATION RESEARCH-GENETIC TOXICOLOGY AND ENVIRONMENTAL MUTAGENESIS
LA English
DT Review
DE Base excision repair; DNA polymerase; Structure; Fidelity; Endogenous
   DNA damage
ID ACTIVE-SITE; FIDELITY; LESION; BETA; 8-HYDROXYGUANINE; OPPOSITE;
   RESIDUE; BYPASS; REPAIR; DAMAGE
AB An aerobic environment burdens DNA polymerase substrates with oxidized substrates (DNA and nucleotide pools). A major promutagenic lesion resulting from oxidative stress is 8-oxo-7,8-dihydro2'-deoxyguanosine (8-oxoG). Guanine oxidation alters the hydrogen bonding properties of the base and glycosidic-preference of the nucleotide. The favored glycosidic syn-conformation exposes the Hoogsteen edge of the base for hydrogen bonding with adenine during DNA synthesis. The cell has recognized the threat of this lesion and has evolved an intricate surveillance system to provide DNA polymerases with unmodified substrates. Failure to do so leads to transversion mutations. Since the mutagenic properties of the base are dictated by the anti-syn-conformation of the nucleotide, the molecular interactions of 8-oxoG in the confines of the DNA polymerase active site are expected to influence its coding potential. Recent structural characterization of DNA polymerases from several families with this lesion in the nascent base pair binding pocket has provided insight to the mutagenic properties of this modified nucleotide. These structures reveal that flexibility around the template-binding pocket can permit 8-oxoG to assume an anti- or syn-conformation and code for cytosine or adenine incorporation, respectively. In contrast, the binding pocket for the incoming nucleotide does not have this flexibility so that 8-oxodGTP insertion opposite cytosine is strongly discouraged. Published by Elsevier B.V.
C1 [Beard, William A.; Batra, Vinod K.; Wilson, Samuel H.] NIEHS, Struct Biol Lab, NIH, Res Triangle Pk, NC 27709 USA.
RP Wilson, SH (reprint author), NIEHS, Struct Biol Lab, NIH, POB 12233, Res Triangle Pk, NC 27709 USA.
EM wilson5@niehs.nih.gov
FU National Institutes of Health, National Institute of Environmental
   Health Sciences [Z01-ES050158, Z01-ES050161]; National Institutes of
   Health [1U19CA105010, P41 RR-01081]
FX This research was supported by Research Project Numbers Z01-ES050158 and
   Z01-ES050161 in the Intramural Research Program of the National
   Institutes of Health, National Institute of Environmental Health
   Sciences and was in association with the National Institutes of Health
   Grant 1U19CA105010. Molecular graphic images were produced using the
   Chimera package [38] from the Resource for Biocomputing, Visualization,
   and Informatics at the University of California, San Francisco
   (supported by NIH P41 RR-01081).
NR 38
TC 39
Z9 39
U1 0
U2 7
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 1383-5718
J9 MUTAT RES-GEN TOX EN
JI Mutat. Res. Genet. Toxicol. Environ. Mutagen.
PD NOV 28
PY 2010
VL 703
IS 1
SI SI
BP 18
EP 23
DI 10.1016/j.mrgentox.2010.07.013
PG 6
WC Biotechnology & Applied Microbiology; Genetics & Heredity; Toxicology
SC Biotechnology & Applied Microbiology; Genetics & Heredity; Toxicology
GA 696NA
UT WOS:000285446900004
PM 20696268
ER

PT J
AU Chun, TW
   Justement, JS
   Murray, D
   Hallahan, CW
   Maenza, J
   Collier, AC
   Sheth, PM
   Kaul, R
   Ostrowski, M
   Moir, S
   Kovacs, C
   Fauci, AS
AF Chun, Tae-Wook
   Justement, J. Shawn
   Murray, Danielle
   Hallahan, Claire W.
   Maenza, Janine
   Collier, Ann C.
   Sheth, Prameet M.
   Kaul, Rupert
   Ostrowski, Mario
   Moir, Susan
   Kovacs, Colin
   Fauci, Anthony S.
TI Rebound of plasma viremia following cessation of antiretroviral therapy
   despite profoundly low levels of HIV reservoir: implications for
   eradication
SO AIDS
LA English
DT Article
DE antiretroviral therapy; discontinuation of therapy; eradication; human
   immunodeficiency virus; viral reservoirs
ID EXTENDED PERIODS; PERSISTENCE; INFECTION; REPLICATION; SUPPRESSION;
   VIRUS
AB Objectives: Sustained suppression of plasma viremia in HIV-infected individuals is attainable with antiretroviral therapy (ART); however, eradication of virus that would allow discontinuation of ART has been hampered by the persistence of HIV reservoirs. It is of great interest to identify individuals who had received ART for prolonged periods of time with extremely low or undetectable HIV reservoirs and monitor plasma viremia following discontinuation of therapy.
   Methods: We measured the size of HIV reservoirs in CD4(+) T cells of individuals on long-term ART and monitored plasma viremia following cessation of ART in one individual with an exceptionally low viral burden after a decade of therapy.
   Results: We demonstrated undetectable levels of HIV DNA in the blood of eight of 45 infected individuals on long-term ART. Among those eight individuals, the frequency of cells carrying infectious virus was significantly lower in those who initiated ART during the early versus the chronic phase of infection. One individual with undetectable HIV DNA in both blood and tissue and a profoundly low level of infectious virus experienced plasma viral rebound 50 days following discontinuation of ART.
   Conclusions: Our data suggest that a significant reduction in the size of viral reservoirs may be achievable in selected individuals who initiate standard ART early in infection. However, given re-emergence of plasma viremia in an individual with an extraordinarily low viral burden, therapeutic strategies aimed at specifically targeting these extremely rare HIV-infected cells with novel interventions may be necessary in order to achieve eradication of virus. (C) 2010 Wolters Kluwer Health vertical bar Lippincott Williams & Wilkins
C1 [Chun, Tae-Wook] NIAID, Immunoregulat Lab, NIH, Bethesda, MD 20892 USA.
   [Maenza, Janine; Collier, Ann C.] Univ Washington, Sch Med, Dept Med, Seattle, WA 98195 USA.
   [Sheth, Prameet M.; Kaul, Rupert; Ostrowski, Mario; Kovacs, Colin] Univ Toronto, Dept Med, Toronto, ON, Canada.
RP Chun, TW (reprint author), NIAID, Immunoregulat Lab, NIH, Bldg 10,Room 6A32,9000 Rockville Pike, Bethesda, MD 20892 USA.
EM twchun@nih.gov
FU Boehringer-Ingelheim; Hoffman-La Roche; Gilead Sciences;
   Schering-Plough; Tibotec-Virco; National Institutes of Health [MO1
   RR-00037, AI41535, AI57005]; National Institute of Allergy and
   Infectious Diseases, National Institutes of Health
FX Potential conflicts of interest: A. C. C. has received research grants
   from Boehringer-Ingelheim, Hoffman-La Roche, Gilead Sciences,
   Schering-Plough, and Tibotec-Virco, and consulted for Glaxo-Smith-Kline,
   Tibotec-Virco, and Pfizer.; Financial support: This research was
   supported in part by the National Institutes of Health grants (MO1
   RR-00037, AI41535, and AI57005) and the Intramural Research Program of
   the National Institute of Allergy and Infectious Diseases, National
   Institutes of Health.
NR 19
TC 112
Z9 114
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 27
PY 2010
VL 24
IS 18
BP 2803
EP 2808
DI 10.1097/QAD.0b013e328340a239
PG 6
WC Immunology; Infectious Diseases; Virology
SC Immunology; Infectious Diseases; Virology
GA 678EU
UT WOS:000284057300006
PM 20962613
ER

PT J
AU Ro, H
   Dawid, IB
AF Ro, Hyunju
   Dawid, Igor B.
TI Lnx-2b restricts gsc expression to the dorsal mesoderm by limiting Nodal
   and Bozozok activity
SO BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
LA English
DT Article
DE Lnx 2b; Nodal; Bozozok; Goosecoid; Dorsal organizer; Dorsal mesoderm
ID HOMEOBOX GENE; ANTERIOR NEUROECTODERM; ZEBRAFISH ORGANIZER; AXIS
   FORMATION; SQUINT; TRANSCRIPTION
AB Coordinated Nodal-related signals and Bozozok (Boz) activity are critical for the initial specification of dorsal mesoderm and anterior neuroectoderm during zebrafish embryogenesis Overexpression of Boz expands gsc expression into the ventro-lateral marginal blastomeres where Nodal signaling is active but is insufficient to Induce ectopic gsc expression in the animal region We found that overexpression of Boz together with depletion of Lnx-2b (previously named Lnx-like Lnx-1) but not each manipulation alone causes robust gsc expression in all blastomeres Furthermore nodal-related signals are required for gsc expression in embryos with elevated Boz activity Through targeted injection into single cells at the 128-cell stage we illustrate the role of maternally deposited Lnx-2b to restrict the expansion of gsc expression into the presumptive ectodermal region This report provides a novel mechanism for limiting dorsal organizer specification to a defined region of the early zebrafish embryo Published by Elsevier Inc
C1 [Ro, Hyunju; Dawid, Igor B.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Mol Genet Lab, Program Genom Differentiat, NIH, Bethesda, MD 20892 USA.
RP Dawid, IB (reprint author), Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Mol Genet Lab, Program Genom Differentiat, NIH, Bethesda, MD 20892 USA.
FU Eunice Kennedy Shriver National Institute of Child Health; Human
   Development National Institutes of Health
FX This work has been supported by the intramural program of the Eunice
   Kennedy Shriver National Institute of Child Health and Human Development
   National Institutes of Health
NR 29
TC 9
Z9 9
U1 0
U2 1
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0006-291X
J9 BIOCHEM BIOPH RES CO
JI Biochem. Biophys. Res. Commun.
PD NOV 26
PY 2010
VL 402
IS 4
BP 626
EP 630
DI 10.1016/j.bbrc.2010.10.070
PG 5
WC Biochemistry & Molecular Biology; Biophysics
SC Biochemistry & Molecular Biology; Biophysics
GA 692QW
UT WOS:000285171200009
PM 20971071
ER

PT J
AU West, LE
   Roy, S
   Lachmi-Weiner, K
   Hayashi, R
   Shi, XB
   Appella, E
   Kutateladze, TG
   Gozani, O
AF West, Lisandra E.
   Roy, Siddhartha
   Lachmi-Weiner, Karin
   Hayashi, Ryo
   Shi, Xiaobing
   Appella, Ettore
   Kutateladze, Tatiana G.
   Gozani, Or
TI The MBT Repeats of L3MBTL1 Link SET8-mediated p53 Methylation at Lysine
   382 to Target Gene Repression
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
ID STATE-SPECIFIC RECOGNITION; DNA-DAMAGE; STRUCTURAL BASIS; HISTONE H4;
   CHROMATIN; PROTEIN; BINDING; METHYLTRANSFERASE; 53BP1; TUDOR
AB The p53 tumor suppressor protein is regulated by multiple post-translational modifications, including lysine methylation. We previously found that monomethylation of p53 at lysine 382 (p53K382me1) by the protein lysine methyltransferase (PKMT) SET8/PR-Set7 represses p53 transactivation of target genes. However, the molecular mechanism linking p53K382 monomethylation to repression is not known. Here we show in biochemical and crystallographic studies the preferential recognition of p53K382me1 by the triple malignant brain tumor (MBT) repeats of the chromatin compaction factor L3MBTL1. We demonstrate that SET8-mediated methylation of p53 at Lys-382 promotes the interaction between L3MBTL1 and p53 in cells, and the chromatin occupancy of L3MBTL1 at p53 target promoters. In the absence of DNA damage, L3MBTL1 interacts with p53K382me1 and p53-target genes are repressed, whereas depletion of L3MBTL1 results in a p53-dependent increase in p21 and PUMA transcript levels. Activation of p53 by DNA damage is coupled to a decrease in p53K382me1 levels, abrogation of the L3MBTL1-p53 interaction, and disassociation of L3MBTL1 from p53-target promoters. Together, we identify L3MBTL1 as the second known methyl-p53 effector protein, and provide a molecular explanation for the mechanism by which p53K382me1 is transduced to regulate p53 activity.
C1 [West, Lisandra E.; Lachmi-Weiner, Karin; Gozani, Or] Stanford Univ, Dept Biol, Stanford, CA 94305 USA.
   [Roy, Siddhartha; Kutateladze, Tatiana G.] Univ Colorado Denver, Dept Pharmacol, Sch Med, Aurora, CO 80045 USA.
   [Hayashi, Ryo; Appella, Ettore] NCI, Cell Biol Lab, NIH, Bethesda, MD 20892 USA.
   [Shi, Xiaobing] Univ Texas MD Anderson Canc Ctr, Dept Biochem & Mol Biol, Houston, TX 77030 USA.
RP Kutateladze, TG (reprint author), 12801 E 17th Ave, Aurora, CO 80045 USA.
EM tatiana.kutateladze@UCHSC.edu; ogozani@stanford.edu
FU National Institutes of Health [GM079641, CA113472]
FX This work was supported, in whole or in part, by Grants GM079641 (to O.
   G.) and CA113472 (to T. G. K.) from the National Institutes of Health
   and the Intramural Research Program of the National Institutes of Health
   (to E. A.).; Supported by a grant from the National Institutes of Health
   Stanford Genome Training Grant.
NR 35
TC 44
Z9 50
U1 0
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 26
PY 2010
VL 285
IS 48
BP 37725
EP 37732
DI 10.1074/jbc.M110.139527
PG 8
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 682ST
UT WOS:000284424000064
PM 20870725
ER

PT J
AU Yang, Y
   Gu, DY
   Aisa, HA
   Ito, Y
AF Yang, Yi
   Gu, Dongyu
   Aisa, Haji Akber
   Ito, Yoichiro
TI Evaluation on the performance of four different column models mounted on
   the compact type-I coil planet centrifuge
SO JOURNAL OF CHROMATOGRAPHY A
LA English
DT Article
DE Compact type-I coil planet centrifuge; Counter current chromatography;
   Mounted column models; DNP-amino acids; Dipeptides; Retention of the
   stationary phase; Resolution
ID COUNTER-CURRENT CHROMATOGRAPHY; DESIGN
AB Optimal positions of coiled separation columns on the type-I centrifuge were determined for four typical two-phase solvent systems to obtain the best separation efficiency (resolution and retention of stationary phase) for each with a suitable set of test samples A set of short coiled columns is connected in series and mounted around the holder hub in four different ways (model A) the tail of one unit with left-handedness was connected to the head of the next unit with right-handedness (TL-HR) (model B) the tail of one unit with left-handedness was connected to the tail of the next unit with right-handedness (TL-TR) (model C) the tail of one unit with left-handedness was connected to the tail of the next unit with left-handedness (TL-TL) (model D) the tail of one unit with left-handedness was connected to the head of the next unit with left-handedness (TL-HL) The results indicated that the performance of model D was the best among the four models High revolution speed (800 rpm) is favorable to separation using the moderately hydrophobic solvent system of hexane-ethyl acetate-methanol-0 1 M HCl (1 1 1 1 v/v) (HEMW) while lower revolution speed (600 rpm) is beneficial to the separation with polar solvent system of 1-butanol-acetic acid-water (19 1 20 v/v) (BAW) Published by Elsevier B V
C1 [Yang, Yi; Gu, Dongyu; Ito, Yoichiro] NHLBI, Bioseparat Technol Lab, Biochem & Biophys Ctr, NIH, Bethesda, MD 20892 USA.
   [Yang, Yi; Gu, Dongyu; Aisa, Haji Akber] Chinese Acad Sci, Key Lab Xinjiang Indigenous Med Plants Resource U, Xinjiang Tech Inst Phys & Chem, Urumqi 830011, Peoples R China.
RP Ito, Y (reprint author), NHLBI, Bioseparat Technol Lab, Biochem & Biophys Ctr, NIH, 10 Ctr Dr,Bldg 10,Room 8N230, Bethesda, MD 20892 USA.
FU Intramural NIH HHS [ZIA HL006022-01]
NR 17
TC 3
Z9 3
U1 0
U2 2
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 26
PY 2010
VL 1217
IS 48
BP 7612
EP 7615
DI 10.1016/j.chroma.2010.10.012
PG 4
WC Biochemical Research Methods; Chemistry, Analytical
SC Biochemistry & Molecular Biology; Chemistry
GA 686BS
UT WOS:000284672400021
PM 21030029
ER

PT J
AU Langer, HF
   Chung, KJ
   Orlova, VV
   Choi, EY
   Kaul, S
   Kruhlak, MJ
   Alatsatianos, M
   DeAngelis, RA
   Roche, PA
   Magotti, P
   Li, XR
   Economopoulou, M
   Rafail, S
   Lambris, JD
   Chavakis, T
AF Langer, Harald F.
   Chung, Kyoung-Jin
   Orlova, Valeria V.
   Choi, Eun Young
   Kaul, Sunil
   Kruhlak, Michael J.
   Alatsatianos, Markella
   DeAngelis, Robert A.
   Roche, Paul A.
   Magotti, Paola
   Li, Xuri
   Economopoulou, Matina
   Rafail, Stavros
   Lambris, John D.
   Chavakis, Triantafyllos
TI Complement-mediated inhibition of neovascularization reveals a point of
   convergence between innate immunity and angiogenesis
SO BLOOD
LA English
DT Article
ID INFLAMMATORY CELL RECRUITMENT; MACULAR DEGENERATION; CHOROIDAL
   NEOVASCULARIZATION; RETINAL NEOVASCULARIZATION; CHEMOATTRACTANT
   RECEPTOR; INDUCED RETINOPATHY; C5A; ACTIVATION; MOUSE; C3A
AB Beyond its role in immunity, complement mediates a wide range of functions in the context of morphogenetic or tissue remodeling processes. Angiogenesis is crucial during tissue remodeling in multiple pathologies; however, the knowledge about the regulation of neovascularization by the complement components is scarce. Here we studied the involvement of complement in pathological angiogenesis. Strikingly, we found that mice deficient in the central complement component C3 displayed increased neovascularization in the model of retinopathy of prematurity (ROP) and in the in vivo Matrigel plug assay. In addition, antibody-mediated blockade of C5, treatment with C5aR antagonist, or C5aR deficiency in mice resulted in enhanced pathological retina angiogenesis. While complement did not directly affect angiogenesis-related endothelial cell functions, we found that macrophages mediated the antiangiogenic activity of complement. In particular, C5a-stimulated macrophages were polarized toward an angiogenesis-inhibitory phenotype, including the up-regulated secretion of the antiangiogenic soluble vascular endothelial growth factor receptor-1. Consistently, macrophage depletion in vivo reversed the increased neovascularization associated with C3- or C5aR deficiency. Taken together, complement and in particular the C5a-C5aR axes are potent inhibitors of angiogenesis. (Blood. 2010;116(22):4395-4403)
C1 [Chung, Kyoung-Jin; Chavakis, Triantafyllos] Univ Clin Carl Gustav Carus Dresden, Div Vasc Inflammat Diabet & Kidney, Dept Med 3, D-01307 Dresden, Germany.
   [Langer, Harald F.; Chung, Kyoung-Jin; Orlova, Valeria V.; Choi, Eun Young; Kaul, Sunil; Kruhlak, Michael J.; Alatsatianos, Markella; Roche, Paul A.; Economopoulou, Matina; Chavakis, Triantafyllos] NCI, Expt Immunol Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
   [Chung, Kyoung-Jin] Tech Univ Dresden, Inst Physiol, Fac Med, D-01307 Dresden, Germany.
   [DeAngelis, Robert A.; Magotti, Paola; Rafail, Stavros; Lambris, John D.] Univ Penn, Dept Pathol & Lab Med, Philadelphia, PA 19104 USA.
   [Li, Xuri] NEI, NIH, Bethesda, MD 20892 USA.
   [Economopoulou, Matina] Univ Clin Carl Gustav Carus Dresden, Dept Ophthalmol, D-01307 Dresden, Germany.
RP Chavakis, T (reprint author), Univ Clin Carl Gustav Carus Dresden, Div Vasc Inflammat Diabet & Kidney, Dept Med 3, Fetscherstr 74, D-01307 Dresden, Germany.
EM lambris@upenn.edu; triantafyllos.chavakis@uniklinikum-dresden.de
RI Magotti, Paola/A-2903-2012; Orlova, Valeria/C-6065-2014; 
OI Orlova, Valeria/0000-0002-1169-2802; Lambris, John/0000-0002-9370-5776
FU NIH [CA112162, AI-068730]; National Cancer Institute; German Academy of
   Sciences Leopoldina
FX This work was supported by the NIH Intramural Research Program, National
   Cancer Institute (T.C.), the German Academy of Sciences Leopoldina
   (H.F.L), and NIH grants CA112162 and AI-068730 (J.D.L.).
NR 58
TC 80
Z9 84
U1 1
U2 10
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 25
PY 2010
VL 116
IS 22
BP 4395
EP 4403
DI 10.1182/blood-2010-01-261503
PG 9
WC Hematology
SC Hematology
GA 685BT
UT WOS:000284599900010
PM 20625009
ER

PT J
AU Hudecek, M
   Schmitt, TM
   Baskar, S
   Lupo-Stanghellini, MT
   Nishida, T
   Yamamoto, TN
   Bleakley, M
   Turtle, CJ
   Chang, WC
   Greisman, HA
   Wood, B
   Maloney, DG
   Jensen, MC
   Rader, C
   Riddell, SR
AF Hudecek, Michael
   Schmitt, Thomas M.
   Baskar, Sivasubramanian
   Lupo-Stanghellini, Maria Teresa
   Nishida, Tetsuya
   Yamamoto, Tori N.
   Bleakley, Marie
   Turtle, Cameron J.
   Chang, Wen-Chung
   Greisman, Harvey A.
   Wood, Brent
   Maloney, David G.
   Jensen, Michael C.
   Rader, Christoph
   Riddell, Stanley R.
TI The B-cell tumor-associated antigen ROR1 can be targeted with T cells
   modified to express a ROR1-specific chimeric antigen receptor
SO BLOOD
LA English
DT Article
ID CHRONIC LYMPHOCYTIC-LEUKEMIA; ACUTE MYELOID-LEUKEMIA; TYROSINE KINASE
   ROR1; GENE-EXPRESSION; CLL CELLS; STEM-CELL; DIFFERENTIATION;
   IMMUNOTHERAPY; LYMPHOMA; TRANSPLANTATION
AB Monoclonal antibodies and T cells modified to express chimeric antigen receptors specific for B-cell lineage surface molecules such as CD20 exert antitumor activity in B-cell malignancies, but deplete normal B cells. The receptor tyrosine kinase-like orphan receptor 1 (ROR1) was identified as a highly expressed gene in B-cell chronic lymphocytic leukemia (B-CLL), but not normal B cells, suggesting it may serve as a tumor-specific target for therapy. We analyzed ROR1-expression in normal nonhematopoietic and hematopoietic cells including B-cell precursors, and in hematopoietic malignancies. ROR1 has characteristics of an oncofetal gene and is expressed in undifferentiated embryonic stem cells, B-CLL and mantle cell lymphoma, but not in major adult tissues apart from low levels in adipose tissue and at an early stage of B-cell development. We constructed a ROR1-specific chimeric antigen receptor that when expressed in T cells from healthy donors or CLL patients conferred specific recognition of primary B-CLL and mantle cell lymphoma, including rare drug effluxing chemotherapy resistant tumor cells that have been implicated in maintaining the malignancy, but not mature normal B cells. T-cell therapies targeting ROR1 may be effective in B-CLL and other ROR1-positive tumors. However, the expression of ROR1 on some normal tissues suggests the potential for toxicity to subsets of normal cells. (Blood. 2010; 116(22): 4532-4541)
C1 [Hudecek, Michael; Schmitt, Thomas M.; Lupo-Stanghellini, Maria Teresa; Nishida, Tetsuya; Yamamoto, Tori N.; Bleakley, Marie; Turtle, Cameron J.; Maloney, David G.; Jensen, Michael C.; Riddell, Stanley R.] Fred Hutchinson Canc Res Ctr, Div Clin Res, Program Immunol, Seattle, WA 98109 USA.
   [Hudecek, Michael] Univ Leipzig, Dept Hematol Oncol & Hemostaseol, Leipzig, Germany.
   [Baskar, Sivasubramanian; Rader, Christoph] NCI, Expt Transplantat & Immunol Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
   [Lupo-Stanghellini, Maria Teresa] Ist Sci San Raffaele, Hematol & Bone Marrow Transplantat Unit, I-20132 Milan, Italy.
   [Bleakley, Marie] Univ Washington, Dept Pediat, Seattle, WA 98195 USA.
   [Turtle, Cameron J.; Greisman, Harvey A.; Wood, Brent; Maloney, David G.; Riddell, Stanley R.] Univ Washington, Dept Med, Seattle, WA 98195 USA.
   [Chang, Wen-Chung] City Hope Natl Canc Ctr, Div Canc Immunotherapeut & Tumor Immunol, Duarte, CA USA.
   [Jensen, Michael C.] Seattle Childrens Res Inst, Ctr Immun & Immunotherapies, Seattle, WA USA.
RP Hudecek, M (reprint author), Fred Hutchinson Canc Res Ctr, Div Clin Res, Program Immunol, D3-100,1100 Fairview Ave N,POB 19024, Seattle, WA 98109 USA.
EM mhudecek@fhcrc.org
RI nishida, tetsuya/I-7300-2014; 
OI Hudecek, Michael/0000-0002-2280-2202
FU Leukemia & Lymphoma Society; National Institutes of Health [CA18029,
   CA136551]; German Research Foundation (Deutsche Forschungsgemeinschaft)
FX This work was supported by grants from the Leukemia & Lymphoma Society
   (S.R.R. and D.G.M.), National Institutes of Health CA18029 and CA136551
   (S.R.R.), and a gift from Rae and Mark Lembersky. M.H. was supported by
   the German Research Foundation (Deutsche Forschungsgemeinschaft).
NR 36
TC 103
Z9 108
U1 1
U2 9
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 25
PY 2010
VL 116
IS 22
BP 4532
EP 4541
DI 10.1182/blood-2010-05-283309
PG 10
WC Hematology
SC Hematology
GA 685BT
UT WOS:000284599900026
PM 20702778
ER

PT J
AU Calattini, S
   Sereti, I
   Scheinberg, P
   Kimura, H
   Childs, RW
   Cohen, JI
AF Calattini, Sara
   Sereti, Irini
   Scheinberg, Philip
   Kimura, Hiroshi
   Childs, Richard W.
   Cohen, Jeffrey I.
TI Detection of EBV genomes in plasmablasts/plasma cells and non-B cells in
   the blood of most patients with EBV lymphoproliferative disorders by
   using Immuno-FISH
SO BLOOD
LA English
DT Article
ID EPSTEIN-BARR-VIRUS; IN-SITU HYBRIDIZATION; ORGAN TRANSPLANT RECIPIENTS;
   HUMAN PLASMA-CELLS; PERIPHERAL-BLOOD; HUMAN THYMOCYTES; INFECTION;
   LYMPHOMA; LYMPHOCYTES; EXPRESSION
AB Epstein-Barr virus (EBV) is present in B cells in the blood of healthy people; few studies have looked for EBV in other cell types in blood from patients with lymphoproliferative disorders. We use a new technique combining immunofluorescent cell-surface staining and fluorescent in situ hybridization to quantify both EBV copy number per cell and cell types in blood from patients with high EBV DNA loads. In addition to CD20(+) B cells, EBV was present in plasmablast/plasma cells in the blood of 50% of patients, in monocytes or T cells in a small proportion of patients, and in "non-B, non-T, non-monocytes" in 69% of patients. The mean EBV copy number in B cells was significantly higher than in plasmablast/plasma cells. There was no correlation between EBV load and virus copy number per cell. Although we detected CD21, the EBV B-cell receptor, on EBV-infected B cells, we could not detect it on virus-infected T cells. These findings expand the range of cell types infected in the blood. Determining the number of EBV genomes per cell and the type of cells infected in patients with high EBV loads may provide additional prognostic information for the development of EBV lymphoproliferative diseases. (Blood. 2010; 116(22): 4546-4559)
C1 [Calattini, Sara; Cohen, Jeffrey I.] NIAID, Med Virol Sect, Infect Dis Lab, NIH, Bethesda, MD 20892 USA.
   [Sereti, Irini] NIAID, Immunoregulat Lab, NIH, Bethesda, MD 20892 USA.
   [Scheinberg, Philip; Childs, Richard W.] NHLBI, Hematol Branch, NIH, Bethesda, MD 20892 USA.
   [Kimura, Hiroshi] Nagoya Univ, Dept Virol, Grad Sch Med, Nagoya, Aichi 4648601, Japan.
RP Cohen, JI (reprint author), NIAID, Med Virol Sect, Infect Dis Lab, NIH, 50 South Dr,Bldg 50,Room 6134, Bethesda, MD 20892 USA.
EM jcohen@niaid.nih.gov
RI Kimura, Hiroshi/I-2246-2012; 
OI Scheinberg, Phillip/0000-0002-9047-4538
FU National Institute of Allergy and Infectious Diseases; National Heart,
   Lung, and Blood Institute; National Cancer Institute
FX This study was supported by the Intramural Research Program of the
   National Institute of Allergy and Infectious Diseases, the National
   Heart, Lung, and Blood Institute, and the National Cancer Institute.
NR 44
TC 17
Z9 17
U1 0
U2 5
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 25
PY 2010
VL 116
IS 22
BP 4546
EP 4559
DI 10.1182/blood-2010-05-285452
PG 14
WC Hematology
SC Hematology
GA 685BT
UT WOS:000284599900028
PM 20699441
ER

PT J
AU Melenhorst, JJ
   Leen, AM
   Bollard, CM
   Quigley, MF
   Price, DA
   Rooney, CM
   Brenner, MK
   Barrett, AJ
   Heslop, HE
AF Melenhorst, J. Joseph
   Leen, Ann M.
   Bollard, Catherine M.
   Quigley, Maire F.
   Price, David A.
   Rooney, Cliona M.
   Brenner, Malcolm K.
   Barrett, A. John
   Heslop, Helen E.
TI Allogeneic virus-specific T cells with HLA alloreactivity do not produce
   GVHD in human subjects
SO BLOOD
LA English
DT Article
ID VERSUS-HOST-DISEASE; LYMPHOPROLIFERATIVE DISEASE; TRANSPLANTATION;
   CYTOMEGALOVIRUS; LYMPHOCYTES; RECIPIENTS; THERAPY; PREVENT; DONOR
AB Adoptive transfer of viral antigen-specific memory T cells can reconstitute antiviral immunity, but in a recent report a majority of virus-specific cytotoxic T-lymphocyte (CTL) linesshowedin vitro cross-reactivity against allo-human leukocyte antigen (HLA) molecules as measured by interferon-gamma secretion. We therefore reviewed our clinical experience with adoptive transfer of allogeneic hematopoietic stem cell transplantation donor-derived virus-specific CTLs in 153 recipients, including 73 instances where there was an HLA mismatch. There was no de novo acute graft-versus-host disease after infusion, and incidence of graft-versus-host disease reactivation was low and not significantly different in recipients of matched or mismatched CTL. However, we found that virus-specific T cell lines recognized up to 10% of a panel of 44 HLA disparate targets, indicating that virus-specific T cells can have cross-reactivity with HLA-mismatched targets in vitro. These data indicate that the adoptive transfer of partially HLA-mismatched virus-specific CTL is safe despite in vitro recognition of recipient HLA molecules. (Blood. 2010; 116(22): 4700-4702)
C1 [Leen, Ann M.; Bollard, Catherine M.; Rooney, Cliona M.; Brenner, Malcolm K.; Heslop, Helen E.] Texas Childrens Hosp, Baylor Coll Med, Ctr Cell & Gene Therapy, Houston, TX 77030 USA.
   [Melenhorst, J. Joseph; Barrett, A. John] NHLBI, Hematol Branch, NIH, Bethesda, MD 20892 USA.
   [Leen, Ann M.; Bollard, Catherine M.; Rooney, Cliona M.; Brenner, Malcolm K.; Heslop, Helen E.] Methodist Hosp, Houston, TX 77030 USA.
   [Quigley, Maire F.; Price, David A.] Cardiff Univ, Sch Med, Cardiff, S Glam, Wales.
   [Quigley, Maire F.; Price, David A.] NIAID, Vaccine Res Ctr, NIH, Bethesda, MD 20892 USA.
RP Heslop, HE (reprint author), Texas Childrens Hosp, Baylor Coll Med, Ctr Cell & Gene Therapy, 1102 Bates St,Suite 1630, Houston, TX 77030 USA.
EM hheslop@bcm.edu
RI Price, David/C-7876-2013
OI Price, David/0000-0001-9416-2737
FU National Heart, Lung, and Blood Institute; National Institutes of Health
   [RO1CA061384, U54HL081007, P01CA094237, P50CA126752]; Leukemia &
   Lymphoma Society; Dan L. Duncan Chair; Fayez Sarofim Chair
FX This work was supported by the National Heart, Lung, and Blood Institute
   (intramural grant; J.J.M., A.J.B.), the National Institutes of Health
   (grants RO1CA061384, U54HL081007, P01CA094237, and P50CA126752), and the
   Leukemia & Lymphoma Society (Specialized Center of Research grant).
   H.E.H. is supported by a Dan L. Duncan Chair. M.K.B. is supported by a
   Fayez Sarofim Chair.
NR 16
TC 87
Z9 88
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 25
PY 2010
VL 116
IS 22
BP 4700
EP 4702
DI 10.1182/blood-2010-06-289991
PG 3
WC Hematology
SC Hematology
GA 685BT
UT WOS:000284599900044
PM 20709906
ER

PT J
AU Gangjee, A
   Zhao, Y
   Lin, L
   Raghavan, S
   Roberts, EG
   Risinger, AL
   Hamel, E
   Mooberry, SL
AF Gangjee, Aleem
   Zhao, Ying
   Lin, Lu
   Raghavan, Sudhir
   Roberts, Elizabeth G.
   Risinger, April L.
   Hamel, Ernest
   Mooberry, Susan L.
TI Synthesis and Discovery of Water-Soluble Microtubule Targeting Agents
   that Bind to the Colchicine Site on Tubulin and Circumvent Pgp Mediated
   Resistance
SO JOURNAL OF MEDICINAL CHEMISTRY
LA English
DT Article
ID III BETA-TUBULIN; CELL LUNG-CANCER; THYMIDYLATE SYNTHASE INHIBITORS;
   DIFFERENTIAL CYTOTOXICITY DATA; MULTIDRUG-RESISTANCE; CHEMOTHERAPY
   RESPONSE; BIOLOGICAL EVALUATION; ANTIMITOTIC AGENTS; ANTITUMOR AGENTS;
   P-GLYCOPROTEIN
AB Two classes of molecules were designed and synthesized based on a 6-CH(3) cyclopenta[d]pyrimidine scaffold and a pyrrolo[2,3-d]pyrimidine scaffold. The pyrrolo[2,3-d]pyrimidines were synthesized by reacting ethyl 2-cyano-4,4-diethoxybutanoate and acetamidine, which in turn was chlorinated and reacted with the appropriate anilines to afford 1 and 2. The cyclopenta[d]pyrimidines were obtained from 3-methyladapic acid, followed by reaction with acetamidine to afford the cyclopenta[d]pyrimidine scaffold. Chlorination and reaction with appropriate anilines afforded (+/-)-3 center dot HCl-(+/-)-7 center dot HCl. Compounds 1 and (+/-)-3 center dot HCl had potent antiproliferative activities in the nanomolar range. Compound (+/-)-3 center dot HCl is significantly more potent than 1. Mechanistic studies showed that I and (+/-)-3 center dot HCl cause loss of cellular microtubules, inhibit the polymerization of purified tubulin, and inhibit colchicine binding. Modeling studies show interactions of these compounds within the colchicine site. The identification of these new inhibitors that can also overcome clinically relevant mechanisms of drug resistance provides new scaffolds for colchicine site agents.
C1 [Gangjee, Aleem; Zhao, Ying; Lin, Lu; Raghavan, Sudhir] Duquesne Univ, Grad Sch Pharmaceut Sci, Div Med Chem, Pittsburgh, PA 15282 USA.
   [Roberts, Elizabeth G.; Risinger, April L.; Mooberry, Susan L.] Univ Texas Hlth Sci Ctr San Antonio, Dept Pharmacol, San Antonio, TX 78229 USA.
   [Hamel, Ernest] NCI, Screening Technol Branch, Dev Therapeut Program, Div Canc Treatment & Diag,NIH, Frederick, MD 21702 USA.
RP Gangjee, A (reprint author), Duquesne Univ, Grad Sch Pharmaceut Sci, Div Med Chem, 600 Forbes Ave, Pittsburgh, PA 15282 USA.
EM gangjee@duq.edu; mooberry@uthscsa.edu
RI zhao, ying/G-7163-2011; Raghavan, Sudhir/C-8871-2011
OI Raghavan, Sudhir/0000-0001-5449-362X
FU National Institutes of Health; National Cancer Institute [CA098850];
   Cowles Fellowship; CTRC Cancer Center Support Grant, CCSG [CA054174]
FX This work was supported, in part, by the National Institutes of Health
   and National Cancer Institute Grant CA098850 (AG). We thank Desiree
   LeBouf and Cara Westbrook for excellent technical assistance. A.L.R. was
   supported by a Cowles Fellowship, and support from the CTRC Cancer
   Center Support Grant, CCSG (CA054174) (S.L.M.) is acknowledged.
NR 59
TC 36
Z9 36
U1 0
U2 4
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 25
PY 2010
VL 53
IS 22
BP 8116
EP 8128
DI 10.1021/jm101010n
PG 13
WC Chemistry, Medicinal
SC Pharmacology & Pharmacy
GA 681CR
UT WOS:000284287200021
PM 20973488
ER

PT J
AU Gopich, IV
   Szabo, A
AF Gopich, Irina V.
   Szabo, Attila
TI FRET Efficiency Distributions of Multistate Single Molecules
SO JOURNAL OF PHYSICAL CHEMISTRY B
LA English
DT Article
ID RESONANCE ENERGY-TRANSFER; FLUORESCENCE SPECTROSCOPY; CONFORMATIONAL
   DYNAMICS; FOLDING DYNAMICS; HETEROGENEITY; MICROSCOPY; DIFFUSION;
   STATES; DNA
AB A simple analytic theory is developed to describe FRET efficiency histograms constructed from a photon trajectory generated by a molecule with multiple conformational states. The histograms are approximated by a sum of Gaussians with the parameters explicitly determined by the FRET efficiencies of the states and the rates of the transitions between the states. The theory, which has been tested against exact histograms for two conformational states and simulated data for three and four conformational states, accurately describes how the peaks in the histograms collapse as the bin time or the transition rates increase.
C1 [Gopich, Irina V.; Szabo, Attila] NIDDKD, Chem Phys Lab, NIH, Bethesda, MD 20892 USA.
RP Gopich, IV (reprint author), NIDDKD, Chem Phys Lab, NIH, Bldg 2, Bethesda, MD 20892 USA.
EM irinag@niddk.nih.gov
RI Szabo, Attila/H-3867-2012
FU National Institutes of Health, NIDDK
FX This work was supported by the Intramural Research Program of the
   National Institutes of Health, NIDDK.
NR 26
TC 31
Z9 31
U1 0
U2 13
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 1520-6106
J9 J PHYS CHEM B
JI J. Phys. Chem. B
PD NOV 25
PY 2010
VL 114
IS 46
BP 15221
EP 15226
DI 10.1021/jp105359z
PG 6
WC Chemistry, Physical
SC Chemistry
GA 681CT
UT WOS:000284287700051
PM 21028764
ER

PT J
AU Kanchanawong, P
   Shtengel, G
   Pasapera, AM
   Ramko, EB
   Davidson, MW
   Hess, HF
   Waterman, CM
AF Kanchanawong, Pakorn
   Shtengel, Gleb
   Pasapera, Ana M.
   Ramko, Ericka B.
   Davidson, Michael W.
   Hess, Harald F.
   Waterman, Clare M.
TI Nanoscale architecture of integrin-based cell adhesions
SO NATURE
LA English
DT Article
ID FOCAL ADHESIONS; ACTIN-FILAMENTS; PROTEIN; FORCE; TALIN; MICROSCOPY;
   PROBES
AB Cell adhesions to the extracellular matrix (ECM) are necessary for morphogenesis, immunity and wound healing(1,2). Focal adhesions are multifunctional organelles that mediate cell-ECM adhesion, force transmission, cytoskeletal regulation and signalling(1-3). Focal adhesions consist of a complex network(4) of trans-plasma-membrane integrins and cytoplasmic proteins that form a <200-nm plaque(5,6) linking the ECM to the actin cytoskeleton. The complexity of focal adhesion composition and dynamics implicate an intricate molecular machine(7,8). However, focal adhesion molecular architecture remains unknown. Here we used three-dimensional super-resolution fluorescence microscopy (interferometric photo-activated localization microscopy)(9) to map nanoscale protein organization in focal adhesions. Our results reveal that integrins and actin are vertically separated by a similar to 40-nm focal adhesion core region consisting of multiple protein-specific strata: a membrane-apposed integrin signalling layer containing integrin cytoplasmic tails, focal adhesion kinase and paxillin; an intermediate force-transduction layer containing talin and vinculin; and an uppermost actin-regulatory layer containing zyxin, vasodilator-stimulated phosphoprotein and alpha-actinin. By localizing amino- and carboxyterminally tagged talins, we reveal talin's polarized orientation, indicative of a role in organizing the focal adhesion strata. The composite multilaminar protein architecture provides a molecular blueprint for understanding focal adhesion functions.
C1 [Kanchanawong, Pakorn; Pasapera, Ana M.; Waterman, Clare M.] NHLBI, NIH, Bethesda, MD 20892 USA.
   [Shtengel, Gleb; Hess, Harald F.] Howard Hughes Med Inst, Ashburn, VA 20147 USA.
   [Ramko, Ericka B.; Davidson, Michael W.] Florida State Univ, Natl High Magnet Field Lab, Tallahassee, FL 32310 USA.
   [Davidson, Michael W.] Florida State Univ, Dept Biol Sci, Tallahassee, FL 32306 USA.
RP Waterman, CM (reprint author), NHLBI, NIH, Bethesda, MD 20892 USA.
EM davidson@magnet.fsu.edu; hessh@janelia.hhmi.org;
   watermancm@nhlbi.nih.gov
OI Waterman, Clare/0000-0001-6142-6775
FU Division of Intramural Research, NHLBI; Howard Hughes Medical Institute
FX We thank J. Lippincott-Schwartz, G. Patterson and M. Parsons for sharing
   DNA; S. Xie for help with automation software; K. Jaqaman for MATLAB
   code; and HHMI Janelia Farm Scientific Computing and NIH Helix systems
   for computing resources. Funding: Division of Intramural Research, NHLBI
   (P.K., A.M.P. and C.M.W.); Howard Hughes Medical Institute (G.S. and
   H.F.H.).
NR 35
TC 454
Z9 464
U1 17
U2 186
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 25
PY 2010
VL 468
IS 7323
BP 580
EP U262
DI 10.1038/nature09621
PG 7
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 684WA
UT WOS:000284584200046
PM 21107430
ER

PT J
AU Chew, EY
   Ambrosius, WT
   Danis, RP
AF Chew, Emily Y.
   Ambrosius, Walter T.
   Danis, Ronald P.
CA ACCORD Study Grp
   ACCORD Eye Study Grp
TI Retinopathy Progression in Type 2 Diabetes REPLY
SO NEW ENGLAND JOURNAL OF MEDICINE
LA English
DT Letter
C1 [Chew, Emily Y.] NIH, Bethesda, MD 20892 USA.
   [Ambrosius, Walter T.] Wake Forest Univ, Bowman Gray Sch Med, Winston Salem, NC USA.
   [Danis, Ronald P.] Univ Wisconsin, Madison, WI USA.
RP Chew, EY (reprint author), NIH, Bldg 10, Bethesda, MD 20892 USA.
EM echew@nei.nih.gov
NR 7
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 25
PY 2010
VL 363
IS 22
BP 2173
EP 2174
PG 2
WC Medicine, General & Internal
SC General & Internal Medicine
GA 684XE
UT WOS:000284587800025
ER

PT J
AU Majerciak, V
   Deng, M
   Zheng, ZM
AF Majerciak, Vladimir
   Deng, Merlyn
   Zheng, Zhi-Ming
TI Requirement of UAP56, URH49, RBM15, and OTT3 in the expression of Kaposi
   sarcoma-associated herpesvirus ORF57
SO VIROLOGY
LA English
DT Article
DE Kaposi sarcoma-associated herpesvirus; Human herpesvirus 8; Gene
   expression; RNA export factors; RNA export; ORF57; Posttranscriptional
   regulation; UAP56; RBM15
ID MESSENGER-RNA EXPORT; TRANSACTIVATOR PROTEIN; NUCLEAR-LOCALIZATION;
   DISTINCT ACTIVITIES; HELICASE UAP56; UNSPLICED RNA; BINDING; VIRUS;
   ACCUMULATION; SPLICEOSOME
AB Transport of mRNA from the nucleus to the cytoplasm is mediated by cellular RNA export factors. In this report, we examined how RNA export factors UAP56 and URH49, and RNA export cofactors RBM15 and OTT3, function in modulating KSHV ORF57 expression. We found that knockdown of each factor by RNAi led to decreased ORF57 expression. Specifically, reduced expression of either UAP56 or RBM15 led to nuclear export deficiency of ORF57 RNA. In the context of the KSHV genome, the near absence of UAP56 or RBM15 reduced the expression of both ORF57 and ORF59 (an RNA target of ORF57), but not ORF50. Collectively, our data indicate that the expression of KSHV ORF57 is regulated by cellular RNA export factors and cofactors at the posttranscriptional level. Published by Elsevier Inc.
C1 [Majerciak, Vladimir; Deng, Merlyn; Zheng, Zhi-Ming] NCI, Tumor Virus RNA Biol Sect, HIV & AIDS Malignancy Branch, Ctr Canc Res,NIH, Bethesda, MD 20892 USA.
RP Zheng, ZM (reprint author), NCI, Tumor Virus RNA Biol Sect, HIV & AIDS Malignancy Branch, Ctr Canc Res,NIH, 10 Ctr Dr 6N106, Bethesda, MD 20892 USA.
EM zhengt@exchange.nih.gov
FU NIH, National Cancer Institute, Center for Cancer Research
FX We thank Evelyne Manet for providing anti-OTT3 antibody, Koichi
   Yamanishi for anti-ORF50 antibody, and Barbara Felber for providing
   UAP56-HA plasmid. We thank Michael Kruhlak for his critical reading of
   our manuscript. This study was supported by the Intramural Research
   Program of NIH, National Cancer Institute, Center for Cancer Research.
NR 30
TC 8
Z9 8
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 0042-6822
J9 VIROLOGY
JI Virology
PD NOV 25
PY 2010
VL 407
IS 2
BP 206
EP 212
DI 10.1016/j.virol.2010.08.014
PG 7
WC Virology
SC Virology
GA 671DJ
UT WOS:000283480100005
PM 20828777
ER

PT J
AU Huang, HS
   Buck, CB
   Lambert, PF
AF Huang, Hao-Shun
   Buck, Christopher B.
   Lambert, Paul F.
TI Inhibition of gamma secretase blocks HPV infection
SO VIROLOGY
LA English
DT Article
DE Human papillomavirus (HPV); gamma Secretase inhibitor; gamma Secretase;
   Infection; Microbicide
ID HUMAN-PAPILLOMAVIRUS; YOUNG-WOMEN; MOUSE MODEL; VACCINE; CANCER; VIRUS
AB Human papillomaviruses (HPV) are common sexually transmitted pathogens that predispose women to cervical and other anogenital cancers. HPV vaccines can prevent infection by some but not other sexually transmitted HPVs but are too costly for use in much of the world at greatest risk to HPV-associated cancers. Microbicides provide an inexpensive alternative to vaccines. In a high throughput screen, drugs that inhibit the cellular protein complex known as gamma secretase were identified as potential HPV microbicides. gamma Secretase inhibitors (GSIs) inhibited the infectivity of HPV pseudoviruses both in human keratinocytes and in mouse cells, with IC(50) values in the picomolar to the nanomolar range. Using a mouse model, we observed that a GSI could inhibit EIPV infection to the same degree as its effectiveness in inhibiting gamma secretase activity in vivo. We conclude that gamma secretase activity is required for HPV infection and that GSIs are effective microbicides against anogenital HPVs. (C) 2010 Elsevier Inc. All rights reserved.
C1 [Huang, Hao-Shun; Lambert, Paul F.] Univ Wisconsin, Sch Med, McArdle Lab Canc Res, Dept Oncol, Madison, WI 53706 USA.
   [Buck, Christopher B.] NCI, Cellular Oncol Lab, Tumor Virus Mol Biol Sect, Bethesda, MD 20892 USA.
RP Lambert, PF (reprint author), Univ Wisconsin, Sch Med, McArdle Lab Canc Res, Dept Oncol, Madison, WI 53706 USA.
EM plambert@wisc.edu
OI Buck, Christopher/0000-0003-3165-8094
FU NIH [CA022443, AI071947]
FX This work was supported by grants from the NIH (CA022443 and AI071947).
NR 16
TC 16
Z9 16
U1 0
U2 1
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0042-6822
J9 VIROLOGY
JI Virology
PD NOV 25
PY 2010
VL 407
IS 2
BP 391
EP 396
DI 10.1016/j.virol.2010.09.002
PG 6
WC Virology
SC Virology
GA 671DJ
UT WOS:000283480100025
PM 20875908
ER

PT J
AU Thomas, R
   de la Torre, L
   Chang, XQ
   Mehrotra, S
AF Thomas, Reuben
   de la Torre, Luis
   Chang, Xiaoqing
   Mehrotra, Sanjay
TI Validation and characterization of DNA microarray gene expression data
   distribution and associated moments
SO BMC BIOINFORMATICS
LA English
DT Article
ID CELL-LINES; BLOOD; VARIABILITY; NETWORKS; CANCER; ARRAYS; ERROR; SEX;
   INHERITANCE; STATISTICS
AB Background: The data from DNA microarrays are increasingly being used in order to understand effects of different conditions, exposures or diseases on the modulation of the expression of various genes in a biological system. This knowledge is then further used in order to generate molecular mechanistic hypotheses for an organism when it is exposed to different conditions. Several different methods have been proposed to analyze these data under different distributional assumptions on gene expression. However, the empirical validation of these assumptions is lacking.
   Results: Best fit hypotheses tests, moment-ratio diagrams and relationships between the different moments of the distribution of the gene expression was used to characterize the observed distributions. The data are obtained from the publicly available gene expression database, Gene Expression Omnibus (GEO) to characterize the empirical distributions of gene expressions obtained under varying experimental situations each of which providing relatively large number of samples for hypothesis testing. All data were obtained from either of two microarray platforms - the commercial Affymetrix mouse 430.2 platform and a non-commercial Rosetta/Merck one. The data from each platform were preprocessed in the same manner.
   Conclusions: The null hypotheses for goodness of fit for all considered univariate theoretical probability distributions (including the Normal distribution) are rejected for more than 50% of probe sets on the Affymetrix microarray platform at a 95% confidence level, suggesting that under the tested conditions a priori assumption of any of these distributions across all probe sets is not valid. The pattern of null hypotheses rejection was different for the data from Rosetta/Merck platform with only around 20% of the probe sets failing the logistic distribution goodness-of-fit test. We find that there are statistically significant (at 95% confidence level based on the F-test for the fitted linear model) relationships between the mean and the logarithm of the coefficient of variation of the distributions of the logarithm of gene expressions. An additional novel statistically significant quadratic relationship between the skewness and kurtosis is identified. Data from both microarray platforms fail to identify with any one of the chosen theoretical probability distributions from an analysis of the l-moment ratio diagram.
C1 [de la Torre, Luis; Mehrotra, Sanjay] Northwestern Univ, Dept Ind Engn & Management Sci, Evanston, IL 60208 USA.
   [Thomas, Reuben; Chang, Xiaoqing] Natl Inst Environm Hlth Sci, Environm Syst Biol Grp, Mol Toxicol Lab, Res Triangle Pk, NC 27709 USA.
RP Mehrotra, S (reprint author), Northwestern Univ, Dept Ind Engn & Management Sci, Evanston, IL 60208 USA.
EM mehrotra@iems.northwestern.edu
RI Mehrotra, Sanjay/B-7477-2009
FU NIH, National Institute of Environmental Health Sciences
FX This research was supported [in part] by the Intramural Research Program
   of the NIH, National Institute of Environmental Health Sciences.
NR 69
TC 7
Z9 7
U1 1
U2 3
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1471-2105
J9 BMC BIOINFORMATICS
JI BMC Bioinformatics
PD NOV 24
PY 2010
VL 11
AR 576
DI 10.1186/1471-2105-11-576
PG 14
WC Biochemical Research Methods; Biotechnology & Applied Microbiology;
   Mathematical & Computational Biology
SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology;
   Mathematical & Computational Biology
GA 695ON
UT WOS:000285381800001
PM 21092329
ER

PT J
AU Luk, E
   Ranjan, A
   FitzGerald, PC
   Mizuguchi, G
   Huang, Y
   Wei, D
   Wu, C
AF Luk, Ed
   Ranjan, Anand
   FitzGerald, Peter C.
   Mizuguchi, Gaku
   Huang, Yingzi
   Wei, Debbie
   Wu, Carl
TI Stepwise Histone Replacement by SWR1 Requires Dual Activation with
   Histone H2A.Z and Canonical Nucleosome
SO CELL
LA English
DT Article
ID CHROMATIN REMODELING COMPLEX; VARIANT H2A.Z; CHROMOSOME STABILITY;
   GENOME; PROMOTERS; EXCHANGE; TRANSCRIPTION; REPLICATION; ATPASE; YEAST
AB Histone variant H2A.Z-containing nucleosomes are incorporated at most eukaryotic promoters. This incorporation is mediated by the conserved SWR1 complex, which replaces histone H2A in canonical nucleosomes with H2A.Z in an ATP-dependent manner. Here, we show that promoter-proximal nucleosomes are highly heterogeneous for H2A.Z in Saccharomyces cerevisiae, with substantial representation of nucleosomes containing one, two, or zero H2A.Z molecules. SWR1-catalyzed H2A.Z replacement in vitro occurs in a stepwise and unidirectional fashion, one H2A.Z-H2B dimer at a time, producing heterotypic nucleosomes as intermediates and homotypic H2A.Z nucleosomes as end products. The ATPase activity of SWR1 is specifically stimulated by H2A-containing nucleosomes without ensuing histone H2A eviction. Remarkably, further addition of free H2A.Z-H2B dimer leads to hyperstimulation of ATPase activity, eviction of nucleosomal H2A-H2B, and deposition of H2A.Z-H2B. These results suggest that the combination of H2A-containing nucleosome and free H2A.Z-H2B dimer acting as both effector and substrate for SWR1 governs the specificity and outcome of the replacement reaction.
C1 [Luk, Ed; Ranjan, Anand; Mizuguchi, Gaku; Huang, Yingzi; Wei, Debbie; Wu, Carl] NCI, Biochem & Mol Biol Lab, NIH, Bethesda, MD 20892 USA.
   [FitzGerald, Peter C.] NCI, Genome Anal Unit, NIH, Bethesda, MD 20892 USA.
RP Luk, E (reprint author), NCI, Biochem & Mol Biol Lab, NIH, Bethesda, MD 20892 USA.
EM luked@mail.nih.gov; carlwu@helix.nih.gov
OI Luk, Ed/0000-0002-6619-2258
FU National Cancer Institute; Leukemia and Lymphoma Society
FX We thank W.H. Wu for the yeast strain SWR1-FL htz1 Delta and J. Landry
   for the yeast strain yJL036. We also thank H. Cam and C. Rubin for
   advice on microarray techniques, F. Pugh and members of the Wu lab for
   critical reading of the manuscript, and anonymous reviewers for helpful
   suggestions. This work was supported by the intramural research program
   of the National Cancer Institute (C.W.) and by the Leukemia and Lymphoma
   Society (E.L. and A.R.).
NR 50
TC 90
Z9 93
U1 0
U2 11
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 0092-8674
J9 CELL
JI Cell
PD NOV 24
PY 2010
VL 143
IS 5
BP 725
EP 736
DI 10.1016/j.cell.2010.10.019
PG 12
WC Biochemistry & Molecular Biology; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA 684VX
UT WOS:000284583500015
PM 21111233
ER

PT J
AU Shibata, Y
   Shemesh, T
   Prinz, WA
   Palazzo, AF
   Kozlov, MM
   Rapoport, TA
AF Shibata, Yoko
   Shemesh, Tom
   Prinz, William A.
   Palazzo, Alexander F.
   Kozlov, Michael M.
   Rapoport, Tom A.
TI Mechanisms Determining the Morphology of the Peripheral ER
SO CELL
LA English
DT Article
ID ENDOPLASMIC-RETICULUM MEMBRANE; SACCHAROMYCES-CEREVISIAE; TRANSLOCON
   COMPLEXES; RIBOSOME RECEPTOR; PROTEINS; ROUGH; BINDING; CELLS;
   MICROTUBULES; IDENTIFICATION
AB The endoplasmic reticulum (ER) consists of the nuclear envelope and a peripheral network of tubules and membrane sheets. The tubules are shaped by the curvature-stabilizing proteins reticulons and DP1/Yop1p, but how the sheets are formed is unclear. Here, we identify several sheet-enriched membrane proteins in the mammalian ER, including proteins that translocate and modify newly synthesized polypeptides, as well as coiled-coil membrane proteins that are highly upregulated in cells with proliferated ER sheets, all of which are localized by membrane-bound polysomes. These results indicate that sheets and tubules correspond to rough and smooth ER, respectively. One of the coiled-coil proteins, Climp63, serves as a "luminal ER spacer'' and forms sheets when overexpressed. More universally, however, sheet formation appears to involve the reticulons and DP1/Yop1p, which localize to sheet edges and whose abundance determines the ratio of sheets to tubules. These proteins may generate sheets by stabilizing the high curvature of edges.
C1 [Shemesh, Tom; Kozlov, Michael M.] Tel Aviv Univ, Sackler Fac Med, Dept Physiol & Pharmacol, IL-69978 Tel Aviv, Israel.
   [Shibata, Yoko; Palazzo, Alexander F.; Rapoport, Tom A.] Harvard Univ, Sch Med, Howard Hughes Med Inst, Boston, MA 02115 USA.
   [Shibata, Yoko] Harvard Univ, Sch Med, Dept Cell Biol, Boston, MA 02115 USA.
   [Prinz, William A.] NIDDK, Lab Cell Biochem & Biol, NIH, Bethesda, MD 20892 USA.
   [Palazzo, Alexander F.] Univ Toronto, Dept Biochem, Toronto, ON M5S 1A8, Canada.
RP Kozlov, MM (reprint author), Tel Aviv Univ, Sackler Fac Med, Dept Physiol & Pharmacol, IL-69978 Tel Aviv, Israel.
EM michk@post.tau.ac.il; tom_rapoport@hms.harvard.edu
RI Palazzo, Alexander/B-1270-2013; Shemesh, Tom/J-5060-2013
OI Palazzo, Alexander/0000-0002-9700-1995; 
FU American Heart Association; National Institute of Diabetes and Digestive
   and Kidney Diseases; Israel Science Foundation (ISF); Marie Curie
   network "Virus Entry"
FX We thank C. Denison, J. Minsteris, and S. Gygi for mass spectrometry
   analysis; J. Baughman for microarray analysis; A. Condon and A. Boye-Doe
   for technical assistance; J. Iwasa for help with illustrations; G.
   Kreibich, K. Ogawa-Goto, L. Lu, and R. Yan for materials; the Nikon
   Imaging Center and the Electron Microscopy facility at HMS for
   microscopy assistance; and R. Klemm and A. Osborne for critical reading
   of the manuscript. Y.S. was supported by the American Heart Association
   and is a Howard Hughes Medical Institute postdoctoral fellow. W.A.P. is
   supported by the Intramural Research Program of the National Institute
   of Diabetes and Digestive and Kidney Diseases. T.A.R. is a Howard Hughes
   Medical Institute Investigator. M.M.K. is supported by the Israel
   Science Foundation (ISF) and the Marie Curie network "Virus Entry.''
NR 38
TC 160
Z9 161
U1 1
U2 28
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 0092-8674
J9 CELL
JI Cell
PD NOV 24
PY 2010
VL 143
IS 5
BP 774
EP 788
DI 10.1016/j.cell.2010.11.007
PG 15
WC Biochemistry & Molecular Biology; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA 684VX
UT WOS:000284583500019
PM 21111237
ER

PT J
AU Matsuki, T
   Matthews, RT
   Cooper, JA
   van der Brug, MP
   Cookson, MR
   Hardy, JA
   Olson, EC
   Howell, BW
AF Matsuki, Tohru
   Matthews, Russell T.
   Cooper, Jonathan A.
   van der Brug, Marcel P.
   Cookson, Mark R.
   Hardy, John A.
   Olson, Eric C.
   Howell, Brian W.
TI Reelin and Stk25 Have Opposing Roles in Neuronal Polarization and
   Dendritic Golgi Deployment
SO CELL
LA English
DT Article
ID MATRIX PROTEIN GM130; APOE RECEPTOR 2; TYROSINE PHOSPHORYLATION; TAU
   PHOSPHORYLATION; BRAIN-DEVELOPMENT; CORTICAL-NEURONS; VLDL RECEPTOR; SAD
   KINASES; POLARITY; MOUSE
AB The Reelin ligand regulates a Dab1-dependent signaling pathway required for brain lamination and normal dendritogenesis, but the specific mechanisms underlying these actions remain unclear. We find that Stk25, a modifier of Reelin-Dab1 signaling, regulates Golgi morphology and neuronal polarization as part of an LKB1-Stk25-Golgi matrix protein 130 (GM130) signaling pathway. Overexpression of Stk25 induces Golgi condensation and multiple axons, both of which are rescued by Reelin treatment. Reelin stimulation of cultured neurons induces the extension of the Golgi into dendrites, which is suppressed by Stk25 overexpression. In vivo, Reelin and Dab1 are required for the normal extension of the Golgi apparatus into the apical dendrites of hippocampal and neocortical pyramidal neurons. This demonstrates that the balance between Reelin-Dab1 signaling and LKB1-Stk25-GM130 regulates Golgi dispersion, axon specification, and dendrite growth and provides insights into the importance of the Golgi apparatus for cell polarization.
C1 [Matsuki, Tohru; Matthews, Russell T.; Olson, Eric C.; Howell, Brian W.] SUNY Upstate Med Univ, Dept Neurosci & Physiol, Syracuse, NY 13210 USA.
   [van der Brug, Marcel P.; Cookson, Mark R.; Hardy, John A.] NIA, Neurogenet Lab, NIH, Bethesda, MD 20892 USA.
   [Cooper, Jonathan A.] Fred Hutchinson Canc Res Ctr, Div Basic Sci, Seattle, WA 98109 USA.
RP Howell, BW (reprint author), SUNY Upstate Med Univ, Dept Neurosci & Physiol, Syracuse, NY 13210 USA.
EM howellb@upstate.edu
RI Hardy, John/C-2451-2009; 
OI Howell, Brian/0000-0002-0204-0773
FU NINDS; SUNY Upstate Medical University; NIH [NS066071, NS069660,
   CA41072]; NIA
FX We would like to thank Zainab Mansaray and Kristin Giamanco for
   experimental assistance, Michael Zuber for comments on the manuscript,
   Hans Clevers for cell lines, Louis Cantley and Jun-ichi Miyazaki for DNA
   vectors, Arvydas Matiukas and Melissa Pepling for assistance with
   confocal microscopy, and Bonnie Lee Howell for editing. This work was
   supported by funds from the NINDS intramural program and SUNY Upstate
   Medical University to B.W.H.; NIH grants NS066071 to E.C.O., NS069660 to
   R.T.M., and CA41072 to J.A.C.; and NIA intramural funds for M.R.C.
NR 57
TC 62
Z9 64
U1 0
U2 4
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 0092-8674
J9 CELL
JI Cell
PD NOV 24
PY 2010
VL 143
IS 5
BP 826
EP 836
DI 10.1016/j.cell.2010.10.029
PG 11
WC Biochemistry & Molecular Biology; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA 684VX
UT WOS:000284583500023
PM 21111240
ER

PT J
AU Godlewski, G
   Alapafuja, SO
   Batkai, S
   Nikas, SP
   Cinar, R
   Offertaler, L
   Osei-Hyiaman, D
   Liu, J
   Mukhopadhyay, B
   Harvey-White, J
   Tam, J
   Pacak, K
   Blankman, JL
   Cravatt, BF
   Makriyannis, A
   Kunos, G
AF Godlewski, Grzegorz
   Alapafuja, Shakiru O.
   Batkai, Sandor
   Nikas, Spyros P.
   Cinar, Resat
   Offertaler, Laszlo
   Osei-Hyiaman, Douglas
   Liu, Jie
   Mukhopadhyay, Bani
   Harvey-White, Judith
   Tam, Joseph
   Pacak, Karel
   Blankman, Jacqueline L.
   Cravatt, Benjamin F.
   Makriyannis, Alexandros
   Kunos, George
TI Inhibitor of Fatty Acid Amide Hydrolase Normalizes Cardiovascular
   Function in Hypertension without Adverse Metabolic Effects
SO CHEMISTRY & BIOLOGY
LA English
DT Article
ID CANNABINOID RECEPTOR; BLOOD-PRESSURE; ENDOCANNABINOID SYSTEM; ENHANCED
   EXPRESSION; ADENYLYL-CYCLASE; NERVOUS-SYSTEM; CB1 RECEPTORS; ANANDAMIDE;
   RATS; FAAH
AB The enzyme fatty acid amide hydrolase (FAAH) catalyzes the in vivo degradation of the endocannabinoid anandamide, thus controlling its action at receptors. A novel FAAH inhibitor, AM3506, normalizes the elevated blood pressure and cardiac contractility of spontaneously hypertensive rats (SHR) without affecting these parameters in normotensive rats. These effects are due to blockade of FAAH and a corresponding rise in brain anandamide levels, resulting in CB, receptor-mediated decrease in sympathetic tone. The supersensitivity of SHR to CB1 receptor-mediated cardiovascular depression is related to increased G protein coupling of CB1 receptors. Importantly, AM3506 does not elicit hyperglycemia and insulin resistance seen with other FAAH inhibitors or in FAAH(-/-) mice, which is related to its inability to inhibit FAAH in the liver due to rapid hepatic uptake and metabolism. This unique activity profile improved therapeutic value in hypertension.
C1 [Alapafuja, Shakiru O.; Nikas, Spyros P.; Makriyannis, Alexandros] Northeastern Univ, Ctr Drug Discovery, Boston, MA 02115 USA.
   [Godlewski, Grzegorz; Batkai, Sandor; Cinar, Resat; Offertaler, Laszlo; Osei-Hyiaman, Douglas; Liu, Jie; Mukhopadhyay, Bani; Harvey-White, Judith; Tam, Joseph; Kunos, George] NIAAA, Lab Physiol Studies, NIH, Rockville, MD 20852 USA.
   [Pacak, Karel] NICHHD, Sect Med Neuroendocrinol, NIH, Bethesda, MD 20892 USA.
   [Blankman, Jacqueline L.; Cravatt, Benjamin F.] Scripps Res Inst, La Jolla, CA 92037 USA.
RP Makriyannis, A (reprint author), Northeastern Univ, Ctr Drug Discovery, 360 Huntington Ave, Boston, MA 02115 USA.
EM a.makriyannis@neu.edu; george.kunos@nih.gov
RI CINAR, Resat/E-5755-2010; Batkai, Sandor/G-3889-2010; Batkai,
   Sandor/H-7983-2014
OI CINAR, Resat/0000-0002-8597-7253; 
FU NIAAA
FX We thank Prof. B. Lutz and Dr. G. Marsicano for providing CBI floxed
   mice used to generate the liver-specific CB<INF>1</INF><SUP>-/-</SUP>
   mice. This work was supported by funds from the intramural program of
   NIAAA.
NR 44
TC 37
Z9 37
U1 0
U2 4
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 1074-5521
J9 CHEM BIOL
JI Chem. Biol.
PD NOV 24
PY 2010
VL 17
IS 11
BP 1256
EP 1266
DI 10.1016/j.chembiol.2010.08.013
PG 11
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 695XD
UT WOS:000285405000015
PM 21095576
ER

PT J
AU Strober, W
AF Strober, Warren
TI The LTi Cell, an Immunologic Chameleon
SO IMMUNITY
LA English
DT Editorial Material
ID NATURAL-KILLER-CELLS; ROR-GAMMA-T; MUCOSAL IMMUNITY; RECEPTOR
AB Lymphoid tissue inducer (LTi) cells are key components of the machinery required for the construction of the lymphoid structures underlying immune responses. In this issue of Immunity,, Vonarbourg et. al. (2010) describe how these cells assume several different guises, each associated with different LTi functions.
C1 NIAID, NIH, Bethesda, MD 20892 USA.
RP Strober, W (reprint author), NIAID, NIH, Bethesda, MD 20892 USA.
EM wstrober@niaid.nih.gov
FU Intramural NIH HHS [Z01 AI000872-08]
NR 11
TC 3
Z9 3
U1 0
U2 0
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 1074-7613
J9 IMMUNITY
JI Immunity
PD NOV 24
PY 2010
VL 33
IS 5
BP 650
EP 652
DI 10.1016/j.immuni.2010.11.016
PG 3
WC Immunology
SC Immunology
GA 704VB
UT WOS:000286082600003
PM 21094460
ER

PT J
AU Lubitz, SA
   Yin, XY
   Fontes, JD
   Magnani, JW
   Rienstra, M
   Pai, M
   Villalon, ML
   Vasan, RS
   Pencina, MJ
   Levy, D
   Larson, MG
   Ellinor, PT
   Benjamin, EJ
AF Lubitz, Steven A.
   Yin, Xiaoyan
   Fontes, Joao D.
   Magnani, Jared W.
   Rienstra, Michiel
   Pai, Manju
   Villalon, Mark L.
   Vasan, Ramachandran S.
   Pencina, Michael J.
   Levy, Daniel
   Larson, Martin G.
   Ellinor, Patrick T.
   Benjamin, Emelia J.
TI Association Between Familial Atrial Fibrillation and Risk of New-Onset
   Atrial Fibrillation
SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION
LA English
DT Article
ID MIDDLE-AGED ADULTS; CARDIOVASCULAR-DISEASE; COMMON VARIANTS; PR
   INTERVAL; AGGREGATION; HISTORY; REGRESSION; COHORT; ZFHX3; SCORE
AB Context Although the heritability of atrial fibrillation (AF) is established, the contribution of familial AF to predicting new-onset AF remains unknown.
   Objective To determine whether familial occurrence of AF is associated with new-onset AF beyond established risk factors.
   Design, Setting, and Participants The Framingham Heart Study, a prospective community-based cohort study started in 1948. Original and Offspring Cohort participants were aged at least 30 years, were free of AF at the baseline examination, and had at least 1 parent or sibling enrolled in the study. The 4421 participants in this analysis (mean age, 54 [SD, 13] years; 54% women) were followed up through December 31, 2007.
   Main Outcome Measures Incremental predictive value of incorporating different features of familial AF (any familial AF, premature familial AF [onset <65 years old], number of affected relatives, and youngest age of onset in a relative) into a risk model for new-onset AF.
   Results Across 11 971 examinations during the period 1968-2007, 440 participants developed AF. Familial AF occurred among 1185 participants (26.8%) and premature familial AF occurred among 351 participants (7.9%). Atrial fibrillation occurred more frequently among participants with familial AF than without familial AF (unadjusted absolute event rates of 5.8% and 3.1%, respectively). The association was not attenuated by adjustment for AF risk factors (multivariable-adjusted hazard ratio, 1.40; 95% confidence interval [CI], 1.13-1.74) or reported AF-related genetic variants. Among the different features of familial AF examined, premature familial AF was associated with improved discrimination beyond traditional risk factors to the greatest extent (traditional risk factors, C statistic, 0.842 [95% CI, 0.826-0.858]; premature familial AF, C statistic, 0.846 [95% CI, 0.831-0.862]; P=.004). Modest changes in integrated discrimination improvement were observed with premature familial AF (2.1%). Net reclassification improvement (assessed using 8-year risk thresholds of <5%, 5%-10%, and >10%) did not change significantly with premature familial AF (index statistic, 0.011; 95% CI, -0.021 to 0.042; P=.51), although categoryless net reclassification was improved (index statistic, 0.127; 95% CI, 0.064-0.189; P=.009).
   Conclusions In this cohort, familial AF was associated with an increased risk of AF that was not attenuated by adjustment for AF risk factors including genetic variants. Assessment of premature familial AF was associated with a very slight increase in predictive accuracy compared with traditional risk factors. JAMA. 2010;304(20):2263-2269 www.jama.com
C1 [Yin, Xiaoyan; Fontes, Joao D.; Magnani, Jared W.; Vasan, Ramachandran S.; Pencina, Michael J.; Levy, Daniel; Larson, Martin G.; Benjamin, Emelia J.] Framingham Heart Dis Epidemiol Study, Framingham, MA 01702 USA.
   [Lubitz, Steven A.; Rienstra, Michiel; Ellinor, Patrick T.] Massachusetts Gen Hosp, Cardiovasc Res Ctr, Charlestown, MA USA.
   [Lubitz, Steven A.] Brigham & Womens Hosp, Div Prevent Med, Boston, MA 02115 USA.
   [Fontes, Joao D.; Magnani, Jared W.; Vasan, Ramachandran S.; Benjamin, Emelia J.] Boston Univ, Sch Med, Cardiol Sect, Boston, MA 02118 USA.
   [Vasan, Ramachandran S.; Benjamin, Emelia J.] Boston Univ, Sch Med, Prevent Med Sect, Boston, MA 02118 USA.
   [Pai, Manju; Villalon, Mark L.] Boston Univ, Sch Med, Dept Med, Boston, MA 02118 USA.
   [Pencina, Michael J.; Larson, Martin G.] Boston Univ, Dept Biostat, Boston, MA 02215 USA.
   [Benjamin, Emelia J.] Boston Univ, Dept Epidemiol, Boston, MA 02215 USA.
   [Larson, Martin G.] Boston Univ, Dept Math & Stat, Boston, MA 02215 USA.
   [Ellinor, Patrick T.] Massachusetts Gen Hosp, Cardiac Arrhythmia Serv, Boston, MA 02114 USA.
   [Rienstra, Michiel] Univ Groningen, Univ Med Ctr Groningen, Dept Cardiol, Groningen, Netherlands.
   [Levy, Daniel] NHLBI, Ctr Populat Studies, Bethesda, MD 20892 USA.
RP Benjamin, EJ (reprint author), Framingham Heart Dis Epidemiol Study, 73 Mt Wayte Ave,Ste 2, Framingham, MA 01702 USA.
EM emelia@bu.edu
OI Ramachandran, Vasan/0000-0001-7357-5970; Benjamin,
   Emelia/0000-0003-4076-2336; Rienstra, Michiel/0000-0002-2581-070X
FU National Institutes of Health (NIH) [T32HL007575, 6R01-NS17950,
   HL092577, R01AG028321, RC1-HL01056, 1R01HL102214, DA027021, HL104156];
   American Heart Association [09FTF2190028]; Netherlands Organization for
   Scientific Research [825.09.020]
FX Dr Lubitz was supported by a National Institutes of Health (NIH)
   training grant in the Epidemiology of Cardiovascular Disease (grant
   T32HL007575). Dr Magnani is supported by American Heart Association
   grant 09FTF2190028. Dr Rienstra is supported by a Rubicon grant from the
   Netherlands Organization for Scientific Research (grant 825.09.020). Dr
   Benjamin is supported by NIH grant 6R01-NS17950. This work was supported
   by grants from the NIH to Drs Benjamin and Ellinor (grant HL092577), Dr
   Benjamin (grants R01AG028321, RC1-HL01056, and 1R01HL102214), and Dr
   Ellinor (grants DA027021 and HL104156).
NR 33
TC 103
Z9 104
U1 0
U2 6
PU AMER MEDICAL ASSOC
PI CHICAGO
PA 515 N STATE ST, CHICAGO, IL 60654-0946 USA
SN 0098-7484
J9 JAMA-J AM MED ASSOC
JI JAMA-J. Am. Med. Assoc.
PD NOV 24
PY 2010
VL 304
IS 20
BP 2263
EP 2269
DI 10.1001/jama.2010.1690
PG 7
WC Medicine, General & Internal
SC General & Internal Medicine
GA 684KI
UT WOS:000284548400025
PM 21076174
ER

PT J
AU Manolio, TA
   Collins, R
AF Manolio, Teri A.
   Collins, Rory
TI Enhancing the Feasibility of Large Cohort Studies
SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION
LA English
DT Editorial Material
ID ENVIRONMENT; GENES
C1 [Manolio, Teri A.] NHGRI, Off Populat Genom, Bethesda, MD 20892 USA.
   [Collins, Rory] Univ Oxford, Clin Trial Serv Unit, Oxford, England.
   [Collins, Rory] Univ Oxford, Epidemiol Studies Unit, Oxford, England.
RP Manolio, TA (reprint author), NHGRI, Off Populat Genom, Bldg 31,Room 4B-09,31 Ctr Dr,MSC 2154, Bethesda, MD 20892 USA.
EM manolio@nih.gov
FU Intramural NIH HHS [Z99 HG999999]; Medical Research Council
   [MC_QA137853, MC_U137686857]
NR 10
TC 29
Z9 30
U1 0
U2 3
PU AMER MEDICAL ASSOC
PI CHICAGO
PA 515 N STATE ST, CHICAGO, IL 60654-0946 USA
SN 0098-7484
J9 JAMA-J AM MED ASSOC
JI JAMA-J. Am. Med. Assoc.
PD NOV 24
PY 2010
VL 304
IS 20
BP 2290
EP 2291
DI 10.1001/jama.2010.1686
PG 2
WC Medicine, General & Internal
SC General & Internal Medicine
GA 684KI
UT WOS:000284548400029
PM 21098774
ER

PT J
AU Simmons, JM
   Minamimoto, T
   Murray, EA
   Richmond, BJ
AF Simmons, Janine M.
   Minamimoto, Takafumi
   Murray, Elisabeth A.
   Richmond, Barry J.
TI Selective Ablations Reveal That Orbital and Lateral Prefrontal Cortex
   Play Different Roles in Estimating Predicted Reward Value
SO JOURNAL OF NEUROSCIENCE
LA English
DT Article
ID PRIMATE ORBITOFRONTAL CORTEX; NEURONAL-ACTIVITY; FRONTAL-CORTEX;
   DECISION-MAKING; WORKING-MEMORY; CONDITIONED REINFORCEMENT; BASOLATERAL
   AMYGDALA; EXPECTED REWARD; ECONOMIC VALUE; LESIONS
AB Subregions of prefrontal cortex are important for estimating reward values and using these values to guide behavior. The present studies directly tested whether orbital prefrontal cortex (O-PFC) and lateral prefrontal cortex (L-PFC) are necessary for evaluating trial-to-trial changes in the reward values predicted by visual cues. We have compared intact rhesus monkeys, those with bilateral O-PFC lesions (n = 3), and those with bilateral L-PFC lesions (n = 3). We used three versions of a visually cued color discrimination task: we varied reward size, delay to reward, or both. O-PFC lesions altered estimations of predicted reward value in all versions of the task. L-PFC lesions disrupted performance only when both reward size and delay to reward were varied together. Neither lesion directly affected basic internal drive states (satiation curves). Our results suggest that O-PFC is essential for establishing independent, context-specific scales with which predicted reward values are measured. L-PFC appears necessary for integration of predicted reward value across these different scales.
C1 [Simmons, Janine M.; Minamimoto, Takafumi; Murray, Elisabeth A.; Richmond, Barry J.] NIMH, Neuropsychol Lab, NIH, US Dept HHS, Bethesda, MD 20892 USA.
   [Minamimoto, Takafumi] Natl Inst Radiol Sci, Mol Imaging Ctr, Dept Mol Neuroimaging, Chiba 2638555, Japan.
RP Richmond, BJ (reprint author), NIMH, Neuropsychol Lab, NIH, US Dept HHS, Bldg 49,Room 1B80, Bethesda, MD 20892 USA.
EM bjr@ln.nimh.nih.gov
RI Minamimoto, Takafumi/D-6610-2012; 
OI Minamimoto, Takafumi/0000-0003-4305-0174; Murray,
   Elisabeth/0000-0003-1450-1642
FU National Institute of Mental Health
FX This work was supported by the Division of Intramural Research Programs
   at the National Institute of Mental Health. We thank Richard Saunders,
   Megan Malloy, Ping-Yu Chen, Dawn Lundgren-Anuszkiewicz, James Peck, and
   Sebastien Bouret.
NR 54
TC 17
Z9 17
U1 0
U2 2
PU SOC NEUROSCIENCE
PI WASHINGTON
PA 11 DUPONT CIRCLE, NW, STE 500, WASHINGTON, DC 20036 USA
SN 0270-6474
J9 J NEUROSCI
JI J. Neurosci.
PD NOV 24
PY 2010
VL 30
IS 47
BP 15878
EP 15887
DI 10.1523/JNEUROSCI.1802-10.2010
PG 10
WC Neurosciences
SC Neurosciences & Neurology
GA 684VF
UT WOS:000284580100017
PM 21106826
ER

PT J
AU Koenigs, M
   Holliday, J
   Solomon, J
   Grafman, J
AF Koenigs, Michael
   Holliday, Jessica
   Solomon, Jeffrey
   Grafman, Jordan
TI Left Dorsomedial Frontal Brain Damage Is Associated with Insomnia
SO JOURNAL OF NEUROSCIENCE
LA English
DT Article
ID SLEEP; REGISTRATION; ACTIVATIONS; SOFTWARE; PET
AB Insomnia is a common sleep disorder, yet its pathophysiological basis remains poorly understood. Studying a group of 192 patients with focal brainlesions, we show a significant association between insomnia and left dorsomedial prefrontal damage. Our findings are the first to demonstrate a link between insomnia and a discrete locus of brain damage, providing novel insight into the neurobiological mechanisms of sleep maintenance.
C1 [Koenigs, Michael; Holliday, Jessica] Univ Wisconsin, Dept Psychiat, Madison, WI 53719 USA.
   [Solomon, Jeffrey] Med Numer Inc, Germantown, MD 20876 USA.
   [Grafman, Jordan] Natl Inst Neurol Disorders & Stroke, Cognit Neurosci Sect, NIH, Bethesda, MD 20892 USA.
RP Koenigs, M (reprint author), Univ Wisconsin, Dept Psychiat, 6001 Res Pk Blvd, Madison, WI 53719 USA.
EM mrkoenigs@wisc.edu; grafmanj@ninds.nih.gov
OI Grafman, Jordan H./0000-0001-8645-4457; Koenigs,
   Michael/0000-0002-5799-4881
FU National Institute of Neurological Disorders and Stroke
FX This work was supported by the National Institute of Neurological
   Disorders and Stroke intramural research program. We thank Sandi
   Bonifant for VHIS data management, Dr. Vanessa Raymont for psychiatric
   evaluations, and Dr. Jose Maisog for developing the chi<SUP>2</SUP>
   false discovery rate software. We thank the veterans for their
   participation in the VHIS.
NR 19
TC 26
Z9 26
U1 0
U2 2
PU SOC NEUROSCIENCE
PI WASHINGTON
PA 11 DUPONT CIRCLE, NW, STE 500, WASHINGTON, DC 20036 USA
SN 0270-6474
J9 J NEUROSCI
JI J. Neurosci.
PD NOV 24
PY 2010
VL 30
IS 47
BP 16041
EP 16043
DI 10.1523/JNEUROSCI.3745-10.2010
PG 3
WC Neurosciences
SC Neurosciences & Neurology
GA 684VF
UT WOS:000284580100033
PM 21106842
ER

PT J
AU Andrei, D
   Salmon, DJ
   Donzelli, S
   Wahab, A
   Klose, JR
   Citro, ML
   Saavedra, JE
   Wink, DA
   Miranda, KM
   Keefer, LK
AF Andrei, Daniela
   Salmon, Debra J.
   Donzelli, Sonia
   Wahab, Azadeh
   Klose, John R.
   Citro, Michael L.
   Saavedra, Joseph E.
   Wink, David A.
   Miranda, Katrina M.
   Keefer, Larry K.
TI Dual Mechanisms of HNO Generation by a Nitroxyl Prodrug of the
   Diazeniumdiolate (NONOate) Class
SO JOURNAL OF THE AMERICAN CHEMICAL SOCIETY
LA English
DT Article
ID NITRIC-OXIDE; ALDEHYDE DEHYDROGENASE; CARDIOVASCULAR-SYSTEM;
   BIOLOGICAL-SYSTEMS; NITROSYL HYDRIDE; AQUEOUS-SOLUTION; N-HYDROXYUREA;
   RELEASE; DONORS; INHIBITORS
AB Here we describe a novel caged form of the highly reactive bioeffector molecule, nitroxyl (HNO). Reacting the labile nitric oxide (NO)- and HNO-generating salt of structure iPrHN-N(O)=NO-Na+ (1, IPA/NO) with BrCH2OAc produced a stable derivative of structure iPrHN-N(O)=NO-CH2OAc (2, AcOM-IPA/NO), which hydrolyzed an order of magnitude more slowly than 1 at pH 7.4 and 37 degrees C. Hydrolysis of 2 to generate HNO proceeded by at least two mechanisms. In the presence of esterase, straightforward dissociation to acetate, formaldehyde, and 1 was the dominant path. In the absence of enzyme, free 1 was not observed as an intermediate and the ratio of NO to HNO among the products approached zero. To account for this surprising result, we propose a mechanism in which base-induced removal of the N-H proton of 2 leads to acetyl group migration from oxygen to the neighboring nitrogen, followed by cleavage of the resulting rearrangement product to isopropanediazoate ion and the known HNO precursor, CH3-C(O)-NO. The trappable yield of HNO from 2 was significantly enhanced over 1 at physiological pH, in part because the slower rate of hydrolysis for 2 generated a correspondingly lower steady-state concentration of HNO, thus, minimizing self-consumption and enhancing trapping by biological targets such as metmyoglobin and glutathione. Consistent with the chemical trapping efficiency data, micromolar concentrations of prodrug 2 displayed significantly more potent sarcomere shortening effects relative to 1 on ventricular myocytes isolated from wild-type mouse hearts, suggesting that 2 may be a promising lead compound for the development of heart failure therapies.
C1 [Salmon, Debra J.; Miranda, Katrina M.] Univ Arizona, Dept Chem & Biochem, Tucson, AZ 85721 USA.
   [Andrei, Daniela; Keefer, Larry K.] NCI, Chem Sect, Comparat Carcinogenesis Lab, Frederick, MD 21702 USA.
   [Donzelli, Sonia; Wahab, Azadeh] Univ Med Ctr Hamburg Eppendorf, Dept Expt & Clin Pharmacol & Toxicol, Hamburg, Germany.
   [Donzelli, Sonia] Univ Med Ctr Hamburg Eppendorf, Dept Neurol, Hamburg, Germany.
   [Donzelli, Sonia] Univ Med Ctr Hamburg Eppendorf, Cardiovasc Res Ctr, Hamburg, Germany.
   [Klose, John R.] SAIC Frederick, Lab Prote & Analyt Technol, Frederick, MD 21702 USA.
   [Citro, Michael L.; Saavedra, Joseph E.] SAIC Frederick, Basic Res Program, Frederick, MD 21702 USA.
   [Wink, David A.] NCI, Radiat Biol Branch, Bethesda, MD 20892 USA.
RP Miranda, KM (reprint author), Univ Arizona, Dept Chem & Biochem, Tucson, AZ 85721 USA.
EM kmiranda@email.arizona.edu; keeferl@mail.nih.gov
RI Miranda, Katrina/B-7823-2009; Keefer, Larry/N-3247-2014
OI Keefer, Larry/0000-0001-7489-9555
FU Marie Curie Intra European Fellowship [PIEF-GA-2008-221666];
   Forschungsforderungsfonds [NWF-08/04]; NIH, National Cancer Institute,
   Center for Cancer Research; NCI [HHSN261200800001E]; National Institutes
   of Health (National Institute on Alcohol Abuse and Alcoholism)
   [R01-GM076247, 1F31AA018069-01A1]
FX This work was supported by: the Marie Curie Intra European Fellowship
   within the 7th European Community Framework Programme
   (PIEF-GA-2008-221666 to S.D.); the Forschungsforderungsfonds (NWF-08/04
   to S.D.); the Intramural Research Program of the NIH, National Cancer
   Institute, Center for Cancer Research; NCI contract HHSN261200800001E;
   National Institutes of Health grants R01-GM076247 to K.M.M. and
   1F31AA018069-01A1 (National Institute on Alcohol Abuse and Alcoholism)
   to D.J.S.
NR 49
TC 31
Z9 31
U1 1
U2 22
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 0002-7863
J9 J AM CHEM SOC
JI J. Am. Chem. Soc.
PD NOV 24
PY 2010
VL 132
IS 46
BP 16526
EP 16532
DI 10.1021/ja106552p
PG 7
WC Chemistry, Multidisciplinary
SC Chemistry
GA 687QC
UT WOS:000284792000044
PM 21033665
ER

PT J
AU Rychlik, MP
   Chon, H
   Cerritelli, SM
   Klimek, P
   Crouch, RJ
   Nowotny, M
AF Rychlik, Monika P.
   Chon, Hyongi
   Cerritelli, Susana M.
   Klimek, Pauline
   Crouch, Robert J.
   Nowotny, Marcin
TI Crystal Structures of RNase H2 in Complex with Nucleic Acid Reveal the
   Mechanism of RNA-DNA Junction Recognition and Cleavage
SO MOLECULAR CELL
LA English
DT Article
ID AICARDI-GOUTIERES-SYNDROME; SUBSTRATE-SPECIFICITY; RIBONUCLEASE-H;
   SACCHAROMYCES-CEREVISIAE; REVERSE TRANSCRIPTION; MUTATIONAL ANALYSES;
   BINDING DOMAIN; RNA/DNA HYBRID; PRIMER REMOVAL; METAL-IONS
AB Two classes of RNase H hydrolyze RNA of RNA/DNA hybrids. In contrast to RNase H1 that requires four ribonucleotides for cleavage, RNase H2 can nick duplex DNAs containing a single ribonucleotide, suggesting different in vivo substrates. We report here the crystal structures of a type 2 RNase H in complex with substrates containing a (5')RNA-DNA(3') junction. They revealed a unique mechanism of recognition and substrate-assisted cleavage. A conserved tyrosine residue distorts the nucleic acid at the junction, allowing the substrate to function in catalysis by participating in coordination of the active site metal ion. The biochemical and structural properties of RNase H2 explain the preference of the enzyme for junction substrates and establish the structural and mechanistic differences with RNase H1. Junction recognition is important for the removal of RNA embedded in DNA and may play an important role in DNA replication and repair.
C1 [Rychlik, Monika P.; Klimek, Pauline; Nowotny, Marcin] Int Inst Mol & Cell Biol, Lab Prot Struct, PL-02109 Warsaw, Poland.
   [Chon, Hyongi; Cerritelli, Susana M.; Crouch, Robert J.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Program Genom Differentiat, NIH, Bethesda, MD 20892 USA.
RP Nowotny, M (reprint author), Int Inst Mol & Cell Biol, Lab Prot Struct, 4 Trojdena St, PL-02109 Warsaw, Poland.
EM mnowotny@iimcb.gov.pl
FU Wellcome Trust [081760]; Eunice Kennedy Shriver National Institute of
   Child Health and Human Development, National Institutes of Health
FX We would like to thank Jadwiga Dyttus and Magdalena Cybulska for
   excellent technical assistance and Prof. Matthias Bochtler, Dr. Honorata
   Czapinska, and Dr. Karolina Gorecka for their help with data collection.
   We thank Dr. Wei Yang for critical reading of the manuscript and
   Maigorzata Figiel for her help in preparation of Figure 4D. We are also
   grateful to the staff of beamlines MX-14 at BESSY, BW6 at DESY, and 14-4
   at ESRF for the assistance with data collection. M.N. is supported by
   Wellcome Trust International Senior Research Fellowship (No. 081760).
   This work was also supported by the Intramural Research Program of the
   Eunice Kennedy Shriver National Institute of Child Health and Human
   Development, National Institutes of Health. H.C. is a Japan Society for
   the Promotion of Science Research Fellow in Biomedical and Behavioral
   Research at the National Institutes of Health.
NR 45
TC 42
Z9 44
U1 1
U2 12
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 1097-2765
J9 MOL CELL
JI Mol. Cell
PD NOV 24
PY 2010
VL 40
IS 4
BP 658
EP 670
DI 10.1016/j.molcel.2010.11.001
PG 13
WC Biochemistry & Molecular Biology; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA 690FR
UT WOS:000284988400017
PM 21095591
ER

PT J
AU Yang, KHS
   Isaev, D
   Morales, M
   Petroianu, G
   Galadari, S
   Oz, M
AF Yang, K. H. S.
   Isaev, D.
   Morales, M.
   Petroianu, G.
   Galadari, S.
   Oz, M.
TI THE EFFECT OF Delta(9)-TETRAHYDROCANNABINOL ON 5-HT3 RECEPTORS DEPENDS
   ON THE CURRENT DENSITY
SO NEUROSCIENCE
LA English
DT Article
DE Delta(9)-tetrahydrocannabinol; cannabinoid; 5-HT3A receptor; Xenopus
   oocytes; nodose ganglion neuron.
ID MEDIATED ION CURRENT; XENOPUS OOCYTES; CANNABINOID RECEPTORS;
   HIPPOCAMPAL-NEURONS; SUBUNIT-A; ANANDAMIDE; INHIBITION; CHANNELS;
   RESPONSES; GANGLION
AB The effects of :Delta(9)-tetrahydrocannabinol (THC), the psychoactive component of cannabis, on the function of 5-HT type 3 (5-HT3) receptors were investigated using a two-electrode voltage clamp technique in Xenopus oocytes, and a whole-cell patch clamp technique in rat nodose ganglion neurons. In oocytes injected with 3 ng cRNA of 5-HT3A receptor, THC reversibly inhibited currents evoked with 5-HT (1 mu M) in a concentration-dependent manner (IC50=1.2 mu M). The extent of THC inhibition was inversely correlated with the amount of cRNA injected and the mean 5-HT3A receptor current densities. Pretreatment with actinomycin D, which inhibits transcription, decreased the mean 5-HT3 receptor current density and increased the extent of THC inhibition on 5-HT3 receptor-mediated currents. The IC50 values for THC increased from 285 nM to 1.2 mu M in oocytes injected with 1 and 3 ng of 5-HT3A cRNA, respectively. In radioligand binding studies on membrane preparations of oocytes expressing 5-HT3A receptors, THC did not alter the specific binding of a 5-HT3A receptor antagonist, [H-3]GR65630. In the presence of 1 mu M THC, the maximum 5-HT-induced response was also inhibited without a significant change in 5-HT potency, indicating that THC acts as a noncompetitive antagonist on 5-HT3 receptors. In adult rat nodose ganglion neurons, application of 1 mu M THC caused a significant inhibition of 5-HT3 receptors, extent of which correlated with the density of 5-HT-induced currents, indicating that the observed THC effects occur in mammalian neurons. The inhibition of 5-HT3 receptors by THC may contribute to its pharmacological actions in nociception and emesis. (C) 2010 Published by Elsevier Ltd on behalf of IBRO.
C1 [Oz, M.] NIDA, Integrat Neurosci Sect, DHHS, NIH,IRP, Baltimore, MD 21224 USA.
   [Yang, K. H. S.] Chapman Univ, Dept Biol Sci, Schmid Coll Sci, Orange, CA 92866 USA.
   [Isaev, D.; Petroianu, G.; Oz, M.] UAE Univ, Fac Med & Hlth Sci, Dept Pharmacol, Lab Funct Lipid, Al Ain, U Arab Emirates.
   [Morales, M.] NIDA, Cellular Neurophysiol Sect, DHHS, NIH,IRP, Baltimore, MD 21224 USA.
   [Galadari, S.] UAE Univ, Fac Med & Hlth Sci, Dept Biochem, Lab Cell Signaling, Al Ain, U Arab Emirates.
RP Oz, M (reprint author), NIDA, Integrat Neurosci Sect, DHHS, NIH,IRP, 333 Cassell Dr, Baltimore, MD 21224 USA.
EM moz@intra.nida.nih.gov
RI Oz, Murat/E-2148-2012
FU National Institutes of Health, National Institute on Drug Abuse;
   FMHS/UAEU
FX The authors wish to thank Dr. David Julius for providing
   5-HT<INF>3A</INF>-cDNA, and Dr. Mary Pfeiffer of NIDA/IRP for careful
   editing of the manuscript. This work was supported in part by the
   Intramural Research Program of the National Institutes of Health,
   National Institute on Drug Abuse, and by start-up grants from FMHS/UAEU.
   The experiments comply with the current laws of the U.S. and the authors
   have no financial interest in or financial conflict with the subject
   matter or materials discussed in the manuscript.
NR 49
TC 7
Z9 7
U1 0
U2 2
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0306-4522
J9 NEUROSCIENCE
JI Neuroscience
PD NOV 24
PY 2010
VL 171
IS 1
BP 40
EP 49
DI 10.1016/j.neuroscience.2010.08.044
PG 10
WC Neurosciences
SC Neurosciences & Neurology
GA 677UC
UT WOS:000284016300005
PM 20800662
ER

PT J
AU Rao, SV
   Kilaru, R
   Povsic, TJ
   Melloni, C
   Melton, L
   Kim, RJ
   Heitner, J
   Raman, S
   Barsness, G
   Ferrucci, L
   Lakatta, EG
   Harrington, RA
   Najjar, SS
AF Rao, Sunil V.
   Kilaru, Rakhi
   Povsic, Thomas J.
   Melloni, Chiara
   Melton, Laura
   Kim, Raymond J.
   Heitner, John
   Raman, Subha
   Barsness, Gregory
   Ferrucci, Luigi
   Lakatta, Edward G.
   Harrington, Robert A.
   Najjar, Samer S.
TI A Randomized Placebo Controlled Trial of Intravenous Erythropoietin to
   Reduce Infarct Size After ST-Segment Elevation Myocardial Infarction:
   Primary Results of the REVEAL Trial
SO CIRCULATION
LA English
DT Meeting Abstract
CT American-Heart-Association Scientific Sessions 2010 on Resuscitation
   Science Symposium
CY NOV 13-17, 2010
CL Chicago, IL
SP Amer Heart Assoc
C1 [Rao, Sunil V.; Kilaru, Rakhi; Povsic, Thomas J.; Melloni, Chiara; Melton, Laura; Harrington, Robert A.] Duke Clin Rsch Inst, Durham, NC USA.
   [Kim, Raymond J.] Duke Cardiovasc Magnet Resonance Cntr, Durham, NC USA.
   [Heitner, John] New York Methodist Hosp, New York, NY USA.
   [Raman, Subha] Ohio State Univ, Med Ctr, Columbus, OH 43210 USA.
   [Barsness, Gregory] Mayo Clin, Rochester, MN USA.
   [Ferrucci, Luigi; Lakatta, Edward G.] NIA, Baltimore, MD 21224 USA.
   [Najjar, Samer S.] Washington Hosp Ctr, Washington, DC 20010 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 23
PY 2010
VL 122
IS 21
BP 2222
EP 2222
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 683JJ
UT WOS:000284471800043
ER

PT J
AU Aufderheide, TP
   Nichol, G
   Rea, TD
   Everson-Stewart, S
   Leroux, B
   Kudenchuk, PJ
   Christenson, J
   Pepe, PE
   Daya, MR
   Dorian, P
   Callaway, CW
   Idris, AH
   Andrusiek, D
   Stephens, SW
   Hostler, D
   Davis, DP
   Dunford, JV
   Pirrallo, RG
   Stiell, IG
   Clement, CM
   Craig, A
   Van Ottingham, L
   Schmidt, TA
   Wang, H
   Weisfeldt, ML
   Ornato, JP
   Sopko, G
AF Aufderheide, Tom P.
   Nichol, Graham
   Rea, Thomas D.
   Everson-Stewart, Siobhan
   Leroux, Brian
   Kudenchuk, Peter J.
   Christenson, Jim
   Pepe, Paul E.
   Daya, Mohamud R.
   Dorian, Paul
   Callaway, Clifton W.
   Idris, Ahamed H.
   Andrusiek, Douglas
   Stephens, Shannon W.
   Hostler, David
   Davis, Daniel P.
   Dunford, James V.
   Pirrallo, Ronald G.
   Stiell, Ian G.
   Clement, Catherine M.
   Craig, Alan
   Van Ottingham, Lois
   Schmidt, Terri A.
   Wang, Henry
   Weisfeldt, Myron L.
   Ornato, Joseph P.
   Sopko, George
CA Resuscitation Outcomes Consortium
TI The Resuscitation Outcomes Consortium ROC) PRIMED Impedance Threshold
   Device (ITD) Cardiac Arrest Trial: A Prospective, Randomized,
   Double-Blind, Controlled Clinical Trial
SO CIRCULATION
LA English
DT Meeting Abstract
CT American-Heart-Association Scientific Sessions 2010 on Resuscitation
   Science Symposium
CY NOV 13-17, 2010
CL Chicago, IL
SP Amer Heart Assoc
C1 [Aufderheide, Tom P.; Pirrallo, Ronald G.] Med Coll Wisconsin, Milwaukee, WI 53226 USA.
   [Nichol, Graham; Rea, Thomas D.; Kudenchuk, Peter J.] Univ Washington, Harborview Cntr Prehosp Emergency Care, Seattle, WA 98195 USA.
   [Everson-Stewart, Siobhan; Leroux, Brian; Van Ottingham, Lois] Univ Washington, Clin Trial Ctr, Seattle, WA 98195 USA.
   [Christenson, Jim] Univ British Columbia, Vancouver, BC V5Z 1M9, Canada.
   [Pepe, Paul E.; Idris, Ahamed H.] UT SW Med Cntr, Dallas, TX USA.
   [Daya, Mohamud R.; Schmidt, Terri A.] Oregon Hlth & Sci Univ, Portland, OR USA.
   [Dorian, Paul] Univ Toronto, Toronto, ON, Canada.
   [Callaway, Clifton W.; Hostler, David] Univ Pittsburgh, Pittsburgh, PA USA.
   [Andrusiek, Douglas] British Columbia Emergency & Hlth Svcs Commiss, Vancouver, BC, Canada.
   [Stephens, Shannon W.; Wang, Henry] Univ Alabama, Birmingham, AL USA.
   [Davis, Daniel P.; Dunford, James V.] Univ Calif San Diego, San Diego, CA 92103 USA.
   [Clement, Catherine M.] Univ Ottawa, Ottawa, ON, Canada.
   [Weisfeldt, Myron L.] Johns Hopkins Sch Med, Baltimore, MD USA.
   [Ornato, Joseph P.] Virginia Commonwealth Univ, Richmond, VA USA.
   [Sopko, George] NHLBI, NIH, Rockville, MD USA.
RI Leroux, Brian/H-2254-2015
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 23
PY 2010
VL 122
IS 21
BP 2225
EP 2225
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 683JJ
UT WOS:000284471800051
ER

PT J
AU Stiell, IG
   Nichol, G
   Leroux, BG
   Rea, TD
   Ornato, JP
   Powell, J
   Christenson, J
   Callaway, CW
   Kudenchuk, PJ
   Aufderheide, TP
   Idris, AH
   Daya, M
   Wang, HE
   Morrison, L
   Davis, D
   Andrusiek, D
   Stephens, S
   Cheskes, S
   Schmicker, RH
   Fowler, R
   Vaillancourt, C
   Hostler, D
   Zive, D
   Pirallo, RG
   Vilke, G
   Sopko, G
   Weisfeldt, M
AF Stiell, Ian G.
   Nichol, Graham
   Leroux, Brian G.
   Rea, Thomas D.
   Ornato, Joseph P.
   Powell, Judy
   Christenson, James
   Callaway, Clifton W.
   Kudenchuk, Peter J.
   Aufderheide, Tom P.
   Idris, Ahamed H.
   Daya, Mohamud
   Wang, Henry E.
   Morrison, Laurie
   Davis, Daniel
   Andrusiek, Dug
   Stephens, Shannon
   Cheskes, Sheldon
   Schmicker, Robert H.
   Fowler, Ray
   Vaillancourt, Christian
   Hostler, David
   Zive, Dana
   Pirallo, Ronald G.
   Vilke, Gary
   Sopko, George
   Weisfeldt, Myron
CA Resuscitation Outcomes Consortium
TI Resuscitation Outcomes Consortium ROC PRIMED Trial of Early Rhythm
   Analysis versus Later Analysis in Out-of-Hospital Cardiac Arrest
SO CIRCULATION
LA English
DT Meeting Abstract
CT American-Heart-Association Scientific Sessions 2010 on Resuscitation
   Science Symposium
CY NOV 13-17, 2010
CL Chicago, IL
SP Amer Heart Assoc
C1 [Stiell, Ian G.; Vaillancourt, Christian] Univ Ottawa, Ottawa, ON, Canada.
   [Nichol, Graham; Rea, Thomas D.] Univ Washington, Harborview Ctr Prehosp Emergency Care, Seattle, WA 98195 USA.
   [Ornato, Joseph P.] Virginia Commonwealth Univ, Richmond, VA USA.
   [Christenson, James; Andrusiek, Dug] Univ British Columbia, Vancouver, BC V5Z 1M9, Canada.
   [Callaway, Clifton W.; Hostler, David] Univ Pittsburgh, Pittsburgh, PA USA.
   [Aufderheide, Tom P.; Pirallo, Ronald G.] Med Coll Wisconsin, Milwaukee, WI 53226 USA.
   [Idris, Ahamed H.; Fowler, Ray] Univ Texas SW Med Ctr Dallas, Dallas, TX 75390 USA.
   [Daya, Mohamud; Zive, Dana] Oregon Hlth & Sci Univ, Portland, OR 97201 USA.
   [Wang, Henry E.; Stephens, Shannon] Univ Alabama, Birmingham, AL USA.
   [Morrison, Laurie; Cheskes, Sheldon] Univ Toronto, Toronto, ON, Canada.
   [Davis, Daniel; Vilke, Gary] Univ Calif San Diego, San Diego, CA 92103 USA.
   [Sopko, George] NHLBI, NIH, Rockville, MD USA.
   [Weisfeldt, Myron] Johns Hopkins Med Insts, Baltimore, MD USA.
RI Leroux, Brian/H-2254-2015
NR 0
TC 1
Z9 1
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 23
PY 2010
VL 122
IS 21
BP 2226
EP 2226
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 683JJ
UT WOS:000284471800055
ER

PT J
AU Adalakha, S
   Greco, BA
   Dart, R
   Shepherd, AM
   Murphy, TP
   Jamerson, KA
   Dworkin, LD
   Henrich, WH
   Reid, D
   Cutlip, DE
   Cooper, CJ
   Tuttle, KR
AF Adalakha, Satjit
   Greco, Barbara A.
   Dart, Richard
   Shepherd, Alexander M.
   Murphy, Timothy P.
   Jamerson, Kenneth A.
   Dworkin, Lance D.
   Henrich, William H.
   Reid, Diane
   Cutlip, Donald E.
   Cooper, Christopher J.
   Tuttle, Katherine R.
TI Blood Pressure Control in Patients with Renal Artery Stenosis,
   Preliminary Results of the CORAL Clinical Trial
SO CIRCULATION
LA English
DT Meeting Abstract
DE Hypertension, renal; Renal circulation; Blood pressure; ACE inhibitor;
   Clinical trials
C1 Univ Toledo, Toledo, OH 43606 USA.
   Baystate Med Cntr, Springfield, MA USA.
   CORAL Study Grp, Toledo, OH USA.
   Univ Texas San Antonio, San Antonio, TX USA.
   Brown Univ, Rhode Isl Hosp, Providence, RI 02903 USA.
   Univ Michigan, Ann Arbor, MI 48109 USA.
   NHLBI, NIH, Bethesda, MD 20892 USA.
   Beth Israel Deaconess Med Cntr, Boston, MA USA.
   Sacred Heart Med Cntr, Spokane, WA USA.
NR 0
TC 1
Z9 1
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 23
PY 2010
VL 122
IS 21
SU S
MA A17234
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA V21UD
UT WOS:000208231602411
ER

PT J
AU Agarwal, S
   Houston, DK
   Tooze, JA
   Bauer, DC
   Cauley, JA
   Harris, TB
   Koster, A
   Womack, C
   Kritchevsky, SB
AF Agarwal, Subhashish
   Houston, Denise K.
   Tooze, Janet A.
   Bauer, Doug C.
   Cauley, Jane A.
   Harris, Tamara B.
   Koster, Annemarie
   Womack, Catherine
   Kritchevsky, Stephen B.
TI Association between 25-hydroxyvitamin D levels and Metabolic Syndrome in
   Older Adults
SO CIRCULATION
LA English
DT Meeting Abstract
DE Vitamins; Metabolic syndrome; Risk factors
C1 Wake Forest Univ, Winston Salem, NC 27109 USA.
   Univ Calif San Francisco, San Francisco, CA 94143 USA.
   Univ Pittsburgh, Pittsburgh, PA USA.
   NIA, Bethesda, MD 20892 USA.
   Univ Tennessee, Memphis, TN USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 23
PY 2010
VL 122
IS 21
SU S
MA A13226
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA V21UD
UT WOS:000208231601199
ER

PT J
AU Agarwal, S
   Rotter, J
   Vaidya, D
   Jorgensen, N
   Jacobs, D
   Sibley, C
   Chen, YDI
   Herrington, D
AF Agarwal, Subhashish
   Rotter, Jerome
   Vaidya, Dhananjay
   Jorgensen, Neal
   Jacobs, David
   Sibley, Christopher
   Chen, Yii-Der Ida
   Herrington, David
TI Metabolic Syndrome and Principal Component Analysis: Multi-Ethnic Study
   of Atherosclerosis (MESA)
SO CIRCULATION
LA English
DT Meeting Abstract
DE Metabolic syndrome; Epidemiologic methods; Risk factors; Cardiovascular
   disease; Cardiovascular disease prevention
C1 Wake Forest Univ, Winston Salem, NC 27109 USA.
   Cedars Sinai Med Cntr, Los Angeles, CA USA.
   Johns Hopkins Univ, Baltimore, MD USA.
   Univ Washington, Seattle, WA 98195 USA.
   Univ Minnesota, Minneapolis, MN USA.
   NIH, Bethesda, MD 20892 USA.
RI Sibley, Christopher/C-9900-2013
NR 0
TC 0
Z9 0
U1 0
U2 3
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 23
PY 2010
VL 122
IS 21
SU S
MA A9113
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA V21UD
UT WOS:000208231600364
ER

PT J
AU Agarwal, S
   Thohan, V
   Shlipak, MG
   Lima, JA
   Bluemke, DA
   Siscovick, D
   Gomes, AS
   Herrington, DM
AF Agarwal, Subhashish
   Thohan, Vinay
   Shlipak, Michael G.
   Lima, Joao A.
   Bluemke, David A.
   Siscovick, David
   Gomes, Antoinette S.
   Herrington, David M.
TI Association between Cystatin C and Left Ventricular Structure and
   Function in the Multi Ethnic Study of Atherosclerosis
SO CIRCULATION
LA English
DT Meeting Abstract
DE Ventricular remodeling; Biomarkers; Diastolic function; Renal function;
   Hypertrophy
C1 Wake Forest Univ, Winston Salem, NC 27109 USA.
   Univ Calif San Francisco, San Francisco, CA 94143 USA.
   Johns Hopkins Univ, Baltimore, MD USA.
   NIH, Bethesda, MD 20892 USA.
   Univ Washington, Seattle, WA 98195 USA.
   Univ Calif Los Angeles, Sch Med, Los Angeles, CA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 23
PY 2010
VL 122
IS 21
SU S
MA A8784
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA V21UD
UT WOS:000208231600313
ER

PT J
AU Almeida, AL
   Teixido-Tura, G
   Choi, EY
   Opdahl, A
   Fernandes, VR
   Wu, CO
   Bluemke, DA
   Lima, JA
AF Almeida, Andre L.
   Teixido-Tura, Gisela
   Choi, Eui-Young
   Opdahl, Anders
   Fernandes, Veronica R.
   Wu, Colin O.
   Bluemke, David A.
   Lima, Joao A.
TI Metabolic Syndrome is Associated with Reduced Myocardial Function
   Assessed by Speckle Tracking Echocardiography: The Multi-Ethnic Study of
   Atherosclerosis
SO CIRCULATION
LA English
DT Meeting Abstract
DE Echocardiography; Metabolic syndrome; Cardiovascular disease; Risk
   factors
C1 Johns Hopkins Univ, Baltimore, MD USA.
   NHLBI, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 23
PY 2010
VL 122
IS 21
SU S
MA A9258
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA V21UD
UT WOS:000208231600376
ER

PT J
AU Bittner, V
   Bartolet, M
   Barraza, R
   Farkouh, ME
   Goldberg, S
   Ramanathan, KB
   Redmon, JB
   Sperling, L
   Rutter, MK
AF Bittner, Vera
   Bartolet, Marnie
   Barraza, Rafael
   Farkouh, Michael E.
   Goldberg, Suzanne
   Ramanathan, Kodangudi B.
   Redmon, James B.
   Sperling, Laurence
   Rutter, Martin K.
TI Risk Factor Control in the Bypass Angioplasty Revascularization
   Investigation 2 Diabetes (BARI 2D) Trial
SO CIRCULATION
LA English
DT Meeting Abstract
DE Risk factors; Smoking; Lipids; Blood pressure
C1 Univ Alabama, Birmingham, AL USA.
   Univ Pittsburgh, Pittsburgh, PA USA.
   Mexican Inst Social Secur, Mexico City, DF, Mexico.
   Mt Sinai Sch Med, New York, NY USA.
   NIH, Bethesda, MD 20892 USA.
   VA Med Cntr Memphis, Memphis, TN USA.
   Univ Minnesota, Minneapolis, MN USA.
   Emory Univ, Atlanta, GA 30322 USA.
   Univ Manchester, Manchester, Lancs, England.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 23
PY 2010
VL 122
IS 21
SU S
MA A12663
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA V21UD
UT WOS:000208231601015
ER

PT J
AU Chen, MY
   Bandettini, WP
   Shanbhag, SM
   Vasu, S
   Booker, OJ
   Lederman, RJ
   Arai, AE
AF Chen, Marcus Y.
   Bandettini, W. P.
   Shanbhag, Sujata M.
   Vasu, Sujethra
   Booker, Oscar J.
   Lederman, Robert J.
   Arai, Andrew E.
TI Vasodilator Stress Cardiac MRI: How Does it Compare with 320-slice
   Coronary CTA?
SO CIRCULATION
LA English
DT Meeting Abstract
DE Cardiac MRI; Cardiac CT; Cardiac imaging; Coronary artery disease;
   Cardiovascular imaging
C1 [Chen, Marcus Y.; Bandettini, W. P.; Shanbhag, Sujata M.; Vasu, Sujethra; Booker, Oscar J.; Lederman, Robert J.; Arai, Andrew E.] NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 23
PY 2010
VL 122
IS 21
SU S
MA A18866
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA V21UD
UT WOS:000208231602962
ER

PT J
AU Chrispin, J
   Jain, A
   Soliman, EZ
   Alonso, A
   Heckbert, SR
   Blumeke, D
   Lima, J
   Nazarian, S
AF Chrispin, Jonathan
   Jain, Aditya
   Soliman, Elsayed Z.
   Alonso, Alvaro
   Heckbert, Susan R.
   Blumeke, David
   Lima, Joao
   Nazarian, Saman
TI Association of Electrocardiographic and Imaging Surrogates of Left
   Ventricular Hypertrophy with Incident Atrial Fibrillation: The
   Multi-Ethnic Study of Atherosclerosis
SO CIRCULATION
LA English
DT Meeting Abstract
DE Atrial fibrillation; Electrocardiography; Magnetic resonance imaging;
   Epidemiology
C1 Johns Hopkins Univ, Sch Med, Baltimore, MD USA.
   Wake Forest Univ, Bowman Gray Sch Med, Winston Salem, NC USA.
   Univ Minnesota, Minneapolis, MN USA.
   Univ Washington, Seattle, WA 98195 USA.
   NIH, Bethesda, MD 20892 USA.
NR 0
TC 1
Z9 1
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 23
PY 2010
VL 122
IS 21
SU S
MA A10989
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA V21UD
UT WOS:000208231600601
ER

PT J
AU Chuang, ML
   Gona, P
   Oyama, N
   Jaffer, FA
   Salton, CJ
   Blease, SJ
   Larson, MG
   Jhaveri, RR
   Lahiri, MK
   Levy, D
   O'Donnell, CJ
   Manning, WJ
AF Chuang, Michael L.
   Gona, Philimon
   Oyama, Noriko
   Jaffer, Farouc A.
   Salton, Carol J.
   Blease, Susan J.
   Larson, Martin G.
   Jhaveri, Rahul R.
   Lahiri, Marc K.
   Levy, Daniel
   O'Donnell, Christopher J.
   Manning, Warren J.
TI Longitudinal Change in Aortic Plaque Volume Using Cardiovascular
   Magnetic Resonance: Clinical Correlates
SO CIRCULATION
LA English
DT Meeting Abstract
DE Arteriosclerosis; Epidemiology; Magnetic resonance imaging; Risk factors
C1 Beth Israel Deaconess Med Cntr, Boston, MA USA.
   NHLBI, Cntr Populat Studies, Framingham, MA USA.
   Hokkaido Univ, Sapporo, Hokkaido, Japan.
   Massachusetts Gen Hosp, Boston, MA 02114 USA.
RI Oyama-Manabe, Noriko/A-5212-2012
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 23
PY 2010
VL 122
IS 21
SU S
MA A13199
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA V21UD
UT WOS:000208231601183
ER

PT J
AU Das, S
   Ferlito, M
   Wang, R
   Liu, DL
   Raghavachari, N
   Munson, P
   Murphy, E
   Steenbergen, C
AF Das, Samarjit
   Ferlito, Marcella
   Wang, Richard
   Liu, Delong
   Raghavachari, Nalini
   Munson, Peter
   Murphy, Elizabeth
   Steenbergen, Charles
TI Existence of microRNA in Heart-Derived Mitochondria
SO CIRCULATION
LA English
DT Meeting Abstract
DE Microrna; Mitochondria; Mitochondrial energetics, heart failure,
   arrhythmias; Apoptosis; Cardiovascular disease prevention
C1 Johns Hopkins Univ, Baltimore, MD USA.
   NHLBI, NIH, Bethesda, MD 20892 USA.
   NIH, Cntr Informat Technol, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 23
PY 2010
VL 122
IS 21
SU S
MA A20624
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA V21UD
UT WOS:000208231603557
ER

PT J
AU Elam, MB
   Lovato, LC
   Byington, RP
   Bonds, D
   Leiter, L
   Crouse, JR
   Linz, P
   Marcovina, S
   O'Connor, PJ
   Ginsberg, HN
AF Elam, Marshall B.
   Lovato, Laura C.
   Byington, Robert P.
   Bonds, Denise
   Leiter, Lawrence
   Crouse, John R.
   Linz, Peter
   Marcovina, Santica
   O'Connor, Patrick J.
   Ginsberg, Henry N.
CA ACCORD Study Grp
TI Hypertriglyceridemia and Low HDL-C Predicts Fenofibrate Response in The
   ACCORD-Lipid Trial
SO CIRCULATION
LA English
DT Meeting Abstract
DE Type 2 Diabetes; Cholesterol lowering drugs; Cardiovascular
C1 Memphis Vet Affairs Med Cntr, Memphis, TN USA.
   Wake Forest Univ, Sch Med, Winston Salem, NC 27109 USA.
   NHLBI, Bethesda, MD 20892 USA.
   St Michaels Hlth Cntr, Toronto, ON, Canada.
   USN, Med Cntr, Div Cardiol, San Diego, CA 92152 USA.
   Univ Washington, Seattle, WA 98195 USA.
   Hlth Partners Rsch Fdn, Minneapolis, MN USA.
   Columbia Univ, Coll Phys & Surg, New York, NY USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 23
PY 2010
VL 122
IS 21
SU S
MA A19724
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA V21UD
UT WOS:000208231603243
ER

PT J
AU Fontes, JD
   Lyass, A
   Massaro, JM
   Schnabel, RB
   Wang, TJ
   Vasan, RS
   Lubitz, SA
   Magnani, JW
   Ellinor, PT
   Fox, CS
   Benjamin, EJ
AF Fontes, Joao D.
   Lyass, Asya
   Massaro, Joseph M.
   Schnabel, Renate B.
   Wang, Thomas J.
   Vasan, Ramachandran S.
   Lubitz, Steven A.
   Magnani, Jared W.
   Ellinor, Patrick T.
   Fox, Caroline S.
   Benjamin, Emelia J.
TI Insulin Resistance Does Not Increase Risk Of Incident Atrial
   Fibrillation: The Framingham Heart Study
SO CIRCULATION
LA English
DT Meeting Abstract
DE Atrial fibrillation; Insulin resistance; Epidemiology; Risk factors
C1 Boston Univ, Framingham, MA USA.
   Boston Univ, Boston, MA 02215 USA.
   Johannes Gutenberg Univ Mainz, Mainz, Germany.
   Massachusetts Gen Hosp, Charlestown, MA USA.
   Massachusetts Gen Hosp, Boston, MA 02114 USA.
   NHLBI, Framingham, MA USA.
NR 0
TC 0
Z9 0
U1 0
U2 2
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 23
PY 2010
VL 122
IS 21
SU S
MA A18418
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA V21UD
UT WOS:000208231602828
ER

PT J
AU Garg, PK
   Liu, K
   Ferrucci, L
   Guralnik, JM
   Criqui, MH
   Tian, L
   Nishida, T
   Tao, HM
   McDermott, MM
AF Garg, Parveen K.
   Liu, Kiang
   Ferrucci, Luigi
   Guralnik, Jack M.
   Criqui, Michael H.
   Tian, Lu
   Nishida, Takashi
   Tao, Huimin
   McDermott, Mary M.
TI Impaired Peroneal Nerve Function is Associated With Adverse Calf Muscle
   Characteristics and Functional Impairment in Peripheral Arterial Disease
SO CIRCULATION
LA English
DT Meeting Abstract
DE Peripheral arterial disease
C1 Northwestern Univ, Chicago, IL 60611 USA.
   NIA, Baltimore, MD 21224 USA.
   Univ Calif San Diego, La Jolla, CA 92093 USA.
   Stanford Univ, Palo Alto, CA 94304 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 23
PY 2010
VL 122
IS 21
SU S
MA A9444
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA V21UD
UT WOS:000208231600406
ER

PT J
AU George, RT
   Arbab-Zadeh, A
   Cerci, RJ
   Vavere, AL
   Kitagawa, K
   Dewey, M
   Rochitte, CE
   Arai, A
   Paul, N
   Rybicki, FJ
   Lardo, AC
   Lima, JA
AF George, Richard T.
   Arbab-Zadeh, Armin
   Cerci, Rodrigo J.
   Vavere, Andrea L.
   Kitagawa, Kakuya
   Dewey, Marc
   Rochitte, Carlos E.
   Arai, Andrew
   Paul, Narinder
   Rybicki, Frank J.
   Lardo, Albert C.
   Lima, Joao A.
TI Combined Non-invasive Coronary Angiography and Myocardial Perfusion
   Imaging Using 320 Row Detector Computed Tomography: CT Perfusion
   Acquisition, Reconstruction, and Analysis Methods of the CORE-320
   Multi-center Cohort Study
SO CIRCULATION
LA English
DT Meeting Abstract
DE Myocardial perfusion; Ischemic heart disease; Computed tomography;
   Noninvasive cardiac imaging; Angiography
C1 Johns Hopkins Univ, Baltimore, MD USA.
   Mie Univ, Tsu, Mie 514, Japan.
   Charite, Berlin, Germany.
   InCor, Sao Paulo, Brazil.
   NIH, Bethesda, MD 20892 USA.
   Univ Toronto, Toronto, ON, Canada.
   Brigham & Womens Hosp, Boston, MA 02115 USA.
NR 0
TC 0
Z9 0
U1 0
U2 2
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 23
PY 2010
VL 122
IS 21
SU S
MA A19969
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA V21UD
UT WOS:000208231603342
ER

PT J
AU Goto, K
   Iso, T
   Hanaoka, H
   Suga, T
   Matsui, H
   Arai, M
   Endo, K
   Gonzalez, FJ
   Kurabayashi, M
AF Goto, Kosaku
   Iso, Tatsuya
   Hanaoka, Hirofumi
   Suga, Toshihiro
   Matsui, Hiroki
   Arai, Masashi
   Endo, Keigo
   Gonzalez, Frank J.
   Kurabayashi, Masahiko
TI Peroxisome Proliferator Activated Receptor-Gamma Regulates
   Trans-endothelial Fatty Acid Transport via Induction of Fatty Acid
   Binding Protein 4 and Fatty Acid Translocase in Capillary Endothelial
   Cells in Heart and Adipose Tissue
SO CIRCULATION
LA English
DT Meeting Abstract
DE Endothelium; Ppar; Energy metabolism; Gene expression; Metabolism
C1 Gunma Univ, Grad Sch Med, Maebashi, Gumma 371, Japan.
   Gunma Univ, Sch Hlth Sci, Maebashi, Gumma 371, Japan.
   NCI, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 23
PY 2010
VL 122
IS 21
SU S
MA A15250
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA V21UD
UT WOS:000208231601802
ER

PT J
AU Hankinson, A
   Daviglus, ML
   Loria, C
   Lewis, CE
   Liu, K
AF Hankinson, Arlene
   Daviglus, Martha L.
   Loria, Catherine
   Lewis, Cora E.
   Liu, Kiang
TI Longer Duration of Overweight/Obesity Associated with Higher Odds of
   Developing Hypertension or Dyslipidemia: The Coronary Artery Risk
   Development in Young Adults (CARDIA) Study
SO CIRCULATION
LA English
DT Meeting Abstract
DE Obesity; Hypertension; Lipids
C1 Northwestern Univ, Chicago, IL 60611 USA.
   NHLBI, Bethesda, MD 20892 USA.
   Univ Alabama, Birmingham, AL USA.
NR 0
TC 0
Z9 0
U1 0
U2 2
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 23
PY 2010
VL 122
IS 21
SU S
MA A16208
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA V21UD
UT WOS:000208231602105
ER

PT J
AU Hanna, EB
   Roe, MT
   Wiviott, SD
   Fox, CS
   Chen, AY
   Saucedo, JF
AF Hanna, Elias B.
   Roe, Matthew T.
   Wiviott, Stephen D.
   Fox, Caroline S.
   Chen, Anita Y.
   Saucedo, Jorge F.
TI Characteristics and In-hospital Outcomes of Patients With Non-ST-Segment
   Elevation Myocardial Infarction and Chronic Kidney Disease Undergoing
   Percutaneous Coronary Intervention
SO CIRCULATION
LA English
DT Meeting Abstract
DE Acute coronary syndromes; Kidney; Percutaneous coronary intervention
C1 Univ Oklahoma, Oklahoma City, OK USA.
   Duke Clin Rsch Inst, Durham, NC USA.
   Brigham & Womens Hosp, Boston, OK USA.
   NHLBI, Framingham Heart Study, Framingham, MA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 23
PY 2010
VL 122
IS 21
SU S
MA A14628
PG 3
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA V21UD
UT WOS:000208231601632
ER

PT J
AU Hochman, JS
   Reynolds, HR
   Dzavik, V
   Buller, CE
   Ruzyllo, W
   Sadowski, ZP
   Maggioni, AP
   Carvalho, AC
   Rankin, JM
   Goldberg, S
   Forman, SA
   Mark, DB
   Lamas, GA
AF Hochman, Judith S.
   Reynolds, Harmony R.
   Dzavik, Vladimir
   Buller, Christopher E.
   Ruzyllo, Witold
   Sadowski, Zygmunt P.
   Maggioni, Aldo P.
   Carvalho, Antonio C.
   Rankin, James M.
   Goldberg, Suzanne
   Forman, Sandra A.
   Mark, Daniel B.
   Lamas, Gervasio A.
CA OAT Invest
TI Persistent Lack of Benefit of Late Revascularization of the Occluded
   Coronary Artery Post-MI - The Occluded Artery Trial (OAT) Long Term
   Results
SO CIRCULATION
LA English
DT Meeting Abstract
DE Interventional cardiology; Percutaneous coronary intervention;
   Myocardial infarction; Clinical trials; Coronary artery disease
C1 NYU, Sch Med, New York, NY USA.
   Univ Hlth Network, Peter Munk Cardiac Cntr, Toronto, ON, Canada.
   Hamilton Gen Hosp, Hamilton, ON, Canada.
   Natl Inst Cardiol, Warsaw, Poland.
   Italian Assoc Hosp Cardiol ANMCO, Rsch Cntr, Florence, Italy.
   Hosp Sao Paulo, Sao Paulo, Brazil.
   Royal Perth Hosp, Perth, WA, Australia.
   NHLBI, NIH, Bethesda, MD 20892 USA.
   Clinical Trials & Surveys Corp, Owings Mills, MD USA.
   Duke Univ, Duke Clin Rsch Inst, Durham, NC USA.
   Mt Sinai Med Ctr, Miami Beach, FL 33140 USA.
NR 0
TC 1
Z9 1
U1 0
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 23
PY 2010
VL 122
IS 21
SU S
MA A13116
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA V21UD
UT WOS:000208231601152
ER

PT J
AU Huang, J
   Sabater-Ileal, M
   Baumert, J
   Shin, SY
   Yang, Q
   Ohrvik, J
   Johnson, AD
   Lohman, K
   Ding, JZ
   Strawbridge, RJ
   Koenig, W
   Soranzo, N
   Liu, YM
   O'Donnell, CJ
   Hamsten, A
AF Huang, Jie
   Sabater-Ileal, Maria
   Baumert, Jens
   Shin, So-Youn
   Yang, Qiong
   Ohrvik, John
   Johnson, Andrew D.
   Lohman, Kurt
   Ding, Jingzhong
   Strawbridge, Rona J.
   Koenig, Wolfgang
   Soranzo, Nicole
   Liu, Yongmei
   O'Donnell, Christopher J.
   Hamsten, Anders
TI Genome-Wide Meta-Analysis of Plasminogen Activator Inhibitor Type 1
   (PAI-1) Identifies a New Locus Independent of the Serpine1 4G/5G
   Polymorphism
SO CIRCULATION
LA English
DT Meeting Abstract
DE Blood coagulation; Thrombosis; Genomics
C1 NHLBI, Framingham Heart Study, Framingham, MA USA.
   Karolinska Inst, Stockholm, Sweden.
   Univ Ulm Med Cntr, Ulm, Germany.
   Wellcome Trust Sanger Inst, Cambridge, England.
   Boston Univ, Sch Publ Hlth, Boston, MA USA.
   Wake Forest Univ, Sch Med, Winston Salem, NC 27109 USA.
RI Johnson, Andrew/G-6520-2013; Yang, Qiong/G-5438-2014
NR 0
TC 0
Z9 0
U1 0
U2 6
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 23
PY 2010
VL 122
IS 21
SU S
MA A17360
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA V21UD
UT WOS:000208231602466
ER

PT J
AU Idris, AH
   Nichols, P
   Schroeder, D
   Everson-Stewart, S
   Powell, JL
   Callaway, CW
   Morrison, L
   Aufderheide, TP
   Rea, T
   Atkins, D
   Berg, R
   Bigham, B
   Davis, D
   Stiell, I
   Sopko, G
   Nichol, G
AF Idris, Ahamed H.
   Nichols, Patrick
   Schroeder, Danielle
   Everson-Stewart, Siobhan
   Powell, Judy L.
   Callaway, Clifton W.
   Morrison, Laurie
   Aufderheide, Tom P.
   Rea, Tom
   Atkins, Dianne
   Berg, Robert
   Bigham, Blair
   Davis, Dan
   Stiell, Ian
   Sopko, George
   Nichol, Graham
CA Resuscitation Outcomes Consortium
TI Chest Compression Rates Used During Out-of-Hospital Cardiopulmonary
   Resuscitation in Nine Resuscitation Outcomes Consortium Regional Sites
SO CIRCULATION
LA English
DT Meeting Abstract
DE Cardiac arrest; Cardiopulmonary resuscitation; Healthcare delivery
   systems
C1 UT SW Med Cntr, Dallas, TX USA.
   UT San Antonio Med Ctr, San Antonio, TX USA.
   Univ Washington, Seattle, WA 98195 USA.
   Univ Pittsburgh, Pittsburgh, PA USA.
   Univ Toronto, Toronto, ON, Canada.
   Med Coll Wisconsin, Milwaukee, WI 53226 USA.
   Univ Iowa, Iowa City, IA USA.
   Univ Penn, Philadelphia, PA 19104 USA.
   Univ Calif Davis, San Diego, CA USA.
   Univ Ottawa, Ottawa, ON, Canada.
   NIH, Bethesda, MD 20892 USA.
   Univ Washington Clin Trial Cntr, Seattle, WA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 23
PY 2010
VL 122
IS 21
SU S
MA A246
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA V21UD
UT WOS:000208231600233
ER

PT J
AU Jain, A
   Liu, K
   Ferrucci, L
   Criqui, MH
   Tian, L
   Guralnik, JM
   Tao, HM
   McDermott, MM
AF Jain, Atul
   Liu, Kiang
   Ferrucci, Luigi
   Criqui, Michael H.
   Tian, Lu
   Guralnik, Jack M.
   Tao, Huimin
   McDermott, Mary M.
TI The Walking Impairment Questionnaire Stair-Climbing Score Predicts
   Mortality in Patients With Peripheral Arterial Disease
SO CIRCULATION
LA English
DT Meeting Abstract
DE Peripheral arterial disease; Cardiovascular disease; Vascular disease;
   Longitudinal studies; Peripheral vasculature
C1 Northwestern Univ, Feinberg Sch Med, Chicago, IL 60611 USA.
   NIA, NIH, Baltimore, MD 21224 USA.
   Univ Calif San Diego, Sch Med, La Jolla, CA 92093 USA.
   Stanford Univ, Stanford, CA 94305 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 23
PY 2010
VL 122
IS 21
SU S
MA A17256
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA V21UD
UT WOS:000208231602418
ER

PT J
AU Kim, JH
   Park, JH
   Choo, K
   Song, SK
   Kim, JS
   Park, YH
   Kim, J
   Chun, KJ
   Lederman, RJ
AF Kim, June-Hong
   Park, Ju-Hyun
   Choo, Kiseok
   Song, Sung-Kook
   Kim, Jung-Su
   Park, Yong-Hyun
   Kim, Jun
   Chun, Kook-Jin
   Lederman, Robert J.
TI Pressure-Wire Based Assessment of Microvascular Resistance Using
   Calibrated Upstream Balloon Obstruction Predicts Myocardial Viability
   After PCI for Acute Coronary Syndrome
SO CIRCULATION
LA English
DT Meeting Abstract
DE Acute coronary syndromes; Vascular resistance; Myocardial infarction;
   Clinical trials; Cardiac MRI
C1 Pusan Natl Univ, Yangsan Hosp, Yangsan, South Korea.
   NHLBI, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 23
PY 2010
VL 122
IS 21
SU S
MA A14026
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA V21UD
UT WOS:000208231601436
ER

PT J
AU Koh, KK
   Quon, M
   Han, S
   Park, Y
   Shin, E
   Shin, K
   Chung, WJ
AF Koh, Kwang K.
   Quon, Michael
   Han, Seung
   Park, Yae
   Shin, Eak
   Shin, Kwen
   Chung, Wook-Jin
TI Significant Differential Metabolic Effects of Rosuvastatin and
   Pravastatin in Hypercholesterolemic Patients
SO CIRCULATION
LA English
DT Meeting Abstract
DE Insulin resistance; Statins
C1 Gachon Univ, Gil Hosp, Inchon, South Korea.
   NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 23
PY 2010
VL 122
IS 21
SU S
MA A15351
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA V21UD
UT WOS:000208231601824
ER

PT J
AU Kohr, MJ
   Sun, JH
   Aponte, A
   Gucek, M
   Murphy, E
   Steenbergen, C
AF Kohr, Mark J.
   Sun, Junhui
   Aponte, Angel
   Gucek, Marjan
   Murphy, Elizabeth
   Steenbergen, Charles
TI Identification of the Myocardial S-nitrosothiol Proteome
SO CIRCULATION
LA English
DT Meeting Abstract
DE Cardioprotection; Ischemia reperfusion; Nitric oxide
C1 Johns Hopkins Med Inst, Baltimore, MD 21205 USA.
   NHLBI, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 2
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 23
PY 2010
VL 122
IS 21
SU S
MA A18132
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA V21UD
UT WOS:000208231602726
ER

PT J
AU Kohr, MJ
   Sun, JH
   Aponte, A
   Gucek, M
   Murphy, E
   Steenbergen, C
AF Kohr, Mark J.
   Sun, Junhui
   Aponte, Angel
   Gucek, Marjan
   Murphy, Elizabeth
   Steenbergen, Charles
TI Critical Cysteine Oxidation is Reduced During Ischemia-Reperfusion
   Injury via S-nitrosothiol Formation
SO CIRCULATION
LA English
DT Meeting Abstract
DE Cardioprotection; Ischemia reperfusion; Nitric oxide; Oxidative stress
C1 Johns Hopkins Med Inst, Baltimore, MD 21205 USA.
   NHLBI, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 23
PY 2010
VL 122
IS 21
SU S
MA A18108
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA V21UD
UT WOS:000208231602715
ER

PT J
AU Lipshultz, SE
   Leister, E
   Shearer, WT
   Rich, K
   Van Dyke, R
   Colan, SD
   Siberry, G
   Jacobson, D
   Kaltman, J
   Dooley, L
   Seage, G
   Specter, S
   Wilkinson, JD
   Williams, P
AF Lipshultz, Steven E.
   Leister, Erin
   Shearer, William T.
   Rich, Kenneth
   Van Dyke, Russell
   Colan, Steven D.
   Siberry, George
   Jacobson, Denise
   Kaltman, Jonathan
   Dooley, Laurie
   Seage, George
   Specter, Stephen
   Wilkinson, James D.
   Williams, Paige
TI Association of Cardiac Structure and Function with In Utero
   Antiretroviral Exposure Among Uninfected Children Born to HIV-Infected
   Mothers in the Pediatric HIV/AIDS Cohort Study
SO CIRCULATION
LA English
DT Meeting Abstract
DE Acquired immunodeficiency syndrome; Pediatric cardiology;
   Echocardiography
C1 Univ Miami, Miami, FL USA.
   Harvard Univ, Sch Publ Hlth, Boston, MA 02115 USA.
   Baylor Coll Med, Houston, TX 77030 USA.
   Texas Childrens Hosp, Houston, TX 77030 USA.
   Univ Illinois, Chicago, IL USA.
   Tulane Univ, New Orleans, LA 70118 USA.
   Childrens Hosp, Boston, MA 02115 USA.
   NICHHD, Bethesda, MD 20892 USA.
   NHLBI, Bethesda, MD 20892 USA.
   Frontier Sci Technol & Rsch Fdn, Amherst, NY USA.
   Univ Calif San Diego, San Diego, CA 92103 USA.
NR 0
TC 1
Z9 1
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 23
PY 2010
VL 122
IS 21
SU S
MA A16026
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA V21UD
UT WOS:000208231602039
ER

PT J
AU Liu, K
   Daviglus, M
   Colangelo, L
   Loria, C
   Lloyd-Jones, D
AF Liu, Kiang
   Daviglus, Martha
   Colangelo, Laura
   Loria, Catherine
   Lloyd-Jones, Donald
TI Maintaining Low Cardiovascular Disease (CVD) Risk Profile from Young
   Adulthood to Middle Age by Healthy Lifestyle: The CARDIA Study
SO CIRCULATION
LA English
DT Meeting Abstract
DE Cardiovascular disease prevention; Risk factors
C1 Northwestern Univ, Sch Med, Chicago, IL USA.
   NHLBI, NIH, Bethesda, MD 20892 USA.
RI Lloyd-Jones, Donald/C-5899-2009
NR 0
TC 0
Z9 0
U1 0
U2 2
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 23
PY 2010
VL 122
IS 21
SU S
MA A12250
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA V21UD
UT WOS:000208231600787
ER

PT J
AU Lovato, LC
   Elam, MB
   Byington, RP
   Sweeney, ME
   Sperl-Hillen, JM
   Fleg, J
   Weiss, D
   Lorber, DL
   Ginsberg, HN
AF Lovato, Laura C.
   Elam, Marshall B., III
   Byington, Robert P.
   Sweeney, Mary E., III
   Sperl-Hillen, Joann M.
   Fleg, Jerome
   Weiss, Daniel
   Lorber, Daniel L.
   Ginsberg, Henry N.
CA ACCORD Study Grp
TI Effect of Fenofibrate Therapy on Cardiovascular Disease in Men versus
   Women with Type 2 Diabetes in the ACCORD-Lipid Trial
SO CIRCULATION
LA English
DT Meeting Abstract
DE Type 2 Diabetes; Cardiovascular disease prevention; Hyperlipidemia;
   Fenofibrate; Cholesterol-lowering drugs
C1 Wake Forest Univ, Bowman Gray Sch Med, Winston Salem, NC USA.
   Vet Affairs Med Cntr Memphis, Memphis, TN USA.
   Vet Affairs Med Cntr Atlanta, Decatur, GA USA.
   Hlth Partners Rsch Fdn, Minneapolis, MN USA.
   NHLBI, Bethesda, MD 20892 USA.
   Your Diabet Endocrine Nutr Grp LLC, Mentor, OH USA.
   Cornell Univ, Weill Med Coll, Flushing, NY USA.
   Columbia Univ Coll Phys & Surg, New York, NY 10032 USA.
NR 0
TC 1
Z9 1
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 23
PY 2010
VL 122
IS 21
SU S
MA A20114
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA V21UD
UT WOS:000208231603395
ER

PT J
AU Michos, ED
   Reis, JP
   Post, WS
   Lutsey, PL
   Gottesman, RF
   Mosley, TH
   Sharrett, AR
   Melamed, ML
AF Michos, Erin D.
   Reis, Jared P.
   Post, Wendy S.
   Lutsey, Pamela L.
   Gottesman, Rebecca F.
   Mosley, Thomas H.
   Sharrett, Albert R.
   Melamed, Michal L.
TI Vitamin D Deficiency is Associated with Increased Risk of Fatal Stroke
   Among Whites but not Blacks: the NHANES-III Linked Mortality Files
SO CIRCULATION
LA English
DT Meeting Abstract
DE Stroke; Vitamins; Epidemiology; Biomarkers
C1 Johns Hopkins Univ, Sch Med, Baltimore, MD USA.
   NHLBI, Bethesda, MD 20892 USA.
   Univ Minnesota, Minneapolis, MN USA.
   Univ Mississippi, Jackson, MS 39216 USA.
   Johns Hopkins Univ, Bloomberg Sch Publ Hlth, Baltimore, MD USA.
   Albert Einstein Coll Med, Bronx, NY 10467 USA.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 23
PY 2010
VL 122
IS 21
SU S
MA A9478
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA V21UD
UT WOS:000208231600414
ER

PT J
AU Nasir, K
   Budoff, MJ
   Post, WS
   Shaw, LJ
   Malik, S
   Polak, JF
   Hoffmann, U
   Bluemke, DA
   Sheuner, MT
   Wong, ND
   Kronmal, R
   Blumenthal, RS
AF Nasir, Khurram
   Budoff, Matthew J.
   Post, Wendy S.
   Shaw, Leslee J.
   Malik, Shaista
   Polak, Joseph F.
   Hoffmann, Udo
   Bluemke, David A.
   Sheuner, Maren T.
   Wong, Nathan D.
   Kronmal, Richard
   Blumenthal, Roger S.
TI Value of Coronary Artery Calcium and Carotid IMT in Predicting
   Cardiovascular Disease Events among Individuals with Family History of
   Heart Disease: The Multi-Ethnic Study of Atherosclerosis.
SO CIRCULATION
LA English
DT Meeting Abstract
DE Genetics; Prevention; Cardiac CT; Carotid arteries
C1 Johns Hopkins Univ, Ciccarone Cntr Prevent, Baltimore, MD 21218 USA.
   Harbor UCLA Med Canter, Torrance, CA USA.
   Los Angeles Biomed Rsch Inst, Torrance, CA USA.
   Emory Univ, Atlanta, GA 30322 USA.
   Univ Calif Irvine, Irvine, CA 92717 USA.
   Tufts Univ, Sch Med, Medford, MA 02155 USA.
   Massachusetts Gen Hosp, Boston, MA 02114 USA.
   Natl Inst Biomed Imaging & Bioengn, Bethesda, MD USA.
   Univ Calif Los Angeles, Cntr Hlth Policy Rsch, Los Angeles, CA USA.
   Univ Washington, Seattle, WA 98195 USA.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 23
PY 2010
VL 122
IS 21
SU S
MA A18549
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA V21UD
UT WOS:000208231602874
ER

PT J
AU Opdahl, A
   Fernandes, VR
   Wu, CO
   Nasir, K
   Choi, EY
   Almeida, AL
   Rosen, B
   Edvardsen, T
   Carvalho, BS
   Bluemke, DA
   Lima, JA
AF Opdahl, Anders
   Fernandes, Veronica R.
   Wu, Colin O.
   Nasir, Khurram
   Choi, Eui-Young
   Almeida, Andre L.
   Rosen, Boaz
   Edvardsen, Thor
   Carvalho, Benilton S.
   Bluemke, David A.
   Lima, Joao A.
TI Resting Heart Rate as Predictor for Development of Heart Failure and
   Left Ventricular Dysfunction: The Multi-Ethnic Study of Atherosclerosis
SO CIRCULATION
LA English
DT Meeting Abstract
DE Cardiac MRI; Heart failure; Heart rate/Heart rate variability
C1 Johns Hopkins Univ, Baltimore, MD USA.
   Harvard Univ, Sch Med, Boston, MA USA.
   NHLBI, Bethesda, MD 20892 USA.
   Univ Utah, Sch Med, Salt Lake City, UT USA.
   Univ Cambridge, Cambridge, England.
   Natl Inst Biomed Imaging & Bioengn, Bethesda, MD USA.
   Univ Oslo, Rikshosp, Oslo Univ Hosp, N-0027 Oslo, Norway.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 23
PY 2010
VL 122
IS 21
SU S
MA A10255
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA V21UD
UT WOS:000208231600467
ER

PT J
AU Pandey, MK
   Bhattacharyya, F
   Belanger, AP
   Wang, SY
   DeGrado, TR
AF Pandey, Mukesh K.
   Bhattacharyya, Falguni
   Belanger, Anthony P.
   Wang, Shuyan
   DeGrado, Timothy R.
TI PET Imaging of Fatty Acid Oxidation and Glucose Uptake in Heart and
   Skeletal Muscle of Rats: Effects of CPT-1 Inhibition
SO CIRCULATION
LA English
DT Meeting Abstract
DE Cardiac metabolism; Cardiovascular imaging; Lipids
C1 Brigham & Womens Hosp, Boston, MA 02115 USA.
   NIH, Rockville, MD USA.
NR 0
TC 0
Z9 0
U1 1
U2 2
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 23
PY 2010
VL 122
IS 21
SU S
MA A12657
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA V21UD
UT WOS:000208231601012
ER

PT J
AU Park, K
   Egelund, E
   Wen, XR
   Cooper-DeHoff, RM
   Merz, CNB
   Handberg, EM
   Johnson, BD
   Sopko, G
   Johnson, J
   Pepine, CJ
AF Park, Ki
   Egelund, Eric
   Wen, Xuerong
   Cooper-DeHoff, Rhonda M.
   Merz, C. N. Bairey
   Handberg, Eileen M.
   Johnson, B. D.
   Sopko, George
   Johnson, Julie
   Pepine, Carl J.
TI Serotonin Transporter Gene Polymorphism in Women with Suspected
   Ischemia: A Report from the NHLBI-sponsored WISE
SO CIRCULATION
LA English
DT Meeting Abstract
DE Biomarkers; Risk factors; Ischemic heart disease
C1 Univ Florida, Gainesville, FL USA.
   Cedars Sinai Heart Inst, Los Angeles, CA USA.
   Univ Pittsburgh, Pittsburgh, PA USA.
   NHLBI, NIH, Bethesda, MD 20892 USA.
NR 0
TC 1
Z9 1
U1 0
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 23
PY 2010
VL 122
IS 21
SU S
MA A20055
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA V21UD
UT WOS:000208231603374
ER

PT J
AU Paynter, N
   Lewis, CE
   Goff, DC
   Loria, CM
   Kiefe, CI
   Lloyd-Jones, DM
AF Paynter, Nina
   Lewis, Cora E.
   Goff, David C.
   Loria, Catherine M.
   Kiefe, Catarina I.
   Lloyd-Jones, Donald M.
TI Cardiovascular Risk Factor Accumulation in Young Adults Over 20 Years of
   Follow-Up: the Coronary Artery Risk Development in Young Adults (CARDIA)
   study
SO CIRCULATION
LA English
DT Meeting Abstract
DE Cardiovascular disease prevention; Risk factors; Longitudinal studies
C1 Brigham & Womens Hosp, Boston, MA 02115 USA.
   Univ Alabama, Birmingham, AL USA.
   Wake Forest Univ, Winston Salem, NC 27109 USA.
   NIH, Bethesda, MD 20892 USA.
   Univ Massachusetts Med Cntr, Worcester, MA USA.
   Northwestern Univ, Chicago, IL 60611 USA.
RI Lloyd-Jones, Donald/C-5899-2009
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 23
PY 2010
VL 122
IS 21
SU S
MA A19558
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA V21UD
UT WOS:000208231603195
ER

PT J
AU Pelter, MM
   Cooper, L
   Moser, DK
   Nesbitt, TS
   Robinson, S
   Dracup, K
AF Pelter, Michele M.
   Cooper, Lawton
   Moser, Debra K.
   Nesbitt, Thomas S.
   Robinson, Susan
   Dracup, Kathleen
TI Are Current Medication Recommendations being Implemented in Rural Heart
   Failure Patients with Impaired Ejection Fraction?
SO CIRCULATION
LA English
DT Meeting Abstract
DE Heart failure; Pharmacology; Physician; Nursing; Quality assessment
C1 Univ Nevada, Reno, NV 89557 USA.
   NIH, Bethesda, MD 20892 USA.
   Univ Kentucky, Lexington, KY USA.
   Univ Calif Davis, Sacramento, CA 95817 USA.
   Univ Calif San Francisco, San Francisco, CA 94143 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 23
PY 2010
VL 122
IS 21
SU S
MA A20676
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA V21UD
UT WOS:000208231603576
ER

PT J
AU Polonsky, TS
   McClelland, RL
   Jorgensen, NW
   Bild, DE
   Burke, GL
   Guerci, AD
   Greenland, P
AF Polonsky, Tamar S.
   McClelland, Robyn L.
   Jorgensen, Neal W.
   Bild, Diane E.
   Burke, Gregory L.
   Guerci, Alan D.
   Greenland, Philip
TI Coronary Artery Calcium Scores and Coronary Risk Coronary Artery Calcium
   Thresholds Are Not Consistent Across Baseline Risk Levels: The
   Multi-Ethnic Study of Atherosclerosis
SO CIRCULATION
LA English
DT Meeting Abstract
DE Subclinical atherosclerosis; Coronary artery disease; Risk factors;
   Prevention
C1 Northwestern Univ, Chicago, IL 60611 USA.
   Univ Washington, Seattle, WA 98195 USA.
   NHLBI, Bethesda, MD 20892 USA.
   Wake Forest Univ, Winston Salem, NC 27109 USA.
   St Francis Hosp, Roslyn, NY USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 23
PY 2010
VL 122
IS 21
SU S
MA A10435
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA V21UD
UT WOS:000208231600525
ER

PT J
AU Preis, SR
   Pencina, MJ
   D'Agostino, RB
   Savage, PJ
   Fox, CS
AF Preis, Sarah R.
   Pencina, Michael J.
   D'Agostino, Ralph B.
   Savage, Peter J.
   Fox, Caroline S.
TI Lifecourse Analysis Reveals Adverse Cardiovascular Disease Risk Factor
   Profiles up to 30 Years Prior to the Diagnosis of Diabetes
SO CIRCULATION
LA English
DT Meeting Abstract
DE Type 2 Diabetes; Risk factors
C1 Framinham Heart Study, Framingham, MA USA.
   Boston Univ, Boston, MA 02215 USA.
   NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 23
PY 2010
VL 122
IS 21
SU S
MA A17105
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA V21UD
UT WOS:000208231602369
ER

PT J
AU Sasaki, T
   Hansford, R
   Zviman, MM
   Berger, RD
   Calkins, H
   Bluemke, DA
   Halperin, HR
   Nazarian, S
AF Sasaki, Takeshi
   Hansford, Rozann
   Zviman, Menekhem M.
   Berger, Ronald D.
   Calkins, Hugh
   Bluemke, David A.
   Halperin, Henry R.
   Nazarian, Saman
TI Quantitative Assessment of Artifacts on Cardiac Magnetic Resonance
   Imaging of Patients with Pacemakers and Implantable Defibrillators
SO CIRCULATION
LA English
DT Meeting Abstract
DE Cardiac MRI; Device; Implantable cardioconvert defibrillator; Pacemakers
C1 Johns Hopkins Univ, Baltimore, MD USA.
   NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 23
PY 2010
VL 122
IS 21
SU S
MA A10366
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA V21UD
UT WOS:000208231600503
ER

PT J
AU Schnabel, RB
   Zeller, T
   Dupuis, J
   Baumert, J
   Wild, PS
   Perret, C
   Castagne, R
   Sinning, CR
   Lubos, E
   Munzel, TF
   Lackner, KJ
   Koenig, W
   Benjamin, EJ
   Tiret, L
   Blankenberg, S
AF Schnabel, Renate B.
   Zeller, Tanja
   Dupuis, Josee
   Baumert, Jens
   Wild, Philipp S.
   Perret, Claire
   Castagne, Raphaele
   Sinning, Christoph R.
   Lubos, Edith
   Munzel, Thomas F.
   Lackner, Karl J.
   Koenig, Wolfgang
   Benjamin, Emelia J.
   Tiret, Laurence
   Blankenberg, Stefan
TI Genetic Variation in the NLRC4 Inflammasome Locus in Relation to
   Interleukin-18 Concentrations and Cardiovascular Disease
SO CIRCULATION
LA English
DT Meeting Abstract
DE Risk factors; Inflammation; Cardiovascular disease prevention; Gene
   expression
C1 Dept Med 2, Mainz, Germany.
   NHLBI, Boston, MA USA.
   Boston Univ, Framingham Heart Study, Boston, MA 02215 USA.
   Helmholtz Zentrum Mnchen, Neuherberg, Germany.
   INSERM, U525, Paris, France.
   Dept Clin Chem & Lab Med, Mainz, Germany.
   Dept Med 2, Ulm, Germany.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 23
PY 2010
VL 122
IS 21
SU S
MA A13387
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA V21UD
UT WOS:000208231601248
ER

PT J
AU Sibley, CT
   Noureldin, RA
   Gai, N
   Nacif, MS
   Mudd, JO
   Halushka, MK
   Bluemke, DA
AF Sibley, Christopher T.
   Noureldin, Radwa A.
   Gai, Neville
   Nacif, Marcelo Souto
   Mudd, James O.
   Halushka, Marc K.
   Bluemke, David A.
TI Cardiac MRI T1 Mapping Noninvasively Predicts Interstitial Myocardial
   Fibrosis in the Absence of Late Gadolinium Enhancement
SO CIRCULATION
LA English
DT Meeting Abstract
DE Cardiac MRI; Cardiomyopathy; Fibrosis
C1 NIH, Bethesda, MD 20892 USA.
   Johns Hopkins Univ, Sch Med, Baltimore, MD USA.
RI Sibley, Christopher/C-9900-2013
NR 0
TC 0
Z9 0
U1 0
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 23
PY 2010
VL 122
IS 21
SU S
MA A19921
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA V21UD
UT WOS:000208231603322
ER

PT J
AU Sibley, CT
   Jain, A
   Schreiner, P
   O'Hare, AM
   Lima, JA
   Tsai, M
   Burke, G
   Michael, CH
AF Sibley, Christopher T.
   Jain, Aditya
   Schreiner, Pamela
   O'Hare, Ann M.
   Lima, Joao A.
   Tsai, Michael
   Burke, Gregory
   Michael, Criqui H.
TI Lipids, Lipoprotein Subclasses, and Ankle Brachial Index in the
   Multi-Ethnic Study of Atherosclerosis
SO CIRCULATION
LA English
DT Meeting Abstract
DE Lipoproteins; Peripheral arterial disease; Epidemiology; Risk factors
C1 NIH, Bethesda, MD 20892 USA.
   Johns Hopkins Univ, Sch Med, Baltimore, MD USA.
   Univ Minnesota, Minneapolis, MN USA.
   Univ Washington, Seattle, WA 98195 USA.
   Wake Forest Univ Hlth Sci, Winston Salem, NC USA.
   Univ Calif San Diego, La Jolla, CA 92093 USA.
RI Sibley, Christopher/C-9900-2013
NR 0
TC 0
Z9 0
U1 0
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 23
PY 2010
VL 122
IS 21
SU S
MA A17130
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA V21UD
UT WOS:000208231602375
ER

PT J
AU Simino, J
   Shi, G
   Jaquish, C
   Paltoo, D
   Weder, AB
   Curb, JD
   Boerwinkle, E
   Hunt, SC
   Rao, DC
AF Simino, Jeannette
   Shi, Gang
   Jaquish, Cashell
   Paltoo, Dina
   Weder, Alan B.
   Curb, J. D.
   Boerwinkle, Eric
   Hunt, Steven C.
   Rao, D. C.
CA Family Blood Pressure Program
TI Five Blood Pressure Loci Identified by an Updated Genome-wide Linkage
   Scan: Meta-analysis of the Family Blood Pressure Program
SO CIRCULATION
LA English
DT Meeting Abstract
DE Hypertension; Blood pressure; Genetics; Epidemiology
C1 Washington Univ, Sch Med, St Louis, MO USA.
   NHLBI, Bethesda, MD 20892 USA.
   Univ Michigan, Ann Arbor, MI 48109 USA.
   Univ Hawaii, Honolulu, HI 96822 USA.
   Univ Texas Hlth Sci Cntr, Houston, TX USA.
   Univ Utah, Salt Lake City, UT USA.
RI Shi, Gang/D-3301-2016
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 23
PY 2010
VL 122
IS 21
SU S
MA A20047
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA V21UD
UT WOS:000208231603372
ER

PT J
AU Sivendran, RT
   Anderson, SA
   Hsu, LY
   Yu, ZX
   Keeran, KJ
   Jeffries, KR
   Clevenger, RR
   Ugander, M
   Arai, AE
AF Sivendran, Rajiv T.
   Anderson, Stasia A.
   Hsu, Li-Yueh
   Yu, Zu Xi
   Keeran, Karen J.
   Jeffries, Kenneth R.
   Clevenger, Randall R.
   Ugander, Martin
   Arai, Andrew E.
TI Late Gadolinium Enhanced MRI Microscopy at Near Cellular Resolution
   Accurately Delineates Infarct Size in Acute MI and Detects Intermediate
   Enhancement in Regions with Histologic Evidence of Edema
SO CIRCULATION
LA English
DT Meeting Abstract
DE Myocardial infarction; Cardiac MRI; Infarct size
C1 [Sivendran, Rajiv T.; Anderson, Stasia A.; Hsu, Li-Yueh; Yu, Zu Xi; Keeran, Karen J.; Jeffries, Kenneth R.; Clevenger, Randall R.; Ugander, Martin; Arai, Andrew E.] NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 23
PY 2010
VL 122
IS 21
SU S
MA A20497
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA V21UD
UT WOS:000208231603516
ER

PT J
AU Stewart, AF
   Dandona, S
   Fan, M
   Almontashiri, N
   Chen, L
   Davies, RW
   Wells, GA
   Tang, W
   Hazen, SL
   Ellix, S
   Reilley, MP
   Epstein, S
   Rader, DJ
   Engert, JC
   Anand, S
   Kathiresan, S
   Cupples, AL
   O'Donnell, CJ
   Shah, S
   Kraus, WE
   Granger, CB
   McPherson, R
   Roberts, R
AF Stewart, Alexandre F.
   Dandona, Sonny
   Fan, Meng
   Almontashiri, Naif
   Chen, Li
   Davies, Robert W.
   Wells, George A.
   Tang, Wilson
   Hazen, Stanley L.
   Ellix, Stephen
   Reilley, Muredach P.
   Epstein, Stephen
   Rader, Daniel J.
   Engert, James C.
   Anand, Sonia
   Kathiresan, Sekar
   Cupples, Adrienne L.
   O'Donnell, Christopher J.
   Shah, Svati
   Kraus, William E.
   Granger, Christopher B.
   McPherson, Ruth
   Roberts, Robert
TI Identification of a Rare Variant Near Neurexin 1 Associated with
   Coronary Artery Disease
SO CIRCULATION
LA English
DT Meeting Abstract
DE Coronary heart disease; Genetics; Epidemiology
C1 Univ Ottawa, Inst Heart, Ottawa, ON, Canada.
   Cleveland Clin, Cleveland, OH 44106 USA.
   Univ Penn, Philadelphia, PA 19104 USA.
   Hosp Cntr, Washington, DC USA.
   McGill Univ, Montreal, PQ, Canada.
   McMaster Univ, Hamilton, ON, Canada.
   MIT, Cambridge, MA 02139 USA.
   Boston Univ, Sch Publ Hlth, Boston, MA USA.
   NHLBI, Framingham, MA USA.
   Duke Univ Med Cntr, Durham, NC USA.
RI Granger, Christopher/D-3458-2014
OI Granger, Christopher/0000-0002-0045-3291
NR 0
TC 0
Z9 0
U1 0
U2 3
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 23
PY 2010
VL 122
IS 21
SU S
MA A17262
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA V21UD
UT WOS:000208231602422
ER

PT J
AU Sun, JH
   Murphy, E
AF Sun, Junhui
   Murphy, Elizabeth
TI Loss of Ischemic Preconditioning-Induced Cardioprotection and Protein
   S-Nitrosylation in Mouse Hearts by Caveolae Disruption via
   Methyl-beta-Cyclodextrin Treatment
SO CIRCULATION
LA English
DT Meeting Abstract
DE Cardioprotection; Ischemia reperfusion; Nitric oxide; Signal
   transduction
C1 [Sun, Junhui; Murphy, Elizabeth] NHLBI, NIH, Bethesda, MD 20892 USA.
RI Sun, Junhui/C-3499-2011
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 23
PY 2010
VL 122
IS 21
SU S
MA A18174
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA V21UD
UT WOS:000208231602740
ER

PT J
AU Ugander, M
   Oki, AJ
   Hsu, LY
   Kellman, P
   Greiser, A
   Chen, MY
   Bandettini, WP
   Aletras, AH
   Arai, AE
AF Ugander, Martin
   Oki, Abiola J.
   Hsu, Li-Yueh
   Kellman, Peter
   Greiser, Andreas
   Chen, Marcus Y.
   Bandettini, W. P.
   Aletras, Anthony H.
   Arai, Andrew E.
TI Myocardial Extracellular Volume Imaging by MRI Quantitatively
   Characterizes Myocardial Infarction and Subclinical Myocardial Fibrosis
SO CIRCULATION
LA English
DT Meeting Abstract
DE Cardiac MRI; Aging; Myocardial infarction; Ejection fraction; Heart
   failure
C1 NIH, Bethesda, MD 20892 USA.
   Siemens AG, Erlangen, Germany.
NR 0
TC 0
Z9 0
U1 0
U2 4
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 23
PY 2010
VL 122
IS 21
SU S
MA A12126
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA V21UD
UT WOS:000208231600751
ER

PT J
AU Vaisman, B
   Ghias, M
   Demosky, SJ
   Stonik, JA
   Amar, MJ
   Sampson, M
   Remaley, AT
AF Vaisman, Boris
   Ghias, Mona
   Demosky, Stephen J.
   Stonik, John A.
   Amar, Marcelo J.
   Sampson, Maureen
   Remaley, Alan T.
TI Role of Endothelial Expression of ABCA1 and SR-BI Genes in HDL
   Metabolism, Cholesterol Trafficking and Protection Against
   Atherosclerosis.
SO CIRCULATION
LA English
DT Meeting Abstract
DE Endothelium; HDL; Arteriosclerosis; Transgenic models
C1 [Vaisman, Boris; Ghias, Mona; Demosky, Stephen J.; Stonik, John A.; Amar, Marcelo J.; Sampson, Maureen; Remaley, Alan T.] NHLBI, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 23
PY 2010
VL 122
IS 21
SU S
MA A18091
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA V21UD
UT WOS:000208231602708
ER

PT J
AU Wang, SN
   Zhou, YF
   Seavey, C
   Hoyt, RF
   Horvath, KA
AF Wang, Suna
   Zhou, Yifu
   Seavey, Caleb
   Hoyt, Robert F.
   Horvath, Keith A.
TI Heart-Type Fatty Acid Binding Protein and C-Reactive Protein are
   Significantly up-Regulated in Bone Marrow-Derived Mesenchymal Stem Cells
   Under Hypoxic Conditions
SO CIRCULATION
LA English
DT Meeting Abstract
DE Hypoxia; Stem cells; Biomarkers
C1 [Wang, Suna; Zhou, Yifu; Seavey, Caleb; Hoyt, Robert F.; Horvath, Keith A.] NHLBI, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 23
PY 2010
VL 122
IS 21
SU S
MA A183
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA V21UD
UT WOS:000208231600172
ER

PT J
AU Whellan, DJ
   Nigam, A
   Starr, AZ
   Hill, JA
   Fletcher, G
   Cooper, LS
   Onwuanyi, A
   Chandler, AB
   Keteyian, SJ
   Ewald, GA
   Kao, AD
   Gheorghiade, M
AF Whellan, David J.
   Nigam, Anil
   Starr, Aijing Z.
   Hill, James A.
   Fletcher, Gerald
   Cooper, Lawton S.
   Onwuanyi, Anekwe
   Chandler, Arthur B.
   Keteyian, Steven J.
   Ewald, Gregory A.
   Kao, Andrew
   Gheorghiade, Mihai
TI Benefit Of Exercise Training Independent Of Heart Failure Severity: The
   HF-action Experience
SO CIRCULATION
LA English
DT Meeting Abstract
DE Heart failure; Cardiac rehabilitation; Clinical trials
C1 Thomas Jefferson Univ, Jefferson Med Coll, Philadelphia, PA 19107 USA.
   Univ Montreal, Montreal, PQ, Canada.
   Duke Clin Rsch Inst, Durham, NC USA.
   Univ Florida, Coll Med, Gainesville, FL USA.
   Mayo Clin, Coll Med, Jacksonville, FL 32224 USA.
   NHLBI, Bethesda, MD 20892 USA.
   Morehouse Sch Med, Atlanta, GA 30310 USA.
   Univ Hosp, Augusta, GA USA.
   Henry Ford Hosp, Detroit, MI 48202 USA.
   St Lukes Hosp, Mid Amer Heart Inst, Kansas City, MO 64111 USA.
   Northwestern Univ, Feinberg Sch Med, Chicago, IL 60611 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 23
PY 2010
VL 122
IS 21
SU S
MA A13154
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA V21UD
UT WOS:000208231601170
ER

PT J
AU Williams, RV
   Zak, V
   Ravishankar, C
   Altmann, K
   Anderson, JB
   Atz, AM
   Dunbar-Masterson, C
   Ghanayem, NS
   Lambert, LM
   Lurito, KJ
   Medoff-Cooper, B
   Margossian, R
   Pemberton, VL
   Russell, J
   Stylianou, M
   Hsu, DT
AF Williams, Richard V.
   Zak, Victor
   Ravishankar, Chitra
   Altmann, Karen
   Anderson, Jeffrey B.
   Atz, Andrew M.
   Dunbar-Masterson, Carolyn
   Ghanayem, Nancy S.
   Lambert, Linda M.
   Lurito, Karen J.
   Medoff-Cooper, Barbara
   Margossian, Renee
   Pemberton, Victoria L.
   Russell, Jennifer
   Stylianou, Mario
   Hsu, Daphne T.
CA Pediat Heart Network Investigators
TI Factors Impacting Growth in Infants with Single Ventricle Physiology in
   the First Year of Life: The Pediatric Heart Network Infant Single
   Ventricle Trial
SO CIRCULATION
LA English
DT Meeting Abstract
DE Congenital heart disease; Nutrition; Pediatric cardiology
C1 Univ Utah, Salt Lake City, UT USA.
   New England Rsch Inst, Watertown, MA USA.
   Childrens Hosp Philadelphia, Philadelphia, PA 19104 USA.
   Columbia Univ, Coll Phys & Surg, New York, NY USA.
   Univ Cincinnati, Cincinnati, OH USA.
   Med Univ S Carolina, Charleston, SC 29425 USA.
   Childrens Hosp, Boston, MA 02115 USA.
   Med Coll Wisconsin, Milwaukee, WI 53226 USA.
   Primary Childrens Med Cntr, Salt Lake City, UT USA.
   E Carolina Univ, Brody Sch Med, Greenville, NC USA.
   NHLBI, Bethesda, MD 20892 USA.
   Hosp Sick Children, Toronto, ON M5G 1X8, Canada.
   Childrens Hosp Montefiore, Bronx, NY USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 23
PY 2010
VL 122
IS 21
SU S
MA A9298
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA V21UD
UT WOS:000208231600381
ER

PT J
AU Xia, JX
   Martinez, C
   Pfeifer, K
   Ebert, S
AF Xia, Jixiang
   Martinez, Celines
   Pfeifer, Karl
   Ebert, Steven
TI Generation of Novel Fluorescent Reporter Cells and Transgenic Mice for
   Identification and Characterization of Cardiomyocytes Derived From
   Adrenergic Progenitor Cells
SO CIRCULATION
LA English
DT Meeting Abstract
DE Biomarkers; Cardiac development; Catecholamines; Stem/progenitor cells;
   Cardiac imaging
C1 Univ Cent Florida, Orlando, FL 32816 USA.
   NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 2
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 23
PY 2010
VL 122
IS 21
SU S
MA A20439
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA V21UD
UT WOS:000208231603498
ER

PT J
AU Yu, Q
   Lambert, G
   Chatterjee, B
   Amar, M
   Cheng, C
   Alpert, D
   Remaley, A
   Pazour, G
   Lo, C
AF Yu, Qing
   Lambert, Gilles
   Chatterjee, Bishwanath
   Amar, Marcelo
   Cheng, Cui
   Alpert, Deanne
   Remaley, Alan
   Pazour, Gregory
   Lo, Cecilia
TI Hypercholesterolemia in a Pcsk5 Mouse Mutant Show P5 Proteolytic
   Degradation of P9 is Essential for Normal Regulation of Serum
   Cholesterol
SO CIRCULATION
LA English
DT Meeting Abstract
DE Lipids; Gene mutations
C1 NHLBI, Bethesda, MD 20892 USA.
   Heart Rsch Inst, Newtown, Tas, Australia.
   Univ Pittsburgh, Sch Med, Pittsburgh, PA USA.
   Univ Massachusetts, Sch Med, Worcester, MA USA.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 23
PY 2010
VL 122
IS 21
SU S
MA A19556
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA V21UD
UT WOS:000208231603194
ER

PT J
AU Zahanich, I
   Li, Y
   Lyashkov, AE
   Lukyanenko, YO
   Vinogradova, TM
   Younes, A
   Lakatta, EG
AF Zahanich, Ihor
   Li, Yue
   Lyashkov, Alexey E.
   Lukyanenko, Yevgeniya O.
   Vinogradova, Tatiana M.
   Younes, Antoine
   Lakatta, Edward G.
TI Protein Phosphatase 1 Regulates Normal Automaticity of the Heart's
   Pacemaker Node Cells by Site-specific Modulation of Phospholamban
   Phosphorylation that Regulates Spontaneous Subsarcolemmal Local Ca2+
   Releases
SO CIRCULATION
LA English
DT Meeting Abstract
DE Pacemakers; Calcium; Phosphatases; Phospholamban; Electrophysiology
C1 [Zahanich, Ihor; Li, Yue; Lyashkov, Alexey E.; Lukyanenko, Yevgeniya O.; Vinogradova, Tatiana M.; Younes, Antoine; Lakatta, Edward G.] NIA, NIH, Baltimore, MD 21224 USA.
NR 0
TC 3
Z9 3
U1 0
U2 3
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 23
PY 2010
VL 122
IS 21
SU S
MA A21546
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA V21UD
UT WOS:000208231603863
ER

PT J
AU Lauer, MS
AF Lauer, Michael S.
TI Misinterpretation of Prostate Cancer Data Reply
SO JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY
LA English
DT Letter
ID MORTALITY
C1 NHLBI, Div Cardiovasc Sci, Bethesda, MD 20892 USA.
RP Lauer, MS (reprint author), NHLBI, Div Cardiovasc Sci, 6701 Rockledge Dr,Room 8128, Bethesda, MD 20892 USA.
EM lauerm@nhlbi.nih.gov
RI Lauer, Michael/L-9656-2013
OI Lauer, Michael/0000-0002-9217-8177
NR 5
TC 0
Z9 0
U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0735-1097
J9 J AM COLL CARDIOL
JI J. Am. Coll. Cardiol.
PD NOV 23
PY 2010
VL 56
IS 22
BP 1862
EP 1863
DI 10.1016/j.jacc.2010.09.006
PG 4
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 681JQ
UT WOS:000284308400017
ER

PT J
AU King, ONF
   Li, XS
   Sakurai, M
   Kawamura, A
   Rose, NR
   Ng, SS
   Quinn, AM
   Rai, G
   Mott, BT
   Beswick, P
   Klose, RJ
   Oppermann, U
   Jadhav, A
   Heightman, TD
   Maloney, DJ
   Schofield, CJ
   Simeonov, A
AF King, Oliver N. F.
   Li, Xuan Shirley
   Sakurai, Masaaki
   Kawamura, Akane
   Rose, Nathan R.
   Ng, Stanley S.
   Quinn, Amy M.
   Rai, Ganesha
   Mott, Bryan T.
   Beswick, Paul
   Klose, Robert J.
   Oppermann, Udo
   Jadhav, Ajit
   Heightman, Tom D.
   Maloney, David J.
   Schofield, Christopher J.
   Simeonov, Anton
TI Quantitative High-Throughput Screening Identifies 8-Hydroxyquinolines as
   Cell-Active Histone Demethylase Inhibitors
SO PLOS ONE
LA English
DT Article
ID HYPOXIA-INDUCIBLE-FACTOR; PROLYL 4-HYDROXYLASES; LYSINE DEMETHYLASES;
   GENE-EXPRESSION; HIF FIH; HYDROXYLASE; METHYLATION; 2-OXOGLUTARATE;
   SPECIFICITY; LIBRARIES
AB Background: Small molecule modulators of epigenetic processes are currently sought as basic probes for biochemical mechanisms, and as starting points for development of therapeutic agents. N-e-Methylation of lysine residues on histone tails is one of a number of post-translational modifications that together enable transcriptional regulation. Histone lysine demethylases antagonize the action of histone methyltransferases in a site-and methylation state-specific manner. N-e-Methyllysine demethylases that use 2-oxoglutarate as co-factor are associated with diverse human diseases, including cancer, inflammation and X-linked mental retardation; they are proposed as targets for the therapeutic modulation of transcription. There are few reports on the identification of templates that are amenable to development as potent inhibitors in vivo and large diverse collections have yet to be exploited for the discovery of demethylase inhibitors.
   Principal Findings: High-throughput screening of a similar to 236,000-member collection of diverse molecules arrayed as dilution series was used to identify inhibitors of the JMJD2 (KDM4) family of 2-oxoglutarate-dependent histone demethylases. Initial screening hits were prioritized by a combination of cheminformatics, counterscreening using a coupled assay enzyme, and orthogonal confirmatory detection of inhibition by mass spectrometric assays. Follow-up studies were carried out on one of the series identified, 8-hydroxyquinolines, which were shown by crystallographic analyses to inhibit by binding to the active site Fe(II) and to modulate demethylation at the H3K9 locus in a cell-based assay.
   Conclusions: These studies demonstrate that diverse compound screening can yield novel inhibitors of 2OG dependent histone demethylases and provide starting points for the development of potent and selective agents to interrogate epigenetic regulation.
C1 [King, Oliver N. F.; Ng, Stanley S.; Beswick, Paul; Oppermann, Udo; Heightman, Tom D.] Univ Oxford, Struct Genom Consortium, Headington, England.
   [Li, Xuan Shirley; Klose, Robert J.] Univ Oxford, Dept Biochem, Oxford OX1 3QU, England.
   [Sakurai, Masaaki; Quinn, Amy M.; Rai, Ganesha; Mott, Bryan T.; Jadhav, Ajit; Maloney, David J.; Simeonov, Anton] NHGRI, Chem Genom Ctr, NIH, Bethesda, MD 20892 USA.
   [Kawamura, Akane; Rose, Nathan R.; Schofield, Christopher J.] Univ Oxford, Dept Chem, Oxford OX1 3QU, England.
   [Kawamura, Akane; Rose, Nathan R.; Schofield, Christopher J.] Univ Oxford, Oxford Ctr Integrat Syst Biol, Oxford OX1 3QU, England.
RP King, ONF (reprint author), Univ Oxford, Struct Genom Consortium, Headington, England.
EM asimeono@mail.nih.gov
RI Rose, Nathan/A-9270-2013; 
OI Rose, Nathan/0000-0002-1871-1156; Schofield,
   Christopher/0000-0002-0290-6565
FU Molecular Libraries Initiative of the National Institutes of Health
   (NIH); NHGRI; NIH; Wellcome Trust; Commonwealth Scholarship Commission
   in the United Kingdom; Biotechnology and Biological Research Council
   (U.K.); Canadian Institutes for Health Research [1097737]; Canadian
   Foundation for Innovation; Genome Canada through the Ontario Genomics
   Institute; GlaxoSmithKline; Karolinska Institutet; Knut and Alice
   Wallenberg Foundation; Ontario Innovation Trust; Ontario Ministry for
   Research and Innovation; Merck Co., Inc.; Novartis Research Foundation;
   Swedish Agency for Innovation Systems; Swedish Foundation for Strategic
   Research
FX This research was supported in part by the Molecular Libraries
   Initiative of the National Institutes of Health (NIH) Roadmap for
   Medical Research and the Intramural Research Program of NHGRI, NIH, The
   Wellcome Trust, The Commonwealth Scholarship Commission in the United
   Kingdom, and the Biotechnology and Biological Research Council (U.K.).
   The Structural Genomics Consortium is a registered charity (number
   1097737) that receives funds from the Canadian Institutes for Health
   Research, the Canadian Foundation for Innovation, Genome Canada through
   the Ontario Genomics Institute, GlaxoSmithKline, Karolinska Institutet,
   the Knut and Alice Wallenberg Foundation, the Ontario Innovation Trust,
   the Ontario Ministry for Research and Innovation, Merck & Co., Inc., the
   Novartis Research Foundation, the Swedish Agency for Innovation Systems,
   the Swedish Foundation for Strategic Research and the Wellcome Trust.
   The funders had no role in study design, data collection and analysis,
   decision to publish, or preparation of the manuscript.
NR 48
TC 98
Z9 99
U1 1
U2 26
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD NOV 23
PY 2010
VL 5
IS 11
AR e15535
DI 10.1371/journal.pone.0015535
PG 12
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 684DM
UT WOS:000284527900023
PM 21124847
ER

PT J
AU Major, JM
   Doubeni, CA
   Freedman, ND
   Park, Y
   Lian, M
   Hollenbeck, AR
   Schatzkin, A
   Graubard, BI
   Sinha, R
AF Major, Jacqueline M.
   Doubeni, Chyke A.
   Freedman, Neal D.
   Park, Yikyung
   Lian, Min
   Hollenbeck, Albert R.
   Schatzkin, Arthur
   Graubard, Barry I.
   Sinha, Rashmi
TI Neighborhood Socioeconomic Deprivation and Mortality: NIH-AARP Diet and
   Health Study
SO PLOS ONE
LA English
DT Article
ID LARGE SOCIAL NETWORK; ALL-CAUSE MORTALITY; UNITED-STATES; RISK-FACTORS;
   FOLLOW-UP; MEN; WOMEN; AREA; INEQUALITIES; GENDER
AB Purpose: Residing in deprived areas may increase risk of mortality beyond that explained by a person's own SES-related factors and lifestyle. The aim of this study was to examine the relation between neighborhood socioeconomic deprivation and all-cause, cancer-and cardiovascular disease (CVD)-specific mortality for men and women after accounting for education and other important person-level risk factors.
   Methods: In the longitudinal NIH-AARP Study, we analyzed data from healthy participants, ages 50-71 years at study baseline (1995-1996). Deaths (n = 33831) were identified through December 2005. Information on census tracts was obtained from the 2000 US Census. Cox models estimated hazard ratios (HRs) and 95% confidence intervals (CIs) for quintiles of neighborhood deprivation.
   Results: Participants in the highest quintile of deprivation had elevated risks for overall mortality (HR(men) = 1.17, 95% CI: 1.10, 1.24; HR(women) = 1.13, 95% CI: 1.05, 1.22) and marginally increased risk for cancer deaths (HR(men) = 1.09, 95% CI: 1.00, 1.20; HR(women) = 1.09, 95% CI: 0.99, 1.22). CVD mortality associations appeared stronger in men (HR = 1.33, 95% CI: 1.19, 1.49) than women (HR = 1.18, 95% CI: 1.01, 1.38). There was no evidence of an effect modification by education.
   Conclusion: Higher neighborhood deprivation was associated with modest increases in all-cause, cancer-and CVD-mortality after accounting for many established risk factors.
C1 [Major, Jacqueline M.; Freedman, Neal D.; Park, Yikyung; Schatzkin, Arthur; Graubard, Barry I.; Sinha, Rashmi] NCI, Div Canc Epidemiol & Genet, NIH, Bethesda, MD 20892 USA.
   [Doubeni, Chyke A.] Univ Massachusetts, Sch Med, Dept Family Med & Community Hlth, Worcester, MA USA.
   [Lian, Min] Washington Univ, Sch Med, Dept Med, St Louis, MO 63110 USA.
   [Hollenbeck, Albert R.] Amer Assoc Retired Persons, Washington, DC USA.
RP Major, JM (reprint author), NCI, Div Canc Epidemiol & Genet, NIH, Bethesda, MD 20892 USA.
EM Jacqueline.major@nih.gov
RI Freedman, Neal/B-9741-2015; Sinha, Rashmi/G-7446-2015; 
OI Freedman, Neal/0000-0003-0074-1098; Sinha, Rashmi/0000-0002-2466-7462;
   Doubeni, Chyke/0000-0001-7495-0285; Park, Yikyung/0000-0002-6281-489X
FU National Cancer Institute, National Institute of Health
FX Supported by the Intramural Research Program of the National Cancer
   Institute, National Institute of Health. The funders had no role in
   study design, data collection and analysis, decision to publish, or
   preparation of the manuscript.
NR 37
TC 42
Z9 42
U1 2
U2 7
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 185 BERRY ST, STE 1300, SAN FRANCISCO, CA 94107 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD NOV 23
PY 2010
VL 5
IS 11
AR e15538
DI 10.1371/journal.pone.0015538
PG 6
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 684DM
UT WOS:000284527900025
PM 21124858
ER

PT J
AU Redon, CE
   Nakamura, AJ
   Gouliaeva, K
   Rahman, A
   Blakely, WF
   Bonner, WM
AF Redon, Christophe E.
   Nakamura, Asako J.
   Gouliaeva, Ksenia
   Rahman, Arifur
   Blakely, William F.
   Bonner, William M.
TI The Use of Gamma-H2AX as a Biodosimeter for Total-Body Radiation
   Exposure in Non-Human Primates
SO PLOS ONE
LA English
DT Article
ID DOUBLE-STRAND BREAKS; PERIPHERAL-BLOOD LYMPHOCYTES; IONIZING-RADIATION;
   DNA-DAMAGE; IN-VIVO; HAIR-FOLLICLES; FOCI; BIOMARKER; SKIN;
   FRAGMENTATION
AB Background: There is a crucial shortage of methods capable of determining the extent of accidental exposures of human beings to ionizing radiation. However, knowledge of individual exposures is essential for early triage during radiological incidents to provide optimum possible life-sparing medical procedures to each person.
   Methods and Findings: We evaluated immunocytofluorescence-based quantitation of gamma-H2AX foci as a biodosimeter of total-body radiation exposure (Co-60 gamma-rays) in a rhesus macaque (Macaca mulatta) model. Peripheral blood lymphocytes and plucked hairs were collected from 4 cohorts of macaques receiving total body irradiation doses ranging from 1 Gy to 8.5 Gy. Each cohort consisted of 6 experimental and 2 control animals. Numbers of residual gamma-H2AX foci were proportional to initial irradiation doses and statistically significant responses were obtained until 1 day after 1 Gy, 4 days after 3.5 and 6.5 Gy, and 14 days after 8.5 Gy in lymphocytes and until 1 day after 1 Gy, at least 2 days after 3.5 and 6.5 Gy, and 9 days after 8.5 Gy in plucked hairs.
   Conclusion: These findings indicate that quantitation of gamma-H2AX foci may make a robust biodosimeter for analyzing total-body exposure to ionizing radiation in humans. This tool would help clinicians prescribe appropriate types of medical intervention for optimal individual outcome. These results also demonstrate that the use of a high throughput gamma-H2AX biodosimeter would be useful for days post-exposure in applications like large-scale radiological events or radiation therapy. In addition, this study validates a possibility to use plucked hair in future clinical trials investigating genotoxic effects of drugs and radiation treatments.
C1 [Redon, Christophe E.; Nakamura, Asako J.; Gouliaeva, Ksenia; Bonner, William M.] NCI, Mol Pharmacol Lab, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
   [Rahman, Arifur; Blakely, William F.] Uniformed Serv Univ Hlth Sci, Armed Forces Radiobiol Res Inst, Bethesda, MD 20814 USA.
RP Redon, CE (reprint author), NCI, Mol Pharmacol Lab, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
EM redonc@mail.nih.gov
FU NIAID; National Cancer Institute, Center for Cancer Research, NIH; Armed
   Forces Radiobiology Research Institute [BD-13 (RBB4AR)]
FX This research was supported by the NIAID Radiation/Nuclear
   Countermeasures Program, the Intramural Research Program of the National
   Cancer Institute, Center for Cancer Research, NIH and under Armed Forces
   Radiobiology Research Institute under research work unit number BD-13
   (RBB4AR). The funders had no role in study design, data collection and
   analysis, decision to publish, or preparation of the manuscript.
NR 33
TC 63
Z9 65
U1 1
U2 7
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD NOV 23
PY 2010
VL 5
IS 11
AR e15544
DI 10.1371/journal.pone.0015544
PG 8
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 684DM
UT WOS:000284527900027
PM 21124906
ER

PT J
AU Schwefel, D
   Frohlich, C
   Eichhorst, J
   Wiesner, B
   Behlke, J
   Aravind, L
   Daumke, O
AF Schwefel, David
   Froehlich, Chris
   Eichhorst, Jenny
   Wiesner, Burkhard
   Behlke, Joachim
   Aravind, L.
   Daumke, Oliver
TI Structural basis of oligomerization in septin-like GTPase of
   immunity-associated protein 2 (GIMAP2)
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
   AMERICA
LA English
DT Article
DE G protein; protein structure
ID IAN FAMILY; CELL-DEVELOPMENT; T-LYMPHOCYTES; GENE; RAT; EXPRESSION;
   MECHANISM; SURVIVAL; BIOLOGY; MODEL
AB GTPases of immunity-associated proteins (GIMAPs) are a distinctive family of GTPases, which control apoptosis in lymphocytes and play a central role in lymphocyte maturation and lymphocyte-associated diseases. To explore their function and mechanism, we determined crystal structures of a representative member, GIMAP2, in different nucleotide-loading and oligomerization states. Nucleotide-free and GDP-bound GIMAP2 were monomeric and revealed a guanine nucleotide-binding domain of the TRAFAC (translation factor associated) class with a unique amphipathic helix alpha 7 packing against switch II. In the absence of alpha 7 and the presence of GTP, GIMAP2 oligomerized via two distinct interfaces in the crystal. GTP-induced stabilization of switch I mediates dimerization across the nucleotide-binding site, which also involves the GIMAP specificity motif and the nucleotide base. Structural rearrangements in switch II appear to induce the release of alpha 7 allowing oligomerization to proceed via a second interface. The unique architecture of the linear oligomer was confirmed by mutagenesis. Furthermore, we showed a function for the GIMAP2 oligomer at the surface of lipid droplets. Although earlier studies indicated that GIMAPs are related to the septins, the current structure also revealed a strikingly similar nucleotide coordination and dimerization mode as in the dynamin GTPase. Based on this, we reexamined the relationships of the septin-and dynamin-like GTPases and demonstrate that these are likely to have emerged from a common membrane-associated dimerizing ancestor. This ancestral property appears to be critical for the role of GIMAPs as nucleotide-regulated scaffolds on intracellular membranes.
C1 [Schwefel, David; Froehlich, Chris; Behlke, Joachim; Daumke, Oliver] Max Delbruck Centrum Mol Med, D-13125 Berlin, Germany.
   [Schwefel, David; Froehlich, Chris] Free Univ Berlin, Inst Chem & Biochem, D-14195 Berlin, Germany.
   [Eichhorst, Jenny; Wiesner, Burkhard] Leibniz Inst Mol Pharmacol, D-13125 Berlin, Germany.
   [Daumke, Oliver] Charite, Inst Med Phys & Biophys, D-10117 Berlin, Germany.
   [Aravind, L.] Natl Lib Med, Natl Ctr Biotechnol Informat, NIH, Bethesda, MD 20894 USA.
RP Daumke, O (reprint author), Max Delbruck Centrum Mol Med, Robert Rossle Str 10, D-13125 Berlin, Germany.
EM oliver.daumke@mdc-berlin.de
FU International Human Frontier Science Program Organization; National
   Institutes of Health
FX We acknowledge advice and assistance by O. Ristau and C. Schilling
   (analytical ultracentrifugation analysis), K. Kochert and S. Mathas
   (cell culture), S. Werner and M. Papst (technical assistance), and the
   Berliner Elektronenspeicherring-Gesellschaft fur Synchrotronstrahlung II
   staff at BL14.1, especially U. Muller (data collection and processing).
   O. D. acknowledges support by a Career Development Award of "The
   International Human Frontier Science Program Organization." L.A. is
   supported by the intramural funds of the National Institutes of Health.
NR 47
TC 23
Z9 24
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 23
PY 2010
VL 107
IS 47
BP 20299
EP 20304
DI 10.1073/pnas.1010322107
PG 6
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 684DT
UT WOS:000284529000031
PM 21059949
ER

PT J
AU Rishi, V
   Bhattacharya, P
   Chatterjee, R
   Rozenberg, J
   Zhao, JF
   Glass, K
   Fitzgerald, P
   Vinson, C
AF Rishi, Vikas
   Bhattacharya, Paramita
   Chatterjee, Raghunath
   Rozenberg, Julian
   Zhao, Jianfei
   Glass, Kimberly
   Fitzgerald, Peter
   Vinson, Charles
TI CpG methylation of half-CRE sequences creates C/EBP alpha binding sites
   that activate some tissue-specific genes
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
   AMERICA
LA English
DT Article
DE gene regulation; EMSA; transcription factor binding site
ID DNA METHYLATION; DIFFERENTIATION; ENHANCER; CELLS; KERATINOCYTES;
   TRANSCRIPTION; EXPRESSION; ISLANDS; PROTEIN; GENOME
AB DNA methylation of the cytosine in the CpG dinucleotide is typically associated with gene silencing. Genomic analyses have identified low CpG promoters that are both methylated and transcriptionally active, but the mechanism underlying the activation of these methylated promoters remains unclear. Here we show that CpG methylation of the CRE sequence (TGACGTCA) enhances the DNA binding of the C/EBP alpha transcription factor, a protein critical for activation of differentiation in various cell types. Transfection assays also show that C/EBP alpha activates the CRE sequence only when it is methylated. The biological significance of this observation was seen in differentiating primary keratinocyte cultures from newborn mice where certain methylated promoters are both bound by C/EBP alpha and activated upon differentiation. Experimental demethylation by either 5-azacytidine treatment or DNMT1 depletion diminished both C/EBP alpha binding and activation of the same methylated promoters upon differentiation suggesting that CpG methylation can localize C/EBP alpha. Transfection studies in cell cultures using methylated tissue-specific proximal promoters identified half-CRE (CGTCA) and half-C/EBP (CGCAA) sequences that need to be methylated for C/EBP alpha mediated activation. In primary dermal fibroblasts, C/EBP alpha activates a different set of methylated tissue-specific promoters upon differentiation into adipocytes. These data identify a new function for methyl CpGs: producing DNA binding sites at half-CRE and half-C/EBP sequences for C/EBP alpha that are needed to activate tissue-specific genes.
C1 [Rishi, Vikas; Bhattacharya, Paramita; Chatterjee, Raghunath; Rozenberg, Julian; Zhao, Jianfei; Vinson, Charles] NCI, Lab Metab, NIH, Bethesda, MD 20892 USA.
   [Glass, Kimberly] Univ Maryland, Dept Phys, College Pk, MD 20742 USA.
   [Fitzgerald, Peter] NCI, Genome Anal Unit, NIH, Bethesda, MD 20892 USA.
RP Vinson, C (reprint author), NCI, Lab Metab, NIH, Bldg 37,Room 3128, Bethesda, MD 20892 USA.
EM vinsonc@mail.nih.gov
NR 34
TC 85
Z9 85
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 23
PY 2010
VL 107
IS 47
BP 20311
EP 20316
DI 10.1073/pnas.1008688107
PG 6
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 684DT
UT WOS:000284529000033
PM 21059933
ER

PT J
AU Dimitriadis, EK
   Weber, C
   Gill, RK
   Diekmann, S
   Dalal, Y
AF Dimitriadis, Emilios K.
   Weber, Christian
   Gill, Rajbir K.
   Diekmann, Stephan
   Dalal, Yamini
TI Tetrameric organization of vertebrate centromeric nucleosomes
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
   AMERICA
LA English
DT Article
DE alternative nucleosomes; cell division; histone variant; regional
   centromeres
ID HISTONE FOLD DOMAIN; VARIANT CENP-A; SACCHAROMYCES-CEREVISIAE;
   CHROMATIN-STRUCTURE; BUDDING YEAST; FISSION YEAST; KINETOCHORE; DNA;
   DEPOSITION; CORE
AB Mitosis ensures equal genome segregation in the eukaryotic lineage. This process is facilitated by microtubule attachment to each chromosome via its centromere. In centromeres, canonical histone H3 is replaced in nucleosomes by a centromere-specific histone H3 variant (CENH3), providing the unique epigenetic signature required for microtubule binding. Due to recent findings of alternative CENH3 nucleosomal forms in invertebrate centromeres, it has been debated whether the classical octameric nucleosomal arrangement of two copies of CENH3, H4, H2A, and H2B forms the basis of the vertebrate centromere. To address this question directly, we examined CENH3 [centromere protein A (CENP-A)] nucleosomal organization in human cells, using a combination of nucleosome component analysis, atomic force microscopy (AFM), and immunoelectron microscopy (immuno-EM). We report that native CENP-A nucleosomes contain centromeric alpha satellite DNA, have equimolar amounts of H2A, H2B, CENP-A, and H4, and bind kinetochore proteins. These nucleosomes, when measured by AFM, yield one-half the dimensions of canonical octameric nucleosomes. Using immuno-EM, we find that one copy of CENP-A, H2A, H2B, and H4 coexist in CENP-A nucleosomes, in which internal C-terminal domains are accessible. Our observations indicate that CENP-A nucleosomes are organized as asymmetric heterotypic tetramers, rather than canonical octamers. Such altered nucleosomes form a chromatin fiber with distinct folding characteristics, which we utilize to discriminate tetramers directly within bulk chromatin. We discuss implications of our observations in the context of universal epigenetic and mechanical requirements for functional centromeres.
C1 [Gill, Rajbir K.; Dalal, Yamini] NCI, Lab Receptor Biol & Gene Express, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
   [Dimitriadis, Emilios K.] Natl Inst Biomed Imaging & Bioengn, Scanning Probe Microscopy Unit, NIH, Bethesda, MD 20892 USA.
   [Weber, Christian; Diekmann, Stephan] Fritz Lipmann Inst, Leibniz Inst Age Res, D-07745 Jena, Germany.
RP Dalal, Y (reprint author), NCI, Lab Receptor Biol & Gene Express, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
EM dalaly@mail.nih.gov
OI Dalal, Yamini/0000-0002-7655-6182
FU Intramural NIH HHS [ZIA BC011207-04, ZIA BC011207-05, ZIA BC011207-01,
   ZIA BC011207-02, ZIA BC011207-06, ZIA BC011207-03]
NR 54
TC 60
Z9 62
U1 0
U2 11
PU NATL ACAD SCIENCES
PI WASHINGTON
PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA
SN 0027-8424
J9 P NATL ACAD SCI USA
JI Proc. Natl. Acad. Sci. U. S. A.
PD NOV 23
PY 2010
VL 107
IS 47
BP 20317
EP 20322
DI 10.1073/pnas.1009563107
PG 6
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 684DT
UT WOS:000284529000034
PM 21059934
ER

PT J
AU Hashimoto, K
   Panchenko, AR
AF Hashimoto, Kosuke
   Panchenko, Anna R.
TI Mechanisms of protein oligomerization, the critical role of insertions
   and deletions in maintaining different oligomeric states
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
   AMERICA
LA English
DT Article
DE homodimer; homooligomer protein; protein structural evolution
ID CRYSTAL-STRUCTURE; QUATERNARY STRUCTURE; EVOLUTION; DOMAIN; AGGREGATION;
   SPECIFICITY; INTERFACES; BINDING; DIMERIZATION; SUPERFAMILY
AB The main principles of protein-protein recognition are elucidated by the studies of homooligomers which in turn mediate and regulate gene expression, activity of enzymes, ion channels, receptors, and cell-cell adhesion processes. Here we explore oligomeric states of homologous proteins in various organisms to better understand the functional roles and evolutionary mechanisms of homooligomerization. We observe a great diversity in mechanisms controlling oligomerization and focus in our study on insertions and deletions in homologous proteins and how they enable or disable complex formation. We show that insertions and deletions which differentiate monomers and dimers have a significant tendency to be located on the interaction interfaces and about a quarter of all proteins studied and forty percent of enzymes have regions which mediate or disrupt the formation of oligomers. We suggest that relatively small insertions or deletions may have a profound effect on complex stability and/or specificity. Indeed removal of complex enabling regions from protein structures in many cases resulted in the complete or partial loss of stability. Moreover, we find that insertions and deletions modulating oligomerization have a lower aggregation propensity and contain a larger fraction of polar, charged residues, glycine and proline compared to conventional interfaces and protein surface. Most likely, these regions may mediate specific interactions, prevent nonspecific dysfunctional aggregation and preclude undesired interactions between close paralogs therefore separating their functional pathways. Last, we show how the presence or absence of insertions and deletions on interfaces might be of practical value in annotating protein oligomeric states.
C1 [Hashimoto, Kosuke; Panchenko, Anna R.] Natl Lib Med, Natl Ctr Biotechnol Informat, NIH, Bethesda, MD 20894 USA.
RP Panchenko, AR (reprint author), Natl Lib Med, Natl Ctr Biotechnol Informat, NIH, Bethesda, MD 20894 USA.
EM panch@ncbi.nlm.nih.gov
FU National Institutes of Health/Department of Health and Human Service
   (DHHS); Japan Society for the Promotion of Science
FX We thank Steve Bryant for insightful discussions and Tom Madej for
   careful reading of the manuscript. This work was supported by National
   Institutes of Health/Department of Health and Human Service (DHHS)
   (Intramural Research program of the National Library of Medicine). K. H.
   was supported by a JSPS Research Fellowship from the Japan Society for
   the Promotion of Science.
NR 58
TC 49
Z9 50
U1 1
U2 15
PU NATL ACAD SCIENCES
PI WASHINGTON
PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA
SN 0027-8424
J9 P NATL ACAD SCI USA
JI Proc. Natl. Acad. Sci. U. S. A.
PD NOV 23
PY 2010
VL 107
IS 47
BP 20352
EP 20357
DI 10.1073/pnas.1012999107
PG 6
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 684DT
UT WOS:000284529000040
PM 21048085
ER

PT J
AU Bagattin, A
   Hugendubler, L
   Mueller, E
AF Bagattin, Alessia
   Hugendubler, Lynne
   Mueller, Elisabetta
TI Transcriptional coactivator PGC-1 alpha promotes peroxisomal remodeling
   and biogenesis
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
   AMERICA
LA English
DT Article
DE organelle biogenesis; adaptive thermogenesis; energy metabolism
ID MITOCHONDRIAL BIOGENESIS; ZELLWEGER-SYNDROME; BETA-OXIDATION;
   RECEPTOR-ALPHA; ERR-ALPHA; BROWN FAT; PROLIFERATION; METABOLISM; PGC-1;
   DIFFERENTIATION
AB Mitochondria and peroxisomes execute some analogous, nonredundant functions including fatty acid oxidation and detoxification of reactive oxygen species, and, in response to select metabolic cues, undergo rapid remodeling and division. Although these organelles share some components of their division machinery, it is not known whether a common regulator coordinates their remodeling and biogenesis. Here we show that in response to thermogenic stimuli, peroxisomes in brown fat tissue (BAT) undergo selective remodeling and expand in number and demonstrate that ectopic expression of the transcriptional coactivator PGC-1 alpha recapitulates these effects on the peroxisomal compartment, both in vitro and in vivo. Conversely, beta-adrenergic stimulation of PGC-1 alpha(-/-) cells results in blunted induction of peroxisomal gene expression. Surprisingly, PPAR alpha was not required for the induction of critical biogenesis factors, suggesting that PGC-1 alpha orchestrates peroxisomal remodeling through a PPAR alpha-independent mechanism. Our data suggest that PGC-1 alpha is critical to peroxisomal physiology, establishing a role for this factor as a fundamental orchestrator of cellular adaptation to energy demands.
C1 [Bagattin, Alessia; Hugendubler, Lynne; Mueller, Elisabetta] NIDDK, Genet Dev & Dis Branch, NIH, Bethesda, MD 20892 USA.
RP Mueller, E (reprint author), NIDDK, Genet Dev & Dis Branch, NIH, Bethesda, MD 20892 USA.
EM elisabettam@niddk.nih.gov
FU National Institute of Diabetes and Digestive and Kidney Diseases,
   National Institutes of Health
FX We are grateful to Richard Proia and to members of the laboratory for
   reading the manuscript and for their helpful suggestions and to Pasha
   Sarraf for critical discussions and comments. We thank Bruce Spiegelman
   (Harvard Medical School, Boston, MA) for the kind gift of P and GFP
   adenoviruses and for the WT and PGC-1 alpha KO brown preadipocyte cell
   lines. We are indebted to Jennifer Lippincott-Schwartz (National
   Institute of Child Health and Human Development, National Institutes of
   Health, Bethesda, MD) for providing us with the RFP-SKL plasmid. We also
   thank Rick Dreyfuss (NIH Medical Arts, Bethesda, MD) for microscopy
   pictures, Morgan Gallazzini for confocal imaging, and Deborah Simon and
   Huiyan Lu for performing tail vein injections. This work was supported
   by the Intramural Research Program of the National Institute of Diabetes
   and Digestive and Kidney Diseases, National Institutes of Health.
NR 24
TC 35
Z9 35
U1 1
U2 5
PU NATL ACAD SCIENCES
PI WASHINGTON
PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA
SN 0027-8424
J9 P NATL ACAD SCI USA
JI Proc. Natl. Acad. Sci. U. S. A.
PD NOV 23
PY 2010
VL 107
IS 47
BP 20376
EP 20381
DI 10.1073/pnas.1009176107
PG 6
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 684DT
UT WOS:000284529000044
PM 21059926
ER

PT J
AU Walseng, E
   Furuta, K
   Bosch, B
   Weih, KA
   Matsuki, Y
   Bakke, O
   Ishido, S
   Roche, PA
AF Walseng, Even
   Furuta, Kazuyuki
   Bosch, Berta
   Weih, Karis A.
   Matsuki, Yohei
   Bakke, Oddmund
   Ishido, Satoshi
   Roche, Paul A.
TI Ubiquitination regulates MHC class II-peptide complex retention and
   degradation in dendritic cells
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
   AMERICA
LA English
DT Article
ID MONOCLONAL-ANTIBODIES; DOWN-REGULATION; INFLAMMATORY STIMULI; IA
   ANTIGENS; IN-VIVO; ENDOCYTOSIS; EXPRESSION; TRANSPORT; RECEPTOR;
   COMPARTMENTS
AB The expression and turnover of MHC class II-peptide complexes (pMHC-II) on the surface of dendritic cells (DCs) is essential for their ability to activate CD4 T cells efficiently. The half-life of surface pMHC-II is significantly greater in activated (mature) DCs than in resting (immature) DCs, but the molecular mechanism leading to this difference remains unknown. We now show that ubiquitination of pMHC-II by the E3 ubiquitin ligase membrane-associated RING-CH 1 (March-I) regulates surface expression, intracellular distribution, and survival of pMHC-II in DCs. DCs isolated from MarchI- KO mice express very high levels of pMHC-II on the plasma membrane even before DC activation. Although ubiquitination does not affect the kinetics of pMHC-II endocytosis from the surface of DCs, the survival of pMHC-II is enhanced in DCs obtained from March-I-deficient and MHC-II ubiquitination-mutant mice. Using pMHC-II-specific mAb, we show that immature DCs generate large amounts of pMHC-II that are remarkably stable under conditions in which pMHC-II ubiquitination is blocked. Thus, the cellular distribution and stability of surface pMHC-II in DCs is regulated by ubiquitin-dependent degradation of internalized pMHC-II.
C1 [Walseng, Even; Furuta, Kazuyuki; Bosch, Berta; Weih, Karis A.; Roche, Paul A.] Natl Canc Inst, Expt Immunol Branch, NIH, Bethesda, MD 20892 USA.
   [Walseng, Even; Bakke, Oddmund] Univ Oslo, Dept Mol Biosci, Ctr Immune Regulat, N-0316 Oslo, Norway.
   [Matsuki, Yohei; Ishido, Satoshi] RIKEN Res Ctr Allergy & Immunol, Lab Infect Immun, Kanagawa 2300045, Japan.
   [Bakke, Oddmund] Univ Bergen, Gade Inst, NO-5020 Bergen, Norway.
RP Roche, PA (reprint author), Natl Canc Inst, Expt Immunol Branch, NIH, Bethesda, MD 20892 USA.
EM rochepa@mail.nih.gov
OI Bakke, Oddmund/0000-0003-4843-7626
FU Norwegian Research Council; Ministry of Education, Culture, Sports,
   Science and Technology of Japan; Japan Society for the Promotion of
   Science; National Institutes of Health
FX We thank Alfred Singer and Richard Hodes for extensive discussions and
   critical reading of this manuscript. We thank Peter Cresswell (Yale
   University School of Medicine), Ron Germain (National Institutes of
   Health), Emil Unanue (Washington University School of Medicine), Sasha
   Rudensky (Memorial Sloan-Kettering Cancer Center), and Diane Mathis
   (Harvard Medical School) for the gifts of reagents used in this study.
   This work is supported by the Norwegian Research Council (E.W. and
   O.B.), the Ministry of Education, Culture, Sports, Science and
   Technology of Japan (S. I.), the Japan Society for the Promotion of
   Science (S. I.), and the Intramural Research Program of the National
   Institutes of Health (P.A.R.).
NR 32
TC 47
Z9 47
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 23
PY 2010
VL 107
IS 47
BP 20465
EP 20470
DI 10.1073/pnas.1010990107
PG 6
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 684DT
UT WOS:000284529000059
PM 21059907
ER

PT J
AU Cairo, S
   Wang, YP
   de Reynies, A
   Duroure, K
   Dahan, J
   Redon, MJ
   Fabre, M
   McClelland, M
   Wang, XW
   Croce, CM
   Buendia, MA
AF Cairo, Stefano
   Wang, Yipeng
   de Reynies, Aurelien
   Duroure, Karine
   Dahan, Jennifer
   Redon, Marie-Jose
   Fabre, Monique
   McClelland, Michael
   Wang, Xin W.
   Croce, Carlo M.
   Buendia, Marie-Annick
TI Stem cell-like micro-RNA signature driven by Myc in aggressive liver
   cancer
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
   AMERICA
LA English
DT Article
DE hepatoblastoma; hepatocellular carcinoma; Myc; signature; stemness
ID HEPATOCELLULAR-CARCINOMA; GENE-EXPRESSION; WNT/BETA-CATENIN; TUMORS;
   TUMORIGENESIS; IDENTIFICATION; HEPATOBLASTOMA; PROLIFERATION;
   CONTRIBUTES; METASTASIS
AB Myc activation has been implicated in the pathogenesis of hepatoblastoma (HB), a rare embryonal neoplasm derived from liver progenitor cells. Here, microRNA (miR) expression profiling of 65 HBs evidenced differential patterns related to developmental stage and Myc activity. Undifferentiated aggressive HBs overexpressed the miR-371-3 cluster with concomitant down-regulation of the miR-100/let-7a-2/miR-125b-1 cluster, evoking an ES cell expression profile. ChIP and Myc inhibition assays in hepatoma cells demonstrated that both miR clusters are regulated by Myc in an opposite manner. We show that the two miR clusters exert antagonistic effects on cell proliferation and tumorigenicity. Moreover, their combined deregulation cooperated in modulating the hepatic tumor phenotype, implicating stem cell-like regulation of Myc-dependent miRs in poorly differentiated HBs. Importantly, a four-miR signature representative of these clusters efficiently stratified HB patients, and when applied to 241 hepatocellular carcinomas (HCCs), it identified invasive tumors with a poor prognosis. Our data argue that Myc-driven reprogramming of miR expression patterns contributes to the aggressive phenotype of liver tumors originating from hepatic progenitor cells.
C1 [Cairo, Stefano; Duroure, Karine; Dahan, Jennifer; Buendia, Marie-Annick] Inst Pasteur, Oncogenesis & Mol Virol Unit, F-75015 Paris, France.
   [Cairo, Stefano; Duroure, Karine; Dahan, Jennifer; Buendia, Marie-Annick] INSERM, U579, F-75015 Paris, France.
   [Wang, Yipeng; McClelland, Michael] Vaccine Res Inst San Diego, San Diego, CA 92121 USA.
   [Wang, Yipeng; McClelland, Michael] Univ Calif Irvine, Dept Pathol & Lab Med, Irvine, CA 92697 USA.
   [de Reynies, Aurelien] Ligue Natl Contre Canc, F-75013 Paris, France.
   [Redon, Marie-Jose; Fabre, Monique] Hop Bicetre, APHP, Serv Anat & Cytol Pathol, F-94275 Le Kremlin Bicetre, France.
   [Fabre, Monique] Univ Paris 11, Unite Pathol, Hop Paul Brousse, APHP,INSERM,U785, F-94800 Villejuif, France.
   [Wang, Xin W.] NCI, Liver Carcinogenesis Sect, Human Carcinogenesis Lab, Ctr Canc Res, Bethesda, MD 20892 USA.
   [Croce, Carlo M.] Ohio State Univ, Dept Mol Virol Immunol & Med Genet, Ctr Comprehens Canc, Med Ctr, Columbus, OH 43210 USA.
RP Buendia, MA (reprint author), Inst Pasteur, Oncogenesis & Mol Virol Unit, F-75015 Paris, France.
EM marie-annick.buendia@pasteur.fr
RI McClelland, Michael/A-8583-2011; Wang, Xin/B-6162-2009; Cairo,
   Stefano/O-2831-2016; 
OI Cairo, Stefano/0000-0002-4725-5970; McClelland,
   Michael/0000-0003-1788-9347
FU Association pour la Recherche contre le Cancer; Nausicaa Association;
   Institut Pasteur; Center for Cancer Research of the National Cancer
   Institute [Z01-BC 010313]
FX We thank C. Trepo (Department of Hepato-gastroenterology, Hotel-Dieu
   Hospital, and Institut National de la Sante et de la Recherche Medicale
   U871, Lyon, France) for providing the HepaRG cell line, S. W. Lowe (Cold
   Spring Harbor Laboratory, Cold Spring Harbor, NY) for miR retroviral
   vector, A. Goga for helpful discussions, and pathologists involved in
   SIOPEL studies. Research was supported by grants from the Association
   pour la Recherche contre le Cancer and the Nausicaa Association. S. C.
   was supported by the Institut Pasteur. X. W. W. was supported by the
   Intramural Research Program Grant Z01-BC 010313 of the Center for Cancer
   Research of the National Cancer Institute.
NR 37
TC 86
Z9 91
U1 0
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 23
PY 2010
VL 107
IS 47
BP 20471
EP 20476
DI 10.1073/pnas.1009009107
PG 6
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 684DT
UT WOS:000284529000060
PM 21059911
ER

PT J
AU Schnabel, RB
   Aspelund, T
   Li, G
   Sullivan, LM
   Suchy-Dicey, A
   Harris, TB
   Pencina, MJ
   D'Agostino, RB
   Levy, D
   Kannel, WB
   Wang, TJ
   Kronmal, RA
   Wolf, PA
   Burke, GL
   Launer, LJ
   Vasan, RS
   Psaty, BM
   Benjamin, EJ
   Gudnason, V
   Heckbert, SR
AF Schnabel, Renate B.
   Aspelund, Thor
   Li, Guo
   Sullivan, Lisa M.
   Suchy-Dicey, Astrid
   Harris, Tamara B.
   Pencina, Michael J.
   D'Agostino, Ralph B., Sr.
   Levy, Daniel
   Kannel, William B.
   Wang, Thomas J.
   Kronmal, Richard A.
   Wolf, Philip A.
   Burke, Gregory L.
   Launer, Lenore J.
   Vasan, Ramachandran S.
   Psaty, Bruce M.
   Benjamin, Emelia J.
   Gudnason, Vilmundur
   Heckbert, Susan R.
TI Validation of an Atrial Fibrillation Risk Algorithm in Whites and
   African Americans
SO ARCHIVES OF INTERNAL MEDICINE
LA English
DT Article
ID CONGESTIVE-HEART-FAILURE; ATHEROSCLEROSIS RISK; PREVALENCE; POPULATION;
   COHORT; ADULTS; PREVENTION; PROGNOSIS; STROKE; TRENDS
AB Background: We sought to validate a recently published risk algorithm for incident atrial fibrillation (AF) in independent cohorts and other racial groups.
   Methods: We evaluated the performance of a Framing-ham Heart Study (FHS)-derived risk algorithm modified for 5-year incidence of AF in the FHS (n= 4764 participants) and 2 geographically and racially diverse cohorts in the age range 45 to 95 years: AGES (the Age, Gene/Environment Susceptibility-Reykjavik Study) (n= 4238) and CHS (the Cardiovascular Health Study) (n= 5410, of whom 874 [16.2%] were African Americans). The risk algorithm included age, sex, body mass index, systolic blood pressure, electrocardiographic PR interval, hypertension treatment, and heart failure.
   Results: We found 1359 incident AF events in 100 074 person-years of follow-up. Unadjusted 5-year event rates differed by cohort (AGES, 12.8 cases/1000 person-years; CHS whites, 22.7 cases/1000 person-years; and FHS, 4.5 cases/1000 person-years) and by race (CHS African Americans, 18.4 cases/1000 person-years). The strongest risk factors in all samples were age and heart failure. The relative risks for incident AF associated with risk factors were comparable across cohorts and race groups. After recalibration for baseline incidence and risk factor distribution, the Framingham algorithm, reported in C statistic, performed reasonably well in all samples: AGES, 0.67 (95% confidence interval [CI], 0.64-0.71); CHS whites, 0.68 (95% CI, 0.66-0.70); and CHS African Americans, 0.66 (95% CI, 0.61-0.71). Risk factors combined in the algorithm explained between 47.0% (AGES) and 63.6% (FHS) of the population-attributable risk.
   Conclusions: Risk of incident AF in community-dwelling whites and African Americans can be assessed reliably by routinely available and potentially modifiable clinical variables. Seven risk factors accounted for up to 64% of risk.
C1 [Schnabel, Renate B.] Johannes Gutenberg Univ Mainz, Dept Med 2, Mainz, Germany.
   [Schnabel, Renate B.; Pencina, Michael J.; Levy, Daniel; Kannel, William B.; Wolf, Philip A.; Vasan, Ramachandran S.; Benjamin, Emelia J.] NHLBI, Framingham Study, Framingham, MA USA.
   [Aspelund, Thor; Gudnason, Vilmundur] Univ Iceland, Heart Prevent Clin & Res Inst, Iceland Heart Assoc, Reykjavik, Iceland.
   [Psaty, Bruce M.; Heckbert, Susan R.] Grp Hlth Res Inst, Grp Hlth Cooperat, Seattle, WA USA.
   [Burke, Gregory L.] Wake Forest Univ, Sch Med, Div Publ Hlth Sci, Winston Salem, NC 27109 USA.
   [Wang, Thomas J.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Div Cardiol, Boston, MA USA.
   [Levy, Daniel] NHLBI, Ctr Populat Studies, Bethesda, MD 20892 USA.
   [Harris, Tamara B.; Launer, Lenore J.] NIA, Lab Epidemiol Demog & Biometry, Intramural Res Program, Bethesda, MD 20892 USA.
   [Li, Guo; Psaty, Bruce M.] Univ Washington, Dept Med, Cardiovasc Hlth Res Unit, Seattle, WA USA.
   [Suchy-Dicey, Astrid; Psaty, Bruce M.; Heckbert, Susan R.] Univ Washington, Dept Epidemiol, Seattle, WA 98195 USA.
   [Kronmal, Richard A.] Univ Washington, Dept Biostat, Seattle, WA 98195 USA.
   [Psaty, Bruce M.] Univ Washington, Dept Hlth Serv, Seattle, WA 98195 USA.
   [Sullivan, Lisa M.; Pencina, Michael J.; D'Agostino, Ralph B., Sr.] Boston Univ, Sch Publ Hlth, Dept Biostat, Boston, MA USA.
   [Kannel, William B.; Benjamin, Emelia J.] Boston Univ, Dept Epidemiol, Boston, MA USA.
   [D'Agostino, Ralph B., Sr.] Boston Univ, Dept Math & Stat, Boston, MA USA.
   [Wolf, Philip A.] Boston Univ, Dept Neurol, Boston, MA USA.
   [Vasan, Ramachandran S.; Benjamin, Emelia J.] Boston Univ, Whitaker Cardiovasc Inst, Evans Mem Med Dept, Cardiol Sect, Boston, MA USA.
   [Vasan, Ramachandran S.; Benjamin, Emelia J.] Boston Univ, Sch Med, Dept Prevent Med, Boston, MA 02118 USA.
RP Heckbert, SR (reprint author), Univ Washington, Cardiovasc Hlth Res Unit, 1730 Minor Ave,Ste 1360, Seattle, WA 98101 USA.
EM heckbert@u.washington.edu
RI Aspelund, Thor/F-4826-2011; Aspelund, Thor/C-5983-2008; Li,
   Guo/E-5613-2012; Schnabel, Renate/F-6527-2014; Gudnason,
   Vilmundur/K-6885-2015; 
OI Benjamin, Emelia/0000-0003-4076-2336; Aspelund,
   Thor/0000-0002-7998-5433; Gudnason, Vilmundur/0000-0001-5696-0084;
   Ramachandran, Vasan/0000-0001-7357-5970
FU National Institutes of Health (NIH) [N01AG-12100, AG028321, AG029451,
   HL092577, RC1 HL101056, R01 NS 17950, 2K24 HL04334]; National Institute
   on Aging Intramural Research Program, Hjartavernd (the Icelandic Heart
   Association); Althingi; National Heart, Lung, and Blood Institute
   (NHLBI) [N01 HC-85079, N01-HC-85086, N01-HC-35129, N01 HC-15103, N01
   HC-55222, U01 HL080295, R01 HL068986, R01 HL087652]; NIH-NHLBI
   [N01-HC-25195]; Deutsche Forschungsgemeinschaft (German Research
   Foundation) [SCHN 1149/1-1]
FX The AGES-Reykjavik study was funded by National Institutes of Health
   (NIH) contract N01-AG-12100, the National Institute on Aging Intramural
   Research Program, Hjartavernd (the Icelandic Heart Association), and the
   Althingi (the Icelandic Parliament). The CHS research reported in this
   article was supported by National Heart, Lung, and Blood Institute
   (NHLBI) grants N01 HC-85079 through N01-HC-85086, N01-HC-35129, N01
   HC-15103, N01 HC-55222, U01 HL080295, R01 HL068986, and R01 HL087652,
   with additional contribution from the National Institute of Neurological
   Disorders and Stroke. The FHS research was supported by NIH-NHLBI
   contract N01-HC-25195 and NIH grants AG028321, AG029451, HL092577, RC1
   HL101056, and R01 NS 17950; NIH Research career award 2K24 HL04334; and
   Deutsche Forschungsgemeinschaft (German Research Foundation) Research
   Fellowship SCHN 1149/1-1.
NR 24
TC 66
Z9 67
U1 1
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 22
PY 2010
VL 170
IS 21
BP 1909
EP 1917
DI 10.1001/archinternmed.2010.434
PG 9
WC Medicine, General & Internal
SC General & Internal Medicine
GA 683MN
UT WOS:000284480000011
PM 21098350
ER

PT J
AU Jimeno-Yepes, AJ
   Aronson, AR
AF Jimeno-Yepes, Antonio J.
   Aronson, Alan R.
TI Knowledge-based biomedical word sense disambiguation: comparison of
   approaches
SO BMC BIOINFORMATICS
LA English
DT Article
AB Background: Word sense disambiguation (WSD) algorithms attempt to select the proper sense of ambiguous terms in text. Resources like the UMLS provide a reference thesaurus to be used to annotate the biomedical literature. Statistical learning approaches have produced good results, but the size of the UMLS makes the production of training data infeasible to cover all the domain.
   Methods: We present research on existing WSD approaches based on knowledge bases, which complement the studies performed on statistical learning. We compare four approaches which rely on the UMLS Metathesaurus as the source of knowledge. The first approach compares the overlap of the context of the ambiguous word to the candidate senses based on a representation built out of the definitions, synonyms and related terms. The second approach collects training data for each of the candidate senses to perform WSD based on queries built using monosemous synonyms and related terms. These queries are used to retrieve MEDLINE citations. Then, a machine learning approach is trained on this corpus. The third approach is a graph-based method which exploits the structure of the Metathesaurus network of relations to perform unsupervised WSD. This approach ranks nodes in the graph according to their relative structural importance. The last approach uses the semantic types assigned to the concepts in the Metathesaurus to perform WSD. The context of the ambiguous word and semantic types of the candidate concepts are mapped to Journal Descriptors. These mappings are compared to decide among the candidate concepts. Results are provided estimating accuracy of the different methods on the WSD test collection available from the NLM.
   Conclusions: We have found that the last approach achieves better results compared to the other methods. The graph-based approach, using the structure of the Metathesaurus network to estimate the relevance of the Metathesaurus concepts, does not perform well compared to the first two methods. In addition, the combination of methods improves the performance over the individual approaches. On the other hand, the performance is still below statistical learning trained on manually produced data and below the maximum frequency sense baseline. Finally, we propose several directions to improve the existing methods and to improve the Metathesaurus to be more effective in WSD.
C1 [Jimeno-Yepes, Antonio J.; Aronson, Alan R.] Natl Lib Med, Bethesda, MD 20894 USA.
RP Jimeno-Yepes, AJ (reprint author), Natl Lib Med, 8600 Rockville Pike, Bethesda, MD 20894 USA.
EM antonio.jimeno@gmail.com
OI Jimeno Yepes, Antonio Jose/0000-0002-6581-094X
FU NIH, National Library of Medicine
FX This work was supported by the Intramural Research Program of the NIH,
   National Library of Medicine. We would like to thank James G. Mork and
   Francois M. Lang for their help and support using the MetaMap tool. We
   would like to thank Chris Lu for his help and support using the JDI
   method.
NR 33
TC 7
Z9 8
U1 1
U2 3
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1471-2105
J9 BMC BIOINFORMATICS
JI BMC Bioinformatics
PD NOV 22
PY 2010
VL 11
AR 569
DI 10.1186/1471-2105-11-569
PG 12
WC Biochemical Research Methods; Biotechnology & Applied Microbiology;
   Mathematical & Computational Biology
SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology;
   Mathematical & Computational Biology
GA 694KU
UT WOS:000285297500001
PM 21092226
ER

PT J
AU Li, LQ
   Lee, JY
   Gross, J
   Song, SH
   Dean, A
   Love, PE
AF Li, LiQi
   Lee, Jan Y.
   Gross, Jennifer
   Song, Sang-Hyun
   Dean, Ann
   Love, Paul E.
TI A requirement for Lim domain binding protein 1 in erythropoiesis
SO JOURNAL OF EXPERIMENTAL MEDICINE
LA English
DT Article
ID TRANSCRIPTION FACTOR GATA-1; ERYTHROID GENE-EXPRESSION; HEMATOPOIETIC
   STEM-CELLS; POSITIVE ROLE; YOLK-SAC; SCL GENE; MICE; DIFFERENTIATION;
   MOUSE; LDB1
AB During erythrocyte development, the nuclear cofactor Lim domain binding protein 1 (Ldb1) functions as a core subunit of multiprotein DNA binding complexes that include the transcription factors Scl and Gata-1 and the Lim-only adapter Lmo2. Scl, Gata-1, and Lmo2 are each required for erythropoiesis, suggesting that Ldb1-nucleated transcription complexes regulate key steps during erythropoiesis. We documented a requirement for Ldb1 in erythropoiesis in mice. Analysis of ldb1(-/-) embryos revealed a critical requirement for Ldb1 during primitive erythropoiesis, and conditional inactivation of ldb1 at later stages of gestation and in adult mice demonstrated that Ldb1 is continuously required for both definitive erythropoiesis and megakaryopoiesis. Down-regulation of Ldb1 in erythroblasts inhibited the expression of multiple erythroid-specific and prosurvival genes. These results represent the first unequivocal demonstration of a role for Ldb1 in erythropoiesis in vivo and establish a critical function for Ldb1-nucleated complexes in regulating the erythroid/megakaryocyte transcriptional program.
C1 [Li, LiQi; Lee, Jan Y.; Gross, Jennifer; Love, Paul E.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Sect Cellular & Dev Biol, NIH, Bethesda, MD 20892 USA.
   [Song, Sang-Hyun; Dean, Ann] NIDDKD, Cellular & Dev Biol Lab, NIH, Bethesda, MD 20892 USA.
RP Love, PE (reprint author), Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Sect Cellular & Dev Biol, NIH, Bethesda, MD 20892 USA.
EM lovep@mail.nih.gov
FU National Institutes of Health; Eunice Kennedy Shriver National Institute
   of Child Health and Human Development; National Institutes of Diabetes
   and Digestive and Kidney Diseases
FX This research was supported by the Intramural Research Program of the
   National Institutes of Health, Eunice Kennedy Shriver National Institute
   of Child Health and Human Development, and National Institutes of
   Diabetes and Digestive and Kidney Diseases.
NR 29
TC 22
Z9 24
U1 0
U2 1
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 22
PY 2010
VL 207
IS 12
BP 2543
EP 2550
DI 10.1084/jem.20100504
PG 8
WC Immunology; Medicine, Research & Experimental
SC Immunology; Research & Experimental Medicine
GA 697HX
UT WOS:000285505000002
PM 21041453
ER

PT J
AU Dawsey, SP
   Tonui, S
   Parker, RK
   Fitzwater, JW
   Dawsey, SM
   White, RE
   Abnet, CC
AF Dawsey, Sonja P.
   Tonui, Stanley
   Parker, Robert K.
   Fitzwater, John W.
   Dawsey, Sanford M.
   White, Russell E.
   Abnet, Christian C.
TI Esophageal Cancer in Young People: A Case Series of 109 Cases and Review
   of the Literature
SO PLOS ONE
LA English
DT Review
ID SQUAMOUS-CELL CARCINOMA; BARRETTS-ESOPHAGUS; SOUTH-AFRICA;
   ADENOCARCINOMA; CHILDHOOD; RISK; IRAN; POPULATION; OESOPHAGUS; MORTALITY
AB Certain geographically distinct areas of the world have very high rates of esophageal cancer (EC). Previous studies have identified western Kenya as a high risk area for EC with an unusual percentage of cases in subjects 30 years of age or younger. To better understand EC in these young patients, we abstracted available data on all 109 young patients diagnosed with EC at Tenwek Hospital, Bomet District, Kenya from January 1996 through June 2009, including age at diagnosis, sex, ethnicity, tumor histology, residence location, and medical interventions. We also attempted to contact all patients or a family member and obtained information on ethnicity, tobacco and alcohol use, family history of cancer, and survival. Sixty (55%) representatives of the 109 young patients were successfully interviewed. The median survival time of these 60 patients was 6.4 months, the most common tumor histology was esophageal squamous cell carcinoma (ESCC) (98%), the M: F ratio was 1.4:1, and only a few subjects used tobacco (15%) or alcohol (15%). Seventy-nine percent reported a family history of cancer and 43% reported having a family history of EC. In summary, this case series describes the largest number of young EC patients reported to date, and it highlights the uniqueness of the EC experience in western Kenya.
C1 [Dawsey, Sonja P.; Dawsey, Sanford M.; Abnet, Christian C.] NCI, Nutr Epidemiol Branch, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA.
   [Tonui, Stanley; White, Russell E.] Tenwek Hosp, Bomet, Kenya.
   [Parker, Robert K.; White, Russell E.] Rhode Isl Hosp, Dept Surg, Providence, RI USA.
   [Parker, Robert K.; White, Russell E.] Brown Univ, Warren Alpert Med Sch, Providence, RI 02912 USA.
   [Fitzwater, John W.] Texas Tech Univ, Hlth Sci Ctr, Sch Med, Dept Surg, Lubbock, TX 79430 USA.
RP Dawsey, SP (reprint author), NCI, Nutr Epidemiol Branch, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA.
EM abnetc@mail.nih.gov
RI Abnet, Christian/C-4111-2015; 
OI Abnet, Christian/0000-0002-3008-7843; Dawsey, Sonja/0000-0003-1605-3994
FU Division of Cancer Epidemiology and Genetics of the National Cancer
   Institute
FX This work was supported in part by intramural funds from the Division of
   Cancer Epidemiology and Genetics of the National Cancer Institute. The
   funders had no role in study design, data collection and analysis,
   decision to publish, or preparation of the manuscript.
NR 58
TC 23
Z9 24
U1 4
U2 8
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 185 BERRY ST, STE 1300, SAN FRANCISCO, CA 94107 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD NOV 22
PY 2010
VL 5
IS 11
AR e14080
DI 10.1371/journal.pone.0014080
PG 6
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 683HW
UT WOS:000284467200013
PM 21124934
ER

PT J
AU Kulandasamy, R
   Adhikari, AV
   Stables, JP
AF Kulandasamy, Ravi
   Adhikari, Airody Vasudeva
   Stables, James P.
TI Design and Synthesis of New Amides and Thioamides Derived from
   3,4-Ethylenedioxythiophene as Potential Anticonvulsants
SO BULLETIN OF THE KOREAN CHEMICAL SOCIETY
LA English
DT Article
DE Thiophene; Thioamide; Amide; Anticonvulsant; Neurotoxicity
ID ANTIEPILEPTIC DRUGS; AGENTS; MICE
AB Five new series of 3,4-ethylenedioxythiophene derivatives carrying important pharamacophores, viz, amide, ester, ether and active secondary aryl moieties have been designed and synthesized through multistep reactions starting from thiodiglycolic ester and diethyl oxalate They have been characterized by elemental and spectral data All the target compounds have been screened for their anticonvulsant activity at three different models viz maximal electroshock (MES), subcutaneous metrazole (scMET), and 6 Hz screen and evaluated for their neurotoxicity in rotorod model Compound 6a emerged as lead with no neurotoxicity All the five series of compounds are safe in the toxicity studies at the maximum dose of 300 mg/kg of body weight Amongst the tested compounds, the ester pharmacophore with thioamide fragment has showed better activity than the other analogs
C1 [Kulandasamy, Ravi; Adhikari, Airody Vasudeva] Natl Inst Technol Karnataka, Dept Chem, Mangalore 575025, Karnataka, India.
   [Stables, James P.] NIH, Preclin Pharmacol Sect, Epilepsy Branch, Bethesda, MD 20892 USA.
RP Adhikari, AV (reprint author), Natl Inst Technol Karnataka, Dept Chem, Mangalore 575025, Karnataka, India.
NR 35
TC 5
Z9 5
U1 0
U2 3
PU KOREAN CHEMICAL SOC
PI SEOUL
PA 635-4 YEOGSAM-DONG, KANGNAM-GU, SEOUL 135-703, SOUTH KOREA
SN 0253-2964
J9 B KOREAN CHEM SOC
JI Bull. Korean Chem. Soc.
PD NOV 20
PY 2010
VL 31
IS 11
BP 3318
EP 3326
DI 10.5012/bkcs.2010.31.11.3318
PG 9
WC Chemistry, Multidisciplinary
SC Chemistry
GA 687QX
UT WOS:000284794100049
ER

PT J
AU Doroshow, JH
AF Doroshow, James H.
TI Selecting Systemic Cancer Therapy One Patient at a Time: Is There a Role
   for Molecular Profiling of Individual Patients With Advanced Solid
   Tumors?
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Editorial Material
ID CLINICAL-TRIAL DESIGN; BREAST-CANCER; ANTICANCER AGENTS; BIOMARKERS;
   CHEMOTHERAPY; BIOPSIES; LEUKEMIA; IMPACT
C1 NCI, Div Canc Treatment & Diag, NIH, Bethesda, MD 20892 USA.
RP Doroshow, JH (reprint author), NCI, Div Canc Treatment & Diag, NIH, Bethesda, MD 20892 USA.
NR 33
TC 24
Z9 24
U1 0
U2 2
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD NOV 20
PY 2010
VL 28
IS 33
BP 4869
EP 4871
DI 10.1200/JCO.2010.31.1472
PG 3
WC Oncology
SC Oncology
GA 681WC
UT WOS:000284353000012
PM 20921466
ER

PT J
AU Morton, LM
   Curtis, RE
   Linet, MS
   Bluhm, EC
   Tucker, MA
   Caporaso, N
   Ries, LAG
   Fraumeni, JF
AF Morton, Lindsay M.
   Curtis, Rochelle E.
   Linet, Martha S.
   Bluhm, Elizabeth C.
   Tucker, Margaret A.
   Caporaso, Neil
   Ries, Lynn A. G.
   Fraumeni, Joseph F., Jr.
TI Second Malignancy Risks After Non-Hodgkin's Lymphoma and Chronic
   Lymphocytic Leukemia: Differences by Lymphoma Subtype
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Article
ID EPIDEMIOLOGY CONSORTIUM INTERLYMPH; LUNG-CANCER; POOLED ANALYSIS;
   SECONDARY MALIGNANCIES; FAMILIAL AGGREGATION; INDOLENT LYMPHOMA;
   CIGARETTE-SMOKING; KIDNEY CANCER; THERAPY; PEOPLE
AB Purpose Previous studies have shown increased risks of second malignancies after non-Hodgkin's lymphoma (NHL) and chronic lymphocytic leukemia (CLL); however, no earlier investigation has quantified differences in risk of new malignancy by lymphoma subtype.
   Patients and Methods We evaluated second cancer and leukemia risks among 43,145 1-year survivors of CLL/small lymphocytic lymphoma (SLL), diffuse large B-cell lymphoma (DLBCL), or follicular lymphoma (FL) from 11 Surveillance, Epidemiology, and End Results (SEER) population-based registries during 1992 to 2006.
   Results Among patients without HIV/AIDS-related lymphoma, lung cancer risks were significantly elevated after CLL/SLL and FL but not after DLBCL (standardized incidence ratio [SIR], CLL/SLL = 1.42, FL = 1.28, DLBCL = 1.00; Poisson regression P for difference among subtypes, P(Diff) = .001). A similar pattern was observed for risk of cutaneous melanoma (SIR: CLL/SLL = 1.92, FL = 1.60, DLBCL = 1.06; P(Diff) = .004). Acute nonlymphocytic leukemia risks were significantly elevated after FL and DLBCL, particularly among patients receiving initial chemotherapy, but not after CLL/SLL (SIR: CLL/SLL = 1.13, FL = 5.96, DLBCL = 4.96; P(Diff) < .001). Patients with HIV/AIDS-related lymphoma (n = 932) were predominantly diagnosed with DLBCL and had significantly and substantially elevated risks for second anal cancer (SIR = 120.50) and Kaposi's sarcoma (SIR = 138.90).
   Conclusion Our findings suggest that differing immunologic alterations, treatments (eg, alkylating agent chemotherapy), genetic susceptibilities, and other risk factors (eg, viral infections, tobacco use) among lymphoma subtypes contribute to the patterns of second malignancy risk. Elucidating these patterns may provide etiologic clues to lymphoma as well as to the second malignancies. J Clin Oncol 28:4935-4944. (c) 2010 by American Society of Clinical Oncology
C1 Div Canc Epidemiol, Rockville, MD USA.
   Div Genet, Rockville, MD USA.
   Canc Control & Populat Sci, Bethesda, MD USA.
   [Morton, Lindsay M.] NCI, Div Canc Epidemiol & Genet, NIH, Dept Hlth & Human Serv, Rockville, MD 20892 USA.
   Washington Hosp Ctr, Gen Internal Med Sect, Washington, DC 20010 USA.
RP Morton, LM (reprint author), NCI, Div Canc Epidemiol & Genet, NIH, Dept Hlth & Human Serv, 6120 Execut Blvd,EPS 7040,MSC 7238, Rockville, MD 20892 USA.
EM mortonli@mail.nih.gov
RI Tucker, Margaret/B-4297-2015; Morton, Lindsay/B-5234-2015
OI Morton, Lindsay/0000-0001-9767-2310
FU National Cancer Institute, National Institutes of Health, Department of
   Health and Human Services
FX Supported by the Intramural Research Program of the National Cancer
   Institute, National Institutes of Health, Department of Health and Human
   Services.
NR 58
TC 64
Z9 70
U1 0
U2 2
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD NOV 20
PY 2010
VL 28
IS 33
BP 4935
EP 4944
DI 10.1200/JCO.2010.29.1112
PG 10
WC Oncology
SC Oncology
GA 681WC
UT WOS:000284353000023
PM 20940199
ER

PT J
AU Shusterman, S
   London, WB
   Gillies, SD
   Hank, JA
   Voss, SD
   Seeger, RC
   Reynolds, CP
   Kimball, J
   Albertini, MR
   Wagner, B
   Gan, J
   Eickhoff, J
   DeSantes, KB
   Cohn, SL
   Hecht, T
   Gadbaw, B
   Reisfeld, RA
   Maris, JM
   Sondel, PM
AF Shusterman, Suzanne
   London, Wendy B.
   Gillies, Stephen D.
   Hank, Jacquelyn A.
   Voss, Stephan D.
   Seeger, Robert C.
   Reynolds, C. Patrick
   Kimball, Jennifer
   Albertini, Mark R.
   Wagner, Barrett
   Gan, Jacek
   Eickhoff, Jens
   DeSantes, Kenneth B.
   Cohn, Susan L.
   Hecht, Toby
   Gadbaw, Brian
   Reisfeld, Ralph A.
   Maris, John M.
   Sondel, Paul M.
TI Antitumor Activity of Hu14.18-IL2 in Patients With Relapsed/Refractory
   Neuroblastoma: A Children's Oncology Group (COG) Phase II Study
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Article
ID COLONY-STIMULATING FACTOR; TARGETED INTERLEUKIN-2 THERAPY;
   MONOCLONAL-ANTIBODY CH14.18; BONE-MARROW-TRANSPLANTATION; HIGH-RISK
   NEUROBLASTOMA; STAGE-IV NEUROBLASTOMA; PLUS INTERLEUKIN-2; CANCER GROUP;
   REFRACTORY NEUROBLASTOMA; CELLULAR CYTOTOXICITY
AB Purpose
   The hu14.18-IL2 fusion protein consists of interleukin-2 molecularly linked to a humanized monoclonal antibody that recognizes the GD2 disialoganglioside expressed on neuroblastoma cells. This phase II study assessed the antitumor activity of hu14.18-IL2 in two strata of patients with recurrent or refractory neuroblastoma.
   Patients and Methods
   Hu14.18-IL2 was given intravenously (12 mg/m(2)/daily) for 3 days every 4 weeks for patients with disease measurable by standard radiographic criteria (stratum 1) and for patients with disease evaluable only by [(123)I] metaiodobenzylguanidine (MIBG) scintigraphy and/or bone marrow (BM) histology (stratum 2). Response was established by independent radiology review as well as BM histology and immunocytology, and durability was assessed by repeat evaluation after more than 3 weeks.
   Results
   Thirty-nine patients were enrolled (36 evaluable). No responses were seen in stratum 1 (n = 13). Of 23 evaluable patients in stratum 2, five patients (21.7%) responded; all had a complete response (CR) of 9, 13, 20, 30, and 35+ months duration. Grade 3 and 4 nonhematologic toxicities included capillary leak, hypoxia, pain, rash, allergic reaction, elevated transaminases, and hyper-bilirubinemia. Two patients required dopamine for hypotension, and one patient required ventilatory support for hypoxia. Most toxicities were reversible within a few days of completing a treatment course and were expected based on phase I results.
   Conclusion
   Patients with disease evaluable only by MIBG and/or BM histology had a 21.7% CR rate to hu14.8-IL2, whereas patients with bulky disease did not respond. Hu14.18-IL2 warrants further testing in children with nonbulky high-risk neuroblastoma.
   J Clin Oncol 28:4969-4975. (C) 2010 by American Society of Clinical Oncology
C1 Dana Farber Canc Inst, Boston, MA 02115 USA.
   Childrens Hosp Boston, Boston, FL USA.
   Childrens Oncol Grp Stat & Data Ctr, Gainesville, FL USA.
   Provenance Biopharmaceut, Waltham, MA USA.
   Univ Wisconsin, Carbone Canc Ctr, Madison, WI USA.
   Childrens Hosp Los Angeles, Los Angeles, CA 90027 USA.
   Scripps Res Inst, La Jolla, CA USA.
   Univ Texas, Lubbock, TX USA.
   Univ Chicago, Chicago, IL 60637 USA.
   NCI, Biol Resources Branch, Frederick, MD 21701 USA.
   Childrens Hosp Philadelphia, Philadelphia, PA 19104 USA.
RP Sondel, PM (reprint author), UW Madison, Wisconsin Inst Med Res, Dept Pediat, MACC Fund Childhood Canc Res Wing 4159, 1111 Highland Ave, Madison, WI 53792 USA.
EM pmsondel@humonc.wisc.edu
OI Reynolds, C. Patrick/0000-0002-2827-8536; Cohn,
   Susan/0000-0001-5749-7650
FU National Institutes of Health (NIH)/National Cancer Institute (NCI)
   [U10CA98543, U10 CA98413, R01-CA-32685-25, CA87025, CA81403, RR03186];
   Midwest Athletes for Childhood Cancer Fund; Crawdaddy Foundation; Evan
   Dunbar Foundation; EMD Pharmaceuticals
FX Supported by National Institutes of Health (NIH)/National Cancer
   Institute (NCI) Grant No. U10CA98543 (Children's Oncology Group [COG]
   Group Chair), NIH/NCI Grant No. U10 CA98413 (COG Statistics and Data
   Center), and NIH/NCI Grants No. R01-CA-32685-25, CA87025, CA81403, and
   RR03186, and grants from the Midwest Athletes for Childhood Cancer Fund,
   the Crawdaddy Foundation, and The Evan Dunbar Foundation. Hu14.18-IL2
   (EMD 273063) was produced through a Material Cooperative Research and
   Development Agreement between the NCI and Merck KGaA.; Mark R.
   Albertini, EMD Pharmaceuticals
NR 43
TC 83
Z9 86
U1 0
U2 11
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD NOV 20
PY 2010
VL 28
IS 33
BP 4969
EP 4975
DI 10.1200/JCO.2009.27.8861
PG 7
WC Oncology
SC Oncology
GA 681WC
UT WOS:000284353000027
PM 20921469
ER

PT J
AU Jankowska, A
   Ko, M
   Huang, Y
   Pape, UJ
   Szpurka, H
   Tahiliani, M
   Bandukwala, HS
   An, J
   Lamperti, ED
   Koh, KP
   Liu, XS
   Aravind, L
   Agarwal, S
   Rao, A
   Maciejewski, JP
AF Jankowska, Anna
   Ko, Myunggon
   Huang, Yun
   Pape, Utz J.
   Szpurka, Hadrian
   Tahiliani, Mamta
   Bandukwala, Hozefa S.
   An, Jungeun
   Lamperti, Edward D.
   Koh, Kian Peng
   Liu, X. Shirley
   Aravind, L.
   Agarwal, Suneet
   Rao, Anjana
   Maciejewski, Jaroslaw P.
TI Impaired Hydroxilation of 5-Methylcytosine In TET2 mutated Patients with
   Myeloid Malignancies
SO BLOOD
LA English
DT Meeting Abstract
CT 52nd Annual Meeting of the American-Society-of-Hematology (ASH)
CY DEC 04-07, 2010
CL Orlando, FL
SP Amer Soc Hematol
C1 [Jankowska, Anna; Szpurka, Hadrian; Maciejewski, Jaroslaw P.] Cleveland Clin, Taussig Canc Inst, Cleveland, OH 44106 USA.
   [Ko, Myunggon; Huang, Yun; Tahiliani, Mamta; Bandukwala, Hozefa S.; An, Jungeun; Lamperti, Edward D.; Koh, Kian Peng; Rao, Anjana] Harvard Univ, Sch Med, Dept Pathol, Immune Dis Inst, Boston, MA 02115 USA.
   [Ko, Myunggon; Huang, Yun; Tahiliani, Mamta; Bandukwala, Hozefa S.; An, Jungeun; Lamperti, Edward D.; Koh, Kian Peng; Rao, Anjana] Program Cellular & Mol Med, Boston, MA USA.
   [Pape, Utz J.; Liu, X. Shirley] Dana Farber Canc Inst, Dept Biostat & Computat Biol, Boston, MA 02115 USA.
   [Pape, Utz J.; Liu, X. Shirley] Harvard Univ, Sch Publ Hlth, Boston, MA 02115 USA.
   [Aravind, L.] NIH, Natl Ctr Biotechnol Informat, Natl Lib Med, Bethesda, MD 20892 USA.
   [Agarwal, Suneet] Childrens Hosp, Div Pediat Hematol, Boston, MA 02115 USA.
NR 0
TC 1
Z9 1
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 19
PY 2010
VL 116
IS 21
BP 3
EP 3
PG 1
WC Hematology
SC Hematology
GA 752BH
UT WOS:000289662200002
ER

PT J
AU Swaminathan, S
   Klemm, L
   Kweon, SM
   Ford, A
   Schwarz, K
   Casellas, R
   Hennighausen, L
   Schatz, DG
   Lieber, MR
   Greaves, MF
   Muschen, M
AF Swaminathan, Srividya
   Klemm, Lars
   Kweon, Soo-mi
   Ford, Anthony
   Schwarz, Klaus
   Casellas, Rafael
   Hennighausen, Lothar
   Schatz, David G.
   Lieber, Michael R.
   Greaves, Mel F.
   Muschen, Markus
TI IL7R alpha Signaling Prevents Premature Expression of AID In Human Pre-B
   Cells: Implications for Clonal Evolution of Childhood Leukemia
SO BLOOD
LA English
DT Meeting Abstract
CT 52nd Annual Meeting of the American-Society-of-Hematology (ASH)
CY DEC 04-07, 2010
CL Orlando, FL
SP Amer Soc Hematol
C1 [Swaminathan, Srividya; Klemm, Lars; Kweon, Soo-mi; Muschen, Markus] Univ Calif San Francisco, Dept Lab Med, San Francisco, CA 94143 USA.
   [Ford, Anthony] Inst Canc Res, Sect Haematol Oncol, Sutton, Surrey, England.
   [Schwarz, Klaus] Univ Hosp Ulm, Inst Transfus Med, Ulm, Germany.
   [Casellas, Rafael] NIAMS, Genome Integr Grp, Bethesda, MD USA.
   [Hennighausen, Lothar] NIDDK, Bethesda, MD USA.
   [Schatz, David G.] Yale Univ, Dept Immunol, New Haven, CT USA.
   [Lieber, Michael R.] Univ So Calif, Los Angeles, CA USA.
   [Greaves, Mel F.] Inst Canc Res, Sect Haematooncol, Surrey, England.
RI Schatz, David/A-6748-2013
OI Schatz, David/0000-0002-5669-1176
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 19
PY 2010
VL 116
IS 21
BP 16
EP 16
PG 1
WC Hematology
SC Hematology
GA 752BH
UT WOS:000289662200027
ER

PT J
AU Krishnan, A
   Pasquini, MC
   Ewell, M
   Stadtmauer, EA
   Alyea, EP
   Antin, JH
   Comenzo, RL
   Goodman, S
   Hari, P
   Negrin, R
   Qazilbash, MH
   Rowley, SD
   Sahebi, F
   Somlo, G
   Vesole, DH
   Vogl, DT
   Weisdorf, DJ
   Geller, N
   Horowitz, MM
   Giralt, S
   Maloney, DG
AF Krishnan, Amrita
   Pasquini, Marcelo C.
   Ewell, Marian
   Stadtmauer, Edward A.
   Alyea, Edwin P., III
   Antin, Joseph H.
   Comenzo, Raymond L.
   Goodman, Stacey
   Hari, Parameswaran
   Negrin, Robert
   Qazilbash, Muzaffar H.
   Rowley, Scott D.
   Sahebi, Firoozeh
   Somlo, George
   Vesole, David H.
   Vogl, Dan T.
   Weisdorf, Daniel J.
   Geller, Nancy
   Horowitz, Mary M.
   Giralt, Sergio
   Maloney, David G.
TI Tandem Autologous Hematopoietic Stem Cell Transplants (AuHCT) with or
   without Maintenance Therapy (auto-auto) Versus Single AuHCT Followed by
   HLA Matched Sibling Non- Myeloablative Allogeneic HCT (auto-allo) for
   Patients with Standard Risk (SR) Multiple Myeloma (MM): Results From the
   Blood and Marrow Transplant Clinical Trials Network (BMT CTN) 0102 Trial
SO BLOOD
LA English
DT Meeting Abstract
CT 52nd Annual Meeting of the American-Society-of-Hematology (ASH)
CY DEC 04-07, 2010
CL Orlando, FL
SP Amer Soc Hematol
C1 [Krishnan, Amrita] City Hope Natl Med Ctr, Hematol & Stem Cell Transplantat, Duarte, CA USA.
   [Hari, Parameswaran] Med Coll Wisconsin, Ctr Int Blood & Marrow Transplant Res, Milwaukee, WI 53226 USA.
   [Ewell, Marian] EMMES Corp, Rockville, MD USA.
   [Stadtmauer, Edward A.] Univ Penn, Myeloma Program, Abramson Canc Ctr, Philadelphia, PA 19104 USA.
   [Antin, Joseph H.] Dana Farber Canc Inst, Div Hematol Malignancies, Boston, MA 02115 USA.
   [Comenzo, Raymond L.] Tufts Med Ctr, Boston, MA USA.
   [Goodman, Stacey; Horowitz, Mary M.] Vanderbilt Univ, Nashville, TN USA.
   [Negrin, Robert] Stanford Univ, Stanford, CA 94305 USA.
   [Qazilbash, Muzaffar H.] UT MD Anderson Canc Ctr, SCT CT Unit 423, Houston, TX USA.
   [Rowley, Scott D.] Hackensack Univ, Med Ctr, John Theurer Canc Ctr, Div Blood & Marrow Transplantat, Hackensack, NJ USA.
   [Sahebi, Firoozeh] City Hope Natl Med Ctr, Kaiser Permanente Med Grp, Duarte, CA 91010 USA.
   [Weisdorf, Daniel J.] Univ Minnesota, Med Ctr, Minneapolis, MN 55455 USA.
   [Geller, Nancy] NHLBI, Bethesda, MD 20892 USA.
   [Giralt, Sergio] Mem Sloan Kettering Canc Ctr, New York, NY 10021 USA.
   [Maloney, David G.] Fred Hutchinson Canc Res Ctr, Seattle, WA 98104 USA.
   [Maloney, David G.] Univ Washington, Seattle, WA 98195 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 19
PY 2010
VL 116
IS 21
BP 24
EP 25
PG 2
WC Hematology
SC Hematology
GA 752BH
UT WOS:000289662200042
ER

PT J
AU Karp, JE
   Pagel, JM
   Smith, BD
   Greer, JM
   Drye, DM
   Smith, KM
   Dorcy, K
   Wright, JJ
   Doyle, LA
   Garrett-Mayer, E
   Estey, EH
AF Karp, Judith E.
   Pagel, John M.
   Smith, B. Douglas
   Greer, Jacqueline M.
   Drye, D. Michelle
   Smith, Kelly M.
   Dorcy, Kathleen
   Wright, John J.
   Doyle, L. Austin
   Garrett-Mayer, Elizabeth
   Estey, Elihu H.
TI Randomized Phase II Study of Two Schedules of Flavopiridol (Alvocidib,
   F) Given as Timed Sequential Therapy (TST) Wtih Ara-C and Mitoxantrone
   (FLAM) for Adults with Newly Diagnosed, Poor-Risk Acute Myelogenous
   Leukemia (AML)
SO BLOOD
LA English
DT Meeting Abstract
CT 52nd Annual Meeting of the American-Society-of-Hematology (ASH)
CY DEC 04-07, 2010
CL Orlando, FL
SP Amer Soc Hematol
C1 [Karp, Judith E.] Kimmel Comprehens Canc Ctr John Hopkins, Div Hematol Malignancies, Baltimore, MD USA.
   [Estey, Elihu H.] Fred Hutchinson Canc Res Ctr, Div Clin Res, Seattle, WA 98104 USA.
   [Smith, B. Douglas; Drye, D. Michelle] Kimmel Canc Ctr, Baltimore, MD USA.
   [Greer, Jacqueline M.] Johns Hopkins Univ, Div Hematol Malignancies, Sidney Kimmel Canc Ctr, Baltimore, MD USA.
   [Smith, Kelly M.] Univ Washington, Med Ctr, Tukwila, WA USA.
   [Wright, John J.; Doyle, L. Austin] NCI, Bethesda, MD 20892 USA.
   [Garrett-Mayer, Elizabeth] Med Univ S Carolina, Charleston, SC 29425 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 19
PY 2010
VL 116
IS 21
BP 85
EP 85
PG 1
WC Hematology
SC Hematology
GA 752BH
UT WOS:000289662200187
ER

PT J
AU Savage, SA
   Zhong, F
   Giri, N
   Jessop, L
   Myers, T
   Chen, R
   Alter, BP
   Artandi, S
AF Savage, Sharon. A.
   Zhong, Franklin
   Giri, Neelam
   Jessop, Lea
   Myers, Timothy
   Chen, Renee
   Alter, Blanche P.
   Artandi, Steven
TI Mutations In TCAB1 Cause Dyskeratosis Congenita
SO BLOOD
LA English
DT Meeting Abstract
CT 52nd Annual Meeting of the American-Society-of-Hematology (ASH)
CY DEC 04-07, 2010
CL Orlando, FL
SP Amer Soc Hematol
C1 [Savage, Sharon. A.; Giri, Neelam] NCI, Clin Genet Branch, Div Canc Epidemiol & Genet, Rockville, MD USA.
   [Zhong, Franklin] Stanford Univ, Sch Med, Stanford, CA 94305 USA.
   [Jessop, Lea; Chen, Renee] NCI, Lab Translat Genom, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA.
   [Myers, Timothy] NCI Frederick, Core Genotyping Facil, SAIC Frederick, Gaithersburg, MD USA.
   [Artandi, Steven] Stanford Univ, Dept Hematol, Stanford, CA 94305 USA.
RI Savage, Sharon/B-9747-2015
OI Savage, Sharon/0000-0001-6006-0740
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 19
PY 2010
VL 116
IS 21
BP 90
EP 91
PG 2
WC Hematology
SC Hematology
GA 752BH
UT WOS:000289662200198
ER

PT J
AU Bjorkholm, M
   Ohm, L
   Eloranta, S
   Derolf, AR
   Hultcrantz, M
   Sjoberg, J
   Andersson, T
   Hoglund, M
   Richter, J
   Landgren, O
   Kristinsson, SY
   Dickman, PW
AF Bjorkholm, Magnus
   Ohm, Lotta
   Eloranta, Sandra
   Derolf, Asa Rangert
   Hultcrantz, Malin
   Sjoberg, Jan
   Andersson, Therese
   Hoglund, Martin
   Richter, Johan
   Landgren, Ola
   Kristinsson, Sigurdur Y.
   Dickman, Paul W.
TI The Success Story of Targeted Therapy In Chronic Myeloid Leukemia: A
   Population-Based Study of 3,173 Patients Diagnosed In Sweden 1973-2008
SO BLOOD
LA English
DT Meeting Abstract
CT 52nd Annual Meeting of the American-Society-of-Hematology (ASH)
CY DEC 04-07, 2010
CL Orlando, FL
SP Amer Soc Hematol
C1 [Bjorkholm, Magnus; Ohm, Lotta; Derolf, Asa Rangert; Hultcrantz, Malin; Sjoberg, Jan; Kristinsson, Sigurdur Y.] Karolinska Univ Hosp, Dept Med, Div Hematol, Stockholm, Sweden.
   [Eloranta, Sandra; Andersson, Therese; Dickman, Paul W.] Karolinska Inst, Dept Med Epidemiol & Biostat, Stockholm, Sweden.
   [Hoglund, Martin] Uppsala Univ, Dept Internal Med, Uppsala, Sweden.
   [Richter, Johan] Lund Univ, Cent Hosp, Lund, Sweden.
   [Landgren, Ola] NCI, Med Oncol Branch, NIH, Bethesda, MD 20892 USA.
RI Kristinsson, Sigurdur /M-2910-2015; Andersson, Therese/E-7107-2016
OI Kristinsson, Sigurdur /0000-0002-4964-7476; Andersson,
   Therese/0000-0001-8644-9041
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 19
PY 2010
VL 116
IS 21
BP 93
EP 94
PG 2
WC Hematology
SC Hematology
GA 752BH
UT WOS:000289662200206
ER

PT J
AU Jacobsohn, DA
   Arora, M
   Klein, JP
   Antin, JH
   Bolwell, BJ
   Boyiadzis, M
   Cahn, JY
   Cairo, M
   Cutler, CS
   Flowers, MED
   Gale, RP
   Hassebroek, A
   Herzig, RH
   Horowitz, MM
   Isola, L
   Klumpp, TR
   Lee, SJ
   Petersdorf, EW
   Santarone, S
   Schouten, HC
   Spellman, S
   Urbano, A
   Weisdorf, DJ
   Wingard, JR
   Pavletic, SZ
AF Jacobsohn, David A.
   Arora, Mukta
   Klein, John P.
   Antin, Joseph H.
   Bolwell, Brian J.
   Boyiadzis, Michael
   Cahn, Jean-Yves
   Cairo, Mitchell S.
   Cutler, Corey S.
   Flowers, Mary E. D.
   Gale, Robert P.
   Hassebroek, Anna
   Herzig, Roger H.
   Horowitz, Mary M.
   Isola, Luis
   Klumpp, Thomas R.
   Lee, Stephanie J.
   Petersdorf, Effie W.
   Santarone, Stella
   Schouten, Harry C.
   Spellman, Stephen
   Urbano, Alvaro
   Weisdorf, Daniel J.
   Wingard, John R.
   Pavletic, Steven Z.
TI Risk Factors for Major Transplant Related Outcomes In Pediatric Patients
   with Chronic Graft-Versus-Host Disease
SO BLOOD
LA English
DT Meeting Abstract
CT 52nd Annual Meeting of the American-Society-of-Hematology (ASH)
CY DEC 04-07, 2010
CL Orlando, FL
SP Amer Soc Hematol
C1 [Jacobsohn, David A.] Childrens Natl Med Ctr, Washington, DC 20010 USA.
   [Klein, John P.] Med Coll Wisconsin, Dept Biostat, Ctr Int Blood & Marrow Transplant Res, Milwaukee, WI 53226 USA.
   [Antin, Joseph H.; Cutler, Corey S.] Dana Farber Canc Inst, Div Hematol Malignancies, Boston, MA 02115 USA.
   [Bolwell, Brian J.] Cleveland Clin, Taussig Canc Inst, Cleveland, OH 44106 USA.
   [Boyiadzis, Michael] Univ Pittsburgh, Inst Canc, Pittsburgh, PA USA.
   [Cahn, Jean-Yves] CHU Grenoble, F-38043 Grenoble, France.
   [Cairo, Mitchell S.] Columbia Univ, New York Presbyterian Morgan Stanley Childrens Ho, New York, NY USA.
   [Flowers, Mary E. D.] Univ Washington, Seattle, WA 98195 USA.
   [Lee, Stephanie J.] Fred Hutchinson Canc Res Ctr, Div Clin Res, Seattle, WA 98104 USA.
   [Gale, Robert P.] Celgene Corp, Summit, NJ USA.
   [Hassebroek, Anna] Ctr Int Blood & Marrow Transplant Res, Minneapolis, MN USA.
   [Herzig, Roger H.] Univ Louisville, James Graham Brown Canc Ctr, BMT, Louisville, KY 40292 USA.
   [Isola, Luis] Mt Sinai Med Ctr, BMT, New York, NY 10029 USA.
   [Klumpp, Thomas R.] Temple Univ, Wynnewood, PA USA.
   [Santarone, Stella] Osped Civile, BMT Ctr, Pescara, Italy.
   [Schouten, Harry C.] Acad Ziekenhuis Maastricht, Maastricht, Netherlands.
   [Urbano, Alvaro] Hosp Clin Barcelona, Dept Hematol, Barcelona, Spain.
   [Weisdorf, Daniel J.] Univ Minnesota, Med Ctr, Minneapolis, MN 55455 USA.
   [Wingard, John R.] Univ Florida, Shands Canc Ctr, Gainesville, FL USA.
   [Pavletic, Steven Z.] NCI, Expt Transplantat & Immunol Branch, Ctr Canc Res, 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 19
PY 2010
VL 116
IS 21
BP 97
EP 98
PG 2
WC Hematology
SC Hematology
GA 752BH
UT WOS:000289662200212
ER

PT J
AU Arai, S
   Jagasia, M
   Arora, M
   Miklos, D
   Chai, XY
   Storer, B
   Martin, PJ
   Cutler, C
   Weisdorf, DJ
   Pidala, J
   Palmer, J
   Flowers, M
   Jacobsohn, D
   Carpenter, PA
   Pavletic, SZ
   Vogelsang, GB
   Lee, SJ
AF Arai, Sally
   Jagasia, Madan
   Arora, Mukta
   Miklos, David
   Chai, Xiaoyu
   Storer, Barry
   Martin, Paul J.
   Cutler, Corey
   Weisdorf, Daniel J.
   Pidala, Joseph
   Palmer, Jeanne
   Flowers, Mary
   Jacobsohn, David
   Carpenter, Paul A.
   Pavletic, Steven Z.
   Vogelsang, Georgia B.
   Lee, Stephanie J.
TI Chronic Gvhd Global Severity According to NIH Consensus Criteria:
   Results From the Chronic Gvhd Consortium
SO BLOOD
LA English
DT Meeting Abstract
CT 52nd Annual Meeting of the American-Society-of-Hematology (ASH)
CY DEC 04-07, 2010
CL Orlando, FL
SP Amer Soc Hematol
C1 [Miklos, David] Stanford Univ, Sch Med, Div Blood & Marrow Transplantat, Stanford, CA 94305 USA.
   [Jagasia, Madan] Vanderbilt Univ, Med Ctr, Nashville, TN USA.
   [Weisdorf, Daniel J.] Univ Minnesota, Med Ctr, Minneapolis, MN 55455 USA.
   [Chai, Xiaoyu; Storer, Barry; Flowers, Mary; Carpenter, Paul A.; Lee, Stephanie J.] Fred Hutchinson Canc Res Ctr, Seattle, WA 98104 USA.
   [Storer, Barry; Flowers, Mary; Carpenter, Paul A.] Univ Washington, Seattle, WA 98195 USA.
   [Martin, Paul J.] FRED HUTCHINSON CNCR RES CT, Seattle, WA USA.
   [Cutler, Corey] Dana Farber Canc Inst, Div Hematol Malignancies, Boston, MA 02115 USA.
   [Pidala, Joseph] H Lee Moffitt Canc Ctr & Res Inst, Tampa, FL USA.
   [Palmer, Jeanne] Childrens Hosp Wisconsin, Milwaukee, WI 53201 USA.
   [Jacobsohn, David] Childrens Mem Hosp, Stem Cell Transplant Program, Chicago, IL 60614 USA.
   [Pavletic, Steven Z.] NCI, Expt Transplantat & Immunol Branch, Ctr Canc Res, NIH, Bethesda, MD USA.
   [Vogelsang, Georgia B.] Johns Hopkins Univ Hosp, Baltimore, MD 21287 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 19
PY 2010
VL 116
IS 21
BP 102
EP 103
PG 2
WC Hematology
SC Hematology
GA 752BH
UT WOS:000289662200221
ER

PT J
AU Kean, L
   Sen, S
   Metzger, ME
   Bonifacino, A
   Singh, K
   Donahue, RE
AF Kean, Leslie
   Sen, Sharon
   Metzger, Mark E.
   Bonifacino, Aylin
   Singh, Karnail
   Donahue, Robert E.
TI Probing the Impact of AMD3100/GCSF Mobilization on the Peripheral Blood
   T Cell Content Using a Rhesus Macaque Model: Increased Proportions of
   FoxP3+/CD4+T Cells Occur After Mobilization and Leukapheresis
SO BLOOD
LA English
DT Meeting Abstract
CT 52nd Annual Meeting of the American-Society-of-Hematology (ASH)
CY DEC 04-07, 2010
CL Orlando, FL
SP Amer Soc Hematol
C1 [Kean, Leslie] Aflac Canc Ctr, Emory Transplant Ctr, Dept Pediat, Atlanta, GA USA.
   [Kean, Leslie] Aflac Canc Ctr, Dept Surg, Atlanta, GA USA.
   [Kean, Leslie] Blood Disorders Serv, Atlanta, GA USA.
   [Sen, Sharon; Singh, Karnail] Emory Univ, Atlanta, GA 30322 USA.
   [Metzger, Mark E.; Bonifacino, Aylin; Donahue, Robert E.] NHLBI, Hematol 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 19
PY 2010
VL 116
IS 21
BP 157
EP 158
PG 2
WC Hematology
SC Hematology
GA 752BH
UT WOS:000289662200351
ER

PT J
AU Switzer, GE
   Harrington, D
   Haagenson, MD
   Drexler, R
   Foley, A
   Confer, DL
   Bishop, M
   Anderlini, P
   Rowley, SD
   Leitman, S
   Anasetti, C
   Wingard, JR
AF Switzer, Galen E.
   Harrington, Donna
   Haagenson, Michael D.
   Drexler, Rebecca
   Foley, Amy
   Confer, Dennis L.
   Bishop, Michelle
   Anderlini, Paolo
   Rowley, Scott D.
   Leitman, Susan
   Anasetti, Claudio
   Wingard, John R.
TI Health-Related Quality-of-Life Among Adult Matched Unrelated Stem Cell
   Donors: A Blood and Marrow Transplant Clinical Trials Network (BMT CTN)
   Randomized Trial of Marrow Versus PBSC Donation
SO BLOOD
LA English
DT Meeting Abstract
CT 52nd Annual Meeting of the American-Society-of-Hematology (ASH)
CY DEC 04-07, 2010
CL Orlando, FL
SP Amer Soc Hematol
C1 [Harrington, Donna] Univ Pittsburgh, Med Ctr, Pittsburgh, PA USA.
   [Drexler, Rebecca] CIBMTR, Natl Marrow Donor Program, Minneapolis, MN USA.
   [Foley, Amy] Univ Minnesota, Dept Orthopaed, Natl Marrow Donor Program, St Paul, MN 55108 USA.
   [Bishop, Michelle] Univ Florida, Gainesville, FL USA.
   [Anderlini, Paolo] Univ Texas MD Anderson Canc Ctr, Houston, TX 77030 USA.
   [Rowley, Scott D.] Hackensack Univ Med Ctr, Div Blood & Marrow Transplantat, John Theurer Canc Ctr, Hackensack, NJ USA.
   [Leitman, Susan] NIH, Dept Transfus Med, Ctr Clin, Bethesda, MD 20892 USA.
   [Anasetti, Claudio] H Lee Moffitt Canc Ctr & Res Inst, Tampa, FL USA.
   [Wingard, John R.] Univ Florida, Shands Canc Ctr, Gainesville, FL 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 19
PY 2010
VL 116
IS 21
BP 165
EP 166
PG 2
WC Hematology
SC Hematology
GA 752BH
UT WOS:000289662200367
ER

PT J
AU Pidala, J
   Kurland, B
   Chai, S
   Majhail, NS
   Weisdorf, DJ
   Cutler, C
   Jagasia, M
   Palmer, J
   Arora, M
   Martin, PJ
   Jacobsohn, D
   Vogelsang, GB
   Pavletic, SZ
   Lee, SJ
AF Pidala, Joseph
   Kurland, Brenda
   Chai, Shawn
   Majhail, Navneet S.
   Weisdorf, Daniel J.
   Cutler, Corey
   Jagasia, Madan
   Palmer, Jeanne
   Arora, Mukta
   Martin, Paul J.
   Jacobsohn, David
   Vogelsang, Georgia B.
   Pavletic, Steven Z.
   Lee, Stephanie J.
TI Quality of Life and Chronic Gvhd Severity According to the NIH Criteria:
   Results From the Chronic Gvhd Consortium
SO BLOOD
LA English
DT Meeting Abstract
CT 52nd Annual Meeting of the American-Society-of-Hematology (ASH)
CY DEC 04-07, 2010
CL Orlando, FL
SP Amer Soc Hematol
C1 [Pidala, Joseph] H Lee Moffitt Canc Ctr & Res Inst, Tampa, FL USA.
   [Kurland, Brenda; Chai, Shawn; Martin, Paul J.; Lee, Stephanie J.] Fred Hutchinson Canc Res Ctr, Seattle, WA 98104 USA.
   [Weisdorf, Daniel J.] Univ Minnesota, Med Ctr, Minneapolis, MN 55455 USA.
   [Cutler, Corey] Dana Farber Canc Inst, Div Hematol Malignancies, Boston, MA 02115 USA.
   [Jagasia, Madan] Vanderbilt Univ, Med Ctr, Nashville, TN USA.
   [Palmer, Jeanne] Childrens Hosp Wisconsin, Milwaukee, WI 53201 USA.
   [Jacobsohn, David] Childrens Mem Hosp, Stem Cell Transplant Program, Chicago, IL 60614 USA.
   [Vogelsang, Georgia B.] Johns Hopkins Univ Hosp, Baltimore, MD 21287 USA.
   [Pavletic, Steven Z.] NCI, Expt Transplantat & Immunol Branch, Ctr Canc Res, NIH, 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 19
PY 2010
VL 116
IS 21
BP 176
EP 176
PG 1
WC Hematology
SC Hematology
GA 752BH
UT WOS:000289662200394
ER

PT J
AU Mullighan, C
   Zhang, JH
   Kasper, LH
   Lerach, S
   Payne-Turner, D
   Phillips, LA
   Collins-Underwood, JR
   Heatley, SL
   Ma, J
   Buetow, K
   Pui, CH
   Brindle, PK
   Downing, JR
AF Mullighan, Charles
   Zhang, Jinghui
   Kasper, Lawryn H.
   Lerach, Stephanie
   Payne-Turner, Debbie
   Phillips, Letha A.
   Collins-Underwood, J. Racquel
   Heatley, Susan L.
   Ma, Jing
   Buetow, Kenneth
   Pui, Ching-Hon
   Brindle, Paul K.
   Downing, James R.
TI CREBBP Mutations In Relapsed Acute Lymphoblastic Leukemia
SO BLOOD
LA English
DT Meeting Abstract
CT 52nd Annual Meeting of the American-Society-of-Hematology (ASH)
CY DEC 04-07, 2010
CL Orlando, FL
SP Amer Soc Hematol
C1 [Ma, Jing] St Jude Childrens Hosp, Hartwell Ctr Bioinformat & Biotechnol, Memphis, TN 38105 USA.
   [Buetow, Kenneth] NCI, Ctr Bioinformat, 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 19
PY 2010
VL 116
IS 21
BP 184
EP 184
PG 1
WC Hematology
SC Hematology
GA 752BH
UT WOS:000289662200414
ER

PT J
AU Keersmaecker, KD
   Real, PJ
   Della Gatta, G
   Palomero, T
   Sulis, ML
   Tosello, V
   Van Vlierberghe, P
   Barnes, K
   Castillo, M
   Sole, X
   Hadler, M
   Lenz, J
   Aplan, P
   Kelliher, M
   Kee, BL
   Pandolfi, PP
   Kappes, D
   Gounari, F
   Petrie, H
   Van der Meulen, J
   Speleman, F
   Paietta, E
   Racevskis, J
   Tallman, M
   Rowe, JM
   Soulier, J
   Avran, D
   Cave, H
   Dastugue, N
   Raimondi, SC
   Meijerink, J
   Cordon-Cardo, C
   Califano, A
   Ferrando, A
AF Keersmaecker, Kim De
   Jose Real, Pedro
   Della Gatta, Giusy
   Palomero, Teresa
   Sulis, Maria Luisa
   Tosello, Valeria
   Van Vlierberghe, Pieter
   Barnes, Kelly
   Castillo, Mireia
   Sole, Xavier
   Hadler, Michael
   Lenz, Jack
   Aplan, Peter
   Kelliher, Michelle
   Kee, Barbara L.
   Pandolfi, Pier Paolo
   Kappes, Dietmar
   Gounari, Fotini
   Petrie, Howard
   Van der Meulen, Joni
   Speleman, Frank
   Paietta, Elisabeth
   Racevskis, Janis
   Tallman, Martin
   Rowe, Jacob M.
   Soulier, Jean
   Avran, David
   Cave, Helene
   Dastugue, Nicole
   Raimondi, Susana C.
   Meijerink, Jules
   Cordon-Cardo, Carlos
   Califano, Andrea
   Ferrando, Adolfo
TI BCL11B Mutations In T-Cell Acute Lymphoblastic Leukemia
SO BLOOD
LA English
DT Meeting Abstract
CT 52nd Annual Meeting of the American-Society-of-Hematology (ASH)
CY DEC 04-07, 2010
CL Orlando, FL
SP Amer Soc Hematol
C1 [Keersmaecker, Kim De; Della Gatta, Giusy; Palomero, Teresa; Sulis, Maria Luisa; Tosello, Valeria; Van Vlierberghe, Pieter; Barnes, Kelly; Castillo, Mireia; Hadler, Michael; Ferrando, Adolfo] Columbia Univ, Inst Canc Genet, New York, NY USA.
   [Jose Real, Pedro] Andalusian Stem Cell Bank, Granada, Spain.
   [Sole, Xavier] IDIBELL Inst Catala Oncol, Barcelona, Spain.
   [Lenz, Jack] Albert Einstein Coll Med, Dept Mol Genet, New York, NY USA.
   [Aplan, Peter] NIH, Bethesda, MD 20892 USA.
   [Kelliher, Michelle] Univ Massachusetts, Sch Med, Dept Canc Biol, Worcester, MA USA.
   [Kelliher, Michelle] Univ Massachusetts, Sch Med, Ctr Canc, Worcester, MA USA.
   [Kee, Barbara L.] Univ Chicago, Dept Pathol, Chicago, IL 60637 USA.
   [Pandolfi, Pier Paolo] Harvard Univ, Sch Med, Beth Israel Deaconess Med Ctr, Boston, MA USA.
   [Kappes, Dietmar] Fox Chase Canc Ctr, Philadelphia, PA 19111 USA.
   [Gounari, Fotini] Univ Chicago, Dept Med, Chicago, IL 60637 USA.
   [Petrie, Howard] Scripps Res Inst, Dept Canc Biol, Jupiter, FL USA.
   [Van der Meulen, Joni; Speleman, Frank] Ghent Univ Hosp, Ctr Med Genet, B-9000 Ghent, Belgium.
   [Paietta, Elisabeth; Racevskis, Janis] Montefiore Med Ctr, New York, NY USA.
   [Tallman, Martin] Mem Sloan Kettering Canc Ctr, Dept Med, New York, NY 10021 USA.
   [Rowe, Jacob M.] Technion Israel Inst Technol, Rambam Med Ctr, Haifa, Israel.
   [Soulier, Jean; Avran, David] Hop St Louis, Hematol Lab, Paris, France.
   [Soulier, Jean; Avran, David] Hop St Louis, INSERM, U944, Paris, France.
   [Cave, Helene] Hop Robert Debre, Dept Genet, F-75019 Paris, France.
   [Dastugue, Nicole] Fac Med Toulouse, INSERM, Ctr Physiopathol Toulouse Purpan, F-31073 Toulouse, France.
   [Raimondi, Susana C.] St Jude Childrens Hosp, Dept Pathol, Memphis, TN 38105 USA.
   [Meijerink, Jules] Sophia Childrens Univ Hosp, Erasmus MC, Rotterdam, Netherlands.
   [Cordon-Cardo, Carlos] Columbia Univ, Dept Pathol, New York, NY USA.
   [Califano, Andrea] Columbia Univ, Joint Ctr Syst Biol, New York, NY USA.
RI Califano, Andrea/F-7239-2012; Van Vlierberghe, Pieter/G-8894-2013;
   Aplan, Peter/K-9064-2016
OI Van Vlierberghe, Pieter/0000-0001-9063-7205; 
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 19
PY 2010
VL 116
IS 21
BP 210
EP 210
PG 1
WC Hematology
SC Hematology
GA 752BH
UT WOS:000289662200472
ER

PT J
AU Pantin, J
   Tian, X
   Geller, N
   Ramos, C
   Cook, L
   Grasmeder, S
   Scheinberg, P
   Young, NS
   Vasu, S
   Donohue, T
   Childs, R
AF Pantin, Jeremy
   Tian, Xin
   Geller, Nancy
   Ramos, Catalina
   Cook, Lisa
   Grasmeder, Sophia
   Scheinberg, Philip
   Young, Neal S.
   Vasu, Sumithira
   Donohue, Theresa
   Childs, Richard
TI Absence of Graft Failure and Excellent Long Term Survival Following
   Fludarabine-Based Reduced Intensity Hematopoietic Stem Cell
   Transplantation In Heavily Transfused Patients with ATG-Refractory
   Severe Aplastic Anemia and Other Bone Marrow Failure Syndromes
SO BLOOD
LA English
DT Meeting Abstract
CT 52nd Annual Meeting of the American-Society-of-Hematology (ASH)
CY DEC 04-07, 2010
CL Orlando, FL
SP Amer Soc Hematol
C1 [Pantin, Jeremy] NIH, Heart Lung & Blood Inst, Hematol Branch, Bethesda, MD 20892 USA.
   [Tian, Xin; Geller, Nancy] NHLBI, Off Biostat, Bethesda, MD 20892 USA.
   [Scheinberg, Philip; Donohue, Theresa; Childs, Richard] NHLBI, NIH, Hematol Branch, Bethesda, MD 20892 USA.
RI Scheinberg, Phillip/H-5251-2012
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 19
PY 2010
VL 116
IS 21
BP 228
EP 229
PG 2
WC Hematology
SC Hematology
GA 752BH
UT WOS:000289662200518
ER

PT J
AU Stadtmauer, EA
   Krishnan, A
   Pasquini, MC
   Ewell, M
   Alyea, EP
   Antin, JH
   Castro-Malaspina, H
   Kassim, AA
   Negrin, R
   Qazilbash, MH
   Rizzo, JD
   Rowley, SD
   Sahebi, F
   Somlo, G
   Vesole, DH
   Vogl, DT
   Weisdorf, DJ
   Geller, N
   Horowitz, MM
   Maloney, DG
   Giralt, S
AF Stadtmauer, Edward A.
   Krishnan, Amrita
   Pasquini, Marcelo C.
   Ewell, Marian
   Alyea, Edwin P., III
   Antin, Joseph H.
   Castro-Malaspina, Hugo
   Kassim, Adetola A.
   Negrin, Robert
   Qazilbash, Muzaffar H.
   Rizzo, J. Douglas
   Rowley, Scott D.
   Sahebi, Firoozeh
   Somlo, George
   Vesole, David H.
   Vogl, Dan T.
   Weisdorf, Daniel J.
   Geller, Nancy
   Horowitz, Mary M.
   Maloney, David G.
   Giralt, Sergio
TI Tandem Autologous Stem Cell Transplants (auto-auto) With or without
   Maintenance Therapy Versus Single Autologous Transplant Followed by
   HLA-Matched Sibling Non- Myeloablative Allogeneic Stem Cell Transplant
   (auto-allo) for Patients (pts) with High Risk (HR) Multiple Myeloma
   (MM): Results From the Blood and Marrow Transplant Clinical Trials
   Network (BMT-CTN) 0102 Trial
SO BLOOD
LA English
DT Meeting Abstract
CT 52nd Annual Meeting of the American-Society-of-Hematology (ASH)
CY DEC 04-07, 2010
CL Orlando, FL
SP Amer Soc Hematol
C1 [Stadtmauer, Edward A.; Vogl, Dan T.] Univ Penn, Abramson Canc Ctr, Philadelphia, PA 19104 USA.
   [Sahebi, Firoozeh] Kaiser Permanente Med Grp, City Hope Natl Med Ctr, Duarte, CA 91010 USA.
   [Rizzo, J. Douglas; Horowitz, Mary M.] Med Coll Wisconsin, Ctr Int Blood & Marrow Transplant Res, Milwaukee, WI 53226 USA.
   [Ewell, Marian] EMMES Corp, Rockville, MD USA.
   [Antin, Joseph H.] Dana Farber Canc Inst, Div Hematol Malignancies, Boston, MA 02115 USA.
   [Castro-Malaspina, Hugo] Mem Sloan Kettering Canc Ctr, New York, NY 10021 USA.
   [Kassim, Adetola A.] Vanderbilt Univ, Med Ctr, Nashville, TN USA.
   [Negrin, Robert] Stanford Univ, Stanford, CA 94305 USA.
   [Qazilbash, Muzaffar H.] Univ Texas MD Anderson Canc Ctr, SCT CT Unit 423, Houston, TX 77030 USA.
   [Rowley, Scott D.] Hackensack Univ, Med Ctr, Div Blood & Marrow Transplantat, John Theurer Canc Ctr, Hackensack, NJ USA.
   [Weisdorf, Daniel J.] Univ Minnesota, Med Ctr, Minneapolis, MN 55455 USA.
   [Geller, Nancy] NHLBI, Bethesda, MD 20892 USA.
   [Maloney, David G.] Fred Hutchinson Canc Res Ctr, Seattle, WA 98104 USA.
   [Maloney, David G.] Univ Washington, Seattle, WA 98195 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 19
PY 2010
VL 116
IS 21
BP 233
EP 234
PG 2
WC Hematology
SC Hematology
GA 752BH
UT WOS:000289662200527
ER

PT J
AU Hardy, NM
   Fellowes, V
   Rose, J
   Fowler, DH
   Gress, RE
   Levine, BL
   June, CH
   Hakim, FT
   Bishop, MR
AF Hardy, Nancy M.
   Fellowes, Vicki
   Rose, Jeremy
   Fowler, Daniel H.
   Gress, Ronald E.
   Levine, Bruce L.
   June, Carl H.
   Hakim, Frances T.
   Bishop, Michael R.
TI Costimulated, Tumor-Derived Donor Lymphocyte (TDL) Infusion for B-Cell
   Tumor Relapse After Allogeneic Hematopoietic Stem Cell Transplantation
SO BLOOD
LA English
DT Meeting Abstract
CT 52nd Annual Meeting of the American-Society-of-Hematology (ASH)
CY DEC 04-07, 2010
CL Orlando, FL
SP Amer Soc Hematol
C1 [Hardy, Nancy M.; Fellowes, Vicki; Rose, Jeremy; Fowler, Daniel H.; Gress, Ronald E.; Hakim, Frances T.; Bishop, Michael R.] NCI, Expt Transplantat & Immunol Branch, Ctr Canc Res, Bethesda, MD 20892 USA.
   [Levine, Bruce L.; June, Carl H.] Univ Penn, Sch Med, Abramson Canc Ctr, Philadelphia, PA 19104 USA.
RI Levine, Bruce/D-1688-2009
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 19
PY 2010
VL 116
IS 21
BP 300
EP 301
PG 2
WC Hematology
SC Hematology
GA 752BH
UT WOS:000289662200684
ER

PT J
AU Davids, MS
   Brown, JR
   Wiestner, A
   Letai, AG
AF Davids, Matthew S.
   Brown, Jennifer R.
   Wiestner, Adrian
   Letai, Anthony G.
TI BH3 Profiling Demonstrates Decreased Mitochondrial Priming for Apoptosis
   In Primary CLL Cells Exposed to Stroma
SO BLOOD
LA English
DT Meeting Abstract
CT 52nd Annual Meeting of the American-Society-of-Hematology (ASH)
CY DEC 04-07, 2010
CL Orlando, FL
SP Amer Soc Hematol
C1 [Davids, Matthew S.; Brown, Jennifer R.; Letai, Anthony G.] Dana Farber Canc Inst, Boston, MA 02115 USA.
   [Wiestner, Adrian] 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 19
PY 2010
VL 116
IS 21
BP 305
EP 305
PG 1
WC Hematology
SC Hematology
GA 752BH
UT WOS:000289662200693
ER

PT J
AU Hanash, AM
   Kappel, LW
   Yim, NL
   Nejat, RA
   Goldberg, GL
   Smith, OM
   Rao, UK
   Dykstra, L
   Na, IK
   Holland, AM
   Liu, C
   Murphy, GF
   Leonard, WJ
   Heller, G
   van den Brink, MRM
AF Hanash, Alan M.
   Kappel, Lucy W.
   Yim, Nury L.
   Nejat, Rebecca A.
   Goldberg, Gabrielle L.
   Smith, Odette M.
   Rao, Uttam K.
   Dykstra, Lindsay
   Na, Il-Kang
   Holland, Amanda M.
   Liu, Chen
   Murphy, George F.
   Leonard, Warren J.
   Heller, Glenn
   van den Brink, Marcel R. M.
TI Abrogation of Donor T Cell IL-21 Signaling Leads to Tissue-Specific
   Modulation of Immunity and Separation of Gvhd From GVL
SO BLOOD
LA English
DT Meeting Abstract
CT 52nd Annual Meeting of the American-Society-of-Hematology (ASH)
CY DEC 04-07, 2010
CL Orlando, FL
SP Amer Soc Hematol
C1 [Hanash, Alan M.] Mem Sloan Kettering Canc Ctr, Dept Med, New York, NY 10021 USA.
   [Kappel, Lucy W.; Yim, Nury L.; Nejat, Rebecca A.; Goldberg, Gabrielle L.; Smith, Odette M.; Rao, Uttam K.; Dykstra, Lindsay; Holland, Amanda M.] Mem Sloan Kettering Canc Ctr, Dept Immunol, New York, NY 10021 USA.
   [Na, Il-Kang] Univ Med Berlin, Charite CBF, Berlin, Germany.
   [Liu, Chen] Univ Florida, Coll Med, Dept Pathol Immunol & Lab Med, Gainesville, FL USA.
   [Murphy, George F.] Harvard Univ, Brigham & Womens Hosp, Sch Med, Prograrn Dermatopathol, Boston, MA 02115 USA.
   [Leonard, Warren J.] NHLBI, Lab Mol Immunol, NIH, Bethesda, MD 20892 USA.
   [Heller, Glenn] Mem Sloan Kettering Canc Ctr, Dept Biostat, New York, NY 10021 USA.
   [van den Brink, Marcel R. M.] Mem Sloan Kettering Canc Ctr, Adult Bone Marrow Transplantat Serv, New York, NY 10021 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 19
PY 2010
VL 116
IS 21
BP 321
EP 322
PG 2
WC Hematology
SC Hematology
GA 752BH
UT WOS:000289662200730
ER

PT J
AU Steiner, LA
   Schulz, VP
   Maksimova, Y
   Mahajan, M
   Bodine, DM
   Gallagher, PG
AF Steiner, Laurie A.
   Schulz, Vincent P.
   Maksimova, Yelena
   Mahajan, Milind
   Bodine, David M.
   Gallagher, Patrick G.
TI Dynamic CO-Localization of GATA1, NFE2, and EKLF and Changes in Gene
   Expression During Hematopoiesis
SO BLOOD
LA English
DT Meeting Abstract
CT 52nd Annual Meeting of the American-Society-of-Hematology (ASH)
CY DEC 04-07, 2010
CL Orlando, FL
SP Amer Soc Hematol
C1 [Steiner, Laurie A.; Gallagher, Patrick G.] Yale Univ, Sch Med, New Haven, CT USA.
   [Mahajan, Milind] Yale Univ, Dept Genet, New Haven, CT USA.
   [Bodine, David M.] NIH, 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 19
PY 2010
VL 116
IS 21
BP 327
EP 327
PG 1
WC Hematology
SC Hematology
GA 752BH
UT WOS:000289662200742
ER

PT J
AU Proto-Siqueira, R
   Santos, MG
   Carvalho, VM
   Maekawa, YH
   Testagrossa, LA
   Andrade, ZR
   Oliveira, JS
   Chauffaille, MDLF
   Zago, MA
   Nagler, A
   Wiestner, A
   Rizzatti, EG
AF Proto-Siqueira, Rodrigo
   Santos, Melina G.
   Carvalho, Valdemir M.
   Maekawa, Yumi H.
   Testagrossa, Leonardo A.
   Andrade, Zelia R.
   Oliveira, Jose Salvador
   Chauffaille, Maria de Lourdes L. F.
   Zago, Marco A.
   Nagler, Arnon
   Wiestner, Adrian
   Rizzatti, Edgar Gil
TI Halofuginone Induces Post-Transcriptional Down-Regulation of Cyclin D1,
   Cell Cycle Arrest and Apoptosis In Mantle Cell Lymphoma Cells through
   Activation of Integrated Stress Response Pathways
SO BLOOD
LA English
DT Meeting Abstract
CT 52nd Annual Meeting of the American-Society-of-Hematology (ASH)
CY DEC 04-07, 2010
CL Orlando, FL
SP Amer Soc Hematol
C1 [Proto-Siqueira, Rodrigo; Santos, Melina G.; Carvalho, Valdemir M.; Maekawa, Yumi H.; Testagrossa, Leonardo A.; Andrade, Zelia R.; Rizzatti, Edgar Gil] Fleury Med & Hlth, Sao Paulo, Brazil.
   [Oliveira, Jose Salvador; Chauffaille, Maria de Lourdes L. F.] UNIFESP EPM, Sect Hematol & Blood Transfus, Dept Clin & Expt Oncol, Sao Paulo, Brazil.
   [Zago, Marco A.] Univ Sao Paulo, Fac Med Ribeirao Preto, Ribeirao Preto, Brazil.
   [Nagler, Arnon] Chaim Sheba Med Ctr, Div Hematol, IL-52621 Tel Hashomer, Israel.
   [Wiestner, Adrian] NHLBI, Hematol Branch, Bethesda, MD 20892 USA.
RI Carvalho, Valdemir/C-5816-2008; de Oliveira, Jose Salvador/M-9322-2015
OI Carvalho, Valdemir/0000-0002-9816-8615; 
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 19
PY 2010
VL 116
IS 21
BP 339
EP 340
PG 2
WC Hematology
SC Hematology
GA 752BH
UT WOS:000289662200774
ER

PT J
AU Tang, WH
   Cushman, M
   Basu, S
   Green, D
   Reiner, AP
   Delaney, JA
   Lange, LA
   Smith, NL
   Tracy, RP
   Wilson, JG
   Tofler, G
   Yang, Q
   Keating, BJ
   Taylor, H
   Jacobs, D
   O'Donnell, CJ
   Folsom, AR
AF Tang, Weihong
   Cushman, Mary
   Basu, Saonli
   Green, David
   Reiner, Alexander P.
   Delaney, Joseph A.
   Lange, Leslie A.
   Smith, Nicholas L.
   Tracy, Russell P.
   Wilson, James G.
   Tofler, Geoffrey
   Yang, Qiong
   Keating, Brendan J.
   Taylor, Herman
   Jacobs, David
   O'Donnell, Christopher J.
   Folsom, Aaron R.
TI Gene-Centric Approach Identifies New and Known Loci for Factor VIII
   Activity and Von Willebrand Factor Antigen In the Candidate Gene
   Association Resource (CARe) Consortium
SO BLOOD
LA English
DT Meeting Abstract
CT 52nd Annual Meeting of the American-Society-of-Hematology (ASH)
CY DEC 04-07, 2010
CL Orlando, FL
SP Amer Soc Hematol
C1 [Tang, Weihong; Jacobs, David; Folsom, Aaron R.] Univ Minnesota, Div Epidemiol & Community Hlth, Minneapolis, MN USA.
   [Cushman, Mary; Tracy, Russell P.] Univ Vermont, Burlington, VT USA.
   [Green, David] NW Feinberg Sch Med, Div Hem Onc, Chicago, IL USA.
   [Reiner, Alexander P.; Smith, Nicholas L.] Univ Washington, Seattle, WA 98195 USA.
   [Delaney, Joseph A.] Univ Florida, Gainesville, FL 32611 USA.
   [Lange, Leslie A.] Univ N Carolina, Chapel Hill, NC 27515 USA.
   [Wilson, James G.; Taylor, Herman] Univ Mississippi, Med Ctr, University, MS 38677 USA.
   [Tofler, Geoffrey] Harvard Univ, Cambridge, MA 02138 USA.
   [Yang, Qiong] Boston Univ, Boston, MA 02215 USA.
   [Keating, Brendan J.] Univ Penn, Philadelphia, PA 19104 USA.
   [O'Donnell, Christopher J.] NHLBI, Framingham Heart Study, Ctr Populat Studies, Framingham, MA USA.
RI Yang, Qiong/G-5438-2014
NR 0
TC 0
Z9 0
U1 0
U2 8
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 19
PY 2010
VL 116
IS 21
BP 353
EP 353
PG 1
WC Hematology
SC Hematology
GA 752BH
UT WOS:000289662200807
ER

PT J
AU Le, RQ
   Melenhorst, JJ
   Hill, B
   Memon, S
   Battiwalla, M
   Savani, BN
   Shenoy, A
   Hensel, NF
   Koklanaris, EK
   Keyvanfar, K
   Hakim, FT
   Douek, DC
   Barrett, AJ
AF Le, Robert Q.
   Melenhorst, J. Joseph
   Hill, Brenna
   Memon, Sarfraz
   Battiwalla, Minoo
   Savani, Bipin N.
   Shenoy, Aarthi
   Hensel, Nancy F.
   Koklanaris, Eleftheria K.
   Keyvanfar, Keyvan
   Hakim, Frances T.
   Douek, Daniel C.
   Barrett, A. John
TI Evolution of the Donor T Cell Repertoire In Allogeneic Stem Cell
   Transplant Recipients In the Second Decade After Transplantation
SO BLOOD
LA English
DT Meeting Abstract
CT 52nd Annual Meeting of the American-Society-of-Hematology (ASH)
CY DEC 04-07, 2010
CL Orlando, FL
SP Amer Soc Hematol
C1 [Le, Robert Q.; Melenhorst, J. Joseph; Battiwalla, Minoo; Shenoy, Aarthi; Hensel, Nancy F.; Koklanaris, Eleftheria K.; Keyvanfar, Keyvan; Barrett, A. John] NHLBI, Hematol Branch, NIH, Bethesda, MD 20892 USA.
   [Hill, Brenna; Douek, Daniel C.] NIAID, Human Immunol Sect, VRC, NIH, Bethesda, MD 20892 USA.
   [Memon, Sarfraz; Hakim, Frances T.] NCI, Expt & Transplantat Immunol Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
   [Savani, Bipin N.] Vanderbilt Univ, Med Ctr, Dept Med, Div Hematol Oncol, Nashville, TN 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 19
PY 2010
VL 116
IS 21
BP 362
EP 362
PG 1
WC Hematology
SC Hematology
GA 752BH
UT WOS:000289662200832
ER

PT J
AU Jagasia, M
   Arora, M
   Flowers, M
   Chao, NJ
   McCarthy, PL
   Antin, JH
   Bolwell, BJ
   Bredeson, C
   Cahn, JY
   Cairo, MS
   Cutler, C
   Gale, RP
   Gupta, V
   Haagenson, MD
   Horowitz, MM
   Lee, SJ
   Litzow, MR
   Pavletic, SZ
   Urbano, A
   Weisdorf, DJ
   Zhang, MJ
   Hahn, T
AF Jagasia, Madan
   Arora, Mukta
   Flowers, Mary
   Chao, Nelson J.
   McCarthy, Philip L.
   Antin, Joseph H.
   Bolwell, Brian J.
   Bredeson, Christopher
   Cahn, Jean-Yves
   Cairo, Mitchell S.
   Cutler, Corey
   Gale, Robert Peter
   Gupta, Vikas
   Haagenson, Michael D.
   Horowitz, Mary M.
   Lee, Stephanie J.
   Litzow, Mark R.
   Pavletic, Steven Z.
   Urbano, Alvaro
   Weisdorf, Daniel. J.
   Zhang, Mei-Jie
   Hahn, Theresa
TI Risk-Factors for Acute Graft-Versus-Host Disease and Survival After
   Hematopoietic Cell Transplantation From Siblings and Unrelated Donors
SO BLOOD
LA English
DT Meeting Abstract
CT 52nd Annual Meeting of the American-Society-of-Hematology (ASH)
CY DEC 04-07, 2010
CL Orlando, FL
SP Amer Soc Hematol
C1 [Jagasia, Madan] Vanderbilt Univ, Med Ctr, Nashville, TN USA.
   [Weisdorf, Daniel. J.] Univ Minnesota, Med Ctr, Minneapolis, MN 55455 USA.
   [Flowers, Mary; Lee, Stephanie J.] Fred Hutchinson Canc Res Ctr, Seattle, WA 98104 USA.
   [Flowers, Mary] Univ Washington, Seattle, WA 98195 USA.
   [Chao, Nelson J.] Duke Univ, Med Ctr, Div Cellular Therapy, Durham, NC USA.
   [McCarthy, Philip L.] Roswell Pk Canc Inst, BMT Program, Buffalo, NY 14263 USA.
   [Antin, Joseph H.; Cutler, Corey] Dana Farber Canc Inst, Div Hematol Malignancies, Boston, MA 02115 USA.
   [Bolwell, Brian J.] Cleveland Clin, Cleveland, OH 44106 USA.
   [Cahn, Jean-Yves] CHU Grenoble, F-38043 Grenoble 09, France.
   [Cairo, Mitchell S.] Columbia Univ, Med Ctr, Div Pediat Hematol & Blood & Marrow Transplantat, New York, NY USA.
   [Gale, Robert Peter] Ctr Adv Studies Leukemia, Los Angeles, CA USA.
   [Gupta, Vikas] Princess Margaret Hosp, Toronto, ON M4X 1K9, Canada.
   [Haagenson, Michael D.] CIBMTR Minneapolis, Minneapolis, MN USA.
   [Horowitz, Mary M.] Med Coll Wisconsin, Ctr Int Blood & Marrow Transplant Res, Milwaukee, WI 53226 USA.
   [Litzow, Mark R.] Mayo Clin, Rochester, MN USA.
   [Pavletic, Steven Z.] NCI, Expt Transplantat & Immunol Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
   [Urbano, Alvaro] Hosp Clin Barcelona, Dept Hematol, Barcelona, Spain.
   [Hahn, Theresa] Roswell Pk Canc Inst, Dept Med, Buffalo, NY 14263 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 19
PY 2010
VL 116
IS 21
BP 394
EP 394
PG 1
WC Hematology
SC Hematology
GA 752BH
UT WOS:000289662200898
ER

PT J
AU Arora, M
   Klein, JP
   Antin, JH
   Bolwell, BJ
   Boyiadzis, M
   Cahn, JY
   Cairo, MS
   Cutler, CS
   Flowers, MED
   Gale, RP
   Hassebroek, A
   Herzig, RH
   Horowitz, MM
   Isola, L
   Jacobsohn, DA
   Klumpp, TR
   Lee, SJ
   Petersdorf, EW
   Santarone, S
   Schouten, HC
   Spellman, S
   Urbano, A
   Weisdorf, DJ
   Wingard, JR
   Pavletic, SZ
AF Arora, Mukta
   Klein, John P.
   Antin, Joseph H.
   Bolwell, Brian J.
   Boyiadzis, Michael
   Cahn, Jean-Yves
   Cairo, Mitchell S.
   Cutler, Corey S.
   Flowers, Mary E. D.
   Gale, Robert P.
   Hassebroek, Anna
   Herzig, Roger H.
   Horowitz, Mary M.
   Isola, Luis
   Jacobsohn, David A.
   Klumpp, Thomas R.
   Lee, Stephanie J.
   Petersdorf, Effie W.
   Santarone, Stella
   Schouten, Harry C.
   Spellman, Stephen
   Urbano, Alvaro
   Weisdorf, Daniel J.
   Wingard, John R.
   Pavletic, Steven Z.
TI Chronic Graft-Versus-Host Disease Risk Score: A CIBMTR Analysis
SO BLOOD
LA English
DT Meeting Abstract
CT 52nd Annual Meeting of the American-Society-of-Hematology (ASH)
CY DEC 04-07, 2010
CL Orlando, FL
SP Amer Soc Hematol
C1 [Arora, Mukta] Univ Minnesota, Minneapolis, MN USA.
   [Klein, John P.] Med Coll Wisconsin, Dept Biostat, Ctr Int Blood & Marrow Transplant Res, Milwaukee, WI 53226 USA.
   [Antin, Joseph H.; Cutler, Corey S.] Dana Farber Canc Inst, Div Hematol Malignancies, Boston, MA 02115 USA.
   [Bolwell, Brian J.] Cleveland Clin, Taussig Canc Inst, Cleveland, OH 44106 USA.
   [Boyiadzis, Michael] Univ Pittsburgh Canc Inst, Pittsburgh, PA USA.
   [Cahn, Jean-Yves] CHU Grenoble, F-38043 Grenoble 09, France.
   [Cairo, Mitchell S.] Columbia Univ, NewYork Presbyterian Morgan Stanley Childrens Hos, New York, NY USA.
   [Lee, Stephanie J.] Fred Hutchinson Canc Res Ctr, Div Clin Res, Seattle, WA 98104 USA.
   [Flowers, Mary E. D.] Univ Washington, Seattle, WA 98195 USA.
   [Gale, Robert P.] Celgene Corp, Summit, NJ USA.
   [Herzig, Roger H.] Univ Louisville, James Graham Brown Canc Ctr, BMT, Louisville, KY 40292 USA.
   [Isola, Luis] Mt Sinai Med Ctr, BMT, New York, NY 10029 USA.
   [Jacobsohn, David A.] Childrens Natl Med Ctr, Washington, DC 20010 USA.
   [Klumpp, Thomas R.] Temple Univ, Wynnewood, PA USA.
   [Santarone, Stella] Osped Civile, BMT Ctr, Pescara, Italy.
   [Schouten, Harry C.] Acad Ziekenhuis, Maastricht, Netherlands.
   [Hassebroek, Anna; Spellman, Stephen] Ctr Int Blood & Marrow Transplant Res, Minneapolis, MN USA.
   [Urbano, Alvaro] Hosp Clin Barcelona, Dept Hematol, Barcelona, Spain.
   [Weisdorf, Daniel J.] Univ Minnesota Med Ctr, Minneapolis, MN USA.
   Univ Florida, Shands Canc Ctr, Gainesville, FL USA.
   [Pavletic, Steven Z.] NCI, Expt Transplantat & Immunol Branch, Canc Res Ctr, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 19
PY 2010
VL 116
IS 21
BP 395
EP 396
PG 2
WC Hematology
SC Hematology
GA 752BH
UT WOS:000289662201001
ER

PT J
AU Barst, RJ
   Kato, GJ
   Sachdev, V
   Nouraie, M
   Machado, RF
   Hassell, K
   Gibbs, S
   Little, J
   Schraufnagel, DE
   Krishnamurti, L
   Girgis, RE
   Morris, CR
   Badesch, DB
   Lanzkron, S
   Castro, O
   Rosenzweig, EB
   Goldsmith, JC
   Gladwin, M
   Gordeuk, VR
AF Barst, Robyn J.
   Kato, Gregory J.
   Sachdev, Vandana
   Nouraie, Mehdi
   Machado, Roberto F.
   Hassell, Kathryn
   Gibbs, Simon
   Little, Jane
   Schraufnagel, Dean E.
   Krishnamurti, Lakshmanan
   Girgis, Reda E.
   Morris, Claudia R.
   Badesch, David B.
   Lanzkron, Sophie
   Castro, Oswaldo
   Rosenzweig, Erika Berman
   Goldsmith, Jonathan C.
   Gladwin, Mark
   Gordeuk, Victor R.
TI Predictors of Six-Minute Walk Distance In Adults with Sickle Cell Anemia
   In the Walk-PHaSST Study
SO BLOOD
LA English
DT Meeting Abstract
CT 52nd Annual Meeting of the American-Society-of-Hematology (ASH)
CY DEC 04-07, 2010
CL Orlando, FL
SP Amer Soc Hematol
ID DISEASE
C1 [Barst, Robyn J.] Columbia Univ, Scarsdale, NY USA.
   [Kato, Gregory J.] NHLBI, Sickle Cell Vasc Dis Sect, NIH, Bethesda, MD 20892 USA.
   [Sachdev, Vandana] NHLBI, Translat Med Branch, NIH, Bethesda, MD 20892 USA.
   [Nouraie, Mehdi] Howard Univ, Ctr Sickle Cell Dis, Washington, DC 20059 USA.
   [Machado, Roberto F.; Schraufnagel, Dean E.; Badesch, David B.] Univ Illinois, Chicago, IL USA.
   [Hassell, Kathryn] Univ Colorado, Hlth Sci Ctr, Denver, CO USA.
   [Gibbs, Simon] UCL, Sch Med, London W1N 8AA, England.
   [Little, Jane] Albert Einstein Coll Med, Bronx, NY 10467 USA.
   [Krishnamurti, Lakshmanan] Childrens Hosp Pittsburgh, Pittsburgh, PA 15213 USA.
   [Girgis, Reda E.] Johns Hopkins Univ, Baltimore, MD USA.
   [Morris, Claudia R.] Childrens Hosp & Res Ctr Oaldand, Oakland, CA USA.
   [Lanzkron, Sophie] Johns Hopkins Sch Med, Baltimore, MD USA.
   [Castro, Oswaldo; Gordeuk, Victor R.] Howard Univ, Ctr Sickle Cell Dis, Potomac, MD USA.
   [Gladwin, Mark] Univ Pittsburgh, Vasc Med Inst, Pittsburgh, PA USA.
   [Rosenzweig, Erika Berman] Columbia Univ, New York, NY USA.
RI Kato, Gregory/I-7615-2014
OI Kato, Gregory/0000-0003-4465-3217
NR 2
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 19
PY 2010
VL 116
IS 21
BP 417
EP 418
PG 2
WC Hematology
SC Hematology
GA 752BH
UT WOS:000289662201050
ER

PT J
AU Novelli, EM
   Kato, GJ
   Ragni, MV
   Hildesheim, ME
   Barge, S
   Meyer, MP
   Hassett, AC
   Gladwin, M
   Isenberg, J
AF Novelli, Enrico M.
   Kato, Gregory J.
   Ragni, Margaret V.
   Hildesheim, Mariana E.
   Barge, Suchitra
   Meyer, Michael P.
   Hassett, Andrea Cortese
   Gladwin, Mark
   Isenberg, Jeffrey
TI Plasma Thrombospondin 1 Is Increased and Associated with Markers of
   Vasculopathy In Sickle Cell Disease
SO BLOOD
LA English
DT Meeting Abstract
CT 52nd Annual Meeting of the American-Society-of-Hematology (ASH)
CY DEC 04-07, 2010
CL Orlando, FL
SP Amer Soc Hematol
C1 [Novelli, Enrico M.; Gladwin, Mark; Isenberg, Jeffrey] Univ Pittsburgh, Vasc Med Inst, Pittsburgh, PA USA.
   [Kato, Gregory J.] NHLBI, Sickle Cell Vasc Dis Sect, NIH, Bethesda, MD 20892 USA.
   [Ragni, Margaret V.] Univ Pittsburgh, Dept Med, Div Hematol Oncol, Pittsburgh, PA USA.
   [Ragni, Margaret V.] Hemophilia Ctr Western Penn, Pittsburgh, PA USA.
   [Hildesheim, Mariana E.] NIH, Dept Crit Care Med, Ctr Clin, Bethesda, MD 20892 USA.
   [Meyer, Michael P.; Hassett, Andrea Cortese] ITXM Diagnost, Pittsburgh, PA 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 19
PY 2010
VL 116
IS 21
BP 417
EP 417
PG 1
WC Hematology
SC Hematology
GA 752BH
UT WOS:000289662201049
ER

PT J
AU Kato, GJ
   Sable, C
   Ensing, G
   Dham, N
   Minniti, C
   Remaley, A
   Campbell, A
   Arteta, M
   Rana, S
   Darbari, D
   Nouraie, M
   Onyekwere, O
   Gladwin, M
   Castro, O
   Gordeuk, VR
AF Kato, Gregory J.
   Sable, Craig
   Ensing, Gregory
   Dham, Niti
   Minniti, Caterina
   Remaley, Alan
   Campbell, Andrew
   Arteta, Manuel
   Rana, Sohail
   Darbari, Deepika
   Nouraie, Mehdi
   Onyekwere, Onyinye
   Gladwin, Mark
   Castro, Oswaldo
   Gordeuk, Victor R.
TI Plasma Level of NT-Pro-BNP In Children with Sickle Cell Disease Is
   Associated with Degree of Anemia and Left Ventricular Measures: The PUSH
   Study
SO BLOOD
LA English
DT Meeting Abstract
CT 52nd Annual Meeting of the American-Society-of-Hematology (ASH)
CY DEC 04-07, 2010
CL Orlando, FL
SP Amer Soc Hematol
C1 [Kato, Gregory J.] NHLBI, Sickle Cell Vasc Dis Sect, NIH, Bethesda, MD 20892 USA.
   [Dham, Niti] Childrens Natl Med Ctr, Dept Cardiol, Washington, DC 20010 USA.
   [Campbell, Andrew; Arteta, Manuel] Univ Michigan, Med Ctr, Ann Arbor, MI USA.
   [Minniti, Caterina; Remaley, Alan] NHLBI, Pulm & Vasc Med Branch, Bethesda, MD 20892 USA.
   [Nouraie, Mehdi; Onyekwere, Onyinye; Gordeuk, Victor R.] Howard Univ, Ctr Sickle Cell Dis, Washington, DC 20059 USA.
   [Darbari, Deepika] Johns Hopkins Univ, NHLBI, Bethesda, MD USA.
   [Gladwin, Mark] Univ Pittsburgh, Vasc Med Inst Pulm, Pittsburgh, PA USA.
   [Castro, Oswaldo] Howard Univ, Ctr Sickle Cell Dis, Potomac, 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 19
PY 2010
VL 116
IS 21
BP 418
EP 418
PG 1
WC Hematology
SC Hematology
GA 752BH
UT WOS:000289662201051
ER

PT J
AU Dunleavy, K
   Chattopadhyay, P
   Kawada, J
   Calattini, S
   Gostick, E
   Price, D
   Roderer, M
   Cohen, J
   Grant, N
   Pittaluga, S
   Janik, JE
   Jaffe, ES
   Wilson, WH
AF Dunleavy, Kieron
   Chattopadhyay, Pratip
   Kawada, Junichi
   Calattini, Sara
   Gostick, Emma
   Price, David
   Roderer, Mario
   Cohen, Jeffrey
   Grant, Nicole
   Pittaluga, Stefania
   Janik, John E.
   Jaffe, Elaine S.
   Wilson, Wyndham H.
TI Immune Characteristics Associated with Lymphomatoid Granulomatosis and
   Outcome Following Treatment with Interferon-Alpha
SO BLOOD
LA English
DT Meeting Abstract
CT 52nd Annual Meeting of the American-Society-of-Hematology (ASH)
CY DEC 04-07, 2010
CL Orlando, FL
SP Amer Soc Hematol
C1 [Dunleavy, Kieron; Cohen, Jeffrey; Grant, Nicole; Pittaluga, Stefania; Janik, John E.; Jaffe, Elaine S.; Wilson, Wyndham H.] NCI, Ctr Canc Res, Bethesda, MD 20892 USA.
   [Chattopadhyay, Pratip; Roderer, Mario] NIAID, Vaccine Res Ctr, Bethesda, MD 20892 USA.
   [Kawada, Junichi; Calattini, Sara] NIAID, Lab Clin Infect Dis, Bethesda, MD 20892 USA.
   [Gostick, Emma; Price, David] Cardiff Univ, Dept Infect Immun & Biochem, Sch Med, Cardiff, S Glam, Wales.
RI Price, David/C-7876-2013
OI Price, David/0000-0001-9416-2737
NR 0
TC 3
Z9 3
U1 0
U2 3
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 19
PY 2010
VL 116
IS 21
BP 424
EP 424
PG 1
WC Hematology
SC Hematology
GA 752BH
UT WOS:000289662201066
ER

PT J
AU Furutani, E
   Su, S
   Smith, A
   Berg, M
   Childs, R
AF Furutani, Elissa
   Su, Su
   Smith, Aleah
   Berg, Maria
   Childs, Richard
TI siRNA Inactivation of the Inhibitory Receptor NKG2A Augments the
   Anti-Tumor Effects of Adoptiyely Transferred NK Cells In Tumor-Bearing
   Hosts
SO BLOOD
LA English
DT Meeting Abstract
CT 52nd Annual Meeting of the American-Society-of-Hematology (ASH)
CY DEC 04-07, 2010
CL Orlando, FL
SP Amer Soc Hematol
C1 [Furutani, Elissa; Su, Su; Smith, Aleah; Berg, Maria; Childs, Richard] NHLBI, Hematol Branch, NIH, Bethesda, MD 20892 USA.
   [Furutani, Elissa] HHMI NIH Res Scholars Program, 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 19
PY 2010
VL 116
IS 21
BP 446
EP 446
PG 1
WC Hematology
SC Hematology
GA 752BH
UT WOS:000289662201118
ER

PT J
AU Muranski, P
   Borman, Z
   Kerkar, S
   Ji, Y
   Gattinoni, L
   Robert, RN
   Sanchez-Perez, L
   Christopher, KA
   Yu, ZY
   Steven, KJ
   Ferreyra, G
   Danner, RL
   Restifo, NP
AF Muranski, Pawel
   Borman, Zachary
   Kerkar, Sid
   Ji, Yun
   Gattinoni, Luca
   Robert, Reger N.
   Sanchez-Perez, Luis
   Christopher, Klebanoff A.
   Yu, Zhiya
   Steven, Kern J.
   Ferreyra, Gabriela
   Danner, Robert L.
   Restifo, Nicholas P.
TI Th17-Derived Memory Cells Are Long-Lived and Retain a Stem-Like
   Molecular Signature
SO BLOOD
LA English
DT Meeting Abstract
CT 52nd Annual Meeting of the American-Society-of-Hematology (ASH)
CY DEC 04-07, 2010
CL Orlando, FL
SP Amer Soc Hematol
C1 [Muranski, Pawel; Borman, Zachary; Kerkar, Sid; Ji, Yun; Gattinoni, Luca; Robert, Reger N.; Sanchez-Perez, Luis; Christopher, Klebanoff A.; Yu, Zhiya; Restifo, Nicholas P.] NCI, NIH, Bethesda, MD 20892 USA.
   [Steven, Kern J.; Ferreyra, Gabriela; Danner, Robert L.] NIH, Ctr Clin, Dept Crit Care Med, Bethesda, MD USA.
RI Restifo, Nicholas/A-5713-2008
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 19
PY 2010
VL 116
IS 21
BP 447
EP 447
PG 1
WC Hematology
SC Hematology
GA 752BH
UT WOS:000289662201121
ER

PT J
AU Kentsis, A
   Sanda, T
   Ngo, V
   Rodig, SJ
   Kutok, J
   Tholouli, E
   Byers, R
   Woude, GV
   Kung, AL
   Staudt, LM
   Look, AT
AF Kentsis, Alex
   Sanda, Takaomi
   Ngo, Vu
   Rodig, Scott J.
   Kutok, Jeffery
   Tholouli, Eleni
   Byers, Richard
   Woude, George Vande
   Kung, Andrew L.
   Staudt, Louis M.
   Look, A. Thomas
TI Aberrant Expression of Hepatocyte Growth Factor Induces Autocrine MET
   Activation Providing a Novel Therapeutic Target In Acute Myeloid
   Leukemia
SO BLOOD
LA English
DT Meeting Abstract
CT 52nd Annual Meeting of the American-Society-of-Hematology (ASH)
CY DEC 04-07, 2010
CL Orlando, FL
SP Amer Soc Hematol
C1 [Kentsis, Alex; Sanda, Takaomi; Kung, Andrew L.; Look, A. Thomas] Harvard Univ, Sch Med, Dana Farber Canc Inst, Childrens Hosp Boston, Boston, MA 02115 USA.
   [Ngo, Vu; Staudt, Louis M.] NCI, NIH, Bethesda, MD USA.
   [Rodig, Scott J.; Kutok, Jeffery] Harvard Univ, Sch Med, Brigham & Womens Hosp, Boston, MA USA.
   [Tholouli, Eleni; Byers, Richard] Cent Manchester Univ Hosp NHS Fdn Trust, Manchester, Lancs, England.
   [Woude, George Vande] Van Andel Res Inst, Grand Rapids, MI USA.
NR 0
TC 0
Z9 0
U1 2
U2 2
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 19
PY 2010
VL 116
IS 21
BP 458
EP 458
PG 1
WC Hematology
SC Hematology
GA 752BH
UT WOS:000289662201145
ER

PT J
AU Pulsipher, MA
   Chitphakdithai, P
   Logan, BR
   Goldstein, SC
   Levine, JE
   Lankiewicz, M
   Stroncek, D
   Confer, DL
AF Pulsipher, Michael A.
   Chitphakdithai, Pintip
   Logan, Brent R.
   Goldstein, Steven C.
   Levine, John E.
   Lankiewicz, Michael
   Stroncek, David
   Confer, Dennis L.
TI Peripheral Blood Stem Cell (PBSC) Donors Experience Higher Levels of
   Pain and Toxicities Early On, While tone Marrow (BM) Donors Experience
   Slower Recovery and More Late Pain: A Prospective Study of the National
   Marrow Donor Program (NMDP)
SO BLOOD
LA English
DT Meeting Abstract
CT 52nd Annual Meeting of the American-Society-of-Hematology (ASH)
CY DEC 04-07, 2010
CL Orlando, FL
SP Amer Soc Hematol
C1 [Pulsipher, Michael A.] Univ Utah, Salt Lake City, UT USA.
   [Chitphakdithai, Pintip] Ctr Int Blood & Marrow Transplant Res, Minneapolis, MN USA.
   [Logan, Brent R.] Med Coll Wisconsin, Milwaukee, WI 53226 USA.
   [Goldstein, Steven C.] Univ Penn, Philadelphia, PA 19104 USA.
   [Levine, John E.] Univ Michigan, Ann Arbor, MI 48109 USA.
   [Lankiewicz, Michael] BloodCtr WI, Milwaukee, WI USA.
   [Stroncek, David] NIH, Ctr Clin, Bethesda, MD 20892 USA.
   [Confer, Dennis L.] Natl Marrow Donor Program, Minneapolis, MN USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 19
PY 2010
VL 116
IS 21
BP 482
EP 482
PG 1
WC Hematology
SC Hematology
GA 752BH
UT WOS:000289662201210
ER

PT J
AU Fasano, RM
   Adams, S
   Smith, A
   Donohue, T
   Bolan, CD
   Sugimoto, K
   Flegel, WA
   Childs, R
AF Fasano, Ross M.
   Adams, Sharon
   Smith, Aleah
   Donohue, Theresa
   Bolan, Charles D., Jr.
   Sugimoto, Kyoko
   Flegel, Willy A.
   Childs, Richard
TI HLA Alloantibody Persistence and De Novo Production of HLA
   Alloantibodies of Donor Origin Following Reduced Intensity Allogeneic
   Hematopoietic Stem Cell Transplantation
SO BLOOD
LA English
DT Meeting Abstract
CT 52nd Annual Meeting and Exposition of the American-Society-of-Hematology
   (ASH)
CY DEC 04-07, 2010
CL Orlando, FL
SP Amer Soc Hematol (ASH)
C1 [Fasano, Ross M.] Childrens Natl Med Ctr, Dept Transfus Med, Washington, DC 20892 USA.
   [Adams, Sharon; Flegel, Willy A.] NIH, Hematol Branch, NIH, Bethesda, MD 20892 USA.
   [Smith, Aleah; Donohue, Theresa; Bolan, Charles D., Jr.; Sugimoto, Kyoko; Childs, Richard] NHLBI, 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 19
PY 2010
VL 116
IS 21
BP 483
EP 483
PG 1
WC Hematology
SC Hematology
GA 752BH
UT WOS:000289662201212
ER

PT J
AU Feng, XM
   Scheinberg, P
   Nunez, O
   Biancotto, A
   Takaku, T
   Mccoy, JP
   Young, NS
AF Feng, Xingmin
   Scheinberg, Phillip
   Nunez, Olga
   Biancotto, Angelique
   Takaku, Tomoiku
   McCoy, J. Philip
   Young, Neal S.
TI Serum Sickness and Plasma Cytokine Profiles After Treatment with
   Antithymocyte Globulin In Severe Aplastic Anemia Patients
SO BLOOD
LA English
DT Meeting Abstract
CT 52nd Annual Meeting of the American-Society-of-Hematology (ASH)
CY DEC 04-07, 2010
CL Orlando, FL
SP Amer Soc Hematol
C1 [Feng, Xingmin; Scheinberg, Phillip; Nunez, Olga; Takaku, Tomoiku; Young, Neal S.] NHLBI, Hematol Branch, NIH, Bethesda, MD 20892 USA.
RI Scheinberg, Phillip/H-5251-2012
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 19
PY 2010
VL 116
IS 21
BP 501
EP 501
PG 1
WC Hematology
SC Hematology
GA 752BH
UT WOS:000289662201265
ER

PT J
AU Calado, R
   Savage, SA
   Peterson, NR
   Takaku, T
   Lansdorp, PM
   Maric, I
   Young, NS
AF Calado, Rodrigo
   Savage, Sharon A.
   Peterson, Nathan R.
   Takaku, Tomoiku
   Lansdorp, Peter M.
   Maric, Irina
   Young, Neal S.
TI TINF2 Mutations In Patients with Aplastic Anemia Result In Low TIN2
   Expression In Hematopoietic Cells and Very Short Telomeres
SO BLOOD
LA English
DT Meeting Abstract
CT 52nd Annual Meeting of the American-Society-of-Hematology (ASH)
CY DEC 04-07, 2010
CL Orlando, FL
SP Amer Soc Hematol
C1 [Takaku, Tomoiku] NHLBI, NIH, Hematol Branch, Bethesda, MD 20892 USA.
   [Savage, Sharon A.] NCI, Clin Genet Branch, Div Canc Epidemiol & Genet, Rockville, MD USA.
   [Lansdorp, Peter M.] British Columbia Canc Res Ctr, Terry Fox Lab, Vancouver, BC V5Z 1L3, Canada.
   [Maric, Irina] NIH, Dept Lab Med, Ctr Clin, Bethesda, MD 20892 USA.
RI Calado, Rodrigo/G-2619-2011; Savage, Sharon/B-9747-2015
OI Savage, Sharon/0000-0001-6006-0740
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 19
PY 2010
VL 116
IS 21
BP 502
EP 503
PG 2
WC Hematology
SC Hematology
GA 752BH
UT WOS:000289662201268
ER

PT J
AU Farrar, JE
   Vlachos, A
   Atsidaftos, E
   Carlson-Donohoe, H
   Ellis, SR
   Markello, TC
   Arceci, RJ
   Lipton, JM
   Bodine, DM
AF Farrar, Jason E.
   Vlachos, Adrianna
   Atsidaftos, Eva
   Carlson-Donohoe, Hannah
   Ellis, Steven R.
   Markello, Thomas C.
   Arceci, Robert J.
   Lipton, Jeffrey M.
   Bodine, David M.
TI SNP Array Genotyping Reveals Constitutional and Mosaic Losses of
   Ribosomal Protein Gene Regions In Patients with Diamond Blackfan Anemia
   without Ribosomal Protein Gene Mutations
SO BLOOD
LA English
DT Meeting Abstract
CT 52nd Annual Meeting of the American-Society-of-Hematology (ASH)
CY DEC 04-07, 2010
CL Orlando, FL
SP Amer Soc Hematol
C1 [Farrar, Jason E.; Arceci, Robert J.] Sidney Kimmel Comprehens Canc Ctr Johns Hopkins, Dept Oncol, Div Pediat Oncol, Baltimore, MD USA.
   [Vlachos, Adrianna; Atsidaftos, Eva; Lipton, Jeffrey M.] Hofstra Univ Sch Med, Div Hematol Oncol & Stem Cell Transplantat, Feinstein Inst Med Res, Steven & Alexandra Cohen Childrens Med Ctr, New Hyde Pk, NY USA.
   [Carlson-Donohoe, Hannah; Markello, Thomas C.] NHGRI, NIH, Med Genet Branch, Bethesda, MD 20892 USA.
   [Ellis, Steven R.] Univ Louisville, Dept Biochem & Mol Biol, Louisville, KY 40292 USA.
   [Bodine, David M.] NHGRI, Hematopoiesis Sect, Genet & Mol Biol Branch, NIH, 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 19
PY 2010
VL 116
IS 21
BP 503
EP 504
PG 2
WC Hematology
SC Hematology
GA 752BH
UT WOS:000289662201271
ER

PT J
AU Scheinberg, P
   Wu, CO
   Scheinberg, P
   Nunez, O
   Sloand, EM
   Young, NS
AF Scheinberg, Phillip
   Wu, Colin O.
   Scheinberg, Priscila
   Nunez, Olga
   Sloand, Elaine M.
   Young, Neal S.
TI Alemtuzumab (Campath) Monotherapy for Severe Aplastic Anemia
SO BLOOD
LA English
DT Meeting Abstract
CT 52nd Annual Meeting of the American-Society-of-Hematology (ASH)
CY DEC 04-07, 2010
CL Orlando, FL
SP Amer Soc Hematol
C1 [Scheinberg, Phillip; Scheinberg, Priscila; Nunez, Olga; Sloand, Elaine M.; Young, Neal S.] NHLBI, Hematol Branch, NIH, Bethesda, MD 20892 USA.
   [Wu, Colin O.] NHLBI, Off Biostat Res, NIH, Bethesda, MD 20892 USA.
RI Scheinberg, Phillip/H-5251-2012
NR 0
TC 0
Z9 0
U1 1
U2 2
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 19
PY 2010
VL 116
IS 21
BP 503
EP 503
PG 1
WC Hematology
SC Hematology
GA 752BH
UT WOS:000289662201270
ER

PT J
AU Giri, N
   Alter, BP
   Savage, SA
   Pan, YJ
   Williams, M
   Kemp, T
   Penrose, K
   Falk, R
   Pinto, L
AF Giri, Neelam
   Alter, Blanche P.
   Savage, Sharon A.
   Pan, Yuanji
   Williams, Markus
   Kemp, Troy
   Penrose, Kerri
   Falk, Roni
   Pinto, Ligia
TI Studies of Immune Function In the Inherited Bone Marrow Failure
   Syndromes
SO BLOOD
LA English
DT Meeting Abstract
CT 52nd Annual Meeting of the American-Society-of-Hematology (ASH)
CY DEC 04-07, 2010
CL Orlando, FL
SP Amer Soc Hematol
C1 [Giri, Neelam; Savage, Sharon A.] NCI, Clin Genet Branch, Div Canc Epidemiol & Genet, Rockville, MD USA.
   [Pan, Yuanji; Williams, Markus; Kemp, Troy; Penrose, Kerri; Pinto, Ligia] NCI, Human Papilloma Virus Immunol Lab, Frederick, MD USA.
   [Falk, Roni] NCI, Hormonal & Reprod Epidemiol Branch, Rockville, MD USA.
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 19
PY 2010
VL 116
IS 21
BP 504
EP 504
PG 1
WC Hematology
SC Hematology
GA 752BH
UT WOS:000289662201272
ER

PT J
AU Stroncek, D
   Jin, P
   Castiello, L
   Tran, K
   Kuznetsov, S
   Balakumaran, A
   Klein, HG
   Robey, P
   Sabatino, M
AF Stroncek, David
   Jin, Ping
   Castiello, Luciano
   Tran, Katherine
   Kuznetsov, Sergei
   Balakumaran, Arun
   Klein, Harvey G.
   Robey, Pamela
   Sabatino, Marianna
TI Tracking Senescence In Human Bone Marrow Stromal Cell (BMSC) Cultures
SO BLOOD
LA English
DT Meeting Abstract
CT 52nd Annual Meeting of the American-Society-of-Hematology (ASH)
CY DEC 04-07, 2010
CL Orlando, FL
SP Amer Soc Hematol
C1 [Stroncek, David; Jin, Ping; Castiello, Luciano; Tran, Katherine; Klein, Harvey G.; Sabatino, Marianna] NIH, Ctr Clin, Bethesda, MD 20892 USA.
   [Balakumaran, Arun; Robey, Pamela] Natl Inst Dent & Craniofacial Res, NIH, Bethesda, MD USA.
RI Robey, Pamela/H-1429-2011
OI Robey, Pamela/0000-0002-5316-5576
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 19
PY 2010
VL 116
IS 21
BP 507
EP 507
PG 1
WC Hematology
SC Hematology
GA 752BH
UT WOS:000289662201282
ER

PT J
AU Melenhorst, JJ
   Leen, AM
   Bollard, CM
   Quigley, MF
   Price, DA
   Rooney, CM
   Brenner, MK
   Barrett, AJ
   Heslop, HE
AF Melenhorst, J. Joseph
   Leen, Ann M.
   Bollard, Catherine M.
   Quigley, Maire F.
   Price, David A.
   Rooney, Cliona M.
   Brenner, Malcolm K.
   Barrett, A. John
   Heslop, Helen E.
TI Allogeneic Virus-Specific T Cells with HLA Alloreactivity Do Not Produce
   Graft-Versus-Host Disease In Human Subjects.
SO BLOOD
LA English
DT Meeting Abstract
CT 52nd Annual Meeting of the American-Society-of-Hematology (ASH)
CY DEC 04-07, 2010
CL Orlando, FL
SP Amer Soc Hematol
C1 [Barrett, A. John] NHLBI, Hematol Branch, NIH, Bethesda, MD 20892 USA.
   [Rooney, Cliona M.; Brenner, Malcolm K.; Heslop, Helen E.] Methodist Hosp, Texas Childrens Hosp, Baylor Coll Med, Ctr Cell & Gene Therapy, Houston, TX 77030 USA.
   [Quigley, Maire F.; Price, David A.] NIAID, 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 19
PY 2010
VL 116
IS 21
BP 537
EP 537
PG 1
WC Hematology
SC Hematology
GA 752BH
UT WOS:000289662201355
ER

PT J
AU Borge, PD
   Theobald, N
   DeCastro, R
   Malech, HL
   Leitman, S
   Kang, EM
AF Borge, P. Dayand, Jr.
   Theobald, Narda
   DeCastro, Rosamma
   Malech, Harry L.
   Leitman, Susan
   Kang, Elizabeth M.
TI Successful Control of Preexistent Active Infection by Granulocyte
   Transfusions During Conditioning Induced Cytopenia In Patients with
   Chronic Granulomatous Disease Undergoing Hematopoietic Stem Cell
   Transplant
SO BLOOD
LA English
DT Meeting Abstract
CT 52nd Annual Meeting of the American-Society-of-Hematology (ASH)
CY DEC 04-07, 2010
CL Orlando, FL
SP Amer Soc Hematol
C1 [Borge, P. Dayand, Jr.; Leitman, Susan] NIH, Dept Transfus Med, Ctr Clin, Bethesda, MD 20892 USA.
   [Theobald, Narda; DeCastro, Rosamma; Malech, Harry L.; Kang, Elizabeth M.] NIAID, Host Def Lab, NIH, 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 19
PY 2010
VL 116
IS 21
BP 569
EP 570
PG 2
WC Hematology
SC Hematology
GA 752BH
UT WOS:000289662201432
ER

PT J
AU Aue, G
   Soto, S
   Valdez, J
   Arthur, DC
   Tian, X
   Wiestner, A
AF Aue, Georg
   Soto, Susan
   Valdez, Janet
   Arthur, Diane C.
   Tian, Xin
   Wiestner, Adrian
TI Phase II Trial of Pulse Dosed Lenalidomide In Previously Treated Chronic
   Lymphocytic Leukemia
SO BLOOD
LA English
DT Meeting Abstract
CT 52nd Annual Meeting of the American-Society-of-Hematology (ASH)
CY DEC 04-07, 2010
CL Orlando, FL
SP Amer Soc Hematol
C1 [Aue, Georg; Soto, Susan; Valdez, Janet] NHLBI, Hematol Branch, NIH, Bethesda, MD 20892 USA.
   [Arthur, Diane C.] NCI, Pathol Lab, NIH, Bethesda, MD 20892 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 19
PY 2010
VL 116
IS 21
BP 595
EP 595
PG 1
WC Hematology
SC Hematology
GA 752BH
UT WOS:000289662201486
ER

PT J
AU Uchida, N
   Bonifacino, A
   Krouse, AE
   Price, SD
   Fasano, RM
   Csako, G
   Leitman, SF
   Metzger, ME
   Hsieh, MM
   Mattapallil, JJ
   Tisdale, JF
   Donahue, RE
AF Uchida, Naoya
   Bonifacino, Aylin
   Krouse, Allen E.
   Price, Sandra D.
   Fasano, Ross M.
   Csako, Gyorgy
   Leitman, Susan F.
   Metzger, Mark E.
   Hsieh, Matthew M.
   Mattapallil, Joseph J.
   Tisdale, John F.
   Donahue, Robert E.
TI Long-Term Reconstitution of Transduced Rhesus CD34+Cells Mobilized by
   G-CSF and Plerixafor.
SO BLOOD
LA English
DT Meeting Abstract
CT 52nd Annual Meeting of the American-Society-of-Hematology (ASH)
CY DEC 04-07, 2010
CL Orlando, FL
SP Amer Soc Hematol
C1 [Uchida, Naoya; Hsieh, Matthew M.; Tisdale, John F.] NHLBI, Mchb, NIH, Bethesda, MD 20892 USA.
   [Bonifacino, Aylin; Krouse, Allen E.; Price, Sandra D.; Metzger, Mark E.; Donahue, Robert E.] NHLBI, Hematol Branch, Bethesda, MD 20892 USA.
   [Fasano, Ross M.; Leitman, Susan F.] NIH, Dept Transfus Med, Ctr Clin, Bethesda, MD 20892 USA.
   [Csako, Gyorgy] NIH, Dept Lab Med, Ctr Clin, Bethesda, MD 20892 USA.
   [Mattapallil, Joseph J.] Uniformed Serv Univ Hlth Sci, Dept Microbiol & Immunol, Bethesda, MD 20814 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 19
PY 2010
VL 116
IS 21
BP 620
EP 621
PG 2
WC Hematology
SC Hematology
GA 752BH
UT WOS:000289662201551
ER

PT J
AU Yokoyama, H
   Harigae, H
   Childs, R
AF Yokoyama, Hisayuki
   Harigae, Hideo
   Childs, Richard
TI Blockade of T Cell Anergy by Tyrosine Kinase Inhibitor, Sorafenib May
   Induce Exacerbation of Gvhd In Allogeneic Hematopoietic Stem Cell
   Transplantation.
SO BLOOD
LA English
DT Meeting Abstract
CT 52nd Annual Meeting of the American-Society-of-Hematology (ASH)
CY DEC 04-07, 2010
CL Orlando, FL
SP Amer Soc Hematol
C1 [Yokoyama, Hisayuki] Natl Hosp Org, Sendai Med Ctr, Dept Hematol, Sendai, Miyagi, Japan.
   [Harigae, Hideo] Tohoku Univ, Grad Sch Med, Sendai, Miyagi 980, Japan.
   [Childs, Richard] NHLBI, Hematol Branch, NIH, 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 19
PY 2010
VL 116
IS 21
BP 624
EP 624
PG 1
WC Hematology
SC Hematology
GA 752BH
UT WOS:000289662201560
ER

PT J
AU Staber, JM
   Burnight, ER
   Korsakov, P
   Kaminski, J
   Craig, NL
   McCray, PB
AF Staber, Janice M.
   Burnight, Erin R.
   Korsakov, Pavel
   Kaminski, Joseph
   Craig, Nancy L.
   McCray, Paul B.
TI A Gene Transfer Approach towards Hemophilia A Correction Using the
   Piggybac Transposon Vector
SO BLOOD
LA English
DT Meeting Abstract
CT 52nd Annual Meeting of the American-Society-of-Hematology (ASH)
CY DEC 04-07, 2010
CL Orlando, FL
SP Amer Soc Hematol
C1 [Staber, Janice M.; Burnight, Erin R.; Korsakov, Pavel; McCray, Paul B.] Univ Iowa Hosp & Clin, Iowa City, IA 52242 USA.
   [Kaminski, Joseph] NIH, Med Coll Georgia, Bethesda, MD 20892 USA.
   [Craig, Nancy L.] Johns Hopkins Univ, Sch Med, Baltimore, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 3
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 19
PY 2010
VL 116
IS 21
BP 631
EP 631
PG 1
WC Hematology
SC Hematology
GA 752BH
UT WOS:000289662201579
ER

PT J
AU Aerbajinai, W
   Chin, K
   Lee, HW
   Zhu, JQ
   Rodgers, GP
AF Aerbajinai, Wulin
   Chin, Kyung
   Lee, Hyun Woo
   Zhu, Jianqiong
   Rodgers, Griffin P.
TI Glia Maturation Factor-Gamma Negatively Modulates TLR4 Signaling In
   Macrophages Induced by Lipopolysaccharide (LPS)
SO BLOOD
LA English
DT Meeting Abstract
CT 52nd Annual Meeting of the American-Society-of-Hematology (ASH)
CY DEC 04-07, 2010
CL Orlando, FL
SP Amer Soc Hematol
C1 [Aerbajinai, Wulin; Chin, Kyung; Lee, Hyun Woo; Zhu, Jianqiong; Rodgers, Griffin P.] NHLBI, NIH, Mol & Clin 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 19
PY 2010
VL 116
IS 21
BP 633
EP 633
PG 1
WC Hematology
SC Hematology
GA 752BH
UT WOS:000289662201584
ER

PT J
AU DiMeglio, LA
   Bolyard, AA
   Marrero, TM
   Alter, BP
   Bonilla, MA
   Boxer, LA
   Link, D
   Newburger, PE
   Rosenberg, PS
   Shimamura, A
   Dale, DC
AF DiMeglio, L. A.
   Bolyard, Audrey Anna
   Marrero, Tracy M.
   Alter, Blanche P.
   Bonilla, Mary Ann
   Boxer, Laurence A.
   Link, Dan
   Newburger, Peter E.
   Rosenberg, Philip S.
   Shimamura, Akiko
   Dale, David C.
TI The Risk of Low Bone Mineral Density with Long-Term G-CSF Therapy for
   Severe Chronic Neutropenia
SO BLOOD
LA English
DT Meeting Abstract
CT 52nd Annual Meeting of the American-Society-of-Hematology (ASH)
CY DEC 04-07, 2010
CL Orlando, FL
SP Amer Soc Hematol
C1 [DiMeglio, L. A.] Indiana Univ, Sch Med, Dept Pediat, Indianapolis, IN 46202 USA.
   [Bolyard, Audrey Anna; Marrero, Tracy M.] Univ Washington, Dept Med, Severe Chron Neutropenia Int Registry, Seattle, WA USA.
   [Alter, Blanche P.] NCI, Rockville, MD USA.
   [Bonilla, Mary Ann] St Josephs Childrens Hosp, Paterson, NJ USA.
   [Boxer, Laurence A.] Univ Michigan, Ann Arbor, MI 48109 USA.
   [Link, Dan] Washington Univ, Sch Med, Div Bone Marrow Transplantat, St Louis, MO USA.
   [Newburger, Peter E.] Univ Massachusetts, Sch Med, Dept Pediat, Worcester, MA USA.
   [Rosenberg, Philip S.] NCI, NIH, Div Canc Epidemiol & Genet, Rockville, MD USA.
   [Shimamura, Akiko] Fred Hutchinson Canc Res Ctr, Seattle, WA 98104 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 19
PY 2010
VL 116
IS 21
BP 634
EP 634
PG 1
WC Hematology
SC Hematology
GA 752BH
UT WOS:000289662201586
ER

PT J
AU Boxer, LA
   Bolyard, AA
   Marrero, TM
   Alter, BP
   Bonilla, MA
   Link, D
   Newburger, PE
   Rosenberg, PS
   Shimamura, A
   Dale, DC
AF Boxer, Laurence A.
   Bolyard, Audrey Anna
   Marrero, Tracy M.
   Alter, Blanche P.
   Bonilla, Mary Ann
   Link, Dan
   Newburger, Peter E.
   Rosenberg, Philip S.
   Shimamura, Akiko
   Dale, David C.
TI Outcomes of Pregnancies for Women with Severe Chronic Neutropenia with
   or without G-CSF Treatment
SO BLOOD
LA English
DT Meeting Abstract
CT 52nd Annual Meeting of the American-Society-of-Hematology (ASH)
CY DEC 04-07, 2010
CL Orlando, FL
SP Amer Soc Hematol
C1 [Boxer, Laurence A.] Univ Michigan, Ann Arbor, MI 48109 USA.
   [Bolyard, Audrey Anna; Marrero, Tracy M.] Univ Washington, Dept Med, Severe Chron Neutropenia Int Registry, Seattle, WA USA.
   [Rosenberg, Philip S.] NCI, NIH, Div Canc Epidemiol & Genet, Rockville, MD USA.
   [Bonilla, Mary Ann] St Josephs Childrens Hosp, Paterson, NJ USA.
   [Link, Dan] Washington Univ, Sch Med, Div Bone Marrow Transplantat, St Louis, MO USA.
   [Newburger, Peter E.] Univ Massachusetts, Sch Med, Dept Pediat, Worcester, MA USA.
   [Shimamura, Akiko] Fred Hutchinson Canc Res Ctr, Seattle, WA 98104 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 19
PY 2010
VL 116
IS 21
BP 635
EP 636
PG 2
WC Hematology
SC Hematology
GA 752BH
UT WOS:000289662201592
ER

PT J
AU Ou, X
   Chae, HD
   Wang, RH
   Shelley, WC
   Cooper, S
   Taylor, T
   Kim, YJ
   Deng, CX
   Yoder, MC
   Broxmeyer, HE
AF Ou, Xuan
   Chae, Hee-Don
   Wang, Rui-Hong
   Shelley, William C.
   Cooper, Scott
   Taylor, Tammi
   Kim, Young-June
   Deng, Chu-Xia
   Yoder, Mervin C.
   Broxmeyer, Hal E.
TI SIRT1 Deficiency Compromises Mouse Embryonic Stem Cell Differentiation,
   and Embryonic and Adult Hematopoiesis In the Mouse
SO BLOOD
LA English
DT Meeting Abstract
CT 52nd Annual Meeting of the American-Society-of-Hematology (ASH)
CY DEC 04-07, 2010
CL Orlando, FL
SP Amer Soc Hematol
C1 [Shelley, William C.] Indiana Univ Sch Med, Dept Pediat, Indianapolis, IN USA.
   [Wang, Rui-Hong; Deng, Chu-Xia] NIDDK, Genet Dev & Dis Branch, NIH, Bethesda, MD USA.
   [Yoder, Mervin C.] Wells Ctr Pediat Res, Canc Res Inst, Indianapolis, IN USA.
   [Broxmeyer, Hal E.] Indiana Univ Sch Med, Res Inst 2, Indianapolis, IN USA.
RI Ou, Xuan/C-4871-2012
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 19
PY 2010
VL 116
IS 21
BP 678
EP 679
PG 2
WC Hematology
SC Hematology
GA 752BH
UT WOS:000289662201714
ER

PT J
AU Nouraie, M
   Barst, RJ
   Rosenzweig, EB
   Sachdev, V
   Machado, RF
   Hassell, K
   Gibbs, JSR
   Little, JA
   Schraufnagel, DE
   Krishnamurti, L
   Novelli, EM
   Girgis, RE
   Morris, CR
   Badesch, DB
   Lanzkron, S
   Castro, O
   Goldsmith, JC
   Gladwin, M
   Gordeuk, VR
   Kato, GJ
AF Nouraie, Mehdi
   Barst, Robyn J.
   Rosenzweig, Erika Berman
   Sachdev, Vandana
   Machado, Roberto F.
   Hassell, Kathryn
   Gibbs, J. Simon R.
   Little, Jane A.
   Schraufnagel, Dean E.
   Krishnamurti, Lakshmanan
   Novelli, Enrico M.
   Girgis, Reda E.
   Morris, Claudia R.
   Badesch, David B.
   Lanzkron, Sophie
   Castro, Oswaldo
   Goldsmith, Jonathan C.
   Gladwin, Mark
   Gordeuk, Victor R.
   Kato, Gregory J.
TI NT-Probnp as a Marker of Cardiopulmonary Compromise and Exercise
   Limitation In Adults with Sickle Cell Anemia In the Walk-PHaSST Study.
SO BLOOD
LA English
DT Meeting Abstract
CT 52nd Annual Meeting of the American-Society-of-Hematology (ASH)
CY DEC 04-07, 2010
CL Orlando, FL
SP Amer Soc Hematol
ID BRAIN NATRIURETIC PEPTIDE; DISEASE
C1 [Nouraie, Mehdi; Gordeuk, Victor R.] Howard Univ, Ctr Sickle Cell Dis, Washington, DC 20059 USA.
   [Barst, Robyn J.; Rosenzweig, Erika Berman] Columbia Univ, New York, NY USA.
   [Sachdev, Vandana] NHLBI, Translat Med Branch, NIH, Bethesda, MD 20892 USA.
   [Machado, Roberto F.; Schraufnagel, Dean E.; Badesch, David B.] Univ Illinois, Chicago, IL USA.
   [Hassell, Kathryn] Univ Colorado, Hlth Sci Ctr, Denver, CO USA.
   [Gibbs, J. Simon R.; Little, Jane A.] Univ London Imperial Coll Sci Technol & Med, Natl Heart & Lung Inst, London, England.
   [Krishnamurti, Lakshmanan] Childrens Hosp Pittsburgh, Pittsburgh, PA 15213 USA.
   [Novelli, Enrico M.] Univ Pittsburgh, Dept Med, Pittsburgh, PA USA.
   [Girgis, Reda E.] Johns Hopkins Univ, Baltimore, MD USA.
   [Morris, Claudia R.] Childrens Hosp, Oakland, CA 94609 USA.
   [Morris, Claudia R.] Res Ctr Oakland, Oakland, CA USA.
   [Lanzkron, Sophie] Johns Hopkins Sch Med, Baltimore, MD USA.
   [Castro, Oswaldo] Howard Univ, Ctr Sickle Cell Dis, Potomac, MD USA.
   [Goldsmith, Jonathan C.] NHLBI, NIH, Rockville, MD USA.
   [Gladwin, Mark] Univ Pittsburgh, Vasc Med Inst Pulm, Pittsburgh, PA USA.
   [Kato, Gregory J.] NHLBI, Sickle Cell Vasc Dis Sect, NIH, Bethesda, MD 20892 USA.
RI Kato, Gregory/I-7615-2014
OI Kato, Gregory/0000-0003-4465-3217
NR 4
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 19
PY 2010
VL 116
IS 21
BP 688
EP 688
PG 1
WC Hematology
SC Hematology
GA 752BH
UT WOS:000289662201740
ER

PT J
AU Castro, O
   Nouraie, M
   Niu, XM
   Rana, S
   Luchtman-Jones, L
   Campbell, A
   Minniti, C
   Kato, G
   Gladwin, M
   Gordeuk, VR
AF Castro, Oswald
   Nouraie, Mehdi
   Niu, Xiaomei
   Rana, Sohail
   Luchtman-Jones, Lori
   Campbell, Andrew
   Minniti, Caterina
   Kato, Gregory
   Gladwin, Mark
   Gordeuk, Victor R.
TI Serum B12 Levels In Children with Sickle Cell Disease Are Lower Than In
   Healthy Control Subjects
SO BLOOD
LA English
DT Meeting Abstract
CT 52nd Annual Meeting of the American-Society-of-Hematology (ASH)
CY DEC 04-07, 2010
CL Orlando, FL
SP Amer Soc Hematol
C1 [Castro, Oswald; Nouraie, Mehdi; Niu, Xiaomei; Gordeuk, Victor R.] Howard Univ, Ctr Sickle Cell Dis, Washington, DC 20059 USA.
   [Luchtman-Jones, Lori] Childrens Natl Med Ctr, Washington, DC 20010 USA.
   [Campbell, Andrew] Univ Michigan, Med Ctr, Ann Arbor, MI USA.
   [Minniti, Caterina] NHLBI, Vasc Med Branch, Bethesda, MD 20892 USA.
   [Kato, Gregory] NHLBI, Sickle Cell Vasc Dis Sect, NIH, Bethesda, MD 20892 USA.
   [Gladwin, Mark] Univ Pittsburgh, Vasc Med Inst Pulm, Pittsburgh, PA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 19
PY 2010
VL 116
IS 21
BP 691
EP 692
PG 2
WC Hematology
SC Hematology
GA 752BH
UT WOS:000289662201748
ER

PT J
AU Darbari, D
   Onyekwere, O
   Nouraie, M
   Kato, GJ
   Minniti, C
   Sable, C
   Ensing, G
   Dham, N
   Campbell, A
   Arteta, M
   Rana, S
   Gladwin, M
   Castro, O
   Gordeuk, VR
AF Darbari, Deepika
   Onyekwere, Onyinye
   Nouraie, Mehdi
   Kato, Gregory J.
   Minniti, Caterina
   Sable, Craig
   Ensing, Gregory
   Dham, Niti
   Campbell, Andrew
   Arteta, Manuel
   Rana, Sohail
   Gladwin, Mark
   Castro, Oswaldo
   Gordeuk, Victor R.
TI Epidemiology and Risk Factors for Pain In Children and Adolescent with
   Sickle Cell Anemia
SO BLOOD
LA English
DT Meeting Abstract
CT 52nd Annual Meeting of the American-Society-of-Hematology (ASH)
CY DEC 04-07, 2010
CL Orlando, FL
SP Amer Soc Hematol
C1 [Darbari, Deepika] Johns Hopkins Univ, NHLBI, Bethesda, MD USA.
   [Onyekwere, Onyinye; Nouraie, Mehdi; Gordeuk, Victor R.] Howard Univ, Ctr Sickle Cell Dis, Washington, DC 20059 USA.
   [Kato, Gregory J.] NHLBI, Sickle Cell Vasc Dis Sect, NIH, Bethesda, MD 20892 USA.
   [Minniti, Caterina] NHLBI, Vasc Med Branch, Bethesda, MD 20892 USA.
   [Dham, Niti] Childrens Natl Med Ctr, Dept Cardiol, Washington, DC 20010 USA.
   [Campbell, Andrew; Arteta, Manuel] Univ Michigan, Med Ctr, Ann Arbor, MI USA.
   [Gladwin, Mark] Univ Pittsburgh, Vasc Med Inst Pulm, Pittsburgh, PA USA.
   [Castro, Oswaldo] Howard Univ, Ctr Sickle Cell Dis, Potomac, 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 19
PY 2010
VL 116
IS 21
BP 693
EP 693
PG 1
WC Hematology
SC Hematology
GA 752BH
UT WOS:000289662201752
ER

PT J
AU Stringaris, K
   Barrett, AJ
   Hills, R
   Linch, DC
   Gale, R
   Allen, C
   Garland, P
   Sargent, R
   de Lavallade, H
   Alsuliman, A
   Khoder, A
   Gabriel, IH
   Sekine, T
   Burnett, A
   Rezvani, K
   Apperley, JF
AF Stringaris, Kate
   Barrett, A. John
   Hills, Robert
   Linch, David C.
   Gale, Rosemary
   Allen, Christopher
   Garland, Paula
   Sargent, Ruhena
   de Lavallade, Hugues
   Alsuliman, Abdullah
   Khoder, Ahmad
   Gabriel, Ian H.
   Sekine, Takuya
   Burnett, Alan
   Rezvani, Katayoun
   Apperley, Jane F.
TI A Distinct Signature of Natural Killer Cell KIR Gene Frequencies In
   Secondary AML Compared with De Novo AML and Normal Controls.
SO BLOOD
LA English
DT Meeting Abstract
CT 52nd Annual Meeting of the American-Society-of-Hematology (ASH)
CY DEC 04-07, 2010
CL Orlando, FL
SP Amer Soc Hematol
C1 [Stringaris, Kate; Garland, Paula; Sargent, Ruhena; de Lavallade, Hugues; Alsuliman, Abdullah; Khoder, Ahmad; Gabriel, Ian H.; Sekine, Takuya; Rezvani, Katayoun; Apperley, Jane F.] Univ London Imperial Coll Sci Technol & Med, Dept Haematol, Hammersmith Hosp, London, England.
   [Barrett, A. John] NHLBI, Hematol Branch, NIH, Bethesda, MD 20892 USA.
   [Hills, Robert; Burnett, Alan] Cardiff Univ, Sch Med, Dept Haematol, Cardiff, S Glam, Wales.
   [Linch, David C.; Gale, Rosemary; Allen, Christopher] UCL, Dept Haematol, Inst Canc, London, England.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 19
PY 2010
VL 116
IS 21
BP 711
EP 712
PG 2
WC Hematology
SC Hematology
GA 752BH
UT WOS:000289662201798
ER

PT J
AU Johnson, NA
   Connors, JM
   Ben-Neriah, S
   Rogic, S
   Savage, KJ
   Steidl, C
   Horsman, DE
   Slack, GW
   Sehn, L
   Chan, WC
   Iqbal, J
   Meyer, PN
   Lenz, G
   Wright, GW
   Rimsza, LM
   Valentino, C
   Brunhoeber, P
   Grogan, T
   Braziel, RM
   Cook, J
   Tubbs, RR
   Weisenburger, DD
   Campo, E
   Rosenwald, A
   Ott, G
   Delabie, J
   Jaffe, E
   Staudt, LM
   Gascoyne, RD
AF Johnson, Nathalie A.
   Connors, Joseph M.
   Ben-Neriah, Susana
   Rogic, Sanja
   Savage, Kerry Joanne
   Steidl, Christian
   Horsman, Douglas E.
   Slack, Graham W.
   Sehn, Laurie
   Chan, Wing-Chung
   Iqbal, Javeed
   Meyer, Paul N.
   Lenz, Georg
   Wright, George W.
   Rimsza, Lisa M.
   Valentino, Carlo
   Brunhoeber, Patrick
   Grogan, Thomas
   Braziel, Rita M.
   Cook, James
   Tubbs, Raymond R.
   Weisenburger, Dennis D.
   Campo, Elias
   Rosenwald, Andreas
   Ott, German
   Delabie, Jan
   Jaffe, Elaine
   Staudt, Louis M.
   Gascoyne, Randy D.
TI Concurrent BCL2 and MYC Protein Expression by Immunohistochemistry
   Determines Clinical Outcome In DLBCL Patients Treated with R-CHOP
SO BLOOD
LA English
DT Meeting Abstract
CT 52nd Annual Meeting of the American-Society-of-Hematology (ASH)
CY DEC 04-07, 2010
CL Orlando, FL
SP Amer Soc Hematol
C1 [Connors, Joseph M.; Ben-Neriah, Susana; Rogic, Sanja] British Columbia Canc Agcy, Vancouver Clin, Vancouver, BC V5Z 4E6, Canada.
   [Slack, Graham W.] British Columbia Canc Agcy, Dept Pathol, Vancouver, BC V5Z 4E6, Canada.
   [Sehn, Laurie] British Columbia Canc Agcy, Dept Med Oncol, Vancouver, BC V5Z 4E6, Canada.
   [Weisenburger, Dennis D.] Univ Nebraska Med Ctr, Dept Pathol, Omaha, NE USA.
   [Lenz, Georg] Univ Hosp Charite, Dept Hematol, Berlin, Germany.
   [Wright, George W.; Jaffe, Elaine] NCI, Ctr Canc Res, Bethesda, MD 20892 USA.
   [Rimsza, Lisa M.; Valentino, Carlo; Brunhoeber, Patrick; Grogan, Thomas] Univ Arizona, Tucson, AZ USA.
   [Braziel, Rita M.] Oregon Hlth & Sci Univ, Portland, OR 97201 USA.
   [Cook, James] Cleveland Clin, Pathol & Lab Med Inst, Cleveland, OH 44106 USA.
   [Tubbs, Raymond R.] Cleveland Clin Fdn, Cleveland, OH 44195 USA.
   [Campo, Elias] Hosp Clin Barcelona, Barcelona, Spain.
   [Rosenwald, Andreas; Ott, German] Univ Wurzburg, Inst Pathol, D-8700 Wurzburg, Germany.
   [Delabie, Jan] Oslo Univ Hosp, Dept Pathol, Oslo, Norway.
   [Staudt, Louis M.] NCI, Metab Branch, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 1
U2 2
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 19
PY 2010
VL 116
IS 21
BP 836
EP 836
PG 1
WC Hematology
SC Hematology
GA 752BH
UT WOS:000289662202228
ER

PT J
AU Jain, S
   Raghavachari, N
   Woodhouse, K
   Kaminski, N
   Gladwin, M
AF Jain, Shilpa
   Raghavachari, Nalini
   Woodhouse, Kimberly
   Kaminski, Naftali
   Gladwin, Mark
TI Characterization of Microrna Expression Profile In Platelets In Sickle
   Cell Disease
SO BLOOD
LA English
DT Meeting Abstract
CT 52nd Annual Meeting of the American-Society-of-Hematology (ASH)
CY DEC 04-07, 2010
CL Orlando, FL
SP Amer Soc Hematol
C1 [Jain, Shilpa] UPMC, Childrens Hosp Pittsburgh, Pittsburgh, PA USA.
   [Raghavachari, Nalini; Woodhouse, Kimberly] NHLBI, Pulm & Vasc Med Branch, Bethesda, MD 20892 USA.
   [Kaminski, Naftali] Univ Pittsburgh, Med Ctr, Pittsburgh, PA USA.
   [Gladwin, Mark] Univ Pittsburgh, Vasc Med Inst Pulm, Pittsburgh, PA USA.
NR 0
TC 0
Z9 0
U1 1
U2 2
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 19
PY 2010
VL 116
IS 21
BP 843
EP 844
PG 2
WC Hematology
SC Hematology
GA 752BH
UT WOS:000289662202253
ER

PT J
AU Lavelle, D
   Vaitkus, K
   Ling, YH
   Smith, N
   Chan, KK
   DeSimone, J
   Saunthararajah, Y
AF Lavelle, Donald
   Vaitkus, Kestis
   Ling, YongHua
   Smith, Nicola
   Chan, Kenneth K.
   DeSimone, Joseph
   Saunthararajah, Yogenthiran
TI Tetrahydrouridine Co-Administration Improves Oral Bioavailability and
   Dampens Inter-Individual Variability of Decitabine Pharmacokinetics In
   Baboons
SO BLOOD
LA English
DT Meeting Abstract
CT 52nd Annual Meeting of the American-Society-of-Hematology (ASH)
CY DEC 04-07, 2010
CL Orlando, FL
SP Amer Soc Hematol
C1 [Lavelle, Donald] Univ Illinois, Dept Med, Jesse Brown VA Med Ctr, Chicago, IL USA.
   [Ling, YongHua; Chan, Kenneth K.] Ohio State Univ, Coll Pharm, Columbus, OH 43210 USA.
   [Smith, Nicola] NCI, Dev Therapeut Program, Bethesda, MD 20892 USA.
   [Saunthararajah, Yogenthiran] Cleveland Clin, Cleveland, OH 44106 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 19
PY 2010
VL 116
IS 21
BP 863
EP 863
PG 1
WC Hematology
SC Hematology
GA 752BH
UT WOS:000289662202304
ER

PT J
AU Capitini, CM
   Guimond, M
   Fry, TJ
AF Capitini, Christian M.
   Guimond, Martin
   Fry, Terry J.
TI Gvhd Increases Apoptosis of CD8(+), but Not CD4(+), T Cells Expanded by
   Vaccines but Is Not Dependent on Fas Ligand
SO BLOOD
LA English
DT Meeting Abstract
CT 52nd Annual Meeting of the American-Society-of-Hematology (ASH)
CY DEC 04-07, 2010
CL Orlando, FL
SP Amer Soc Hematol
C1 [Capitini, Christian M.; Fry, Terry J.] NCI, Pediat Oncol Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
   [Guimond, Martin] Univ Montreal, Maisonneuve Rosemont Hosp, Montreal, 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 19
PY 2010
VL 116
IS 21
BP 870
EP 870
PG 1
WC Hematology
SC Hematology
GA 752BH
UT WOS:000289662202321
ER

PT J
AU Salzer, W
   Asselin, B
   Supko, J
   Devidas, M
   Kaiser, N
   Plourde, PV
   Winick, N
   Reaman, G
   Raetz, E
   Carroll, WL
   Hunger, S
AF Salzer, Wanda
   Asselin, Barbara
   Supko, Jeffrey
   Devidas, Meenakshi
   Kaiser, Nicole
   Plourde, Paul V.
   Winick, Naomi
   Reaman, Gregory
   Raetz, Elizabeth
   Carroll, William L.
   Hunger, Stephen
TI Administration of Erwinia Asparaginase (Erwinase (R)) Following Allergy
   to PEG-Asparaginase In Children and Young Adults with Acute
   Lymphoblastic Leukemia Treated on AALL07P2 Achieves Therapeutic Nadir
   Serum Asparaginase Activity: A Report From the Children's Oncology Group
   (COG).
SO BLOOD
LA English
DT Meeting Abstract
CT 52nd Annual Meeting of the American-Society-of-Hematology (ASH)
CY DEC 04-07, 2010
CL Orlando, FL
SP Amer Soc Hematol
C1 [Salzer, Wanda] NCI, Bethesda, MD 20892 USA.
   [Asselin, Barbara] Univ Rochester, Sch Med, Dept Pediat, Golisano Childrens Hosp URMC, Rochester, NY 14642 USA.
   [Supko, Jeffrey] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Boston, MA USA.
   [Devidas, Meenakshi] Univ Florida, Coll Med, Dept Biostat, Childrens Oncol Grp, Gainesville, FL USA.
   [Kaiser, Nicole] Childrens Hosp, Aurora, CO USA.
   [Plourde, Paul V.] EUSA Pharma, Langhorne, PA USA.
   [Winick, Naomi] Univ Texas SW Med Ctr Dallas, Div Pediat Hematol Oncol, Dallas, TX 75390 USA.
   [Reaman, Gregory] Childrens Natl Med Ctr, Dept Hematol Oncol, Washington, DC 20010 USA.
   [Raetz, Elizabeth] NYU, Langone Med Ctr, New York, NY USA.
   [Hunger, Stephen] Childrens Hosp, Aurora, CO USA.
   [Hunger, Stephen] Univ Colorado, Sch Med, Pediat Heme Onc BMT, Aurora, CO USA.
   [Carroll, William L.] NYU, Inst Canc, New York, NY USA.
NR 0
TC 2
Z9 2
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 19
PY 2010
VL 116
IS 21
BP 882
EP 882
PG 1
WC Hematology
SC Hematology
GA 752BH
UT WOS:000289662202357
ER

PT J
AU Alter, BP
   Giri, N
   Lansdorp, PM
   Baerlocher, GM
   Rosenberg, PS
   Savage, S
AF Alter, Blanche P.
   Giri, Neelam
   Lansdorp, Peter M.
   Baerlocher, Gabriela M.
   Rosenberg, Philip S.
   Savage, Sharon
TI Longitudinal Changes In Telomere Length In Patients with Dyskeratois
   Congenita.
SO BLOOD
LA English
DT Meeting Abstract
CT 52nd Annual Meeting of the American-Society-of-Hematology (ASH)
CY DEC 04-07, 2010
CL Orlando, FL
SP Amer Soc Hematol
C1 [Giri, Neelam] NCI, Clin Genet Branch, Div Canc Epidemiol & Genet, Rockville, MD USA.
   [Lansdorp, Peter M.] BC Canc Res Ctr, Terry Fox Lab, Vancouver, BC, Canada.
   [Baerlocher, Gabriela M.] Univ Bern, Inselspital Bern, Bern, Switzerland.
   [Rosenberg, Philip S.] NCI, Biostat Branch, Rockville, MD USA.
   [Savage, Sharon] NCI, Clin Genet Branch, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 19
PY 2010
VL 116
IS 21
BP 917
EP 918
PG 2
WC Hematology
SC Hematology
GA 752BH
UT WOS:000289662202453
ER

PT J
AU Rochowski, A
   Rosenberg, PS
   Alonzo, TA
   Gerbing, RB
   Lange, B
   Alter, BP
AF Rochowski, Andrzej
   Rosenberg, Philip S.
   Alonzo, Todd A.
   Gerbing, Robert B.
   Lange, Beverly
   Alter, Blanche P.
TI The Prevalence of Fanconi Anemia Among Patients with De Novo Acute
   Myelogenous Leukemia.
SO BLOOD
LA English
DT Meeting Abstract
CT 52nd Annual Meeting of the American-Society-of-Hematology (ASH)
CY DEC 04-07, 2010
CL Orlando, FL
SP Amer Soc Hematol
C1 [Rochowski, Andrzej] Childrens Natl Med Ctr, Ctr Canc & Blood Disorders, Washington, DC 20010 USA.
   [Rosenberg, Philip S.] NCI, Biostat Branch, Rockville, MD USA.
   [Alonzo, Todd A.] Univ So Calif, Keck Sch Med, Los Angeles, CA 90033 USA.
   [Gerbing, Robert B.] Childrens Oncol Grp, Arcadia, CA USA.
   [Lange, Beverly] Childrens Hosp Philadelphia, 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 19
PY 2010
VL 116
IS 21
BP 918
EP 918
PG 1
WC Hematology
SC Hematology
GA 752BH
UT WOS:000289662202455
ER

PT J
AU Slager, S
   Rabe, K
   Achenbach, S
   Vachon, C
   Goldin, L
   Strom, S
   Lanasa, MC
   Spector, LG
   Rassenti, LZ
   Leis, J
   Camp, N
   Glenn, M
   Kay, NE
   Cunningham, JM
   Hanson, CA
   Marti, GE
   Weinberg, JB
   Morrison, VA
   Link, B
   Call, T
   Caporaso, N
   Cerhan, J
AF Slager, Susan
   Rabe, Kari
   Achenbach, Sara
   Vachon, Celine
   Goldin, Lynn
   Strom, Sara
   Lanasa, Mark C.
   Spector, Logan G.
   Rassenti, Laura Z.
   Leis, Jose
   Camp, Nicola
   Glenn, Martha
   Kay, Neil E.
   Cunningham, Julie M.
   Hanson, Curtis A.
   Marti, Gerald E.
   Weinberg, J. Brice
   Morrison, Vicki A.
   Link, Brian
   Call, Timothy
   Caporaso, Neil
   Cerhan, James
TI Investigation of CLL-Susceptibility Loci with Monoclonal B-Cell
   Lymphocytosis (MBL) Risk and Confirmation of Recently Reported
   CLL-Susceptibility Loci
SO BLOOD
LA English
DT Meeting Abstract
CT 52nd Annual Meeting of the American-Society-of-Hematology (ASH)
CY DEC 04-07, 2010
CL Orlando, FL
SP Amer Soc Hematol
C1 [Hanson, Curtis A.] Mayo Clin, Div Hematopathol, Rochester, MN USA.
   [Goldin, Lynn] NCI, Div Canc Epidemiol & Genet, NIH, Bethesda, MD 20892 USA.
   [Strom, Sara] UT MD Anderson Canc Ctr, Houston, TX USA.
   [Lanasa, Mark C.] Duke Univ, Med Ctr, Durham, NC USA.
   [Spector, Logan G.] Univ Minnesota, Minneapolis, MN USA.
   [Rassenti, Laura Z.] UCSD, Moores Canc Ctr, La Jolla, CA USA.
   [Leis, Jose] Mayo Clin Arizona, Scottsdale, AZ USA.
   [Glenn, Martha] Univ Utah, Huntsman Canc Inst, Salt Lake City, UT USA.
   [Marti, Gerald E.] NHLBI, Hematol Branch, NIH, Potomac, MD USA.
   [Weinberg, J. Brice] VA & Duke Med Ctr, Durham, NC USA.
   [Morrison, Vicki A.] Univ Minnesota, VA Med Ctr, Minneapolis, MN USA.
   [Link, Brian] Univ Iowa, Iowa City, IA USA.
   [Cerhan, James] Mayo Fdn, 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 19
PY 2010
VL 116
IS 21
BP 1014
EP 1014
PG 1
WC Hematology
SC Hematology
GA 752BH
UT WOS:000289662202666
ER

PT J
AU Stumpel, DJPM
   Schotte, D
   Lange-Turenhout, EAM
   Schneider, P
   Seslija, L
   de Menezes, RX
   Marquez, VE
   Pieters, R
   Den Boer, ML
   Stam, R
AF Stumpel, Dominique J. P. M.
   Schotte, Diana
   Lange-Turenhout, Ellen A. M.
   Schneider, Pauline
   Seslija, Lidija
   de Menezes, Renee X.
   Marquez, Victor E.
   Pieters, Rob
   Den Boer, Monique L.
   Stam, Ronald
TI Methylation of Specific Microrna Genes In MLL-Rearranged Infant Acute
   Lymphoblastic Leukemia: Major Matters at a Micro Scale
SO BLOOD
LA English
DT Meeting Abstract
CT 52nd Annual Meeting of the American-Society-of-Hematology (ASH)
CY DEC 04-07, 2010
CL Orlando, FL
SP Amer Soc Hematol
C1 [Stumpel, Dominique J. P. M.; Schotte, Diana; Lange-Turenhout, Ellen A. M.; Schneider, Pauline; Seslija, Lidija; de Menezes, Renee X.; Den Boer, Monique L.; Stam, Ronald] Erasmus MC Sophia Childrens Hosp, Rotterdam, Netherlands.
   [Marquez, Victor E.] NCI, NIH, Ctr Canc Res, Biol Chem Lab, Frederick, MD 21701 USA.
   [Pieters, Rob] Sophia Childrens Hosp Rotterdam, Erasmus MC, Dept Pediat Hem Onc, Rotterdam, Netherlands.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 19
PY 2010
VL 116
IS 21
BP 1030
EP 1030
PG 1
WC Hematology
SC Hematology
GA 752BH
UT WOS:000289662202706
ER

PT J
AU Patel, C
   Gillet, JP
   Stenke, L
   Lindberg, M
   Bjorkholm, M
   Sjoberg, J
   Viktorsson, K
   Lewensohn, R
   Landgren, O
   Gottesman, MM
AF Patel, Chirayu
   Gillet, Jean-Pierre
   Stenke, Leif
   Lindberg, Marita
   Bjorkholm, Magnus
   Sjoberg, Jan
   Viktorsson, Kristina
   Lewensohn, Rolf
   Landgren, Ola
   Gottesman, Michael M.
TI Individualized Multidrug Resistance In Acute Myeloid Leukemia.
SO BLOOD
LA English
DT Meeting Abstract
CT 52nd Annual Meeting of the American-Society-of-Hematology (ASH)
CY DEC 04-07, 2010
CL Orlando, FL
SP Amer Soc Hematol
C1 [Patel, Chirayu; Gillet, Jean-Pierre; Gottesman, Michael M.] NCI, NIH, Cell Biol Lab, CCR, Bethesda, MD 20892 USA.
   [Bjorkholm, Magnus] Karolinska Univ Hosp, Div Hematol, Dept Med, Stockholm, Sweden.
   [Patel, Chirayu; Gillet, Jean-Pierre; Gottesman, Michael M.] Karolinska Inst, Stockholm, Sweden.
   [Landgren, Ola] NCI, NIH, Med Oncol Branch, Bethesda, MD 20892 USA.
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 19
PY 2010
VL 116
IS 21
BP 1033
EP 1033
PG 1
WC Hematology
SC Hematology
GA 752BH
UT WOS:000289662202714
ER

PT J
AU Novak, RL
   Harper, DP
   Caudell, DL
   Beachy, SH
   Chung, YJ
   Wolff, L
   Aplan, P
AF Novak, Rachel L.
   Harper, David P.
   Caudell, David L.
   Beachy, Sarah H.
   Chung, Yang Jo
   Wolff, Linda
   Aplan, Peter
TI Use of CALM-AF10 and NUP98-HOXD13 fusions to Identify Oncogenic Pathways
   That Collaborate with HOXA9 Overexpression.
SO BLOOD
LA English
DT Meeting Abstract
CT 52nd Annual Meeting of the American-Society-of-Hematology (ASH)
CY DEC 04-07, 2010
CL Orlando, FL
SP Amer Soc Hematol
C1 [Novak, Rachel L.; Beachy, Sarah H.; Chung, Yang Jo; Aplan, Peter] NCI, NIH, Genet Branch, Bethesda, MD 20892 USA.
   [Harper, David P.] Madigan Army Med Ctr, Dept Pediat, Tacoma, WA 98431 USA.
   [Caudell, David L.] Virginia Tech, Coll Vet Med Pathobiol, Blacksburg, VA USA.
   [Wolff, Linda] NCI, NIH, Cellular Oncol Lab, Bethesda, MD 20892 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 19
PY 2010
VL 116
IS 21
BP 1036
EP 1036
PG 1
WC Hematology
SC Hematology
GA 752BH
UT WOS:000289662202722
ER

PT J
AU Kreitman, RJ
   Tallman, MS
   Coutre, S
   Robak, T
   Wilson, WH
   Stetler-Stevenson, M
   Noel, P
   Fitz-Gerald, DJ
   Buzoianu, M
   Lechleider, RJ
   Pastan, I
AF Kreitman, Robert J.
   Tallman, Martin S.
   Coutre, Steven
   Robak, Tadeusz
   Wilson, Wyndham H.
   Stetler-Stevenson, Maryalice
   Noel, Pierre
   Fitz-Gerald, David J.
   Buzoianu, Manuela
   Lechleider, Robert J.
   Pastan, Ira
TI A Phase 1 Study of Moxetumomab Pasudotox, An Anti-CD22 Recombinant
   Immunotoxin, In Relapsed/Refractory Hairy Cell Leukemia (HCL): Updated
   Results.
SO BLOOD
LA English
DT Meeting Abstract
CT 52nd Annual Meeting of the American-Society-of-Hematology (ASH)
CY DEC 04-07, 2010
CL Orlando, FL
SP Amer Soc Hematol
C1 [Kreitman, Robert J.; Fitz-Gerald, David J.; Pastan, Ira] NCI, Mol Biol Lab, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
   [Tallman, Martin S.] Northwestern Univ, Sch Med, Chicago, IL USA.
   [Coutre, Steven] Stanford Univ, Sch Med, Stanford, CA 94305 USA.
   [Robak, Tadeusz] Med Univ Lodz, Dept Hematol, Lodz, Poland.
   [Stetler-Stevenson, Maryalice] NCI, Pathol Lab, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
   [Noel, Pierre] NIH, Dept Lab Med, Ctr Clin, Bethesda, MD 20892 USA.
   [Buzoianu, Manuela; Lechleider, Robert J.] MedImmune LLC, Gaithersburg, 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 19
PY 2010
VL 116
IS 21
BP 1042
EP 1043
PG 2
WC Hematology
SC Hematology
GA 752BH
UT WOS:000289662202739
ER

PT J
AU White, JG
   Gunay-Aygun, M
AF White, James G.
   Gunay-Aygun, Merel
TI The York Platelet Syndrome: A Third Case and New Findings.
SO BLOOD
LA English
DT Meeting Abstract
CT 52nd Annual Meeting of the American-Society-of-Hematology (ASH)
CY DEC 04-07, 2010
CL Orlando, FL
SP Amer Soc Hematol
C1 [White, James G.] Univ Minnesota, Lab Med Pathol & Pediat, Minneapolis, MN USA.
   [Gunay-Aygun, Merel] NIH, Bethesda, MD 20892 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 19
PY 2010
VL 116
IS 21
BP 1047
EP 1047
PG 1
WC Hematology
SC Hematology
GA 752BH
UT WOS:000289662202749
ER

PT J
AU Krishnamurti, L
   Goel, R
   Castro, O
   Barst, RJ
   Rosenzweig, EB
   Sachdev, V
   Machado, RF
   Gibbs, S
   Little, JA
   Schraufnagel, DE
   Girgis, RE
   Morris, CR
   Badesch, DB
   Lanzkron, S
   Goldsmith, JC
   Gordeuk, VR
   Kato, GJ
   Gladwin, M
   Hassell, K
AF Krishnamurti, Lakshmanan
   Goel, Ruchika
   Castro, Oswaldo
   Barst, Robyn J.
   Rosenzweig, Erika Berman
   Sachdev, Vandana
   Machado, Roberto F.
   Gibbs, Simon
   Little, Jane A.
   Schraufnagel, Dean E.
   Girgis, Reda E.
   Morris, Claudia R.
   Badesch, David B.
   Lanzkron, Sophie
   Goldsmith, Jonathan C.
   Gordeuk, Victor R.
   Kato, Gregory J.
   Gladwin, Mark
   Hassell, Kathryn
TI Chronic Pain Is An Independent Predictor of Lower 6 Minute Walk Distance
   In Patients with Sickle Cell Disease: Results From Walk-PHaSST Study
SO BLOOD
LA English
DT Meeting Abstract
CT 52nd Annual Meeting of the American-Society-of-Hematology (ASH)
CY DEC 04-07, 2010
CL Orlando, FL
SP Amer Soc Hematol
C1 [Krishnamurti, Lakshmanan; Goel, Ruchika] UPMC, Childrens Hosp Pittsburgh, Div Hematol Oncol BMT, Pittsburgh, PA USA.
   [Castro, Oswaldo] Howard Univ, Ctr Sickle Cell Dis, Potomac, MD USA.
   [Barst, Robyn J.; Rosenzweig, Erika Berman] Columbia Univ, New York, NY USA.
   [Sachdev, Vandana] NHLBI, Translat Med Branch, NIH, Bethesda, MD 20892 USA.
   [Machado, Roberto F.; Schraufnagel, Dean E.] Univ Illinois, Chicago, IL USA.
   [Gibbs, Simon] UCL, Sch Med, London W1N 8AA, England.
   [Little, Jane A.] Albert Einstein Coll Med, Bronx, NY 10467 USA.
   [Girgis, Reda E.] Johns Hopkins Univ, Baltimore, MD USA.
   [Morris, Claudia R.] Childrens Hosp & Res Ctr Oakland, Oakland, CA USA.
   [Badesch, David B.] Univ Illinois, Chicago, IL USA.
   [Lanzkron, Sophie] Johns Hopkins Sch Med, Baltimore, MD USA.
   [Goldsmith, Jonathan C.] NHLBI, NIH, Rockville, MD USA.
   [Gordeuk, Victor R.] Howard Univ, Ctr Sickle Cell Dis, Washington, DC 20059 USA.
   [Kato, Gregory J.] NHLBI, Sickle Cell Vasc Dis Sect, NIH, Bethesda, MD 20892 USA.
   [Gladwin, Mark] Univ Pittsburgh, Vasc Med Inst Pulm, Pittsburgh, PA USA.
   [Hassell, Kathryn] Univ Colorado, Hlth Sci Ctr, Denver, CO 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 19
PY 2010
VL 116
IS 21
BP 1096
EP 1097
PG 2
WC Hematology
SC Hematology
GA 752BH
UT WOS:000289662202881
ER

PT J
AU Minniti, C
   Alam, S
   Kato, GJ
   Nouraie, M
   Sable, C
   Ensing, G
   Campbell, A
   Rana, S
   Darbari, D
   Gladwin, M
   Castro, O
   Gordeuk, VR
AF Minniti, Caterina
   Alam, Shoaib
   Kato, Gregory J.
   Nouraie, Mehdi
   Sable, Craig
   Ensing, Gregory
   Campbell, Andrew
   Rana, Sohail
   Darbari, Deepika
   Gladwin, Mark
   Castro, Oswaldo
   Gordeuk, Victor R.
TI Evaluation of Exercise Capacity In Children with SCD by Six Minute Walk
   Test
SO BLOOD
LA English
DT Meeting Abstract
CT 52nd Annual Meeting of the American-Society-of-Hematology (ASH)
CY DEC 04-07, 2010
CL Orlando, FL
SP Amer Soc Hematol
C1 [Minniti, Caterina] NHLBI, Pulm & Vasc Med Branch, Bethesda, MD USA.
   [Kato, Gregory J.] NHLBI, Sickle Cell Vasc Dis Sect, NIH, Bethesda, MD 20892 USA.
   [Nouraie, Mehdi; Gordeuk, Victor R.] Howard Univ, Ctr Sickle Cell Dis, Washington, DC 20059 USA.
   [Sable, Craig] Childrens Natl Med Ctr, Washington, DC 20010 USA.
   [Campbell, Andrew] Univ Michigan, Med Ctr, Ann Arbor, MI 48109 USA.
   [Darbari, Deepika] Johns Hopkins Univ, NHLBI Pulm & Vasc Med, NHLBI, Bethesda, MD USA.
   [Gladwin, Mark] Univ Pittsburgh, Vasc Med Inst Pulm, Pittsburgh, PA USA.
   [Castro, Oswaldo] Howard Univ, Ctr Sickle Cell Dis, Potomac, 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 19
PY 2010
VL 116
IS 21
BP 1099
EP 1099
PG 1
WC Hematology
SC Hematology
GA 752BH
UT WOS:000289662202887
ER

PT J
AU Dampier, C
   Smith, WR
   Wager, C
   Bell, M
   Eckman, JR
   Hsu, LL
   McClish, D
   McKinlay, S
   Minitti, C
   Molokie, R
   Smith-Whitley, K
   Telen, MJ
   Weiner, D
   Miller, S
AF Dampier, Carlton
   Smith, Wally R.
   Wager, Carrie
   Bell, Margaret
   Eckman, James R.
   Hsu, Lewis L.
   McClish, Donna
   McKinlay, Sonja
   Minitti, Caterina
   Molokie, Robert
   Smith-Whitley, Kim
   Telen, Marilyn J.
   Weiner, Debra
   Miller, Scott
TI Initial Experience with the IMPROVE Trial-a Phase III Analgesic Trial
   for Hospitalized Sickle Cell Painful Episodes
SO BLOOD
LA English
DT Meeting Abstract
CT 52nd Annual Meeting of the American-Society-of-Hematology (ASH)
CY DEC 04-07, 2010
CL Orlando, FL
SP Amer Soc Hematol
C1 [Dampier, Carlton] Emory Univ, Atlanta, GA 30322 USA.
   [Smith, Wally R.; McClish, Donna] Virginia Commonwealth Univ, Richmond, VA USA.
   [Wager, Carrie; Bell, Margaret; McKinlay, Sonja] Emory Univ, Med Ctr, New England Res Inst, Atlanta, GA 30322 USA.
   [Eckman, James R.] Emory Univ, Med Ctr, Dept Hematol & Med Oncol, Atlanta, GA 30322 USA.
   [Hsu, Lewis L.] Childrens Natl Med Ctr, Washington, DC 20010 USA.
   [Minitti, Caterina] Univ Illinois, NIH, Ctr Clin, Chicago, IL USA.
   [Smith-Whitley, Kim] Childrens Hosp Phila, Div Hematol, Philadelphia, PA USA.
   [Telen, Marilyn J.] Duke Univ, Dept Med, Div Hematol, Durham, NC USA.
   [Weiner, Debra] Childrens Hosp Boston, New York, NY USA.
   [Miller, Scott] SUNY, New York, NY 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 19
PY 2010
VL 116
IS 21
BP 1100
EP 1100
PG 1
WC Hematology
SC Hematology
GA 752BH
UT WOS:000289662202890
ER

PT J
AU Mehari, A
   Tian, X
   Alam, S
   Xu, DH
   Seamon, C
   Gladwin, MT
   Machado, RF
   Kato, GJ
AF Mehari, Alem
   Tian, Xin
   Alam, Shoaib
   Xu, Dihua
   Seamon, Catherine
   Gladwin, Mark T.
   Machado, Roberto F.
   Kato, Gregory J.
TI Hemodynamic Parameters Predict Mortality In Sickle Cell Disease-Related
   Pulmonary Hypertension
SO BLOOD
LA English
DT Meeting Abstract
CT 52nd Annual Meeting of the American-Society-of-Hematology (ASH)
CY DEC 04-07, 2010
CL Orlando, FL
SP Amer Soc Hematol
C1 [Mehari, Alem; Alam, Shoaib; Seamon, Catherine; Kato, Gregory J.] NHLBI, Pulm & Vasc Med Branch, Bethesda, MD 20892 USA.
   [Tian, Xin; Xu, Dihua] NHLBI, Off Biostat Res, Bethesda, MD 20892 USA.
   [Gladwin, Mark T.] Univ Pittsburgh, Vasc Med Inst, Pittsburgh, PA USA.
   [Gladwin, Mark T.] Univ Pittsburgh, Crit Care Med Div, Pittsburgh, PA USA.
   [Machado, Roberto F.] Univ Illinois, Sect Pulm Crit Care Med Sleep & Allergy, Chicago, IL USA.
RI Kato, Gregory/I-7615-2014
OI Kato, Gregory/0000-0003-4465-3217
NR 0
TC 0
Z9 0
U1 0
U2 3
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 19
PY 2010
VL 116
IS 21
BP 1100
EP 1100
PG 1
WC Hematology
SC Hematology
GA 752BH
UT WOS:000289662202891
ER

PT J
AU Morton, LM
   Gilbert, ES
   Lynch, CF
   Hall, P
   Dores, GM
   Curtis, RE
   Storm, HH
   Johannesen, TB
   Stovall, M
   Smith, SA
   Weathers, R
   Aleman, BM
   Kleinerman, RA
   Fraumeni, JF
   Holowaty, EJ
   Pukkala, E
   Kaijser, M
   Hauptmann, M
   Fossa, SD
   Joensuu, H
   Andersson, M
   van den Belt-Dusebout, AW
   Vaalavirta, L
   Langmark, F
   Travis, LB
   van Leeuwen, FE
AF Morton, Lindsay M.
   Gilbert, Ethel S.
   Lynch, Charles F.
   Hall, Per
   Dores, Graca M.
   Curtis, Rochelle E.
   Storm, Hans H.
   Johannesen, Tom Borge
   Stovall, Marilyn
   Smith, Susan A.
   Weathers, Rita
   Aleman, Berthe M.
   Kleinerman, Ruth A.
   Fraumeni, Joseph F., Jr.
   Holowaty, Eric J.
   Pukkala, Eero
   Kaijser, Magnus
   Hauptmann, Michael
   Fossa, Sophie D.
   Joensuu, Heikki
   Andersson, Michael
   van den Belt-Dusebout, Alexandra W.
   Vaalavirta, Leila
   Langmark, Froydis
   Travis, Lois B.
   van Leeuwen, Flora E.
TI Risk of Treatment-Related Stomach Cancer Among Hodgkin Lymphoma
   Survivors.
SO BLOOD
LA English
DT Meeting Abstract
CT 52nd Annual Meeting of the American-Society-of-Hematology (ASH)
CY DEC 04-07, 2010
CL Orlando, FL
SP Amer Soc Hematol
C1 [Morton, Lindsay M.; Gilbert, Ethel S.; Curtis, Rochelle E.; Kleinerman, Ruth A.; Fraumeni, Joseph F., Jr.] NCI, NIH, DHHS, Rockville, MD USA.
   [Lynch, Charles F.] Univ Iowa, Dept Epidemiol, Iowa City, IA USA.
   [Hall, Per] Karolinska Inst, Dept Med Epidemiol & Biostat, Stockholm, Sweden.
   [Dores, Graca M.] Dept Vet Affairs Med Ctr, Med Serv, Oklahoma City, OK USA.
   [Storm, Hans H.] Danish Canc Soc, Copenhagen, Denmark.
   [Johannesen, Tom Borge; Langmark, Froydis] Canc Registry Norway, Oslo, Norway.
   [Stovall, Marilyn; Smith, Susan A.; Weathers, Rita] Univ Texas MD Anderson Canc Ctr, Dept Radiat Phys, Houston, TX 77030 USA.
   [Aleman, Berthe M.] Netherlands Canc Inst, Dept Radiotherapy, Amsterdam, TX, Netherlands.
   [Holowaty, Eric J.] Canc Care Ontario, Populat Studies & Surveillance, Toronto, ON, Canada.
   [Pukkala, Eero] Finnish Canc Registry, Inst Stat & Epidemiol Canc Res, FIN-00170 Helsinki, Finland.
   [Kaijser, Magnus] Karolinska Inst, Dept Med, Clin Epidemiol Unit, Stockholm, Sweden.
   [Hauptmann, Michael] Netherlands Canc Inst, Dept Bioinformat & Stat, Amsterdam, Netherlands.
   [Fossa, Sophie D.] Oslo Univ Hosp, Dept Oncol, Oslo, Norway.
   [Fossa, Sophie D.] Univ Oslo, Oslo, Norway.
   [Joensuu, Heikki; Vaalavirta, Leila] Univ Helsinki, Cent Hosp, Dept Oncol, Helsinki, Finland.
   [Andersson, Michael] Copenhagen Univ Hosp, Dept Oncol, Copenhagen, Denmark.
   [van den Belt-Dusebout, Alexandra W.; van Leeuwen, Flora E.] Netherlands Canc Inst, Dept Epidemiol, Amsterdam, Netherlands.
   [Travis, Lois B.] Univ Rochester, Med Ctr, Dept Radiat Oncol, Rochester, NY 14642 USA.
RI Morton, Lindsay/B-5234-2015
OI Morton, Lindsay/0000-0001-9767-2310
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 19
PY 2010
VL 116
IS 21
BP 1104
EP 1105
PG 2
WC Hematology
SC Hematology
GA 752BH
UT WOS:000289662203011
ER

PT J
AU Zhang, JH
   Mullighan, C
   Harvey, R
   Carroll, WL
   Chen, IML
   Devidas, M
   Larsen, E
   Edmonson, M
   Buetow, K
   Gerhard, DS
   Loh, ML
   Reaman, GH
   Relling, MV
   Smith, MA
   Downing, JR
   Willman, CL
   Hunger, S
AF Zhang, Jinghui
   Mullighan, Charles
   Harvey, Richard
   Carroll, William L.
   Chen, I-Ming L.
   Devidas, Meenakshi
   Larsen, Eric
   Edmonson, Michael
   Buetow, Ken
   Gerhard, Daniela S.
   Loh, Mignon L.
   Reaman, Gregory H.
   Relling, Mary V.
   Smith, Malcolm A.
   Downing, James R.
   Willman, Cheryl L.
   Hunger, Stephen
TI Lack of Somatic Sequence Mutations In Protein Tyrosine Kinase Genes
   Other Than the JAK Kinase Family In High Risk B-Precursor Childhood
   Acute Lymphoblastic Leukemia (ALL): A Report From the Children's
   Oncology Group (COG) High-Risk (HR) ALL TARGET Project
SO BLOOD
LA English
DT Meeting Abstract
CT 52nd Annual Meeting of the American-Society-of-Hematology (ASH)
CY DEC 04-07, 2010
CL Orlando, FL
SP Amer Soc Hematol
C1 [Zhang, Jinghui; Mullighan, Charles; Downing, James R.] St Jude Childrens Hosp, Memphis, TN 38105 USA.
   [Chen, I-Ming L.] Univ New Mexico, Ctr Canc, Albuquerque, NM 87131 USA.
   [Carroll, William L.] NYU, Med Ctr, Inst Canc, New York, NY 10016 USA.
   [Devidas, Meenakshi] Univ Florida, Coll Med, Dept Biostat, Gainesville, FL USA.
   [Larsen, Eric] Maine Childrens Canc Program, Scarborough, ME USA.
   [Edmonson, Michael] NCI, Lab Populat Genet, Bethesda, MD 20892 USA.
   [Buetow, Ken] NCI, Ctr Bioinformat, Rockville, MD USA.
   [Gerhard, Daniela S.] NCI, Office Canc Genom, Bethesda, MD 20892 USA.
   [Loh, Mignon L.] Univ Calif San Francisco, Div Pediat Hematol Oncol, San Francisco, CA 94143 USA.
   [Reaman, Gregory H.] George Washington Univ, Childrens Natl Med Ctr, Washington, DC USA.
   [Relling, Mary V.] St Jude Childrens Hosp, Memphis, TN 38105 USA.
   [Willman, Cheryl L.] Univ New Mexico, Ctr Canc, UNM Canc Res Facil, Albuquerque, NM 87131 USA.
   [Hunger, Stephen] Univ Colorado, Coll Med, Pediat Hem Onc BMT, Aurora, CO USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 19
PY 2010
VL 116
IS 21
BP 1135
EP 1135
PG 1
WC Hematology
SC Hematology
GA 752BH
UT WOS:000289662203084
ER

PT J
AU Hultcrantz, M
   Kristinsson, SY
   Andersson, TML
   Eloranta, S
   Derolf, AR
   Landgren, O
   Dickman, PW
   Bjorkholm, M
AF Hultcrantz, Malin
   Kristinsson, Sigurdur Y.
   Andersson, Therese M-L
   Eloranta, Sandra
   Derolf, Asa Rangert
   Landgren, Ola
   Dickman, Paul W.
   Bjorkholm, Magnus
TI Patterns of Survival and Causes of Death In 9,384 Patients with
   Myeloproliferative Neoplasms Diagnosed In Sweden Between 1973 and 2008
SO BLOOD
LA English
DT Meeting Abstract
CT 52nd Annual Meeting of the American-Society-of-Hematology (ASH)
CY DEC 04-07, 2010
CL Orlando, FL
SP Amer Soc Hematol
C1 [Hultcrantz, Malin; Kristinsson, Sigurdur Y.; Derolf, Asa Rangert; Bjorkholm, Magnus] Karolinska Univ Hosp, Div Hematol, Dept Med, Stockholm, Sweden.
   [Andersson, Therese M-L; Eloranta, Sandra] Karolinska Inst, Dept Med Epidemiol & Biostat, Stockholm, Sweden.
   [Landgren, Ola] NCI, Med Oncol Branch, NIH, Bethesda, MD 20892 USA.
   [Dickman, Paul W.] Karolinska Univ Hosp, Dept Med Epidemiol & Biostat, Stockholm, Sweden.
RI Kristinsson, Sigurdur /M-2910-2015; Andersson, Therese/E-7107-2016
OI Kristinsson, Sigurdur /0000-0002-4964-7476; Andersson,
   Therese/0000-0001-8644-9041
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 19
PY 2010
VL 116
IS 21
BP 1266
EP 1267
PG 2
WC Hematology
SC Hematology
GA 752BH
UT WOS:000289662203403
ER

PT J
AU Roschewski, M
   Weniger, M
   Kurdziel, K
   Pittaluga, S
   Tian, X
   Tweito, M
   Dunleavy, K
   Wilson, WH
   Wiestner, A
AF Roschewski, Mark
   Weniger, Marc
   Kurdziel, Karen
   Pittaluga, Stefania
   Tian, Xin
   Tweito, Megan
   Dunleavy, Kieron
   Wilson, Wyndham H.
   Wiestner, Adrian
TI FDG-PET as a Marker of tumor proliferation Compared to Gene-Expression
   Proliferation Scores, MIB1%, and LDH In Untreated Mantle Cell Lymphoma
   (MCL)
SO BLOOD
LA English
DT Meeting Abstract
CT 52nd Annual Meeting of the American-Society-of-Hematology (ASH)
CY DEC 04-07, 2010
CL Orlando, FL
SP Amer Soc Hematol
C1 [Roschewski, Mark] Walter Reed Army Med Ctr, Dept Hematol Oncol, Washington, DC 20307 USA.
   [Weniger, Marc; Wiestner, Adrian] NHLBI, Hematol Branch, Bethesda, MD 20892 USA.
   [Tweito, Megan; Dunleavy, Kieron; Wilson, Wyndham H.] NCI, CCR, NIH, Bethesda, MD 20892 USA.
NR 0
TC 1
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 19
PY 2010
VL 116
IS 21
BP 1275
EP 1276
PG 2
WC Hematology
SC Hematology
GA 752BH
UT WOS:000289662203425
ER

PT J
AU Sanda, T
   Tyner, JW
   Gutierrez, A
   Ngo, VN
   Moriggl, R
   Ahn, Y
   Glover, JM
   Chang, BH
   Willis, SG
   Staudt, LM
   Druker, BJ
   Look, AT
AF Sanda, Takaomi
   Tyner, Jeffrey W.
   Gutierrez, Alejandro
   Ngo, Vu N.
   Moriggl, Richard
   Ahn, Yebin
   Glover, Jason M.
   Chang, Bill H.
   Willis, Stephanie G.
   Staudt, Louis M.
   Druker, Brian J.
   Look, A. Thomas
TI Pathway Dependence on the Tyrosine Kinase TYK2 and Its Mediator STAT1 In
   T-Cell Acute Lymphoblastic Leukemia
SO BLOOD
LA English
DT Meeting Abstract
CT 52nd Annual Meeting of the American-Society-of-Hematology (ASH)
CY DEC 04-07, 2010
CL Orlando, FL
SP Amer Soc Hematol
C1 [Gutierrez, Alejandro; Look, A. Thomas] Childrens Hosp, Dana Farber Canc Inst, Dept Pediat Oncol, Boston, MA 02115 USA.
   [Tyner, Jeffrey W.; Willis, Stephanie G.; Druker, Brian J.] Oregon Hlth & Sci Univ, Knight Canc Inst, Div Hematol & Med Oncol, Portland, OR 97201 USA.
   [Ngo, Vu N.; Staudt, Louis M.] NCI, Metab Branch, NIH, Bethesda, MD 20892 USA.
   [Moriggl, Richard] Ludwig Boltzmann Inst Canc Res, Vienna, Austria.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 19
PY 2010
VL 116
IS 21
BP 1298
EP 1298
PG 1
WC Hematology
SC Hematology
GA 752BH
UT WOS:000289662203486
ER

PT J
AU Phelan, JD
   Khandanpour, C
   Horman, S
   Gaudreau, MC
   Zhu, JF
   Paul, WE
   Duhrsen, U
   Grimes, HL
   Moroy, T
AF Phelan, James D.
   Khandanpour, Cyrus
   Horman, Shane
   Gaudreau, Marie-Claude
   Zhu, Jinfang
   Paul, William E.
   Duehrsen, Ulrich
   Grimes, H. Leighton
   Moroy, Tarik
TI Growth Factor Independent-1 (Gfi1) Is Critically Required for T-Cell
   Acute Lymphoblastic Leukemia (T-ALL) Tumor Initiation and Maintenance
SO BLOOD
LA English
DT Meeting Abstract
CT 52nd Annual Meeting of the American-Society-of-Hematology (ASH)
CY DEC 04-07, 2010
CL Orlando, FL
SP Amer Soc Hematol
C1 [Phelan, James D.; Horman, Shane; Grimes, H. Leighton] Cincinnati Childrens Hosp, Med Ctr, Div Immunobiol, Cincinnati, OH USA.
   [Khandanpour, Cyrus; Gaudreau, Marie-Claude; Moroy, Tarik] IRCM, Montreal, PQ, Canada.
   [Zhu, Jinfang; Paul, William E.] NIAID, NIH, Essen, Germany.
   [Duehrsen, Ulrich] Univ Hosp Essen, D-45122 Essen, Germany.
   [Grimes, H. Leighton] Cincinnati Childrens Hosp, Med Ctr, Div Expt Hematol & Canc Biol, Cincinnati, OH 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 19
PY 2010
VL 116
IS 21
BP 1299
EP 1299
PG 1
WC Hematology
SC Hematology
GA 752BH
UT WOS:000289662203487
ER

PT J
AU Adams, NB
   Lutsey, P
   Folsom, A
   Herrington, D
   Sibley, CT
   Zakai, N
   Ades, S
   Burke, G
   Cushman, M
AF Adams, Nathan B.
   Lutsey, Pamela
   Folsom, Aaron
   Herrington, David
   Sibley, Christopher T.
   Zakai, Neil
   Ades, Steven
   Burke, Gregory
   Cushman, Mary
TI Statin Therapy and Levels of Thrombosis Risk Factors In a Healthy
   Population: the Multi-Ethnic Study of Atherosclerosis
SO BLOOD
LA English
DT Meeting Abstract
CT 52nd Annual Meeting of the American-Society-of-Hematology (ASH)
CY DEC 04-07, 2010
CL Orlando, FL
SP Amer Soc Hematol
C1 [Adams, Nathan B.; Zakai, Neil; Ades, Steven; Cushman, Mary] Univ Vermont, Burlington, VT USA.
   [Lutsey, Pamela; Folsom, Aaron] Univ Minnesota, Minneapolis, MN USA.
   [Herrington, David; Burke, Gregory] Wake Forest Univ, Bowman Gray Sch Med, Winston Salem, NC USA.
   [Sibley, Christopher T.] NIH, Ctr Clin, Bethesda, MD 20892 USA.
RI Sibley, Christopher/C-9900-2013
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 19
PY 2010
VL 116
IS 21
BP 1306
EP 1306
PG 1
WC Hematology
SC Hematology
GA 752BH
UT WOS:000289662203509
ER

PT J
AU Schechter, AN
   Srihirun, S
   Sriwantana, T
   Unchern, S
   Noulsri, E
   Pattanapanyasat, K
   Fucharoen, S
   Piknova, B
   Sibmooh, N
AF Schechter, Alan N.
   Srihirun, Sirada
   Sriwantana, Thanaporn
   Unchern, Supeenun
   Noulsri, Egarit
   Pattanapanyasat, Kovit
   Fucharoen, Suthat
   Piknova, Barbora
   Sibmooh, Nathawut
TI Platelet Aggregation Is Inhibited by Nitrite Reduction to Nitric Oxide
   In Blood
SO BLOOD
LA English
DT Meeting Abstract
CT 52nd Annual Meeting of the American-Society-of-Hematology (ASH)
CY DEC 04-07, 2010
CL Orlando, FL
SP Amer Soc Hematol
C1 [Schechter, Alan N.; Piknova, Barbora] NIDDK, NIH, Bethesda, MD USA.
   [Srihirun, Sirada; Sriwantana, Thanaporn; Unchern, Supeenun; Sibmooh, Nathawut] Mahidol Univ, Fac Sci, Dept Pharmacol, Bangkok 10400, Thailand.
   [Noulsri, Egarit; Pattanapanyasat, Kovit] Mahidol Univ, Siriraj Hosp, Fac Med, Off Res & Dev, Bangkok 10700, Thailand.
   [Fucharoen, Suthat] Mahidol Univ, Inst Sci & Technol Res & Dev, Thalassemia Res Ctr, Nakhon Pathom, Thailand.
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 19
PY 2010
VL 116
IS 21
BP 1310
EP 1311
PG 2
WC Hematology
SC Hematology
GA 752BH
UT WOS:000289662203520
ER

PT J
AU Lacerda, SH
   Semberova, J
   Holada, K
   Simakova, O
   Simak, J
AF Lacerda, Silvia H.
   Semberova, Jana
   Holada, Karel
   Simakova, Olga
   Simak, Jan
TI Carbon Nanotubes Activate Store Operated Calcium Entry (SOCE) In Human
   Platelets Manifested by STIM1 Capping
SO BLOOD
LA English
DT Meeting Abstract
CT 52nd Annual Meeting of the American-Society-of-Hematology (ASH)
CY DEC 04-07, 2010
CL Orlando, FL
SP Amer Soc Hematol
C1 [Lacerda, Silvia H.; Simak, Jan] US FDA, Lab Cellular Hematol, CBER, Rockville, MD 20857 USA.
   [Semberova, Jana] Inst Care Mother & Child, Prague, Czech Republic.
   [Holada, Karel] Charles Univ Prague, Inst Microbiol & Immunol, Fac Med 1, Prague, Czech Republic.
   [Simakova, Olga] NIH, Dept Lab Med, Ctr Clin, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 3
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 19
PY 2010
VL 116
IS 21
BP 1311
EP 1311
PG 1
WC Hematology
SC Hematology
GA 752BH
UT WOS:000289662203521
ER

PT J
AU Dayes, MH
   Hunger, S
   Linda, SB
   Bowman, WP
   Seibel, NL
   Sung, L
   Devidas, M
AF Dayes, Marla H.
   Hunger, Stephen
   Linda, Stephen B.
   Bowman, W. Paul
   Seibel, Nita L.
   Sung, Lillian
   Devidas, Meenakshi
TI Longer Time to the Start of Continuation Therapy Is Associated with
   Improved Survival In High Risk Pediatric Acute Lymphoblastic Leukemia
   (ALL): A Report From the Children's Oncology Group (COG)
SO BLOOD
LA English
DT Meeting Abstract
CT 52nd Annual Meeting of the American-Society-of-Hematology (ASH)
CY DEC 04-07, 2010
CL Orlando, FL
SP Amer Soc Hematol
C1 [Dayes, Marla H.] Baylor Coll Med, Dept Pediat, TX Childrens Canc Ctr, Houston, TX 77030 USA.
   [Dayes, Marla H.] Baylor Coll Med, Hem Serv, Houston, TX 77030 USA.
   [Dayes, Marla H.] Baylor Coll Med, VA Hlth Serv Res & Dev Ctr, Houston, TX 77030 USA.
   [Dayes, Marla H.] Texas Childrens Hosp, Houston, TX 77030 USA.
   [Hunger, Stephen] Univ Colorado, Sch Med, Aurora, CO USA.
   [Hunger, Stephen] Childrens Hosp, Aurora, CO USA.
   [Linda, Stephen B.; Devidas, Meenakshi] Univ Florida, Coll Med, Dept Biostat, Gainesville, FL USA.
   [Bowman, W. Paul] Cook Childrens Med Ctr, Dept Hematol Oncol, Ft Worth, TX USA.
   [Seibel, Nita L.] NCI, Div Canc Treatment, Canc Therapy Evaluat Program, Bethesda, MD 20892 USA.
   [Sung, Lillian] Hosp Sick Children, Dept Pediat, Div Hem Onc, Toronto, ON M5G 1X8, 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 19
PY 2010
VL 116
IS 21
BP 1322
EP 1322
PG 1
WC Hematology
SC Hematology
GA 752BH
UT WOS:000289662203554
ER

PT J
AU Wayne, A
   Bhojwani, D
   Richards, K
   Stetler-Stevenson, M
   Silverman, LB
   Jeha, S
   Pui, CH
   McDevitt, J
   FitzGerald, DJ
   Kreitman, RJ
   Lechleider, RJ
   Pastan, I
AF Wayne, Alan
   Bhojwani, Deepa
   Richards, Kelly
   Stetler-Stevenson, Maryalice
   Silverman, Lewis. B.
   Jeha, Sima
   Pui, Ching-Hon
   McDevitt, Jennifer
   FitzGerald, David J.
   Kreitman, Robert J.
   Lechleider, Robert J.
   Pastan, Ira
TI Complete Remissions In 3 of 12 Patients with Pediatric Acute
   Lymphoblastic Leukemia (ALL) During Phase I Testing of the Anti-CD22
   Immunotoxin Moxetumomab Pasudotox
SO BLOOD
LA English
DT Meeting Abstract
CT 52nd Annual Meeting of the American-Society-of-Hematology (ASH)
CY DEC 04-07, 2010
CL Orlando, FL
SP Amer Soc Hematol
C1 [Wayne, Alan; Richards, Kelly] NCI, Pediat Oncol Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
   [Bhojwani, Deepa; Jeha, Sima; Pui, Ching-Hon] St Jude Childrens Hosp, Memphis, TN 38105 USA.
   [Stetler-Stevenson, Maryalice] NCI, Pathol Lab, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
   [Silverman, Lewis. B.] Childrens Hosp, Dana Farber Canc Inst, Boston, MA 02115 USA.
   [FitzGerald, David J.; Kreitman, Robert J.; Pastan, Ira] NCI, Mol Biol Lab, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
   [McDevitt, Jennifer; Lechleider, Robert J.] Medimmune Inc, Gaithersburg, MD 20878 USA.
NR 0
TC 0
Z9 0
U1 0
U2 4
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 19
PY 2010
VL 116
IS 21
BP 1331
EP 1331
PG 1
WC Hematology
SC Hematology
GA 752BH
UT WOS:000289662203577
ER

PT J
AU Lee, DW
   Kochenderfer, JN
   Rader, C
   Orentas, RJ
   Mackall, CL
AF Lee, Daniel W.
   Kochenderfer, James N.
   Rader, Christoph
   Orentas, Rimas J.
   Mackall, Crystal L.
TI Novel Antigen-Specific Expansion of T Cells Transduced with a CD19
   Chimeric Antigen Receptor
SO BLOOD
LA English
DT Meeting Abstract
CT 52nd Annual Meeting of the American-Society-of-Hematology (ASH)
CY DEC 04-07, 2010
CL Orlando, FL
SP Amer Soc Hematol
C1 [Lee, Daniel W.] NCI, Pediat Oncol Branch, Bethesda, MD 20892 USA.
   [Kochenderfer, James N.] NCI, Surg Branch, Bethesda, MD 20892 USA.
   [Rader, Christoph] NCI, Expt Transplantat & Immunol Branch, Ctr Canc Res, Bethesda, MD 20892 USA.
   [Orentas, Rimas J.; Mackall, Crystal L.] NCI, Pediat Oncol Branch, Ctr Canc Res, NIH, 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 19
PY 2010
VL 116
IS 21
BP 1337
EP 1337
PG 1
WC Hematology
SC Hematology
GA 752BH
UT WOS:000289662203593
ER

PT J
AU Karp, JE
   Pratz, KW
   Litzow, MR
   Ji, JP
   Chen, A
   Rudek, M
   Kaufmann, SH
AF Karp, Judith E.
   Pratz, Keith W.
   Litzow, Mark R.
   Ji, Juping
   Chen, Alice
   Rudek, Michelle
   Kaufmann, Scott H.
TI Phase I Trial of the Oral Poly (ADP-ribose) Polymerase (PARP) Inhibitor
   Veliparib (ABT-888, V) Combined Wtih Topoecan (T) and Carboplatin (C)
   for Adults with Relapsed and Refractory Acute Leukemias
SO BLOOD
LA English
DT Meeting Abstract
CT 52nd Annual Meeting of the American-Society-of-Hematology (ASH)
CY DEC 04-07, 2010
CL Orlando, FL
SP Amer Soc Hematol
C1 [Karp, Judith E.] Sidney Kimmel Comprehens Canc Ctr John Hopkins, Div Hematol Malignancies, Baltimore, MD USA.
   [Pratz, Keith W.; Rudek, Michelle] Johns Hopkins Sidney Kimmel Comprehens Canc Ctr, Baltimore, MD USA.
   [Litzow, Mark R.; Kaufmann, Scott H.] Mayo Clin, Rochester, MN USA.
   [Ji, Juping] NCI, Bethesda, MD 20892 USA.
   [Chen, Alice] NCI, Idb, CTEP, Rockville, MD USA.
NR 0
TC 1
Z9 1
U1 0
U2 2
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 19
PY 2010
VL 116
IS 21
BP 1342
EP 1343
PG 2
WC Hematology
SC Hematology
GA 752BH
UT WOS:000289662203607
ER

PT J
AU Yong, ASM
   Stephens, N
   Keyvanfar, K
   Savani, BN
   Eniafe, R
   Berg, M
   Sloand, EM
   Childs, R
   Barrett, AJ
AF Yong, Agnes S. M.
   Stephens, Nicole
   Keyvanfar, Keyvan
   Savani, Bipin N.
   Eniafe, Rhoda
   Berg, Maria
   Sloand, Elaine M.
   Childs, Richard
   Barrett, A. John
TI Killing of Quiescent and Cycling Chronic Myeloid Leukemia CD34+Cells by
   Autologous Ex-Vivo Expanded Natural Killer Cells Is Enhanced by
   Bortezomib Treatment
SO BLOOD
LA English
DT Meeting Abstract
CT 52nd Annual Meeting of the American-Society-of-Hematology (ASH)
CY DEC 04-07, 2010
CL Orlando, FL
SP Amer Soc Hematol
C1 [Yong, Agnes S. M.; Stephens, Nicole; Keyvanfar, Keyvan; Eniafe, Rhoda; Berg, Maria; Sloand, Elaine M.; Childs, Richard; Barrett, A. John] NHLBI, Hematol Branch, NIH, Bethesda, MD 20892 USA.
   [Savani, Bipin N.] Vanderbilt Univ, Med Ctr, Dept Med, Div Hematol Oncol, Nashville, TN 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 19
PY 2010
VL 116
IS 21
BP 1389
EP 1390
PG 2
WC Hematology
SC Hematology
GA 752BH
UT WOS:000289662203726
ER

PT J
AU Pantin, J
   Tian, X
   Geller, N
   Ramos, C
   Cook, L
   Grasmeder, S
   Scheinberg, P
   Young, NS
   Vasu, S
   Donohue, T
   Childs, R
AF Pantin, Jeremy
   Tian, Xin
   Geller, Nancy
   Ramos, Catalina
   Cook, Lisa
   Grasmeder, Sophia
   Scheinberg, Philip
   Young, Neal S.
   Vasu, Sumithira
   Donohue, Theresa
   Childs, Richard
TI Long-Term Follow-up of Reduced Intensity Allogeneic Hematopoietic Stem
   Cell Transplantation for Severe Paroxysmal Nocturnal Hemoglobinuria
SO BLOOD
LA English
DT Meeting Abstract
CT 52nd Annual Meeting of the American-Society-of-Hematology (ASH)
CY DEC 04-07, 2010
CL Orlando, FL
SP Amer Soc Hematol
C1 [Pantin, Jeremy; Scheinberg, Philip; Donohue, Theresa; Childs, Richard] NHLBI, Hematol Branch, NIH, Bethesda, MD 20892 USA.
RI Scheinberg, Phillip/H-5251-2012
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 19
PY 2010
VL 116
IS 21
BP 1440
EP 1440
PG 1
WC Hematology
SC Hematology
GA 752BH
UT WOS:000289662203836
ER

PT J
AU Sun, K
   Sckisel, G
   Tietze, J
   Li, MH
   Sayers, T
   Blazar, BR
   Murphy, WJ
AF Sun, Kai
   Sckisel, Gail
   Tietze, Julia
   Li, Minghui
   Sayers, Thomas
   Blazar, Bruce R.
   Murphy, William J.
TI Organ-Specific Protection from CD8(+) T Cell-Mediated Acute Skin GVHD by
   Bortezomib Administration Correlates with Decreased IL-6
SO BLOOD
LA English
DT Meeting Abstract
CT 52nd Annual Meeting of the American-Society-of-Hematology (ASH)
CY DEC 04-07, 2010
CL Orlando, FL
SP Amer Soc Hematol
C1 [Sun, Kai; Sckisel, Gail; Tietze, Julia; Murphy, William J.] UC Davis Sch Med, Dept Dermatol, Sacramento, CA USA.
   [Li, Minghui] Univ Nevada, Reno Sch Med, Dept Microbiol & Immunol, Reno, NV 89557 USA.
   [Sayers, Thomas] NCI, Canc & Inflammat Program, SAIC Frederick Inc, Frederick, MD 21701 USA.
   [Blazar, Bruce R.] Univ Minnesota, Masonic Canc Ctr, Dept Pediat, Div Blood & Marrow Transplantat, Minneapolis, MN USA.
   [Murphy, William J.] UC Davis Sch Med, Dept Internal Med, Sacramento, CA USA.
RI Sayers, Thomas/G-4859-2015
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 19
PY 2010
VL 116
IS 21
BP 1532
EP 1532
PG 1
WC Hematology
SC Hematology
GA 752BH
UT WOS:000289662204155
ER

PT J
AU Ozaki, K
   Meguro, A
   Hatanaka, K
   Oh, I
   Matsu, H
   Tatara, R
   Sato, K
   Leonard, WJ
   Ozawa, K
AF Ozaki, Katsutoshi
   Meguro, Akiko
   Hatanaka, Keiko
   Oh, Iekuni
   Matsu, Haruko
   Tatara, Raine
   Sato, Kazuya
   Leonard, Warren J.
   Ozawa, Keiya
TI Lack of IL-21 Signal Attenuates Graft-Versus-Leukemia Effect In the
   Absence of CD8 T-Cells
SO BLOOD
LA English
DT Meeting Abstract
CT 52nd Annual Meeting of the American-Society-of-Hematology (ASH)
CY DEC 04-07, 2010
CL Orlando, FL
SP Amer Soc Hematol
C1 [Ozaki, Katsutoshi; Meguro, Akiko; Hatanaka, Keiko; Oh, Iekuni; Matsu, Haruko; Tatara, Raine; Sato, Kazuya; Ozawa, Keiya] Jichi Med Univ, Div Hem, Shimotsuke, Japan.
   [Leonard, Warren J.] Lmi NHLBI, NIH, 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 19
PY 2010
VL 116
IS 21
BP 1534
EP 1534
PG 1
WC Hematology
SC Hematology
GA 752BH
UT WOS:000289662204159
ER

PT J
AU Coghill, JM
   West, ML
   Cook, DN
   Serody, JS
AF Coghill, James M.
   West, Michelle L.
   Cook, Donald N.
   Serody, Jonathan S.
TI The Absence of CC-Chemokine Receptor 8 on Donor Regulatory T Cells
   Impairs Their Ability to Prevent Lethal Acute Gvhd
SO BLOOD
LA English
DT Meeting Abstract
CT 52nd Annual Meeting of the American-Society-of-Hematology (ASH)
CY DEC 04-07, 2010
CL Orlando, FL
SP Amer Soc Hematol
C1 [Coghill, James M.; Serody, Jonathan S.] Univ N Carolina, Lineberger Comprehens Canc Ctr, Dept Internal Med, Chapel Hill, NC 27599 USA.
   [Cook, Donald N.] NIH, Durham, 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 19
PY 2010
VL 116
IS 21
BP 1535
EP 1536
PG 2
WC Hematology
SC Hematology
GA 752BH
UT WOS:000289662204163
ER

PT J
AU Han, KL
   Walker, S
   Malech, HL
   Kang, EM
AF Han, Kyu Lee
   Walker, Sherry
   Malech, Harry L.
   Kang, Elizabeth M.
TI Adenosine A(2A) Receptor Agonist Mediated Prevention of Graft-Versus
   Host Disease In the Mouse Is Associated with An Increase of T-Regulatory
   Cells In Target Organs
SO BLOOD
LA English
DT Meeting Abstract
CT 52nd Annual Meeting of the American-Society-of-Hematology (ASH)
CY DEC 04-07, 2010
CL Orlando, FL
SP Amer Soc Hematol
C1 [Han, Kyu Lee; Walker, Sherry; Malech, Harry L.; Kang, Elizabeth M.] NIAID, Host Def Lab, NIH, 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 19
PY 2010
VL 116
IS 21
BP 1536
EP 1536
PG 1
WC Hematology
SC Hematology
GA 752BH
UT WOS:000289662204164
ER

PT J
AU Zhu, JQ
   Chin, K
   Aerbajinai, W
   Trainor, CD
   Perter, G
   Rodgers, GP
AF Zhu, Jianqiongz
   Chin, Kyung
   Aerbajinai, Wulin
   Trainor, Cecelia D.
   Perter, Gao
   Rodgers, Griffin P.
TI Recombinant Erythroid Kruppel-Like Factor Fused to GATA1 up-Regulates
   delta-Globin Expression In Erythroid Cells
SO BLOOD
LA English
DT Meeting Abstract
CT 52nd Annual Meeting of the American-Society-of-Hematology (ASH)
CY DEC 04-07, 2010
CL Orlando, FL
SP Amer Soc Hematol
C1 [Zhu, Jianqiongz; Chin, Kyung; Aerbajinai, Wulin] NHLBI, NIH, Bethesda, MD 20892 USA.
   [Trainor, Cecelia D.; Rodgers, Griffin P.] NIDDK, Bethesda, MD USA.
   [Perter, Gao] NIAAA, NIH, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 19
PY 2010
VL 116
IS 21
BP 1538
EP 1538
PG 1
WC Hematology
SC Hematology
GA 752BH
UT WOS:000289662204172
ER

PT J
AU Li, WL
   Yan, M
   Liu, YQ
   Coleman, WG
   Rodgers, GP
AF Li, Wenli
   Yan, Ming
   Liu, Yueqin
   Coleman, William G., Jr.
   Rodgers, Griffin P.
TI Olfactomedin 4 Down-Regulates Neutrophil Killing of Gram-Positive and
   Gram-Negative Bacteria
SO BLOOD
LA English
DT Meeting Abstract
CT 52nd Annual Meeting of the American-Society-of-Hematology (ASH)
CY DEC 04-07, 2010
CL Orlando, FL
SP Amer Soc Hematol
C1 [Li, Wenli; Rodgers, Griffin P.] NHLBI, Mol & Clin Hematol Branch, NIH, Bethesda, MD 20892 USA.
   [Yan, Ming; Coleman, William G., Jr.] NIDDKD, Bethesda, MD 20892 USA.
   [Liu, Yueqin] NIH, Crit Care Dept, Ctr Clin, 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 19
PY 2010
VL 116
IS 21
BP 1546
EP 1546
PG 1
WC Hematology
SC Hematology
GA 752BH
UT WOS:000289662204197
ER

PT J
AU Giger, U
   Pratt, SM
   Palena, C
   Kennedy, DR
   Bauer, TR
AF Giger, Urs
   Pratt, Suzanne M.
   Palena, Christina
   Kennedy, Doug R.
   Bauer, Thomas R.
TI Feline Leukocyte Adhesion Deficiency
SO BLOOD
LA English
DT Meeting Abstract
CT 52nd Annual Meeting of the American-Society-of-Hematology (ASH)
CY DEC 04-07, 2010
CL Orlando, FL
SP Amer Soc Hematol
C1 [Giger, Urs; Kennedy, Doug R.] Univ Penn, Med Genet Sect, Philadelphia, PA 19104 USA.
   [Pratt, Suzanne M.] Antech Diagnost, Portland, RI USA.
   [Palena, Christina] Mt View Vet Hosp, Vancouver, WA USA.
   [Bauer, Thomas R.] NCI, NIH, CCR, ETIB, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 1
U2 4
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 19
PY 2010
VL 116
IS 21
BP 1547
EP 1547
PG 1
WC Hematology
SC Hematology
GA 752BH
UT WOS:000289662204199
ER

PT J
AU Owen, AN
   Steiner, LA
   Gallagher, PG
   Bodine, DM
AF Owen, Ashley N.
   Steiner, Laurie A.
   Gallagher, Patrick G.
   Bodine, David M.
TI An Active Chromatin Hub Involving the Three Alternate Promoter/First
   Exons of the Ankyrin-1 (ANK-1) Gene
SO BLOOD
LA English
DT Meeting Abstract
CT 52nd Annual Meeting of the American-Society-of-Hematology (ASH)
CY DEC 04-07, 2010
CL Orlando, FL
SP Amer Soc Hematol
C1 [Owen, Ashley N.; Bodine, David M.] NIH, Bethesda, MD 20892 USA.
   [Steiner, Laurie A.; Gallagher, Patrick G.] Yale Univ, Sch Med, New Haven, CT USA.
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 19
PY 2010
VL 116
IS 21
BP 1579
EP 1579
PG 1
WC Hematology
SC Hematology
GA 752BH
UT WOS:000289662204282
ER

PT J
AU Yang, T
   Lou, Y
   Jian, W
   Bungert, J
   Noguchi, CT
   Huang, SM
   Qiu, Y
AF Yang, Tao
   Lou, Yi
   Jian, Wei
   Bungert, Jorg
   Noguchi, Constance Tom
   Huang, Suming
   Qiu, Yi
TI Regulation of HDAC1 Histone Deacetylase Activity During Hematopoesis
SO BLOOD
LA English
DT Meeting Abstract
CT 52nd Annual Meeting of the American-Society-of-Hematology (ASH)
CY DEC 04-07, 2010
CL Orlando, FL
SP Amer Soc Hematol
C1 [Huang, Suming] Univ Florida, Coll Med, Shands Canc Ctr Biochem & Mol Biol, Gainesville, FL USA.
   [Noguchi, Constance Tom] NIDDK, Mol Med Branch, NIH, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 19
PY 2010
VL 116
IS 21
BP 1581
EP 1582
PG 2
WC Hematology
SC Hematology
GA 752BH
UT WOS:000289662204289
ER

PT J
AU Kim, YS
   Shin, DM
   Wang, HS
   Morse, H
AF Kim, Yong-Soo
   Shin, Dong-Mi
   Wang, Hongsheng
   Morse, Herbert, III
TI MAZ Is a Substrate for the Deubiquitinating Enzyme DUB1
SO BLOOD
LA English
DT Meeting Abstract
CT 52nd Annual Meeting of the American-Society-of-Hematology (ASH)
CY DEC 04-07, 2010
CL Orlando, FL
SP Amer Soc Hematol
C1 [Kim, Yong-Soo; Shin, Dong-Mi; Wang, Hongsheng; Morse, Herbert, III] NIH, Natl Inst Allergy & Infect Dis, 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 19
PY 2010
VL 116
IS 21
BP 1597
EP 1597
PG 1
WC Hematology
SC Hematology
GA 752BH
UT WOS:000289662204333
ER

PT J
AU Tabe, Y
   Jin, LH
   Kojima, K
   Zhou, YX
   Pittaluga, S
   Konopleva, M
   Miida, T
   Raffeld, M
AF Tabe, Yoko
   Jin, Linhua
   Kojima, Kensuke
   Zhou, Yixin
   Pittaluga, Stefania
   Konopleva, Marina
   Miida, Takashi
   Raffeld, Mark
TI MDM2 Antagonist Nutlin-3 Enhances Bortezomib-Mediated Mitochondrial
   Apoptosis In TP53-Mutated Mantle Cell Lymphoma
SO BLOOD
LA English
DT Meeting Abstract
CT 52nd Annual Meeting of the American-Society-of-Hematology (ASH)
CY DEC 04-07, 2010
CL Orlando, FL
SP Amer Soc Hematol
C1 [Tabe, Yoko; Jin, Linhua; Zhou, Yixin; Miida, Takashi] Juntendo Univ, Sch Med, Sportol Ctr, Dept Clin,Lab Med, Tokyo 113, Japan.
   [Kojima, Kensuke] Univ Texas MD Anderson Canc Ctr, Dept Stem Cell Transplantat & Cellular Therapy, Houston, TX 77030 USA.
   [Pittaluga, Stefania; Raffeld, Mark] NCI, Dept Pathol, Bethesda, MD USA.
   [Konopleva, Marina] Univ Texas MD Anderson Canc Ctr, MD Anderson Canc Ctr, Houston, TX 77030 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 19
PY 2010
VL 116
IS 21
BP 1599
EP 1599
PG 1
WC Hematology
SC Hematology
GA 752BH
UT WOS:000289662204340
ER

PT J
AU Gerbitz, A
   Sukumar, M
   Helm, F
   Wilke, A
   Friese, C
   Fahrenwaldt, C
   Lehmann, F
   Loddenkemper, C
   Kammertons, T
   Mautner, J
   Blankenstein, T
   Bornkamm, G
AF Gerbitz, Armin
   Sukumar, Madhusudhanan
   Helm, Florian
   Wilke, Andrea
   Friese, Christian
   Fahrenwaldt, Cornelia
   Lehmann, Frank
   Loddenkemper, Christoph
   Kammertoens, Thomas
   Mautner, Josef
   Blankenstein, Thomas
   Bornkamm, Georg
TI Stromal Cross-Presentation and Host Interferon-gamma Signaling and Are
   Required for Elimination of Antigen-Loss Variants of High-Grade B Cell
   Lymphomas: Implications for Adoptive T Cell Therapy
SO BLOOD
LA English
DT Meeting Abstract
CT 52nd Annual Meeting of the American-Society-of-Hematology (ASH)
CY DEC 04-07, 2010
CL Orlando, FL
SP Amer Soc Hematol
C1 [Gerbitz, Armin] Univ Erlangen Nurnberg, Erlangen, Germany.
   [Sukumar, Madhusudhanan] NIH, Clin Res Ctr, Bethesda, MD USA.
   [Helm, Florian; Wilke, Andrea; Friese, Christian; Fahrenwaldt, Cornelia; Kammertoens, Thomas; Blankenstein, Thomas] Charite, Immunol CBF, Berlin, Germany.
   [Lehmann, Frank; Bornkamm, Georg] Helmholtz Ctr Munich, Munich, Germany.
   [Loddenkemper, Christoph; Mautner, Josef] Tech Univ Munich, Munich, Germany.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 19
PY 2010
VL 116
IS 21
BP 1601
EP 1602
PG 2
WC Hematology
SC Hematology
GA 752BH
UT WOS:000289662204347
ER

PT J
AU Venkatakrishnan, K
   Ramanathan, RK
   Sarantopoulos, J
   Mulkerin, DL
   Shibata, SI
   Hamilton, A
   Dowlati, A
   Mani, S
   Rudek, MA
   Ivy, P
   Takimoto, CH
   Neuwirth, R
   Parasuraman, S
   LoRusso, PM
AF Venkatakrishnan, Karthik
   Ramanathan, Ramesh K.
   Sarantopoulos, John
   Mulkerin, Daniel L.
   Shibata, Stephen I.
   Hamilton, Anne
   Dowlati, Afshin
   Mani, Sridhar
   Rudek, Michelle A.
   Ivy, Percy
   Takimoto, Chris H.
   Neuwirth, Rachel
   Parasuraman, Sudha
   LoRusso, Patricia M.
TI Pharmacokinetics and Safety of Bortezomib In Patients with Advanced
   Malignancies and Varying Degrees of Liver Dysfunction: Results of the
   Phase 1 National Cancer Institute Organ Dysfunction Working Group Study
   NCI 6432
SO BLOOD
LA English
DT Meeting Abstract
CT 52nd Annual Meeting of the American-Society-of-Hematology (ASH)
CY DEC 04-07, 2010
CL Orlando, FL
SP Amer Soc Hematol
C1 [Venkatakrishnan, Karthik] Millennium Pharmaceut Inc, Clin Pharmacol, Cambridge, MA USA.
   [Ramanathan, Ramesh K.] Univ Pittsburgh Canc Inst, Pittsburgh, PA USA.
   [Sarantopoulos, John; Takimoto, Chris H.] Univ Texas Hlth Sci Ctr San Antonio, Canc Therapy & Res Ctr, San Antonio, TX 78229 USA.
   [Mulkerin, Daniel L.] Univ Wisconsin Paul P Carbone Comprehens Canc Ctr, Madison, WI USA.
   [Shibata, Stephen I.] City Hope Comprehens Canc Ctr, Dept Med Oncol & Therapeut Res, Duarte, CA USA.
   [Hamilton, Anne] Univ Sydney, Sydney Canc Ctr, Sydney, NSW 2006, Australia.
   [Dowlati, Afshin] Case Western Reserve Univ, Case Comprehens Canc Ctr, Cleveland, OH 44106 USA.
   [Mani, Sridhar] Albert Einstein Coll Med, Albert Einstein Canc Ctr, Bronx, NY 10467 USA.
   [Rudek, Michelle A.] Johns Hopkins Univ, Sidney Kimmel Comprehens Canc Ctr, Baltimore, MD USA.
   [Ivy, Percy] NCI, Invest Drug Branch, Canc Therapy Evaluat Program, Div Canc Treatment & Diag, Bethesda, MD USA.
   [Neuwirth, Rachel] Millennium Pharmaceut Inc, Biostat, Cambridge, MA USA.
   [Parasuraman, Sudha] Millennium Pharmaceut Inc, Clin Res, Cambridge, MA USA.
   [LoRusso, Patricia M.] Karmanos Canc Inst, Detroit, MI 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 19
PY 2010
VL 116
IS 21
BP 1621
EP 1621
PG 1
WC Hematology
SC Hematology
GA 752BH
UT WOS:000289662204395
ER

PT J
AU Caceres, G
   Robey, RW
   Sokol, L
   Rocha, K
   Fulp, WJ
   Clark, J
   Lawrence, NJ
   Sebti, S
   Bates, SE
   List, AF
AF Caceres, Gisela
   Robey, Robert W.
   Sokol, Lubomir
   Rocha, Kathy
   Fulp, William J.
   Clark, Justine
   Lawrence, Nicholas J.
   Sebti, Said
   Bates, Susan E.
   List, Alan F.
TI In Vitro and In Vivo Inhibition of P-Glycoprotein (ABCB1) by a Novel
   Non-Substrate Compound: HG-829.
SO BLOOD
LA English
DT Meeting Abstract
CT 52nd Annual Meeting of the American-Society-of-Hematology (ASH)
CY DEC 04-07, 2010
CL Orlando, FL
SP Amer Soc Hematol
C1 [Caceres, Gisela; Sokol, Lubomir; Rocha, Kathy; Fulp, William J.; Clark, Justine; Lawrence, Nicholas J.; Sebti, Said; List, Alan F.] Univ S Florida, H Lee Moffitt Canc Ctr, Tampa, FL 33682 USA.
   [Robey, Robert W.] NIH, Canc Therapeut Branch, Ctr Canc Res, Bethesda, MD 20892 USA.
   [Rocha, Kathy] Univ S Florida, Canc Biol PhD Program, Tampa, FL USA.
   [Bates, Susan E.] NCI, Med Oncol Branch, NIH, 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 19
PY 2010
VL 116
IS 21
BP 1625
EP 1625
PG 1
WC Hematology
SC Hematology
GA 752BH
UT WOS:000289662204406
ER

PT J
AU Silverman, LR
   Kaza, A
   Sloand, EM
   Greenberg, PL
   Wilhelm, FE
AF Silverman, Lewis R.
   Kaza, Azra
   Sloand, Elaine M.
   Greenberg, Peter L.
   Wilhelm, Frandois E.
TI Overall Survival In Myelodysplastic Syndrome or Acute Myeloid Leukemia
   Patients Treated with On 01910.Na Correlates with Bone Marrow Blast
   Response.
SO BLOOD
LA English
DT Meeting Abstract
CT 52nd Annual Meeting of the American-Society-of-Hematology (ASH)
CY DEC 04-07, 2010
CL Orlando, FL
SP Amer Soc Hematol
C1 [Silverman, Lewis R.] Mt Sinai Sch Med, Div Hematol Oncol, New York, NY USA.
   [Kaza, Azra] St Vincents Comprehens Canc Ctr, New York, NY USA.
   [Sloand, Elaine M.] NHLBI, Hematol Branch, NIH, Bethesda, MD 20892 USA.
   [Greenberg, Peter L.] Stanford Univ, Div Hematol, Stanford Canc Ctr, Stanford, CA 94305 USA.
   [Wilhelm, Frandois E.] Onconova Therapeut Inc, Newtown, 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 19
PY 2010
VL 116
IS 21
BP 1629
EP 1630
PG 2
WC Hematology
SC Hematology
GA 752BH
UT WOS:000289662204418
ER

PT J
AU Kristinsson, SY
   Min, T
   Pfeiffer, R
   Bjorkholm, M
   Goldin, L
   Blimark, C
   Mellqvist, UH
   Wahlin, A
   Turesson, I
   Landgren, O
AF Kristinsson, Sigurdur Y.
   Min, Tang
   Pfeiffer, Ruth
   Bjorkholm, Magnus
   Goldin, Lynn
   Blimark, Cecilie
   Mellqvist, Ulf-Henrik
   Wahlin, Anders
   Turesson, Ingemar
   Landgren, Ola
TI Monoclonal Gammopathy of Undetermined Significance and Risk of
   Infections: A Population-Based Study.
SO BLOOD
LA English
DT Meeting Abstract
CT 52nd Annual Meeting of the American-Society-of-Hematology (ASH)
CY DEC 04-07, 2010
CL Orlando, FL
SP Amer Soc Hematol
C1 [Kristinsson, Sigurdur Y.; Bjorkholm, Magnus] Karolinska Univ Hosp, Div Hematol, Dept Med, Stockholm, Sweden.
   [Kristinsson, Sigurdur Y.; Bjorkholm, Magnus] Karolinska Inst, Stockholm, Sweden.
   [Min, Tang; Pfeiffer, Ruth; Goldin, Lynn] NCI, Div Canc Epidemiol & Genet, NIH, Bethesda, MD 20892 USA.
   [Blimark, Cecilie; Mellqvist, Ulf-Henrik] Sahlgrens Univ Hosp, Gothenburg, Sweden.
   [Wahlin, Anders] Univ Hosp, Dept Hematol, Umea, Sweden.
   [Turesson, Ingemar] Skane Univ Hosp Malmo, Malmo, Sweden.
   [Landgren, Ola] NCI, Med Oncol Branch, NIH, Bethesda, MD 20892 USA.
RI Pfeiffer, Ruth /F-4748-2011; Wahlin, Anders/F-6043-2013; Kristinsson,
   Sigurdur /M-2910-2015
OI Wahlin, Anders/0000-0001-6402-0463; 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 19
PY 2010
VL 116
IS 21
BP 1652
EP 1652
PG 1
WC Hematology
SC Hematology
GA 752BH
UT WOS:000289662204473
ER

PT J
AU Rogers, HM
   Teng, RF
   Noguchi, CT
AF Rogers, Heather Marie
   Teng, Ruifeng
   Noguchi, Constance Tom
TI Glucose Metabolism and Erythropoietin Stimulation of Erythroid
   Progenitor Cells
SO BLOOD
LA English
DT Meeting Abstract
CT 52nd Annual Meeting of the American-Society-of-Hematology (ASH)
CY DEC 04-07, 2010
CL Orlando, FL
SP Amer Soc Hematol
C1 [Rogers, Heather Marie; Teng, Ruifeng; Noguchi, Constance Tom] NIDDK, Mol Med Branch, NIH, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 19
PY 2010
VL 116
IS 21
BP 1719
EP 1719
PG 1
WC Hematology
SC Hematology
GA 752BH
UT WOS:000289662204651
ER

PT J
AU Nagai, K
   Fujiwara, H
   Ochi, T
   An, J
   Shirakata, T
   Mineno, J
   Kuzushirna, K
   Shiku, H
   Melenhorst, JJ
   Gostic, E
   Price, DA
   Yasukawa, M
AF Nagai, Kozo
   Fujiwara, Hiroshi
   Ochi, Toshiki
   An, Jun
   Shirakata, Toshiaki
   Mineno, Junichi
   Kuzushirna, Kiyotaka
   Shiku, Hiroshi
   Melenhorst, J. Joseph
   Gostic, Enima
   Price, David A.
   Yasukawa, Masaki
TI Engineering of Human T-Cells with a Novel Aurora-A Kinase-Specific
   T-Cell Receptor Gene Transfer Confers Anti-Leukemia Reactivity
SO BLOOD
LA English
DT Meeting Abstract
CT 52nd Annual Meeting of the American-Society-of-Hematology (ASH)
CY DEC 04-07, 2010
CL Orlando, FL
SP Amer Soc Hematol
C1 [Nagai, Kozo; Fujiwara, Hiroshi; Ochi, Toshiki; An, Jun; Shirakata, Toshiaki; Yasukawa, Masaki] Ehime Univ, Grad Sch Med, Toon, Japan.
   [Mineno, Junichi] Takara Bio Inc, Ctr Cell & Gene Therapy, Otsu, Shiga, Japan.
   [Kuzushirna, Kiyotaka] Aichi Canc Ctr, Res Inst, Nagoya, Aichi 464, Japan.
   [Shiku, Hiroshi] Mie Univ, Dept Canc Vaccine & ImmunoGene Therapy, Grad Sch Med, Tsu, Mie 514, Japan.
   [Melenhorst, J. Joseph] NHLBI, NIH, Bethesda, MD 20892 USA.
   [Gostic, Enima; Price, David A.] Cardiff Univ, Dept Infect Immun & Biochem, Sch Med, Cardiff, S Glam, Wales.
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 19
PY 2010
VL 116
IS 21
BP 1741
EP 1741
PG 1
WC Hematology
SC Hematology
GA 752BH
UT WOS:000289662204709
ER

PT J
AU Cohen, KS
   Cheng, S
   Larson, MG
   Cupples, LA
   McCabe, EL
   Wang, YA
   Martin, RP
   Klein, RJ
   Hashmi, B
   O'Donnell, CJ
   Ramachandran, VS
   Shaw, SY
   Wang, TJ
AF Cohen, Kenneth S.
   Cheng, Susan
   Larson, Martin G.
   Cupples, L. Adrienne
   McCabe, Elizabeth L.
   Wang, Ying A.
   Martin, Roderick P.
   Klein, Rachael J.
   Hashmi, Basma
   O'Donnell, Christopher J.
   Ramachandran, Vasan S.
   Shaw, Stanley Y.
   Wang, Thomas J.
TI CD34+Circulating Progenitor Cell Frequency Is Highly Heritable.
SO BLOOD
LA English
DT Meeting Abstract
CT 52nd Annual Meeting of the American-Society-of-Hematology (ASH)
CY DEC 04-07, 2010
CL Orlando, FL
SP Amer Soc Hematol
C1 [Cohen, Kenneth S.] Univ Chicago, Hematol Oncol Sect, Chicago, IL 60637 USA.
   [Cheng, Susan] Harvard Univ, Brigham & Womens Hosp, Sch Med, Div Cardiovasc Med, Boston, MA 02115 USA.
   [Larson, Martin G.; Cupples, L. Adrienne; Wang, Ying A.] Boston Univ, Dept Math & Biostat, Framingham Heart Study, Boston, MA 02215 USA.
   [McCabe, Elizabeth L.; Wang, Thomas J.] Massachusetts Gen Hosp, Div Cardiol, Framingham Heart Study, Boston, MA 02114 USA.
   [Martin, Roderick P.; Klein, Rachael J.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Ctr Regenerat Med, Boston, MA USA.
   [Hashmi, Basma] Harvard Univ, Dept Bioengn, Boston, MA 02115 USA.
   [O'Donnell, Christopher J.] NHLBI, Ctr Populat Studies, Framingham Heart Study, Framingham, MA USA.
   [Shaw, Stanley Y.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Ctr Syst Biol, Boston, MA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 19
PY 2010
VL 116
IS 21
BP 1748
EP 1748
PG 1
WC Hematology
SC Hematology
GA 752BH
UT WOS:000289662204728
ER

PT J
AU de Cabo, R
AF de Cabo, Rafael
TI Calorie Restriction and Aging
SO BLOOD
LA English
DT Meeting Abstract
CT 52nd Annual Meeting of the American-Society-of-Hematology (ASH)
CY DEC 04-07, 2010
CL Orlando, FL
SP Amer Soc Hematol
C1 [de Cabo, Rafael] NIA, NIH, Baltimore, MD 21224 USA.
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 19
PY 2010
VL 116
IS 21
BP 1755
EP 1755
PG 1
WC Hematology
SC Hematology
GA 752BH
UT WOS:000289662204742
ER

PT J
AU Green, ED
AF Green, Eric D.
TI Genomics in 2K10: Fulfilling the Promise of a Sequenced Human Genome.
SO BLOOD
LA English
DT Meeting Abstract
CT 52nd Annual Meeting of the American-Society-of-Hematology (ASH)
CY DEC 04-07, 2010
CL Orlando, FL
SP Amer Soc Hematol
C1 [Green, Eric D.] NHGRI, NIH, 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 19
PY 2010
VL 116
IS 21
BP 1758
EP 1758
PG 1
WC Hematology
SC Hematology
GA 752BH
UT WOS:000289662204756
ER

PT J
AU Rouault, T
AF Rouault, Tracey
TI Multiple Causes of Iron Overload In Tissues, Cells and Subcellular
   Compartments.
SO BLOOD
LA English
DT Meeting Abstract
CT 52nd Annual Meeting of the American-Society-of-Hematology (ASH)
CY DEC 04-07, 2010
CL Orlando, FL
SP Amer Soc Hematol
ID DISEASE
C1 [Rouault, Tracey] Natl Inst Child Hlth & Dev, NIH, Bethesda, MD USA.
NR 5
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 19
PY 2010
VL 116
IS 21
BP 1761
EP 1761
PG 1
WC Hematology
SC Hematology
GA 752BH
UT WOS:000289662204767
ER

PT J
AU Kato, GJ
AF Kato, Gregory J.
TI Risk Factors for Echocardiography-Determined Cardiopulmonary
   Abnormalities In Sickle Cell Anemia In the Walk-PHaSST Study
SO BLOOD
LA English
DT Meeting Abstract
CT 52nd Annual Meeting of the American-Society-of-Hematology (ASH)
CY DEC 04-07, 2010
CL Orlando, FL
SP Amer Soc Hematol
ID DISEASE; DEATH
C1 [Kato, Gregory J.] NHLBI, Sickle Cell Vasc Dis Sect, NIH, Bethesda, MD 20892 USA.
RI Kato, Gregory/I-7615-2014
OI Kato, Gregory/0000-0003-4465-3217
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 19
PY 2010
VL 116
IS 21
BP 119
EP 120
PG 2
WC Hematology
SC Hematology
GA 752BH
UT WOS:000289662200261
ER

PT J
AU Quinn, CT
   McKinstry, RC
   Dowling, MM
   Ball, WS
   Kraut, MA
   Casella, JF
   Dlamini, N
   Ichord, RN
   Jordan, LC
   Kirkham, FJ
   Noetzel, MJ
   Roach, ES
   Hirtz, D
   DeBaun, MR
AF Quinn, Charles T.
   McKinstry, Robert C.
   Dowling, Michael M.
   Ball, William S.
   Kraut, Michael A.
   Casella, James F.
   Dlamini, Nomazulu
   Ichord, Rebecca N.
   Jordan, Lori C.
   Kirkham, Fenella J.
   Noetzel, Michael J.
   Roach, E. Steve
   Hirtz, Deborah
   DeBaun, Michael R.
TI Acute Silent Cerebral Ischemia Occurs More Frequently Than Silent
   Cerebral Infarction In Children with Sickle Cell Anemia
SO BLOOD
LA English
DT Meeting Abstract
CT 52nd Annual Meeting of the American-Society-of-Hematology (ASH)
CY DEC 04-07, 2010
CL Orlando, FL
SP Amer Soc Hematol
C1 [Quinn, Charles T.; Ball, William S.] Cincinnati Childrens Hosp Med Ctr, Cincinnati, OH USA.
   [McKinstry, Robert C.; Noetzel, Michael J.] Washington Univ, Sch Med, St Louis, MO USA.
   [Dowling, Michael M.] UT SW Med Ctr, Dallas, TX USA.
   [Casella, James F.] Johns Hopkins Univ, Sch Med, Dept Pediat, Div Pediat Hematol, Baltimore, MD 21205 USA.
   [Dlamini, Nomazulu; Kirkham, Fenella J.] UCL Inst Child Hlth, Neurosci Unit, London, England.
   [Ichord, Rebecca N.] Childrens Hosp Philadelphia, Philadelphia, PA 19104 USA.
   [Jordan, Lori C.] Johns Hopkins Univ, Sch Med, Dept Neurol, Div Pediat Neurol, Baltimore, MD 21205 USA.
   [Roach, E. Steve] Nationwide Childrens Hosp, Columbus, OH USA.
   [Hirtz, Deborah] NINDS, Div Extramural Res, NIH, Bethesda, MD 20892 USA.
RI Kirkham, Fenella/C-2442-2009
OI Kirkham, Fenella/0000-0002-2443-7958
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 19
PY 2010
VL 116
IS 21
BP 122
EP 123
PG 2
WC Hematology
SC Hematology
GA 752BH
UT WOS:000289662200269
ER

PT J
AU Mossoba, ME
   Mariotti, J
   Yan, XY
   Gangopadhyay, A
   Winterton, M
   Sabatino, M
   Hanh, K
   Fellowes, V
   Hakim, FT
   Stroncek, D
   Leitman, S
   Levine, BL
   June, CH
   Fowler, DH
AF Mossoba, Miriam E.
   Mariotti, Jacopo
   Yan, Xiao-Yi
   Gangopadhyay, Anu
   Winterton, Mathew
   Sabatino, Marianna
   Hanh Khuu
   Fellowes, Vicki
   Hakim, Frances T.
   Stroncek, David
   Leitman, Susan
   Levine, Bruce L.
   June, Carl H.
   Fowler, Daniel H.
TI T-Rapa Cell Clinical Products Contain a Balance of Minimally
   Differentiated Th2/Th1 Effector Cells Depleted of Treg Cells
SO BLOOD
LA English
DT Meeting Abstract
CT 52nd Annual Meeting of the American-Society-of-Hematology (ASH)
CY DEC 04-07, 2010
CL Orlando, FL
SP Amer Soc Hematol
C1 [Mossoba, Miriam E.; Yan, Xiao-Yi; Gangopadhyay, Anu; Winterton, Mathew; Fellowes, Vicki; Hakim, Frances T.; Fowler, Daniel H.] NCI, Expt Transplantat & Immunol Branch, NIH, Ctr Canc Res, Bethesda, MD 20892 USA.
   [Mariotti, Jacopo] Fdn IRCCS Ist Nazl Tumori, Milan, Italy.
   [Sabatino, Marianna; Hanh Khuu; Stroncek, David; Leitman, Susan] NIH, Dept Transfus Med, Ctr Clin, Bethesda, MD 20892 USA.
   [Levine, Bruce L.] Univ Penn, Sch Med, Philadelphia, PA 19104 USA.
   [June, Carl H.] Univ Penn, Abramson Canc Ctr, Philadelphia, PA 19104 USA.
RI Levine, Bruce/D-1688-2009
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 19
PY 2010
VL 116
IS 21
BP 158
EP 159
PG 2
WC Hematology
SC Hematology
GA 752BH
UT WOS:000289662200353
ER

PT J
AU Fowler, DH
   Mossoba, ME
   Schuver, BB
   Layton, P
   Hakim, FT
   Kurlander, R
   Gea-Banacloche, J
   Sportes, C
   Hardy, NM
   Pavletic, SZ
   Steinberg, SM
   Khuu, H
   Sabatino, M
   Stroncek, D
   Leitmnan, S
   Rowley, SD
   Donato, ML
   Goy, A
   Friedman, T
   Korngold, R
   Pecora, AL
   Levine, BL
   June, CH
   Gress, RE
   Bishop, MR
AF Fowler, Daniel H.
   Mossoba, Miriam E.
   Schuver, Bazetta Blacklock
   Layton, Paula
   Hakim, Frances T.
   Kurlander, Roger
   Gea-Banacloche, Juan
   Sportes, Claude
   Hardy, Nancy M.
   Pavletic, Steven Z.
   Steinberg, Seth M.
   Khuu, Hanh
   Sabatino, Marianna
   Stroncek, David
   Leitmnan, Susan
   Rowley, Scott D.
   Donato, Michele L.
   Goy, Andre
   Friedman, Thea
   Korngold, Robert
   Pecora, Andrew L.
   Levine, Bruce L.
   June, Carl H.
   Gress, Ronald E.
   Bishop, Michael R.
TI Adoptive Transfer of Treg-Depleted Donor Th1 and Th2 Cells Safely
   Accelerates Alloengraftment After Low-Intensity Chemotherapy
SO BLOOD
LA English
DT Meeting Abstract
CT 52nd Annual Meeting of the American-Society-of-Hematology (ASH)
CY DEC 04-07, 2010
CL Orlando, FL
SP Amer Soc Hematol
C1 [Hakim, Frances T.] NCI, Expt Transplantat & Immunol Branch, NIH, Ctr Canc Res, Bethesda, MD 20892 USA.
   [Leitmnan, Susan] NIH, Dept Transfus Med, Ctr Clin, Bethesda, MD 20892 USA.
   [Rowley, Scott D.; Donato, Michele L.; Pecora, Andrew L.] Hackensack Univ Med Ctr, John Theurer Canc Ctr, Div Blood & Marrow Transplantat, Hackensack, NJ USA.
   [Friedman, Thea] Hackensack Univ Med Ctr, Ctr Canc, Hackensack, NJ USA.
   [June, Carl H.] Univ Penn, Sch Med, Abramson Canc Ctr, Philadelphia, PA 19104 USA.
RI Levine, Bruce/D-1688-2009
NR 0
TC 1
Z9 1
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 19
PY 2010
VL 116
IS 21
BP 230
EP 231
PG 2
WC Hematology
SC Hematology
GA 752BH
UT WOS:000289662200522
ER

PT J
AU Slape, CI
   Saw, J
   Failla, LM
   Aplan, PD
   Jane, SM
   Curtis, DJ
AF Slape, Christopher I.
   Saw, Jesslyn
   Failla, Laura M.
   Aplan, Peter D.
   Jane, Stephen M.
   Curtis, David J.
TI Dissecting the Mechanism of Apoptosis and Leukemic Transformation In
   Myelodysplasia
SO BLOOD
LA English
DT Meeting Abstract
CT 52nd Annual Meeting of the American-Society-of-Hematology (ASH)
CY DEC 04-07, 2010
CL Orlando, FL
SP Amer Soc Hematol
C1 [Slape, Christopher I.; Saw, Jesslyn; Failla, Laura M.; Jane, Stephen M.; Curtis, David J.] Royal Melbourne Hosp, Bone Marrow Res Labs, Parkville, Vic 3050, Australia.
   [Aplan, Peter D.] NIH, 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 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 19
PY 2010
VL 116
IS 21
BP 268
EP 268
PG 1
WC Hematology
SC Hematology
GA 752BH
UT WOS:000289662200611
ER

PT J
AU Sloand, EM
   Loeliger, K
   Pfannes, L
   Poon, A
   Calado, R
   Feng, XM
   Padilla-Nash, H
   Chen, JC
   Young, NS
AF Sloand, Elaine M.
   Loeliger, Kelsey
   Pfannes, Loretta
   Poon, Andrea
   Calado, Rodrigo
   Feng, Xingmin
   Padilla-Nash, Hesed
   Chen, Jichun
   Young, Neal S.
TI Does a Chronic Inflammatory Process Underlie Clonal Progression In
   Aplastic Anemia?- In Vitro and In Vivo Evidence That Inflammation
   Produces Aneuploidy for Chromosomes 7 and 8 In Replicating Cells
SO BLOOD
LA English
DT Meeting Abstract
CT 52nd Annual Meeting of the American-Society-of-Hematology (ASH)
CY DEC 04-07, 2010
CL Orlando, FL
SP Amer Soc Hematol
C1 [Sloand, Elaine M.] NIH, Div Intramural Res, Bethesda, MD 20892 USA.
   [Poon, Andrea; Chen, Jichun] NHLBI, NIH, Hematol Branch, Bethesda, MD 20892 USA.
   [Padilla-Nash, Hesed] NCI, Bethesda, MD 20892 USA.
RI Calado, Rodrigo/G-2619-2011
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 19
PY 2010
VL 116
IS 21
BP 281
EP 282
PG 2
WC Hematology
SC Hematology
GA 752BH
UT WOS:000289662200642
ER

PT J
AU Korde, N
   Loeliger, K
   Simakova, O
   Zingone, A
   Childs, R
   Landgren, O
   Noel, P
   Sloand, EM
   Maric, I
AF Korde, Neha
   Loeliger, Kelsey
   Simakova, Olga
   Zingone, Adriana
   Childs, Richard
   Landgren, Ola
   Noel, Pierre
   Sloand, Elaine M.
   Maric, Irina
TI Pure Red Cell Aplasia Associated with Plasma Cell Myeloma: Does
   Monoclonal Protein Inhibit Erythropoiesis?
SO BLOOD
LA English
DT Meeting Abstract
CT 52nd Annual Meeting of the American-Society-of-Hematology (ASH)
CY DEC 04-07, 2010
CL Orlando, FL
SP Amer Soc Hematol
C1 [Korde, Neha; Loeliger, Kelsey; Childs, Richard; Sloand, Elaine M.] NHLBI, Hematol Branch, NIH, Bethesda, MD 20892 USA.
   [Simakova, Olga; Noel, Pierre; Maric, Irina] NIH, Dept Lab Med, Ctr Clin, Bethesda, MD 20892 USA.
   [Zingone, Adriana; Landgren, Ola] NCI, Med Oncol Branch, NIH, 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 19
PY 2010
VL 116
IS 21
BP 282
EP 282
PG 1
WC Hematology
SC Hematology
GA 752BH
UT WOS:000289662200643
ER

PT J
AU Eberle, FC
   Rodriguez-Canales, J
   Wei, L
   Hanson, JC
   Killian, JK
   Sun, HW
   Adams, LG
   Hewitt, SM
   Wilson, WH
   Meltzer, PS
   Staudt, LM
   Emmert-Buck, MR
   Pittaluga, S
   Jaffe, ES
AF Eberle, Franziska C.
   Rodriguez-Canales, Jaime
   Wei, Lai
   Hanson, Jeffrey C.
   Killian, J. Keith
   Sun, Hong-Wei
   Adams, Lisa G.
   Hewitt, Stephen M.
   Wilson, Wyndham H.
   Meltzer, Paul S.
   Staudt, Louis M.
   Emmert-Buck, Michael R.
   Pittaluga, Stefania
   Jaffe, Elaine S.
TI Methylation Profiling of Mediastinal Gray Zone Lymphoma Reveals a
   Distinctive Signature with Elements Shared by Classical Hodgkin's
   Lymphoma and Mediastinal Large B-Cell Lymphoma
SO BLOOD
LA English
DT Meeting Abstract
CT 52nd Annual Meeting of the American-Society-of-Hematology (ASH)
CY DEC 04-07, 2010
CL Orlando, FL
SP Amer Soc Hematol
C1 [Eberle, Franziska C.; Rodriguez-Canales, Jaime; Hanson, Jeffrey C.; Hewitt, Stephen M.; Emmert-Buck, Michael R.; Pittaluga, Stefania; Jaffe, Elaine S.] NCI, Pathol Lab, Bethesda, MD 20892 USA.
   [Wei, Lai] NEI, Immunol Lab, Bethesda, MD 20892 USA.
   [Killian, J. Keith; Adams, Lisa G.; Meltzer, Paul S.] NCI, Genet Branch, Bethesda, MD 20892 USA.
   [Sun, Hong-Wei] NIAMSD, Biodata Min & Discovery Sect, Bethesda, MD 20892 USA.
   [Wilson, Wyndham H.; Staudt, Louis M.] NCI, Metab Branch, Bethesda, MD 20892 USA.
RI Wei, Lai/D-1088-2014
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 19
PY 2010
VL 116
IS 21
BP 328
EP 329
PG 2
WC Hematology
SC Hematology
GA 752BH
UT WOS:000289662200748
ER

PT J
AU Lopez, R
   Sellers, S
   Dunbar, CE
   Childs, R
AF Lopez, Rebecca
   Sellers, Stephanie
   Dunbar, Cynthia E.
   Childs, Richard
TI IL-15 Administration to In-Vivo Expand Adoptively Transferred NK Cells
   In Rhesus Macaques
SO BLOOD
LA English
DT Meeting Abstract
CT 52nd Annual Meeting of the American-Society-of-Hematology (ASH)
CY DEC 04-07, 2010
CL Orlando, FL
SP Amer Soc Hematol
C1 [Lopez, Rebecca] NIH, Heart Lung & Blood Inst, Hematol Branch, Bethesda, MD 20892 USA.
   [Childs, Richard] NHLBI, Hematol Branch, NIH, 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 19
PY 2010
VL 116
IS 21
BP 422
EP 423
PG 2
WC Hematology
SC Hematology
GA 752BH
UT WOS:000289662201063
ER

PT J
AU Lopez, R
   Zerbe, C
   Vasu, S
   Cullis, H
   Childs, R
AF Lopez, Rebecca
   Zerbe, Christa
   Vasu, Sumithira
   Cullis, Herb
   Childs, Richard
TI A Novel Method to Expand Viral Reactive CTL From a Selectively Accessed
   Portion of a Cryopreserved Cord Unit to Prevent Viral Infections After
   Transplantation
SO BLOOD
LA English
DT Meeting Abstract
CT 52nd Annual Meeting of the American-Society-of-Hematology (ASH)
CY DEC 04-07, 2010
CL Orlando, FL
SP Amer Soc Hematol
C1 [Lopez, Rebecca; Zerbe, Christa] NIH, Heart Lung & Blood Inst, Hematol Branch, Bethesda, MD 20892 USA.
   [Childs, Richard] NHLBI, Hematol Branch, NIH, Bethesda, MD 20892 USA.
   [Cullis, Herb] Amer Fluoroseal Corp, Gaithersburg, 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 19
PY 2010
VL 116
IS 21
BP 422
EP 422
PG 1
WC Hematology
SC Hematology
GA 752BH
UT WOS:000289662201061
ER

PT J
AU Olnes, MJ
   Poon, A
   Tucker, Z
   Young, NS
   Sloand, EM
AF Olnes, Matthew J.
   Poon, Andrea
   Tucker, Zachary
   Young, Neal S.
   Sloand, Elaine M.
TI JAK2 Inhibition with TG101348 Inhibits Monosomy 7 Myelodysplastic
   Syndromes (MDS) Bone Marrow Cells In Vitro: a Potential Targeted Therapy
   for Monosomy 7 MDS
SO BLOOD
LA English
DT Meeting Abstract
CT 52nd Annual Meeting of the American-Society-of-Hematology (ASH)
CY DEC 04-07, 2010
CL Orlando, FL
SP Amer Soc Hematol
C1 [Olnes, Matthew J.; Poon, Andrea; Tucker, Zachary; Young, Neal S.; Sloand, Elaine M.] NHLBI, NIH, 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 19
PY 2010
VL 116
IS 21
BP 428
EP 429
PG 2
WC Hematology
SC Hematology
GA 752BH
UT WOS:000289662201076
ER

PT J
AU Salit, RB
   Pavletic, SZ
   Fowler, DH
   Wilder, J
   Bryant, K
   Steinberg, SM
   Hakim, FT
   Bishop, MR
AF Salit, Rachel B.
   Pavletic, Steven Z.
   Fowler, Daniel H.
   Wilder, Jennifer
   Bryant, Kelly
   Steinberg, Seth M.
   Hakim, Frances T.
   Bishop, Michael R.
TI Pilot Randomized Trial Comparing the Effects of Alemtuzumab and
   Cyclosporine Versus Tacrolimus, Methotrexate and Sirolimus on Graft
   Versus Host Disease Prevention, Engraftment and Immune Reconstitution
   After Reduced Intensity Unrelated Donor Transplantation.
SO BLOOD
LA English
DT Meeting Abstract
CT 52nd Annual Meeting of the American-Society-of-Hematology (ASH)
CY DEC 04-07, 2010
CL Orlando, FL
SP Amer Soc Hematol
C1 [Salit, Rachel B.] NCI, Med Oncol Branch, Bethesda, MD 20892 USA.
   [Pavletic, Steven Z.; Fowler, Daniel H.; Bryant, Kelly; Hakim, Frances T.; Bishop, Michael R.] NCI, Expt Transplantat & Immunol Branch, Bethesda, MD 20892 USA.
   [Wilder, Jennifer] SAIC Frederick, Frederick, MD USA.
   [Steinberg, Seth M.] NCI, Biostat & Data Management Sect, 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 19
PY 2010
VL 116
IS 21
BP 533
EP 534
PG 2
WC Hematology
SC Hematology
GA 752BH
UT WOS:000289662201348
ER

PT J
AU McIver, ZA
   Grim, A
   Naguib, N
   Khuu, H
   Battiwalla, M
   Stroncek, D
   Barrett, AJ
AF McIver, Zachariah A.
   Grim, Andrew
   Naguib, Nicolas
   Khuu, Hahn
   Battiwalla, Minoo
   Stroncek, David
   Barrett, A. John
TI Selective Depletion of T Cell Alloresponses Using a Photodepletion
   Strategy Preferentially Targets CD4+T Cells
SO BLOOD
LA English
DT Meeting Abstract
CT 52nd Annual Meeting of the American-Society-of-Hematology (ASH)
CY DEC 04-07, 2010
CL Orlando, FL
SP Amer Soc Hematol
C1 [McIver, Zachariah A.; Grim, Andrew; Naguib, Nicolas; Battiwalla, Minoo; Barrett, A. John] NHLBI, NIH, 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 19
PY 2010
VL 116
IS 21
BP 627
EP 628
PG 2
WC Hematology
SC Hematology
GA 752BH
UT WOS:000289662201569
ER

PT J
AU Boztug, K
   Rosenberg, PS
   Bohm, M
   Moulton, T
   Curtin, J
   Rezaei, N
   Corns, J
   Innis, J
   Avci, Z
   Tran, HC
   Pellier, I
   Gatti, S
   Fruge, R
   Parvaneh, N
   Darbyshire, P
   Buchanan, GR
   Alter, BP
   Boxer, L
   Donadieu, J
   Welte, K
   Klein, C
AF Boztug, Kaan
   Rosenberg, Philip S.
   Boehm, Marie
   Moulton, Thomas
   Curtin, Julie
   Rezaei, Nima
   Corns, John
   Innis, Jeffrey
   Avci, Zekai
   Tran, Hung Chi
   Pellier, Isabelle
   Gatti, Simona
   Fruge, Rachel
   Parvaneh, Nima
   Darbyshire, Phil
   Buchanan, George R.
   Alter, Blanche P.
   Boxer, Larry
   Donadieu, Jean
   Welte, Karl
   Klein, Christoph
TI Extended Molecular and Clinical Phenotype of Human G6PC3 Deficiency
SO BLOOD
LA English
DT Meeting Abstract
CT 52nd Annual Meeting of the American-Society-of-Hematology (ASH)
CY DEC 04-07, 2010
CL Orlando, FL
SP Amer Soc Hematol
C1 [Boztug, Kaan; Boehm, Marie; Welte, Karl; Klein, Christoph] Hannover Med Sch, D-3000 Hannover, Germany.
   [Rosenberg, Philip S.] NCI, NIH, Rockville, MD USA.
   [Moulton, Thomas] Bronx Lebanon Hosp Ctr, Bronx, NY USA.
   [Curtin, Julie] Childrens Hosp Westmead, Sydney, NSW, Australia.
   [Rezaei, Nima; Parvaneh, Nima] Univ Tehran Med Sci, Tehran, Iran.
   [Corns, John] Nationwide Childrens Hosp, Columbus, OH USA.
   [Innis, Jeffrey; Boxer, Larry] Univ Michigan, Ann Arbor, MI 48109 USA.
   [Avci, Zekai] Kecioren Res & Training Hosp, Ankara, Turkey.
   [Tran, Hung Chi] Childrens Hosp Angeles, Los Angeles, CA USA.
   [Pellier, Isabelle] CHU Angers, Angers, France.
   [Gatti, Simona] Polytech Univ Marche, Marche, Italy.
   [Fruge, Rachel] Univ Texas SW Med Ctr Dallas, Dallas, TX 75390 USA.
   [Darbyshire, Phil] Birmingham Childrens Hosp, Birmingham, W Midlands, England.
   [Buchanan, George R.] Univ Texas Dallas, Dallas, TX 75230 USA.
   [Donadieu, Jean] Hop Trousseau, F-75571 Paris, France.
RI Rezaei, Nima/B-4245-2008; isabelle, pellier/L-5683-2015
OI Rezaei, Nima/0000-0002-3836-1827; 
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 19
PY 2010
VL 116
IS 21
BP 637
EP 637
PG 1
WC Hematology
SC Hematology
GA 752BH
UT WOS:000289662201597
ER

PT J
AU Zhou, YX
   Jin, LH
   Pittaluga, S
   Raffeld, M
   Miida, T
   Tabe, Y
AF Zhou, Yixin
   Jin, Linhua
   Pittaluga, Stefania
   Raffeld, Mark
   Miida, Takashi
   Tabe, Yoko
TI PI3K a Selective Inhibitor Induces Growth Inhibition In Mantle Cell
   Lymphoma.
SO BLOOD
LA English
DT Meeting Abstract
CT 52nd Annual Meeting of the American-Society-of-Hematology (ASH)
CY DEC 04-07, 2010
CL Orlando, FL
SP Amer Soc Hematol
C1 [Zhou, Yixin; Miida, Takashi; Tabe, Yoko] Juntendo Univ, Sch Med, Dept Clin Lab Med, Tokyo 113, Japan.
   [Jin, Linhua] Juntendo Univ, Sch Med, Clin Lab Med, Sportol Ctr, Tokyo 113, Japan.
   [Pittaluga, Stefania; Raffeld, Mark] NCI, Dept Pathol, Bethesda, MD 20892 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 19
PY 2010
VL 116
IS 21
BP 757
EP 757
PG 1
WC Hematology
SC Hematology
GA 752BH
UT WOS:000289662202036
ER

PT J
AU Sripichal, O
   Lee, YT
   Meier, ER
   Byrnes, C
   Miller, JL
AF Sripichal, Orapan
   Lee, Y. Terry
   Meier, Emily R.
   Byrnes, Colleen
   Miller, Jeffery L.
TI HbF-Inducing Cytokines and BCL11A shRNA Have Combined Effects Upon
   Globin Gene Reprogramming In Adult Human Erythroblasts.
SO BLOOD
LA English
DT Meeting Abstract
CT 52nd Annual Meeting of the American-Society-of-Hematology (ASH)
CY DEC 04-07, 2010
CL Orlando, FL
SP Amer Soc Hematol
C1 [Sripichal, Orapan; Lee, Y. Terry; Meier, Emily R.; Byrnes, Colleen; Miller, Jeffery L.] NIDDK, Mol Med Branch, NIH, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 19
PY 2010
VL 116
IS 21
BP 861
EP 861
PG 1
WC Hematology
SC Hematology
GA 752BH
UT WOS:000289662202299
ER

PT J
AU Battiwalla, M
   McIver, ZA
   Haggerty, J
   Koklanaris, EK
   Chawla, K
   Superata, J
   Childs, R
   Kurlander, R
   Stroncek, D
   Khuu, H
   Citrin, D
   Sabatino, M
   Leitman, S
   Barrett, AJ
AF Battiwalla, Minoo
   McIver, Zachariah A.
   Haggerty, Janice
   Koklanaris, Eleftheria K.
   Chawla, Kamna.
   Superata, Jeanine
   Childs, Richard
   Kurlander, Roger
   Stroncek, David
   Khuu, Hanh
   Citrin, Deborah
   Sabatino, Marianna
   Leitman, Susan
   Barrett, A. John
TI 4-Log Ex-Vivo T-Lymphocyte Depleted Myeloablative HLA-Matched Sibling
   Transplants; a Platform for Adoptive Immunotherapy
SO BLOOD
LA English
DT Meeting Abstract
CT 52nd Annual Meeting of the American-Society-of-Hematology (ASH)
CY DEC 04-07, 2010
CL Orlando, FL
SP Amer Soc Hematol
C1 [Battiwalla, Minoo; Haggerty, Janice; Koklanaris, Eleftheria K.; Chawla, Kamna.; Superata, Jeanine; Childs, Richard; Barrett, A. John] NHLBI, Hematol Branch, NIH, Bethesda, MD 20892 USA.
   [McIver, Zachariah A.] NHLBI NIH, Rockville, MD USA.
   [Kurlander, Roger] NIH, CC DLM Hematol, Bethesda, MD 20892 USA.
   [Leitman, Susan] NIH, Ctr Clin, Dept Transfus Med, Bethesda, MD 20892 USA.
   [Khuu, Hanh] NCI, NIH, 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 19
PY 2010
VL 116
IS 21
BP 867
EP 868
PG 2
WC Hematology
SC Hematology
GA 752BH
UT WOS:000289662202314
ER

PT J
AU Rosenberg, PS
   Tamary, H
   Alter, BP
AF Rosenberg, Philip S.
   Tamary, Hannah
   Alter, Blanche P.
TI How Rare Is Rare? Carrier Frequencies for Fanconi Anemia In the United
   States and Israel.
SO BLOOD
LA English
DT Meeting Abstract
CT 52nd Annual Meeting of the American-Society-of-Hematology (ASH)
CY DEC 04-07, 2010
CL Orlando, FL
SP Amer Soc Hematol
C1 [Rosenberg, Philip S.] NCI, Biostat Branch, Rockville, MD USA.
   [Tamary, Hannah] Schneider Childrens Med Ctr, Petah Tiqwa, Israel.
   [Alter, Blanche P.] NCI, Clin Genet Branch, Potomac, 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 19
PY 2010
VL 116
IS 21
BP 917
EP 917
PG 1
WC Hematology
SC Hematology
GA 752BH
UT WOS:000289662202452
ER

PT J
AU Fowler, CJ
   Yau, YY
   Bolan, CD
   Leitman, S
AF Fowler, Cedar J.
   Yau, Yu Ying
   Bolan, Charles D., Jr.
   Leitman, Susan
TI Analysis of Donor Demographic and Laboratory Parameters Affecting
   CD34(+) Cell Mobilization In Healthy Allogeneic Pediatric Peripheral
   Blood Stem Cell (PBSC) Donor.
SO BLOOD
LA English
DT Meeting Abstract
CT 52nd Annual Meeting of the American-Society-of-Hematology (ASH)
CY DEC 04-07, 2010
CL Orlando, FL
SP Amer Soc Hematol
C1 [Fowler, Cedar J.] NIAID, Lab Clin Infect Dis, Bethesda, MD 20892 USA.
   [Yau, Yu Ying; Leitman, Susan] NIH, Dept Transfus Med, Ctr Clin, Bethesda, MD 20892 USA.
   [Bolan, Charles D., Jr.] NHLBI, Hematol Branch, NIH, 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 19
PY 2010
VL 116
IS 21
BP 929
EP 929
PG 1
WC Hematology
SC Hematology
GA 752BH
UT WOS:000289662202482
ER

PT J
AU Gormley, NJ
   Smith, A
   Berg, M
   Cook, L
   Ramos, C
   Grasmeder, S
   Donohue, T
   Childs, R
AF Gormley, Nicole J.
   Smith, Aleah
   Berg, Maria
   Cook, Lisa
   Ramos, Catalina
   Grasmeder, Sophia
   Donohue, Theresa
   Childs, Richard
TI In Vitro Assessment of Tolerance and Rejection Occurring After
   Co-Transplantation of Allogeneic Umbilical Cord Blood and Haploidentical
   CD34+Cells as Treatment for Severe Aplastic Anemia.
SO BLOOD
LA English
DT Meeting Abstract
CT 52nd Annual Meeting of the American-Society-of-Hematology (ASH)
CY DEC 04-07, 2010
CL Orlando, FL
SP Amer Soc Hematol
C1 [Smith, Aleah; Berg, Maria; Cook, Lisa; Ramos, Catalina; Grasmeder, Sophia; Donohue, Theresa; Childs, Richard] NHLBI, Hematol Branch, NIH, 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 19
PY 2010
VL 116
IS 21
BP 972
EP 972
PG 1
WC Hematology
SC Hematology
GA 752BH
UT WOS:000289662202575
ER

PT J
AU Capitini, CM
   Meadors, JL
   Cho, MM
   Orentas, RJ
   Mackall, CL
   Fry, TJ
AF Capitini, Christian M.
   Meadors, Joanna L.
   Cho, Monica M.
   Orentas, Rimas J.
   Mackall, Crystal L.
   Fry, Terry J.
TI 4-1BBL-Expressing aAPCs Attenuate IL-15-Induced NK Cell Expansion and
   Cytokine Production In Vitro but Induce NK Cell-Mediated Gvhd In Vivo.
SO BLOOD
LA English
DT Meeting Abstract
CT 52nd Annual Meeting of the American-Society-of-Hematology (ASH)
CY DEC 04-07, 2010
CL Orlando, FL
SP Amer Soc Hematol
C1 [Capitini, Christian M.; Meadors, Joanna L.; Cho, Monica M.; Orentas, Rimas J.; Mackall, Crystal L.; Fry, Terry J.] NCI, Pediat Oncol Branch, Ctr Canc Res, NIH, 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 19
PY 2010
VL 116
IS 21
BP 1050
EP 1051
PG 2
WC Hematology
SC Hematology
GA 752BH
UT WOS:000289662202759
ER

PT J
AU Qin, HY
   Meadors, JL
   Fry, TJ
AF Qin, Haying
   Meadors, Joanna L.
   Fry, Terry J.
TI Adoptive Transfer of Primed CD62L+T Cells Mediate Selective GVL In a
   Murine Model of Pediatric ALL.
SO BLOOD
LA English
DT Meeting Abstract
CT 52nd Annual Meeting of the American-Society-of-Hematology (ASH)
CY DEC 04-07, 2010
CL Orlando, FL
SP Amer Soc Hematol
C1 [Qin, Haying; Meadors, Joanna L.; Fry, Terry J.] NCI, Pediat Oncol Branch, CCR, NIH, 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 19
PY 2010
VL 116
IS 21
BP 1050
EP 1050
PG 1
WC Hematology
SC Hematology
GA 752BH
UT WOS:000289662202758
ER

PT J
AU Meier, ER
   Byrnes, C
   Weissman, M
   Lee, YT
   Noel, P
   Luban, NLC
   Miller, JL
AF Meier, Emily R.
   Byrnes, Colleen
   Weissman, Maxine
   Lee, Y. Terry
   Noel, Pierre
   Luban, Naomi L. C.
   Miller, Jeffery L.
TI Stressed Erythropoiesis In Children with Sickle Cell Disease Is An
   Indicator of Low Fetal Hemoglobin Production and Increased Disease
   Severity
SO BLOOD
LA English
DT Meeting Abstract
CT 52nd Annual Meeting of the American-Society-of-Hematology (ASH)
CY DEC 04-07, 2010
CL Orlando, FL
SP Amer Soc Hematol
C1 [Meier, Emily R.] Childrens Natl Med Ctr, Div Hematol, Washington, DC 20010 USA.
   [Meier, Emily R.] NIDDK, Mol Med Branch, NIH, Washington, DC USA.
   [Byrnes, Colleen; Lee, Y. Terry; Miller, Jeffery L.] NIDDK, Mol Med Branch, NIH, Bethesda, MD USA.
   [Weissman, Maxine; Noel, Pierre] NIH, Dept Lab Med, Ctr Clin, Bethesda, MD 20892 USA.
   [Luban, Naomi L. C.] Childrens Natl Med Ctr, Div Lab Med, Washington, DC 20010 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 19
PY 2010
VL 116
IS 21
BP 1099
EP 1100
PG 2
WC Hematology
SC Hematology
GA 752BH
UT WOS:000289662202889
ER

PT J
AU Kochenderfer, JN
   Dudley, ME
   Stetler-Stevenson, M
   Wilson, WH
   Janik, JE
   Nathan, DAN
   Maric, I
   Raffeld, M
   Feldman, SA
   Morgan, RA
   Rosenberg, SA
AF Kochenderfer, James N.
   Dudley, Mark E.
   Stetler-Stevenson, Maryalice
   Wilson, Wyndham H.
   Janik, John E.
   Nathan, Debbie-Ann N.
   Maric, Irina
   Raffeld, Mark
   Feldman, Steven A.
   Morgan, Richard A.
   Rosenberg, Steven A.
TI A Phase I Clinical Trial of Treatment of B-Cell Malignancies with
   Autologous Anti-CD19-CAR-Transduced T Cells
SO BLOOD
LA English
DT Meeting Abstract
CT 52nd Annual Meeting of the American-Society-of-Hematology (ASH)
CY DEC 04-07, 2010
CL Orlando, FL
SP Amer Soc Hematol
C1 [Dudley, Mark E.] NCI, Surg Branch, NIH, Bethesda, MD 20892 USA.
   [Stetler-Stevenson, Maryalice] NCI, Pathol Lab, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
   [Wilson, Wyndham H.] NCI, CCR, NIH, Bethesda, MD 20892 USA.
   [Janik, John E.] NCI, Metab Branch, Bethesda, MD 20892 USA.
   [Maric, Irina] NIH, Dept Lab Med, Ctr Clin, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 1
U2 2
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 19
PY 2010
VL 116
IS 21
BP 1179
EP 1180
PG 2
WC Hematology
SC Hematology
GA 752BH
UT WOS:000289662203197
ER

PT J
AU Dunleavy, K
   Reiter, BLW
   Grant, CM
   Shovlin, M
   Wright, GW
   Fleisher, TA
   Wilson, WH
AF Dunleavy, Kieron
   Reiter, Benjamin L. W.
   Grant, Cliona M.
   Shovlin, Margaret
   Wright, George W.
   Fleisher, Thomas A.
   Wilson, Wyndham H.
TI Rituximab Is Associated with Prolonged Immunoglobulin Deficiency In
   Newly Diagnosed Patients with Aggressive B-Cell Lymphoma Receiving
   Immunochemotherapy
SO BLOOD
LA English
DT Meeting Abstract
CT 52nd Annual Meeting of the American-Society-of-Hematology (ASH)
CY DEC 04-07, 2010
CL Orlando, FL
SP Amer Soc Hematol
C1 [Dunleavy, Kieron; Reiter, Benjamin L. W.; Grant, Cliona M.; Shovlin, Margaret; Wright, George W.; Wilson, Wyndham H.] NCI, Ctr Canc Res, Bethesda, MD 20892 USA.
   [Fleisher, Thomas A.] NIH, Dept Lab 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 19
PY 2010
VL 116
IS 21
BP 1187
EP 1187
PG 1
WC Hematology
SC Hematology
GA 752BH
UT WOS:000289662203213
ER

PT J
AU Bishop, MR
   Steinberg, S
   Hardy, NM
   Pavletic, SZ
   Gress, RE
   Salit, RB
   Layton, P
   Fowler, DH
AF Bishop, Michael R.
   Steinberg, Seth
   Hardy, Nancy M.
   Pavletic, Steven Z.
   Gress, Ronald E.
   Salit, Rachel B.
   Layton, Paula
   Fowler, Daniel H.
TI Incidence, Risks, and Outcomes of Relapse Following Reduced-Intensity
   Allogeneic Hematopoietic Stem Cell Transplantation for Non-Hodgkin's
   Lymphoma
SO BLOOD
LA English
DT Meeting Abstract
CT 52nd Annual Meeting of the American-Society-of-Hematology (ASH)
CY DEC 04-07, 2010
CL Orlando, FL
SP Amer Soc Hematol
C1 [Bishop, Michael R.; Hardy, Nancy M.; Pavletic, Steven Z.; Gress, Ronald E.; Salit, Rachel B.; Layton, Paula; Fowler, Daniel H.] NCI, Expt Transplantat & Immunol Branch, NIH, Bethesda, MD 20892 USA.
   [Steinberg, Seth] NCI, Dept Biostat, NIH, Rockville, 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 19
PY 2010
VL 116
IS 21
BP 1416
EP 1417
PG 2
WC Hematology
SC Hematology
GA 752BH
UT WOS:000289662203782
ER

PT J
AU Shaffer, BC
   Modric, M
   Liewehr, D
   Stetlter-Stevenson, M
   Arthur, DC
   Steinberg, S
   Hakim, FT
   Bryant, K
   Odom, J
   Layton, P
   Salit, RB
   Rader, C
   Gress, RE
   Fowler, DH
   Bishop, MR
   Pavletic, SZ
AF Shaffer, Brian C.
   Modric, Marko
   Liewehr, David
   Stetlter-Stevenson, Maryalice
   Arthur, Diane C.
   Steinberg, Seth
   Hakim, Frances T.
   Bryant, Kelly
   Odom, Jeanne
   Layton, Paula
   Salit, Rachel B.
   Rader, Christoph
   Gress, Ronald E.
   Fowler, Daniel H.
   Bishop, Michael R.
   Pavletic, Steven Z.
TI Allogeneic Hematopoetic Transplantation for CLL: Results of Combination
   Chemotherapy as Pre-Transplant Targeted Lymphocyte Depletion on Disease
   Response, Donor Chimerism, and Transplantation Outcomes
SO BLOOD
LA English
DT Meeting Abstract
CT 52nd Annual Meeting of the American-Society-of-Hematology (ASH)
CY DEC 04-07, 2010
CL Orlando, FL
SP Amer Soc Hematol
C1 [Shaffer, Brian C.; Modric, Marko; Hakim, Frances T.; Bryant, Kelly; Odom, Jeanne; Layton, Paula; Salit, Rachel B.; Rader, Christoph; Gress, Ronald E.; Fowler, Daniel H.; Bishop, Michael R.; Pavletic, Steven Z.] NCI, Expt Transplantat & Immunol Branch, Ctr Canc Res, Bethesda, MD 20892 USA.
   [Liewehr, David; Steinberg, Seth] Dept Biostat, Biostat & Data Management Sect, Rockville, MD USA.
   [Stetlter-Stevenson, Maryalice; Arthur, Diane C.] NCI, Pathol Lab, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
NR 1
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 19
PY 2010
VL 116
IS 21
BP 1428
EP 1428
PG 1
WC Hematology
SC Hematology
GA 752BH
UT WOS:000289662203807
ER

PT J
AU Salit, RB
   Pavletic, SZ
   Fowler, DH
   Wilder, J
   Bryant, K
   Steinberg, SM
   Hakim, FT
   Bishop, MR
AF Salit, Rachel B.
   Pavletic, Steven Z.
   Fowler, Daniel H.
   Wilder, Jennifer
   Bryant, Kelly
   Steinberg, Seth M.
   Hakim, Frances T.
   Bishop, Michael R.
TI Use of Targeted Lymphocyte Depletion as a Personalized Approach to
   Improve Engraftment and Disease Control Following Reduced-Intensity
   Allogeneic Hematopoietic Stem Cell Transplantation Using HLA-Matched
   Unrelated Donors.
SO BLOOD
LA English
DT Meeting Abstract
CT 52nd Annual Meeting of the American-Society-of-Hematology (ASH)
CY DEC 04-07, 2010
CL Orlando, FL
SP Amer Soc Hematol
C1 [Salit, Rachel B.] NIH, Med Oncol Branch, Bethesda, MD 20892 USA.
   [Pavletic, Steven Z.; Fowler, Daniel H.; Bryant, Kelly; Hakim, Frances T.; Bishop, Michael R.] NCI, Expt Transplantat & Immunol Branch, Bethesda, MD 20892 USA.
   [Wilder, Jennifer] SAIC Frederick, Frederick, MD USA.
   [Steinberg, Seth M.] NCI, Biostat & Data Management Sect, 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 19
PY 2010
VL 116
IS 21
BP 1451
EP 1451
PG 1
WC Hematology
SC Hematology
GA 752BH
UT WOS:000289662203861
ER

PT J
AU Shin, DM
   Lee, CH
   Morse, H
AF Shin, Dong-Mi
   Lee, Chang-Hoon
   Morse, Herbert, III
TI The Transcriptional Network Governed by Interferon Regulatory Factor
   (IRF8) In Germinal Center B Cell Lymphomas
SO BLOOD
LA English
DT Meeting Abstract
CT 52nd Annual Meeting of the American-Society-of-Hematology (ASH)
CY DEC 04-07, 2010
CL Orlando, FL
SP Amer Soc Hematol
C1 [Shin, Dong-Mi; Lee, Chang-Hoon; Morse, Herbert, III] NIAID, Immunopathol Lab, NIH, 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 19
PY 2010
VL 116
IS 21
BP 1496
EP 1496
PG 1
WC Hematology
SC Hematology
GA 752BH
UT WOS:000289662204058
ER

PT J
AU Barese, C
   King, C
   Sellers, S
   Krouse, AE
   Metzger, ME
   Traversari, C
   Bordignon, C
   Kornblau, SM
   Marini, F
   Donahue, RE
   Dunbar, CE
AF Barese, Cecilia
   King, Connor
   Sellers, Stephanie
   Krouse, Allen E.
   Metzger, Mark E.
   Traversari, Catia
   Bordignon, Claudio
   Kornblau, Steven M.
   Marini, Frank, III
   Donahue, Robert E.
   Dunbar, Cynthia E.
TI Suicide Gene (HSVtk) Ablation of Hematopoietic Stem Cells and Their
   Progeny In the Rhesus Macaque Model: An Approach to Deletion of
   Dangerous Clones
SO BLOOD
LA English
DT Meeting Abstract
CT 52nd Annual Meeting of the American-Society-of-Hematology (ASH)
CY DEC 04-07, 2010
CL Orlando, FL
SP Amer Soc Hematol
C1 [Barese, Cecilia; King, Connor; Sellers, Stephanie; Dunbar, Cynthia E.] NHLBI, NIH, Bethesda, MD 20892 USA.
   [Krouse, Allen E.; Metzger, Mark E.; Donahue, Robert E.] NHLBI, Hematol Branch, Rockville, MD USA.
   [Traversari, Catia] MolMed SpA, Canc Therapy, Milan, Italy.
   [Bordignon, Claudio] Univ Vita Salute San Raffaele, Milan, Italy.
   [Kornblau, Steven M.; Marini, Frank, III] Univ Texas MD Anderson Canc Ctr, Houston, TX 77030 USA.
RI BARESE, CECILIA/G-8843-2011
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 19
PY 2010
VL 116
IS 21
BP 1540
EP 1541
PG 2
WC Hematology
SC Hematology
GA 752BH
UT WOS:000289662204179
ER

PT J
AU Bouchkouj, N
   Larabee, S
   Qin, HY
   Meadors, JL
   Mackall, CL
   Fry, TJ
AF Bouchkouj, Najat
   Larabee, Shannon
   Qin, Haying
   Meadors, Joanna Louise
   Mackall, Crystal L.
   Fry, Terry J.
TI Dipeptidyl Peptidase Inhibition Alters Myeloid Derived Suppressor Cell
   Phenotype and Induces Regression of Pediatric Sarcomas
SO BLOOD
LA English
DT Meeting Abstract
CT 52nd Annual Meeting of the American-Society-of-Hematology (ASH)
CY DEC 04-07, 2010
CL Orlando, FL
SP Amer Soc Hematol
C1 [Bouchkouj, Najat; Larabee, Shannon; Qin, Haying; Meadors, Joanna Louise; Mackall, Crystal L.; Fry, Terry J.] NCI, Pediat Oncol Branch, NIH, 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 19
PY 2010
VL 116
IS 21
BP 1551
EP 1552
PG 2
WC Hematology
SC Hematology
GA 752BH
UT WOS:000289662204212
ER

PT J
AU Wang, HS
   Shin, DM
   Qi, CF
   Morse, H
AF Wang, Hongsheng
   Shin, Dong Mi
   Qi, Chenfeng
   Morse, Herbert, III
TI CXCR7 Regulates Retention of Splenic Marginal Zone B Cells and
   Availability of SDF-1/CXCL12
SO BLOOD
LA English
DT Meeting Abstract
CT 52nd Annual Meeting of the American-Society-of-Hematology (ASH)
CY DEC 04-07, 2010
CL Orlando, FL
SP Amer Soc Hematol
C1 [Morse, Herbert, III] NIAID, Immunopathol Lab, NIH, 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 19
PY 2010
VL 116
IS 21
BP 1593
EP 1593
PG 1
WC Hematology
SC Hematology
GA 752BH
UT WOS:000289662204322
ER

PT J
AU Price, S
   Shaw, P
   Kirk, J
   Davis, J
   Perkins, K
   Gill, F
   Fleisher, T
   Rao, VK
AF Price, Susan
   Shaw, Pamela
   Kirk, Jennifer
   Davis, Joie
   Perkins, Katie
   Gill, Fred
   Fleisher, Thomas
   Rao, V. Koneti
TI Causes and Consequences of Splenectomy In ALPS-FAS
SO BLOOD
LA English
DT Meeting Abstract
CT 52nd Annual Meeting of the American-Society-of-Hematology (ASH)
CY DEC 04-07, 2010
CL Orlando, FL
SP Amer Soc Hematol
C1 [Price, Susan; Davis, Joie; Perkins, Katie; Rao, V. Koneti] NIAID, ALPS Unit, LCID, NIH, Bethesda, MD 20892 USA.
   [Shaw, Pamela; Kirk, Jennifer] NIAID, Biostat Res Branch, NIH, Bethesda, MD 20892 USA.
   [Gill, Fred; Fleisher, Thomas] NIH, Ctr Clin, Bethesda, MD 20892 USA.
NR 1
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 19
PY 2010
VL 116
IS 21
BP 1595
EP 1595
PG 1
WC Hematology
SC Hematology
GA 752BH
UT WOS:000289662204328
ER

PT J
AU Kumkhaek, C
   Aerbajinai, W
   Liu, WL
   Zhu, JQ
   Uchida, N
   Hsieh, MM
   Tisdale, JF
   Rodgers, GP
AF Kumkhaek, Chutima
   Aerbajinai, Wulin
   Liu, Wenli
   Zhu, Jianqiong
   Uchida, Naoya
   Hsieh, Matthew M.
   Tisdale, John F.
   Rodgers, Griffin P.
TI MASL1 Induces Erythroid Differentiation In Human
   Erythropoietin-Dependent CD34(+) Cells Involving Raf/MEK/ERK Signaling
   Pathway
SO BLOOD
LA English
DT Meeting Abstract
CT 52nd Annual Meeting of the American-Society-of-Hematology (ASH)
CY DEC 04-07, 2010
CL Orlando, FL
SP Amer Soc Hematol
C1 [Kumkhaek, Chutima; Aerbajinai, Wulin; Liu, Wenli; Zhu, Jianqiong; Uchida, Naoya; Hsieh, Matthew M.; Tisdale, John F.] NHLBI, Mol & Clin Hematol Branch, NIH, Bethesda, MD 20892 USA.
   [Rodgers, Griffin P.] NIDDK, 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 19
PY 2010
VL 116
IS 21
BP 1718
EP 1718
PG 1
WC Hematology
SC Hematology
GA 752BH
UT WOS:000289662204647
ER

PT J
AU Noh, SJ
   Byrnes, C
   Lee, YT
   Miller, JL
AF Noh, Seung-Jae
   Byrnes, Colleen
   Lee, Y. Terry
   Miller, Jeffery L.
TI Molecular and Cellular Specialization of Iron Regulation In Human
   Erythroid Progenitor Cells Prior to Hemoglobin Production
SO BLOOD
LA English
DT Meeting Abstract
CT 52nd Annual Meeting of the American-Society-of-Hematology (ASH)
CY DEC 04-07, 2010
CL Orlando, FL
SP Amer Soc Hematol
C1 [Noh, Seung-Jae; Byrnes, Colleen; Lee, Y. Terry; Miller, Jeffery L.] NIDDKD, Mol Med Branch, NIH, Bethesda, MD 20892 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 19
PY 2010
VL 116
IS 21
BP 1727
EP 1727
PG 1
WC Hematology
SC Hematology
GA 752BH
UT WOS:000289662204674
ER

PT J
AU Smith, A
   Khuu, H
   Betters, DM
   Cook, L
   Ramos, C
   Grasmeder, S
   Berg, M
   Lopez, R
   Su, S
   Fellowes, V
   Stroncek, D
   Pantin, J
   Vasu, S
   Donohue, T
   Keyvanfar, K
   Childs, R
AF Smith, Aleah
   Khuu, Hahn
   Betters, Dawn M.
   Cook, Lisa
   Ramos, Catalina
   Grasmeder, Sophia
   Berg, Maria
   Lopez, Rebecca
   Su, Su
   Fellowes, Vicki
   Stroncek, David
   Pantin, Jeremy
   Vasu, Sumi
   Donohue, Theresa
   Keyvanfar, Keyvan
   Childs, Richard
TI Adoptive Transfer of Escalating Doses of Ex Vivo Expanded Autologous
   Natural Killer (NK) Cells In Patients with Advanced Malignancies
   Following Bortezomib Treatment to Sensitize to NK-TRAIL Cytotoxicity.
SO BLOOD
LA English
DT Meeting Abstract
CT 52nd Annual Meeting of the American-Society-of-Hematology (ASH)
CY DEC 04-07, 2010
CL Orlando, FL
SP Amer Soc Hematol
C1 [Smith, Aleah; Betters, Dawn M.; Cook, Lisa; Ramos, Catalina; Grasmeder, Sophia; Berg, Maria; Lopez, Rebecca; Su, Su; Pantin, Jeremy; Vasu, Sumi; Donohue, Theresa; Keyvanfar, Keyvan; Childs, Richard] NHLBI, Hematol Branch, NIH, 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 19
PY 2010
VL 116
IS 21
BP 1743
EP 1744
PG 2
WC Hematology
SC Hematology
GA 752BH
UT WOS:000289662204715
ER

PT J
AU Bates, SE
AF Bates, Susan E.
TI Epigenetic Modulation and Therapy of Lymphoid Malignancies.
SO BLOOD
LA English
DT Meeting Abstract
CT 52nd Annual Meeting of the American-Society-of-Hematology (ASH)
CY DEC 04-07, 2010
CL Orlando, FL
SP Amer Soc Hematol
C1 [Bates, Susan E.] NCI, Med Oncol Branch, NIH, 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 19
PY 2010
VL 116
IS 21
BP 1762
EP 1762
PG 1
WC Hematology
SC Hematology
GA 752BH
UT WOS:000289662204770
ER

PT J
AU Restifo, NP
   Sukumar, M
   Gattinoni, L
AF Restifo, Nicholas P.
   Sukumar, Madhu
   Gattinoni, Luca
TI Improving Adoptive Immunotherapy Using Less-Differentiated T Cells.
SO BLOOD
LA English
DT Meeting Abstract
CT 52nd Annual Meeting of the American-Society-of-Hematology (ASH)
CY DEC 04-07, 2010
CL Orlando, FL
SP Amer Soc Hematol
C1 [Restifo, Nicholas P.; Sukumar, Madhu; Gattinoni, Luca] NCI, NIH, Bethesda, MD 20892 USA.
RI Restifo, Nicholas/A-5713-2008
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 19
PY 2010
VL 116
IS 21
BP 1766
EP 1767
PG 2
WC Hematology
SC Hematology
GA 752BH
UT WOS:000289662204789
ER

PT J
AU Liu, ML
   Wilk, SA
   Wang, AP
   Zhou, LJ
   Wang, RH
   Ogawa, W
   Deng, CX
   Dong, LQ
   Liu, F
AF Liu, Meilian
   Wilk, Sarah Ann
   Wang, Anping
   Zhou, Lijun
   Wang, Rui-Hong
   Ogawa, Wataru
   Deng, Chuxia
   Dong, Lily Q.
   Liu, Feng
TI Resveratrol Inhibits mTOR Signaling by Promoting the Interaction between
   mTOR and DEPTOR
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
ID ACTIVATED PROTEIN-KINASE; MAMMALIAN TARGET; CELL-GROWTH; AMPK
   ACTIVATION; AMINO-ACIDS; INSULIN; RAPAMYCIN; PHOSPHORYLATION;
   METABOLISM; MECHANISM
AB Resveratrol (RSV) is a naturally occurring polyphenol that has been found to exert antioxidant, anti-inflammatory, and neuroprotective properties. However, how RSV exerts its beneficial health effects remains largely unknown. Here, we show that RSV inhibits insulin-and leucine-stimulated mTOR signaling in C2C12 fibroblasts via a Sirt1-independent mechanism. Treating C2C12 cells with RSV dramatically inhibited insulin-stimulated Akt, S6 kinase, and 4E-BP1 phosphorylation but had little effect on tyrosine phosphorylation of the insulin receptor and activation of the p44/42MAPK signaling pathway. RSV treatment also partially blocked mTOR and S6 kinase phosphorylation in TSC1/2-deficient mouse embryonic fibroblasts, suggesting the presence of an inhibitory site downstream of TSC1/2. Knocking out PDK1 or suppressing AMP-activated protein kinase had little effect on leucine-stimulated mTOR signaling. On the other hand, RSV significantly increased the association between mTOR and its inhibitor, DEPTOR. Furthermore, the inhibitory effect of RSV on leucine-stimulated mTOR signaling was greatly reduced in cells in which the expression levels of DEPTOR were suppressed by RNAi. Taken together, our studies reveal that RSV inhibits leucine-stimulated mTORC1 activation by promoting mTOR/DEPTOR interaction and thus uncover a novel mechanism by which RSV negatively regulates mTOR activity.
C1 [Liu, Feng] Univ Texas Hlth Sci Ctr San Antonio, Dept Pharmacol, San Antonio, TX 78229 USA.
   [Dong, Lily Q.] Univ Texas Hlth Sci Ctr San Antonio, Dept Cellular & Struct Biol, San Antonio, TX 78229 USA.
   [Liu, Feng] Univ Texas Hlth Sci Ctr San Antonio, Dept Biochem, San Antonio, TX 78229 USA.
   [Dong, Lily Q.; Liu, Feng] Univ Texas Hlth Sci Ctr San Antonio, Barshop Ctr Longev & Aging Studies, San Antonio, TX 78229 USA.
   [Wang, Rui-Hong; Deng, Chuxia] NIDDK, Mammalian Genet Sect, Genet Dev & Dis Branch, NIH, Bethesda, MD 20892 USA.
   [Ogawa, Wataru] Kobe Univ, Grad Sch Med, Div Diabet Endocrinol & Kidney Dis, Dept Internal Med, Kobe, Hyogo 6500017, Japan.
EM lium2@uthscsa.edu; liuf@uthscsa.edu
RI Zhou, Lijun/H-2229-2011; deng, chuxia/N-6713-2016
FU National Institutes of Health [RO1 DK76902, RO1 DK80344]
FX This work was supported, in whole or in part, by National Institutes of
   Health Grants RO1 DK76902 (to F.L.) and RO1 DK80344 (to L.Q.D.).
NR 44
TC 81
Z9 84
U1 1
U2 18
PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA
SN 0021-9258
J9 J BIOL CHEM
JI J. Biol. Chem.
PD NOV 19
PY 2010
VL 285
IS 47
BP 36387
EP 36394
DI 10.1074/jbc.M110.169284
PG 8
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 679FE
UT WOS:000284146100080
PM 20851890
ER

PT J
AU Smith, LK
   Shah, RR
   Cidlowski, JA
AF Smith, Lindsay K.
   Shah, Ruchir R.
   Cidlowski, John A.
TI Glucocorticoids Modulate MicroRNA Expression and Processing during
   Lymphocyte Apoptosis
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
ID ACUTE LYMPHOBLASTIC-LEUKEMIA; REGULATED MICRORNAS; INDUCE APOPTOSIS;
   DICER; CELLS; THYMOCYTES; AUTOIMMUNITY; ACTIVATION; PATHWAYS; CLEAVAGE
AB Glucocorticoids modulate immune development and function through the induction of lymphocyte apoptosis via mechanisms requiring alterations in gene expression. Recently, short, noncoding, microRNAs have been identified as key regulators of lymphocyte function; however, it is unknown whether glucocorticoids regulate noncoding microRNAs and whether this regulation contributes to lymphocyte apoptosis. We now show by both microarray and deep sequencing analysis that microRNAs are substantially repressed during glucocorticoid-induced apoptosis of primary rat thymocytes. Mechanistic studies revealed that primary microRNA transcripts were not repressed, whereas the expression of the key microRNA processing enzymes: Dicer, Drosha, and DGCR8/Pasha, were significantly reduced at both the mRNA and protein levels during glucocorticoid-induced apoptosis. To delineate the role of Dicer depletion and microRNA repression in apoptosis, we silenced Dicer expression in two human leukemic cell lines and demonstrated that Dicer depletion significantly enhanced glucocorticoid-induced apoptosis in both model systems. Finally, in vitro and in vivo overexpression of the conserved miR-17-92 polycistron, which was repressed significantly by dexamethasone treatment in both our microarray and deep sequencing studies, blunted glucocorticoid-induced apoptosis. These studies provide evidence of altered post-transcriptional microRNA expression and the repression of the microRNA bioprocessing pathway during glucocorticoid-induced apoptosis of lymphocytes, suggesting a role for microRNA processors and specific microRNAs in cell life/death decisions.
C1 NIEHS, Mol Endocrinol Grp, Lab Signal Transduct, NIH,Dept Hlth & Human Serv, Res Triangle Pk, NC 27709 USA.
   [Smith, Lindsay K.] Univ N Carolina, Chapel Hill, NC USA.
   [Shah, Ruchir R.] SRA Int, Durham, NC 27713 USA.
RP Cidlowski, JA (reprint author), 111 TW Alexander Dr,Rm F349, Res Triangle Pk, NC 27709 USA.
EM cidlows1@niehs.nih.gov
FU National Institutes of Health [Z01E5090057-12]
FX This work was supported, in whole or in part, by National Institutes of
   Health Grant Z01E5090057-12.
NR 42
TC 44
Z9 46
U1 2
U2 6
PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA
SN 0021-9258
EI 1083-351X
J9 J BIOL CHEM
JI J. Biol. Chem.
PD NOV 19
PY 2010
VL 285
IS 47
BP 36698
EP 36708
DI 10.1074/jbc.M110.162123
PG 11
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 679FE
UT WOS:000284146100076
PM 20847043
ER

PT J
AU Xiao, CY
   Kim, HS
   Lahusen, T
   Wang, RH
   Xu, XL
   Gavrilova, O
   Jou, W
   Gius, D
   Deng, CX
AF Xiao, Cuiying
   Kim, Hyun-Seok
   Lahusen, Tyler
   Wang, Rui-Hong
   Xu, Xiaoling
   Gavrilova, Oksana
   Jou, William
   Gius, David
   Deng, Chu-Xia
TI SIRT6 Deficiency Results in Severe Hypoglycemia by Enhancing Both Basal
   and Insulin-stimulated Glucose Uptake in Mice
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
ID PROTEIN-KINASE-B; DEPENDENT GENE-EXPRESSION; IN-VIVO; TUMOR-SUPPRESSOR;
   TRANSPORTERS; GLUT1; METABOLISM; SIRTUINS; ROLES; MOUSE
AB Glucose homeostasis in mammals is mainly regulated by insulin signaling. It was previously shown that SIRT6 mutant mice die before 4 weeks of age, displaying profound abnormalities, including low insulin, hypoglycemia, and premature aging. To investigate mechanisms underlying the pleiotropic phenotypes associated with SIRT6 deficiency, we generated mice carrying targeted disruption of SIRT6. We found that 60% of SIRT6(-/-) animals had very low levels of blood glucose and died shortly after weaning. The remaining animals, which have relatively higher concentrations of glucose, survived the early post-weaning lethality, but most died within one year of age. Significantly, feeding the mice with glucose-containing water increased blood glucose and rescued 83% of mutant mice, suggesting that the hypoglycemia is a major cause for the lethality. We showed that SIRT6 deficiency results in more abundant membrane association of glucose transporters 1 and 4, which enhances glucose uptake. We further demonstrated that SIRT6 negatively regulates AKT phosphorylation at Ser-473 and Thr-308 through inhibition of multiple upstream molecules, including insulin receptor, IRS1, and IRS2. The absence of SIRT6, consequently, enhances insulin signaling and activation of AKT, leading to hypoglycemia. These data uncover an essential role of SIRT6 in modulating glucose metabolism through mediating insulin sensitivity.
C1 [Xiao, Cuiying; Kim, Hyun-Seok; Lahusen, Tyler; Wang, Rui-Hong; Xu, Xiaoling; Deng, Chu-Xia] NIDDK, Genet Dev & Dis Branch, Bethesda, MD 20892 USA.
   [Gavrilova, Oksana; Jou, William] NIDDK, Mouse Metab Core Lab, Bethesda, MD 20892 USA.
   [Kim, Hyun-Seok; Gius, David] NCI, Radiat Oncol Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
RP Deng, CX (reprint author), 10 Ctr Dr, Bethesda, MD 20892 USA.
EM chuxiad@bdg10.niddk.nih.gov
RI deng, chuxia/N-6713-2016
FU NIDDK, National Institutes of Health
FX This work was supported, in whole or in part, by the Intramural Research
   Program of NIDDK, National Institutes of Health.
NR 44
TC 82
Z9 86
U1 1
U2 5
PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA
SN 0021-9258
J9 J BIOL CHEM
JI J. Biol. Chem.
PD NOV 19
PY 2010
VL 285
IS 47
BP 36776
EP 36784
DI 10.1074/jbc.M110.168039
PG 9
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 679FE
UT WOS:000284146100051
PM 20847051
ER

PT J
AU Wang, Y
   Liu, L
   Davies, DR
   Segal, DM
AF Wang, Yan
   Liu, Lin
   Davies, David R.
   Segal, David M.
TI Dimerization of Toll-like Receptor 3 (TLR3) Is Required for Ligand
   Binding
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
ID DOUBLE-STRANDED-RNA; CRYSTAL-STRUCTURE; STRUCTURAL BASIS; RECOGNITION;
   ECTODOMAIN; ACTIVATION; COMPLEX; SITE
AB TLR3 (Toll-like receptor 3) recognizes dsRNA, a potent indicator of viral infection. The extracellular domain of TLR3 dimerizes when it binds dsRNA, and the crystal structure of the dimeric complex reveals three sites of interaction on each extracellular domain, two that bind dsRNA and one that is responsible for dimer formation. The goal of this study was to determine which amino acid residues are essential for forming a stable receptor.ligand complex and whether dimerization of TLR3 is required for dsRNA binding. Using a novel ELISA to analyze dsRNA binding by mutant TLR3 constructs, we identified the essential interacting residues and determined that the simultaneous interaction of all three sites is required for ligand binding. In addition, we show that TLR3 is unable to bind dsRNA when dimerization is prevented by mutating residues in the dimerization site or by immobilizing TLR3 at low density. We conclude that dimerization of TLR3 is essential for ligand binding and that the three TLR3 contact sites individually interact weakly with their binding partners but together form a high affinity receptor.ligand complex.
C1 [Segal, David M.] NCI, Expt Immunol Branch, NIH, Bethesda, MD 20892 USA.
   [Liu, Lin; Davies, David R.] NIDDK, Mol Biol Lab, NIH, Bethesda, MD 20892 USA.
RP Segal, DM (reprint author), NCI, Expt Immunol Branch, NIH, Bldg 10,Rm 4B36,9000 Rockville Pike, Bethesda, MD 20892 USA.
EM dave_segal@nih.gov
FU National Institutes of Health (NCI and NIDDK); National Institutes of
   Health/Food and Drug Administration, NIAID
FX This work was supported, in whole or in part, by the Intramural Research
   Program of the National Institutes of Health (NCI and NIDDK) and by a
   National Institutes of Health/Food and Drug Administration intramural
   biodefense award from NIAID.
NR 18
TC 23
Z9 24
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 19
PY 2010
VL 285
IS 47
BP 36836
EP 36841
DI 10.1074/jbc.M110.167973
PG 6
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 679FE
UT WOS:000284146100041
PM 20861016
ER

PT J
AU Ma, BY
   Nussinov, R
AF Ma, Buyong
   Nussinov, Ruth
TI Polymorphic C-terminal beta-Sheet Interactions Determine the Formation
   of Fibril or Amyloid beta-derived Diffusible Ligand-like Globulomer for
   the Alzheimer A beta 42 Dodecamer
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
ID SOLID-STATE NMR; ION CHANNELS; EXPERIMENTAL CONSTRAINTS;
   MOLECULAR-DYNAMICS; SOLVENT PROTECTION; OXIDATIVE STRESS; EMERGING ROLE;
   PROTEIN; OLIGOMERS; PEPTIDE
AB The relationship between amyloid deposition and cellular toxicity is still controversial. In addition to fibril-forming oligomers, other soluble A beta forms (amyloid beta-derived diffusible ligands (ADDLs)) were also suggested to form and to present different morphologies and mechanisms of toxicity. One ADDL type, the "globulomer," apparently forms independently of the fibril aggregation pathway. Even though many studies argue that such soluble A beta oligomers are off fibril formation pathways, they may nonetheless share some structural similarity with protofibrils. NMR data of globulomer intermediates, "preglobulomers," suggested parallel in-register C-terminal beta-sheets, with different N-terminal conformations. Based on experimental data, we computationally investigate four classes of A beta dodecamers: fibril, fibril oligomer, prefibril/preglobulomer cluster, and globulomer models. Our simulations of the solvent protection of double-layered fibril and globulomer models reproduce experimental observations. Using a single layer A beta fibril oligomer beta-sheet model, we found that the C-terminal beta-sheet in the fibril oligomer is mostly curved, preventing it from quickly forming a fibril and leading to its breaking into shorter pieces. The simulations also indicate that beta-sheets packed orthogonally could be the most stable species for A beta dodecamers. The major difference between fibril-forming oligomers and ADDL-like oligomers (globulomers) could be the exposure of Met-35 patches. Although the Met-35 patches are necessarily exposed in fibril-forming oligomers to allow their maturation into fibrils, the Met-35 patches in the globulomer are covered by other residues in the orthogonally packed A beta peptides. Our results call attention to the possible existence of certain "critical intermediates" that can lead to both seeds and other soluble ADDL-like oligomers.
C1 [Ma, Buyong; Nussinov, Ruth] NCI, Basic Sci Program, SAIC Frederick Inc, Ctr Canc Res Nanobiol Program, Frederick, MD 21702 USA.
   [Nussinov, Ruth] 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), NCI, Basic Sci Program, SAIC Frederick Inc, Ctr Canc Res Nanobiol Program, Bldg 469,Rm 151, Frederick, MD 21702 USA.
EM mabuyong@mail.nih.gov
RI Ma, Buyong/F-9491-2011
OI Ma, Buyong/0000-0002-7383-719X
FU National Cancer Institute, National Institutes of Health
   [HHSN261200800001E]; National Institutes of Health, NCI, Center for
   Cancer Research
FX This work was supported, in whole or in part, by the National Cancer
   Institute, National Institutes of Health under contract number
   HHSN261200800001E and by the Intramural Research Program of the National
   Institutes of Health, NCI, Center for Cancer Research.
NR 56
TC 22
Z9 22
U1 0
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 19
PY 2010
VL 285
IS 47
BP 37102
EP 37110
DI 10.1074/jbc.M110.133488
PG 9
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 679FE
UT WOS:000284146100066
PM 20847046
ER

PT J
AU Mouw, KW
   Steiner, AM
   Ghirlando, R
   Li, NS
   Rowland, SJ
   Boocock, MR
   Stark, WM
   Piccirilli, JA
   Rice, PA
AF Mouw, Kent W.
   Steiner, Andrew M.
   Ghirlando, Rodolfo
   Li, Nan-Sheng
   Rowland, Sally-J.
   Boocock, Martin R.
   Stark, W. Marshall
   Piccirilli, Joseph A.
   Rice, Phoebe A.
TI Sin Resolvase Catalytic Activity and Oligomerization State are Tightly
   Coupled
SO JOURNAL OF MOLECULAR BIOLOGY
LA English
DT Article
DE site-specific recombination; DNA topology; serine recombinase;
   resolvase; 3 '-bridging phosphorothiolate-modified DNA
ID GAMMA-DELTA-RESOLVASE; SITE-SPECIFIC RECOMBINATION; VELOCITY ANALYTICAL
   ULTRACENTRIFUGATION; TN3 RESOLVASE; SEDIMENTATION-VELOCITY; SYNAPTIC
   COMPLEX; DNA TOPOISOMERASE; INTEGRATIVE RECOMBINATION;
   STAPHYLOCOCCUS-AUREUS; BACTERIOPHAGE-LAMBDA
AB Serine recombinases promote specific DNA rearrangements by a cut-and-paste mechanism that involves cleavage of all four DNA strands at two sites recognized by the enzyme. Dissecting the order and timing of these cleavage events and the steps leading up to them is difficult because the cleavage reaction is readily reversible. Here, we describe assays using activated Sin mutants and a DNA substrate with a 3'-bridging phosphorothiolate modification that renders Sin-mediated DNA cleavage irreversible. We find that activating Sin mutations promote DNA cleavage rather than simply stabilize the cleavage product. Cleavage events at the scissile phosphates on complementary strands of the duplex are tightly coupled, and the overall DNA cleavage rate is strongly dependent on Sin concentration. When combined with analytical ultracentrifugation data, these results suggest that Sin catalytic activity and oligomerization state are tightly linked, and that activating mutations promote formation of a cleavage-competent oligomeric state that is normally formed only transiently within the full synaptic complex. (C) 2010 Elsevier Ltd. All rights reserved.
C1 [Mouw, Kent W.; Steiner, Andrew M.; Li, Nan-Sheng; Piccirilli, Joseph A.; Rice, Phoebe A.] Univ Chicago, Dept Biochem & Mol Biol, Chicago, IL 60637 USA.
   [Piccirilli, Joseph A.] Univ Chicago, Dept Chem, Chicago, IL 60637 USA.
   [Rowland, Sally-J.; Boocock, Martin R.; Stark, W. Marshall] Univ Glasgow, Fac Biomed & Life Sci, Glasgow G12 8QQ, Lanark, Scotland.
   [Ghirlando, Rodolfo] NIDDKD, Mol Biol Lab, NIH, Bethesda, MD 20892 USA.
RP Rice, PA (reprint author), Univ Chicago, Dept Biochem & Mol Biol, 920 E 58Th St, Chicago, IL 60637 USA.
EM PRice@uchicago.edu
RI Ghirlando, Rodolfo/A-8880-2009; Boocock, Martin/K-5825-2012; 
OI Stark, Marshall/0000-0001-8086-2572
FU NIH [GM086826]; Wellcome Trust [072552]; Medical Scientist National
   Research Service Award [5 T32 G07281]; Howard Hughes Medical Institute;
   NIH, National Institute of Diabetes and Digestive and Kidney Diseases
FX We thank Katrine Whiteson for comments on the manuscript, Selene Koo for
   help with figures, and Elena Solomaha at the University of Chicago
   bio-physical core facility for help with the collection and analysis of
   preliminary analytical ultracentrifugation data. We are very grateful to
   Rick Cosstick (Liverpool) for providing 3'-S-modified site I substrates,
   which will be used in future studies. This work was funded, in part, by
   NIH grant GM086826 (to P.A.R.), Wellcome Trust Project grant 072552 (to
   W.M.S., S-J.R. and M.R.B), Medical Scientist National Research Service
   Award 5 T32 G07281 (to K.W.M.), the Howard Hughes Medical Institute
   (J.A.P.) and the Intramural Research Program of the NIH, National
   Institute of Diabetes and Digestive and Kidney Diseases (R.G.).
NR 55
TC 9
Z9 9
U1 0
U2 2
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 19
PY 2010
VL 404
IS 1
BP 16
EP 33
DI 10.1016/j.jmb.2010.08.057
PG 18
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 686CI
UT WOS:000284674000002
PM 20868695
ER

PT J
AU Saneyoshi, H
   Deschamps, JR
   Marquez, VE
AF Saneyoshi, Hisao
   Deschamps, Jeffrey R.
   Marquez, Victor E.
TI Synthesis of Conformationally Locked L-Deoxythreosyl Phosphonate
   Nucleosides Built on a Bicyclo[3.1.0]hexane Template
SO JOURNAL OF ORGANIC CHEMISTRY
LA English
DT Article
ID NUCLEOTIDE ANALOGS; ANTIVIRAL ACTIVITY; CYCLOPROPYLAMINES; VERSATILE;
   HIV
AB Two conformationally locked versions of L-deoxythreosyl phosphonate nucleosides (2 and 3) were synthesized to investigate the preference of HIV reverse transcriptase for a conformation displaying either a fully diaxial or fully diequatorial disposition of substituents Synthesis of the enantiomeric 4-(6-amino-9H-purin-9-yl)bicyclo[3 1 0]hexan-2-ol carbocyclic nucleoside precursors (diaxially disposed) proceeded straightforwardly from commercially available (1R,4S)-4-hydroxy-2-cyclopent-2-enyl-1-yl acetate employing a hydroxyl-directed Simmons-Smith cyclopropanation that culminated with a Mitsunobu coupling of the purine base For the more complicated 1-(6-amino-9H-punn-9-yl)bicyclo[3 1 0]hexan-3-ol carbocyclic nucleoside precursors (diequatorially disposed), the obligatory linear approach required the syntheses of key 1-aminobicyclo[3 1 0]hexan-3-yl benzoate precursors that were assembled via the amide variant of the Kulinkovich reaction involving the intramolecular cyclopropanation of a substituted delta-vinylamide Completion of the purine ring was achieved by conventional approaches but with much improved yields through the use of a microwave reactor The syntheses of the phosphonates and the corresponding diphosphates were achieved by conventional means None of the diphosphates, which were supposed to act as nucleoside triphosphate mimics, could compete with dATP even when present in a 10-fold excess
C1 [Saneyoshi, Hisao; Marquez, Victor E.] NCI, Biol Chem Lab, Ctr Canc Res, NIH, Frederick, MD 21702 USA.
   [Deschamps, Jeffrey R.] USN, Res Lab, Washington, DC 20375 USA.
RP Marquez, VE (reprint author), NCI, Biol Chem Lab, Ctr Canc Res, NIH, Frederick, MD 21702 USA.
OI Deschamps, Jeffrey/0000-0001-5845-0010
FU NIH, National Cancer Institute, Center for Cancer Research
FX We express their gratitude to Drs Stephen H Hughes, Paul Boyer, and B
   Christie Vu of the HIV Drug Resistant Program at NCI for the biological
   testing The advice and help of Dr Stefan G Sarafianos of the Department
   of Microbiology at the University of Missouri-Columbia is also
   appreciated This research was supported by the Intramural Research
   Program of the NIH, National Cancer Institute, Center for Cancer
   Research
NR 20
TC 8
Z9 8
U1 0
U2 5
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 0022-3263
J9 J ORG CHEM
JI J. Org. Chem.
PD NOV 19
PY 2010
VL 75
IS 22
BP 7659
EP 7669
DI 10.1021/jo101475p
PG 11
WC Chemistry, Organic
SC Chemistry
GA 678MO
UT WOS:000284080300019
PM 20964394
ER

PT J
AU Saito, M
   Kumamoto, K
   Robles, AI
   Horikawa, I
   Furusato, B
   Okamura, S
   Goto, A
   Yamashita, T
   Nagashima, M
   Lee, TL
   Baxendale, VJ
   Rennert, OM
   Takenoshita, S
   Yokota, J
   Sesterhenn, IA
   Trivers, GE
   Hussain, SP
   Harris, CC
AF Saito, Motonobu
   Kumamoto, Kensuke
   Robles, Ana I.
   Horikawa, Izumi
   Furusato, Bungo
   Okamura, Shu
   Goto, Akiteru
   Yamashita, Taro
   Nagashima, Makoto
   Lee, Tin-Lap
   Baxendale, Vanessa J.
   Rennert, Owen M.
   Takenoshita, Seiichi
   Yokota, Jun
   Sesterhenn, Isabell A.
   Trivers, Glenwood E.
   Hussain, S. Perwez
   Harris, Curtis C.
TI Targeted Disruption of Ing2 Results in Defective Spermatogenesis and
   Development of Soft-Tissue Sarcomas
SO PLOS ONE
LA English
DT Article
ID HISTONE-DEACETYLASE INHIBITOR; CHROMOSOME LONG ARM; TUMOR-SUPPRESSOR;
   GERM-CELL; CHROMATIN MODIFICATION; TESTICULAR CANCER; EPIGENETIC EVENTS;
   MEIOTIC PROPHASE; MALE-INFERTILITY; GENE-EXPRESSION
AB ING2 (inhibitor of growth family, member 2) is a member of the plant homeodomain (PHD)-containing ING family of putative tumor suppressors. As part of mSin3A HDAC corepressor complexes, ING2 binds to tri-methylated lysine 4 of histone H3 (H3K4me3) to regulate chromatin modification and gene expression. ING2 also functionally interacts with the tumor suppressor protein p53 to regulate cellular senescence, apoptosis and DNA damage response in vitro, and is thus expected to modulate carcinogenesis and aging. Here we investigate the developmental and physiological functions of Ing2 through targeted germline disruption. Consistent with its abundant expression in mouse and human testes, male mice deficient for Ing2 showed abnormal spermatogenesis and were infertile. Numbers of mature sperm and sperm motility were significantly reduced in Ing2(-/-) mice (similar to 2% of wild type, P<0.0001 and similar to 10% of wild type, P<0.0001, respectively). Their testes showed degeneration of seminiferous tubules, meiotic arrest before pachytene stage with incomplete meiotic recombination, induction of p53, and enhanced apoptosis. This phenotype was only partially abrogated by concomitant loss of p53 in the germline. The arrested spermatocytes in Ing2(-/-) testes were characterized by lack of specific HDAC1 accumulation and deregulated chromatin acetylation. The role of Ing2 in germ cell maturation may extend to human ING2 as well. Using publicly available gene expression datasets, low expression of ING2 was found in teratozoospermic sperm (>3-fold reduction) and in testes from patients with defective spermatogenesis (>7-fold reduction in Sertoli-cell only Syndrome). This study establishes ING2 as a novel regulator of spermatogenesis functioning through both p53- and chromatin-mediated mechanisms, suggests that an HDAC1/ING2/H3K4me3-regulated, stage-specific coordination of chromatin modifications is essential to normal spermatogenesis, and provides an animal model to study idiopathic and iatrogenic infertility in men. In addition, a bona fide tumor suppressive role of Ing2 is demonstrated by increased incidence of soft-tissue sarcomas in Ing2(-/-) mice.
C1 [Saito, Motonobu; Kumamoto, Kensuke; Robles, Ana I.; Horikawa, Izumi; Okamura, Shu; Goto, Akiteru; Yamashita, Taro; Nagashima, Makoto; Trivers, Glenwood E.; Hussain, S. Perwez; Harris, Curtis C.] NCI, Human Carcinogenesis Lab, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
   [Furusato, Bungo; Sesterhenn, Isabell A.] Armed Forces Inst Pathol, Dept Genitourinary Pathol, Washington, DC 20306 USA.
   [Saito, Motonobu; Kumamoto, Kensuke; Takenoshita, Seiichi] Fukushima Med Univ, Sch Med, Dept Organ Regulatory Surg, Fukushima, Japan.
   [Lee, Tin-Lap; Baxendale, Vanessa J.; Rennert, Owen M.] NICHHD, Lab Clin & Dev Genom, Program Reprod & Adult Endocrinol, NIH, Bethesda, MD 20892 USA.
   [Yokota, Jun] Natl Canc Ctr, Div Biol, Tokyo, Japan.
RP Saito, M (reprint author), NCI, Human Carcinogenesis Lab, Ctr Canc Res, NIH, Bldg 37, Bethesda, MD 20892 USA.
EM curtis_harris@nih.gov
RI Lee, Tin-Lap/A-7853-2009; 
OI Lee, Tin-Lap/0000-0002-6654-0988; Furusato, Bungo/0000-0003-4614-9882
FU National Cancer Institute, National Institutes of Health; JA-Fukushima,
   Japan
FX This research was supported in part by the Intramural Research Program
   of the National Cancer Institute, National Institutes of Health. MS was
   supported by a scholarship from the JA-Fukushima, Japan. The funders had
   no role in study design, data collection and analysis, decision to
   publish, or preparation of the manuscript.
NR 68
TC 18
Z9 18
U1 0
U2 1
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD NOV 19
PY 2010
VL 5
IS 11
AR e15541
DI 10.1371/journal.pone.0015541
PG 15
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 682JY
UT WOS:000284400100019
PM 21124965
ER

PT J
AU Chien, EYT
   Liu, W
   Zhao, QA
   Katritch, V
   Han, GW
   Hanson, MA
   Shi, L
   Newman, AH
   Javitch, JA
   Cherezov, V
   Stevens, RC
AF Chien, Ellen Y. T.
   Liu, Wei
   Zhao, Qiang
   Katritch, Vsevolod
   Han, Gye Won
   Hanson, Michael A.
   Shi, Lei
   Newman, Amy Hauck
   Javitch, Jonathan A.
   Cherezov, Vadim
   Stevens, Raymond C.
TI Structure of the Human Dopamine D3 Receptor in Complex with a D2/D3
   Selective Antagonist
SO SCIENCE
LA English
DT Article
ID PROTEIN-COUPLED RECEPTORS; ANGSTROM CRYSTAL-STRUCTURE; 2ND EXTRACELLULAR
   LOOP; DRUG-SEEKING BEHAVIOR; BINDING-SITE CREVICE; D-3 RECEPTOR;
   BETA(2)-ADRENERGIC RECEPTOR; INDUCED REINSTATEMENT; COCAINE-SEEKING;
   IONIC LOCK
AB Dopamine modulates movement, cognition, and emotion through activation of dopamine G protein-coupled receptors in the brain. The crystal structure of the human dopamine D3 receptor (D3R) in complex with the small molecule D2R/D3R-specific antagonist eticlopride reveals important features of the ligand binding pocket and extracellular loops. On the intracellular side of the receptor, a locked conformation of the ionic lock and two distinctly different conformations of intracellular loop 2 are observed. Docking of R-22, a D3R-selective antagonist, reveals an extracellular extension of the eticlopride binding site that comprises a second binding pocket for the aryl amide of R-22, which differs between the highly homologous D2R and D3R. This difference provides direction to the design of D3R-selective agents for treating drug abuse and other neuropsychiatric indications.
C1 [Chien, Ellen Y. T.; Liu, Wei; Zhao, Qiang; Han, Gye Won; Cherezov, Vadim; Stevens, Raymond C.] Scripps Res Inst, Dept Mol Biol, La Jolla, CA 92037 USA.
   [Katritch, Vsevolod] Univ Calif San Diego, Skaggs Sch Pharm & Pharmaceut Sci, La Jolla, CA 92093 USA.
   [Katritch, Vsevolod] Univ Calif San Diego, San Diego Supercomp Ctr, La Jolla, CA 92093 USA.
   [Hanson, Michael A.] Receptos, San Diego, CA 92121 USA.
   [Shi, Lei] Cornell Univ, Weill Cornell Med Coll, Dept Physiol & Biophys, New York, NY 10021 USA.
   [Shi, Lei] Cornell Univ, Weill Cornell Med Coll, HRH Prince Alwaleed Bin Talal Bin Abdulaziz Alsau, New York, NY 10021 USA.
   [Newman, Amy Hauck] Natl Inst Drug Abuse, Med Chem Sect, Intramural Res Program, Baltimore, MD 21224 USA.
   [Javitch, Jonathan A.] Columbia Univ Coll Phys & Surg, Ctr Mol Recognit, New York, NY 10032 USA.
   [Javitch, Jonathan A.] Columbia Univ Coll Phys & Surg, Dept Psychiat, New York, NY 10032 USA.
   [Javitch, Jonathan A.] Columbia Univ Coll Phys & Surg, Dept Pharmacol, New York, NY 10032 USA.
RP Stevens, RC (reprint author), Scripps Res Inst, Dept Mol Biol, 10550 N Torrey Pines Rd, La Jolla, CA 92037 USA.
EM stevens@scripps.edu
RI Liu, Wei/F-1820-2011; Cherezov, Vadim/L-9812-2013; Katritch,
   Vsevolod/Q-8357-2016; 
OI Cherezov, Vadim/0000-0002-5265-3914; Katritch,
   Vsevolod/0000-0003-3883-4505
FU Protein Structure Initiative (PSI) [U54 GM074961, U54 GM094618]; NIH
   Roadmap [P50 GM073197]; NIH [R21 RR025336, GM075915]; Pfizer; National
   Institute on Drug Abuse [DA022413, MH54137, DA023694]; National Science
   Foundation [IIS0308078]; Science Foundation Ireland [02-IN1-B266];
   National Cancer Institute [Y1-CO-1020]; National Institute of General
   Medical Sciences [Y1-GM-1104]
FX This work was supported in part by Protein Structure Initiative (PSI)
   grant U54 GM074961 and PSI: Biology grant U54 GM094618 for structure
   production, NIH Roadmap grant P50 GM073197 for technology development,
   NIH grant R21 RR025336 (V. C.), and Pfizer. Additional support was
   provided by the National Institute on Drug Abuse Intramural Research
   Program (A.H.N.), grants DA022413 and MH54137 (J.A.J.), and grant
   DA023694 (L. S.). The content is solely the responsibility of the
   authors and does not necessarily represent the official views of the
   National Institute of General Medical Science or the NIH. We thank J.
   Velasquez for help with molecular biology, T. Trinh and K. Allin for
   help with baculovirus expression, D. Gray for assistance with
   eticlopride synthesis, M. Griffor for large-scale production of the
   receptor, X. Qiu for suggestions, and A. Walker for assistance with
   manuscript preparation. We acknowledge Y. Zheng, The Ohio State
   University and M. Caffrey, Trinity College (Dublin, Ireland), for the
   generous loan of the in meso robot (built with support from NIH grant
   GM075915), the National Science Foundation (grant IIS0308078), and
   Science Foundation Ireland (grant 02-IN1-B266); and J. Smith, R.
   Fischetti, and N. Sanishvili at the GM/CA-CAT beamline at the Advanced
   Photon Source, for assistance in development and use of the minibeam and
   beamtime. The GM/CA-CAT beamline (23-ID) is supported by the National
   Cancer Institute (grant Y1-CO-1020) and the National Institute of
   General Medical Sciences (grant Y1-GM-1104). Atomic coordinates and
   structure factors have been deposited in the Protein Data Bank with
   identification code 3PBL. A. H. N. is an inventor on a patent
   application from the National Institutes of Health that covers the use
   of R-22 and analogs as D3 receptor selective agents. R. C. S. is on the
   Board of Directors of Receptos, which does structure-directed drug
   discovery on GPCRs.
NR 39
TC 616
Z9 625
U1 7
U2 80
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 19
PY 2010
VL 330
IS 6007
BP 1091
EP 1095
DI 10.1126/science.1197410
PG 5
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 682BU
UT WOS:000284374700040
PM 21097933
ER

PT J
AU Manolio, TA
AF Manolio, Teri A.
TI Genomewide Association Studies and Assessment of Risk of Disease REPLY
SO NEW ENGLAND JOURNAL OF MEDICINE
LA English
DT Letter
C1 NHGRI, Bethesda, MD 20892 USA.
RP Manolio, TA (reprint author), NHGRI, Bethesda, MD 20892 USA.
EM manolio@nih.gov
NR 4
TC 1
Z9 1
U1 0
U2 3
PU MASSACHUSETTS MEDICAL SOC
PI WALTHAM
PA WALTHAM WOODS CENTER, 860 WINTER ST,, WALTHAM, MA 02451-1413 USA
SN 0028-4793
J9 NEW ENGL J MED
JI N. Engl. J. Med.
PD NOV 18
PY 2010
VL 363
IS 21
BP 2077
EP 2077
PG 1
WC Medicine, General & Internal
SC General & Internal Medicine
GA 681KC
UT WOS:000284310000029
ER

PT J
AU Koonin, EV
   Wolf, YI
AF Koonin, Eugene V.
   Wolf, Yuri I.
TI The common ancestry of life
SO BIOLOGY DIRECT
LA English
DT Article
ID ADAPTIVE EVOLUTION; LYSOZYMES; PROTEINS; SETS
AB Background: It is common belief that all cellular life forms on earth have a common origin. This view is supported by the universality of the genetic code and the universal conservation of multiple genes, particularly those that encode key components of the translation system. A remarkable recent study claims to provide a formal, homology independent test of the Universal Common Ancestry hypothesis by comparing the ability of a common-ancestry model and a multiple-ancestry model to predict sequences of universally conserved proteins.
   Results: We devised a computational experiment on a concatenated alignment of universally conserved proteins which shows that the purported demonstration of the universal common ancestry is a trivial consequence of significant sequence similarity between the analyzed proteins. The nature and origin of this similarity are irrelevant for the prediction of "common ancestry" of by the model-comparison approach. Thus, homology (common origin) of the compared proteins remains an inference from sequence similarity rather than an independent property demonstrated by the likelihood analysis.
   Conclusion: A formal demonstration of the Universal Common Ancestry hypothesis has not been achieved and is unlikely to be feasible in principle. Nevertheless, the evidence in support of this hypothesis provided by comparative genomics is overwhelming.
   Reviewers: this article was reviewed by William Martin, Ivan Iossifov (nominated by Andrey Rzhetsky) and Arcady Mushegian. For the complete reviews, see the Reviewers' Report section.
C1 [Koonin, Eugene V.; Wolf, Yuri I.] NIH, Natl Ctr Biotechnol Informat, Natl Lib Med, Bethesda, MD 20894 USA.
RP Koonin, EV (reprint author), NIH, Natl Ctr Biotechnol Informat, Natl Lib Med, Bethesda, MD 20894 USA.
EM koonin@ncbi.nlm.nih.gov
FU US Department of Health and Human Services (National Library of
   Medicine, NIH)
FX We thank Douglas Theobald for helpful discussions. The authors' research
   is supported by intramural funds of the US Department of Health and
   Human Services (National Library of Medicine, NIH).
NR 19
TC 9
Z9 9
U1 3
U2 17
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1745-6150
J9 BIOL DIRECT
JI Biol. Direct
PD NOV 18
PY 2010
VL 5
AR 64
DI 10.1186/1745-6150-5-64
PG 5
WC Biology
SC Life Sciences & Biomedicine - Other Topics
GA 686HA
UT WOS:000284686200001
PM 21087490
ER

PT J
AU Kochenderfer, JN
   Wilson, WH
   Janik, JE
   Dudley, ME
   Stetler-Stevenson, M
   Feldman, SA
   Maric, I
   Raffeld, M
   Nathan, DAN
   Lanier, BJ
   Morgan, RA
   Rosenberg, SA
AF Kochenderfer, James N.
   Wilson, Wyndham H.
   Janik, John E.
   Dudley, Mark E.
   Stetler-Stevenson, Maryalice
   Feldman, Steven A.
   Maric, Irina
   Raffeld, Mark
   Nathan, Debbie-Ann N.
   Lanier, Brock J.
   Morgan, Richard A.
   Rosenberg, Steven A.
TI Eradication of B-lineage cells and regression of lymphoma in a patient
   treated with autologous T cells genetically engineered to recognize CD19
SO BLOOD
LA English
DT Article
ID CHIMERIC ANTIGEN RECEPTOR; HUMAN BONE-MARROW; IN-VIVO; ADOPTIVE
   IMMUNOTHERAPY; ANTITUMOR-ACTIVITY; LYMPHOCYTES; ANTIBODY;
   DIFFERENTIATION; PERSISTENCE; EFFICACY
AB Adoptive transfer of genetically modified T cells is an attractive approach for generating antitumor immune responses. We treated a patient with advanced follicular lymphoma by administering a preparative chemotherapy regimen followed by autologous T cells genetically engineered to express a chimeric antigen receptor (CAR) that recognized the B-cell antigen CD19. The patient's lymphoma underwent a dramatic regression, and B-cell precursors were selectively eliminated from the patient's bone marrow after infusion of anti-CD19-CAR-transduced T cells. Blood B cells were absent for at least 39 weeks after anti-CD19-CAR-transduced T-cell infusion despite prompt recovery of other blood cell counts. Consistent with eradication of B-lineage cells, serum immunoglobulins decreased to very low levels after treatment. The prolonged and selective elimination of B-lineage cells could not be attributed to the chemotherapy that the patient received and indicated antigen-specific eradication of B-lineage cells. Adoptive transfer of anti-CD19-CAR-expressing T cells is a promising new approach for treating B-cell malignancies. This study is registered at www.clinicaltrials.gov as #NCT00924326. (Blood.2010;116(20):4099-4102)
C1 [Kochenderfer, James N.; Maric, Irina] NIH, Dept Lab Med, Ctr Clin, Bethesda, MD 20892 USA.
   [Kochenderfer, James N.; Dudley, Mark E.; Feldman, Steven A.; Nathan, Debbie-Ann N.; Lanier, Brock J.; Morgan, Richard A.; Rosenberg, Steven A.] NCI, Surg Branch, Bethesda, MD 20892 USA.
   [Wilson, Wyndham H.; Janik, John E.] NCI, Metab Branch, Bethesda, MD 20892 USA.
   [Stetler-Stevenson, Maryalice; Raffeld, Mark] NCI, Pathol Lab, Bethesda, MD 20892 USA.
RP Kochenderfer, JN (reprint author), NIH, Dept Lab Med, Ctr Clin, 10 Ctr Dr,CRC Rm 3-3888, Bethesda, MD 20892 USA.
EM kochendj@mail.nih.gov
FU Center for Cancer Research, National Cancer Institute, National
   Institutes of Health
FX This work was supported by the Center for Cancer Research, National
   Cancer Institute, National Institutes of Health (intramural funding).
NR 25
TC 379
Z9 396
U1 6
U2 48
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 18
PY 2010
VL 116
IS 20
BP 4099
EP 4102
DI 10.1182/blood-2010-04-281931
PG 4
WC Hematology
SC Hematology
GA 681YC
UT WOS:000284359400016
PM 20668228
ER

PT J
AU Harris, LD
   Klatt, NR
   Vinton, C
   Briant, JA
   Tabb, B
   Ladell, K
   Lifson, J
   Estes, JD
   Price, DA
   Hirsch, VM
   Brenchley, JM
AF Harris, Levelle D.
   Klatt, Nichole R.
   Vinton, Carol
   Briant, Judith A.
   Tabb, Brian
   Ladell, Kristin
   Lifson, Jeffrey
   Estes, Jacob D.
   Price, David A.
   Hirsch, Vanessa M.
   Brenchley, Jason M.
TI Mechanisms underlying gamma delta T-cell subset perturbations in
   SIV-infected Asian rhesus macaques
SO BLOOD
LA English
DT Article
ID HUMAN-IMMUNODEFICIENCY-VIRUS; ACTIVE ANTIRETROVIRAL THERAPY;
   INFLAMMATORY-BOWEL-DISEASE; HIV-1 INFECTION; MICROBIAL TRANSLOCATION;
   HIV-1-INFECTED PATIENTS; GASTROINTESTINAL-TRACT; IMMUNE ACTIVATION;
   PERIPHERAL-BLOOD; SOOTY MANGABEYS
AB T cells that express the gamma delta T-cell receptor, which recognize microbial or stress-induced antigens, represent a minority of blood T cells but constitute a major proportion of intraepithelial lymphocytes in the gastrointestinal mucosa. As microbial products have been shown to translocate from the gastrointestinal tract into circulation in chronically HIV/Simian immunodeficiency virus (SIV)-infected individuals, we conducted a study of V delta 1 and V delta 2 T-cell frequency, phenotype, and function in blood, spleen, lymph nodes, gastrointestinal mucosa, and bronchoalveolar lavage of uninfected and chronically SIVsmE543-infected rhesus macaques (RMs). We found: (1) SIV-associated inversion of V delta 1/V delta 2 T cells occurs in blood and in several tissues; (2) gamma delta T cells are not infected by SIV in vivo; (3) the V delta 1/V delta 2 inversion involves expansion of V delta 1 T cells; (4) expanded V delta 1 T cells are phenotypically and functionally different from V delta 1 T cells from uninfected RMs; and (5) the stimulus underlying expansion of V delta 1 T cells appears to be microbial translocation. These data highlight the importance of microbial translocation-induced immune activation in chronically infected individuals and provide new insights into an immune dysregulation phenomenon that is a hallmark of HIV/SIV infection. These findings may lead to novel therapeutic interventions that improve the immune responses against microbial antigens, and thus, decrease microbial translocation-induced immune activation. (Blood.2010;116(20):4148-4157)
C1 [Harris, Levelle D.; Klatt, Nichole R.; Vinton, Carol; Briant, Judith A.; Hirsch, Vanessa M.; Brenchley, Jason M.] NIAID, Mol Microbiol Lab, NIH, Bethesda, MD 20892 USA.
   [Tabb, Brian; Lifson, Jeffrey; Estes, Jacob D.] NIH, AIDS & Canc Virus Program, SAIC Frederick Inc, Frederick, MD USA.
   [Ladell, Kristin; Price, David A.] Cardiff Univ, Sch Med, Cardiff, S Glam, Wales.
RP Brenchley, JM (reprint author), NIAID, Mol Microbiol Lab, NIH, 4 Ctr Dr,Rm 301,9000 Rockville Pike, Bethesda, MD 20892 USA.
EM jbrenchl@mail.nih.gov
RI Ladell, Kristin/K-2475-2013; Price, David/C-7876-2013; Ladell,
   Kristin/C-8301-2013
OI Price, David/0000-0001-9416-2737; Ladell, Kristin/0000-0002-9856-2938
FU National Institute of Allergy and Infectious Diseases, National
   Institutes of Health (NIH); National Cancer Institute, NIH
   [HHSN266200400088C]
FX These studies were supported by the intramural National Institute of
   Allergy and Infectious Diseases, National Institutes of Health (NIH)
   program and with federal funds from the National Cancer Institute, NIH,
   under contract HHSN266200400088C. J.A.B. is a Howard Hughes Medical
   Institute Medical Fellow. D.A.P. is a Medical Research Council (United
   Kingdom) Senior Clinical Fellow.
NR 53
TC 21
Z9 22
U1 0
U2 3
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 18
PY 2010
VL 116
IS 20
BP 4148
EP 4157
DI 10.1182/blood-2010-05-283549
PG 10
WC Hematology
SC Hematology
GA 681YC
UT WOS:000284359400022
PM 20660793
ER

PT J
AU de Latour, RP
   Visconte, V
   Takaku, T
   Wu, C
   Erie, AJ
   Sarcon, AK
   Desierto, MJ
   Scheinberg, P
   Keyvanfar, K
   Nunez, O
   Chen, JC
   Young, NS
AF de Latour, Regis Peffault
   Visconte, Valeria
   Takaku, Tomoiku
   Wu, Colin
   Erie, Andrew J.
   Sarcon, Annahita K.
   Desierto, Marie J.
   Scheinberg, Phillip
   Keyvanfar, Keyvan
   Nunez, Olga
   Chen, Jichun
   Young, Neal S.
TI Th17 immune responses contribute to the pathophysiology of aplastic
   anemia
SO BLOOD
LA English
DT Article
ID BONE-MARROW FAILURE; REGULATORY T-CELLS; GROWTH-FACTOR-BETA;
   CLINICAL-RELEVANCE; FAMILY-MEMBERS; MOUSE MODEL; IL-17; DISEASE;
   INTERLEUKIN-17; INFLAMMATION
AB T helper type 17 (Th17) cells have been characterized based on production of interleukin-17 (IL-17) and association with autoimmune diseases. We studied the role of Th17 cells in aplastic anemia (AA) by isolating Th17 cells from patients blood (n = 41) and bone marrow (BM) mononuclear cells (n = 7). The frequency and total number of CD3(+)CD4(+)IL-17-producing T cells were increased in AA patients at presentation compared with healthy controls (P = .0007 and .02, respectively) and correlated with disease activity. There was an inverse relationship between the numbers of Th17 cells and CD4(+)CD25(high)FoxP3(+) regulatory T cells (Tregs) in the blood of AA patients. Concomitant with the classical Th1 response, we detected the presence of CD4(+) and CD8(+) IL-17-producing T cells in a mouse model of lymph node infusion-induced BM failure. Although anti-IL-17 treatment did not abrogate BM failure, early treatment with the anti-IL-17 antibody reduced the severity of BM failure with significantly higher platelet (P < .01) and total BM cell (P < .05) counts at day 10. Recipients that received anti-IL-17 treatment had significantly fewer Th1 cells (P < .01) and more Treg cells (P < .05) at day 10 after lymph node infusion. Th17 immune responses contribute to AA pathophysiology, especially at the early stage during disease progression. (Blood.2010;116(20):4175-4184)
C1 [de Latour, Regis Peffault] NHLBI, Hematol Branch, NIH, Clin Res Ctr, Bethesda, MD 20892 USA.
   [de Latour, Regis Peffault] Greffe Hop St Louis, Serv Hematol, Paris, France.
   [Wu, Colin] NHLBI, Off Biostat Res, NIH, Bethesda, MD 20892 USA.
RP de Latour, RP (reprint author), NHLBI, Hematol Branch, NIH, Clin Res Ctr, Bldg 10,Rm 3E-5232,10 Ctr Dr, Bethesda, MD 20892 USA.
EM regis.peffaultdelatour@sls.aphp.fr
RI Scheinberg, Phillip/H-5251-2012; 
OI Scheinberg, Phillip/0000-0002-9047-4538
FU National Institutes of Health; AA; Myelodysplastic Syndrome
   International Foundation; France HPN
FX This work was supported by the Intramural Research Program of the
   National Institutes of Health. R.P.d.L. received a bursary award from
   the AA and Myelodysplastic Syndrome International Foundation and a grant
   from France HPN.
NR 50
TC 47
Z9 51
U1 0
U2 4
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 18
PY 2010
VL 116
IS 20
BP 4175
EP 4184
DI 10.1182/blood-2010-01-266098
PG 10
WC Hematology
SC Hematology
GA 681YC
UT WOS:000284359400025
PM 20733158
ER

PT J
AU Liu, X
   Ryland, L
   Yang, J
   Liao, AJ
   Aliaga, C
   Watts, R
   Tan, SF
   Kaiser, J
   Shanmugavelandy, SS
   Rogers, A
   Loughran, K
   Petersen, B
   Yuen, J
   Meng, FX
   Baab, KT
   Jarbadan, NR
   Broeg, K
   Zhang, RR
   Liao, JS
   Sayers, TJ
   Kester, M
   Loughran, TP
AF Liu, Xin
   Ryland, Lindsay
   Yang, Jun
   Liao, Aijun
   Aliaga, Cesar
   Watts, Rebecca
   Tan, Su-Fern
   Kaiser, James
   Shanmugavelandy, Sriram S.
   Rogers, Andrew
   Loughran, Kathleen
   Petersen, Bailey
   Yuen, Jonathan
   Meng, Fanxue
   Baab, Kendall Thomas
   Jarbadan, Nancy Ruth
   Broeg, Kathleen
   Zhang, Ranran
   Liao, Jason
   Sayers, Thomas Joseph
   Kester, Mark
   Loughran, Thomas P., Jr.
TI Targeting of survivin by nanoliposomal ceramide induces complete
   remission in a rat model of NK-LGL leukemia
SO BLOOD
LA English
DT Article
ID GRANULAR LYMPHOCYTE LEUKEMIA; INDUCED APOPTOSIS; IN-VIVO; PROTEIN
   EXPRESSION; CELL-DIVISION; CANCER CELLS; TUMOR-GROWTH; FAS LIGAND;
   DELIVERY; DEATH
AB The natural killer (NK) type of aggressive large granular lymphocytic (LGL) leukemia is a fatal illness that pursues a rapid clinical course. There are no effective therapies for this illness, and pathogenetic mechanisms remain undefined. Here we report that the survivin was highly expressed in both aggressive and chronic leukemic NK cells but not in normal NK cells. In vitro treatment of human and rat NK-LGL leukemia cells with cell-permeable, short-chain C-6-ceramide (C-6) in nanoliposomal formulation led to caspase-dependent apoptosis and diminished survivin protein expression, in a time-and dose-dependent manner. Importantly, systemic intravenous delivery of nanoliposomal ceramide induced complete remission in the syngeneic Fischer F344 rat model of aggressive NK-LGL leukemia. Therapeutic efficacy was associated with decreased expression of survivin in vivo. These data suggest that in vivo targeting of survivin through delivery of nanoliposomal C-6-ceramide may be a promising therapeutic approach for a fatal leukemia. (Blood. 2010;116(20):4192-4201)
C1 [Liu, Xin; Ryland, Lindsay; Yang, Jun; Liao, Aijun; Aliaga, Cesar; Watts, Rebecca; Tan, Su-Fern; Rogers, Andrew; Loughran, Kathleen; Petersen, Bailey; Yuen, Jonathan; Meng, Fanxue; Baab, Kendall Thomas; Jarbadan, Nancy Ruth; Broeg, Kathleen; Zhang, Ranran; Liao, Jason; Kester, Mark; Loughran, Thomas P., Jr.] Penn State Univ, Coll Med, Penn State Hershey Canc Inst, Hershey, PA 17033 USA.
   [Ryland, Lindsay; Kaiser, James; Shanmugavelandy, Sriram S.; Kester, Mark] Penn State Univ, Coll Med, Dept Pharmacol, Hershey, PA 17033 USA.
   [Liao, Aijun] China Med Univ, Shengjing Hosp, Dept Hematol, Shenyang, Peoples R China.
   [Sayers, Thomas Joseph] NCI, SAIC Frederick, Expt Immunol Lab, Frederick, MD 21701 USA.
RP Liu, X (reprint author), Penn State Univ, Coll Med, Penn State Hershey Canc Inst, CH74,Rm 4401,500 Univ Dr,POB 850, Hershey, PA 17033 USA.
EM Xliu2@hmc.psu.edu
RI Sayers, Thomas/G-4859-2015
FU National Institutes of Health [CA133525, CA098472]; Pennsylvania Tobacco
   Settlement Fund; National Cancer Institute, National Institutes of
   Health [NO1-CO-12400, HSN261200800001E]; Center for Cancer Research,
   National Cancer Institute, National Institutes of Health
FX This study was supported by National Institutes of Health grant nos.
   CA133525 and CA098472 (to T. P. L.) and Pennsylvania Tobacco Settlement
   Fund (to M. K.). This project has been also funded in part with federal
   funds from the National Cancer Institute, National Institutes of Health,
   under contracts NO1-CO-12400 and HSN261200800001E (to T.J.S.).; The
   content of this publication does not necessarily reflect the views or
   policies of the Department of Health and Human Services, nor does
   mention of trade names, commercial products, or organizations imply
   endorsement by the US Government. This research was supported in part by
   the Intramural Research Program of the Center for Cancer Research,
   National Cancer Institute, National Institutes of Health.
NR 50
TC 49
Z9 51
U1 1
U2 7
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 18
PY 2010
VL 116
IS 20
BP 4192
EP 4201
DI 10.1182/blood-2010-02-271080
PG 10
WC Hematology
SC Hematology
GA 681YC
UT WOS:000284359400027
PM 20671121
ER

PT J
AU Turner, JJ
   Morton, LM
   Linet, MS
   Clarke, CA
   Kadin, ME
   Vajdic, CM
   Monnereau, A
   Maynadie, M
   Chiu, BCH
   Marcos-Gragera, R
   Costantini, AS
   Cerhan, JR
   Weisenburger, DD
AF Turner, Jennifer J.
   Morton, Lindsay M.
   Linet, Martha S.
   Clarke, Christina A.
   Kadin, Marshall E.
   Vajdic, Claire M.
   Monnereau, Alain
   Maynadie, Marc
   Chiu, Brian C-H.
   Marcos-Gragera, Rafael
   Costantini, Adele Seniori
   Cerhan, James R.
   Weisenburger, Dennis D.
TI InterLymph hierarchical classification of lymphoid neoplasms for
   epidemiologic research based on the WHO classification (2008): update
   and future directions
SO BLOOD
LA English
DT Article
ID NON-HODGKIN-LYMPHOMA; B-CELL LYMPHOMA; GENE-EXPRESSION; POOLED ANALYSIS;
   UNDETERMINED SIGNIFICANCE; MONOCLONAL GAMMOPATHY; CONSORTIUM INTERLYMPH;
   FOLLICULAR LYMPHOMAS; PROGNOSTIC INDEX; UNITED-STATES
AB After publication of the updated World Health Organization (WHO) classification of tumors of hematopoietic and lymphoid tissues in 2008, the Pathology Working Group of the International Lymphoma Epidemiology Consortium (InterLymph) now presents an update of the hierarchical classification of lymphoid neoplasms for epidemiologic research based on the 2001 WHO classification, which we published in 2007. The updated hierarchical classification incorporates all of the major and provisional entities in the 2008 WHO classification, including newly defined entities based on age, site, certain infections, and molecular characteristics, as well as borderline categories, early and "in situ" lesions, disorders with limited capacity for clinical progression, lesions without current International Classification of Diseases for Oncology, 3rd Edition codes, and immunodeficiency-associated lymphoproliferative disorders. WHO subtypes are defined in hierarchical groupings, with newly defined groups for small B-cell lymphomas with plasmacytic differentiation and for primary cutaneous T-cell lymphomas. We suggest approaches forapplying the hierarchical classification in various epidemiologic settings, including strategies for dealing with multiple coexisting lymphoma subtypes in one patient, and cases with incomplete pathologic information. The pathology materials useful for state-of-the-art epidemiology studies are also discussed. We encourage epidemiologists to adopt the updated InterLymph hierarchical classification, which incorporates the most recent WHO entities while demonstrating their relationship to older classifications. (Blood.2010;116(20):e90-e98)
C1 [Turner, Jennifer J.] Douglass Hanly Moir Pathol, Dept Histopathol, N Ryde, NSW 2113, Australia.
   [Turner, Jennifer J.] Macquarie Univ, Australian Sch Adv Med, Sydney, NSW 2109, Australia.
   [Morton, Lindsay M.; Linet, Martha S.] NCI, Div Canc Epidemiol & Genet, NIH, Dept Hlth & Human Serv, Rockville, MD USA.
   [Clarke, Christina A.] Canc Prevent Inst Calif, Fremont, CA USA.
   [Kadin, Marshall E.] Boston Univ, Sch Med, Dept Dermatol & Skin Surg, Roger Williams Med Ctr, Providence, RI USA.
   [Vajdic, Claire M.] Univ New S Wales, Prince Wales Clin Sch, Sydney, NSW 2052, Australia.
   [Vajdic, Claire M.] Univ New S Wales, Lowy Canc Res Ctr, Sydney, NSW 2052, Australia.
   [Monnereau, Alain] Bergonie Inst, Hematol Malignancies Registry Gironde, Bordeaux, France.
   [Monnereau, Alain] Univ Paris Sud, Inserm, UMRS Environm Epidemiol Canc 1018, Paris, France.
   [Maynadie, Marc] Univ Burgundy, Hematol Malignancies Registry Cote Or, Dijon, France.
   [Chiu, Brian C-H.] Univ Chicago, Dept Hlth Studies, Chicago, IL 60637 USA.
   [Marcos-Gragera, Rafael] Inst Biomed Invest, Epidemiol Unit, Canc Registry Girona, Dept Hlth, Girona, Spain.
   [Costantini, Adele Seniori] Canc Res & Prevent Inst Epidemiol, Florence, Italy.
   [Cerhan, James R.] Mayo Clin, Div Epidemiol, Coll Med, Rochester, MN USA.
   [Weisenburger, Dennis D.] Univ Nebraska Med Ctr, Dept Pathol & Microbiol, Omaha, NE USA.
RP Turner, JJ (reprint author), Douglass Hanly Moir Pathol, Dept Histopathol, 14 Giffnock Ave,Macquarie Pk, N Ryde, NSW 2113, Australia.
EM jtur8838@bigpond.net.au
RI Monnereau, Alain/L-1249-2014; Morton, Lindsay/B-5234-2015; 
OI Monnereau, Alain/0000-0002-5056-1397; Morton,
   Lindsay/0000-0001-9767-2310; Vajdic, Claire/0000-0002-3612-8298; Cerhan,
   James/0000-0002-7482-178X; Marcos-Gragera, Rafael/0000-0001-9824-3657
FU National Cancer Institute, National Institutes of Health, Department of
   Health and Human Services, Bethesda, MD; National Institutes of Health
   [P20RR018757]; National Cancer Institute [R01 CA92153, R01 CA97274]
FX This work was supported, in part, by the Intramural Research Program of
   the National Cancer Institute, National Institutes of Health, Department
   of Health and Human Services, Bethesda, MD, National Cancer Institute
   grants R01 CA92153 and R01 CA97274 (to J.R.C.), and National Institutes
   of Health grant P20RR018757 (M.E.K.).
NR 43
TC 96
Z9 109
U1 0
U2 9
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 18
PY 2010
VL 116
IS 20
BP E90
EP E98
DI 10.1182/blood-2010-06-289561
PG 9
WC Hematology
SC Hematology
GA 681YC
UT WOS:000284359400002
PM 20699439
ER

PT J
AU Lui, SH
   Miller-Randolph, S
   Crown, D
   Moayeri, M
   Sastalla, I
   Okugawa, S
   Leppla, SH
AF Lui, Shihui
   Miller-Randolph, Sharmina
   Crown, Devorah
   Moayeri, Mahtab
   Sastalla, Inka
   Okugawa, Shu
   Leppla, Stephen H.
TI Anthrax Toxin Targeting of Myeloid Cells through the CMG2 Receptor Is
   Essential for Establishment of Bacillus anthracis Infections in Mice
SO CELL HOST & MICROBE
LA English
DT Article
ID CAPILLARY MORPHOGENESIS PROTEIN-2; LETHAL TOXIN; MACROPHAGE SENSITIVITY;
   KINASE-KINASE; SUSCEPTIBILITY; INACTIVATION; SUFFICIENT; ANTIBODY
AB Bacillus anthracis kills through a combination of bacterial infection and toxemia. Anthrax toxin working via the CMG2 receptor mediates lethality late in infection, but its roles early in infection remain unclear. We generated myeloid-lineage specific CMG2-deficient mice to examine the roles of macrophages, neutrophils, and other myeloid cells in anthrax pathogenesis. Macrophages and neutrophils isolated from these mice were resistant to anthrax toxin. However, the myeloid-specific CMG2-deficient mice remained fully sensitive to both anthrax lethal and edema toxins, demonstrating that targeting of myeloid cells is not responsible for anthrax toxin-induced lethality. Surprisingly, the myeloid-specific CMG2-deficient mice were completely resistant to B. anthracis infection. Neutrophil depletion experiments suggest that B. anthracis relies on anthrax toxin secretion to evade the scavenging functions of neutrophils to successfully establish infection. This work demonstrates that anthrax toxin uptake through CMG2 and the resulting impairment of myeloid cells are essential to anthrax infection.
C1 [Lui, Shihui; Miller-Randolph, Sharmina; Crown, Devorah; Moayeri, Mahtab; Sastalla, Inka; Okugawa, Shu; Leppla, Stephen H.] NIAID, Bacterial Toxins & Therapeut Sect, Lab Bacterial Dis, NIH, Bethesda, MD 20892 USA.
RP Lui, SH (reprint author), NIAID, Bacterial Toxins & Therapeut Sect, Lab Bacterial Dis, NIH, 9000 Rockville Pike, Bethesda, MD 20892 USA.
EM shliu@niaid.nih.gov; sleppla@niaid.nih.gov
FU National Institute of Allergy and Infectious Diseases, National
   Institutes of Health
FX This research was supported by the intramural research program of the
   National Institute of Allergy and Infectious Diseases, National
   Institutes of Health. We thank Rasem Fattah for assistance in protein
   purification. We also thank Zonglin Hu and Stephen Chow for construction
   of A35 mutant strains. None of the authors of this manuscript haves
   financial interest related to this work.
NR 34
TC 1
Z9 1
U1 1
U2 3
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 1931-3128
J9 CELL HOST MICROBE
JI Cell Host Microbe
PD NOV 18
PY 2010
VL 8
IS 5
BP 455
EP 462
DI 10.1016/j.chom.2010.10.004
PG 8
WC Microbiology; Parasitology; Virology
SC Microbiology; Parasitology; Virology
GA 694DE
UT WOS:000285274400009
ER

EF